40a edizione Scivac Rimini

40째

congressonazionalescivac M O N T E C AT I N I PA L A Z Z O D E I C O N G R E S S I 30 MARZO - 2 APRILE 2000

1

FEDERATION OF EUROPEAN COMPANION ANIMAL VETERINARY ASSOCIATIONS

THE

dal Presidente SCIVAC Caro collega, il calendario SCIVAC per il 2000 è particolarmente fitto di attività, per questo motivo la Commissione Scientifica si è dovuta impegnare a fondo per far risaltare nella maniera adeguata quello che per la nostra associazione è l’appuntamento più importante dell’anno. È stato quindi confezionato un programma molto invitante articolato su quattro giornate, dal Giovedì alla Domenica, e strutturato secondo la formula multisala in grado di soddisfare svariate esigenze di aggiornamento.

Saranno proposti in simultanea su quattro sale argomenti di cardiologia, chirurgia generale, citologia, dermatologia, diagnostica per immagini, medicina degli animali esotici, problemi comportamentali, oncologia, ortopedia, practice management, comunicazioni libere, comunicazioni dalle industrie.

I suddetti argomenti saranno trattati da uno staff di ventisei relatori di grande qualità che interverranno, oltre che dall’Italia, da Olanda e Stati Uniti. In particolare, alcuni di questi come Barclay Slocum per l’ortopedia, Bob Hamlin per la cardiologia, Nicholas Dodman per le malattie comportamentali, Theresa Lightfoot e Elliot Jacobson per gli animali esotici e Kerstin Hansson per la diagnostica per immagini rappresentano una attesa novità per l’Italia. Altri, come Denny DeNicola per la citologia e Ton Willemse per la dermatologia rappresentano un piacevole ritorno. Tutti comunque contribuiranno sicuramente a rendere ancora più interessante e ricco di contenuti il nostro 40° Congresso.

Come in tutti i nostri meeting ci sarà occasione per incontrare colleghi e scambiare con loro idee ed informazioni, per di più, in questo congresso rispettando una nostra tradizione, si terrà alla fine dei lavori congressuali della giornata di Sabato l’Assemblea Annuale SCIVAC a cui ti invito caldamente ad intervenire.

Al di là della mia breve introduzione, leggendo nel dettaglio il programma che segue troverai molti motivi per ritenere che questa è una occasione da non perdere, per cui in attesa di incontrarti a Montecatini ti porgo i miei più cordiali saluti.

Dr. Pier Mario Piga Presidente SCIVAC

scivac Presidente PIERMARIO PIGA

-

SOCIETÀ CULTURALE ITALIANA VETERINARI

Presidente Senior CARLO SCOTTI

Vice Presidente ERMENEGILDO BARONI

Segretario UGO LOTTI

PER

Tesoriere MATTEO SPALLAROSSA

ANIMALI

DA

Consigliere MASSIMO BARONI

COMPAGNIA Consigliere MICHELA ROMANELLI

Uffici: Palazzo Trecchi - 26100 Cremona - Tel. O (0372) 460440 - Telefax (0372) 457091 - E MAIL: info@scivac.it - Partita I.V.A. 00861330199

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40째

COMMISSIONI

congresso nazionale scivac

DIRETTIVO SCIVAC Consiglio Direttivo SCIVAC 1998-2001

PIERMARIO PIGA CARLO SCOTTI GILDO BARONI UGO LOTTI MATTEO SPALLAROSSA MASSIMO BARONI MICHELA ROMANELLI

Presidente Presidente Senior Vice Presidente Segretario Tesoriere Consigliere Consigliere

COMITATO CONGRESSUALE Presidente

GIORGIO ROMANELLI CLAUDIO BUSSADORI MARCO CALDIN ALESSANDRA FONDATI CLAUDIO PERUCCIO STEFANO PIZZIRANI CARLO SCOTTI ALDO VEZZONI

Med Vet, Dipl ECVS Med Vet, Dipl ECVIM-CA Med Vet Med Vet, Dipl ECVD Med Vet, Dipl ECVO Med Vet, Dipl ECVS Med Vet Med Vet, Dipl ECVS

Coordinatore Congressuale

FULVIO STANGA

Med Vet

Segreteria Congressuale

LUDOVICA BELLINGERI SCIVAC Via Trecchi 20, 26100 Cremona Tel 0372 460440 Fax 0372 457091 e mail: fstanga@scivac.it Web site: www.scivac.it

ORGANIZZAZIONE CONGRESSUALE New Team Via Ghiretti 2, 43100 Parma Tel 0521 293913 - Fax 0521 294036 - e mail: newteam.parma@iol.it ORGANIZZAZIONE ALBERGHIERA Pinocchio Viaggi e Turismo srl Viale Amendola 2, 51016 - Montecatini Terme (PT) Tel 0572 75209 - 75861 - Fax 0572 910400 26

40°

congresso nazionale scivac

RELATORI Click on the picture for the abstract

MASSIMO BARONI

MARIO CANIATTI

MedVet, Dipl ECVN Libero Professionista Genova

MedVet, Dipl ECVP Università di Milano

MICHELE BORGARELLI

DAVIDE DE LORENZI

MedVet, Dipl ECVIM-CA (Card) Libero Professionista Torino

MedVet Libero Professionista Forlì

PAOLO BURACCO

DENNIS DE NICOLA

MedVet, Dipl ECVS Università di Torino

DVM, PhD, Dipl ACVP Purdue University Indiana, USA

CLAUDIO BUSSADORI

NICHOLAS H. DODMAN

MedVet, Dipl ECVIM-CA (Card) Libero Professionista Milano

BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB Tufts University, Massachussets, USA

MARCO CALDIN

FABRIZIO FABBRINI

MedVet Libero Professionista Padova

MedVet, Dipl CES Derm Libero Professionista Milano

5

40°

congresso nazionale scivac

RELATORI AL Click on the picture for the abstract

STEVE GARNER

ELLIOT JACOBSON

DVM, Dipl AVBS League City, Texas, USA

DVM, PhD College of Veterinary Medicine University of Florida, Gainesville, USA

GIOVANNI GHIBAUDO

THERESA LIGHTFOOT

MedVet Libero Professionista Milano

DVM, Dipl ABVP (Avian Practice) Largo, Florida, USA

OSCAR GRAZIOLI

MASSIMO MILLEFANTI

MedVet Libero Professionista Reggio Emilia

MedVet Libero Professionista Milano

MASSIMO GUALTIERI

CARLO MARIA MORTELLARO

MedVet Università di Milano

MedVet Università di Milano

ROBERT HAMLIN

CHIARA NOLI

DVM The Ohio State University Columbus, Ohio, USA

MedVet, Dipl ECVD Libero Professionista Milano

KERSTIN HANSSON MedVet School of Veterinary Medicine University of Uppsala, SVEZIA 6

CONGRESSO Click on the picture for the abstract CRISTINA OSELLA

CANDACE A. SOUSA

MedVet Libero Professionista Torino

DVM, Dipl ABVP, Dipl ACVD El Macero, California, USA

YANNICK POUBANNE

MATTEO TOMMASINI

MedVet, MS Versailles, FRANCIA

MedVet, Dipl ECVS Libero Professionista Roma

PAOLA ROCCABIANCA

ALDO VEZZONI

MedVet Università di Padova

MedVet, Dipl ECVS Libero Professionista Cremona

GIORGIO ROMANELLI

FABIO VIGANÒ

MedVet, Dipl ECVS Libero Professionista Milano

MedVet Libero Professionista San Giorgio Legnano (MI)

ROBERTO SANTILLI

MASSIMO VIGNOLI

MedVet, Dipl ECVIM-CA (Card) Libero Professionista Milano

MedVet Libero Professionista Bologna

BARCLAY SLOCUM

TON WILLEMSE

DVM Slocum Clinic Eugene, Oregon, USA

DVM, PhD, Dipl ECVD University of Utrecht Olanda

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40°

PROGRAMMA

congresso nazionale scivac

Giovedì Mattina 30 Marzo 2000 SALA D’INGRESSO REGISTRAZIONE

8.00 TEATRO VERDI 1300 DERMATOLOGIA SIDEV

Gruppo di Studio Chairperson: Gino D’Agnolo

Chairperson: Alessandra Fondati

9.30 Dermatite atopica nel cane

Ton Willemse (NL)

10.30

Chairperson: Maurizio Pasinato

Esame fisico dell’apparato cardiovascolare Diagnosi differenziale delle principali malattie cardiopolmonari attraverso osservazione, palpazione, percussione e auscultazione

Aggressività del cane

Bob Hamlin (USA)

Nicholas Dodman (USA)

CARDIOLOGIA Gruppo di Studio Chairperson: Gino D’Agnolo

Chairperson: Alessandra Fondati

11.30 Malattie simil-atopiche nel gatto (40’)

Ton Willemse (NL)

Animal Health

Diagnosi differenziale e trattamento delle dermatosi parassitarie nel cane e nel gatto (40’)

Candace A. Sousa (USA)

I principi di fisiologia clinica necessari per la diagnosi e il trattamento delle malattie cardiopolmonari Una discussione sui metodi di misurazione e sulle basi fisiopatologiche delle alterazioni di frequenza cardiaca, forza contrattile, flusso ematico attraverso il letto arterioso, elasticità miocardica e consumo di ossigeno

Novità diagnostiche in dermatologia veterinaria (40’)

Fabrizio Fabbrini (I)

13.30

SALA VENERE 170 MEDICINA COMPORTAMENTALE SISCA L’aggressività legata a dominanza e le conclusioni di nuove indagini che indicano i risultati a lungo termine della

modificazione del comportamento, gli effetti del contenuto proteico della dieta e la risposta ai farmaci

SALA MARTE 40 ANIMALI ESOTICI Sessione Specialistica Chairperson: Massimo Millefanti What's new in reptile virology (60’) Elliott Jacobson (USA) e Francesco Origgi (I)

Mycoplasma infection of tortoises (30’) Elliott Jacobson (USA)

PAUSA CAFFÈ ED ESPOSIZIONE COMMERCIALE DERMATOLOGIA SIDEV

12.30

AUDITORIUM 700 CARDIOLOGIA

Bob Hamlin (USA)

MEDICINA COMPORTAMENTALE SISCA

PAUSA CAFFÈ

Chairperson: Maurizio Pasinato Comportamento del cane legato alla paura L’ansia da separazione, la sua eziologia, diagnosi e trattamento con antidepressivi (40’) Nicholas Dodman (USA) Epidemiologia dell’ansia da separazione in Italia Risultati di un’indagine

Mycotic infections of reptiles: Diagnosis and treatment (30’) Elliott Jacobson (USA) Diagnostic techniques in reptile medicine (90’)

nazionale (40’) Cristina Osella (I) Disturbi ossessivocompulsivi del cane Una panoramica completa sui disturbi ossessivo-compulsivi, a livello di diagnosi e terapia (40’) Nicholas Dodman (USA)

Elliott Jacobson (USA) e Francesco Origgi (I)

PA U S A P R A N Z O E D E S P O S I Z I O N E C O M M E R C I A L E

Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

SCIENTIFICO Giovedì Pomeriggio 30 Marzo 2000 TEATRO VERDI 1300 DERMATOLOGIA SIDEV

AUDITORIUM 700 CARDIOLOGIA Gruppo di Studio Chairperson: Gino D’Agnolo

Chairperson: Alessandra Fondati

14.30 Alopecia e dermatite psicogene nel cane e nel gatto

Elettrocardiografia con 2 derivazioni Approccio semplificato all’interpretazione di un tracciato ECG a due derivazioni per il riconoscimento delle alterazioni cardiopolmonari nel cane e nel gatto

Ton Willemse (NL)

Chairperson: Maurizio Pasinato Aggressività del gatto: il “gatto alfa” Una nuova sindrome aggressiva e le cause organiche di aggressività nel gatto

SALA MARTE 40 ANIMALI ESOTICI Sessione Specialistica Chairperson: Marta Avanzi Approach to the clinically ill psittacine (90’)

Nicholas Dodman (USA)

Bob Hamlin (USA)

Hill’s*

15.30 Novità terapeutiche in dermatologia veterinaria

Approccio diagnostico e criteri terapeutici delle più comuni malattie cardiovascolari nel cane Come operare la migliore scelta terapeutica sulla base di criteri diagnostici obiettivi

Giovanni Ghibaudo (I)

16.30

SALA VENERE 170 MEDICINA COMPORTAMENTALE SISCA

Bob Hamlin (USA)

Ansia e marcatura con urina del gatto Terapia ansiolitica, modificazioni ambientali e utilizzazione dei feromoni per la lettiera, una nuova arma nella lotta all’eliminazione inappropriata Nicholas Dodman (USA)

Teresa Lightfoot (USA)

Chelonian shell repair (30’) Teresa Lightfoot (USA)

PA U S A C A F F È E D E S P O S I Z I O N E C O M M E R C I A L E DERMATOLOGIA SIDEV

CARDIOLOGIA Gruppo di Studio Chairperson: Gino D’Agnolo

Chairperson: Alessandra Fondati

17.30 Malattie cutanee autoimmuni negli animali da compagnia

Ton Willemse (NL)

Bob Hamlin (USA)

18.30 Malattie di recente descrizione in dermatologia veterinaria

Chiara Noli (I)

Diagnosi e principi di scelta terapeutica delle tre “IPER” del gatto: cardiomiopatia IPERtrofica, IPERtiroidismo, IPERtensione

Management delle emergenze cardiopolmonari Approccio diagnostico e terapeutico a tachicardia ventricolare, insufficienza cardiaca acuta, bronchite ostruttiva acuta con fibrosi polmonare e bradiaritmia Bob Hamlin (USA)

MEDICINA COMPORTAMENTALE SISCA Chairperson: Maurizio Pasinato

ANIMALI ESOTICI Sessione Specialistica Chairperson: Marta Avanzi

Disturbi ossessivo-compulsivi del gatto Alopecia psicogena, suzione della lana e iperestesia felina/tail-chasing (rincorrersi la coda) Nicholas Dodman (USA)

Medical problems of bearded dragons, chameleons and iguanid lizards (60’)

Psicofarmacologia Concetti di base nel trattamento dell’aggressività, della paura e delle forme compulsive

Emergency presentations in birds (60’)

Nicholas Dodman (USA)

Teresa Lightfoot (USA)

Elliot Jacobson (USA)

INTERRUZIONE

19.30 Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

40°

congresso nazionale scivac

PROGRAMMA Venerdì Mattina 31 Marzo 2000 SALA D’INGRESSO REGISTRAZIONE

8.30 TEATRO VERDI 1300

AUDITORIUM 700

CITOLOGIA

ORTOPEDIA

Gruppo di Studio Chairperson: Mario Caniatti

Gruppo di Studio Chairperson: Gildo Baroni

9.30 Principi interpretativi di citologia oncologica

Allineamento dell’arto posteriore deviato

Davide De Lorenzi (I)

Barclay Slocum (USA) e Theresa Devine (USA)

SALA VENERE 170 ANIMALI ESOTICI SIVAE

Workshop Specialistico 10.00-13.30 Chairperson: Chiara Noli e Ton Willemse

Chairperson: Leonardo Brunetti Patologie gastroenteriche del furetto (Mustela putorius furo)

11.30

ORTOPEDIA

Gruppo di Studio Chairperson: Mario Caniatti

Gruppo di Studio Chairperson: Gildo Baroni

I principi di citologia esfoliativa per l’analisi dei versamenti neoplastici

Sarcomi indotti da trauma

Prima parte: terapia dell’atopia Introduzione e problemi potenziali (20’) T. Willemse Risultati di uno studio pilota sull’uso del palmidrol

ANIMALI ESOTICI SIVAE

nel gatto (20’) F. Scarampella Risultati dell’iposensibilizzazione in 100 cani con dermatite atopica (20’) R. Tognetti Risultati preliminari di uno studio controllato a doppio cieco sull’efficacia ed il dosaggio più efficace dell’olio di semi di ribes nero in cani con dermatitie atopica (30’) C. Noli

Chairperson: Leonardo Brunetti

PA U S A C A F F È

Teresa Lightfoot (USA)

10.30 PAUSA CAFFÈ ED ESPOSIZIONE COMMERCIALE CITOLOGIA

SALA MARTE 40 DERMATOLOGIA

Neoplasie del furetto e relativi protocolli terapeutici

Seconda parte: terapia delle malattie batteriche Introduzione e problemi potenziali (20’) C. Noli Risultati preliminari di uno studio sull’uso dell’autovaccino nella piodermite ricorrente del cane F. Fabbrini

Giorgio Romanelli (I) Teresa Lightfoot (USA)

Hill’s*

12.30

Possibilità terapeutiche in caso di UAP (mancata unione del processo anconeo)

Dennis De Nicola (USA)

13.30

Aldo Vezzoni (I)

Tutto quello che sappiamo di medicina canina e felina ma non dobbiamo applicare per curare conigli & co.

Massimo Millefanti (I)

Risultati di uno studio controllato multicentrico sull’effetto del cefadroxil a dosaggio onogiornaliero nelle piodermiti superficiali e profonde del cane A. Oseliero Efficacia della terapia topica con clorexidina nelle piodermiti di superficie e superficiali S. Colombo Utilizzo della clorexidina gel nelle dermatiti delle pieghe cutanee L. Cornegliani Discussione

PA U S A P R A N Z O E D E S P O S I Z I O N E C O M M E R C I A L E

Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

SCIENTIFICO Venerdì Pomeriggio 31 Marzo 2000 TEATRO VERDI 1300

AUDITORIUM 700

CITOLOGIA

ORTOPEDIA

Gruppo di Studio Chairperson: Carlo Masserdotti

Gruppo di Studio Chairperson: Gildo Baroni

14.30 Citologia delle

Lussazione della rotula

neoformazioni cutanee

Barclay Slocum (USA) e Theresa Devine (USA)

Mario Caniatti (I)

SALA MARTE 40 COMUNICAZIONI LIBERE

Chairperson: Leonardo Brunetti Tecniche cliniche in alcuni piccoli mammiferi esotici: cincillà, cani della prateria e ricci africani

Teresa Lightfoot (USA)

Hill’s*

15.30

16.30

SALA VENERE 170 ANIMALI ESOTICI SIVAE

Citologia e tumori nasali

TPO: follow up, risultati e complicazioni

Lesioni neoplastiche in piccoli roditori, lagomorfi e furetti: aspetti clinici e quadri microscopici a confronto

Mario Caniatti (I) e Carlo M. Mortellaro (I)

Aldo Vezzoni (I)

Paola Roccabianca (I)

PA U S A C A F F È E D E S P O S I Z I O N E C O M M E R C I A L E CITOLOGIA

ORTOPEDIA

Gruppo di Studio Chairperson: Carlo Masserdotti

Gruppo di Studio Chairperson: Gildo Baroni

17.30 Citologia oncologica delle masse toraco-addominali

Osteotomia livellante del piatto tibiale (TPLO) per il trattamento delle lesioni del legamento crociato craniale

ANIMALI ESOTICI SIVAE

COMUNICAZIONI LIBERE

Chairperson: Leonardo Brunetti Conigli: problemi medici e pasteurellosi

Teresa Lightfoot (USA)

18.30 Panoramica delle più comuni infezioni batteriche nei rettili e dei relativi trattamenti antimicrobici

Dennis De Nicola (USA)

Barclay Slocum (USA) e Theresa Devine (USA)

Elliot Jacobson (USA)

INTERRUZIONE

19.30 Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

40°

congresso nazionale scivac

PROGRAMMA Sabato Mattina 1 Aprile 2000

TEATRO VERDI 1300 DIAGNOSTICA PER IMMAGINI Gruppo di Studio Chairperson: David Chiavegato

8.30 Diagnostica ultrasonografica: quando, come, perché e per che cosa impiegarla nella clinica degli animali d’affezione

AUDITORIUM 700

SALA VENERE 170

CHIRURGIA

ORTOPEDIA

Gruppo di Studio Chairperson: Giorgio Romanelli

Sessione Specialistica Chairperson: Aldo Vezzoni

Polipi del rinofaringe, dell’orecchio medio e dell’orecchio esterno del gatto: prendi tre e paghi uno

Opzioni chirurgiche per la displasia dell’anca

SALA MARTE 40 COMUNICAZIONI LIBERE

Carlo M. Mortellaro (I)

GRUPPO

9.30

ESAOTE

Hill’s* Otite terminale nel cane e nel gatto (40’) Indicazioni e limiti della TECALBO (Total Ear Canal Ablation and Lateral Bulla Osteotomy)

Carlo M. Mortellaro (I)

Kerstin Hansson (S)

10.30

Barclay Slocum (USA) e Theresa Devine (USA)

PA U S A C A F F È E D E S P O S I Z I O N E C O M M E R C I A L E DIAGNOSTICA PER IMMAGINI Gruppo di Studio Chairperson: David Chiavegato

11.30 Anatomia normale radiografica dei distretti toracici

CHIRURGIA

CARDIOLOGIA

Gruppo di Studio Chairperson: Giorgio Romanelli

Sessione Interattiva Chairperson: Carlo Scotti

Diagnosi e trattamento delle neoplasie gastrointestinali

Confronto tra mezzi diagnostici tradizionali e mezzi diagnostici innovativi in cardiologia veterinaria Dove finisce il fonendoscopio e dove comincia l’ecocardiografo

COMUNICAZIONI LIBERE

Massimo Vignoli (I) Animal Health

12.30

Diagnostica per immagini del trauma toracico L’importanza delle tecniche radiografiche impiegate.

Come riconoscere le situazioni a rischio

Kerstin Hansson (S)

13.30

Massimo Gualtieri (I)

Claudio Bussadori (I) e Bob Hamlin (USA)

PA U S A P R A N Z O E D E S P O S I Z I O N E C O M M E R C I A L E

Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

SCIENTIFICO Sabato Pomeriggio 1 Aprile 2000 TEATRO VERDI 1300 DIAGNOSTICA PER IMMAGINI Gruppo di Studio Chairperson: David Chiavegato

14.30 Ecografia dell’apparato riproduttore maschile e femminile nel cane

AUDITORIUM 700

SALA VENERE 170

SALA MARTE 40

CHIRURGIA

CITOLOGIA

ZOOANTROPOLOGIA

Gruppo di Studio Chairperson: Pier Mario Piga

Sessione Specialistica Chairperson: Davide De Lorenzi

Chairperson: Maurizio Pasinato

Sarcomi vaccino indotti nel gatto Ipotesi patogenetiche, diagnosi e trattamento

Classificazione citologica dei linfomi

Il veterinario e gli animalisti: un rapporto difficile, ma indispensabile (30’) Luisella Battaglia

Hill’s* Paolo Buracco (I) e Giorgio Romanelli (I)

Kerstin Hansson (S)

15.30

Dennis De Nicola (USA)

PA U S A C A F F È E D E S P O S I Z I O N E C O M M E R C I A L E DIAGNOSTICA PER IMMAGINI Gruppo di Studio Chairperson: David Chiavegato

16.30 Vantaggi e limiti dell’ecografia nella diagnosi delle malattie gastroenteriche

CHIRURGIA

CITOLOGIA

PRACTICE MANAGEMENT

Gruppo di Studio Chairperson: Pier Mario Piga

Sessione Interattiva Chairperson: Davide De Lorenzi

Workshop Interattivo Chairperson: Giorgio Romanelli

Sfide in chirurgia oncologica Come demolire e ricostruire la testa nel cane e nel gatto

È un tumore o non è un tumore?!

Internet utile per il medico veterinario Come accedere in modo semplice agli impieghi di internet per il veterinario: le ricerche bibliografiche nella letteratura scientifica mondiale, i siti nella rete più interessanti, la telemedicina, ecc.

Michele Borgarelli (I)

GRUPPO

17.30

Il ruolo del veterinario nella società e la sua funzione educativa (30’) Roberto Marchesini (I)

ESAOTE

Hill’s*

Ruolo dell’ecografia nella diagnosi dell’ipercalcemia

Roberto Santilli (I)

Paolo Buracco (I) e Giorgio Romanelli (I)

Hill’s*

Dennis De Nicola (USA)

Yannick Poubanne (F)

18.30

INTERRUZIONE

18.45

A S S E M B L E A A N N UA L E S C I VAC

Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

40°

PROGRAMMA

congresso nazionale scivac

Domenica Mattina 2 Aprile 2000 TEATRO VERDI 1300

AUDITORIUM 700

DIAGNOSTICA PER IMMAGINI

DILATAZIONE-TORSIONE GASTRICA

Gruppo di Studio Chairperson: David Chiavegato

Gruppo di Lavoro Chairperson: Giorgio Romanelli

8.30 Uso di CT e RM nella diagnostica delle malattie del SNC

Protocollo di stabilizzazione del paziente con GDV (30’) Fabio Viganò (I) GDV / Corpi estranei / Torsione di milza / Volvolo intestinale: diverse facce della stessa medaglia (30’) Luca Formaggini (I)

Massimo Baroni (I)

GRUPPO

9.30

Chairperson: Pier Mario Piga

Fattori prognostici del paziente in corso di GDV (30’) Marco Caldin (I)

Anestesia del paziente in GDV (30’) Oscar Grazioli (I)

Roberto Santilli (I)

Un nuovo modello di ambulatorio veterinario basato sulla messa in opera di elevati standard di prestazioni e cambiamenti di attitudini – al di sopra della norma. Come la capacità di fornire un servizio costituisca spesso il fattore limitante la crescita di una struttura veterinaria.

Steve Garner (USA)

Hill’s* “The Bond” ovvero “il legame” è il carburante per il successo nella comunicazione veterinaria Oggiorno il prerequisito per potere praticare con successo la medicina veterinaria è mostrare di apprezzare il legame affettivo tra gli esseri umani e I loro animali da compagnia.

Steve Garner (USA)

PA U S A C A F F È E D E S P O S I Z I O N E C O M M E R C I A L E DIAGNOSTICA PER IMMAGINI

DILATAZIONE-TORSIONE GASTRICA

Gruppo di Studio Chairperson: David Chiavegato

Gruppo di Lavoro Chairperson: Luca Formaggini

11.30 Impiego della diagnostica per immagini nel paziente con ematuria

Chirurgia della GDV: come e perché (30’) Matteo Tommasini (I) Monitoraggio e trattamento nel post-operatorio (30’) Fabio Viganò (I)

Kerstin Hansson (S)

PRACTICE MANAGEMENT Chairperson: Pier Mario Piga

COMUNICAZIONI LIBERE

La comunicazione – trattare con i clienti ed i collaboratori Sapere come gestire la comunicazione in alcune situazioni- chiave quali: il costo dei servizi, il telefono, ricevere messaggi, gestire clienti sconvolti, comunicazioni interpersonali … è essenziale per una struttura di successo

Steve Garner (USA)

GRUPPO

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SALA MARTE 40 COMUNICAZIONI LIBERE

Progetto per una nuova professione veterinaria

Animal Health

ESAOTE Principi di scintigrafia negli animali da compagnia

10.30

SALA VENERE 170 PRACTICE MANAGEMENT

ESAOTE

Hill’s*

Impiego dell’ecografia nella diagnosi e nel trattamento delle patologie prostatiche

Discussione interattiva

Il servizio-clienti quale obiettivo per il veterinario di successo Lo sviluppo di una cultura di servizi si basa sul porre il cliente al centro delle interazioni della struttura veterinaria. Concentratevi su come il vostro servizio sia fornito al cliente, non su cosa sia fornito.

Michele Borgarelli (I)

Steve Garner (USA)

TERMINE DEL CONGRESSO

13.30 Livello Aggiornamento

Livello Avanzato

Relazione sullo Stato dell’Arte

Sessione Specialistica

Sessione Interattiva

Per le sessioni specialistiche e interattive è richiesta una quota di iscrizione aggiuntiva.

40° Congresso Nazionale SCIVAC

Authors’ list click on the name for the abstract

Abramo F. Adamo P.F. Allione A. Baroni E. Baroni M. Beni A. Bernardini M. Bianciardi P. Bo P. Bollo E. Borgarelli M. Borghi M. Brusa F. Buracco P. Caldin M. Caniatti M. Colombo S. Cornegliani L. Corazza M. De Lorenzi D. DeNicola D. Dodman N. Fabbrini F. Fontaine J. Formaggini L. Garner S. Gabellini G. Gerboni G. Ghibaudo G. Gilardini R. Grazioli O. Gualtieri M. Hamlin R. Hansson K.

Jacobson E. Lightfoot T. Maggio F. Manzini M. Militerno G. Miolo A. Mortellaro C.M. Noli C. Origgi F. Orsi R. Oseliero A. Osella M.C. Osuna G.L. Peirone B Petazzoni M. Poubanne Y. Roccabianca P. Romanelli G. Rovesti G. Santilli R. Scarampella F. Schmidt K. Slocum B. Slocum Devine T. Sousa C. Squarzoni P. Tognetti R. Tommasini Degna M. Vercelli A. Vezzoni A. Vignoli M. Viganò F. Willemse T.

40° Congresso Nazionale SCIVAC

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CURRICULUM VITAE DEI RELATORI click on the picture for the abstract

MASSIMO BARONI Dipl ECVN, Genova Laureato con lode presso la Facoltà di Medicina Veterinaria dell’Università di Pisa nel 1987. Membro SINVET dal 1989 e componente del Consiglio direttivo dal 1992 al 1995. Membro ESVN (European Society of Veterinary Neurology) e ESVOT (European Society of Veterinary Orthopeadic and Traumatology). Dal 1992 al 1994 frequenta il corso specialistico ESAVS (European Society for Advanced Veterinary Studies) in Neurologia. Dal 1993 al 1995 svolge un Non Conforming Residency in Neurologia presso l’Istituto di Neurologia dell’Università di Berna. Nel 1995 compie un periodo di studio in Neurologia dei grossi animali presso l’Università di Edimburgo. Nell’Ottobre dello stesso anno ottiene il Diploma dell’ECVN (European College of Veterinary Neurology). Ha presentato relazioni a vari congressi a carattere nazionale ed internazionale. È inoltre autore di varie pubblicazioni a carattere neurologico ed ortopedico. Attualmente svolge la libera professione a Genova occupandosi esclusivamente di Neurologia ed Ortopedia.

MICHELE BORGARELLI Med Vet, Dipl ECVIM – CA (Cardiology) Si è laureato presso l’Università di Torino nel 1989 con una tesi di fisiologia. Dal 1990 si occupa di cardiologia e di ecografia nei piccoli animali. Da allora ha seguito numerosi periodi di aggiornamento in Italia e all’estero. È stato professore a contratto in ecocardiografia per gli anni 1996-97 e 1998-99 presso la Facoltà di Medicina Veterinaria di Torino. Nel 1999 si è diplomato al College Europeo di Medicina Interna (Cardiologia).

Ha tenuto numerosi seminari scientifici e corsi di perfezionamento su argomenti riguardanti la cardiologia e l’ecografia internistica nei piccoli animali ed ha presentato i risultati dei suoi esperimenti ed esperienze cliniche in congressi nazionali ed internazionali. È segretario e tesoriere della Società Europea di Cardiologia Veterinaria.

È autore di numerose pubblicazioni di cardiologia ed ecografia internistica su riviste nazionali ed internazionali.

Attualmente collabora con la Facoltà di Medicina Veterinaria di Torino in programmi di ricerca sulla miocardiopatia dilatativa nel cane.

PAOLO BURACCO Med Vet, Dipl ECVS È nato a Torino il 16-8-1956. È professore associato di Semeiotica Chirurgica Veterinaria presso la Facoltà di Med. Vet. di Torino. Nel periodo settembre 1987-dicembre 1988 è stato Visiting Assistant Professor presso la School of Vet. Med. (Purdue University, Indiana), con Borsa di Perfezionamento A.I.R.C. È diplomato dal giugno 1998 al Collegio Europeo dei Chirurghi Veterinari, piccoli animali (E.C.V.S.). È membro della Veterinary Cancer Society, della Società Ital. di Chir. Vet., dell’Europ. Soc. of Vet. Oncology e dell’European College of Veterinary Surgeons. È stato relatore in numerosi convegni nazionali ed internazionali ed è autore di circa 100 pubblicazioni su riviste italiane ed estere, comprese le comunicazioni congressuali.

MARCO CALDIN Med Vet Laureato alla Facoltà di Veterinaria di Bologna, con una tesi in “Diagnostica Strumentale nella Cardiologia dei Piccoli Animali”. Ha rivestito il ruolo di coordinatore del Gruppo di Studio SCIVAC di “Diagnostica per immagini” dal 1988 al 1990. Ha partecipato come relatore a vari congressi, corsi e seminari. Professore a contratto alla Facoltà di Veterinaria di Pisa per l’anno accademico 1994-1995 e alla Facoltà di Veterinaria di Padova per l’anno accademico 1996-1998 e Professore Incaricato per l’anno 1998-1999. Attualmente è Coordinatore del Gruppo di studio di Medicina Interna. Svolge la libera professione a Padova presso la Clinica Veterinaria Privata San Marco, della quale è Direttore Sanitario.

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MARIO CANIATTI Med Vet, Dipl ECVP Laureato all’Università di Milano dove lavora dal 1990 nell’Istituto di Anatomia Patologica. È Diplomato all’European College of Veterinary Pathology. La sua attività è concentrata sulla citologia diagnostica e sulla patologia comparata delle neoplasia cutanee e delle malattie linfoproliferative. Ha pubblicato oltre 40 articoli su riviste scientifiche italiane e internazionali.

DAVIDE DE LORENZI Med Vet Laureato in Medicina Veterinaria a Bologna il 28 ottobre 1988, con lode; ha conseguito nel 1992 la specializzazione in Clinica e Patologia degli Animali da Affezione presso la Facoltà di Medicina Veterinaria di Pisa. È stato ideatore ed è l’attuale coordinatore del Gruppo di studio SCIVAC di Citologia Diagnostica ed inoltre è relatore ed istruttore del Corso di Citologia Diagnostica della SCIVAC. Da alcuni anni tiene un seminario di Citologia Diagnostica alla Scuola di Specializzazione in Clinica e Patologia degli animali da Affezione della Facoltà di Medicina Veterinaria di Pisa. È autore e coautore di alcuni articoli e comunicazioni aventi come oggetto la patologia clinica e la citologia diagnostica.

Dal 1993 compie regolari periodi di aggiornamento in Olanda presso la Facoltà di Medicina Veterinaria di Utrecht (Dipartimento Animali da Compagnia); presso la medesima Facoltà ha portato a termine un corso triennale, organizzato dall’ESAVS, avente come soggetto la medicina interna.

Esercita come libero professionista a Forlì occupandosi prevalentemente di Chirurgia e Citologia Diagnostica.

40° Congresso Nazionale SCIVAC

I suoi principali interessi professionali sono la citologia diagnostica, l’ematologia diagnostica, la biochimica clinica. Tiene corsi di patologia clinica a studenti, veterinari, assistenti, residenti e patologi. È co-autore del testo “Veterinary Hematology: Atlas of Common Domestic Species” e di oltre 15 monografie e capitoli di libri riguardanti la citologia, l’ematologia e la biochimica clinica. Ha pubblicato oltre 50 articoli su riviste scientifiche veterinarie referate. È stato invitato ad oltre 100 congressi tra nazionali ed internazionali. È appassionato di fotografia, adora viaggiare (soprattutto in Europa) e ha una passione per i clown.

NICHOLAS DODMAN BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB Si è laureato in veterinaria nel 1970 all’Università di Glasgow, Scozia. Dal 1972 al 1981 ha tenuto corsi di anestesia all’Università di Glasgow. Nel 1981 si è trasferito a North Grafton nel Massachussets, presso la Tuft University, ricoprendo inizialmente l’incarico di Assistant Professor e quindi di Associate Professor di Anestesia e di Responsabile del servizio anestesiologico.

Nel 1975 ha ottenuto il Diploma del Royal College of Veterinary Surgeons in Anestesia. Nel 1982 si è diplomato al College Americano di Anestesia Attualmente le sue ricerche sono concentrate sulle alterazioni del comportamento nel cane e nel cavallo, oltre che al trattamento farmacologico dell’ansietà e dell’aggressività. Ha pubblicato oltre 80 articoli scientifici su riviste referate ed ha all’attivo una ventina di capitoli di libri e testi riguardanti ile patologie comportamentali. Dal 1996 è diplomato al College Americano di Comportamento Animale. Dal 1990 è Professore del Dipartimento di Scienze Cliniche e Direttore della Clinica Comportamentale della Tufts University School of Veterinary Medicine.

FABRIZIO FABBRINI Med Vet, Dipl CES Derm DENNIS B. DENICOLA DVM, PhD, Dipl ACVP Laureato alla Purdue University nel 1978, dove ottiene un PhD nel 1981. È Professore di Patologia Clinica Veterinaria. Direttore del Veterinary Clinical Pathology Laboratory, Direttore del Veterinary Clinical Pathology Residency Training Program e Direttore del National Veterinary Cytology Resource Center. Nel 1983 si diploma all’American College of Veterinary Pathologists (ACVP).

Laureatosi a pieni voti presso l’Università Statale di Milano nel 1981 si occupa, come libero professionista, dei piccoli animali da compagnia.

Dal 1987 il suo interesse verte verso la dermatologia veterinaria prendendo parte a diverse attività del gruppo di studio di dermatologia della SCIVAC (organizzare seminari, presentare relazioni ad incontri nazionali e ai corsi di base di Dermatologia).

Ha ottenuto il Diploma Francese in Dermatologia (C.E.S.) frequentando nel Triennio 93-95 le Facoltà Veterinarie di Lyon e Nantes.

40° Congresso Nazionale SCIVAC

Attualmente lavora a Milano, dove segue corsi di dermatologia anche riferiti.

Ha presentato relazioni e case report di dermatologia in congressi nazionali ed europei; ha scritto articoli di dermatologia in riviste nazionali e partecipa dal 1994 in qualità di relatore ai corsi di base di dermatologia organizzati dalla SCIVAC. Il Dr. Fabbrini è full member della ESVD, uno dei promotori e soci fondatori della SIDEV (Società italiana di Dermatologia Veterinaria) nella quale riveste attualmente la carica di tesoriere.

LUCA FORMAGGINI Med Vet Laureato a Milano nel 1991, frequenta nello stesso anno come tirocinante il Centro Veterinario “Gregorio VII” in Roma e con una Borsa di Studio la Clinica Chiurgica della Facoltà di Medicina Veterinaria di Zurigo per un periodo di due mesi. Dal 1992 al 1994 lavora presso la Clinica Veterinaria “Città di Pavia” occupandosi principalmente di chirurgia e pronto soccorso. Dal 1994 al 1996 entra a far parte dello staff chirurgico del Centro Veterinario “Gregorio VII” in Roma sotto la guida del Dr Tommasini svolgendo altresì ruoli di Medico di Pronto Soccorso nella stessa struttura.

Da fine 1996 è socio fondatore della Clinica Veterinaria “Lago Maggiore”. I principali campi di interesse sono la chirurgia generale, ortopedica e la medicina e chirurgia d’emergenza. È membro SCIVAC e BSAVA e ricopre ruoli di relatore e istruttore nei corsi di Chirurgia e Fissazione Esterna ed è Collaboratore nel Gruppo di Studio di Chirurgia Generale SCIVAC.

STEVEN GARNER DVM, Dipl ABVP Laureato in veterinaria nel 1983, ha conseguito nel 1992 il Diploma dell’American Board of Veterinary Practitioners con specializzazione in animali da compagnia. Steven Garner è stato un pioniere nel campo delle applicazioni di internet in medicina veterinaria ed ha sviluppato vari prodotti tra cui il Veterinary Specialist Network, un servizio di telemedicina, teleradiologia e telecitologia e VISION, un sistema di videoconferenza veterinaria. Steven Garner è proprietario e lavora in una clinica privata di Houston, in Texas, che è stata definita come la clinica veterinaria più produttiva del mondo. In questa clinica ha sviluppato con successo l’impiego di particolari software da lui stesso creati, alcuni dei quali dedicati all’educazione dei proprietari.

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GIOVANNI GHIBAUDO Med Vet Laureato presso la Facoltà di Medicina Veterinaria di Milano nel 1994; all’Istituto di Microbiologia ed Immunologia con una tesi sul sistema immunitario del cane e del gatto. Lavora presso la Clinica Veterinaria Malpensa di Samarate (Varese), occupandosi in particolare di medicina interna, dermatologia, citologia ed oncologia. Ha svolto il corso di Dermatologia dell’ESAVS (1996-98). Membro dell’ESVD e ECVIM. Sta svolgendo la prima parte del Diploma Europeo in dermatologia ECVD. Autore di diversi articoli su riviste nazionali ed estere. Ha presentato alcune relazioni in occasione di riunioni SCIVAC di dermatologia (SIDEV) e citologia (GdS).

OSCAR GRAZIOLI Med Vet Oscar Grazioli, conseguita la maturità classica, si è laureato in Medicina Veterinaria presso l’Università degli studi di Parma nel 1978. I suoi principali campi di interesse sono l’anestesiologia, la medicina interna e la patologia degli animali esotici, con particolare riferimento ai rettili. Autore di diverse pubblicazioni scientifiche è stato relatore a numerosi congressi e seminari. Dal 1992 è ordinary member della Association of Veterinary Anaesthetists (AVA) inglese. Nel triennio 1996 1998 è stato coordinatore del gruppo SCIVAC di Anestesia, Rianimazione, Medicina d’emergenza e terapia del dolore di cui è tuttora collaboratore. Oscar Grazioli è anche giornalista pubblicista e recentemente scrittore, avendo esordito nel campo letterario con un libro intitolato “Quello che gli animali non dicono”, che ha ottenuto unanime consenso di pubblico e di critica. Vive e lavora a Reggio Emilia.

MASSIMO GUALTIERI Med Vet Massimo Gualtieri si è laureato presso la Facoltà di Medicina Veterinaria di Milano nel 1983. Nel 1987 consegue il diploma della Scuola di Specializzazione in Clinica delle Malattie dei Piccoli Animali. Nel 1991 ottiene la nomina a Ricercatore presso l’Istituto di Clinica Chirurgica dell’Università di Milano.

Dal 1992 è docente presso il “Centro de Cirurgia de Minima Invasion” della Facoltà di Caceres (Spagna) per il “Corso Internazionale Teorico-Pratico di Endo-

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scopia nei Piccoli Animali” e dove, dal 1997, è direttore e organizzatore del “Corso Teorico-Pratico di Endoscopia Flessibile nei piccoli Animali” per Veterinari italiani.

Dal 1995 è docente presso la Scuola di Specializzazione in Patologia e Clinica degli animali d’affezione della Facoltà di Medicina Veterinaria di Milano.

Dal 1996 è docente per il Corso di Medicina Operatoria che ha in affidamento presso la Facoltà di Medicina Veterinaria di Milano. È stato docente invitato per l’anno 98/99 presso la Facoltà di Medicina Veterinaria di Liegi per un ciclo di lezioni riguardanti la Chirurgia dell’Apparato Gastroenterico. Dal 1998 è Presidente della European Society of Comparative Gastroenterology (ESCG) della quale è inoltre membro fondatore. È autore e coautore di più di 75 pubblicazioni su riviste italiane ed estere.

40° Congresso Nazionale SCIVAC

ELLIOTT R. JACOBSON DVM, MS, PhD Laureato in veterinaria presso la University of Missouri, Columbia, nel 1975 ottiene un PhD nello stesso anno in endocrinologia. Dal 1985 fa parte del board di specializzazione dell’American College of Zoological Medicine. Dal 1975 al 1977 è Assistant Professor del Department of Veterinary Science, University of Maryland. Dal 1979 lavora presso il College of Veterinary Medicine della University of Florida a Gainesville, al Department of Small Animal Clinical Sciences, dove dal 1990 è Professor of Wildlife and Zoological Medicine. I suoi interessi di ricerca sono le malattie infettive e non infettive dei rettili, la farmacocinetica degli antibiotici nei rettili e l’immunologia dei rettili. È autore di 159 articoli referati e di 31 capitoli di libri.

ROBERT HAMLIN DVM, PhD, Dipl ACVIM Laureato nel 1958 alla Ohio State University. Presso la stessa Università ha conseguito un Master of Sciences nel 1960 e un PhD nel 1952. Attualmente ricopre gli incarichi di Professore di Bioscienze Veterinarie e Professore di Ingegneria Biomedica. È autore di oltre 250 articoli scientifici e oltre 50 capitoli di libri. I suoi interessi di ricerca includono la fisiopatologia cardiovascolare, l’elettrocardiografia comparativa, la farmacologia delle malattie cardiovascolari e la biomeccanica polmonare. Ha ricevuto numerosi riconoscimenti per la sua attività scientifica e didattica, tra cui il Robert Kirk Award e l’Insegnante dell’anno. È stato Presidente dell’American College of Veterinary Internal Medicine. È anche stato nominato membro dell’Accademia di Medicina Veterinaria degli Stati Uniti.

KERSTIN HANSSON Dr Med Vet Laurea nel 1984. Dal 1987 lavora nel Dipartimento di Clinica Raduiologica della Swedish University of Agricultural Sciences di Uppsala, dove ricopre vari incarichi nei settori di ricerca, insegnamento e amministrazione. Dal 92 al 96 è stata Responsabile del settore clinico e dal 96 al 99 Responsabile del Dipartimento.

Nel 92 ha conseguito il British Certificate in Veterinary Radiology. Ha tenuto numerosi corsi di aggiornamneto per veterinari in vari aspetti di diagnostica per immagini. I suoi interessi professionali sono concentrati nell’ecografia diagnostica. Pratica lo sci aplino ed in generale gli sport all’aria aperta.

TERESA LIGHTFOOT DVM, Dipl ABVP Si è laureata all’Università del Missouri nel 1980. Quindi ha seguito un programma di externship allo Zoo di St. Louis e ha iniziato la pratica veterinaria a Largo, in Florida. Nel 1987 ha aperto un ospedale veterinario per uccelli e animali esotici. Ha quindi costituito una società con la collega Lucy Bartlett nel 1989.Dalla sua costituzione nel 1993 è diplomata dell’American Board of Veterinary Practitioners, con specializzazione in medicina aviare e attualmente la clinica dove lavora ha ottenuto un programma di residency per l’ABVP. Fa parte dello staff veterinario del Suncoast Seabird Sanctuary. Ha presieduto l’Education Committee della AAV, l’Association of Avian Veterinarians. È autrice di numerosissimi articoli sulla medicina aviare e degli animali esotici. È stata votata come migliore relatrice “esotica” al Congresso della North American Veterinary Conference del 1998. I suoi principali settori di ricerca sono la reintroduzione di tartarughe indigene nel loro ambiente e le patologie comportamentali degli uccelli.

CARLO MARIA MORTELLARO Med Vet Nato a Rivolta d’Adda, Cremona, il 5 Febbraio 1950, si è laureato in Medicina Veterinaria presso la Facoltà di Medicina Veterinaria dell’Università degli Studi di Milano nel 1974. È stato professore di Anestesiologia Veterinaria presso la stessa Università dal 1976 al 1979.

Dal 1980 al 1992 ha ricoperto il ruolo di Professore As-

40° Congresso Nazionale SCIVAC

sociato di Patologia Chirurgica Veterinaria e Podologia e nel 1993 è stato nominato Professore Ordinario di Patologia Chirurgica Veterinaria, ruolo che tuttora ricopre. I suoi principali interessi scientifici sono rappresentati dalle patologie di orecchio, naso e gola nel cane e nel gatto, lesioni del cavo orale, endoscopia delle vie aeree superiori ed infine patologie della regione anale e circumanale (da un estremo all’altro del corpo senza transitare in mezzo). In questi ultimi anni un interesse particolare è stato rivolto alle patologie osteo-articolari distrofico-displastiche (nota la sua avversione per le forme”carenziali”) del cane e del gatto. È Presidente in carica dell’IVENTA (International Veterinary Ear Nose and Throat Association. È referee scientifico del Gruppo di Studio di Ortopedia della SCIVAC. È autore-coautore di 160 pubblicazioni. È stato relatore in numerosi congressi e seminari di aggiornamento post-universitario in Italia ed all’Estero. Talvolta suona (le tastiere).

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dia e dell’Emilia, lavorando presso la sezione di Milano fino alla fine del 1995 sulla diagnostica delle leptospirosi animali. Nel febbraio del 1996 è stato ammesso ad un training clinico presso il “Wildlife and Zoological Medicine Service” del College of Veterinary Medicine dell’Università della Florida sotto la guida del professor Elliott Jacobson. Dal 1996 si occupa di clinica e patologia dei rettili. Nel 1997 è tornato come consulente a contratto presso la sezione di Milano dell’Istituto Zooprofilattico. Nel 1998 ha vinto la Fulbright scholarship ed è stato ammesso al programma di PhD presso i dipartimenti di “Pathobiology and Small Animal Clinical Sciences” del College of Veterinary Medicine dell’Università della Florida (Major professor Dr Jacobson). Ha presentato i risultati delle sue ricerche nell’ambito di congressi nazionali ed internazionali ed è autore di pubblicazioni riguardanti la clinica e la patologia dei rettili su riviste internazionali. Attualmente sta perseguendo il suo PhD presso l’Università della Florida, con una ricerca focalizzata sullo sviluppo di sistemi diagnostici sierologici e molecolari per l’evidenziazione delle infezioni da herpesvirus nelle tartarughe.

CHIARA NOLI Med Vet Dipl ECVD Laureata all’Università di Milano nel 1990, è specialista in Malattie dei Piccoli Animali dal 1995. Dopo due anni di soggiorni all’estero in Spagna (1989-1990), e in Germania (1991-1992), per apprendere la dermatologia, ha ottenuto un residency di tre anni in dermatologia veterinaria presso l’Università di Utrecht, Paesi Bassi (1992-1995). Successivamente ha passato sei mesi nell’Istituto di Patologia Veterinaria dell’Università di Berna (nel 1995), per perfezionare la dermatopatologia. Nel 1996 ha conseguito il Diploma del College Europeo di Dermatologia Veterinaria (Dip. ECVD). Dal 1996 lavora in Italia eseguendo esclusivamente consulenze dermatologiche e letture dermatopatologiche, e nel 1999 ha aperto un suo studio dermatologico veterinario a Milano. È past-president della Società Italiana di Dermatologia Veterinaria (SIDEV), membro del Consiglio Direttivo della ESVD (Società Europea di Dermatologia Veterinaria) e Full Member della AAVD (Accademia Americana di Dermatologia Veterinaria). È autrice di numerosi articoli italiani e internazionali e di tre capitoli di libri. Ha inoltre tenuto relazioni a numerosi congressi in Italia e all’estero.

FRANCESCO ORIGGI Med Vet Si è laureato presso l’Università di Milano nel 1994 con una tesi sperimentale in patologia.

Alla fine del 1994 ha vinto una borsa di studio bandita dall’Istituto Zooprofilattico Sperimentale della Lombar-

MARIA CRISTINA OSELLA Med Vet Laureata in Medicina Veterinaria con la Tesi “Il comportamento aggressivo del cane” e Dottore di Ricerca in Medicina Interna con la Tesi: “Problemi comportamentali nel cane e nel gatto: approccio clinico-diagnostico e terapeutico”, presso la Facoltà di Medicina Veterinaria di Torino, coordinatore Prof. F. Monti, presso cui continua l’attività di ricerca, con il supporto della Borsa di Studio S.I.S.Vet. (Società Italiana delle Scienze Veterinarie) di perfezionamento post-dottorato. Promotrice di alcune iniziative di Pet-Therapy, tra cui il progetto sull’impiego terapeutico degli animali d’affezione in strutture psichiatriche. Socio fondatore SISCA (Società Italiana delle Scienze Comportamentali Applicate). Relatore e Direttore di Corsi SCIVAC, Corsi dell’OMS/FAO, relatore e coordinatore di incontri di aggiornamento rivolti ai colleghi ed agli studenti, sostenitore di iniziative varie a carattere divulgativo. Libero professionista operante nel settore della Clinica Comportamentale del cane e del gatto.

YANNICK POUBANNE Med Vet Laureatosi in medicina veterinaria nel 1984 ha esercitato la libera professione nei piccoli animali prima di iniziare a collaborare nel 1988 con la Hill’s Pet Nutrition in Francia. Dopo aver ricoperto vari incarichi per la Hill’s in Francia e Spagna, ha iniziato una propria atti-

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vità nel 95, offrendo servizi di consulenza a numerose aziende in Europa. È anche responsabile del programma di management alla Facoltà di Veterinaria di Maison Alfort di Parigi. È Vice-Presidente del European Group for Veterinary Practice Management e membro del direttivo del GERM, il gruppo di studio francese di management in medicina veterinaria. Ha ottenuto il Business School Certificates ed il Master in Statistica all’Università di Lille in Francia. Attualmente sta terminando un PhD in Scienze del management, specializzazione Marketing presso l’Università di Aix-en-Provence.

PAOLA ROCCABIANCA Med Vet Nel Luglio 1991 ottiene la Laurea in Medicina Veterinaria (110/110 cum laude). Nel triennio 1991-1994 svolge il Dottorato in Patologia Comparata degli Animali Domestici presso l’Isituto di Anatomia Patologica Veterinaria dell’Università di Milano con un programma dal titolo: “Citodiagnostica in patologia animale”.

Nel 1994 risulta vincitrice della Borsa J. Fullbright del Governo Americano e di una Borsa di Studio Ministeriale per Specializzazione all’Estero e risiede presso la Scuola di Medicina Veterinaria di Davis, California. In questa sede segue il servizio di dermatopatologia e di patologia clinica e, presso il laboratorio del Prof P. Moore, svolge ricerche di immunopatologia e studia le patologie linfoproliferative dei piccoli animali. Nel 1996 ottiene la borsa di post-dottorato in Scienze Mediche Veterinarie e Biologia Applicata, continuando l’attività presso l’Università di Davis. Dal 1998 ad oggi occupa la posizione di Ricercatore presso l’Istituto di Patologia ed Igiene Veterinaria della Facoltà di Medicina Veterinaria di Padova.

GIORGIO ROMANELLI Med Vet, Dipl ECVS Laureato alla Facoltà di Veterinaria di Milano nel 1981. Conseguita la laurea ha lavorato ad un programma di Chirurgia sperimentale sul trapianto di cuore nei maiali e di pancreas nei cani. Lavora a Milano come libero professionista. Si occupa principalmente di Chirurgia Generale ed Ortopedia e di Oncologia Clinica e Chirurgica. Diplomato dal luglio 1993 all’European College of Veterinary Surgeons. Autore del video SCIVAC sulla fissazione esterna. Ha ricoperto dal 1993 al 1995 la carica di Presidente SCIVAC. Oltre che della SCIVAC è membro di AAHA, BSAVA, ECVS, AOI, SINVET, ESVN, Veterinary Cancer Society.

40° Congresso Nazionale SCIVAC

ROBERTO SANTILLI Med Vet, Dipl ECVIM CA (Cardiology) Laureato presso la Facoltà di Medicina Veterinaria di Milano nel 1990. Si è diplomato all’European College of Veterinary Internal Medicine -Companion Animals (Specialty of Cardiology) nel 1999. Lavora presso la Clinica Veterinaria Malpensa in Samarate (Varese) e la Clinica Veterinaria Fiera in Milano. È stato professore a contratto in cardiologia felina per l’anno 1997-1998 presso la Scuola di Specializzazione in Patologia e Clinica degli animali d’affezione dell’Università degli Studi di Milano. Dal 1992 al 1998 ha svolto programmi di aggiornamento in cardiologia ed ecografia addominale presso la North Carolina State University, l’Ohio State University, University of California, Cornell University e Missouri State University. È istruttore ai corsi S.C.I.V.A.C. di cardiologia ed ecografia addominale. È autore di numerose pubblicazioni di ecografia addominale e cardiologia su riviste nazionali ed internazionali. Il suo principale settore di ricerca sono le cardiomiopatie e l’ipertensione arteriosa del gatto.

BARCLAY SLOCUM DVM Laureato alla Colorado State University nel 1970. Internship all’Università di Saskatoon in Canada e Residency prima a Davis, California e quindi alla Ohio State University. Svolge la professione veterinaria da oltre 20 anni. Ha sviluppato numerose tecniche ortopediche innovative, tra cui l’steotomia livellante del piatto tibiale (TPLO) per il trattamento della rottura del crociato craniale nel cane, l’allungamento del collo femorale, la recessione trocleare, e il trasferimento del retto femorale. Ha tenuto numerose relazioni su temi di ortopedia sia negli Stati Uniti che in America. Ha ricevuto molti riconoscimenti per la sua attività professionale, tra cui il Practitioner Research Award dall’AVMA e l’Outstanding Small Animal Practitioner Award dalla AAHA.

CANDACE SOUSA DVM, Dipl ABVP, Dipl ACVD Laureata all’Università di Davis California nel 1977.

Dopo alcuni anni come libero professionista a Sacramento è ritornata all’Università della California dove ha completato un programma di residency alternativo della durata di 2 anni e mezzo continuando l’attività di libera professione. Nel 1983 ha ottenuto il diploma del-

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l’American Board of Veterinary Practitioners e dal 1991 ha la specializzazione in clinica canina e felina.

Dal 1985 è diplomata all’American College of Veterinary Dermatology. Ha pubblicato numerosi articoli di dermatologia veterinaria e ha tenuto relazioni sia in congressi nazionali che internazionali. Attualmente ha un’attività di referenza in dermatologia a Sacramento e ha un contratto di Adjunct Clinical Professor in dermatologia all’Università di Davis.

MATTEO TOMMASINI DEGNA Med Vet, Dipl ECVS Laureato alla Facoltà di Veterinaria di Pisa nel 1982.

Specialista in Malattie dei Piccoli Animali. Membro attivo della AO VET International. Socio ASAMI, Associazione per lo Studio e Applicazione della Metodica di Ilizarov. Tiene relazioni al corso veterinario ASAMI organizzato da SCIVAC. Membro del Comitato di Fondazione e Diplomato dell’European College of Veterinary Surgeons. Svolge la libera professione a Roma presso il Centro Veterinario Gregorio VII. Ha ricoperto il ruolo di Coordinatore del Gruppo di Studio di Chirurgia dalla sua formazione fino al 1994.

ALDO VEZZONI Med Vet, Dipl ECVS Laureato nel 1975 presso la facoltà di Veterinaria dell’Università di Milano, ha ottenuto il titolo di Specialista in Medicina dei Piccoli Animali nel 1978 presso la stessa facoltà. Dal 1976 lavora a Cremona come libero professionista nella propria clinica veterinaria. Si è Diplomato al College Europeo di Chirurgia a Cambridge nel 1993. Ha tenuto diverse relazioni sia in Italia che all’estero su temi riguardanti la filariosi canina, l’ortopedia, la chirurgia e l’odontostomatologia. Autore di numerosi articoli scientifici sulla filariosi e sulla chirurgia e ortopedia nei piccoli animali. Autore e co-autore di un testo sulla filariosi canina e del prontuario SCIVAC, è stato anche curatore di numerose edizioni italiane di testi stranieri. Dal 1994 è membro del Comitato Centrale FNOVI di cui riveste dal 1997 la carica di Segretario. Dallo stesso anno è anche Presidente dell’Ordine dei Veterinari di Cremona.

MASSIMO VIGNOLI Med Vet Il Dott. Massimo Vignoli è nato a Bologna il 24/04/64.

Iscritto alla Facoltà di Medicina Veterinaria di Bologna

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nell’Anno Acc. 87/88 e laureato nel giugno 93. Ha trascorso alcuni periodi all’estero in Europa e USA. Diplomato in radiologia veterinaria nell’Ottobre 1997.

Fa parte del coordinamento del gruppo di studio di diagnostica per immagini della SCIVAC. Ha all’attivo diverse pubblicazioni nazionali ed internazionali riguardanti la diagnostica per immagini e la chirurgia.

Settore di particolare interesse: radiologia scheletrica; tecnica radiologica.

Al momento svolge attività libero professionale a Sasso Marconi (BO) dove si occupa prevalentemente di radiologia e chirurgia.

FABIO VIGANÒ Med Vet, Spec Mal PA Il Dott. Fabio Viganò laureato e specializzato (in Malattie dei piccoli Animali) a Milano rispettivamente nel 1987 e nel 1995. Dal 1987 ad oggi esercita la libera professione ed effettua soggiorni di studio in Università e cliniche private dedite al pronto soccorso ed alla terapia intensiva negli Stati Uniti. Dal 1993 è membro e partecipa a tutti i meeting annuali della società americana Veterinary Emergency and Critical Care Society. Relatore in diversi congressi, Direttore Scientifico ed unico relatore di corsi riguardanti il pronto soccorso e la terapia intensiva per medici veterinari. Dal 1995 è responsabile del settore medicina d’urgenza del gruppo di studio d’anestesia e rianimazione della SCIVAC. Nel 1997 è stato Coordinatore Scientifico del 33° Congresso SCIVAC “Medicina d’urgenza e terapia intensiva nei piccoli animali”. Attualmente è Titolare e Direttore Sanitario della Clinica Veterinaria San Giorgio, Via Roma, 54 san Giorgio su Legnano (MI).

TON WILLEMSE DVM, PhD, Dipl ECVD Laureato in veterinaria nel 1974 all’Università di Utrecht, dove dal 1978 è responsabile dell’unità dermatologica del Dipartimento di Scienze Cliniche in Animali da Compagnia per le attività di insegnamento, ricerca e clinica. Nel 1984 ha terminato un PhD e dal 1986 è Professore Associato di dermatologia. È anche chairman della divisione medica del Dipartimento. È autore di oltre 70 articoli scientifici su riviste referate oltre a numerosi capitoli di libri. È membro fondatore del College Europeo di Dermatologia Veterinaria di cui è stato presidente. È amante della lettura, della musica classica, del golf, gli piace prendere il sole e cucinare.

SPONSOR La SCIVAC ringrazia le Aziende sponsor per il sostegno e il contributo prestati alla realizzazione di questo Congresso.

La sponsorizzazione ha permesso di contenere le quote di iscrizione.

Animal Health

Hill’s* 27

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Uso di CT e RM nella diagnostica delle malattie del SNC Massimo Baroni Med. Vet., Dipl. ECVN - Libero Professionista - Genova

Riassunto Tomografia Computerizzata (CT) e Risonanza Magnetica (RM) hanno ormai una applicazione routinaria in neurologia umana e trovano sempre più ampi spazi in campo veterinario, certamente ancora penalizzato dal costo elevato di tali attrezzature.

Lo scopo della presente trattazione vuole essere quello di esporre i principi fondamentali su cui si basano le suddette procedure e discutere le principali loro attuali applicazioni in Neurologia Veterinaria.

CT e MR NELLA DIAGNOSTICA INTRACRANICA Sebbene la CT rivesta ancora un ruolo molto importante nella diagnostica delle malattie intracraniche del cane e del gatto a causa del costo relativamente accessibile rispetto alla RM, quest’ultima si è rivelata di gran lunga più sensibile nella diagnostica delle malattie cerebrali e ha quasi totalmente soppiantato la Tomografia computerizzata in medicina umana.

La CT è comunque idonea alla diagnosi di processi riguardanti la volta cranica o comunque i tessuti duri, compreso l’orecchio interno, le masse occupanti spazio ubicate in fossa posteriore, le lesioni di tipo vascolare nelle loro primissime fasi, alcune lesioni infiammatorie occupanti spazio (ascessi, GME), alcune anomalie (idrocefalo). Non è invece sensibile nella diagnostica di lesioni ubicate in fossa posteriore a causa del notevole spessore osseo che causa perdita di definizione.

La RM offre una notevole sensibilità diagnostica sia nel campo delle lesioni espansive che infiammatorie e degenerative oltreché nelle anomalie congenite. Permette una ottima visione delle strutture della fossa posteriore e dell’orecchio medio e interno. Non è idonea per la visualizzazione di lesioni riguardanti i tessuti duri.

UTILIZZO DELLA CT E DELLA RM NELLA DIAGNOSTICA MIDOLLARE A causa sia di fattori tecnici (dimensioni ridotte del midollo spinale), sia di fattori di costi, la mielografia rimane ancora l’indagine di scelta nella diagnosi delle principali lesioni spinali.

Tuttavia CT e RM trovano anche in questo campo precise indicazioni e sicuramente saranno di applicazione crescente nel prossimo futuro.

La CT è ideale per lo studio dei processi infiammatori, degenerativi e malformativi che riguardano la colonna vertebrale. Può inoltre essere utilizzata con successo nella diagnosi delle ernie discali ed è di notevole ausilio nella diagnosi di Sindrome da Cauda Equina, soprattutto per lo studio di osteofitosi foraminali. Una tecnica estremamente interessante è la mielo-CT, che consente di identificare in maniera precisa compressioni extradurali. È di notevole aiuto in lesioni particolari, come, ad esempio, la Spondilopatia Cervicale Caudale nell’alano.

La RM è al momento attuale la procedura di scelta per la diagnosi di neoplasie midollari sia extra che intradurali (meningiomi, gliomi, tumori delle guaine dei nervi periferici).

Molto utile potrà rivelarsi in futuro nella diagnosi di discopatie e nella diagnosi di compressioni intraforaminali in corso di sindrome da cauda equina.

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Nell’ambito della diagnostica neurologica, più che in altri campi, lo sviluppo di nuove metodiche di diagnosi per immagini, ha costituito una vera e propria pietra miliare per l’approfondimento della conoscenza di moltissime patologie e per la messa a punto di un efficace trattamento. In particolare Tomografia Computerizzata (CT) e Risonanza Magnetica (RM) hanno ormai una applicazione routinaria in neurologia umana e trovano sempre più ampi spazi in campo veterinario, certamente ancora penalizzato dal costo elevato di tali attrezzature.

Lo scopo della presente trattazione vuole essere quello di esporre i principi fondamentali su cui si basano le suddette procedure e discutere le principali loro attuali applicazioni in Neurologia Veterinaria.

TOMOGRAFIA COMPUTERIZZATA Principi base La Tomografia Computerizzata è una diretta evoluzione della Tomografia convenzionale classica, nella quale una sorgente di raggi ruota intorno all’oggetto da esaminare, permettendo di visualizzare sulla radiografia solamente lo strato del corpo che si vuole esaminare attenuando sia gli strati sottostanti che sovrastanti.

Anche nella CT, esiste una sorgente di raggi X che ruotando attraversa il corpo da esaminare. Sul lato opposto esistono dei rilevatori che captano il fascio di raggi x. A seconda della disposizione dei rivelatori si distinguono varie generazioni di macchine CT. In quelle di quarta generazione, il tuobo radiogeno ruota attorno al paziente e i rivelatori, di tipo statico, sono posti in numero di 300-4000 su tutti i 360° intorno al paziente stesso. Un computer riceve le informazioni percepite dai rilevatori ed elabora un’immagine basata sul grado di attenuazione di una scala di grigi.

L’immagine bidimensionale che appare sullo schermo è un’insieme di “Pixel” che rappresentano le caratteristiche di attenuazione di un certo volume di tessuto chiamato “Voxel”. Ad ogni pixel è attribuito un numero di attenuazione che si basa su una calibrazione che va dal numero dell’acqua (0) a quello dell’aria (1000).

La scala di grigi visualizzata può essere variata, ottenendo immagini con “finestra” idonea alla visualizzazione dei soli tessuti duri e immagini con “finestra” adatta alla visualizzazione dei tessuti molli. Il paziente viene esaminato secondo scansioni contigue di spessore variabile: un solo piano viene direttamente esaminato, anche se gli altri due piani dello spazio possono essere ricostruiti dal computer.

Mezzi di contrasto ionici iniettati endovena (Iopamidolo, ioexolo) vengono utilizzati per migliorare la visualizzazione di lesioni che presentano una rottura della barriera ematoencefalica o che sono particolarmente vascolarizzate.

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come piccoli dipoli magnetici. Se essi non sono sottoposti ad alcun campo magnetico, sono orientati in maniera random.

Tra i vari, i protoni Idrogeno sono quelli di maggiore importanza per l’applicazione biologica della MR. In una macchina per MR, è presente un magnete che determina un campo magnetico Bo parallelamente al quale si orientano i piccoli dipoli magnetici presenti nell’organismo.

Un segnale a radio-frequenza viene quindi emesso e determina un nuovo campo magnetico B1 cambiando l’orientamento dei dipoli secondo la direzione del nuovo campo.

Quando cessa il segnale i dipoli tendono a riacquistare l’orientamento primitivo Bo, emettendo l’energia prima assorbita, la quale viene captata come radiosegnale. Il tempo che occorre ai dipoli per riacquistare l’orientamento primitivo viene chiamato Tempo di Rilassamento T1. Oltre ad interagire con Bo, i dipoli interagiscono anche fra di loro, emettendo un radio segnale. Il tempo di durata di questo segnale viene chiamato Rilassamento T2.

Le caratteristiche di un tessuto in termini di Densità Protonica, Rilassamento T1 e Rilassamento T2, sono utilizzate da un computer per elaborare l’immagine. A seconda del tipo di radiofrequenza utilizzata verranno enfatizzate una delle tre caratteristiche, per cui avremo immagini T1, T2 e a densità protonica.

Nelle immagini T1, tutti i tessuti ricchi in acqua appaiono ipointensi (scuri), mentre i tessuti poveri in acqua appaiono iperintensi (bianchi). Quindi il CSF appare nero, la sostanza bianca appare più intensa di quella grigia. Nelle immagini T2, avviene il contrario, per cui risultano iperintensi il CSF e la sostanza grigia.

Come per la CT, anche nella MR, il corpo del paziente viene esaminato secondo scansioni di spessore variabile: Tutti e tre i piani dello spazio, coronale, assiale e sagittale possono essere direttamente esaminati.

Mezzi di contrasto paramagnetici(gadolinio) vengono utilizzati per enfatizzare alcuni tipi di lesione.

STUDIO DELL’ANATOMIA NORMALE CT e MR Anche in Neurologia Veterinaria sono ormai a disposizione varie fonti di Letteratura riguardanti la normale anatomia CT e MR, la descrizione della quale esula dalla presente trattazione. È tuttavia necessario puntualizzare che solo una precisa e profonda conoscenza di essa, consente di avvicinarsi correttamente alla diagnostica, motivo per cui si stimola il lettore ad uno studio della letteratura suddetta prima di affrontare un approccio diretto con queste metodiche di diagnostica per immagine.

CT e MR NELLA DIAGNOSTICA INTRACRANICA RISONANZA MAGNETICA Principi base All’interno di un organismo, i nuclei atomici che posseggono in diverso numero protoni e neutroni si comportano

Sebbene la CT rivesta ancora un ruolo molto importante nella diagnostica delle malattie intracraniche del cane e del gatto a causa del costo relativamente accessibile rispetto alla RM, quest’ultima si è rivelata di gran lunga più sensibile nella diagnostica delle malattie cerebrali e ha quasi total-

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mente soppiantato la Tomografia computerizzata in medicina umana.

La CT è comunque idonea alla diagnosi di processi riguardanti la volta cranica o comunque i tessuti duri, compreso l’orecchio interno, le masse occupanti spazio ubicate in fossa posteriore, le lesioni di tipo vascolare nelle loro primissime fasi, alcune lesioni infiammatorie occupanti spazio (ascessi, GME), alcune anomalie (idrocefalo). Non è invece sensibile nella diagnostica di lesioni ubicate in fossa posteriore a causa del notevole spessore osseo che causa perdita di definizione.

La RM offre una notevole sensibilità diagnostica sia nel campo delle lesioni espansive che infiammatorie e degenerative oltreché nelle anomalie congenite. Permette una ottima visione delle strutture della fossa posteriore e dell’orecchio medio e interno. Non è idonea per la visualizzazione di lesioni riguardanti i tessuti duri.

NEOPLASIE Alcuni tipi di tumori mostrano caratteristiche tipiche che si rivelano spesso diagnostiche:

GLIOMI Si mostrano come zone ipointense in T1 ed iperintense in T2, a margini non definiti, a localizzazione intrassiale, con “Contrast enhancement” ad anello o disomogeneo. Alcuni gliomi a basso indice di malignità non prendono contrasto.

Esercitano solitamente notevole effetto massa.

MENINGIOMI Hanno localizzazioni tipiche (meningiomi della volta, della base cranica, della falce, dell’angolo cerebello-pontino), presentano margini molto netti, spesso con chiara distinzione dal parenchima circostante, si presentano isointensi in T1 e iperintensi in T2, hanno contrast enhancement intenso ed omogeneo che si estende spesso alle meningi adiacenti (meningeal tail). Spesso presentano aree calcifiche.

TUMORI DEI PLESSI CORIOIDEI Sono a localizzazione intraventricolare, sono ben definiti ed assumono intensamente ed uniformemente il contrasto.

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LESIONI INFIAMMATORIE Le sequenze T2 sono solitamente le più sensibili nell’identificare le lesioni infiammatorie, le quali appaiono iperintense in queste sequenze, mentre appaiono isointense o ipointense in T1. Decisa ipointensità si coglie in T1 nelle lesioni che portano a malacia. Il contrast enhancement delle lesioni infiammatorie varia a seconda della gravità della rottura della barriera ematoencefalica.

Anche in caso di demielinizzazione, come avviene ad esempio nell’infezione cimurrosa, si possono avere aree di ipersegnale in T2 associate ad aree ipointense in T1.

LESIONI VASCOLARI Lesioni emorragiche acute associate ad edema possono provocare iperintensità T2.

Con la trasformazione dell’ossiemoglobina in desossiemoglobina e in metaemoglobina, si ha un’iperintensità T1 ed un’ipointensità T2.

UTILIZZO DELLA CT E DELLA RM NELLA DIAGNOSTICA MIDOLLARE A causa sia di fattori tecnici (dimensioni ridotte del midollo spinale), sia di fattori di costi, la mielografia rimane ancora l’indagine di scelta nella diagnosi delle principali lesioni spinali.

Tuttavia CT e RM trovano anche in questo campo precise indicazioni e sicuramente saranno di applicazione crescente nel prossimo futuro.

La CT è ideale per lo studio dei processi infiammatori, degenerativi e malformativi che riguardano la colonna vertebrale. Può inoltre essere utilizzata con successo nella diagnosi delle ernie discali ed è di notevole ausilio nella diagnosi di Sindrome da Cauda Equina, soprattutto per lo studio di osteofitosi foraminali. Una tecnica estremamente interessante è la mielo-CT, che consente di identificare in maniera precisa compressioni extradurali. È di notevole aiuto in lesioni particolari, come, ad esempio, la Spondilopatia Cervicale Caudale nell’alano.

La RM è al momento attuale la procedura di scelta per la diagnosi di neoplasie midollari sia extra che intradurali (meningiomi, gliomi, tumori delle guaine dei nervi periferici).

Molto utile potrà rivelarsi in futuro nella diagnosi di discopatie e nella diagnosi di compressioni intraforaminali in corso di sindrome da cauda equina.

ADENOMI, ADENOCARCINOMI IPOFISARI CONCLUSIONI A partenza dalla sella turcica si estendono verso il talamo. Hanno margini ben definiti e buona ed omogenea presa di contrasto. Spesso è difficile una differenziazione con il meningioma della base. A tale scopo può essere utile associare alla RM uno studio CT per la messa in evidenza di eventuali calcificazioni, elemento che fa propendere la diagnosi verso il meningioma.

CT e RM stanno rivoluzionando anche in medicina veterinaria l’approccio al paziente neuroleso aprendo nuovi affascinanti orizzonti diagnostici e terapeutici. Uno studio approfondito e specialistico di queste metodiche è quindi necessario, così come si ritiene utile una conoscenza dei loro principi di base da parte del veterinario pratico.

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Vantaggi e limiti dell’ecografia nella diagnosi delle malattie gastroenteriche Michele Borgarelli Med. Vet., Dipl. ECVIM-CA (Cardiology) - Libero Professionista - Torino

Riassunto Recentemente, l’esame ecografico è divenuto parte integrante del complesso degli esami per la valutazione dei pazienti affetti da patologie dell’apparato gastroenterico. L’ecografia, infatti, si è dimostrata una metodica versatile e sensibile per la valutazione delle lesioni morfologiche a carico di tale apparato e degli organi annessi quali pancreas e linfonodi.

Rispetto alle altre metodiche di diagnostica per immagini quali l’esame radiologico in bianco e con mezzo di contrasto, l’endoscopia, la tomografia assiale computerizzata e la scintigrafia, la metodica ecografica presenta alcuni vantaggi rappresentati dal minor rapporto costo/tempo d’esecuzione e dai minori rischi biologici per l’operatore, dalla possibilità di eseguire facilmente esami seriali, dal richiedere raramente una sedazione, dalla possibilità di osservare la parete del tratto gastrointestinale a tutto spessore e non solo la mucosa, e dalla possibilità di valutare la peristalsi.

I principali limiti dell’esame ecografico sono rappresentati dagli artefatti (ombre acustiche e ring down) prodotti dalla presenza di gas e feci nello stomaco e nell’intestino che in alcuni casi ne impediscono la completa e soddisfacente visualizzazione, dall’assenza di specificità delle lesioni osservate, e dalla difficoltà di determinare nella maggior parte dei casi la loro precisa localizzazione.

Per quanto concerne le patologie gastriche e intestinali l’esame ecotomografico presenta una buona sensibilità nel riconoscere alterazioni morfologiche della parete che nell’uomo raggiunge l’82% per quanto concerne le lesioni parietali gastriche. Tuttavia la presenza di gas, di cibo e di feci normalmente presente nel tratto gastro enterico dei nostri animali, diminuisce in modo significativo la sensibilità della metodica che in casi dubbi deve sempre essere seguita da altri accertamenti quali l’esame endoscopico. Quadri ecografici caratteristici sono stati riportati per quanto concerne la gastropatia uremica e la gastropatia ipertrofica cronica pilorica, e l’invaginamento intestinale. Le neoplasie gastro intestinali presentano spesso invece quadri ecografici comuni, con lesioni morfologicamente non distinguibili da altre situazioni patologiche quali stati infiammatori severi o infiltrazioni granulomatose. In questi casi però l’ecografia permette, con relativa sicurezza, in modo mininvasivo e solo con una blanda sedazione di eseguire aghi aspirati o biopsie mirate dalle lesioni osservate aumentando in questo modo la specificità diagnostica della metodica. L’esame ecografico rappresenta inoltre un’ eccellente metodica per la stadiazione clinica delle neoplasie.

INTRODUZIONE Recentemente, l’esame ecografico è divenuto parte integrante del complesso degli esami per la valutazione dei pazienti affetti da patologie dell’apparato gastroenterico. L’ecografia, infatti, si è dimostrata una metodica versatile e sensibile per la valutazione delle lesioni morfologiche a carico di tale apparato e degli organi annessi quali pancreas e linfonodi 1 .

Rispetto alle altre metodiche di diagnostica per immagini quali l’esame radiologico in bianco e con mezzo di contrasto, l’endoscopia, la tomografia assiale computerizzata e la scintigrafia, la metodica ecografica presenta alcuni vantaggi rappresentati dal minor rapporto costo/tempo d’esecuzione e dai minori rischi biologici per l’operatore, dalla possibilità di eseguire facilmente esami seriali, dal richiedere raramente una sedazione, dalla possibilità di osservare la parete del tratto gastrointestinale a tutto spessore e non solo la

mucosa, e dalla possibilità di valutare la peristalsi. Inoltre l’ecografia permette, con relativa sicurezza, di eseguire aghi aspirati o biopsie mirate dalle lesioni osservate in modo mininvasivo e solo con una blanda sedazione 2 aumentando in questo modo la specificità diagnostica della metodica.

I principali limiti dell’esame ecografico sono rappresentati dagli artefatti (ombre acustiche e ring down) prodotti dalla presenza di gas e feci nello stomaco e nell’intestino che in alcuni casi ne impediscono la completa e soddisfacente visualizzazione, dall’assenza di specificità delle lesioni osservate, e dalla difficoltà di determinare nella maggior parte dei casi la loro precisa localizzazione3.

ASPETTO NORMALE Il caratteristico aspetto di tutto il tratto gastroenterico è quello di una struttura pluristratificata; tale aspetto è di nor-

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ma ben visibile utilizzando sonde ad elevata frequenza e definizione. L’aspetto stratificato con alternanza di linee iper ed ipoecogene appare determinato da una combinazione tra la produzione di eco che originano dalle differenti interfacie presenti (ad es. lume e mucosa), e dalla differente ecogenicità degli strati istologici 1. Il piccolo intestino di norma presenta uno spessore relativo della mucosa maggiore rispetto agli altri strati della parete, tale ipertrofia non si osserva invece nel colon e nel retto, e può quindi costituire elemento differenziale per quanto concerne la localizzazione delle lesioni eventualmente osservate. La scomparsa del normale aspetto stratificato della parete costituisce in genere un segno di patologia. Lo spessore normale della parete gastrica è di 3-5 mm, mentre quello della parete intestinale è di 2-3 mm; tutte le misure debbono essere eseguite in una sezione trasversale del tratto in esame. Di norma è possibile osservare da 3 a 5 contrazioni peristaltiche al minuto nello stomaco e nel duodeno, mentre il piccolo intestino presenta da 1 a 3 peristalsi al minuto 4. Nell’ambito di un esame volto alla valutazione dell’apparato gastroenterico è di estrema importanza la valutazione dei linfonodi regionali (gastrici, epatici, splenici, pancreatico-duodenali, digiunali, e colici), perché spesso rappresentano l’unico marker ecografico di una patologia di tale apparato.

STOMACO Le gastriti lievi e moderate spesso sono associate a quadri ecografici normali. A volte è possibile evidenziare una lieve linfoadenopatia regionale. Nelle forme più severe è possibile osservare un ispessimento della parete gastrica (maggiore di 7 mm) con aspetto stratificato in genere conservato4. Nell’uomo l’esame ecografico si è inoltre dimostrato altamente sensibile per il riconoscimento o l’esclusione di lesioni infiammatorie associate a ulcere peptiche 5. Tuttavia nel cane la presenza di gas e di residui alimentari, o la difficoltà di riempire in modo adeguato lo stomaco con acqua senza ricorrere alla sedazione, rendono difficile l’osservazione di tutta la parete gastrica. L’esame endoscopico resta quindi ancora oggi la metodica più sensibile per l’identificazione delle ulcere 6 , e, deve sempre seguire l’esame ecotomografico nel caso esso non evidenzi lesioni morfologiche della parete gastrica in pazienti con anamnesi (assunzione di farmaci antiinfiammatori) e sintomatologia riconducibili ad ulcera gastrica 1. I quadri ecografici di più frequente riscontro sono rappresentati da: ispessimento localizzato della parete gastrica, perdita dell’aspetto stratificato della parete, difetto di parete o cratere, aumentata quantità di contenuto liquido, e diminuita motilità gastrica 6.

La gastropatia uremica presenta un quadro ecografico tipico rappresentato dall’aspetto iperecogeno della mucosa in seguito a fenomeni di mineralizzazione della stessa. Altre patologie diverse dall’insufficienza renale possono determinare una mineralizzazione della mucosa gastrica tra cui neoplasie, iperparatiroidismo primario, e altre patologie causanti calcificazioni distrofiche 7.

Un’altra patologia che presenta un quadro ecografico caratteristico è rappresentata dalla gastropatia ipertrofica pilorica cronica. La malattia colpisce in genere cani di piccola

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taglia anziani ed è caratterizzata da vomito cronico. La malattia è caratterizzata da 3 gradi istologici di gravità correlati alle lesioni ecografiche. I soggetti con grado istologico 1 o 2 della patologia, presentano un aumento dello spessore dello strato muscolare (> 4mm) che appare come un anello ipoecogeno che circonda il piloro. I pazienti con lesioni istologiche più avanzate presentano invece un aumento severo dello spessore parietale (> 9 mm) 8. L’esame ecotomografico rappresenta inoltre un esame utile per la valutazione della funzionalità pilorica post correzione chirurgica.

Le neoplasie gastriche rappresentano un evento relativamente raro nel cane e nel gatto (< 1% di tutte le neoplasie) e colpiscono prevalentemente soggetti anziani 9. L’aspetto ecografico delle lesioni neoplastiche è in genere quello di un ispessimento della parete associata alla perdita dell’aspetto stratificato 10. In un recente studio su 21 casi di neoplasia gastrica si è evidenziato che il rinvenimento di masse focali localizzate nell’antro, associate a ispessimento dello strato muscolare, può essere riferito con maggiore frequenza a leiomioma e a leiomiosarcoma, mentre l’estensione della lesione oltre lo strato della sierosa è maggiormente suggestivo di carcinoma. Nello stesso studio inoltre era osservato come il grado di ispessimento della mucosa, la presenza di ulcere e di linfoadenopatie regionali non permettesse di distinguere tra i diversi tipi di neoplasia 11. La possibilità di eseguire prelievi bioptici mirati permette inoltre di aumentare in modo considerevole la sensibilità diagnostica della metodica, mentre l’osservazione di linfoadenopatie regionali e di eventuali lesioni metastatiche in altre sedi quali il fegato, fa dell’ecografia la metodica di elezione in Medicina Veterinaria per la stadiazione clinica della neoplasia 12.

L’aspetto ecografico dei corpi estranei gastrici, è una conseguenza della loro capacità di riflettere o di essere attraversati dagli ultrasuoni. La maggior parte dei corpi estranei gastrici sia radiopachi che radiotrasparenti presentano in genere un’ombra acustica posteriore più o meno accentuata 4.

Gli oggetti che possono essere attraversati dagli ultrasuoni (palline o oggetti di gomma) in genere sono di più facile riconoscimento, dal momento che l’immagine ecografica ne ripete la forma 13.

INTESTINO Le enteriti non sono di solito associate rilievi ecografici di rilievo se non, in alcuni casi, la presenza di una modesta linfoadenopatia regionale. Nel caso invece il processo infiammatorio determini delle modificazioni parietali, queste sono rappresentate in genere dalla presenza di un ispessimento più o meno generalizzato della parete con conservazione dell’aspetto stratificato.

Di solito tale reperto è associato a diminuzione dell’attività peristaltica. Alcune forme virali (parvovirosi) determinano come unico reperto ecografico un quadro di ileo paralitico avanzato non associato a modificazioni morfologiche a carico della parete 4. Un aspetto particolare, indicativo di infiammazione intestinale, è rappresentato dall’aspetto “corrugato” del duodeno che si osserva in corso di pancreatite 1,3.

Si ricorda che tale reperto è normale nel gatto e può anche essere associato a ileo meccanico nelle regioni a monte del-

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l’ostruzione 4.

Altri aspetti caratteristici ecografici sono quelli prodotti dall’invaginamento intestinale. In tale situazione l’ecografia evidenzia la presenza di lesioni pluristratificate con aspetto a “bersaglio” nelle sezioni trasversali, e di “tridente” in quelle longitudinali. In caso di soggetti anziani deve essere posta particolare attenzione nell’individuazione delle possibili cause dell’intussuscezione quali la presenza di neoplasie, o di corpi estranei 14. Per quanto concerne l’identificazione di corpi estranei, l’esame ecotomografico può essere di particolare aiuto soprattutto per l’identificazione di quelli filiformi in genere associati a alla presenza di un aspetto “corrugato” dovuto all’aumento della peristalsi.

La maggior parte delle neoplasie intestinali sono caratterizzate da un ispessimento parietale associato a perdita del normale aspetto stratificato 4. La sensibilità dell’esame ecografico rispetto a quello radiologico per il riconoscimento delle neoplasie intestinali appare superiore. In uno studio su 13 casi di tumore intestinale nel cane, l’ecografia risultò in grado di riconoscere correttamente una massa addominale in 12 soggetti, e l’origine intestinale di tale massa in 10 soggetti, mentre l’esame radiologico fu in grado di evidenziare la presenza di una lesione a tipo massa in addome in soli 5 soggetti 15. L’esame ecografico tuttavia non presenta in genere aspetti tipici in grado di differenziare tra le diverse neoplasie, sebbene la possibilità di eseguire prelievi bioptici mirati dalle lesioni osservate consenta di aumentare in modo significativo la specificità diagnostica. L’adenocarcinoma si presenta in genere come una massa eccentrica ad ecogenicità mista con perdita del normale aspetto stratificato. Le lesioni a volte appaiono però di tipo simmetrico con aspetti simili a quelli del linfoma alimentare 16. Il leiomioma ed il leiomiosarcoma sono neoplasie a partenza dallo strato muscolare di relativo raro riscontro nel cane e nel gatto. Da un punto di vista ecografico nell’uomo tali neoplasie sono caratterizzate dalla presenza di aree di necrosi, emorragie e degenerazione mixoide che appaiono come aree ipo/anaecogene all’interno della massa neoplastica 17. Tale quadro è stato riportato anche nel 75% dei cani colpiti da leiomioma e leiomiosarcoma 16 . Il linfoma alimentare si presenta invece tipicamente come un ispessimento simmetrico della parete con perdita del normale aspetto stratificato; il tratto colpito appare in genere ipo/anecogeno e con diminuzione della peristalsi 18. Il linfoma alimentare è considerato la neoplasia di più frequente ri-

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scontro nel gatto. In uno studio preliminare del nostro gruppo il linfoma alimentare rappresentava l’83% di tutte le neoplasie intestinali individuate nel gatto. Analogamente a quanto riportato nell’uomo anche nel gatto il linfoma alimentare può presentarsi con altri aspetti quali ispessimento eccentrico segmentale, infiltrazione nodulare, massa eccentrica, o infiltrazione mucosale 18.

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Lamb CR, (1999), Recent developments in diagnostic imaging of the gastrointestinal tract of the dog and cat, Vet. Clin. Of North Am. Small Anim. Pract., 29: 307-341.

Crystal MA et al., (1993), Use of ultrasound-guided fine needle aspiration biopsy and automated core biopsy for the diagnosis of gastrointestinal disease in small animals, Vet. Radiol. & US, 34: 438-444.

Borgarelli M et al., (1997), Esame ecografico dell’apparato gastroenterico (parte I): anatomia ecografica e reperti normali, Veterinaria 10 (3): 43-51.

Green RW, (1996), Small animal ultrasound, Lippincot-Raven, Philadelphia, 149-175.

Worlicek H et al., (1989), Ultrasonic examination of the fluid-filled stomach, Journ. Of Clinic.Ultr. 17: 5-14.

Penninck D et al., (1997), Ultrasonography of gastric ulceration in the dog, Vet. Radiol. & US, 38: 308-312.

Grooters AM et al., (1994), Sonographic appearance of uremic gastropathy in four dogs, Vet. Radiol. & US, 35: 35-40.

Biller DS et al., (1994), Ultrasonographic appearance of chronic hypertrophic pyloric gastropathy in the dog, Vet. Radiol. & US, 35: 3033.

Ettinger SJ & Feldman EC, (1995), Textbook of veterinary internal medicine, WB Saunders, Philadelphia, 1143-1168.

Rivers BJ et al., (1997), Canine gastric neoplasia: utility of ultrasonography in diagnosis, J. Am. Anim. Hosp. Assoc., 33: 144-155.

Lamb CR & Grierson J, (1999), Ultrasonographic appearance of primary gastric neoplasia in 21 dogs, J. Small Anim. Pract., 40: 211-215.

Penninck DG et al., (1998), Ultrasonography of canine gastric epithelial neoplasia, Vet. Radiol. & US, 39: 342-348.

Tidwell AS & Penninck DG, (1992), Ultrasonography of gastrointestinal foreign bodies, Vet. Radiol. & US, 33: 160-169.

Lamb CR & mantis P, (1998), Ultrasonographic features of intestinal intussusception in 10 dogs, J. Small Anim. Pract. 39: 437-441.

Meyers III NC & Penninck DG, (1994), Ultrasonographic diagnosis of gastrointestinal smooth muscle tumors in the dog, Vet. Radiol. & US, 35: 391-397.

Rivers BJ & al., (1997), Ultrasonographic features of intestinal adenocarcinoma in five cats, Vet. Radiol. & US, 38: 300-306.

Rowley VA & Cooberg PL, (1982), The ultrasonographic appearance of abdominal leiomyosarcoma, J. Can. Ass. of Rad. 33: 94-97.

Penninck DG et al., (1994), Ultrasonography of alimentary lymphosarcoma in the cat, Vet. Radiol. & US, 35: 299-304.

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Impiego dell’ecografia nella diagnosi e nel trattamento delle patologie prostatiche Michele Borgarelli Med. Vet., Dipl. ECVIM-CA (Cardiology) - Libero Professionista - Torino

Riassunto Rispetto alle metodiche classiche (palpazione e esame radiologico) lo studio ecografico della prostata presenta il vantaggio di permettere una misurazione attendibile e ripetibile delle dimensioni dell’organo e di valutarne la morfologia in modo non invasivo. I limiti dello studio ultrasonografico sono da associare alla mancanza di specificità delle lesioni osservate. Tuttavia il quadro clinico e gli eventuali reperti di laboratorio associati ai rinvenimenti ecografici consentono di raggiungere una diagnosi nella maggior parte dei casi. In caso di sussistenza di dubbi diagnostici, l’esame ecografico consentendo l’esecuzione di aghi aspirati o di biopsie mirate, permette di raggiungere una diagnosi definitiva in modo mini-invasivo e con bassi rischi di complicazioni.

L’aspetto normale della prostata è quello di una struttura uniforme moderatamente iperecogena caratterizzata da echi fitti e grossolani. La ghiandola presenta un aspetto bilobato con margini lisci e capsula iperecogena che appare solo parzialmente visibile nella singola scansione. Normalmente l’uretra prostatica appare visibile solo in condizione di replezione della vescica e si presenta come una struttura tubulare anaecogena che attraversa l’organo in senso cranio caudale. Le dimensioni normali della prostata variano in relazione all’età e al peso dei soggetti tuttavia è necessario ricordare che virtualmente tutti i soggetti interi sopra i 2,5 anni sviluppano una iperplasia prostatica benigna.

Gli aspetti ecografici delle diverse patologie prostatiche sono in genere associati ad aumento delle dimensioni dell’organo con aspetti di iperecogenicità di disomogeneità parenchimale. Frequente è il reperto di cavità cistiche singole o multiple di diversa dimensione. Il reperto di foci di mineralizzazione è in genere associato a prostatite cronica batterica e a neoplasia. Il reperto di una prostata con aspetto disomogeneo e/o di dimensioni aumentate in soggetti castrati è altamente sospetta di neoplasia.

L’esame ecografico oltre che per la descrizione delle lesioni e la valutazione delle dimensioni dell’organo, si dimostra un’ottima tecnica anche per la valutazione del follow-up dei pazienti sottoposti a terapia. Inoltre esso permette di drenare con relativa sicurezza cavità cistiche di grosse dimensioni e ascessi che colpiscano la prostata.

INTRODUZIONE La prostata è l’unica ghiandola sessuale accessoria del cane maschio. Essa è un organo muscolo ghiandolare bilobato retroperitoneale, che circonda l’uretra prossimale tra la sua porzione membranosa e il collo della vescica 1. La posizione della prostata nell’addome caudale dipende dall’età, dallo stadio di replezione della vescica e dalla presenza di eventuali patologie.

Poiché la prostata è soggetta a numerose patologie non necessariamente associate a sintomatologia clinica o a rilievi di laboratorio significativi per periodi anche prolungati, ma che possono spesso esitare in situazioni di malattia anche severa, è importante disporre di indagini strumentali che permettano di riconoscere precocemente tali patologie.

Nel cane la maggior parte delle malattie che affliggono la prostata determina o un aumento delle dimensioni o modificazioni del suo profilo, e le metodiche utilizzate per valutare tali alterazioni sono rappresentate dalla palpazione transrettale, dagli esami radiografici in bianco e con mezzo di contrasto

e dall’esame ecografico. Rispetto alle metodiche classiche (palpazione e esame radiologico) lo studio ecografico presenta il vantaggio di permettere una misurazione attendibile e ripetibile delle dimensioni dell’organo e di valutarne la morfologia in modo non invasivo 1,2,3. I limiti dello studio ultrasonografico sono da associare alla mancanza di specificità delle lesioni osservate. Tuttavia il quadro clinico, gli eventuali reperti di laboratorio associati ai rinvenimenti ecografici consentono di raggiungere una diagnosi nella maggior parte dei casi. In caso di sussistenza di dubbi diagnostici, l’esame ecografico consentendo l’esecuzione di aghi aspirati o di biopsie mirate, permette di raggiungere una diagnosi definitiva in modo mini-invasivo e con bassi rischi di complicazioni 1, 4.

TECNICHE DI ESAME E ASPETTO NORMALE L’esame ecografico della prostata può essere eseguito attraverso l’approccio transaddominale o trasperineale. In al-

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ternativa possono essere utilizzati sia l’approccio transrettale o quello endouretrale 1. L’approccio maggiormente utilizzato nella specie canina è rappresentato da quello transaddominale con il trasduttore posto ai lati del prepuzio. Tale approccio permette un esame ottimo o soddisfacente della ghiandola nella maggior parte dei casi, mentre la presenza di una vescica in moderato o completo stato di replezione, facilita la visualizzazione della prostata poiché ne determina una localizzazione addominale.

L’aspetto normale della prostata è quello di una struttura uniforme moderatamente iperecogena caratterizzata da echi fitti e grossolani 1, 5. La ghiandola presenta un aspetto bilobato con margini lisci e capsula iperecogena che appare solo parzialmente visibile nella singola scansione. Normalmente l’uretra prostatica appare visibile solo in condizione di replezione della vescica e si presenta come una struttura tubulare anaecogena che attraversa l’organo in senso cranio caudale. Nelle sezioni trasversali l’uretra appare come una struttura centrale iperecogena spesso circondata da un’area ipoecogena probabilmente determinata dalla presenza di cellule muscolari lisce (zona ilare). Sempre nelle sezioni trasversali è stata descritta un’area iperecoica centrale a forma di farfalla, con aree ipoecogene dorsali e ventrali, tale area corrisponderebbe nelle sezioni sagittali ad una zona iperecogena con morfologia ovoidale. Tale regione appare correlata alla presenza di una maggiore quantità di collagene, mentre le regioni ipoecogene sono caratterizzate da una maggiore quantità di tessuto ghiandolare 6.

La misurazione ecografica delle dimensioni prostatiche si è rivelata una metodica precisa e ripetibile. Diversi lavori hanno dimostrato l’influenza che età, e peso corporeo esercitano sulle dimensioni della prostata. In genere soggetti anziani e di peso maggiore tendono ad avere una prostata di maggiori dimensioni 2, 7. Tuttavia tale correlazione appare non essere presenti nei soggetti di età inferiore l’anno. Deve anche essere considerato il fatto che l’iperplasia prostatica benigna appare svilupparsi virtualmente in tutti i cani di età superiore ai 2,5 anni influenzando così in modo significativo la correlazione tra dimensioni ed età. In uno studio eseguito su 77 cani, infatti, è stato evidenziato che un sottogruppo di 17 soggetti di età e peso diversi con prostata istologicamente normale non presentava tale correlazione 7. In accordo a tali considerazioni è possibile che qualsiasi ghiandola che misura più di 3-3,5 cm in lunghezza, larghezza e spessore dovrebbe essere considerata patologica 7,8.

ASPETTI ECOGRAFICI PATOLOGICI L’iperplasia prostatica benigna (IPB) è la più comune patologia prostatica del cane. Virtualmente tutti i soggetti anziani maschi non castrati sono colpiti dalla malattia 9. In genere l’IPB compare nei soggetti di età superiore ai 2,5 anni come iperplasia ghiandolare semplice. A questo stadio l’esame ecografico evidenzia un semplice aumento delle dimensioni della ghiandola con profilo conservato. Il parenchima in genere tende ad evidenziare una maggiore ecogenicità associata alla scomparsa della zona ilare. Con il progredire dell’ipertrofia possono svilupparsi delle piccole cisti (cisti da ritenzione). In questo caso lo studio ecotomografico evidenzia

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un organo aumentato di volume, con presenza di piccole cavità anecogene in genere di dimensioni inferiori al centimetro (IPB cistica). La coalescenza di più cavità cistiche può dare origine a cisti di maggiori dimensioni spesso comunicanti con l’uretra e responsabili dello scolo uretrale emorragico presente comunemente nelle forme più severe. La diagnosi presuntiva di IPB può essere in genere espressa accompagnando il dato clinico con l’esame ecografico. Tuttavia deve essere sottolineato che la patologia spesso è presente insieme con altre malattie prostatiche con quadri ultrasonografici simili (metaplasia squamosa, prostatite batterica cronica, neoplasia in stadio iniziale). Nei casi dubbi è necessario effettuare ulteriori accertamenti diagnostici quali l’esame del liquido prostatico, la biopsia con ago sottile o con tru cut 1, 3, 9.

La metaplasia squamosa è una patologia della prostata conseguente ad iperestrogenismo sia endogeno (Sertolioma) sia esogeno (somministrazione di estrogeni per la terapia dell’IPB).

Da un punto di vista ecografico i quadri possono essere diversi. In genere le dimensioni dell’organo appaiono diminuite o comunque inferiori a quelle attese per l’età dei soggetti esaminati. Tuttavia, poiché l’esposizione prolungata agli estrogeni determina tra gli altri effetti collaterali sistemici anche crescita dello stroma fibromuscolare della ghiandola e stasi secretoria 3, in alcuni casi la prostata può apparire aumentata di dimensioni e con presenza di cisti da ritenzione con quadro ecografico del tutto simile a quello dell’IPB o delle prostatiti croniche. L’anamnesi e il contemporaneo esame dei testicoli in questi casi può permettere di formulare una diagnosi presuntiva.

La prostatite batterica acuta si presenta in genere con sintomatologia clinica importante determinata dallo stato setticemico. In questi casi l’esame ecografico evidenzia in genere un organo di dimensioni normali con aspetto ipoecogeno. In alcuni casi si può osservare un aspetto disomogeneo con presenza di alcune piccole aree focali ipo/anaecogene riferibili a edema focale 1.

La prostatite batterica cronica presenta invece quadri ecografici simili all’iperplasia prostatica cistica benigna. Poiché la patologia, analogamente all’IPB, presenta spesso decorso asintomatico per lunghi periodi, il riscontro di una prostata aumentata di dimensioni con parenchima iperecogeno disomogeneo e presenza di cisti multiple deve sempre dar luogo a successivi accertamenti diagnostici per escludere la presenza di una prostatite batterica cronica. In uno studio è stato riportato che la maggiore parte dei cani maschi con infezioni del tratto urinario presenta anche prostatite cronica 10, di conseguenza un esame culturale delle urine può essere dirimente. Altro reperto ecografico a volte visibile nei soggetti con prostatite cronica è rappresentato dalla presenza di foci mineralizzati. Tale rilievo dovrebbe sempre essere seguito dall’esecuzione di una biopsia dell’organo perché spesso rappresenta rinvenimento frequente anche nelle neoplasie 1.

L’ascesso prostatico è in genere il risultato di una prostatite batterica cronica o della localizzazione metastatica secondaria di focolai di infezione in altri distretti dell’organi-

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smo. Da un punto di vista ecografico esso appare come una struttura anaecogena priva di contenuto corpuscolato o con echi irregolari più o meno fitti occupanti la cavità. Di solito i margini appaiono irregolari e le dimensioni sono variabili.

Nei casi di cavità di grosse dimensioni il profilo prostatico può essere alterato 1.

Le neoplasie della prostata presentano una relativa bassa incidenza (5% di tutti i soggetti con patologia prostatica). La neoplasia più frequente è rappresentata dall’adenocarcinoma, seguito dal carcinoma delle cellule di transizione. Non sono state riportate neoplasie benigne prostatiche in letteratura 3. Il rilievo ecografico tipico è rappresentato dalla presenza di una prostata aumentata di volume, con parenchima disomogeneo, foci di mineralizzazione e margini irregolari 1, 11 . In soggetti orchiectomizzati tale reperto può essere altamente indicativo di neoplasia della prostata poiché, a differenza delle altre patologie prostatiche, le neoplasie possono colpire anche i soggetti castrati.

Nei casi di patologie neoplastiche prostatiche lo studio Color Doppler può costituire un ulteriore elemento differenziale. Nell’uomo, infatti, i soggetti affetti da neoplasia presentano un aumento del numero dei segnali Color che assumono spesso aspetto caotico. Tale rilievo è stato descritto anche in caso di prostatite. Nel cane tuttavia non apparirebbero differenze per lo studio Doppler tra normali e quelli con prostatite, mentre non esistono dati riferibili agli studi con Color Doppler 5.

Le cisti paraprostatiche possono derivare dalle rimanenze del dotto di Mueller, da cisti prostatiche da ritenzione o ematomi prostatici 3. In genere le formazioni di derivazione dall’utero mascolino sono localizzate dorsalmente alla linea mediana della prostata. In questi casi la prostata appare normale. Nel caso di cisti di origine prostatica invece spesso la prostata presenta i quadri tipici dell’IPB associata o meno ad altre patologie. Le cisti paraprostatiche di qualunque origine presentano l’aspetto ultrasonografico di grosse strutture anaecogene spesso multiloculate 1.

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metodica di tipo terapeutico nel senso di permetterne il drenaggio e la successiva alcolizzazione in modo mini invasivo.

Nella nostra esperienza il drenaggio ecoguidato di cisti prostatiche seguito dalla alcolizzazione con alcool assoluto della cavità rappresenta un utile modo di ridurre eventuali sequele del trattamento farmacologico e chirurgico (orchiectomia) delle forme più severe di iperplasia cistica benigna.

Ricordiamo che i farmaci e la castrazione non agiscono sulle formazioni cistiche 3, che se di grandi dimensioni possono continuare a essere responsabili di eventuale sintomatologia quale lo scolo emorragico o possono successivamente essere infettate da infezioni delle vie urinarie con trasformazione in ascesso.

Per quanto concerne il drenaggio degli ascessi prostatici è stato riportato che la metodica può presentare rischi di infezione retroperitoneale legata al passaggio di germi lungo il tragitto dell’ago, o di shock settico provocato dall’assorbimento di batteri e delle loro tossine 3. Sebbene tale metodica sia comunemente utilizzata in medicina umana, in medicina veterinaria è ancora consigliato il drenaggio chirurgico con metodiche diverse3. Anche nel trattamento chirurgico sono comunque riportati frequenti complicanze post intervento 12. Recentemente il nostro gruppo ha pubblicato uno studio condotto su 45 casi di ascesso prostatico drenato per via transaddominale sotto guida ecografica. In nessuno dei soggetti di tale studio si sono osservate complicanze a seguito della patologia e solo 4 soggetti hanno presentato recidive ad 1 mese risoltesi comunque con un secondo trattamento (follow up a 6 mesi). Sulla base di tali dati è nostra opinione che il drenaggio percutaneo degli ascessi prostatici possa essere considerato se eseguito da mani esperte un’ottima tecnica di rapida esecuzione e con risultati duraturi, alternativa alla chirurgia.

Bibliografia 1.

2.

3.

UTILITÀ DELL’ECOGRAFIA NELLA TERAPIA DELLE PATOLOGIE PROSTATICHE

4.

Poiché l’esame ecotomografico si è dimostrato una metodica ripetibile ed accurata per la valutazione delle dimensioni prostatiche, essa riveste un ruolo di primaria importanza nel follow up dei pazienti trattati (riduzione delle dimensioni, regressione delle cisti da ritenzione). Inoltre essa permette l’individuazione di eventuali eventi complicanti il normale decorso della patologia. Ad esempio i pazienti trattati con estrogeni per IPB possono presentare quadri di metaplasia squamosa facilmente individuabile con l’esame ecotomografico.

Un discorso particolare deve infine essere fatto per quanto concerne il trattamento delle cisti prostatiche di dimensioni maggiori di 2 cm e degli ascessi prostatici. In caso di tali patologie, infatti, la metodica ecografica permette da un lato una diagnosi precisa per quanto concerne la localizzazione e le dimensioni delle lesioni, dall’altro rappresenta una

6.

5.

7.

8.

9.

10.

11.

12.

13.

Green RW (1996), Small animal ultrasound, Lippincot-Raven, Philadelphia, 237-250 Ruel Y et al.(1998), Ultrasonographic evaluation of the prostate in healthy intact dog, Vet. Radiol & US, 39, 212-216 Ettinger SJ & Feldman EC (1995), Textbook of veterinary internal medicine, WB Saunders, Philadelphia, 1662-1685 Burkhard MJ & Meyer DJ (1996), Invasive cytology of internal organs, Vet. Clin. Of North Am. (Small Anim. Pract.), 26, 1203-1222 Newell SM et al. (1998), Doppler ultrasound of the prostate in normal dogs and in dogs with chronic lymphocytic-lymphoplasmocytic prostatis, Vet. Radiol & US, 39, 332-336 Cooney JC et al. (1992), Ultrasonography of the canine prostate with histologic correlation, Theriogen, 38, 877-895 Atalan G et al. (1999), Ultrasonographic estimation of prostatic size in canine cadavers, Res. In Vet. Scien., 67, 7-15 Lijour L (1993), Echographie de la prostate, Proceed. II International Symposium of Vet. Echography, Nice, March 11-13, 30-36 Barsanti JA (1999), Prostatic hyperplasia: medical therapy, Proceed.

17th ACVIM, Chicago, June 10-13, 536-538 Krawiec DR & Heflin D (1992), Study of prostatic disease in dogs:177 cases (1981-1986), JAVMA, 200, 1119-1122 Bell FW et al. (1991), Clinical and pathological features of prostatic adenocarcinoma in sexually intact and castrated dogs: 31 cases (1970-1987), JAVMA, 199, 1623-1630 Mullen HS et al. (1990), Results of surgery and postoperative complications in 92 dogs treated for prostatic abscessation by a multiple penrose drain technique, JAAHA, 26, 369-379 Bussadori C. et al. (1999), Drenaggio percutaneo degli ascessi prostatici nel cane, La Radiol. Medica in stampa

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Sarcomi iniezione-indotti nel gatto: ipotesi patogenetiche, diagnosi e trattamento Paolo Buracco Med. Vet., Dipl. ECVS - Dipartimento di Patologia Animale - Università di Torino

Giorgio Romanelli Med. Vet., Dipl. ECVS - Libero Professionista - Milano

Riassunto Dagli anni ’80 si è rilevato un aumento di sarcomi felini, specie fibrosarcomi, in sede di inoculo SC di vaccini ed altri preparati. Il rischio è, dopo vaccinazione a virus spento per FeLV e rabbia, 50% in più dopo 1, 127% dopo 2 e 175% dopo 3 inoculi nella stessa sede. L’incidenza è di 20/100.000 gatti; il rischio in Italia è forse più alto perchè non solo i vaccini sono inoculati SC. Sembra oggi accertato che ogni stimolo cronico (vaccini, iniezioni ritardo, corpi estranei) in grado di determinare un’infiammazione granulomatosa può esitare, in soggetti presunti predisposti, in tumore entro 1,56 mesi/3-7 anni. In caso di noduli cutanei a comparsa improvvisa, persistenti da oltre 21 gg, a rapida crescita (> 2 cm) e localizzati nelle sedi di inoculo, si procede a biopsia; l’esame citologico è utile in metà dei casi. L’alto tasso di recidiva (62-86% entro 6 mesi dopo chirurgia incompleta) implica interventi radicali con anche asportazione dell’osso sottostante. La sola chirurgia è stata utilizzata in 14 gatti: sopravvivenza media 533 gg, mediana 365 gg, a 6 mesi 71.4%, a 12 mesi 58.3%, a 2 anni 33.3%, metastasi 0% e recidive 50%. I risultati di chirurgia/radioterapia adiuvante sono discordanti, anche se alcuni Aa. segnalano una diminuzione delle recidive dal 70 al 50%. La nostra casistica (11 gatti, 4560 Gy totali) non è incoraggiante (sopravvivenza a 6 mesi 72%, a 1 anno 27%, a 2 anni 18%, media 368 e mediana 243 gg, recidiva 72%, metastasi 18%). L’associazione di chirurgia radicale/chemioterapia è in studio. La casistica personale è relativa a 19 gatti (doxorubicina ogni 21 gg per 4 volte -1 mg/kg ev.-, chirurgia 10 gg dopo il 2o trattamento): sopravvivenza a 6 e 12 mesi, 90.9 e 80%, media 212 gg, mediana 121 gg; 18 gatti tuttora in vita e “liberi da malattia”.

Per la profilassi, è quindi opportuno a) evitare ogni inoculo interscapolare; b) non usare più vaccini contemporaneamente e nella stessa sede (linee guida della “task-force” americana); 3) immunizzare per rabbia e FeLV solo i gatti a rischio; 4) un adeguato intervallo per i vaccini relativi alle malattie respiratorie/panleucopenia. La chirurgia, per essere efficace, deve essere radicale ed eseguita su lesioni già “biopsiate”; ulteriori terapie (radio-chemio) sono associate in base a condizioni dell’animale, localizzazione del sarcoma e disponibilità del proprietario.

I sarcomi dei tessuti molli rappresentano il 12-25% dei tumori cutanei e sottocutanei felini. Dalla seconda metà degli anni 80 si è però rilevato, prima in USA e poi in Europa, un progressivo aumento (25-61% a seconda della fonte) di sarcomi localizzati nelle sedi di inoculo SC di vaccini ed altre preparazioni iniettabili (regione interscapolare, costato, regione glutea). La forma più comune è il fibrosarcoma (FSA); altri fenotipi sono il condrosarcoma, l’istiocitoma fibroso maligno, l’osteosarcoma extrascheletrico, il sarcoma miofibroblastico, il rabdomiosarcoma, il sarcoma indifferenziato e l’emangiosarcoma. La prima segnalazione al riguardo è di Hendrick e Goldschmidt1; da allora si è molto pubblicato sull’argomento, con anche l’istituzione in USA di una “task force” (VAFSTF) volta ad approfondirne patogenesi, diagnosi e terapia. Gli Aa. americani hanno associato l’au-

mentata incidenza dei sarcomi all’obbligo di vaccinazione antirabbica dei gatti ed alla concomitante diffusione dell’immunizzazione contro FeLV. In USA le uniche inoculazioni sottocutanee praticate sono quelle vaccinali. Gli studi intrapresi hanno evidenziato un incremento di rischio a seguito di vaccinazioni a virus spento contro FeLV (probabilità di 2,82-5) e rabbia (probabilità 1,99). Il rischio è del 50% in più rispetto ai soggetti non vaccinati, passando al 127% dopo 2 e al 175% dopo 3 inoculazioni nella stessa sede2. L’incidenza di tali neoplasie è di 20/100.000 gatti, ma in Europa il rischio è probabilmente più alto perchè non solo i vaccini sono inoculati sottocute. Tra le varie ipotesi patogenetiche, alcune attribuiscono potere carcinogenetico all’idrossido di alluminio, adiuvante nella maggior parte dei vaccini felini inattivati3,4. Tale ipotesi è stata prima avvalorata dal suo re-

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perimento, al M.E., nei macrofagi frammisti alle cellule sarcomatose per essere poi contraddetta dal segnalamento di sarcomi a seguito di vaccinazioni con preparati privi della sostanza. Si è allora supposto che la trasformazione tumorale fosse indotta da processi infiammatori cronici causati da vaccini contenenti adiuvanti anche diversi4. Nuovo significato patogenetico assumevano i quadri istologici di pannicolite focale granulomatosa necrotizzante nella sede di iniezione, prima per lo più interpretati come semplici “reazioni vaccinali”. Lo stimolo cronico come fattore causale era comunque avvalorato dai casi di sarcoma oculare felino a seguito di traumi anche pregressi5; così come, nell’uomo e negli animali, dalla possibile induzione neoplastica dopo impianto di corpi estranei diversi6. Alcuni Aa. hanno tuttavia sostenuto che fosse la stimolazione antigenica specifica ad aumentare la probabilità di sviluppo tumorale sottolineando che, benchè fosse il vaccino antirabbico ad indurre le più gravi risposte infiammatorie, i rischi maggiori si rilevavano dopo vaccinazione anti-FeLV7: ciò per il fatto che gli antigeni vaccinali sono in grado di stimolare la formazione di citochine o di fattori di crescita più facilmente soggetti a trasformazione tumorale. In realtà, laddove la vaccinazione anti-FeLV e antirabbica è poco diffusa (Europa e Giappone), l’incidenza di sarcomi post-immunizzazione per panleucopenia e virus respiratori è in aumento. Qualsiasi stimolo irritativo cronico (vaccini, soprattutto se ripetuti; iniezioni long-acting8, corpi estranei, compresi i fili non riassorbibili nei piani profondi) può quindi determinare granulomi o stati di infiammazione cronica in grado di interferire con la normale riparazione del connettivo, esitando eventualmente in sarcoma. L’immunoistochimica evidenzia spesso un fenotipo mioblastico/miofibroblastico, stadio di transizione di fibroblasti e/o macrofagi e normale componente del processo di guarigione delle ferite4, con anche aree di transizione (infiammazione/tessuto tumorale). La trasformazione neoplastica si verifica in 1,5-6 mesi-3 anni (per alcuni fino a 7). Ciò implica un’accurata anamnesi per risalire anche a singole inoculazioni, eseguite anche molto tempo prima. Rimane tuttavia oscura l’ipotesi di una predisposizione individuale visto che solo in 2 gatti su 10.000 si verifica il tumore7. L’ infiammazione post-iniezione non è prerogativa del gatto, ma questa specie sarebbe unica per sensibilità e capacità di attivazione di oncogeni. Si sono infatti rilevate effettive mutazioni della p53 (gene oncosoppressore coinvolto nella cancerogenesi) anche in aree di tessuto morfologicamente normale alla periferia dei sarcomi.

Per la diagnosi, la VAFSTF ha elaborato linee guida volte a definire il comportamento da adottare per i noduli comparsi improvvisamente nelle sedi di inoculo, a rapida crescita (oltre 2-4 cm alla presentazione), persistenti da oltre 3 settimane, eventualmente adesi ai piani profondi, di forma irregolare e a margini poco definiti. Si esegue in questi casi una biopsia incisionale o con tru-cut, scegliendo un’area poi facilmente rimovibile nella successiva chirurgia. La biopsia ad ago sottile fornisce indicazioni solo nel 50% dei casi; nei rimanenti è dubbia a causa della scarsa cellularità, della necrosi o del prelievo di liquido cistico. L’esame istologico permette la diagnosi definitiva, differenziando tra l’altro i sarcomi “iniezione-” da quelli “non-iniezione indotti”. I primi infatti originano più in profondità (sottocute e fascia) e

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sono caratterizzati da indice mitotico più elevato, pleomorfismo cellulare variabile e marcata reazione infiammatoria (linfociti e macrofagi, eventuale materiale fagocitato); possono inoltre rilevarsi aree di necrosi e colliquazione. È bene poi effettuare la palpazione dei linfonodi regionali (raramente colpiti) e l’esame Rx del torace (LL dx e sx) per escludere metastasi e per valutare l’eventuale estensione alle vertebre. A differenza dei sarcomi non-iniezione indotti dove il tasso metastatico è del 20-25%, in quelli post-iniettivi si rilevano metastasi nel 20-70% dei casi9-10. Opportuni, infine, lo screening ematologico preoperatorio e i tests per FIV e FeLV, gli ultimi in genere negativi.

Il trattamento è tuttora oggetto di valutazione. Il problema principale è l’elevato grado di infiltrazione locale della neoplasia e, di conseguenza, l’elevato tasso di recidiva locale (62-86% entro 6 mesi dall’asportazione non corretta, contro il 14-20% in caso di sarcomi non-iniezione indotti). La recidiva potrebbe comunque spiegarsi anche sulla base dell’ampia area di tessuto attivato dal processo infiammatorio: la nuova lesione potrebbe quindi provenire da un’ulteriore sede di induzione neoplastica. Questo giustifica l’escissione del tumore con un margine di 3 cm almeno su tutti i piani, compreso quello osseo profondo se necessario (processi spinosi, coste, porzioni di pelvi o scapola), fino all’amputazione dell’arto. In molti casi è necessario operare la chiusura mediante plastiche cutanee o miocutanee. La casistica degli Aa. inerente l’utilizzo della sola chirurgia è relativa a 12 gatti con FSA e a 2 con rabdomiosarcoma post-iniettivi. La sopravvivenza media è risultata di 533 giorni (75-1401) e la mediana di 365, con percentuale di sopravvivenza a 6 mesi del 71.4%, a 12 mesi del 58.3% e a 2 anni del 33.3%. La percentuale di metastasi è risultata 0, mentre quello di recidiva del 50%. Di questi (7), 3 (42,8%) erano già stati riferiti per lesioni conseguenti a precedenti interventi. Tre gatti (30%) sono morti per cause non correlate al tumore.

In diversi studi, alla chirurgia si sono associate la radioo la chemioterapia od una combinazione delle due. I risultati di chirurgia-radioterapia adiuvante sono discordanti. Secondo alcuni si avrebbe diminuzione del tasso di recidiva dal 70 al 50% con dosi totali di radiazioni di 45-50 Gy, erogate in frazioni quotidiane o a giorni alterni con apparecchi a megavoltaggio11. Altri segnalano risultati migliori con dosi più basse (30-35 Gy in 4-5 frazioni). La nostra personale casistica, ottenuta irradiando 11 gatti precedentemente sottoposti a chirurgia con dosi totali di 45-60 Gy, 12 frazioni a giorni alterni con apparecchio ad ortovoltaggio12, ha dato risultati poco incoraggianti. La sopravvivenza a 6 mesi è stata del 72%, ma è scesa al 27% ad 1 anno e a 18% a 2 anni; dei 2 soggetti ancora vivi (827 e 1172 giorni), uno ha sviluppato recidiva locale dopo 283 giorni ed è stato operato altre 2 volte e sottoposto a chemioterapia con doxorubicina (1 mg/kg), mentre il secondo è tuttora libero da malattia. I 9 gatti deceduti sono stati soppressi per recidiva locale ad eccezione di uno, morto per cause non correlate al tumore dopo 210 giorni; in 2 casi (entrambi con istiocitoma fibroso maligno) sono state rilevate anche metastasi polmonari. Il tasso di recidiva locale è risultato del 72%, quello metastatico del 18%; la sopravvivenza media di 368 giorni (97-1172) e la mediana di 243. L’elevato tasso di insuccesso può in parte giustificarsi per il fatto che 6 dei 9 gatti nei quali si è avuta reci-

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diva (66.6%) erano già stati riferiti per recidive conseguenti a chirurgia incompleta. Recentemente si è proposta la brachiterapia adiuvante al fine di erogare alte dosi di radiazione senza danneggiare eccessivamente i tessuti sani circostanti.

Risultati incoraggianti derivano dall’associazione chirurgia radicale-chemioterapia. Tra i farmaci proposti (doxorubicina, carboplatino, mitoxantrone, ciclofosfamide), il protocollo attualmente utilizzato dagli Aa. prevede doxorubicina (1 mg/kg e.v.) ogni 21 giorni per 4 volte; la chirurgia è pianificata 10 giorni dopo il secondo trattamento. Sono per ora disponibili i dati relativi a 19 gatti: follow-up di 65-456 giorni, sopravvivenza a 6 e 12 mesi rispettivamente del 90.9 e 80%. Solo 1 gatto (con istiocitoma fibroso maligno già recidivo alla presentazione) ha sviluppato recidiva e metastasi ed è stato soppresso dopo 128 giorni. La sopravvivenza media è di 212 giorni, la mediana di 121, 18 soggetti sono ancora in vita e “liberi da malattia”.

Sperimentazioni condotte da molti Aa. prevedono oggi la chirurgia (caposaldo terapeutico) e l’associazione con modulatori di immunità e biologici, terapie geniche e trattamenti fotodinamici.

Per i sarcomi iniezione-indotti felini, occorre quindi una profilassi che escluda le iniezioni SC interscapolari optando, se proprio necessario, per il sottocute della regione laterale del torace (più facilmente aggredibile dalla chirurgia). La VAFSTF consiglia, per standardizzare gli studi, di vaccinare per la rabbia SC nella gamba destra, per la leucemia nella sinistra e per le malattie respiratorie/panleucopenia nella spalla destra, evitando più vaccini contemporaneamente. L’insorgenza di sarcomi a livello muscolare è possibile; questi, essendo più profondi, sono diagnosticati più tardivamente13.

L’immunizzazione per rabbia e FeLV è consigliata solo nei soggetti realmente a rischio; per le malattie respiratorie/panleucopenia, secondo invece uno schema temporale adeguato (durata effettiva della copertura anticorpale). Le lesioni persistenti per più di 6 settimane vanno sottoposte a biopsia in

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quanto la maggior probabilità di successo si ha al primo intervento e su noduli di piccole dimensioni. La chirurgia deve essere radicale su ogni piano mentre la scelta di associare ulteriori terapie (radiazioni o chemioterapici) potrà variare in base alle condizioni generali dell’animale, alla localizzazione del sarcoma ed alla disponbilità del proprietario.

BIBLIOGRAFIA (limitata; il resto disponibile presso gli autori) 1) 2)

3)

4) 5) 6) 7) 8) 9)

10)

11) 12)

13)

Hendrick MJ, Goldschmidt MH, (1991), Do injection site reactions induce fibrosarcomas in cats? JAVMA, 99: 968.

Kass PH et al., (1993), Epidemiologic evidence for a causal relation between vaccination and fibrosarcoma tumorigenesis in cats. JAVMA, 203: 396-405.

Hendrick MJ et al., (1992), Postvaccinal sarcomas in the cat: epidemiology and electron probe microanalytical identification of aluminum. Cancer Res, 52: 5391-5394.

Hendrick MJ, Brooks JJ, (1994), Postvaccinal sarcomas in the cat: histology and immunohistochemistry. Vet Pathol, 31: 126-129.

Dubielzig RR, (1984) Ocular sarcoma following trauma in three cats.

JAVMA, 184: 578-581.

Sinibaldi K et al., (1976), Tumors associated with metallic implants in animals. Clin Orthop Rel Res: 118, 257-266.

Macy DW, (1995), The potential role and mechanisms of FeLV vaccine-induced neoplasm. Seminars in Vet Med and Surg, 10: 234-237.

Esplin DG et al., (1999), Fibrosarcoma at the site of a Lufenuron injection in a cat. Vet Cancer Soc Newsletter 23(2): 8-9.

Hendrick MJ et al., (1994), Comparison of fibrosarcomas that developed at vaccination sites and non vaccination sites in cats: 239 cases (1991-1992). JAVMA 205: 1425-1429.

Couto CG, (1998), Selected neoplasm in cats and dogs. In: Small animal internal medicine, a cura di Nelson RW & Couto GC, Mosby, St. Louis, Baltimore, Boston, Carlsbad, Chicago, Minneapolis, New York, Philadelphia, Portland, London, Mila, Sydney, Tokyo, Toronto, sec. ediz., 1153-1154.

Cronin K et al., (1998), Radiation therapy and surgery for fibrosarcoma in 33 cats. Vet Radiol and Ultrasound, 39: 51-56.

Martano M et al. (1999), La radioterapia nel trattamento delle neoplasie del cane e del gatto. Parte I: principi di applicazione. Veterinaria (5): 25-39.

Macy DW, (1999), Current understandig of vaccination site-associated sarcomas in the cat. J Feline Med and Surg 1: 15-21.

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Sfide in chirurgia oncologica: come demolire e ricostruire la testa nel cane e nel gatto Paolo Buracco Med. Vet., Dipl. ECVS - Dipartimento di Patologia Animale - UniversitĂ di Torino

Giorgio Romanelli Med. Vet., Dipl. ECVS - Libero Professionista - Milano

Riassunto Gli autori, attraverso una rassegna di casi clinici, presentano diversi aspetti di chirurgia demolitiva e ricostruttiva per lesioni (per lo piĂš neoplasie) a diversa localizzazione a livello della testa. Verranno pertanto proposti casi di risoluzione chirurgica a livello di palpebra, labbro, guancia, naso, bocca (compresa lingua) ed orecchio; saranno inoltre descritti interventi per lesioni tumorali di alcune ossa craniche.

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Citologia delle neoformazioni cutanee Mario Caniatti Med. Vet., Dipl. ECVP - Istituto di Anatomia Patologica Veterinaria e Patologia Aviare - Università di Milano

Riassunto Le lesioni cutanee sono tra i più comuni problemi per il veterinario nella sua pratica quotidiana.

ESPERIENZE PERSONALI1 - In uno studio retrospettivo sono stati valutati 222 aspirati, colorati con una colorazione tipo Romanowsky, di neoformazioni cutanee nel cane (182 casi) e nel gatto (40 casi). I tutti i casi era disponibile un esame istologico di controllo. La diagnosi citologica era definita nel modo seguente: inadeguato (43, 19,4%); positivo per neoplasia (117 casi, 52,7%) e negativo per neoplasia (62 casi, 27,9%). I campioni definiti come inadeguati (18 processi infiammatori, 10 neoplasie benigne, 10 sarcomi e 5 tumori epiteliali maligni) erano dovuti a scarsa cellularità, cattiva conservazione del campione o necrosi. Questi campioni erano esclusi dallo studio comparativo e perciò la percentuale di recupero è stata del 80,6%. I 117 casi citologicamente diagnosticati come neoplastici erano: 41 tumori maligni a cellule fusate; 39 tumori a cellule rotonde (23 mastocitomi); 31 tumori epiteliali (7 benigni); 3 melanomi; 3 neoplasie indifferenziate (sarcomi all’esame istologico). Non erano mai eseguite diagnosi false positive per neoplasia. Interessante notare come negli emangiopericitomi si siano evidenziate cellule giganti multinucleate, da noi chiamate “crown cells” (cellule a corona), tipiche e patognomoniche per la disposizione dei nuclei in quasi perfetto cerchio ai margini della membrana citoplasmatica. In 34 casi la diagnosi citologica negativa per neoplasia era in accordo con l’istologia, mentre in 28 casi (14 tumori epiteliali e 14 tumori a cellule fusate) veniva fatta una diagnosi citologica falsa negativa. Sulla base dei 179 casi in cui era fatta una diagnosi citologica, i nostri risultati hanno mostrato un complessivo accordo tra diagnosi citologica e istologica dell’84,4% (151/179). La sensibilità è stata del 80,7%, la specificità e il valore predittivo dei risultati positivi (neoplasie) sono state del 100%, mentre il valore predittivo dei risultati negativi (lesione non neoplastica) è stato del 54,8%. Questi risultati confermano il valore dell’aspirazione con ago sottile nella gestione clinica delle neoformazioni cutanee, particolarmente nei riguardi della diagnosi delle forme neoplastiche.

Bibliografia -1. Caniatti M, Ceruti R, Ghisleni G et al., (1999), Correlations between fine needle aspiration (FNA) and histology in 222 palpable cutaneous lesions of dogs and cats, Abstracts XVII Meeting European Society of Veterinary Pathology, Nantes, September 14-17, pag. 121.

Le lesioni superficiali, coinvolgenti i tessuti cutanei e sottocutanei sono tra i più comuni problemi con i quali si confronta il veterinario nella sua pratica quotidiana. La valutazione citologica di queste lesioni può essere diagnostica in un buon numero di casi, oppure può portare ad una parziale caratterizzazione del processo. Tale caratterizzazione sarà comunque utile al clinico perché restringerà il campo delle ipotesi diagnostiche differenziali e condurrà a scegliere mirate indagini addizionali (biopsia, coltura, radiografia ecc.).

Non va dimenticato che, in un certo numero di casi, l’esame citologico di lesioni cutanee non porterà alcuna informazione utile per la diagnosi o per la gestione del paziente; in questi casi si può procedere nel work-up senza aver perso molto in termini di tempo e denaro.

La collezione del campione è relativamente facile e normalmente avviene per apposizione, scarificazione o prelievo con ago sottile in funzione dei caratteri clinici della lesione da valutare (es. un’ulcera può essere valutata con apposizione o scarificazione, una neoformazione va campionata con ago sottile). Per quanto riguarda i prelievi con ago sottile può essere scelta una tecnica aspirativa o meno (infissione) in funzione del gusto e sensibilità dell’operatore non essendoci dati scientifici che sicuramente fanno ritenere una delle due tecniche superiore all’altra.

Nel corso di questa trattazione si farà particolare riferimento alla citologia delle neoformazioni cutanee tralasciando, o affrontando marginalmente, i campioni citologici ottenuti da lesioni cutanee di stretto interesse dermatologico (es. piodermiti, pemfigo ecc.).

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40° Congresso Nazionale SCIVAC

REPERTI CITOLOGICI NORMALI

Lesioni non infiammatorie/non neoplastiche

In citologia la conoscenza del quadro citologico normale per un determinato organo o tessuto è particolarmente importante e basilare per poter affrontare lo studio di un campione patologico.

La cute in questo senso fa eccezione in quanto in condizioni normali un prelievo citologico risulterà “praticamente acellulare” oppure conterrà occasionali e rari reperti riferibili a cellule cheratinizzate o frammenti di annessi cutanei (peli, ghiandole). In caso contrario (campione adeguatamente cellulare), tutto ciò che osserviamo nel vetrino è espressione, primitiva o secondaria, della patologia sottesa.

Cisti cheratiniche o dermoidi sono neoformazioni molto comuni e di facile diagnosi citologica in termini di benignità. Molto più difficile, se non impossibile, la diagnosi differenziale con tumori benigni del follicolo pilifero, anch’essi fortunatamente caratterizzati da comportamento benigno.

La calcinosis circumscripta è caratteristica dei soggetti giovani (soprattutto nel cane, ma anche nel gatto è descritta), in particolare nel pastore tedesco. Importante il reperto macroscopico, virtualmente diagnostico, di materiale di aspetto biancastro “gessoso” sul vetrino.

Gli eritrociti una volta che hanno lasciato il letto vasale vengono considerati corpi estranei e sono fagocitati dai macrofagi e da questi degradati. Gli ematomi hanno caratteri citologici diversi in relazione alla loro età in quanto l’eritrofagocitosi può essere distinta in recente (fagocitosi di eritrociti ben conservati) o di più vecchia data (presenza di prodotti di degradazione come emosiderina e ematoidina).

Il mucocele cede materiale fluido viscoso che citologicamente è di solito caratterizzato da un moderato numero di macrofagi schiumosi su di un fondo di materiale rosato proteinaceo.

REPERTI PATOLOGICI Lesioni infiammatorie Il quadro citologico in corso di flogosi (suppurativo, piogranulomatoso ecc.) ed eventuali aspetti degenerativi leucocitari possono dare indicazioni sul tipo di agente, infettivo o meno, eventualmente presente primariamente o secondariamente nella lesione.

Flogosi ad eziologia infettiva: Nel caso di forme infettive (batteriche, micotiche e virali), la presenza numerosa o meno dei microrganismi nel campione citologico è assai variabile e in funzione delle caratteristiche dell’ospite, della patogenicità del microrganismo e di eventuali trattamenti antimicrobici cui il paziente è stato sottoposto nei giorni antecedenti il prelievo.

Con le classiche colorazioni tipo Romanowsky (Hemacolor, Diff-Quik, Giemsa, Wright ecc.) la maggior parte dei batteri si colora in blu indipendentemente da come si colora con la colorazione di Gram. La morfologia dei singoli batteri può essere molto importante per la diagnosi o per indirizzare l’esame colturale (es. Nocardia, Actinomyces, Dermatophilus congolensis ecc.). I micobatteri non si colorano con le classiche colorazioni tipo Romanowsky, ma questo è di grande significato diagnostico in quanto appaiono come immagini negative nel citoplasma dei macrofagi che li hanno fagocitati.

Le infezioni fungine hanno la caratteristica di evocare nella maggior parte dei casi una flogosi mista prevalentemente macrofagica e in parte neutrofilica con eventuale presenza di varie altre cellule infiammatorie, soprattutto linfociti, plasmacellule e eosinofili, nonché fusate reattive. Ne consegue che in caso di reperti citologico di questo tipo deve essere fatta un’attenta ricerca nei confronti di eventuali agenti micotici.

Flogosi ad eziologia non infettiva: Un certo numero di condizioni infiammatorie della cute e dei tessuti sottocutanei sono il risultato di una causa non infettiva anche se, purtroppo, spesso presentano un’infezione batterica secondaria che complica e rende difficile la diagnosi citologica. Tra queste, le forme più comuni sono la pannicolite (flogosi del grasso sottocutaneo) che comunque può essere causata anche da agenti infettivi, ma più spesso è sterile, nonché le forme di flogosi eosinofilica.

Neoplasie Come regola generale, dal punto di vista citologico possono essere diagnosticati tre tipi di neoplasie: epiteliali, a cellule fusate e a cellule rotonde.

Tumori epiteliali: sono comuni. La diagnosi citologica di queste neoplasie si basa sul reperto di gruppi di cellule coesive che mostrano segni di malignità citologica. Tra i più comuni tumori epiteliali della cute si annoverano il carcinoma squamoso, gli epiteliomi e gli adenomi perianali (questi ultimi citologicamente indistinguibili dall’iperplasia). Nei carcinomi squamosi, la cui diagnosi è spesso resa difficile dalla concomitante flogosi neutrofilica (vuoi perché tendono ad ulcerare e quindi a infettarsi, vuoi perché la cheratina è un potente stimolo flogogeno), il reperto più caratteristico è quello della maturazione asincrona della cellula (nucleo di aspetto giovanile in cellula con citoplasma ampiamente cheratinizzato). Gli epteliomi sono caratterizzati dalla presenza di gruppi uniformi di cellule relativamente piccole e con un elevato rapporto nucleo:citoplasmatico. Gli adenomi delle ghiandole epatoidi sono facilmente riconoscibili per l’aspetto citologico delle singole cellule che, voluminose e con abbondante citoplasma granuloso, ricordano assai da vicino gli epatociti. Questo aiuta anche nella diagnosi di neoplasie di ghiandole epatodi ectopiche che sono relativamente comuni a livello di coscia, prepuzio, coda ecc.

Tumori a cellule fusate: Di non facile diagnosi citologica in quanto esfoliano con difficoltà. I lipomi non sono diagnosticabili come tali con l’esame citologico in quanto sono indistinguibili dal normale grasso sottocutaneo. Di solito i tumori a cellule fusate vengono definiti citologicamente come tali, ma generalmente non si ritiene sia possibile definire meglio citologicamente queste entità anche se eccezioni sono descritte.

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Tumori a cellule rotonde: In sede cutanea i più comuni tra questi tumori sono senz’altro il mastocitoma e l’istiocitoma del cane giovane. La diagnosi di queste forme è piuttosto agevole sul campione citologico in quanto si tratta in generale di campioni molto cellulari, con eccezione di alcuni istiocitomi, in cui le cellule sono di solito facili da riconoscere come citotipo.

Melanomi Le cellule dei melanomi, tipicamente caratterizzate dalla presenza di granuli citoplasmatici di pigmento melanico, possono assumere aspetti assai variabili sotto forma di cellule rotonde, fusate o similepiteliali. Ciò crea grossi problemi in quei melanomi caratterizzati da pigmento scarsissimo o assente (melanomi amelanotici).

ESPERIENZE PERSONALI1 In uno studio retrospettivo sono stati valutati 222 aspirati di neoformazioni cutanee nel cane (182 casi) e nel gatto (40 casi). I tutti i casi studiati (aspirati prelevati da clinici, fissati all’aria e colorati con una colorazione tipo Romanowsky) era disponibile un esame istologico di controllo per valutare la bontà della diagnosi citologica.

La diagnosi citologica era definita nel modo seguente: inadeguato (43 casi, 19,4%); positivo per neoplasia (117 casi, 52,7%) e negativo per neoplasia (62 casi, 27,9%).

I campioni definiti come inadeguati (18 processi infiammatori, 10 neoplasie benigne, 10 sarcomi e 5 tumori epiteliali maligni) erano dovuti a scarsa cellularità, cattiva conservazione del campione o necrosi. Questi campioni erano esclusi dallo studio comparativo e perciò la percentuale di recupero è stata del 80,6%.

I 117 casi citologicamente diagnosticati come neoplastici erano: 41 tumori maligni a cellule fusate; 39 tumori a cellule rotonde (23 mastocitomi); 31 tumori epiteliali (7 beni-

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gni); 3 melanomi; 3 neoplasie indifferenziate (tutti e tre sarcomi all’esame istologico). Non erano mai eseguite diagnosi false positive per neoplasia. La cellularità del campione ed evidenti segni di malignità sono i cardini su cui si basa la prevenzione di possibili diagnosi citologiche false positive per neoplasia. Interessante notare come negli emangiopericitomi si siano evidenziate cellule giganti multinucleate, da noi definite “crown cells” (cellule a corona), tipiche e patognomoniche per la disposizione dei nuclei in quasi perfetto cerchio ai margini della membrana citoplasmatica.

In 34 casi la diagnosi citologica negativa per neoplasia era in accordo con l’istologia, mentre in 28 casi (14 tumori epiteliali e 14 tumori mesenchimali a cellule fusate) veniva fatta una diagnosi citologica falsa negativa. Una buona percentuale delle diagnosi false negative, come pure dei campioni definiti come inadeguati, potrebbero essere una conseguenza del campionamento che non è seguito dall’immediata valutazione del campione al solo scopo di determinarne l’adeguatezza in termini di cellularità e conservazione del materiale.

Sulla base dei 179 casi in cui era definita una diagnosi citologica, i nostri risultati hanno mostrato un complessivo accordo tra diagnosi citologica e istologica dell’84,4% dei casi (151/179). La sensibilità è stata del 80,7%, la specificità e il valore predittivo dei risultati positivi (neoplasie) sono state del 100%, mentre il valore predittivo dei risultati negativi (lesione non neoplastica) è stato del 54,8%.

Questi risultati confermano il valore dell’aspirazione con ago sottile nella gestione clinica delle neoformazioni cutanee, particolarmente nei riguardi della diagnosi delle forme neoplastiche.

Bibliografia 1.

Caniatti M, Ceruti R, Ghisleni G et al., (1999), Correlations between fine needle aspiration (FNA) and histology in 222 palpable cutaneous lesions of dogs and cats, Abstracts XVII Meeting European Society of Veterinary Pathology, Nantes, September 14-17, pag.121.

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Citologia e tumori nasali Mario Caniatti Med. Vet., Dipl. ECVP - Istituto di Anatomia Patologica Veterinaria e Patologia Aviare - Università di Milano

Carlo Maria Mortellaro Med. Vet. - Istituto di Clinica Chirurgica e Radiologia Veterinaria - Università di Milano

Riassunto PREMESSA: Le patologie croniche del cavo nasale sono piuttosto comuni nel cane e gatto, tuttavia i segni clinici associati sono aspecifici e quindi non correlabili ad una precisa eziologia e anche l’ausilio radiografico non è determinante nel precisare la diagnosi. Quindi, nella maggior parte dei casi di rinite cronica, una diagnosi definitiva necessita di una biopsia. Negli ultimi anni, numerose tecniche definite “non chirurgiche” sono state messe a punto per ottenere campioni bioptici. Fra queste vi sono tecniche istologiche (pinch biopsy, core biopsy) e citologiche (lavaggi, tamponi, spazzolati).

ESPERIENZE PERSONALI: Sono stati condotti studi sui caratteri cito-istologici di patologie nasali croniche del gatto e del cane1-4. In questi era valutata la bontà dell’indagine citologica per brushing soprattutto nella diagnosi di neoplasie. Nel gatto2 sono stati valutati 53 brush nasali: 36 casi erano classificati come infiammatori e, in 30 di questi, la diagnosi citologica era confermata dal dato istologico e di follow-up (6 falsi negativi). 17 casi erano classificati come neoplastici e in 16 di questi la diagnosi citologica era confermata dal dato istologico o di follow-up. In un caso (falso positivo) veniva diagnosticata come neoplasia una forma flogistica cronica linfoplasmacellulare. Sulla base di questi risultati si è osservato un 86.8% (46/53 casi) di accordo nella diagnosi di flogosi vs neoplasia, con sensibilità del 72,7%, specificità del 96,8%, valore predittivo dei risultati positivi del 94,1% e valore predittivo dei risultati negativi del 83,3%.

Nel cane4 sono stati valutati 94 soggetti. La diagnosi citologica di flogosi era in accordo con i dati istologici e di followup in 51 su 66 casi (15 falsi negativi), mentre la diagnosi citologica di neoplasia è stata confermata in tutti i 28 casi valutati. La procedura ha mostrato un 84,0% di accordo nella diagnosi di flogosi vs neoplasia, con sensibilità del 65,1%, specificità del 100%, valore predittivo dei risultati positivi del 100% e valore predittivo dei risultati negativi del 77,3%.

Bibliografia: (1)Caniatti M, Trabucco M, Mortellaro CM et al., (1994), Abstracts XII Meeting European Society of Veterinary Pathology, Mondovì, September 18-22, pag.120. (2)Caniatti M, Roccabianca P, Ghisleni G et al., (1998), J Small Anim Pract, 39: 73-77. (3)Caniatti M, Roccabianca P, Scanziani E et al., (1998), Vet Rec, 142: 334-338. (4)Caniatti M, Mortellaro CM, Ghisleni G et al., (1999), Abstracts IX Annual Congress European Society of Veterinary Internal Medicine, Perugia, October 14-16, pag. 103-104.

Le malattie ad andamento cronico delle cavità e dei seni nasali sono piuttosto comuni nella specie canina e felina, tuttavia i segni clinici associati (es. starnuti, scolo di essudati, epistassi, dispnea ecc.) sono aspecifici e quindi non direttamente correlabili ad una precisa eziologia infiammatoria o neoplastica. Inoltre, anche l’ausilio dell’indagine radiografica, pur utile nello stabilire una diagnosi di malattia e soprattutto la sua estensione, non è determinante nel precisare la diagnosi eziologica.

Ne consegue che nella maggior parte dei casi di rinite cronica, un tentativo di diagnosi definitiva necessita di un prelievo bioptico. Per questi motivi negli ultimi anni, nu-

merose tecniche definite “non chirurgiche” sono state messe a punto per ottenere campioni bioptici. Fra queste vi sono tecniche istologiche (pinch biopsy, core biopsy) e citologiche (lavaggi, tamponi, spazzolati). Tra le tecniche citologiche gli spazzolati, grazie al fatto che il prelievo viene eseguito spesso sotto guida endoscopica, si sono decisamente affermati. Per contro, lavaggi e tamponi sono in via di abbandono a causa di difficoltà tecniche (lavaggi) e povertà dei campioni raccolti in termini di cellularità. Anche per quanto riguarda l’uso del sussidio endoscopico possono essere fatte considerazioni analoghe a quelle espresse nei confronti dell’indagine radiografica. L’esame endoscopico, nel-

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la maggior parte dei casi, permette di fare una corretta diagnosi differenziale fra forme infiammatorie e neoplastiche, tuttavia ha una relativamente inferiore capacità di definire, nell’ambito delle forme neoplastiche, il possibile citotipo d’origine (epiteliale, fusato, rotondocellulare). Per questi motivi, in alcuni centri di referenza che si occupano della diagnosi e dello studio delle patologie nasali croniche, è ormai invalso l’utilizzo combinato della tecnica endoscopica associata ad un prelievo citologico (brushing) o cito-istologico (brushing + pinch biopsy). In questa nota ci si soffermerà in particolare sugli aspetti citologici di campioni raccolti con la tecnica dello spazzolato (brushing) in corso di patologie nasali croniche con particolare riferimento alle condizioni neoplastiche.

REPERTI CITOLOGICI NORMALI In condizioni normali un prelievo citologico del cavo nasale contiene un numero di cellule da lieve a moderato. Dette cellule sono costituite da epiteliali squamose (porzione rostrale del cavo nasale), cilindriche ciliate, occasionali caliciformi mucipare (non ciliate, contengono granuli di muco), scarsi globuli rossi e cellule nucleate del sangue.

REPERTI PATOLOGICI I quadri patologici rilevabili citologicamente a livello di cavità nasali sono riconducibili a due grandi catergorie: riniti e neoplasie.

Riniti Dal punto di vista citologico le riniti vengono classificate secondo i tipi di cellule infiammatorie prevalenti: Flogosi neutrofilica: primitiva (es. da batteri o da miceti) o secondaria ad altre lesioni, in genere di natura neoplastica. Gli aspetti degenerativi dei nuclei granulocitari (cariolisi, carioressi) possono essere spia di un’eziologia batterica, ma germi poco patogeni o una terapia antibiotica possono rendere difficoltosa una precisa diagnosi eziologica su base citologica.

Tra i miceti, reperti di flogosi neutrofilica nasale sono tipicamente causati da microrganismi del Gen. Aspergillus che spesso sono poco visibili nei preparati citologici. Ne consegue che in caso di intensa flogosi neutrofilica nasale è spesso utile una colorazione speciale (es. PAS: Acido periodico-reattivo di Schiff) per evidenziare l’eventuale presenza di miceti. Anche Rhinosporidium seeberi è causa, nella specie canina, di una flogosi eminentemente neutrofilica cui è associata iperplasia e metaplasia squamosa dell’epitelio nasale.

Flogosi eosinofilica: relativamente frequente nel cane e nel gatto, è espressione di fenomeni di ipersensibilità.

Può essere associata una componente neutrofilica o macrofagica.

Flogosi macrofagica: quasi mai pura, più spesso associata alle componenti neutrofilica e linfoplasmocitica. Tra le

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cause note ricordiamo: corpi estranei, miceti e parassiti come, ad esempio, leishmania.

Flogosi linfoplasmacellulare: relativamente comune, soprattutto nel gatto, è espressione di flogosi cronica aspecifica.

Flogosi miste: assai comuni in caso di eziologia micotica (es. Criptococcosi), corpi estranei, ma più spesso si rilevano in corso di riniti croniche aspecifiche in cui non c’è evidenza citologica di una particolare eziologia.

Neoplasie Spesso sono associate a processo infiammatorio che può sovrastare il quadro neoplastico e rendere la diagnosi impossibile o difficoltosa. Infatti neoplasie epiteliali ben differenziate potrebbero essere interpretate come fenomeni reattivi dell’epitelio nei confronti dell’essudato. Le neoplasie sono nella maggior parte dei casi primitive, ma alcuni tumori (es. carcinomi squamosi, melanomi) possono originare dal cavo orale ed estendersi per contiguità a quello nasale.

Dal punto di vista citologico possono essere diagnosticati tre tipi di neoplasie: epiteliali, a cellule fusate e a cellule rotonde.

Tumori epiteliali: sono i più comuni. La diagnosi citologica di queste neoplasie si basa sul reperto di gruppi di cellule coesive che mostrano segni di malignità citologica . Negli adenocarcinomi tali cellule possono mostrare vacuolizzazioni citoplasmatiche, mentre in caso di carcinoma squamoso è tipico il reperto di cellule cheratinizzate nelle quali permane un nucleo di aspetto immaturo. Va comunque sottolineato come cellule squamose possano essere espressione di fenomeni iperplastici e metaplastici dell’epitelio respiratorio conseguenti a flogosi.

Tumori a cellule fusate: fibro-, condro- e osteosarcomi sono relativamente comuni, ma di non facile diagnosi citologica in quanto esfoliano con difficoltà e, nei prelievi per spazzolato, possono cedere abbastanza materiale solo quando l’epitelio sovrastante viene eroso. Le cellule dei melanomi, tipicamente caratterizzate dalla presenza di granuli citoplasmatici di pigmento, spesso assumono aspetto fusato.

Tumori a cellule rotonde: il più comune tra questi tumori è senz’altro il linfoma nel gatto. La diagnosi citologica è basata sul reperto di una prevalente popolazione pleomorfa di cellule linfoidi immature, ma falsi positivi possono essere causati da flogosi croniche linfoplasmocitiche.

Nel cane non è rara la localizzazione nasale del tumore venereo trasmissibile (TVT). In questa sede, la diagnosi differenziale fra TVT e linfoma è senz’altro più agevole con l’indagine citologica rispetto a quella istologica. Il tumore ha reperti citologici tipici e costituiti da una popolazione pleomorfa di cellule rotonde caratterizzate da un relativamente abbondante citoplasma grigiastro in cui sono spesso presenti piccoli e netti vacuoli perinucleari. Frequenti sono anche le mitosi atipiche e l’infiltrato linfoplasmacellulare.

Sempre nel cane è di occasionale riscontro il mastocitoma che va differenziato con attenzione dalle molto più comuni riniti eosinofiliche nelle quali è spesso presente una componente mastocitica.

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ESPERIENZE PERSONALI Negli ultimi anni sono stati condotti alcuni studi sui caratteri cito-istologici di patologie nasali croniche del gatto e del cane1-4 nei quali veniva sottolineata la validità dell’indagine citologica per brushing nella diagnosi delle patologie croniche nasali con particolare riferimento alle condizioni neoplastiche.

Nel gatto2 sono stati valutati 53 soggetti portatori di patologie nasali croniche. 36 casi erano citologicamente classificati come infiammatori e, in 30 di questi, la diagnosi citologica era confermata dal dato istologico e di follow-up (6 casi falsi negativi). 17 casi erano classificati come neoplastici e in 16 di questi la diagnosi citologica era confermata dal dato istologico o di follow-up. In un caso di adenocarcinoma la diagnosi citologica era di neoplasia benigna, mentre in un caso (falso positivo) veniva diagnosticata come neoplasia una forma flogistica cronica linfoplasmacellulare. Sulla base di questi risultati si è osservato un 86.8% (46/53 casi) di accordo nella diagnosi di flogosi vs neoplasia, con sensibilità del 72,7%, specificità del 96,8%, valore predittivo dei risultati positivi del 94,1% e valore predittivo dei risultati negativi del 83,3%.

Nel cane4 sono stati valutati 94 soggetti. La diagnosi citologica di flogosi era in accordo con i dati istologici e di

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follow-up in 51 su 66 casi (15 falsi negativi), mentre la diagnosi citologica di neoplasia è stata confermata in tutti i 28 casi valutati (17 carcinomi, 8 sarcomi, un linfoma, un melanoma, un tumore venereo trasmissibile).

La procedura ha mostrato un 84,0% di accordo nella diagnosi di flogosi vs neoplasia, con sensibilità del 65,1%, specificità del 100%, valore predittivo dei risultati positivi del 100% e valore predittivo dei risultati negativi del 77,3%.

Bibliografia 1.

2.

3.

4.

Caniatti M, Trabucco M, Mortellaro CM et al., (1994), Diagnosis of nasal tumors in dogs: value of rhinoscopy-assisted biopsies, Abstracts XII Meeting European Society of Veterinary Pathology, Mondovì, September 18-22, pag.120.

Caniatti M, Roccabianca P, Ghisleni G et al., (1998), Evaluation of brush cytology in the diagnosis of chronic intranasal disease in cats, J Small Anim Pract, 39: 73-77.

Caniatti M, Roccabianca P, Scanziani E et al., (1998), Nasal rhinosporidiosis in dogs: four cases from Europe and a review of the literature, Vet Rec, 142: 334-338.

Caniatti M, Mortellaro CM, Ghisleni G et al., (1999), Evaluation of brush cytology in the diagnosis of chronic intranasal disease in dogs, Abstracts IX Annual Congress European Society of Veterinary Internal Medicine, Perugia, October 14-16, pag. 103-104.

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Efficacia della clorexidina digluconato shampoo al 2% e soluzione allo 0,45% nelle piodermiti di superficie e superficiali del cane Silvia Colombo Istituto di Patologia Speciale e Clinica Medica Veterinaria - Facoltà di Medicina Veterinaria di Milano

Luisa Cornegliani Libero Professionista - Milano

Giovanni Ghibaudo Clinica Veterinaria Malpensa - Samarate (VA)

INTRODUZIONE La terapia topica è ampiamente utilizzata come terapia collaterale delle infezioni batteriche cutanee del cane, associata all’uso di antibiotici per via generale. La Clorexidina digluconato è uno dei principi attivi più frequentemente prescritti per la sua efficacia nei confronti dello Staphylococcus Intermedius, che è l’agente eziologico più comunemente isolato nelle piodermiti.

Gli obiettivi del presente lavoro sono stati i seguenti: stabilire se le piodermiti di superficie e superficiale del cane possono essere trattate con la sola terapia topica; valutare l’efficacia, la praticità d’impiego e gli eventuali effetti collaterali della Clorexidina digluconato.

MATERIALI E METODI 24 soggetti di diversa razza, sesso ed età, previo consenso dei proprietari, sono stati selezionati per lo studio. Tutti i soggetti inclusi risultavano affetti da piodermiti di superficie o superficiali in base all’esito di una visita dermatologica, di raschiati cutanei multipli e di tricogrammi o esami colturali per dermatofiti negativi e di esami citologici compatibili con le suddette patologie. Sono stati esclusi dallo studio cani affetti da piodermiti profonde, da patologie concomitanti (Demodicosi, Dermatofitosi, Dermatite da Malassezia), cani trattati con antiinfiammatori, antistaminici, antibiotici o glucocorticoidi topici o per via orale da meno di due settimane o trattati con corticosteroidi iniettabili da meno di sei settimane. I soggetti inclusi sono stati casualmente assegnati a due differenti gruppi di trattamento. I soggetti inclusi nel gruppo A (12 cani: 6 con piodermite di superficie, 6 con piodermite superficiale) sono stati trattati con Clorexidina digluconato shampoo al 2% due volte la settimana e con Clorexidina digluconato soluzione allo 0,45% BID per un pe-

riodo di 21 giorni; i soggetti del gruppo B (12 cani: 3 con piodermite superficiale, 9 con piodermite superficiale) sono stati trattati topicamente con lo stesso protocollo sopra descritto con l’aggiunta di Cefalessina 25 mg/kg BID PO. Tutti i cani sono stati sottoposti a visite di controllo a 7, 14 e 21 giorni dall’inizio della terapia e 7 e 14 giorni dopo la sospensione della terapia stessa. I parametri controllati durante ciascun esame clinico sono stati i seguenti: condizioni generali, temperatura, gravità delle lesioni (scala 1-10) ed intensità del prurito (scala 1-10).

RISULTATI Nel gruppo A (12 cani) sono stati inclusi 6 soggetti affetti da piodermite di superficie (Dermatite piotraumatica) e 6 soggetti affetti da piodermite superficiale (Follicolite superficiale). In tutti i soggetti (6 cani) affetti da piodermite di superficie il trattamento ha portato a completa risoluzione delle lesioni e scomparsa del prurito. Nei soggetti (6 cani) affetti da piodermite superficiale, invece, la risposta alla terapia è stata giudicata ottima in 1 soggetto, modesta in 3 soggetti e scarsa in 2 soggetti. Al termine dello studio i 5 cani in cui non si era ottenuta la completa guarigione delle lesioni sono stati trattati con Cefalessina 25 mg/kg BID PO. Il gruppo B (12 cani) comprendeva 3 soggetti affetti da piodermite di superficie (Dermatite piotraumatica) e 9 soggetti affetti da piodermite superficiale (Follicolite superficiale). In tutti i soggetti appartenenti al gruppo B la risposta alla terapia è stata giudicata ottima. In 7 cani su 24 compessivamente trattati con Clorexidina digluconato shampoo al 2% e soluzione allo 0,45% sono stati osservati effetti collaterali, descritti come irritazione ed eritema dopo le prime 2 applicazioni dello shampoo.

Tali manifestazioni non si sono più presentate nonostante la prosecuzione del trattamento. Nessun effetto collaterale è stato invece riferito dopo l’applicazione della soluzione.

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Gruppo A: Clorexidina digluconato shampoo 2% - Clorexidina digluconato soluzione 0,45% Caso n°

Segnalamento

Patologia

Prurito (0-10)

Gravità lesioni (0-10)

Risultato

Effetti Collaterali

Patologia sospettata

1

Terranova M 5a

Dermatite Piotraumatica

5

5

Ottimo

Nessuno

DAP

2

P. T. F 3,5a

Follicolite Superficiale

6

4

Modesto

Eritema

Atopia

3

Dogue B. F 1,5a

Follicolite Superficiale

6

4

Modesto

Nessuno

DAP

4

Pitbull FS 1,5a

Follicolite Superficiale

7

5

Ottimo

Nessuno

AA

5

Boxer F 3a

Follicolite Superficiale

10

8

Lost to follow up

6

Fox T. M 7a

Follicolite Superficiale

10

6

Modesto

Irritazione

Allergie

7

Dogue B. M 1a

Follicolite Superficiale

3

5

Lost to follow up

8

Bassotto F 8a

Follicolite Superficiale

0

4

Scarso

Nessuno

9

Bassotto F 13a

Dermatite Piotraumatica

5

3

Ottimo

Nessuno

10

Shih Tzu M 9a

Follicolite Superficiale

0

8

Scarso

Irritazione

11

P. T. M 5a

Dermatite Piotraumatica

6

4

Ottimo

Nessuno

12

Meticcio M 4a

Dermatite Piotraumatica

6

2

Ottimo

Nessuno

13

Meticcio F 2,5a

Dermatite Piotraumatica

4

2

Ottimo

Nessuno

AtopiaDAP

14

Chow M 4,5a

Dermatite Piotraumatica

5

2

Ottimo

Nessuno

AtopiaDAP

AtopiaDAP

Pio di superficie 6/14 Pio superficiali 8/14 Lost to follow up: 2 Totale 12 casi. 6/12 e 6/12 Risultati: Pio di superficie ottima 6/6 Pio superficiali ottima 1/6, modesta 3/6, scarsa 2/6 Effetti collaterali: 3/12

Gruppo B: Clorexidina digluconato shampoo 2% - Clorexidina digluconato soluzione 0,45% - Cefalessina 25 mg/kg BID PO Caso n°

Segnalamento

Patologia

Prurito (0-10)

Gravità lesioni (0-10)

Risultato

Effetti Collaterali

Patologia sospettata

1

P. T. M 4a

Dermatite Piotraumatica

8

7

Ottimo

Nessuno

DAP

2

P.T. M 5a

Dermatite Piotraumatica

9

9

Ottimo

Eritema

3

Bassotto FS 5a

Follicolite Superficiale

8

3

Ottimo

Nessuno

4

P. T. M 7a

Dermatite Piotraumatica

8

7

Ottimo

Nessuno

Allergie

5

Terranova F 2a

Follicolite Superficiale

8

6

Ottimo

Nessuno

DAP

6

Meticcio M 3a

Follicolite Superficiale

10

7

Ottimo

Nessuno

Atopia

7

Labrador F 1,5a

Follicolite Superficiale

0

5

Ottimo

Eritema

8

Yorksh. T. F 4a

Follicolite Superficiale

6

5

Ottimo

Irritazione

Atopia

9

Pitbull F 2,5a

Follicolite Superficiale

5

6

Ottimo

Nessuno

Allergie

10

Dalmata M 3a

Follicolite Superficiale

5

4

Modesto

Irritazione

Atopia

11

P. T. F 5a

Follicolite Superficiale

7

6

Ottimo

Nessuno

AtopiaDAP

12

Meticcio M 9a

Follicolite Superficiale

6

5

Ottimo

Nessuno

DAP

13

Meticcio M 4,5a

Dermatite Piotraumatica

4

2

Lost to follow up

Pio di superficie: 4/13 Pio superficiali: 9/13 Lost to follow up:1 Totale casi: 3/12 e 9/12 Risultati: Pio di superficie ottima 3/3 Pio superficiali ottima 8/9, modesta 1/9 Effetti collaterali: 4/12

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CONCLUSIONI L’utilizzazione associata di Clorexidina digluconato come shampoo al 2% e come soluzione allo 0,45% si è rivelata estremamente efficace nel trattamento delle piodermiti di superficie (dermatite piotraumatica) del cane come unica terapia prescritta. Per quanto concerne invece le piodermiti superficiali (follicolite superficiale), la terapia topica da sola non è risultata sufficientemente efficace, richiedendo in quasi tutti i soggetti la successiva somministrazione di Cefalessina. In questi cani, la terapia topica ha portato ad un “controllo” dell’infezione batterica con progressivo miglioramento delle lesioni osservabili e dell’intensità del prurito, seguito però da una recidiva non appena il trattamento è stato interrotto. L’efficacia del protocollo applicato nel presente lavoro andrebbe quindi valutata nel trattamento di forme

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ricorrenti di follicolite superficiale, in cui potrebbe rivelarsi utile nel controllo delle recidive. Le formulazioni utilizzate si sono dimostrate di pratico impiego da parte dei proprietari, e gli effetti collaterali sono stati modesti e non si sono più manifestati con la prosecuzione del trattamento, probabilmente in seguito alla progressiva guarigione delle lesioni presenti.

Bibliografia Guaguere E.: Topical treatmente of canine and feline pyoderma. Veterinary Dermatology 7:145-151, 1996.

Ihrke P. J.: Bacterial Skin Disease in the Dog - A Guide to Canine Pyoderma. Bayer AG, 1996.

Scott D. W., Miller W. H., Griffin C. E.: Mueller & Kirk’s Small Animal Dermatology, 5th Edition. W. B. Saunders Co., Philadelphia, 1995.

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Uso della clorexidina 0,45% in gel nella dermatite delle pieghe cutanee Luisa Cornegliani Libero Professionista - Milano

Silvia Colombo Istituto di Patologia Speciale e Clinica Medica Veterinaria - Facoltà di Medicina Veterinaria di Milano

Giovanni Ghibaudo Clinica Veterinaria Malpensa - Samarate (VA)

INTRODUZIONE La Clorexidina è una biguanidina ad azione antisettica e disinfettante efficace nei confronti delle maggior parte dei batteri e di molti funghi. Non è inattivata dalla presenza di materiale organico; non è irritante ed è efficace formulata in shampoo, pomata, soluzione in formulazione a concentrazioni da 0.5 a 2%. A concentrazioni inferiori vicine allo 0.01% viene comunemente impiegata nell’irrigazione delle ferite cutanee. Per queste caratteristiche si è voluto testarne l’efficacia antibatterica ed antifungina nella dermatite delle pieghe o intertrigo utilizzando un gel allo 0.45%. L’uso in tale formulazione è stato deciso in base alla maggior facilità di applicazione ed alla maggior persistenza sulla cute. Si è voluto in questo modo valutare anche i potenziali effetti tossici locali per una maggior persistenza della Clorexidina sulla cute e la potenzialità antibatterica a concentrazione inferiore a 0.5%.

MATERIALI E METODI Un gruppo di 40 cani di differenti razze ed età è stato selezionato per lo studio. I soggetti inclusi nel gruppo sono stati scelti seguendo i suddetti parametri di inclusione: consenso del proprietario, nessun trattamento topico o sistemico nel mese precedente, buono stato di salute generale, visita dermatologica. Quest’ultima non doveva rilevare nessuna causa sottostante la patologia eccezione fatta per la conformazione anatomica: cani con malattie da ipersensibilità, parassitarie o riconducibili a malattie metaboliche or-

monali sono stati esclusi. Per ogni cane un campione citologico venne prelevato da lesioni infiammatorie eritematose, delle pliche facciali e vulvari, per apposizione diretta e/o per impressione su nastro adesivo trasparente. Ogni campione citologico venne poi allestito con colorazione rapida (Hemacolor). In tutti i prelievi esaminati l’esame citologico mostrò detriti superficiali, un gran numero di batteri (cocchi>20/HPF) e numerosi lieviti (malassezia spp.>10/ HPF). La Clorexidina digluconato in gel allo 0.45% venne applicata sulle lesioni cutanee due volte al giorno per 10 giorni. Tutti i soggetti inclusi vennero testati clinicamente e citologicamente al giorno 4 e al giorno 10. Di seguito venne mantenuta una terapia locale con applicazione bisettimanale per i quattro mesi successivi.

RISULTATI Il miglioramento clinico risultò evidente con diminuzione di prurito, eritema ed infiammazione. L’esame citologico di controllo per apposizione e/o impressione con nastro adesivo trasparente, ripetuto ad ogni controllo, mostrò una diminuzione significativa della sovrainfezione batterica e della popolazione di lieviti (cocchi e malassezie <5/HPF). Tutti i soggetti furono seguiti nei quattro mesi successivi e la dermatite delle pieghe rimase in remissione con applicazioni locali di gel due volte alla settimana, senza effetti collaterali. Questo approccio terapeutico fu mantenuto in tutti i casi in cui il proprietario preferì il trattamento sintomatico a lungo termine in alternativa alla chirurgia plastica correttiva delle pieghe.

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CONCLUSIONI L’applicazione topica di Clorexidina digluconato in gel allo 0.45% è risultato essere, in questo gruppo di studio, un trattamento soddisfacente nel controllo completo della sovracrescita della flora batterica e dei lieviti. Dato che batteri e lieviti giocano un ruolo centrale nella patogenesi della dermatite delle pieghe il loro controllo è sufficiente ad evitarne le manifestazioni cliniche principali; eritema, infiammazione e successivo prurito non si manifestano in questi soggetti quantunque non vengano modificati le altre componenti che causano la patologia (pieghe cutanee, aumentata umidità, scarsa igiene, ecc.). La Clorexidina agisce nei confronti di

40° Congresso Nazionale SCIVAC

batteri e lieviti a seconda della concentrazione e del tempo di contatto con l’agente patogeno nei confronti del quale vengono impiegati. La preparazione in gel allo 0.45% permette di aumentare il tempo di contatto e quindi di antisettico della molecola senza però causare i ben noti effetti citotossici.

Bibliografia Scott DW, Miller WH, Griffin CE: Dermatologic therapy. In Muller and Kirk’s Small Animal Dermatology, 5th ed. WB Saunders Company, Philadelphia 1995, pp. 174-227.

Ihrke PJ.: Surface pyoderma. In Bacterial Skin Diseases in theDog. A guide to canine Pyoderma. Bayer AG 1996, pp 21-25.

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Principi interpretativi in citologia oncologica Davide De Lorenzi Medico Veterinario, Specialista in “Clinica e Patologia degli Animali da Affezione” - Forlì

Riassunto L’esame citologico rappresenta una tecnica di oramai consolidata importanza anche in Medicina Veterinaria; la valutazione delle linee cellulari implicate nel processo patologico permette al clinico di eseguire un rapido screening ed anche se una diagnosi definitiva non viene, a volte, emessa tuttavia la natura generale del problema può essere individuata rapidamente se viene impiegato un approccio ragionato e metodico al campione esaminato.

Quando una diagnosi definitiva non viene raggiunta, il risultato dell’esame citologico ci permette comunque di indirizzare i successivi eventuali approfondimenti diagnostici (ad es. esame colturale, istologico, radiologico, ecografico, chirurgia esplorativa, ecc...).

Sicuramente, la prima e più importante informazione che è possibile ottenere dall’analisi del campione citologico è l’identificare la lesione come infiammatoria o come neoplastica.

Una volta identificata la natura neoplastica della lesione, risulta di particolare importanza cercare di definirne il comportamento biologico, in altre parole di classificare il tumore come “benigno” oppure “maligno”.

Da un punto di vista didattico, i criteri di malignità possono essere divisi come segue: 1) Criteri di malignità a livello della singola cellula: a) a livello di nucleo cellulare; b) a livello di citoplasma cellulare; 2) Criteri di malignità a livello della popolazione cellulare; 3) Criteri di malignità indiretti; La relazione illustra i principali criteri di malignità citologica, focalizzando specificamente la trattazione sul significato patologico delle modificazioni citomorfologiche in corso di neoplasia.

INTRODUZIONE L’esame citologico rappresenta una tecnica di oramai consolidata importanza anche in Medicina Veterinaria; la valutazione delle linee cellulari implicate nel processo patologico permette al clinico di eseguire un rapido screening ed anche se una diagnosi definitiva non viene, a volte, emessa tuttavia la natura generale del problema può essere individuata rapidamente se viene impiegato un approccio ragionato e metodico al campione esaminato.

Quando una diagnosi definitiva non viene raggiunta, il risultato dell’esame citologico ci permette comunque di indirizzare i successivi eventuali approfondimenti diagnostici (ad es. esame colturale, istologico, radiologico, ecografico, chirurgia esplorativa, ecc...).

Sicuramente, la prima e più importante informazione che è possibile ottenere dall’analisi del campione citologico è l’identificare la lesione come infiammatoria o come neoplastica.

Un classico algoritmo per l’approccio al campione citologico viene illustrato nella Tabella 1.

Una volta identificata la natura neoplastica della lesione, risulta di particolare importanza cercare di definirne il comportamento biologico, in altre parole di classificare il tumore come “benigno” oppure “maligno”.

Questa relazione ha lo scopo di valutare i principali criteri citologici di malignità e di spiegarne il significato.

La prima, importantissima valutazione che dobbiamo fare, analizzando un campione citologico, è stimare l’adeguatezza dello striscio; in altre parole, devono essere valutate la cellularità generale, la conservazione delle cellule, la qualità della colorazione e che il nome del proprietario e la sede del prelievo siano scritti sulla banda sabbiata del vetrino e sul modulo di accompagnamento. Se anche uno solo di questi elementi appare inadeguato o mancante, bisogna evitare di dare una diagnosi, limitandosi ad indicare il motivo dell’inadeguatezza del campione e ripetendo l’agoaspirazione.

Una altro concetto importante è quello della rappresentatività del campione che stiamo analizzando; infatti, a seconda della zona che abbiamo aspirato, possiamo ritrovare,

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40° Congresso Nazionale SCIVAC

Tabella 1 - Approccio al campione citologico: la valutazione dei criteri di malignità rappresenta un passaggio obbligato, una volta stabilita la natura neoplastica della patologia.

in percentuali variamente rappresentate sul vetrino cellule infiammatorie, neoplastiche, tissutali normali oppure necrosi.

Proprio per questo motivo, prima di emettere una diagnosi citologica, è obbligatorio valutare tutti i vetrini che abbiamo a disposizione.

Nessuna delle valutazioni che saranno il soggetto di questa relazione può e deve essere fatta se non si è sicuri della adeguatezza e della rappresentatività del campione citologico in esame.

CRITERI DI MALIGNITÀ La morfologia delle cellule è espressione della loro attività biologica; essa, infatti, da una parte ci indica il comportamento genetico e molecolare della cellula stessa, mentre dall’altra riflette quello che è lo stato biologico del tessuto e dell’ospite al quale appartiene.

Come conseguenza di queste considerazioni, possiamo certamente affermare che lo studio della morfologia cellulare rappresenta un passaggio fondamentale per lo studio e la comprensione di quella miriade di processi fisiologici e patologici che coinvolgono la cellula, il tessuto e quindi l’ospite.

Anche se questi processi sono innumerevoli, le cellule reagiscono con un limitato numero di risposte, che possono essere catalogate in alcune classi generali, per una migliore e più facile comprensione dei processi patologici.

In particolare, l’attività biologica generale della cellula viene indicata dalle caratteristiche nucleari, mentre la specifica attività funzionale viene meglio descritta dalla morfologia citoplasmatica, che manifesta le differenziazioni caratteristiche di una particolare attività cellulare.

Da un punto di vista didattico, i criteri di malignità possono essere divisi come segue: 1) Criteri di malignità a livello della singola cellula: a) a livello di nucleo cellulare; b) a livello di citoplasma cellulare; 2) Criteri di malignità a livello della popolazione cellulare; 3) Criteri di malignità indiretti; IMPORTANTE: In citologia diagnostica, esiste un solo ed indiscutibile criterio di malignità, e cioè il ritrovare cellule estranee (e cioè metastatiche) a livello di un tessuto o di un fluido ove queste non dovrebbero esistere. In assenza di

40° Congresso Nazionale SCIVAC

questo reperto, nessuno dei criteri che descriveremo, permetterà da solo di esprimere un criterio definitivo di malignità o benignità. Il giudizio finale dipenderà dalla somma e dall’importanza dei criteri di malignità evidenziati, anche in relazione al tipo di neoplasia sospettata.

In linea generale, i più forti criteri di malignità sono quelli evidenziati a livello di nucleo , di mitosi e di architetture cellulari.

Una ultima considerazione di ordine generale: se è vero che un campione che presenta molti ed importanti criteri di malignità spesso è in effetti un tumore maligno, il non ritrovarne non può mai permetterci di escludere al 100% la presenza di una malignità, e questo come conseguenza delle particolari caratteristiche del campione citologico, che può essere più o meno rappresentativo del tessuto analizzato.

Esistono, inoltre, neoplasie (come alcuni carcinomi tiroidei nel cane ) che, pur non presentando nessuno dei caratteri classici di malignità, hanno un comportamento biologico assolutamente maligno.

A) Criteri di malignità a livello dalla singola cellula a) a livello di nucleo Rientrano, in questa categoria, alcuni fra i più importanti e significativi criteri di interpretazione delle caratteristiche di malignità delle cellule.

Prima di parlare di queste caratteristiche, facciamo un breve ripasso delle strutture che si trovano dentro il nucleo evidenziandone, in particolare, la loro funzione: potremo in questo modo capire meglio perché alterazioni presenti a questo livello diventano così importanti nel giudizio finale di malignità. Accenneremo anche al concetto di euplasia, ovvero di normalità cellulare, poiché solo conoscendo le caratteristiche fisiologiche delle cellule sarà possibile evidenziare gli aspetti patologici. *Nucleoli: essi sono costituiti da RNA e proteine associate al RNA, e sono il sito di sintesi dei ribosomi.

Con le colorazioni tipo Romanowsky (MGG, DQ, Wright) essi appaiono colorati in azzurro o blu chiaro, con margini generalmente non perfettamente definiti, mentre con la colorazione di Papanicolaou essi appaiono a limiti netti e precisi e di colore variabile rosso-arancio.

La quantità di materiale nucleolare è direttamente proporzionale alla quantità di proteine prodotte in quel momento dalla cellula: vi sono cellule che, fisiologicamente, hanno nucleoli prominenti poiché la loro produzione proteica è costantemente alta (ad es. gli epatociti e le cellule intestinali) mentre vi sono cellule che hanno minuscoli nucleoli (ad es. le cellule prostatiche normali).

Nelle infiammazioni croniche e nei tessuti cicatriziali è reperto comune il rilevare cellule mesenchimali con nucleoli molto grandi e prominenti, come conseguenza della notevole richiesta di materiale proteico nel sito interessato dal processo patologico. *Cromatina: è costituita da DNA e proteine associate al DNA; rappresenta il contenuto cromosomico delle cellule in

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fase metabolica, non in mitosi. Durante la mitosi, la cromatina si addensa a formare i cromosomi.

Nella fase intermitotica, la cromatina si organizza a formare la cromatina marginale (eterocromatina), la trama cromatinica e la paracromatina (intercromatina).

La cromatina marginale rappresenta quella cromatina biologicamente inattiva che si addensa contro la superficie interna della membrana nucleare; per questa ragione, prima che il Microscopio Elettronico permettesse una più esatta conoscenza della microanatomia cellulare, la cromatina marginale veniva impropriamente compresa nella denominazione “membrana nucleare”, perché la risoluzione del Microscopio Ottico (M.O.) non permetteva di distinguere fra la membrana nucleare vera e l’eterocromatina. In realtà, la membrana nucleare vera è talmente sottile che non è rilevabile durante l’osservazione al M.O. ma la sua forma è evidenziata con precisione dalla eterocromatina disposta contro di essa. Inoltre, anche il minore o maggiore spessore che è possibile rilevare con il M.O. non è da attribuire alla membrana nucleare, ma alla quantità di eterocromatina addensata.

La trama cromatinica rappresenta quel “reticolato” di eterocromatina addensata ed inattiva che si estende attraverso tutto il nucleo, in diretta continuazione con la cromatina marginale. Questa può disporsi a formare filamenti (da sottilissimi a più spessi e grossolani) o granuli detti anche “cromocentri” che possono essere finissimi e conferire al nucleo l’aspetto del vetro molato oppure sempre più grossolani, fino ad assumere l’aspetto di agglomerati irregolari e disomogenei.

La paracromatina è quella minima parte di cromatina biologicamente attiva sempre presente nel nucleo della cellula. La paracromatina si colora pochissimo, con ogni tipo di colorante e rappresenta la porzione chiara del nucleo, quella che si intravede fra le maglie della trama cromatinica (Paracromatina significa “che sta vicino alla cromatina”) .

IL CONCETTO DI EUPLASIA, ovvero LA CELLULA NORMALE: viene definita “normale” quella cellula che si trova in “pace ed armonia” con le altre cellule, con l’ambiente che la circonda ed in assenza di processi patologici che la coinvolgano e la modifichino.

In condizione di euplasia, le caratteristiche delle principali strutture nucleari, se osservare al microscopio ottico, sono le seguenti: >) rotonde o arrotondate: nucleo, nucleoli, cromocentri >) uniformi e regolari: pattern cromatinico, distribuzione paracromatina, spessore della cromatina marginale) >) sovrapponibili da un nucleo all’altro in un frammento multicellulare di tessuto oppure da un nucleo all’altro di una cellula multinucleata.

Analizziamo ora le principali modificazioni morfologiche del nucleo correlate alla presenza di neoplasia maligna; 1) Irregolarità della membrana nucleare Gravi irregolarità di forma della membrana cellulare sono abbastanza frequenti nelle cellule neoplastiche, mentre sono assolutamente poco comuni nelle cellule non tumorali.

Come già affermato in precedenza, non possiamo vedere la membrana nucleare vera e propria, ma possiamo valutare con precisione il suo profilo guardando la cromatina margi-

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nale che si addensa contro il margine interno della membrana stessa.

Queste anomalie di profilo fanno assumere al nucleo aspetti bizzarri, per la presenza di spicole appuntite che si proiettano verso l’esterno, incisure profonde che assomigliano a “morsi” o a tagli e comunque qualsiasi altro aspetto non spiegabile con lo stato di normalità (euplasia), regressione (retroplasia) od incrementata attività (proplasia) cellulare.

2) Anomalie a carico del contenuto (ipercromatismo) e della distribuzione della cromatina Queste anomalie si riscontrano spessissimo in associazione fra di loro e per questo vengono trattate insieme.

Con il termine ipercromatismo si intende un percettibile aumento di intensità di colorazione del nucleo al microscopio ottico e questo come conseguenza sia di una maggiore concentrazione di DNA che di una maggiore tingibilità dell’eterocromatina.

Questo è dovuto principalmente al fatto che le cellule neoplastiche sono in genere polipliodi ovvero, presentano una anomalia cromosomica dovuta alla presenza di un numero di cromosomi maggiore di un multiplo intero del normale assetto euploide; essendovi più DNA, vi saranno più proteine ad esso collegate e sono queste che, una volta colorate, determinano l’ipercromatismo nucleare così spesso rilevabile nelle cellule neoplastiche.

L’ipercromatismo è frequentemente associato alla distribuzione irregolare della cromatina: viene abbandonata quella disposizione regolare ed uniforme presente nelle cellule in euplasia e la cromatina si addensa a formare numerosi cromocentri sotto forma di ammassi irregolari e filamenti grossolani casualmente distribuiti in tutta la trama cromatinica.

Particolarmente evidenti sono le anomalie a carico della cromatina marginale che, a volte, assume l’aspetto di spessi agglomerati alternati ad aree dove essa è così sottile da non essere evidenziabile al microscopio ottico. La marginalizzazione della cromatina nucleare ha un significato preciso: essa, infatti, è un segno precoce di degenerazione cellulare.

Per contro, la paracromatina può apparire ancora più chiara fino a diventare otticamente vuota, risaltando notevolmente con le aree ipercromatiche circostanti; questo esagerato pleomorfismo nucleare, appare ancora più evidente se il nucleo viene ipoteticamente diviso in quattro settori ed ogni settore viene paragonato agli altri: in una cellula normale, la distribuzione è omogenea e le 4 sezioni sono praticamente sovrapponibili fra di loro, come densità e distribuzione di cromatina, mentre nel nucleo della cellula neoplastica, le differenze sono molto ben evidenti fra settore e settore.

3) Anomale a carico dei nucleoli In seguito a vari tipi di stimoli patologici, si possono avere alterazioni nel volume, regolarità, forma e numero dei nucleoli presenti nel nucleo.

Nucleoli anche di cospicue dimensioni (≥ a 5 µ), si possono incontrare ogniqualvolta la cellula sia impegnata nella produzione di proteine come, ad esempio, a seguito di flogosi acuta o cronica oppure di processi riparativi. Nella cellula neoplastica, al contrario, i nucleoli aumentano di volume come conseguenza del blocco nel trasporto dei prodotti nucleolari verso il citoplasma.

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Sempre come conseguenza di una forte richiesta nella produzione di proteine, i nucleoli possono essere numerosi (≥ 5-6) e di dimensioni diverse nella stessa cellula, per cui anche l’anisonucleolisi non rappresenta, di per sé, un criterio molto importante di malignità.

Al contrario, non esiste nessuna motivazione al di fuori della presenza di una neoplasia maligna, per spiegare la presenza di nucleoli di forme bizzarre, con spicole o margini retti ed angolati; questo aspetto, specialmente se in associazione ai due sopra menzionati, rappresenta sicuramente un forte ed importante indizio di malignità.

4) Molteplicità nucleare La presenza di più nuclei all’interno di una stessa cellula, non rappresenta, di per sé, un criterio di malignità; esistono infatti numerosi esempi di cellule multinucleate in popolazioni cellulari del tutto normali.

Ricordiamo, ad esempio, le cellule transizionali delle vie urinarie, le cellule mesoteliali, le cellule ciliate bronchiali, gli osteoclasti, le cellule giganti da corpo estraneo, i megacariociti, ecc.; Tuttavia, quando all’interno dei vari nuclei troviamo le caratteristiche descritte ai punti 1, 2 e 3, un sospetto di malignità deve essere emesso; nella cellula neoplastica, infatti, la multinuclearità è conseguenza di divisioni nucleari (normali, ma più spesso anomale) non seguite da divisione citoplasmatica oppure, più raramente, da fusione di due o più cellule neoplastiche. I nuclei risultanti, saranno perciò colpiti in varia maniera dalle anomalie a carico di cromatina, nucleoli e membrana nucleare.

5) Macrocariosi ed aumentato rapporto nucleo/citoplasma (N/C) Un nucleo avente diametro superiore ai 10-12 µ deve essere considerato come “sospetto”; nelle cellule neoplastiche, infatti, le dimensioni del nucleo possono aumentare sia come conseguenza della poliploidia e del relativo aumento di DNA, sia come aumento dell’idratazione conseguente alle difficoltà di scambio di ioni e molecole fra i due versanti della membrana nucleare (c.d. edema nucleare funzionale).

La relazione fra volume nucleare e citoplasmatico rimane entro limiti costanti nelle cellule normali. L’aumento della componente nucleare di questo rapporto è uno dei caratteri più distintivi della malignità ed inoltre ci fornisce anche un indice del grado di differenziazione delle cellule neoplastiche, infatti, in generale, più le cellule neoplastiche sono indifferenziate più il rapporto N/C è elevato.

Un aumento di volume del nucleo può essere presente anche in cellule non maligne come risultato di vari processi patologici (infiammazione, processi riparativi, metaplasia); in questi casi, tuttavia, l’aumento del nucleo è accompagnato da un aumento globale del volume cellulare ed il rapporto N/C si mantiene entro limiti costanti di benignità.

Vale la pena di ricordare che le cellule della linea linfoide presentano fisiologicamente un elevato rapporto N/C. 6) Mitosi anomale Un altro importante criterio di malignità identificabile a livello di nucleo è il riconoscimento di mitosi anomale.

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Come conseguenza delle gravi alterazioni a livello di materiale cromatinico, il regolare svolgimento della mitosi viene impedito ed il risultato sarà quello di una divisione anomala e bizzarra del nucleo.

I quadri più frequentemente osservabili sono quelli di divisione asimmetrica del materiale cromatinico, divisioni multipolari, cromosomi addensati ai poli del nucleo (c.d. cromosomi polari), ritardo di migrazione dei cromosomi in anafase.

Come conseguenza di queste aberrazioni, si avranno cellule multipolari con varie anomalie a livello nucleare oppure nuclei giganti, abnormi, mostruosi. b) a livello di citoplasma Le modificazioni a carico del citoplasma, spesso facilmente evidenziabili e fortemente suggestive di malignità, devono tuttavia essere sempre considerate di secondaria importanza e come elementi complementari alle più importanti modificazioni coinvolgenti il nucleo ed i suoi elementi costitutivi.

Come già detto in precedenza, la specifica attività funzionale viene meglio descritta dalla morfologia citoplasmatica, che manifesta le differenziazioni caratteristiche di una particolare attività cellulare. È importante avere chiaro il concetto di differenziazione o maturazione cellulare: con questo termine si intende indicare il processo che, sotto il controllo genetico del nucleo, porta alle modificazioni morfofunzionali che permettono alla cellula di specializzarsi ed esplicare il compito per la quale essa è richiesta dall’organismo. Questo comporterà particolari differenziazioni a carico della matrice citoplasmatica e della membrana cellulare; fra le prime ricordiamo lo sviluppo di tonofibrille (nelle cellule squamose dell’epidermide), di miofibrille (nelle cellule muscolari) e di neurofilamenti (nelle cellule nervose), mentre fra le seconde ricordiamo la formazione di desmosomi (che permettono la giunzione fra cellule di uno stesso tessuto permettendo un passaggio selettivo delle più svariate sostanze), di orletti striati, di cilia, ed altro ancora.

Nella differenziazione cellulare normale, ad esempio, l’epitelio squamoso pluristratificato va incontro a maturazione diretta dalle cellule basali alle cellule superficiali corneificate: si può dire, di conseguenza, che queste ultime sono più differenziate delle cellule basali.

1) Dedifferenziazione cellulare Anche le cellule neoplastiche sottostanno al processo della differenziazione, ma questo può essere incompleto o aberrante; il concetto di differenziazione relativo a cellule neoplastiche, è rappresentato dalla somiglianza delle cellule tumorali al tessuto di origine corrispondente, per cui si definisce “differenziato” dal punto di vista citologico, un tumore le cui cellule presentino caratteristiche morfologiche tali da permettere facilmente di individuare la linea cellulare colpita: un esempio classico è quello del mastocitoma di Grado I nel quale tutte le cellule neoplastiche presentano abbondanti granulazioni a livello citoplasmatico.

Al contrario, si definisce “indifferenziato” dal punto di vista citologico, un tumore le cui cellule abbiano perso a tal

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punto le caratteristiche morfologiche delle cellule originarie da renderne difficile, se non impossibile, l’attribuzione del tessuto di origine: un classico esempio è quello del melanoma amelanotico, dove vengono a mancare quasi totalmente le granulazioni citoplasmatiche nero-verdastre che caratterizzano il melanocita maturo.

Il massimo livello di dedifferenziazione viene chiamato anaplasia.

Non sempre, comunque, il grado di differenziazione è inversamente proporzionale alla malignità della neoplasia: esistono carcinomi mucosecernenti (cioè così ben differenziati da produrre addirittura muco, come le cellule normali) che hanno un comportamento biologico molto maligno mentre il basalioma ha un comportamento biologico certamente meno maligno del carcinoma squamocellulare, pur essendo un tumore che colpisce cellule meno differenziate della stessa linea evolutiva.

2) Cellule ad anello con castone (“signet ring cells”) In alcuni adenocarcinomi, specialmente in quelli di derivazione gastrica, intestinale o mammaria, è possibile identificare cellule neoplastiche che presentano un grosso vacuolo omogeneo che colma tutto lo spazio citoplasmatico spingendo il nucleo contro la membrana citoplasmatica, deformandolo.

L’aspetto finale sarà quello tipico di un anello con castone o a sigillo.

Questo materiale è muco ed è generalmente positivo con la colorazione di PAS. Pur essendo un aspetto piuttosto tipico, non è tuttavia patognomonico di adenocarcinoma; soprattutto in corso di versamenti cavitari, le cellule mesoteliali reattive possono, in fase di degenerazione, assumere l’aspetto morfologico appena descritto e questo non crea certo problemi interpretativi di poco conto, se si tiene presente la frequenza con la quale molti adenocarcinomi metastatizzano a livello di membrane sierose e di organi interni.

Il significato di questa anomalia è da ricercarsi nel fatto che queste cellule neoplastiche, pur mantenendo la capacità di produrre muco, non sono in grado di secernerlo per cui si riempiono e degenerano senza riuscire a liberarlo.

3) Iperbasofilia L’aumentata basofilia citoplasmatica è un rilievo piuttosto frequente all’osservazione con il microscopio ottico, di cellule neoplastiche.

Questa alterata tingibilità del citoplasma è conseguenza di una attività sintetica abnorme ed esagerata; l’RNA ed i prodotti di sintesi che si addensano, in modo afinalistico, a livello di citoplasma sono responsabili di questo fenomeno.

B) Criteri di malignità a livello di popolazione cellulare Mentre le valutazioni fino a qui fatte, relative a nucleo e citoplasma, posso essere definite come citologia del medio e forte ingrandimento, le considerazioni relative alla popolazione cellulare possono essere definite come citologia del piccolo e medio ingrandimento.

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Infatti, i criteri di malignità a questo livello vengono analizzati sia paragonando le cellule fra di loro, nella globalità dello striscio disponibile, sia valutando le caratteristiche dei frammenti di tessuto neoplastico raccolti con l’agoaspirazione.

1) Pleomorfismo Uno dei caratteri più salienti di malignità riscontrabile a carico di una popolazione cellulare è dato dal pleomorfismo, ovvero dalla marcata variazione di forma e volume delle cellule ed in particolare dei nuclei e del loro contenuto.

In particolare, si definisce anisocitosi la differenza in forma e volume di cellule di una stessa popolazione; anisocariosi la differenza in forma e volume dei nuclei cellulari; anisonucleolisi la differenza in numero, forma e volume dei nucleoli presenti nei nuclei cellulari.

Queste modificazioni, a volte tanto marcate da potere essere definite drammatiche, sono la conseguenza del controllo aberrante oppure mancante, da parte del nucleo neoplastico, della crescita e della differenziazione cellulare.

Un altro aspetto importante di pleomorfismo, già descritto in precedenza, è il rilievo della variazione del rapporto N/C nell’ambito della popolazione cellulare.

2) Ipercellularità Questo parametro è fortemente influenzato dal tipo di tumore che stiamo analizzando.

Infatti, il rilievo di moltissime cellule è assolutamente comune in presenza di neoplasie a cellule rotonde, frequente in presenza di neoplasie di origine epiteliale ma poco comune in presenza di neoplasie di origine mesenchimale.

Il rilievo di ipercellularità a carico di una popolazione di cellule di origine mesenchimale, anche in assenza di criteri di malignità importanti, deve sempre fare sospettare una neoplasia; questo avviene perché le cellule neoplastiche mesenchimali tendono a perdere la forte coesione intercellulare, dovuta alla presenza di sostanza fondamentale, che caratterizza i tessuti connettivali.

3) “Cannibalismo” cellulare Il cannibalismo o pseudofagocitosi cellulare rappresenta il fenomeno per cui una cellula è contenuta nel citoplasma di un’altra cellula.

Questo fenomeno è stato spiegato, dai primi citologi, come un vero e proprio quadro di fagocitosi fra cellule neoplastiche, da qui il termine di “cannibalismo”.

In realtà, le cose avvengono in maniera diversa: i contatti abnormi che si stabiliscono fra cellule neoplastiche contigue e che hanno perduto l’inibizione da contatto possono causare profonde invaginazioni del citoplasma con il risultato che una cellula sferica sembri fagocitata all’interno di una seconda la quale, invece, la circonda con lunghe propaggini citoplasmatiche.

Questa interpretazione è confermata dal fatto che le membrane che delimitano le due cellule sono perfettamente integre presentando lo sviluppo di desmosomi normali.

Da sottolineare il fatto che questi quadri di pseudofagocitosi rappresentano rapporti intercellulari che si possono ritrovare nelle cellule mesoteliali reattive e non neoplastiche.

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4) Indice mitotico Questo indice esprime il rapporto fra il numero totale delle cellule presenti ed il numero delle cellule in mitosi.

Pur essendo un parametro molto utile ed affidabile in istologia, non lo è altrettanto in citologia perché l’assenza di coesione fra le cellule e la variabilità della densità di queste ultime sul vetrino permette unicamente valutazioni di tipo empirico e soggettivo, che possono risentire in modo notevole dell’area dello striscio che si sta analizzando.

Dal punto di vista citologico, risulta molto più indicativo di malignità il rilievo di alcune mitosi anomale che di numerose mitosi normali.

5) Citoarchitetture Un concetto relativamente nuovo in medicina veterinaria, anche se caposaldo dell’interpretazione citologica in medicina umana da moltissimo tempo, è quello della valutazione citologica delle architetture, ovvero della disposizione reciproca delle cellule appartenenti allo stesso tessuto.

Ogni tessuto normale manifesta una determinata disposizione architetturale, conseguenza del comportamento biologico e del controllo genetico delle cellule che lo compongono.

La disposizione architettonica amplifica e razionalizza la biologia di ogni singola cellula ed infatti, le cellule di un determinato tessuto non solo nascono con la capacità di esprimere determinate capacità metaboliche ma anche con una programmazione per disporsi reciprocamente in maniera da ottimizzare le loro potenzialità.

Quando un determinato tessuto va incontro ad una patologia neoplastica, specialmente in presenza di neoplasie mediamente o ben differenziate, è possibile rilevare nello striscio che stiamo analizzando frammenti multicellulari che conservano disposizioni architetturali tipiche del tessuto di origine, permettendoci così di aggiungere informazioni preziose e complementari a quelle derivanti dall’analisi morfologica delle singole cellule. È altresì vero che nelle neoplasie indifferenziate, il tessuto tumorale cresce in maniera caotica ed afinalistica, assumendo disposizioni spaziali ed architettoniche che non permettono il riconoscimento esatto del tessuto di origine: anche in citologia, come in istologia, si può parlare, in presenza di questi quadri, di “perdità di polarità” ed il suo rilievo deve sempre fare sospettare una patologia neoplastica.

(Una trattazione completa delle citoarchitetture non è nelle finalità di questa relazione; questo interessante argomento è stato approfondito nel corso di una giornata del Gruppo di Studio di Citologia per cui, chi fosse interessato all’argomento, può chiedere il testo della relazione al suo Autore, il Dr. Masserdotti di Brescia oppure al sottoscritto).

C) Criteri indiretti di malignità Tutte le considerazioni fino a qui fatte, sono relative alle cellule che noi sospettiamo appartenenti alla neoplasia.

Esistono tuttavia dei criteri valutativi che, pur non basandosi sulla presenza o assenza di cellule sospette, possono fare insorgere al citologo il sospetto di una neoplasia in atto:

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si parla di criteri “indiretti” di malignità. La loro identificazione da parte del citologo permette, se non di emettere una diagnosi di malignità, sicuramente di aumentare l’attenzione per cercare di individuare la causa della loro presenza.

1) Presenza di eritrociti e di macrofagi carichi di emosiderina La presenza sul vetrino di numerosi eritrociti può suggerire fenomeni emorragici secondari, fra le altre cose, a forme tumorali ed il suo significato è del tutto sovrapponibile a quello della ricerca del sangue occulto nelle feci e nelle urine.

Ovviamente si tratta di un segno di nessuna importanza nei preparati ottenuti per abrasione o spazzolatura ma assume un significato particolare in campioni che derivano da versamenti cavitari, urine, liquor cefalorachidiano e lavaggio broncoalveolare.

Come conseguenza della emorragia, possono essere evidenti numerosi siderofagi, ovvero macrofagi che hanno fagocitato eritrociti ed hanno, al loro interno, depositi di emosiderina e di ematina: la loro presenza ci indica che l’emorragia è presente da un certo periodo di tempo e che, pertanto, non può essere stata causata dalle manovre eseguite per raccogliere i campioni da esaminare.

2) Fondo necrotico Il rilievo di un fondo composto da detriti cellulari necrotici, precipitati proteici e macrofagi ripieni di questi detriti, deve fare sospettare la presenza di una neoplasia in fase avanzata, pur essendo la necrosi fenomeno comune anche a patologie non tumorali.

Questo fenomeno detto “diatesi tumorale”, è conseguenza sia della rapida morte e degenerazione delle cellule neoplastiche, che non sono in grado di replicarsi normalmente e di svolgere le fisiologiche attività metaboliche che spetterebbero alle cellule dalle quali derivano, sia dal fatto che il tumore , crescendo e sviluppandosi in maniera afinalistica e caotica, presenterà aree con insufficiente od assente apporto vascolare destinate ad ischemia e necrosi.

3) Presenza di popolazioni cellulari reattive La presenza di una popolazione cellulare reattiva può rappresentare la risposta dell’organismo a certi tipi di neoplasia.

In particolare, la presenza di moltissimi granulociti eosinofili in un versamento può, fra le altre ipotesi, farci sospettare la presenza di un mastocitoma, così come la presenza di una forte reazione mesoteliale, in assenza di concomitante flogosi che ne giustifichi la presenza, deve farci insospettire riguardo la presenza di una sottostante patologia neoplastica.

ALTERAZIONI CELLULARI SIMULANTI LA MALIGNITÀ Esistono una serie di situazioni patologiche non neoplastiche che possono simulare quadri di malignità citologica.

La loro conoscenza è pertanto fondamentale, per non incorrere in errori le cui conseguenze possono essere drammatiche.

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**Proliferazione infiammatoria Lo stimolo infiammatorio può determinare una attiva proliferazione cellulare come risposta diretta ad un agente patogeno: come conseguenza di questa intensa proliferazione si possono osservare quadri di ingrandimento nucleare, polinucleosi, ipercromatismo, marginalizzazione della cromatina e presenza di macronucleoli.

L’interpretazione delle modificazioni cellulari infiammatorie deve focalizzarsi sulle alterazioni del citoplasma e delle strutture cromatiniche. Il volume citoplasmatico tende ad aumentare, parallelamente a quello nucleare, con un minimo spostamento del rapporto nucleo-citoplasmatico.

I nuclei possono essere polimorfi, per effetto della degenerazione cellulare indotta dalla flogosi; si possono avere anche nuclei con contorni irregolari, cromatina addensata alla periferia, carioressi e picnosi.

Di fatto, in presenza di flogosi cronica, si possono rilevare cellule tissutali fortemente sospette: per questo motivo, in presenza di linee cellulari reattivo-flogisitche (neutrofili, linfociti, macrofagi, fibroblasti, ecc,) le valutazioni di malignità devono essere estremamente caute.

L’esame deve essere eventualmente ripetuto dopo un ciclo di terapia antibiotica e, se permangono dubbi, deve essere proposta una biopsia per una valutazione istologica. ***Iperplasia ed ipertrofia Si definisce con iperplasia un aumento volumetrico di organi o tessuti conseguente all’aumento numerico delle cellule che li compongono mentre si definisce ipertofia un aumento volumetrico delle singole cellule.

Questi fenomeni, spesso associati, si possono rilevare in vari tipi di epiteli e mucose (cilindrico, squamoso, transizione) come conseguenza di stimoli irritativi cronici oppure in tessuti ghiandolari (mammella, prostata) come conseguenza di attività ormonale.

Dal punto di vista citologico, le cellule epiteliali e mucose iperplastiche benigne, sono caratterizzate da un aumento delle dimensioni nucleari, con contorni regolari e cromatina a trama delicata e distribuzione uniforme.

Il rapporto nucleo-citoplasma è praticamente costante.

Riparazione e rigenerazione Le reazioni riparative che interessano i tessuti, si manifestano con ipertrofia nucleare e prominenza dei nucleoli, potendo così simulare la malignità.

La rigenerazione o la riparazione delle superfici epiteliali e mucose che seguono ad una lesione tissutale, avvengono mediante tessuto di granulazione. La riepitelizzazione inizia a partire dai margini della lesione e ricopre progressivamente il neoformato tessuto di granulazione con un singolo strato di cellule immature che si differenzieranno in un secondo momento.

Le cellule in attiva rigenerazione presentano caratteri morfologici simili a quelli già descritti al punto ***, spesso associati ad alterazioni di tipo infiammatorio.

Dal punto di vista citologico, i nuclei sono ingranditi ed ipercromatici, con macronucleoli evidenti; tuttavia, la disposizione della cromatina è uniforme, finemente granulare, senza formazione di aggregati grossolani ed irregolari con membrana nucleare regolare omogenea e ben distinta. ●

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Cellule multinucleate Uno dei segni citologici di malignità è dato dalla presenza di cellule giganti, con marcata ipertrofia nucleare e nuclei multipli o plurilobati. Questo aspetto non va confuso con la multinuclearità che si può osservare in cellule benigne.

Cellule multinucleate maligne: come già detto, nelle neoplasie maligne la multinuclearità è conseguente a mitosi anomale multipolari; i criteri che permettono di riconoscere cellule di questo tipo come maligne sono: aumento del rapporto N/C, ipercromatismo con presenza di addensamenti cromatinici grossolani, contorno nucleare irregolare, nucleoli prominenti e nuclei di forma e dimensioni diverse.

Cellule istiocitarie multinucleate : si tratta di sincizi cellulari multinucleati ad attività fagocitaria che si possono rinvenire in corso di flogosi croniche, generalmente di tipo non settico.

I nuclei multipli sono rotondi od ovali, di dimensioni uniformi, situati centralmente, a volte sovrapposti fra loro e con cromatina finemente granulare.

In generale, le membrane nucleari sono regolari e ben definite, il citoplasma è abbondante, a volte con vacuoli fagocitari, limiti poco distinguibili.

Cellule giganti di tipo osteoclastico: cellule giganti multinucleate sono segnalate negli aspirati provenienti da lesioni displasiche di osso e sinovia, nonché da tumori benigni della gengiva del cane (epulidi). Anche qui, i nuclei sono regolarmente rotondi od ovali, in posizione centrale e contorno ben delineato. Le caratteristiche citoplasmatiche, che si presenta privo di vacuoli ed a limiti netti e definiti, permette la distinzione di queste cellule da quelle istiocitarie multinucleate. ❍

Per concludere, vorrei ripetere ancora una volta quanto già espresso all’inizio di questa relazione, poiché considero questi concetti di importanza fondamentale: 1) In citologia diagnostica, esiste un solo ed indiscutibile criterio di malignità, e cioè il ritrovare cellule estranee (e cioè metastatiche) a livello di un tessuto o di un fluido ove queste non dovrebbero esistere. In assenza di questo reperto, nessuno dei criteri che sono stati descritti, permetterà da solo di esprimere un criterio definitivo di malignità o benignità. Il giudizio finale dipenderà dalla somma e dall’importanza dei criteri di malignità evidenziati, anche in relazione al tipo di neoplasia sospettata.

2) Nessuna delle valutazioni che sono state il soggetto di questa relazione può e deve essere fatta se non si è sicuri della adeguatezza e della rappresentatività del campione citologico in esame.

Letture consigliate Bibbo M. Comprehensive Cytopathology 2nd edition, WB Saunders, Philadelphia, 1997.

Fournel-Fleury C., Magnol J-P, Guelfi J.F., Color Atlas of Cancer Cytology of the Dog and the Cat Conference Nationale des Veterinaires Spécialisés en Petit Animaux, Paris, 1994.

Takahashi M., Citologia del Cancro Verduci editore, Roma, 1987.

Koss L.G. Aspiration biopsy: Cytologic Interpretation and Histologic Bases Lippincott & Wilkins ed., Baltimora, 1992.

DeMay R.M., The Art and Science of Cytopathology ASCP Press, Chicago, 1996.

Baker R., Lumsden J.H., Color Atlas of Cytology of the Dog and Cat Mosby ed, St Louis (MI), 1999.

Cowell R.L., Tyler R.D., Meinkoth J.H., Diagnostic Cytology and Hematology of the dog and the cat 2nd ed, Mosby, St.Louis, 1999.

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Cytology of Neoplastic Effusions I principi di citologia esfoliativa per l’analisi dei versamenti neoplastici

Dennis B. DeNicola DVM, PhD, Diplomate ACVP - Purdue University - Department of Veterinary Pathobiology - Indiana - USA

Riassunto L’identificazione di un versamento neoplastico può essere relativamente semplice. Si utilizzano gli abituali criteri citomorfologici di malignità per caratterizzare le singole popolazioni cellulari all’interno del versamento. Inoltre, il riscontro di un numero elevato di cellule non infiammatorie o di tipi cellulari anomali nel versamento, indipendentemente dai criteri morfologici di malignità può essere estremamente utile per identificare un versamento neoplastico. In alcuni casi, a livello di cavità toracica o addominale questa identificazione può essere problematica, a causa di una popolazione cellulare molto particolare, le cellule mesoteliali, tipicamente presenti sia nei versamenti neoplastici che in quelli non neoplastici. Queste cellule normali che rivestono la sierosa spesso diventano iperplastiche e displasiche ed assumono caratteristiche morfologiche che simulano i criteri citomorfologici di malignità. Questi elementi si esfoliano liberamente nella cavità corporea e si osservano sia nei versamenti infiammatori che in quelli neoplastici.

I due versamenti neoplastici più facilmente diagnosticati sono quelli associati al linfosarcoma ed al carcinoma.

I primi presentano comunemente una popolazione accentuata di cellule non infiammatorie isolate e tondeggianti.

Nella maggior parte dei linfosarcomi si riscontrano tipi cellulari intermedi o di grandi dimensioni e risulta quindi facile effettuare la differenziazione dai versamenti chilosi, dove predominano i piccoli linfociti. I versamenti determinati dai carcinomi mostrano comunemente un’accentuata popolazione di cellule mononucleari tondeggianti, raggruppate in grappoli adesi e associate ad un processo infiammatorio meno evidente. Nella maggior parte dei casi, sulla base della sola valutazione citologica è impossibile distinguere i versamenti carcinomatosi da quelli causati da un mesotelioma. Questi versamenti ed altri verranno illustrati nel corso della relazione facendo riferimento a casi clinici. Inoltre, verrà presa in considerazione l’analisi di base dei fluidi, compresa la caratterizzazione del conteggio degli elementi nucleati, del contenuto proteico e della valutazione chimica selettiva. Infine, verranno trattati i processi infiammatori secondari, la formazione del versamento chiloso ed altri argomenti.

The identification of a neoplastic effusion can be relatively simple. Routine cytomorphologic criteria of malignancy are used to characterize individual cell populations within the effusion. In addition, the finding of either high numbers of non-inflammatory cells or abnormal types of cells in the effusion regardless of cytomorphologic criteria of malignancy can be extremely helpful in characterizing a neoplastic effusion. Some neoplastic effusions of the thoracic and abdominal cavity can be problematic because of a unique population of cells, the mesothelial cell, typically present with both neoplastic and non-neoplastic effusions. These normal serosal-lining cells often become hyperplastic and dysplastic with morphologic features that mimic the cytomorphologic criteria of malignancy.

These cells exfoliate freely into the body cavity and are seen in both inflammatory and neoplastic effusions.

The two most easily diagnosed neoplastic effusions are effusions associated with lymphosarcoma and carcinoma. Lymphosarcoma effusions commonly present with a prominent population of discrete round non-inflammatory cells. Most lymphosarcoma are intermediate to large cell type and are therefore easily differentiated from chylous effusions with predominantly small lymphocytes. Carcinoma effusions commonly present with a prominent population of round mononuclear cells in cohesive clusters associated with a less prominent inflammatory process. Distinction between carcinomatous and mesothelioma-related effusions is impossible in most cases by only cytologic evaluation. These effusions and others will be demonstrated during the presentation in a case-based format. In addition, basic fluid analysis including characterization of nucleated cell counts, protein content and selective chemical evaluation will be included. Secondary inflammatory processes, chylous effusion formations, and others will be discussed also.

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Effusions associated with neoplastic disease can be a result of any of the primary causes of abdominal and thoracic fluid formation. The four primary causes of abnormal fluid accumulation include 1) decreased plasma colloidal oncotic pressure resulting in a loss of the “pulling” force of particulate matter in the plasma keeping fluid within the vasculature, 2) increased vascular permeability allowing excessive fluid to pass from the vasculature into the body cavity, 3) increased hydrostatic pressure forcing the water phase of the plasma into the body cavity, and 4) obstruction of lymphatic flow needed for normal fluid removal from the body cavity. The table below briefly reviews the major physical, quantitative cytologic and qualitative cytologic features of each of these types of fluid formation.

Transudates are most commonly associated with a decreased in the plasma colloidal oncotic pressure through diseases resulting in a decreased plasma albumin concentration.

Protein losing nephropathy and hepatic insufficiency are the two conditions typically placed high in a differential diagnosis list but severe protein losing enteropathy and severe malnutrition can also result in similar fluid formation. Both primary and secondary (metastatic) disease of the kidney and liver could easily result in transudate fluid formation. The presence or absence of neoplastic cells in the effusion is dependent upon the type of neoplastic process involved and the location of the neoplastic tissue. Epithelial neoplasms (carcinoma) and discrete cell neoplasms (lymphosarcoma, histiocytic neoplasia, mast cell tumor, etc.) tend to exfoliate well.

If these neoplastic tissues are in contact with the mesothelial surface, there is the potential of finding neoplastic cells in the effusion associated with the typical low numbers of mature nondegenerate neutrophils and macrophages.

Exudates are caused by any process resulting in increased permeability to blood vasculature. They are typically associated with active inflammatory disease or true hemorrhage, which are commonly found with many neoplastic conditions. Non-infectious inflammatory disease or hemorrhage associated with neoplasm invasion into normal tissue and tissue necrosis within neoplastic tissue itself or the tissue being invaded are common. If this process is close in proximity to the mesothelial surface of thoracic or abdominal cavities, this inflammatory process will be reflected in

the formation of an exudate. As with the transudative processes, the finding of neoplastic cells in the effusion is directly related to the type of neoplastic process seen and the location of the neoplasm relative to the mesothelial surface.

Passive congestion related to either congestive heart failure with potential thoracic and / or abdominal effusion formation or with local passive congestion related to conditions such as severe primary liver disease can be associated with neoplastic conditions. Neoplastic conditions can be associated with either primary or secondary disease processes. As with transudate and exudate fluid formation, the finding of neoplastic cells in the fluid is dependent upon the type of neoplastic process seen and the location of the neoplasm relative to the mesothelial surface. Obstruction of lymphatic drainage can be easily understood relative to primary neoplastic disease. Space-occupying lesions in either the thoracic or abdominal cavities can result in interference of lymphatic drainage and secondary chylous fluid accumulation.

Besides idiopathic chylous fluid effusion, neoplastic disease / space-occupying disease is the most common cause for chylous effusion formation. In many of these conditions, there is direct shedding of neoplastic cells into the body cavity involved and cytologic evaluation of the fluid is a critical component to the effusion formation.

Application of standard cytomorphologic criteria of malignancy is of value in recognizing the neoplastic process, but the general criteria of malignancy including cellularity and lack of a significant inflammatory cell population become of most value in recognizing neoplastic effusions. The finding of an abnormal, non-inflammatory cell population even without significant cytomorphologic criteria of malignancy is of extreme value. Lymphosarcoma (Figure 1), carcinoma (Figure 2) and mesothelioma (Figure 3) are the most commonly identified neoplastic effusions in veterinary medicine. In the case of lymphosarcoma, the finding of a prominent population of intermediate to large and immature appearing lymphocytes allow easy differentiation from simple chylous effusions where normal small lymphocytes should be the predominant lymphocyte population. In the case of carcinomas or mesotheliomas, the finding of large numbers epithelial or mesothelial cells in very large cohesive clusters allows easy identification of the neoplastic process.

General Features of Thoracic and Abdominal Fluid Formation Transudate

Exudate

Hemorrhage

Passive Congestive

Chylous

Color

Colorless

White, Yellow, or Pink

Red

Slightly Yellow to Pink

Colorless, White, or Pink

Turbidity

Clear

Turbid

Turbid

Turbid

Clear to Turbid

Protein (g/dl)

< 3.0

> 3.0

> 3.0

> 3.0

> 3.0

Specific Gravity

< 1.017

> 1.017

> 1.017

> 1.017

> 1.017

Nucleated Cells (/µl)

< 1,500

> 5,000

1,500 – 10,000

1,500 – 10,000

1,500 – 10,000

RBC (/µl)

Rare

Variable

Dependent upon degree of hemorrhage

< 5,000

Variable

Nucleated Cell Types

Mature neutrophils and macrophages with few mesothelial cells

Primarily neutrophils and macrophages dependent upon cause

Macrophages with variable numbers of neutrophils

Macrophages with variable numbers of neutrophils

Mature neutrophils, small lymphocytes and variable numbers of macrophages

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Figure 1 - Abdominal fluid with lymphosarcoma; four large immature appearing neoplastic lymphocytes mixed with one small lymphocyte and one neutrophil.

Figure 2 - Thoracic fluid with metastatic carcinoma effusion; primarily neoplastic cells present in large cohesive clusters.

Figure 3 - Thoracic fluid from a dog with malignant mesothelioma. Note the large, highly pleomorphic mononuclear and multinucleated neoplastic mesothelial cells surrounded by erythrocytes and mixed inflammatory cell types.

Figure 4 - Thoracic fluid with severe mixed neutrophilic / macrophagic inflammation and marked mesothelial cell hyperplasia / dysplasia; mesothelial cells actually only represent less than 1% of the total nucleated cell populations.

Figure 5 - Thoracic fluid from a dog with a pure transudate. Multiple benign hyperplastic / dysplastic mesothelial cells with a high mitotic rate are present. The total cellularity of the fluid is low. This specimen was prepared from a very concentrated cellular pellet.

Figure 6 - Thoracic fluid from a dog with a pure transudate.

Multiple benign hyperplastic / dysplastic mesothelial cells are present. The total cellularity of the fluid is low. This specimen was prepared from a very concentrated cellular pellet.

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The primary problem with recognizing neoplastic effusions is when there is significant active inflammation associated with the process. If a prominent inflammatory process is present, caution to prevent over-interpretation of the effusion is strongly recommended. In the face of any type of active inflammatory process within the thoracic or abdominal cavities, there is typically a response by the mesothelial surfaces. Benign mesothelial cell hypertrophy, hyperplasia and dysplasia are commonly seen in any type of effusion formed and many of the morphologic features of dysplastic / hyperplastic mesothelial cells are similar to the cytomorphologic criteria of malignancy.

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Some of the commonly seen morphologic similarities include anisocytosis, anisokaryosis, variation in nuclear/cytoplasmic ratios, present of prominent and multiple nucleoli, presence of prominent numbers of mesothelial cells, etc. When inflammation is present and there is an understanding that a significant mesothelial cell response is likely, identification of neoplastic disease based upon the evaluation of low numbers of suspected neoplastic cells should be avoided (Figure 4, 5 and 6). Investigation into other diagnostic modalities including localization of a space-occupying lesion and direct fine needle aspiration or biopsy for cytologic or histologic assessment is warranted.

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Cytologic Analysis of Neoplastic Diseases of Thoraco-Abdominal Masses Citologia oncologica delle masse toracoaddominali

Dennis B. DeNicola DVM, PhD, Diplomate ACVP - Purdue University - Department of Veterinary Pathobiology - Indiana - USA

Riassunto Grazie agli sviluppi relativamente recenti delle tecniche di diagnostica per immagini, ed in particolare, della caratterizzazione ecografica della cavità addominale e di quella toracica, ed al miglioramento delle procedure di prelievo diretto di campioni bioptici, è diventata prassi comune l’esame di materiale citologico proveniente da vari organi interni.

Nella maggior parte dei casi, si applicano i metodi di routine per la valutazione dei campioni citologici. Per la caratterizzazione delle malattie a carattere nodulare degli organi interni, sono estremamente importanti i criteri generali di malignità, come l’identificazione di singole popolazioni di tipi cellulari non infiammatori che non appartengono al particolare tessuto da cui è stato effettuato il prelievo. Inoltre, i criteri generali di malignità vengono completati da quelli standard nucleari e citoplasmatici, per cercare di caratterizzare un processo neoplastico.

Poiché l’identificazione di una “popolazione anomala” di cellule da una particolare sede anatomica è molto importante ai fini dell’analisi citologica, per la valutazione dei campioni prelevati dagli organi interni assume un ruolo critico la certezza della localizzazione anatomica del prelievo. L’identificazione di una popolazione di grandi cellule epiteliali mononucleari poligonali in un tentativo di prelievo per aspirazione da un nodulo del campo polmonare toracico caudale porta ad un’interpretazione di carcinoma, dal momento che queste cellule non appartengono al polmone. Tuttavia, la semplice e comune aspirazione di tessuto epatico durante l’esecuzione degli aspirati polmonari caudali può determinare facilmente la comparsa di grandi cellule epiteliali mononucleari poligonali, rappresentate da normali epatociti.

Nel corso di questa relazione verranno illustrati i principi basilari dell’analisi citologica dei campioni prelevati da organi interni. Verranno anche prese in considerazione alcune delle caratteristiche citologiche “normali” dei più comuni organi interni sottoposti a prelievo per questo tipo di esame. Infine, verranno trattati i comuni problemi di interpretazione nei differenti organi.

With the relatively recent advances in diagnostic imaging particularly related to ultrasonographic characterization of the abdomen and thoracic cavity and the advancement of directed biopsy procedures, collection of cytologic material from various internal organs have become common. In most cases, application of routine methods of evaluating the cytologic specimen is applied. General criteria of malignancy including identification of single populations of non-inflammatory cell types that do not belong in the particular tissue being sampled are extremely important in the characterization of nodular diseases of internal organs. In addition, standard nuclear and cytoplasmic criteria of malignancy complement the general criteria of malignancy when attempting to characterize a neoplastic process.

Because identification of an “abnormal population” of cells from a particular anatomic location is very important in the cytologic analysis, confidence in biopsy location is critical when evaluating cytologic specimens of internal organs.

The identification of a population of large polygonal mononuclear epithelial cells in an attempted aspirate of a nodule in the caudal thoracic lung field could lead to the interpretation of carcinoma since these cells do not belong in the lung.

However, the simple and common aspiration of liver tissue during caudal pulmonary aspirates could easily have large polygonal mononuclear epithelial cells that are normal hepatocytes.

The basic principles of cytologic analysis of internal organ cytologic specimens will be discussed during the presentation. Review of some of the “normal” cytologic features of the more common internal organs sampled for cytologic evaluation will be included. Discussion of common problem areas of interpretation for different organs will be included also.

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Before attempting to identify neoplastic disease of masses in the abdominal or thoracic cavity, there must be a good familiarity with the “normal” cytology of tissues that are going to be sampled. Some of the more standard cytologic criteria of malignancy that should be used in evaluating thoraco-abdominal mass evaluation are listed in tabular form below. These are very useful in working with masses from the thoracic and abdominal cavities, but certain criteria of malignancy are normal features of selected tissues and if this was not known, over-interpretation of the cytologic specimen is possible.

Several of the more common thoraco-abdominal mass cytologic specimens will be discussed briefly below. In each tissue discussed, the “normal” cytologic features are presented first with a general comment regarding “abnormal” features specifically related to neoplastic conditions of these tissues.

Lung – Cytologic evaluation of solid mass involvement of the lung is often best characterized with fine needle aspiration of the lung. Normal aspirates of the pulmonary parenchyma are hypocellular containing cell-free lipid material mixed with low numbers of alveolar macrophages and very few epithelial cells lining the airways. The simple identification of relatively high numbers of non-inflammatory cells from a directed aspirate of a mass in the pulmonary field is extremely supportive of neoplastic disease. Normally, the use of cytomorphologic criteria of malignancy to differentiate between benign neoplasia and malignant neoplasia is very helpful. With the presence of a radiographically identifiable mass within the pulmonary parenchyma, benign hyperplasia should not be a significant concern since this benign response typically does not present with space-occupying lesions. Carcinomatous (primary and metastatic) and lymphosarcoma involvement in the lung are the most common neoplastic conditions seen in veterinary medicine and these neoplasm types typically exfoliate well giving good diagnostic quality specimens to evaluate. The finding of high numbers of epithelial cells with or without significant cytomorphologic criteria of malignancy and the finding of a prominent population of intermediate to large and immature appearing lymphocytes (Figure 1) is highly diagnostic of neoplastic disease. Whenever there is significant active inflammation (with or without the presence of an underlying infectious etiologic agent), caution should be taken to avoid over-interpretation. When inflammatory disease is present, benign epithelial cell hyperplasia / dysplasia of alveolar lining and bronchioles is generally seen and morphologic features of these epithelial cells can mimic criteria of malignancy. Knowledge of normal hepatic cytologic features is important since aspiration of liver instead of pulmonary tissue can easily occur with attempted transabdominal aspirates of the caudal lung field.

Liver – Aspirates and impression smears of biopsy material from the liver are common cytologic specimens. Normal cytologic features of hepatic parenchymal tissue includes the finding of a prominent population of hepatocytes (Figure 2) mixed with very few other normal cellular elements from the liver including bile ductular epithelial cells, endothelial cells, fibrocytes and very few mixed inflammatory cell

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types. The predominating hepatocytes are generally present individually and in cohesive clusters of varying sizes. These cells are large round to polygonal cells with 1-2, uniform, round, eccentric nuclei and moderate to abundant amounts of granular, blue cytoplasm. Few small clear or indistinct cytoplasmic vacuoles and very few small, fine to coarse, green-black pigment granules representative of intracytoplasmic accumulation of bile pigment may be present also.

Normal hepatocytes typically have one (occasionally two) large, round and prominent nucleolus. Minimal variation in nuclear/cytoplasmic ratios is common for normal hepatocytes also. Hyperplastic hepatocytes may have a mild degree of anisokaryosis and the nuclear/cytoplasmic ratios may be slightly increased also. Both of these features are common with and may be the only cytomorphologic features of malignancy in well differentiated benign and malignant hepatocellular neoplasia. Therefore, accurate cytologic diagnosis of well differentiated hepatocellular neoplasia is difficult if not impossible. Histologic assessment of hepatic lobular architecture, or the lack of hepatic normal lobular architecture, is required to make a definitive diagnosis in these cases.

Metastatic carcinoma or highly pleomorphic primary hepatocellular carcinoma and primary bile ductular carcinoma and sarcoma or lymphosarcoma are relatively easy to identify in hepatic cytologic specimens. In the first case, the identification of an abnormal population of epithelial cells with good cytomorphologic criteria of malignancy is readily identified.

In the case of primary bile ductular carcinoma, a high number of “abnormal” epithelial cells even without good cytomorphologic criteria of malignancy is a helpful finding. Bile ductular epithelial cells typically have a much higher nuclear/cytoplasmic ratio, a much more deeply blue staining cytoplasm, and a less course cytoplasm compared to hepatocytes. In the case of sarcoma or lymphosarcoma, identification of an “abnormal” population of lymphocytes or mesenchymal cells with or without good criteria of malignancy is a strong criterion for underlying mesenchymal neoplasia (Figures 3 and 4). Since mesenchymal cells typically do not exfoliate well at all, finding any mesenchymal cells in an aspirate of liver is highly suspicious for neoplastic disease. Benign bile ductular epithelial cell hyperplasia and benign fibroplasia may be seen with inflammatory and degenerative changes within the liver and in these conditions, increased numbers of these cellular elements may be seen. However, the collection of high numbers of primarily bile ductular epithelial cells or a prominent population of mesenchymal cells with no significant active inflammatory component or hepatocyte population are extremely strong criteria for characterizing the process as a neoplastic process.

Spleen – Aspiration of normal splenic tissue typically reveals large numbers of lymphoid elements with normal small lymphocytes predominating and low numbers of reactive lymphocytes, plasmacytoid lymphocytes, well differentiated plasma cells, and intermediate to large and immature appearing lymphocytes. Samples should appear as normal lymph node aspirate material. In addition to the lymphoid elements, there is typically a minor background population of normal hematopoietic cellular elements, particularly in some species such as the ferret and hedgehog. Nodular / space-oc-

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Figure 1 - Fine needle aspirate of consolidated lung lobe with lymphosarcoma. Note the single population of intermediate to large and immature appearing lymphocytes.

Figure 2 - Fine needle aspirate of normal canine liver with a predominating population of large round to polygonal mononuclear epithelial cells with eccentric round nuclei, single round prominent nucleoli, and moderate amounts of granular blue cytoplasm.

Figure 3 - Fine needle aspirate of an enlarged liver in a dog with disseminated lymphosarcoma. Note the prominent population of intermediate to large and immature appearing neoplastic lymphocytes.

Figure 4 - Fine needle aspirate of a nodule in the liver with poorly differentiated sarcoma, probable hemangiosarcoma.

Figure 5 - Fine needle aspirate of a large space-occupying lesion in the spleen of a dog with hemangiosarcoma. Note the prominent population of pleomorphic mesenchymal appearing cells.

Figure 6 - Fine needle aspirate of an enlarged spleen from a dog with disseminated malignant histiocytosis. Note the large pleomorphic mononuclear and multinucleated cells that show erythrophagocytosis and cytophagia.

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cupying disease of the spleen is relatively common in our domestic species. In most cases, this is representative of benign lymphoid hyperplasia. Cytologic features are exactly as is seen in lymph node reactive hyperplasia where there is a relative increase in numbers of reactive and immature appearing lymphoid elements. Even in these cases, the normal small lymphocyte should predominate. Lymphosarcoma and hemangiosarcoma are among the most common neoplastic processes sampled in splenic specimens. Lymphosarcoma is usually an easy task related to the identification of large numbers of intermediate to large and immature appearing lymphocytes with no significant heterogeneity in the lymphoid populations seen. Cytologic and histologic diagnosis of hemangiosarcoma (Figure 5) of the spleen can be a very difficult task. In many of these cases where there is a very large identified mass within the splenic parenchyma, there are large areas of congestion, hemorrhage, and tissue necrosis associated with only a very small region of malignant neoplastic tissue. Accurate ultrasonographic identification of the more viable neoplastic tissue is not simple and randomly collected biopsy specimens prove non-diagnostic since they most commonly sample the areas of congestion, hem-

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orrhage and necrosis. If neoplastic tissue is sampled, pleomorphic plump spindle cells with good cytomorphologic criteria of malignancy are present. With other neoplastic conditions such as disseminated mastocytosis, disseminated histiocytic neoplasia (Figure 6) metastatic carcinoma and primary and secondary sarcomas, a homogeneous population of representative neoplastic cells typically with good cytomorphologic criteria of malignancy are easily found if the specific mass / nodule is sampled.

Collection and evaluation of masses in other internal organs including kidney, adrenal gland, the gastrointestinal tract and mesenteric lymph nodes can be a simple process if there is good knowledge of the â&#x20AC;&#x153;normalâ&#x20AC;? cytology of these tissues and a standard pattern of evaluation is followed. The presentation of a good diagnostic quality cytologic sample with high numbers of primarily a single population of noninflammatory cells that do not belong in the tissue being sampled is the most important criteria of malignancy possible. Many of these cases will have good cytomorphologic features of malignancy also and attempting to identify at least four nuclear criteria of malignancy before making a cytologic diagnosis of malignancy is a good recommendation.

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Cytologic Classification of Lymphosarcoma Classificazione citologica dei linfomi

Dennis B. DeNicola DVM, PhD, Diplomate ACVP - Purdue University - Department of Veterinary Pathobiology - Indiana - USA

Riassunto La diagnosi citologica del linfosarcoma è generalmente semplice in medicina veterinaria, perché di solito i nostri pazienti ci vengono presentati quando il processo patologico ha raggiunto uno stadio relativamente avanzato.

Al momento della visita, la maggior parte del tessuto linfoide normale è stato sostituito da tessuto neoplastico. Nella più comune presentazione del linfosarcoma nel cane, rappresentata dall’aumento generale di dimensione dei linfonodi, si osserva una notevole predominanza di una singola popolazione di linfociti intermedi o grandi e di aspetto immaturo. In altri casi di ingrossamento linfonodale, come l’iperplasia linfoide reattiva, l’infiammazione del tessuto linfoide e le metastasi a carico del tessuto stesso, si osserva un’evidente mescolanza di differenti tipi di linfociti, quali piccoli linfociti, linfociti reattivi, plasmacellule e linfociti di aspetto immaturo.

Il problema primario che ci si pone di fronte in caso di linfosarcoma in medicina veterinaria è la classificazione delle differenti forme. In medicina umana, sono stati utilizzati vari schemi citologici ed istologici di classificazione, basati sulla morfologia delle cellule neoplastiche e sull’architettura istologica dei tessuti tumorali, per prevedere la prognosi e la risposta al trattamento. La differenziazione fra linfosarcoma di basso grado, di grado intermedio e di grado elevato è più facile in medicina umana che in veterinaria, a causa della variazione istologica osservata e del grado di differenze di dimensioni del tipo di linfociti nell’uomo rispetto agli animali. Durante la relazione verranno illustrate e dimostrate le caratteristiche di base delle classificazioni citologiche del linfosarcoma, particolarmente nel cane. Verranno anche descritti altri tipi di classificazione del linfosarcoma come l’immunofenotipizzazione e la caratterizzazione dell’indice proliferativo. Questi vari schemi di classificazione saranno utilizzati per differenziare i quadri più difficili di linfosarcoma dalle forme atipiche di risposte linfoidi iperplastiche che possono essere difficili anche per un citologo esperto.

The cytologic diagnosis of lymphosarcoma is generally simple in veterinary medicine because the majority of the time our patients are presented at a relatively late stage of the disease process. At presentation, most of the normal lymphoid tissue has been replaced by neoplastic tissue. In the more common general lymph node enlargement presentation of lymphosarcoma in the dog, there is a vast predominance of a single population of intermediate to large and immature appearing lymphocytes. In other causes of lymph node enlargement including reactive lymphoid hyperplasia, inflamed lymphoid tissue, and metastatic disease to lymphoid tissue, there is a prominent mixture of different types of lymphocytes including small lymphocytes, reactive lymphocytes, plasma cells, and immature appearing lymphocytes.

The primary problem we are presented with regarding lymphosarcoma in veterinary medicine is the classification of the different forms. In human medicine various cytologic and histologic schemes of classification based upon neoplastic cell morphology and histologic architecture of the neoplastic tissue are used to predict prognosis and treatment response. Differentiation into low-grade, intermediate-grade and high-grade lymphosarcoma is easier in human medicine than veterinary medicine because of the histologic variance seen and the degree of size differences of the types of lymphocytes in human medicine compared to veterinary medicine. Basic features of cytologic classifications of lymphosarcoma, particularly in the dog, will be discussed and demonstrated during the presentation.

Other types of lymphosarcoma classification including immunophenotyping and proliferative index characterization will be discussed also. These various schemes of classification will be used to differentiate the more difficult presentations of lymphosarcoma from atypical forms of lymphoid hyperplastic responses that can be difficult for even the experienced cytologist.

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Lymphosarcoma is one of the more common neoplastic conditions in veterinary medicine where the veterinarian should be able to develop confidence in making the correct diagnosis with relatively little experience. The key to making the correct diagnosis is to understand the primary cytologic presentations in other conditions that could result in enlargement of the lymph node (lymphadenomegaly) regardless whether it is a peripheral or internal lymph node. Most cases of lymphosarcoma present with a homogeneous population of intermediate to large and immature appearing lymphocytes in contrast to the presence of a heterogeneous population of lymphoid cellular elements seen in the vast majority of all benign conditions of lymphadenomegaly. Some of the more common causes for lymphadenomegaly include benign reactive lymphoid hyperplasia, lymphadenitis, and edema. Regarding the lymphoid elements seen during these conditions, a similar pattern of lymphocyte heterogeneity is noted. Even with metastatic neoplastic disease to the lymph node, the identifiable lymphocyte populations present with a heterogeneous grouping of lymphocytes in different stages of differentiation.

The normal lymph node (Figure 1) cytologically presents with a very heterogeneous population of lymphocytes. In all normal peripheral and internal lymph nodes, normal small lymphocytes morphologically similar to the lymphocytes predominating in the peripheral blood vastly predominate. These cells typically represent greater than 85-95% of the total nucleated cells present depending upon which lymph node is sampled. Intermixed with these small lymphocytes, there are low numbers of reactive lymphocytes, plasmacytoid lymphocytes, well differentiated plasma cells, intermediate to large and immature appearing lymphocytes, and few macrophages and miscellaneous mixed inflammatory cell types.

Benign reactive lymphoid hyperplasia (Figure 2) presents with a similar heterogeneity of lymphoid elements, but the relative numbers of reactive and immature appearing lymphocytes increases compared to normal. Even in most of these cases, unless there is extreme reactive lymphoid hyperplasia, the normal small lymphocytes should be the predominating cell type seen.

In cases of lymphadenitis, the relative numbers of inflammatory cell types increases dependent upon the cause of the inflammatory process. Significant numbers of neutrophils are classically seen in cases of bacterial disease and they may be associated with degeneration of neutrophils and the cytological identification of bacterial organisms. Macrophages are commonly associated with inflammation associated with fungal infections, foreign bodies, tissue necrosis and hemorrhage. Eosinophils are seen in cases of hypersensitivity responses or parasitic infections. The lymphoid elements typically seen in cases of primary inflammatory disease of the lymph node usually are similar to those seen with simple benign reactive lymphoid hyperplasia.

In cases of simple lymphedema as a cause of lymphadenomegaly, the lymphoid response can be quite varied dependent upon the cause of the edema. If there is simple obstruction of lymphatic flow, the lymphocyte cellular pic-

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ture is similar to that of normal lymph node tissue with normal small lymphocytes vastly predominating. If there is an underlying inflammatory process with or without the presence of an infectious etiologic agent as the primary cause for the obstruction, there may be a relatively significant degree of benign reactive lymphoid hyperplasia.

Most cases of lymphosarcoma in veterinary medicine present in a relatively late stage of the disease development. Upon presentation, the veterinarian is dealing with significant lymphadenomegaly and in most cases, there is enlargement of multiple lymph nodes either peripherally or internally. Commonly at this stage of disease development, a single population of neoplastic lymphocytes has replaced the normal lymphoid elements. The cytologic diagnosis of lymphosarcoma, small cell type is a diagnostic challenge since this cell type represents up to 95% of the cellularity in the normal lymph node. Luckily in veterinary medicine, lymphosarcoma most commonly presents with intermediate to large and immature appearing neoplastic lymphocytes. The recognition of vastly predominating large and immature appearing lymphocytes is a relatively simple process for even the novice cytologist. Again, the key point to recognizing the presence of lymphosarcoma is the identification of a vastly predominating population of a single cell type in contrast to the classic presentation of lymphocyte heterogeneity seen with the various benign causes for lymph node enlargement.

Even with the uncommon presentation of small cell lymphosarcoma, a logical approach to the cytologic interpretation will usually lead to the correct diagnosis. If a veterinarian is presented with cytologic material from multiple peripheral lymph nodes that are approximately 2-4 times the size of normal and 95-100% of the nucleated cells seen are normal small lymphocytes, a relatively safe diagnosis of lymphosarcoma can be made. Other conditions including benign reactive lymphoid hyperplasia, lymphadenitis, edema and metastatic neoplasia will have a prominent heterogeneity of lymphoid elements, not a monotonous population of one lymphocyte type. If there is question, excisional biopsy and histologic assessment of nodal histologic architecture is warranted.

The specific classification of lymphosarcoma can be a relatively confusing and difficult task. Over the years there have been multiple classification schemes developed with hopes of being able to accurately predict biologic behavior or response to treatment. In human medicine, the classification of non-Hodgkinâ&#x20AC;&#x2122;s lymphosarcoma has evolved into the development of an attempted universal classification scheme identified as the International Working Formulation. This scheme appears to allow relatively good prediction of biological behavior and is based upon neoplastic lymphocyte size and shape as well as histologic pattern within the neoplastic tissue.

In veterinary medicine, many of the schemes that have been developed over the years for human medicine have been applied but good correlation with responsiveness to therapy or biologic behavior and survivability has not been well documented. Differentiation into low-grade, intermediate-grade and high-grade lymphosarcoma is easier in human medicine than veterinary medicine because of the his-

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Figure 1 - Normal lymph node with predominantly normal small lymphocytes mixed with very few large and immature appearing lymphocytes.

Figure 2 - Benign reactive lymphoid hyperplasia with prominent heterogeneity of lymphoid elements and the presence of significant numbers of plasmacytoid lymphocytes and well differentiated plasma cells.

Figure 3 - Lymphosarcoma with the more common variant of large immature appearing neoplastic lymphocytes replacing normal lymphoid elements.

Figure 4 - Lymphosarcoma with the much less common variant of large immature appearing and highly pleomorphic neoplastic lymphocytes replacing normal lymphoid elements.

tologic variance seen and the degree of size differences of the types of lymphocytes in human medicine compared to veterinary medicine.

The two primary histologic patterns of lymphosarcoma are “diffuse” and “follicular”. The follicular lymphosarcomas prove to be less malignant in human medicine, but this variant of lymphosarcoma is rare based upon most recent reviews of canine lymphosarcoma grading. The question of progression of follicular to diffuse lymphosarcoma type is always present, particularly in veterinary medicine since we often only see our animals with more severe progressive stages of disease. The diffuse variant of lymphosarcoma is when there is no normal nodal histologic architecture present in cross section of the node.

Beyond the specific pattern of distribution of the neoplastic lymphoid populations, there are attempts at critically evaluating cellular morphology with an emphasis on cell size, nuclear size and nuclear shape. The basic outline of the International Working Formulation classification

scheme for human medicine that is being attempted to be utilized in veterinary medicine (specifically the dog) is identified in tabular form below.

Immunophenotype classification of lymphosarcoma has become more common in recent years also. Unlike with human medicine, morphologic presentation does not predict immunophenotyping. Again, the lack of significant variation in cell size and differences in nuclear morphology, proves to be a restriction in veterinary medicine. A broad generality suggests that T-cell lymphosarcoma is of greater malignancy than B-cell lymphosarcoma. In the future, the sub-type classification of T-cell and B-cell lymphosarcoma may prove helpful in predicting biologic behavior in veterinary medicine as it has proven helpful in human medicine.

Regardless how lymphosarcoma is classified, the initial identification of lymphosarcoma is something the veterinarian is faced with regularly. The application of the simple outline presented at the beginning of this section should

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prove effective in identifying lymphosarcoma in most cases. The novice veterinary cytologist should be aware that there are variants of lymphosarcoma that are occasionally observed. All lymphosarcomas do not present with â&#x20AC;&#x153;typicalâ&#x20AC;? large round mononuclear cells with eccentric round to slightly indented nuclei and scant amounts of variably blue cytoplasm (Figure 3). Variants of mixed cellular lymphosarcoma (small and intermediate or large cell types), well differentiated plasmacytoid lymphosarcoma, lymphosarcoma

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cells with large prominent cytoplasmic granules, and extremely pleomorphic forms (Figure 4) of lymphosarcoma are all possible. In many of these cases, confirmation by evaluation by a veterinary pathologist trained in diagnostic cytology may be required to make a definitive diagnosis. In some of these cases, additional investigations including immunophenotyping and ultrastructural evaluation of the neoplastic cell population in question may be required also.

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Is It A Tumor or Not? È un tumore o non è un tumore?

Dennis B. DeNicola DVM, PhD, Diplomate ACVP - Purdue University - Department of Veterinary Pathobiology - Indiana - USA

Riassunto By following specific guidelines regarding the evaluation of any cytologic specimen, we can often easily differentiate neoplastic disease from non-neoplastic disease. In addition, differentiation between malignant neoplastic and benign neoplastic conditions are relatively easy in most situations. Abilities in diagnostic cytology are directly related to an individual’s knowledge of the “normal” cytologic features of the particular tissue being sampled, the cytologist’s logical approach to the cytologic specimen, and proper sample collection with assurance that the lesion in question is being sampled in a representative manner. In most of the cytologic specimens we see, differentiation of neoplastic and non-neoplastic diseases is based upon the relative numbers of either inflammatory or non-inflammatory cell types present. One of most difficult situations for even the well-trained cytologist is when there is a significant mixture of both inflammatory and non-inflammatory cellular elements. Whenever a mixed inflammatory and non-inflammatory cytologic specimen is seen, extreme caution should be taken. Hyperplastic / dysplastic “reactive” changes are commonly present with various epithelial linings and connective tissue elements associated with an inflammatory process. The morphologic features of these changes can be very similar to the cytomorphologic features of malignancy.

In the presentation, a series of cases will be used to emphasize some of the basic principles of diagnostic cytology related to the diagnosis of neoplastic disease as well as demonstrate some difficult mixed inflammatory and neoplastic diseases. This interactive session should allow the veterinarian to evaluate his or her level of understanding of diagnostic cytology and to identify the value of diagnostic cytology as a rapid mode of diagnosis in the veterinary practice setting.

This session should serve as either a starting or intermediary point in the participants’ life-long education in the area of diagnostic cytology.

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Canine aggression Aggressività del cane

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto Esistono diverse cause di comportamento aggressivo nel cane. Poiché il trattamento di ognuna di esse è differente, è importante conoscere i tipi di aggressività che un cane può esprimere prima di poter applicare un trattamento logico.

I tipi fondamentali di aggressività canina che verranno trattati sono i seguenti: 1. DA DOMINANZA - è il tipo più comune di aggressività nel cane - diretto solo verso i membri della famiglia o i componenti dello stesso nucleo familiare (membri del branco del cane) 2. RIVALITÀ TRA FRATELLI (compresa l’aggressività da parentela) - è il più comune tipo di aggressione fra cani che vivono nello stesso nucleo familiare - è un tipo di aggressività da dominanza 3. TERRITORIALE - protezione della proprietà - di solito rivolta verso gli estranei 4. DA PAURA - aggressione verso gli estranei sia all’interno che fuori dal proprio territorio - basata sull’apprendimento 5. INDOTTA DAL DOLORE - reazione istantanea al dolore 6. REINDIRIZZATA - aggressione diretta verso un membro inferiore del gruppo sociale e non verso quello che ha suscitato la risposta aggressiva 7. SESSUALE - aggressione associata ai comportamenti di accoppiamento/corteggiamento 8. MATERNA - protezione dei giovani 9. PREDATORIA - afferrare e uccidere una preda - altamente sviluppata nelle razze terrier e da combattimento - differisce dagli altri tipi perché l’assunzione di un comportamento sottomesso da parte dell’aggredito non spegne il comportamento aggressivo (cioè, la sequenza completa comprende l’uccisione).

10. DI GRUPPO - un membro di un gruppo stimola e induce una risposta comportamentale aggressiva in altri membri del gruppo - un tipo di facilitazione sociale 11. APPRESA - addestramento ad attaccare - può aumentare o diminuire qualsiasi tipo di comportamento in seguito all’esperienza 12. DI TIPO MEDICO - connessa, ad esempio, a crisi convulsive parziali, ipotiroidismo,…

13. IDIOPATICA - può essere analoga alle crisi convulsive parziali There are several causes of aggressive behavior in dogs. Because the treatment for each is different, it is important to know the type of aggression being expressed by the dog before logical treatment can be applied.

The basic types of canine aggression will be discussed as follows: 1. DOMINANCE - most common type of aggression in dogs - directed to family members or house-mates only (members of the dog’s pack) 2. SIBLING RIVALRY (including alliance aggression) - most common type of aggression between house-mates - type of dominance aggression 3. TERRITORIAL - protection of property - usually directed toward strangers 4. FEAR-INDUCED - aggression to strangers on or off territory - based on learning 5. PAIN-INDUCED - instantaneous reaction to pain 6. REDIRECTED - aggression directed toward a lower member of the social group and not to the one inducing the aggression 7. SEXUAL - aggression associated with mating/courtship 8. MATERNAL - protection of young 9. PREDATORY - catching and killing prey - highly developed in fighting and terrier breeds - differs from other types because submissive behavior does not turn the aggression off (i.e. the complete action sequence includes killing).

10.GROUP - one group member stimulates and escalates aggressive behavior in other group members - a type of social facilitation 11.LEARNED - attack training - can increase or decrease any type of behavior as a result of experience 12.MEDICALLY - linked e.g. partial seizures, hypothyroidism 13.IDIOPATHIC - may be the same as partial seizures

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1. DOMINANCE AGGRESSION Dogs have evolved from wolves and therefore live in social groups. As such, they accept humans as pack members in a linear dominance order. Dogs do not understand or expect equality. Depending on their internal level of dominance, they strive to attain the highest social position possible within their pack. As they see it, a group without a leader will die.

Many owners try to use excessive petting, spoiling, and allowing the dog to have its own way to win over their pet.

Dominant dogs see this as submissive behavior and subsequently assume the “alpha” position. A dog so disposed then expects its owner to respect its wishes and to follow its directions. The problem usually comes to a head when the dog views a pack member (family member) as trying to challenge a position he has established and maintained with subtle cues. Dominance is not an abnormal behavior but an integral, important component of canine social dynamics.

Important Facts Concerning Dominance a. Dominance aggression appears unprovoked, fast and without threats. Some dogs seem to have a glazed-eye appearance and appear remorseful immediately after the attack. b. Dominance aggression is complicated because it varies according to time, place and circumstance. But under similar conditions, dominance is consistent and quite stable. c. A dominant dog may be psychologically dominant but physically submissive (ie. trained submission). d. Once established, dominance is relatively permanent. e. Standing over the dog with hand over his back is often interpreted as a threat to dominance. f. Dominance is not fully expressed until behavioral maturity at 18 months to 2 years. g. Dominant dogs may only show 1 or 2 signs of dominance (see below). h. 85% of dominant dogs are males but castration has little effect.

I. The drive for dominance is inherited but dominance has a learned component. j. Dominance is usually directed toward family members or familiar people within its social group. k. Aggression is only shown to “pack” members of similar dominance status. Very submissive people or children under 1 year old are rarely attacked.

Signs of Dominance In most cases, 1 to 3 of the following signs are shown.

The * indicates the most common signs seen in dominant dogs. a. Resists -*standing over, hands over head or back - hand over muzzle - handling of feet, tail or testicles - being picked up -*discipline b.* Protects food, toys, sleeping areas, members of its social group and territory.

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c. Mounts people or jumps on them. d. Steals food in the owner’s presence. e. Pushy personality. f. Leg lifts inside the house. g.* Maintains prolonged eye contact. h. Rarely exhibits submissive postures. i. May bite if awoken suddenly or disturbed while resting. j. May demand touch or be aloof.

Treating Dominance Aggression There are two objectives in treating a dominant dog. The first priority is to gain control of the dog and the second is to alter the dog’s place in the social group. The dog must learn that nothing in life is free. All valued assets must be earned. Generally the most dominant person in the household (i.e. the person the dog is least likely to growl at) should initiate the procedures below and then the training should be generalized to include all family members. It is very important that all of the procedures in the following protocol are adhered to by all concerned.

1. Obedience training- food training is best because it avoids confrontation.

2. Remove all valued assets- i.e. toys, bones etc.

- the dog must learn that these assets are controlled by you, and besides, you are removing items that could elicit aggression.

3. Anything the dog enjoys doing is on allowed following a correct response to a command.

- do a sit-stay before feeding or allowing the dog into the backyard.

4. Lots of exercise on leash- freedom is a valued asset.

5. DO NOT PUNISH OR CONFRONT the dog- one lost battle and you have lost your hard work.

The “alpha roll” or collar scruff.

DO NOT advise your clients to perform these acts on their dominant dog. They may work reasonably well on puppies, but a dog that has established a top position will see this as a challenge. In these cases, the acts will escalate aggression and you are asking to get bitten. In older dogs, these methods can be effective if you are absolutely positive you will win; you must be prepared to battle to the death. Understandably, most owners are not willing to do this. Besides, the other steps in this program will change the dog’s position in the social group and, therefore, these two procedures are not necessary.

6. Go through doors first.

7. Do not touch the dog for several weeks- dominant dogs demand attention.

- this is often hard for a client to accept but it is very important.

8. Do not play tug-of-war or play fight.

Although some progress will be seen in the first week, it takes 6 to 8 weeks to establish a new social place for the dog using this method. Once the new place is established, the owner can return valued assets one step at a time. However they must always watch for returning signs of dominance and be prepared to reinstitute the program as necessary. Usually it is necessary to maintain some aspects of the dominance program more or less indefinitely.

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2. SIBLING RIVALRY

How to Recognize Alliance Aggression

Dogs in the same household will fight only if they are at similar dominance levels. Housemates will fight in two distinct situations.

In the first, there may be a change in dominance because the usual “alpha” dog becomes old or the younger dog reaches behavioral maturity (18 months to 3 years of age).

Fights are usually not life-threatening and a new dominance hierarchy will work itself out within 2 to 3 weeks. Occasionally fights can last longer than 3 weeks because the dogs cannot seem to establish a hierarchy. Typically the dogs are the same sex and one of the dogs has just reached behavioral maturity. Any breed may develop this problem but it is more common in terriers. Aggressive incidents are isolated to one or two circumstances (for example when penned together, at feeding, or over possessions). Treatment consists of avoiding the eliciting situations until a new hierarchy is formed.

The owner may try to establish an artificial dominant individual by consistently feeding and greeting one dog before the second. Unfortunately the prognosis for resolution of this condition is quite poor. In many cases, one of the two dogs will have to leave the home.

The second and much more common situation occurs because of an alliance between the owner and the submissive dog. This condition is termed Alliance Aggression. These fights can be much more dangerous and will persist for a considerable time. The fighting happens when a kind owner will not allow a pecking order to be established because he continually punishes the bully. This lowers the dominance of the dominant dog and escalates that of the submissive one, effectively potentiating the fighting.

a. The dogs fight only in the presence of the owner. When left alone in the back yard, for instance, the dogs do not fight. b. The fights may be vicious (ie blood is drawn). c. Fighting has occurred for over 3 weeks.

D O M I N A N C E

1 1 <———-2 + OWNER 2

Treating Alliance Aggression The first step in the treatment of alliance aggression is to determine which of the two dogs should be dominant. This decision is based on the behavior, age, health, and tenacity of the two dogs. In almost all cases, both dogs are dominant over the owner as the presence of a dominant individual in the pack suppresses aggression in other pack members. The object of treatment is to get the owner to dominate both dogs but especially dog #2.

1. The dogs should be separated for feeding.

2. If the owner must give attention to the alpha dog (e.g. for bathing, grooming, nail clipping) a good idea is to crate dog #2 while the owner interacts with dog #1 in front of the crate.

3. Show both dogs that you recognize the hierarchy by feeding, interacting, grooming dog #1 before dog #2.

4. The use of a halter system to dominate dog #2 should be recommended. The collar and a 3 foot leash should be left on the dog when the owner is home.

5. The owner should physically leave the room if fighting occurs. This may be difficult for the owner because he is concerned about the safety of the dogs.

6. The dogs should be separated when the owner is not home.

Toys and food should be removed to prevent aggression.

7. The owner should assert his/her dominance over both dogs.

Once the dominance hierarchy is rearranged (owner>dog #1>dog #2), the owner can go back to a more normal relationship with the two dogs. However, dog #1 must always be greeted, fed, groomed, & exercised first and dog #1 must never be punished for being dominant over dog #2.

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Canine fear-based conditions Comportamento del cane legato alla paura

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto In termini di prevalenza, le condizioni basate sulla paura sono seconde solo all’aggressività. Per trattarle in modo soddisfacente è importante riconoscere la causa della paura o dell’ansia, modificare il modo in cui viene tenuto l’animale per ridurre la sua esposizione alle proprie paure ed avviare un programma di riaddestramento volto a ridurre la paura specifica del cane.

In questa relazione verranno discussi i vari tipi di paura, raggruppabili sotto le voci generali di: 1) paure animate, 2) paure inanimate e 3) paure determinate dalla situazione. Le paure animate sono rappresentate dal timore di esseri viventi, come l’uomo e altri animali. La risposta del cane può variare dalla tendenza a nascondersi o scappare via ad una ipersottomissione per arrivare infine all’aggressione. Le paure inanimate sono tipicamente rappresentate dalle fobie da rumori e verrà illustrata quella classica nota come paura dei tuoni. Le paure determinate dalla situazione vengono scatenate da molteplici impulsi. La varietà più classica è l’ansia da separazione, che verrà utilizzata come principale esempio per questo tipo di paure. Saranno descritti sia il trattamento di tutti i tipi di paure mediante desensibilizzazione sistematica e controcondizionamento che l’integrazione dell’addestramento di base con la terapia farmacologica.

Fear based conditions are second only to aggression in terms of their prevalence. In order to treat these conditions satisfactorily it is important to recognize the cause of fear or anxiety, to change management to reduce the dog’s exposure to its fear and to engage a retraining program designed to reduce the dog’s specific fear.

In this lecture, the various types of fears will be discussed under the general headings of: 1) Animate fears, 2) Inanimate fears, and 3) situational fears. Animate fears involve fears of living things including people and other animals. The dog’s response can range from hiding or running away to super-submission and even aggression. Inanimate fears are typified by noise phobias and the classical noise phobia of thunderstorm phobia will be discussed. Situational fears are precipitated by multiple input. The most classical variety is separation anxiety, which will be used as the primary example of this type of fear. Treatment of all types of fears by systematic desensitization and counterconditioning, and supplementation of basic retraining by pharmacological therapy will be discussed.

CANINE FEAR-BASED CONDITIONS Fear is not listed as a disorder in the human diagnostic and statistical manual of psychiatry. Fear is regarded as being a normal reaction to a fear-inducing circumstance or event. Only abnormal or excessive fears are regarded as being problematic and these are termed phobias. In veterinary medicine when we talk about a fear based condition we are referring really to phobic conditions i.e. abnormal, excessive or irrational fears rather than just plain simple fears.

One example of a genetic fear is provided by a nervous strain of pointers down at the National Institute of Mental Health. These dogs show a genetic tendency for excess fearfulness and will bark or collapse when confronted by strangers or open spaces. Another example of genetic nervousness is provided by reference to certain known anxious breeds. For example German Shepherds are often of a ner-

vous disposition and show behaviors that are built from this foundation (e.g. fear aggression, territorial-fear aggression, etc.). Environmental influences can also play a major role in the development of fears and in this respect the critical period of development is extremely important. The critical period as it was termed is probably better referred to as the sensitive period of development and is usually prescribed to the first 3-12 (or 14) weeks of life. Before the sensitive period comes the infantile period week one and the transitional period week two during which the pup emerges from a sightless hearingless dependent to a socially interactive individual. It is after this metamorphosis that the sensitive period of learning occurs. The first three weeks of the sensitive period (from weeks 3-6) is regarded as the period of socialization of the pup without its members of its litter. In this period it learns it’s social graces. In the 6-8 week of life fears start to develop i.e. the pup is not all accepting but becomes

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discriminating and will bark when faced with unfamiliar animals or objects. It is from the 6-8 week until the 12-14 week that serious damage can be done if the pup has adverse experiences e.g. is separated and frightened etc. Following the sensitive period learning does not cease but continues at a slower pace and is still relatively rapid through the juvenile period which lasts until adolescence. As a stable learning base evolves the young dog learns to interpret novel events, even adverse events, as unique rather than as the rule. This is the opposite of what occurs very early on.

vely.

4. When the owner has good control over the dog and the head halter is fully operational the desensitization program can begin.

5. First there dog is put into a sit stay or down stay or instructed to relax (“watch me”) and a mildly fear inducing person is introduced at a distance.

6. The dog should be praised and rewarded for remaining calm and relaxed.

The types of fears that can develop are: 1. Animate fears (fears of the same or different species) 2. Inanimate fears (usually fear of sounds) 3. Situational fears (most commonly separation anxiety but also other situations) We will now consider these fears independently though the basic mechanism for each is essentially the same.

Animate Fears: Like other fears, animate fears are acquired most readily during the sensitive period of learning. One adverse experience at say 10 weeks of age can produce permanent deleterious effects. For example a dog that has a negative encounter with a man with a beard at this age may grow up to generalize its fear to include all men with beards. Typically if humans are the subject of fearfulness, men and children are the usually subjects. Sometimes the fears are very specific e.g. men with beards or rather generalized e.g. all men.

Another common manifestation of animate fears is fear of other dogs (e.g. fear of the same species). The chief presenting sign of this type of fear is that the fearfulness (which often manifest as aggression) is directed towards either all dogs or all dogs of a certain category (e.g. all large dogs).

Dogs can also sometimes develop a fear of flying insects as a result of adverse experiences in early life.

Treatment: The treatment of animate fears involves systematic desensitization with counter conditioning. The steps are as follows.

1. Make sure that the owner has good control over his/her own dog. Sometimes it is necessary to implement some stricter control over the dog (e.g. activate a dominance control program).

2. Increase the owner’s authority over the dog. On it’s own this type of control system goes some ways towards reducing a dog’s fear.

3. Often the increased authority is improved by regular obedience training. In this respect a gentle leader head halter (or other type of head halter) can be used effecti-

7. If success is achieved at this level the person is asked to move closer to the dog and their procedure is repeated.

Alternatively the dog can be moved closer to the person or even walked around them in wide but decreasing circles. The important thing is that control is maintained throughout the procedure and that the dog is only rewarded for remaining calm.

8. When the dog is close to the person the person should shuck out some food treats onto the ground near the dog and hopefully it will be relaxed enough to eat them. This means that some level of success has been achieved.

9. Progressively more adventurous moves should be engaged upon by the person for example walking around, raising hands in the air, talking slightly loudly and so on rewarding the dog all the time for remaining calm.

10. Once desensitization is achieved to this person another mildly fair inducing person is introduced in the same way probably on another occasion.

11. This procedure is repeated for a group of mildly fair inducing people before progressing to the next level: the moderately fearful person.

12. The procedure is repeated for a group of moderately fear inducing people and finally for the top category of fear inducing person e.g. the man with the beard.

During the entire desensitization program the dog should be prevented from encountering the fair inducing stimulus i.e. it should be protected from encounters with strangers so that fearful reactions are circumvented.

The above desensitization program can be practiced with any animate fear inducing stimulus whether it is a person another dog or flies. Sometimes these programs are not affective on their own and pharmacological treatment is necessary to facilitate or expedite the process.

Drugs that reduce fear include the anti-depressants (fluoxetine, clomipramine, and amitriptyline), buspirone, and beta blockers.

As background therapy for the treatment of any fear basing condition it is important to increase a dogs level of exercise to a minimum of 20-30 minutes of aerobic exercise daily.

Also it is helpful in some cases to feed the dog a low pro-

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tein preservative free diet.

beta-blocker (popranolol) used in combination by recently we have had some success with the serotonin re-uptake and inhibitor drugs.

Inanimate Fears: The archetypal inanimate fear is thunderstorm phobia.

Although sometimes regarded as a simple sound phobia the exact situation which thunderstorm phobia is far from clear.

Genetics seems to play some role in its development as it affects certain breeds primarily. Susceptible breeds include German Shepherds, Labrador Retrievers and Northern breeds and the fear can first be appreciated when the dog is quite young. Sometimes in the early stages the fear is rather mild and simply takes the form of the dog staying close to the owner during a storm. At some time after the onset of adulthood (2-3 years of age) there is a sudden exasperation of thunderstorm phobia from uncomplicated fearfulness to frank phobic proportions. The escalation often occurs? During a particularly noise overhead storm. When severely affected dogs pace and pant and salivate, becoming extremely distraught and either seeking the owner’s attention or hiding, sometimes in sinks or bathroom tubs. Many dogs with thunderstorm phobia show fear of other sounds as well, so they may, for example, have a fear of sonic booms, quarry blasting or cars backfiring. They also develop secondary fears of flashing lights, rain and wind noise. Inquiring into their history it is often found that they display other fears too for example fear of strangers or separation anxiety.

Treatment: 1. Assuming that the primary phobic reaction is toward fear, the goal standard of treatment would be systematic desensitization and counter conditioning to the sound of thunderstorms. Owners are often advised to obtain a high quality recording of a thunderstorm and to play it at progressively increasing volumes and making sure that the dog remains comfortable at each increase in volume.

As with desensitizing to fear of people, it is important to assure that the dog remains calm and relaxed at each stage of the procedure. This can be engaged by the dog’s willingness to accept food treats or play (which is part of the counter conditioning strategy). As with fear of strangers however desensitization to thunderstorm phobia cannot be accomplished while a dog is being exposed to real storms and therefore should only be attempted during the non-storm season. The sad truth about thunderstorm phobia is that it is just about the only phobia that does not respond well to desensitization. Even if a dog is desensitized to fear of thunderstorm sounds over the winter it will often deteriorate into its original phobic state the minute it is exposed to a real storm. No one is really on why desensitization to thunderstorms does not work well but theories are numerous ranging from the fact that the primary fear may be one involving static electricity to changes in biometric pressure.

2. Pharmacological adjunctive treatment to desensitization or frank pharmacological suppression of the phobic reaction may be the only way to go. Success has been achieved with medications such as alprazolam (Xanax) and a

3. As usual all of the background supportive measure should be engaged including increase in the dogs exercise, changing it’s diet, and engaging in regular obedience training to structure relationships within the home and build the dogs confidence. Harsh training methods should not be used.

Situational Fears: The most distressing situational fear is separation anxiety.

This condition affects 4% of the 54 million dogs in the United States. There is suggestion that genetic influences may be involved in the development of this condition however environment seems to play a most important role. Affected dogs have usually been subjected to a dysfunctional environment in their early lives. They have either been separated early from the bitch, been isolated through travel or in pet stores, shelters or pounds, or have had multiple owners. Separation anxiety is entirely predictable in dogs adopted from shelters on the basis of three simple tests (one involving the dogs clinical history, one involving an evaluation by kennel staff, and one involving a brief period of separation). The problem is thus one comes with the dog and not one that is created and by new owners. However new owners can influence their behavior in different ways. Strangely, overly indulgent owners might promote the condition and contribute towards its maintenance and even its exasperation. More matter of fact owners might help instill confidence in the dog thus circumventing the worst throws of the problem and permitting its gradual resolution. The signs of separation are as follows: • • • • • • • • •

Dysfunctional history Following the owners around the house Pre-departure anxiety Vocalization while the dog is left alone Destruction of property while the dog is alone Urination or defecation only while the dog is left alone Anorexia while the dog is left alone Excessive self licking while the dog is alone Exuberant greeting on the owners return

The occurrence of any 3 or more of the above symptoms at a moderate or severe level in any one dog is probably indicative of the disorder though subclinical levels of separation anxiety may exist in many dogs.

Treatment: 1. Systematic desensitization in counter conditioning.

This procedure is extremely lengthily and requires phenomenal owner compliance and understanding of the retraining method. Because of this and because of the requirement the dog is not left along during the retraining program we rarely advise it here at Tufts. Essentially the owner works on the pre-departure queues first, standing

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up and jingling keys or putting on a coat and so on until the dog finally realized that these queues do not mean that the owner is going to leave. Following that the owner may attempt to approach the door but not actually open it, then touch the doorknob open the door step outside and so on in increments over several days or weeks until the dog is comfortable at each new level. It is important not to progress to quickly and sometimes it is helpful to randomize the challenge i.e. do not always increase the time for which the dog is left sometimes reduce the time so the dog is confused and never really knows when your coming back. The early stages of a desensitization program once you’ve stepped out of the door are really tedious involving leaving the dog for a few seconds at a time then for fractions of a minute couple of minutes and so on until it is comfortable for these brief periods. Following the success of brief departures the time period can gradually be increased up until 20-30 minutes where after a more substantial increments of time left alone can be attempted.

2. Independence training. This type of training does not necessitate and that the dog is never left alone during the retaining program but does often rely on pharmacological control of anxiety. The idea is that the owner teaches the dog independence while they are with it. They teach it for example to sit stay while they move progressively further away from it and finally out of the room. On their return they reward the dog for remaining calm, composed and obedient. Possible they will try to discourage the dog from following them around the house by placing a training lead on it and constantly taking it to a comfortable area and praising it for being there. They will be instructed not to permit the dog to lean up against them or rest on them while they are watching television but other times and not to indulge the dog with constant petting or hugging. It’s also important for them not to have the dog in bed with them at night but rather to have it on a dog bed or blanket inside the room and praise it for remaining at a distance from them.

In addition to the above independence training the dog should be totally ignored for 20 minutes before the people leave and when they return home. This is to level the emotional rollercoaster that lengthily departures and exuberant greeting rituals promote.

Prior to the 20 minutes of ignoring the dog on departure some sustained release food treat should be put down for the dog. This aspect of the retraining program is sometimes termed counter conditioning as it is conditioning the dog to expect a different experience associated with the owners departure. Instead of feeling anxious it will be in an appetitive frame of mind. A typical sustained released food treat might be a nylon bone with holes drilled in it and peanut butter or cheese whiz wedged inside the honey comb cavities.

Constant positive training exercise and dietary manipulations (low protein preservative free diet) might be helpful in reducing the dog’s anxieties that it had learned later on in the above program 3. Pharmacological treatment. Pharmacological treatment can be used in conjunction with systematic desensitization or independence training although it is a more vital part of the latter. Several drugs have been recommended over the eons but amitriptyline seems to have emerged as the gold standing for comparison. Amitriptyline is dosed at 4 milligrams per kilogram twice a day given with food. Side effects include depression of appetite, slight? Possible increased aggression, and rarely, seizures. An off the market version of amitriptyline is clomipramine. This is dosed at 2 milligrams per kilogram twice a day. Studies have demonstrated that clomipramine is an effective treatment for separation anxiety though the improvement may not be great. Side affects are similar to amitriptyline. Fluoxetine has also been used with the same modest success as clomipramine. Side affects are along similar lines to the other drugs though perhaps less severe. Another drug that can be tried is the anti anxiety medication buspirone which is effective in some cases. The dose is 5, 10, or 20 milligrams given 3 times a day for a small, medium and large size dog respectively (10, 20 and 40 kilogram dog respectively). Finally the beta blocker propranolol can be used successfully to treat this condition either alone or more normally in combination with one of the anti-depressants above. Some people have recommended the use of benzodiazepine such as a diazepam (Valium) chlorazepate (tranxene) or alprazolam (Xanax). These latter drugs should not be selected lightly or for more than a short term as they are addictive, will produce withdrawal, produce serious changes in appetite, weight gain, lethargy, etc. If at all possible use one of the other drugs mentioned above. The only true indication for this type of drug might be if short term immediate control is necessary e.g. if a dog is going to be kenneled over a weekend or some such.

The above is a brief summary of the 3 basic types of fear which as mentioned are often and comorbid (i.e. they exist together). As such they represent different manifestations of an underlined fearfulness of character which as mentioned will be produced by genetic or environmental influences.

Recently we have found that sub-clinical hypothyroidism can contribute to anxiety and supseptable breeds or in dogs showing other signs of hypothyroidism (excess shedding, recurrence infections, alopecia, irregular estrus, etc.) we check thyroid common levels by means of a thyroid panel and will treat with synthetic thyroid hormone (syloxin 0.1 milligram per 12-15 pds. bodyweight). Improvement is seen in 5 days to 5 weeks if it is to be effective, if not the dog can be tapered off and some other treatment tried.

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Canine compulsive behavior Disturbi ossessivo-compulsi del cane

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto È stato recentemente riconosciuto che molti dei disturbi ripetitivi, inesplicabili e difficili da trattare che i cani manifestano sono in realtà la conseguenza di una forma di disordine ossessivo-complusivo. Questi disturbi vengono scatenati da ansia primaria e ambiente stressante e interessano una varietà di specie animali, compreso il cane, il gatto e gli animali da zoo, ma sono derivati da comportamenti normali come l’assunzione del cibo, la toelettatura e la predazione; tuttavia, vengono attuati in modo ripetitivo e fuori dal contesto. Per illustrare l’eziologia, le manifestazioni e il trattamento di questi disordini, verranno utilizzati esempi tipici come la dermatite da leccamento delle estremità (granuloma da leccamento), il rincorrersi la coda e la tendenza ad acchiappare luci/ombre.

It has been recognized recently that many of the previously inexplicable and difficult to treat repetitive disorders that dogs display are, in fact, the result of a form of obsessive compulsive disorder. These disorders are precipitated by underlying anxiety and environment stressed and afflict a variety of animals species including dogs, cats, and zoo animals but are derived from normal behaviors such as eating, grooming, and predation but are performed repetitively and out of context. Typical examples such as acral-lick dermatitis (lick granuloma), tail chasing, and light chasing/shadow chasing will be used to illustrate the causation, manifestation, and treatment of these disorders.

This particular compulsion is related to grooming and has many features in common with obsessive compulsive disorder (OCD) in humans. In humans, obsessive-compulsive disorders are often associated with grooming events, such as repetitive hand washing. ALD is characterized by repetitive licking of the lower extremities of the fore or hind legs that results in physical injury. Bald spots appear first and if the frequency of licking continues to be excessive, the skin may become abraded causing formation of deep skin ulcers that may result in secondary infection. In extreme cases, the underlying bone can become infected necessitating amputation.

ALD can be confused with some medical conditions so before you make a psychogenic diagnosis, you must first rule out any underlying medical cause. Any condition that causes physical discomfort can stimulate excessive grooming. Potential differential diagnoses include allergies, fleas, skin infections, trauma (foreign bodies, fractures, prior injury), arthritis, or tumors. However, even once the primary medical cause is resolved, a susceptible dog (i.e. one that is predisposed to anxiety conditions) may continue to excessively groom the previously affected area. At this point the condition may be viewed as psychogenic and should be treated accordingly.

Licking usually first appears in young adulthood or middle age (2-5 years of age), oftentimes in conjunction with exposure to situations that could be construed as stressful.

Such anxiety-provoking triggers can include separation anxiety or any situation that disrupts the dog’s bond with its owner, noise phobias, a change in the dog’s physical or social environment, or a continual lack of appropriate releasing stimuli for normal (innate) tendencies. This maladaptive grooming behavior can wax and wane in response to prevailing stressors in the sense that when the dog is experiencing stress the condition may worsen, but when the dog is not anxious the behavior may temporarily improve. True to form for a compulsive behavior, once the licking pattern is well established, it will be performed out of context, in other words when the dog is not anxious. Dogs that have been punished for excessive grooming may purposely remove themselves to a remote area away from the owner to engage in the behavior, suggesting there is an uncontrollable, if not obsessive, quality to this condition. Once the behavior is engrained, the condition is usually refractory to all forms of traditional veterinary therapy including anti-inflammatory drugs, topical therapy, anxiolytics and sedatives, and mechanical restraint. Although Elizabethan collars will allow some resolution while the collar is on, such mechanical re-

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straint does nothing to address the underlying anxiety-driven condition. Therefore, it is not surprising that once the collar is removed the dog will resort to licking.

ALD has genetic components in the sense that (a) it is a grooming disorder and aspects of grooming are hard-wired, and (b) it is more prevalent in certain breeds and perhaps within certain breeding lines. ALD is most common in large breeds (> 50lbs) and active breeds that have been selected to work closely with people and form strong attachments. Not surprisingly, many dogs with ALD also have other anxiety related behavior conditions such as separation anxiety, thunderstorm phobia, or fear-based territorial aggression. Many affected dogs have nervous or anxious temperaments. The breeds most commonly affected include, but are not limited to, Dobermans, Labrador Retrievers, Great Danes, and German Shepherds. Interestingly, smaller breeds are less prone to develop ALD, but rather engage in compulsive chewing of the digital pads or toenails. Keep in mind that although ALD has potential genetic underpinnings, environmental influences are often necessary for the full expression of the condition.

Light Chasing (Shadow Chasing) Light chasing is a compulsive behavior that is likely related to a displaced predatory drive. The behavior is characterized by staring, biting, leaping, chasing, and barking at shadows or lights. There is frequently a history that the owner has initiated and reinforced the behavior by playing with a flashlight, but subsequently the dog is unable to control the behavior. Owners may continue to reinforce this behavior by reprimanding or trying to calm the dog, thus further encouraging any attention seeking components of this behavior. It is our impression that dogs that develop this behavior are under a certain amount of environmental stress and engaging in this behavior may provide some temporary relief. Humans with OCD frequently report that they engage in compulsive behavior to relieve the anxiety caused by their obsessions.

Light (shadow) chasing may have a genetic basis since (a) in terms of appearance, it seems to stem from hard-wired predatory behavior and (2) it appears to occur more frequently in certain breeds including Wire-haired Fox Terriers, Old English Sheepdogs, Schnauzers, Rottweilers, and Golden Retrievers. Owners of shadow chasers appear to be less likely to seek behavior consultations, presumably because these dogs rarely injure themselves in the process. Only when the behavior becomes disturbing to the owner is a consultation requested. Therefore, as opposed to other compulsive behaviors that result in physical injury to the dog, we have comparatively little information on shadow chasers regarding age of onset, genetic family information, or response to treatment.

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rapid movement of the eyes, head and body toward the “flies”. In essence, the dogs behave somewhat frantically, as if they were being pursued by a swarm of gnats. Fly-snapping behavior has traditionally been thought to be a form of psychomotor epilepsy. In cases where there is a seizure origin, there is often a pre-ictal mood change, the bouts are of short duration, and salivation, defecation, urination, and a post-ictal stage (lethargy, disorientation) may be observed following an episode. In other cases, fly-snapping appears to be compulsive in nature and is thought to be related to predatory behavior “gone awry”. Fly-snapping is considered to be compulsive when the bouts are frequent, disruptive to the animal’s functioning, continue for prolonged periods of time, are associated with anxiety, and no aura or other symptoms compatible with a diagnosis of psychomotor epilepsy are evident. It is also possible that a seizure focus may be responsible for triggering the compulsion. Like other compulsive behaviors, fly-snapping may also have attention-seeking components and may easily be reinforced by the owner’s attention. Compulsive fly-snapping may have a genetic basis, as certain breeds seem more predisposed to develop this condition. These breeds include, but are not limited to, Cavalier King Charles Spaniels, Dobermans, Bernese Mountain dogs, English Springer Spaniels, Labrador Retrievers, German Shepherds, and various terrier breeds. Little data is available for the age of onset although the Cavalier King Charles Spaniel breed club reports that onset in this breed is typically 8-18 months of age. As with light chasing, because this behavior is frequently reported to be more frustrating for the owner than injurious to the dog, owners may be less motivated to seek professional help and as a consequence data are sparse at this time.

Flank-sucking Flank-biting or flank-sucking is thought to be related to displaced nursing behavior although some dogs lope in circles as they attempt to mouth their flanks giving a somewhat displaced predatory appearance to the behavior. Repetitive mouthing and sucking of the flank region resulting in anything from a rough, dampened coat to raw, open sores characterizes the behavior. In addition to self mutilation (lesions), an affected dog also may show a decrease in appetite and become unresponsive, or even worse aggressive, towards the owner when it is approached while flank sucking.

The onset of this condition is usually observed sometime between puberty to young adulthood and the onset and exacerbation of the condition is often associated with exposure to anxiety provoking conditions. Flank-sucking is thought to have a genetic basis since (a) it appears to be a displaced nursing behavior which is hard-wired and (b) certain breeds appear to be predisposed to developing this condition, particularly Doberman Pinschers.

Fly-snapping Fly-snapping behavior is another compulsive behavior that may have displaced predatory underpinnings. Fly-snapping is characterized by staring at invisible insects, snapping at the air and flank area, head shaking and scratching, and

Other Compulsive Behaviors Repetitive circling, fence running, digging and pacing are also common manifestations of compulsive behavior.

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Some breeds, especially retrievers and terriers, are prone to developing dysfunctional chewing, chasing, and carrying of inedible objects. Compulsive behavior with objects differs from play behavior or normal breed tendencies. The dogs may engage in these behaviors for hours or until they collapse from exhaustion. If the owner prevents the dog from performing the unwanted behavior, the dog may resort to a different but equally compulsive behavior. Thus the compulsion is merely transferred and not eliminated. These dogs may experience weight loss, worn teeth, abraded footpads, and abrasions to the nose and mouth. In severe cases, these behaviors can seriously interfere with the dog’s relationship with its owner and its ability to function normally. While excessive barking is typically diagnosed as a nuisance behavior stemming from inappropriate management or anxiety, certain forms of rhythmic barking may be compulsive.

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cally occurs between 6-16 months of age although it can occur anytime in response to a stressful trigger. The age range of onset we have observed extends from 2 months to 10 years of age. The onset may be sudden with no apparent eliciting trigger, particularly in young dogs. In other cases the onset may be sudden but associated with exposure to a clearly identifiable trigger. Alternatively, the onset may be gradual with the dog showing mild, occasional, and easily interrupted tail chasing bouts that over time and in response to environmental pressures gradually erupt into the fullfledged condition. Both the dog’s genetic background and environmental influences likely influence the variation in development. Tail chasing is considered to have a genetic basis because (a) it appears to be a displaced predatory behavior, (b) it is particularly prevalent in terriers and herding breeds especially Bull Terriers and German Shepherd Dogs, and (c) extensive data on Bull Terriers strongly suggest the disorder is familial at least in this breed.

Tail-chasing/Spinning Tail chasing appears to be a displaced predatory behavior. The condition is characterized by a slow to moderate rotation while focused on the tail to rapid spinning bouts with no apparent focus. The dog may snap, grab, and bite the tail while engaged in this behavior. Breeders often differentiate between tail chasing and spinning and argue that tail chasing is a separate condition and of less concern. However, our research demonstrates that these 2 somewhat different manifestations are one and the same thing. Most dogs express tail chasing and spinning interchangeably and we often find that chasing focused on the tail precedes rapid spinning bouts. When fully engaged in their compulsion, tail chasing dogs appear to be dissociated from their environment. They often can not be distracted, are unresponsive to the owner’s commands, and seem unaware of their surroundings. Some dogs may become irritable or aggressive if restrained. In rare cases, continuous tail chasing associated with hysteria and frenzied vocalizations can progress to a rage-like aggression directed toward the environment, the owners, or other household pets. Injuries incurred while tail chasing include self-mutilation of the tail, tail fractures while banging into walls or furniture, weight loss, exhaustion, and abrasion of digital pads.

Through our research, we have identified two behavioral categories of tail chasers that differ in the frequency and degree of expression of this behavior, subclinical and clinical tail chasers. Some mildly affected dogs (subclinical) may only tail chase occasionally and in response to specific triggers. These dogs can readily be interrupted, seem aware of their surroundings, and the behavior can be controlled by eliminating the offending trigger. These dogs generally are not a concern from a behavioral standpoint and you will rarely see them in your practice. The uninformed owner often views mild tail chasing as normal (“cute”) behavior, not realizing that exposure to stress can often exacerbate the condition. Other dogs (clinical) may tail chase anywhere from 2-3 times per day to up to 80% of their waking hours on a daily basis. These moderately to severely affected dogs are often unable to function normally and their relationship with their owner is impaired. The onset of tail chasing typi-

TREATMENT OF CANINE COMPULSIVE BEHAVIOR 1. Identify the Conflict Reducing stress by identifying methods of decreasing the sources of arousal and conflict are the first aspects of treatment that should be explored. It is important to identify when, and in what situation, the behavior occurred for the first time, and under what circumstances it is currently performed. Unfortunately it is not always possible to identify the conflict, and if identified, it may be difficult or impossible to remove it. In the latter case, the owner will need to try to desensitize the dog to the stressful situation. Conditions known to trigger anxiety in susceptible dogs include benign experiences that would not have a negative impact on most dogs. Potential triggers for a susceptible dog include: Environmental and Social Conflict - Any conditions that increase arousal or conflict (owner departures and returns, food preparation, changes in social or physical environment) - Lack of opportunity to express species-typical behavior (lack of mental and physical stimulation appropriate for the breed and age of the dog) - Temporary or permanent move to an unfamiliar environment (change in residence or boarding at kennel) - An unpredictable environment - Change in social group (introduction or departure of people or pets; change in social interaction with owners or conspecifics) - Confinement to small areas (crates, small rooms, kennel) - Sensitivity to particular sounds (storms, vacuums, yard machinery, telephones, microwave bells, running water) Physical Discomfort - Estrus - Parturition - Routine surgery - Fleas, allergies, impacted anal sacs, and any physical trauma.

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Regarding physical conditions that initially trigger the compulsive behavior, once you successfully treat the original cause, susceptible dogs may continue to show the behavior. At this point, you will need to address the psychogenic aspects of the condition. Finally, what initially triggers the behavior may not be what maintains the behavior.

Once the behavior has become engrained and the threshold for performance is lowered, compulsions may be exhibited with or without the presence of any of a variety of presumed stressful triggers. Temporary pharmacological intervention is usually indicated at this stage.

2. Environmental Enrichment As a form of occupational therapy, give the dog distracting toys to keep it busy during times it is prone to engaging in compulsive behavior. Dogs that are motivated by food often like hollow bones or Kong toys filled with peanut butter, liverwurst, or cream cheese. The food may take longer to extract if the food filled toy is frozen first. If the dog enjoys chasing objects, a large Boomer Ball can be made more interesting with rabbit scent (available to train hunting dogs) and the dog can push it around the yard or house.

There are also a variety of “food puzzle” toys available in pet stores and through pet catalogues. A “Buster Cube” (a hard plastic cube that can be filled with dry kibble) is such a device. It must be rolled a few times for food to be released.

Buster Cubes are appropriate for dogs that are not prone to destroying or ingesting objects. Boomer Balls are also available as food puzzles and are virtually indestructible. They can be ordered by calling 1-888-858-9529 (toll free). Ask for a ball with holes drilled to release kibble. The owner may need to start by filling the toy with the dog’s favorite food treats to generate enthusiasm. To keep the dog mentally stimulated; the owner can provide daily meals in one of these food puzzles. After all, our dog’s ancestors spent a good portion of their active time “chasing down meals”.

Why shouldn’t our domestic dogs have the opportunity to express this “natural” approach to feeding?

It is very important to remember that dogs are pack animals and as such are inherently social. Like people, dogs suffer emotionally, and sometimes physically, when they do not receive sufficient and appropriate social interaction. The optimum treatment strategy is to spend as much quality time with the dog as it needs, though the hustle and bustle of modern life does not always permit this luxury. Failing the owner’s ability to provide a rich and diversified life of interesting and entertaining experiences for the dog, the owner should consider engaging the services of others who have more time on their hands. The owner might hire a professional dog walker or a neighbor to visit their dog when they are away for long hours. Also, doggie day-care can provide an otherwise lonely dog with company and entertainment.

The take home message is that dogs are living creatures and need something to occupy their time, just as we do. Many of the modern-day canine psychoses seem to stem from or be aggravated by an inappropriate lifestyle that is unstimulating. It benefits dogs to be gainfully employed in something, to have a job to do. In the process of designing a job for the

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dog, make sure the owner incorporates breed-specific needs, such as herding-type activities for herding breeds, lure coursing for terriers and sight hounds, and retrieving games for sporting dogs.

3. Exercise Just like in people, regular, brisk, daily exercise is an effective means to reduce a dog’s anxiety. Twenty to thirty minutes of sustained, aerobic exercise once or preferably twice per day is recommended. A brisk walk or games of fetch are good forms of exercise. It is aerobic (running) exercise that is really indicated, not just a twice-daily saunter around the block. The owners will need to promote and supervise their dog’s exercise program. Simply turning the dog out in the backyard is usually insufficient, as most dogs do not tire themselves out this way. They may run a bit, rest a bit, and so on, not really pushing themselves to the maximum. They need the owner, their personal trainer, to make it all come together.

4. Diet The definitive work on what constitutes an appropriate diet has yet to be published, but we are currently researching this aspect of treatment for compulsive behavior. Theoretically, low protein diets should offer advantages over higher protein equivalents in terms of mood stabilization and the minimization of anxiety because low protein diets should promote the endogenous formation of serotonin. If appropriate for the dog’s age and activity level, we recommend feeding an all natural (no artificial preservatives) low protein diet (16-22% protein) for a trial period of 2-4 weeks to see if there is any improvement in the dog’s condition. Nature’s Recipe Senior is a good choice. Recent research from our clinic suggests that a low protein diet may stabilize mood and decrease anxiety and aggression in some dogs and we are hopeful that similar positive results will be obtained regarding a decrease in compulsive behavior in response to low protein diets.

5. Daily Structure Dogs feel more secure, and consequently less anxious, when they have a predictable routine. The owner should try to maintain a consistent daily schedule for feeding, exercise, training, and play so the dog can anticipate the activities and attention.

6. Attention Withdrawal It is particularly important to ignore the dog, unless it is in danger of injuring itself, when it is engaged in compulsive behavior, since any attention given at this time will reinforce the unwanted behavior. The dog is conditioned to respond to many cues that the owner may inadvertently be giving, and

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only by ignoring the dog’s behavior can the owner eliminate the possibility of giving such cues. The dog may consider any form of attention, even punishment, as a reward. In addition, punishment may actually increase the dog’s anxiety and intensify the behavior. This step is essential in the initial stage of treatment, but may be relaxed, once the obedience training has had some effect. Ignoring the dog, in conjunction with obedience training, will help reduce the incidence of compulsive behavior.

What should the owner do if they cannot distract the dog from the unwanted behavior? Once the dog begins to show the compulsive behavior, the owner should make a novel sound (blow a whistle or duck call, shake a can of pennies) and leave the room. Hopefully the sound will distract the dog, it will stop the unwanted behavior and follow the owner from the room. Ideally the dog should learn to associate the performance of a particular behavior with the sound and the owner’s subsequent departure. The owner’s departure functions as a form of punishment for the dog and will help decrease the frequency of the behavior. If there is an attention-seeking component to the dog’s compulsive behavior, the owner may notice an increase in the frequency and/or intensity of the behavior when the owner begins this portion of the program, then it should decrease. It is very important that the owner is consistent and does not reward the dog’s compulsion with attention or the dog will become more persistent.

To be effective, this technique must be used every time the dog shows an intention to perform the compulsive behavior. When supervision is impossible, the dog should be put in a situation where it cannot or likely will not engage in the compulsive behavior.

7. No Discipline Once compulsive behavior is engrained, it becomes an activity over which the dog no longer has any form of selfcontrol. At this stage, any form of punishment could be construed as being inhumane. Discipline is very complex, and if not used properly, may increase the dog’s anxiety by increasing the unpredictability of the owner’s interactions with the dog. Dogs that are punished for compulsive behavior may learn to engage in the behavior only in the owner’s absence (they may go to a remote location in the house) or they may engage in a different form of compulsive behavior that is more “acceptable” to the owner. For example, a tail chaser may begin to pace in large circles or may engage in repetitive behavior with toys. While this behavior may be less disturbing for the owner, the underlying anxiety still has not been addressed and the compulsion has merely been transferred, not eliminated. Therefore, we strongly recommend that discipline should not be used in dogs suffering from compulsive disorders.

8. Obedience Training Formal obedience training, at home, is an invaluable aid to the treatment of compulsive dogs. Two short, 5 minute sessions daily of obedience exercises are usually sufficient.

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Be sure to use treats and praise for motivation. Obedience training will make the interaction between the owner and the dog more consistent, and make the dog’s environment more predictable which will help decrease the dog’s anxiety. Regular obedience training will also stimulate the dog mentally, much like having a job. The owner will also need to use obedience commands for the counterconditioning techniques that may be recommended later in treatment. If the owner is inexperienced at dog training, we recommend you direct the owner to the assistance of a trainer well versed in positive training techniques.

9. Counterconditioning Counterconditioning interrupts unwanted behavior by training the dog to respond to a command which is incompatible with continuing performance of the compulsive behavior. This technique is most effective when you can identify and predict the situations that trigger the dog’s compulsive behavior. Counterconditioning is most successfully implemented later in the treatment program after the dog’s anxiety level is reduced (via management changes and pharmacological treatment) and response to obedience commands is well established.

The first step to counterconditioning is to teach the dog to relax on command by responding to verbal and visual cues from the owner. Under non-stressful conditions, teach the dog to sit and watch the owner in order to receive praise or a food treat. Have the owner say “sit” and as they move their finger to their face as a visual cue say “watch me”. If the dog responds by paying attention to the owner in a relaxed and focused manner, reward the dog with a small food treat or praise lavishly. Perform this relaxation exercise daily for the first 5 days. Each day increase the amount of time that the dog must pay attention to the owner in a relaxed pose before they give a reward. By the end of the fifth day, the dog should be able to sit while focused on the owner for 25-30 seconds no matter what the distraction. At this stage, when the owner senses the dog is about to engage in compulsive behavior, they can use this counterconditioning technique to interrupt the behavior before it is initiated. It is important to practice this exercise on a periodic basis to ensure its effectiveness when the owner needs it.

As an alternative strategy, once the dog can perform a long “down-stay”, the owner can train the dog to lie on a special dog bed or mat that is used for counterconditioning.

Train the dog to lie on the mat when it is relaxed and not likely to engage in compulsive behavior. Initially, reward the dog every 10 seconds it lies still, then every 20, then 30, and so on. Later on in training, the owner will want to institute intermittent rewards. If the dog leaves the mat, attach a no reward mark such as “AH! AH!” on the misbehavior then escort the dog back to the mat. The dog will soon learn that if the “stay” command is broken, it is going to be put back anyway, but if it holds the stay on its own, it has a fair chance of being rewarded with a treat. Gradually train the dog to relax and lie on the mat when the owner is no longer in the room.

Now the owner is ready to intervene before the dog engages in compulsive activity by commanding it to lie on the train-

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ing mat or bed which should, by the way, be located in a safe and quiet area.

10. Pharmacological Therapy If the compulsive behavior has been going on for some time, removing the cause of the conflict in conjunction with the other steps in the treatment program may not be enough to eliminate the problem. In these cases, use of drugs, usually temporary, is indicated to normalize the brain chemistry

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and stabilize the dogâ&#x20AC;&#x2122;s mood. Although no drugs are approved for the treatment of compulsive behavior in dogs, some success has been achieved using drugs prescribed for the treatment of similar disorders in humans. Our first treatment choice is either clomipramine or fluoxetine. Both of these medications are human anti-depressants that have certain anti-obsessional effects. In theory they operate by inhibiting the re-uptake of serotonin in the brain. Owners should be advised that use of medication, without the management changes and behavioral modification techniques outlined above, is inevitably ineffective.

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Feline aggression Aggressività del gatto: il “gatto alfa”

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto L’aggressività è al secondo posto in ordine di frequenza fra i problemi comportamentali del gatto, preceduta solo dall’eliminazione inappropriata. Come nel caso del cane, esistono diversi tipi differenti di aggressività ed è importante identificare quello coinvolto per attuare il trattamento opportuno, dal momento che la terapia varia. In questa relazione verranno presi in considerazione i seguenti tipi di aggressività.

1) Aggressività da dominanza del gatto – tipo di aggressività rivolto contro i proprietari che si occupano di loro.

2) Aggressività territoriale – un’altra varietà di aggressività da dominanza che si manifesta fra gatti che vivono nello stesso nucleo familiare.

3) Aggressività indotta dalla paura – rivolta contro gli estranei.

4) Aggressività reindirizzata – conseguente ad un elevato livello di eccitazione, si scatena improvvisamente fra una coppia di gatti o fra un gatto ed un essere umano.

5) Aggressività predatoria – un comportamento naturale che talvolta può essere erroneamente indirizzato.

6) Aggressività da cause mediche – come quella scatenata da crisi convulsive parziali, ipertiroidismo e tumori cerebrali.

Nella relazione, ciascun tipo di aggressività verrà illustrato attraverso l’esposizione di casi clinici e la descrizione del trattamento, compreso quello farmacologico.

Aggression is the second most common feline behavior problem, second only to inappropriate elimination. As with canine aggression there are several different types and it is important to identify what type of aggression is involved for instituting treatment as treatments vary. In this lecture the following types of aggression will be discussed.

1) Feline dominance aggression – the type of aggression directed against caring owners.

2) Territorial aggression – another variety of dominance aggression exhibited between cats living in the same household.

3) Fear induced aggression – directed toward strangers.

4) Redirected aggression – a result of high arousal and occurring precipitously between a pair of cats or between a cat and a human being.

5) Predatory aggression – a natural behavior that can sometimes be misdirected.

6) Medically linked aggression – including that precipitated by partial seizures, hyperthyroidism, and brain tumors.

In the lecture, each type of aggression will be illustrated with reference to case material and treatment including pharmacologic treatment will be outlined.

Aggression is the number two feline behavior problem reported to behaviorists, second only to inappropriate elimination. As with canine aggression there are several different types and the treatment depends on what is causing the aggression. Aggression in cats (as in other animals) has been variously classified, although a system analogous to that used in dogs permits some comparisons to be made. Therefore, classification of aggression into dominance-related, fear, or redirected aggression, etc. is quite reasonable. An al-

ternative classification, which is helpful when it comes to planning pharmacologic treatment, is the so-called Reis classification in which aggression is considered as two main types: a) Affective (offensive or defensive), b) Predatory aggression. All types of aggression where emotions are evident and there is associated autonomic activation fall into the affective category, whereas predatory aggression is non-affective and sometimes referred to as the “quiet biting attack” type of aggression.

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DOMINANCE AGGRESSION (Status-related Aggression) In the past people have not really regarded cats as evidencing dominance aggression. This is because cats do not have dominance hierarchies like dogs but are thought of more as an anti-social, solitary species. Lately this concept of cat society has been changing and it is now known that cats will live in large dynamic groups with a loose social structure as long as there is an abundant food supply. Two social structures have been put forward, one being a sort of despotic hierarchy (with one dominant leader and everybody else equal second in command with occasional pariah cats) and the other being far more dynamic and interactive. This latter hierarchy involves dominant actions by leader cats to assert their position, time sharing, and some prioritization.

Also, within the social group there are preferred associates and other cats who actively avoid each other. The whole social dynamic is similar to what occurs in people, where group leadership may not initially be apparent.

As it turns out cats do have the same sorts of requirements as dogs and more dominant ones will protect food, objects, or territory and will repel unwanted gestures made towards them, reacting in a hostile way to admonishments or punishments. Cats of this disposition may be less common than the equivalent type of dog but they do occur. In the past there was a type of aggression in cats known as “petting-induced aggression” which was reported to occur between cats and their owners. The very orientation of this aggression is suggestive of dominance and it has parallels in the canine world. Cats that exhibit this type of aggression may show other signs of pushiness, too, such as insisting on being fed, waking the owner up in the morning, preventing the owner from resting in a chair, or meowing excessively for attention.

Key Points • • • •

Dominant cats have a pushy nature Petting-induced aggression may be the presenting sign First appears in kittenhood but persists throughout life Affected cats may resist grooming, nail clipping, and discipline • Affected cats may be possessive/protective of food and toys • Owners are often kindly individuals who have “spoiled” their cat

Treatment 1) Train the cat to perform “tricks” e.g. to sit to receive food or assume a certain position. This can be accomplished quite easily by “click and treat training”. For information on this training method a video is available by Karen Pryor. (It can be purchased from 1-800-47CLICK).

2) Train the cat to perform one new “trick” per month.

3) Use the training acquired as above to insist on certain behavior prior to the cat receiving food or attention from the owner (e.g. train the cat to sit to receive food or petting).

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4) Exercise the cat daily with moving toys (e.g. cat dancer, laser mouse, objects on a string). At least twenty minutes of playing per day will help the cat blow off steam and reduce its level of aggression.

5) If the owner is really intimidated by the cat, a water pistol or air horn can be used as a punishment and for self defense.

Timing of punishment is critical. It should be delivered immediately after the first aggressive signs are noticed.

6) If aggression occurs during petting: a) the owners should stand and let the cat fall to the ground. b) For severe cases, suggest that cats do not need to be petted. c) With systematic desensitization and counterconditioning these cats can be taught to accept petting.

Start petting the cat at the level of the shoulder and reward with a small food treat. Over a period of weeks the owner should expect to pet the cat more and more for the treat.

FEAR AGGRESSION Like dogs, cats can become fearful of people or other animals and under these circumstances may choose to slink away and hide. However, some cats are more proactive in dealing with their fears and will attack when frightened. The concept here is that a good offense offers the best defense.

Fear aggressive cats are more likely to attack when cornered and unable to escape.

Important facts about fear aggression • Usually acquired although there may be genetic influences.

• Cats have been shown to inherit about 50% of their disposition from their sires. Inappropriate experiences in an early period of learning are particularly important when it comes to generating fear-based conditions. The critical period of development in cats is from two until seven weeks of age. Adverse experiences, particularly towards the end of this period (and to some extent beyond) will have permanent adverse effects. Cats that have not been socialized to people before seven weeks rarely become fully accepting of people’s company. (especially feral cats) • Fearful cats display typical signs of fear including dilated pupils, flattening of the ears, open mouth threats, hissing, batting with paws, piloerection (especially bushy tail).

• Cats that have been exposed to a fear-inducing stimulus and have become riled can remain in that state for several hours and can be dangerous to handle.

Treatment As with all other fears the essence of behavioral treatment is systematic desensitization with counterconditioning.

The cat should be exposed gradually to the fearful stimulus while it is being engaged in some distracting/pleasant activity (e.g. receiving food treats).

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If the cat is refractory to desensitization techniques then pharmacological desensitization can be attempted. Drugs that are useful for this purpose include the anti-anxiety drug, buspirone, and the serotonin reuptake inhibitors, such as clomipramine and fluoxetine. Beta-blockers (like propranolol) may also be helpful.

INTER-CAT AGGRESSION Aggression is the number two feline behavior problem reported to behaviorists, second only to inappropriate elimination. Cats show several different types of aggression toward other cats including status-related (dominance) aggression, fear aggression, territorial aggression, and redirected aggression.

1. Territorial Aggression Cats are solitary hunters, not pack animals by nature.

However, when food is plentiful, as it is in most of our homes, multiple cats can live harmoniously most of the time.

Nevertheless, even well fed cats retain their instinct to define and defend a territory. Outdoor cats mark their territory with urine, feces and pheromones from scent glands. Scent marking serves to indicate the territory is occupied and reduces encounters between cats. In close quarters, though, cats often negotiate subtle territorial rules including respecting distinct territories within a single room such as a couch or window perch. Moreover, some feline housemates learn to “time share” favored locations with one cat taking the front window in the morning and the other taking it over in the afternoon. Unfortunately, anything that disturbs the “agreed upon” rules can lead to a confrontation and what occasionally starts as a minor feline spat can erupt into a full blown feud unless you can intervene. It is important to keep in mind that when cats are confined indoors, they have little chance to avoid each other and aggression is all too frequently the end result.

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to equal status.

2. Non-Recognition Aggression In other instances, feline housemates have a good relationship until something occurs and they do not recognize one another. For example, non-recognition can be triggered when one cat in the family returns from the veterinarian’s office or the groomer and smells and behaves differently. The cat that has been away may also release a scent from its anal sacs that signals fear and may cause the other cat to respond aggressively. If a fight ensues, it can sometimes irreparably damage the relationship.

3. Redirected Aggression Aggression intended for an outdoor intruder that is redirected onto a feline housemate can also severely damage the social bond between cats that have previously cohabited in harmony. A typical scenario is of one cat resting by a window.

The second cat sees an intruder cat outside the window and rushes to attack it. The first cat sees its housemate rushing toward it in an aggressive manner and becomes defensive. The second cat redirects its attack on its housemate. Theories as to why cats redirect fall into two main categories. One theory is that one cat adopts an offensive strategy but being unable to attack the unwelcome visitor who is on the other side of a window turns around and attacks the cat next to it instead. The second theory argues that one of the two cats becomes extremely frightened and assumes a defensive posture pupils dilated, claws unsheathed, crouched body posture, ears flattened accompanied by hissing and perhaps swatting. The second cat observes this and believes it is about to be attacked and takes the offensive and a fight ensues.

Another scenario is when two cats are resting in the same vicinity when a frightening incident occurs such as an unusual and particularly loud noise. Both cats are startled and assume a defensive posture. When they see each other in this stance, they assume the other is ready to launch an attack.

Each cat responds defensively, a fight erupts, and they remain fearful and aggressive toward each other afterwards.

In cases of redirected aggression, the cats should be separated immediately. If this is done and they are given several hours, if not overnight, to cool off you may be able to reintroduce them the next day over a bowl of food.

Problems with territorial aggression are most common when a new cat is added to the household. If sudden introductions lead to aggression, this can set the stage for future battles and does not bode well for the future. The way to avoid this problem is to gradually introduce the cats to each other across a closed door. A gradual introduction of a new cat to the household may take 2-3 weeks.

General Recommendations

Territorial aggression between cats already living in the same household tends to develop gradually. The more confident cat may begin to guard various resources and threaten its feline housemate over the slightest infraction. Gradually the threats may progress to attacks and the victim may become progressively more frightened. Depending on the “victim’s” temperament it may choose to retaliate or hide, only making an appearance when the territorial cat is not around.

Occasionally litterbox problems may arise because the fearful cat is too afraid to leave its hiding place. Additional problems of spraying/marking may occur if both cats are of close

1. Neuter all cats.

2. Keep nails trimmed as short as possible to lessen the chance of injury when your cats are reintroduced.

3. Set aside 10-15 minutes every day for each cat for interactive playtime. Encourage continuous aerobic play with laser pens, feather wands, or toys on strings to reduce anxiety and release energy.

4. Place bells on the cats so you can locate them. The bells must be loud and have different tones allowing you to individually distinguish the cats. This will also allow the cats to know each other’s whereabouts so there will be

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less chance for a surprise attack.

5. On a daily basis, rub each cat with a towel that has the other cat’s scent to familiarize each cat with the other’s scent.

6. If the cats end up in a fight, do not reach between them as you could be seriously injured. Instead, separate them with a blanket, broom, or whatever is handy. Alternatively, make a loud noise to startle them by dropping a pan or book. Cats become extremely agitated after an aggressive event and respond best to isolation until they become calm. You should banish the aggressor to a less desirable area. They may need to be separated for as long as 12 hours.

Reintroduction: Counterconditioning and Desensitization We recommend two related techniques, systematic desensitization and counterconditioning, that are used to treat fear-based problems. Systematic desensitization accustoms a cat to the thing it fears. Counterconditioning rewards the cat, when it is in the presence of the thing it fears, with something it needs or wants, such as food or attention. Over time, these techniques work together to make a formerly stressful experience pleasant and rewarding. Time is the key word here. This two-step program can take months and will require considerable persistence and patience on your part.

Throughout this process, be prepared to go back to the previous stage at any sign of hostile behavior, and then advance to the next stage again.

Neither cat should show anxiety or aggression during the reintroduction process. If they do, go back to the distance where both cats were comfortable. Look for signs of anxiety from the victim and aggression by the aggressor. Signs of anxiety may include not finishing the food, eating quickly and leaving, avoiding eye contact, hiding or trembling.

Warning signs of impending aggression may include staring, tail quivering, flattening of the ears, growling, hissing, stiff body posture, or piloerection. Banish the aggressor if this behavior is observed.

Reward the cats for ignoring each other. If the aggressive cat averts its gaze, it should be rewarded. If the cat that has been attacked makes direct eye contact with the aggressor, reward that response. Do not give food treats or praise to either cat if they are showing fear or aggression. You only want to reward positive interactions between the cats.

STEP I 1. Completely separate the cats in 2 different environments within your house. Perhaps one cat could have the upstairs, designated environment A, and the other could have the downstairs, environment B. Initially relegate the aggressor to a neutral or less desirable area that is less emotive. Water and litterboxes should be accessible to all cats at all times. Make sure each cat is aware of the other’s presence on the other side of the closed door, but confuse their tendency for territoriality by switching “environments” on a daily basis.

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In other words, the cat that was relegated to environment A should be put in environment B and vice versa.

2. As an alternative strategy based on the logistics of your household, you may elect to isolate the aggressive cat in a specific room and allow the other cat to have free range of the house. Select 2 or more rooms with doors that you can close securely. Relocate the aggressive cat between the rooms on alternate days, leaving the door to the currently unused room open. The cat that has the run of the house will investigate the unused room and smell the scent of its feline housemate. Likewise, when the cat in custody returns to one of these rooms on the following day, it will smell its free-ranging estranged companion’s scent. The daily exchange of scents maintains cat-to-cat familiarity in a non-threatening environment and prevents either cat from becoming territorially protective toward a particular environment.

STEP II If pharmacological treatment is recommended, it is preferable to have that aspect of therapy in place before you move on to Step II. Now you can begin the process of desensitization and counterconditioning to ensure that “familiarity does not breed contempt”. If you are accustomed to feeding your cats “free-choice”, you will have to abandon this practice for the time being. During the retraining period, all cats should be meal fed in the morning and at night, so they will be hungry enough to want to participate in the “program”. If your schedule permits, it would be advantageous to give the cats a small amount of food and feed them frequently throughout the day so you will have numerous socialization opportunities.

1. Use mealtimes as an opportunity to reward both cats for relaxed behavior. Also pet and play with them when they are on opposite sides of the door to reinforce that only pleasurable events occur when they are together. You should withhold all food and rewards except for training sessions so the cats learn to associate the presence of the other cat with food and play rather than anxiety.

To begin, feed the cats simultaneously on either side of a closed door so they can hear and smell each other while they are eating. At this stage the food should be highly palatable, perhaps their preferred canned food. You may also choose to feed small bits of tuna, chicken or other delectable treats.

Start by placing the bowls as far apart as necessary so the cats remain comfortable. After the cats have been eating comfortably for a few days, you can begin gradually inching the bowls closer towards the door. Once they have been relaxed being on opposite sides of the door for at least 1 week, you can proceed to the next phase of reintroduction.

2. When your cats are able to eat next to each other on opposite sides of a closed door, you can crack the door open 1-2 inches and secure it with a doorstop or hook and eye.

After they are happy getting occasional glimpses of each other through the crack, open the door 4-6 inches and insert a narrow screen to prevent any physical contact. The

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screen should have newspaper taped on to only reveal a 4 -inch strip of space. The “strip’ can gradually be enlarged to afford the cats increased visual access until the whole screen is free of newspaper. Remember to continue to give the cats time to get used to each other before proceeding to the next step.

3. Completely open the door, but again, insert a screen so they can not have any direct physical contact.

STEP III 1. Once your cats are able to eat near each other across the screen, the next step is to reintroduce them to each other for a short while in the same room. At first they should be restrained on harnesses and held in complete control by one person each or be confined in separate cat carriers. Bring them to opposite sides of the same room for as long as they remain relaxed, 10-15 minutes at a time.

Give them meals, treats, attention, or toys, whatever they prefer most, in order to make this an enjoyable experience for all. Each day, assuming things are still peaceful, bring them a little closer to each other and begin to extend the time they are together. The primary goal is to have them eating side by side and ignoring each other’s presence in the same room.

2. Once they are eating peacefully side by side on harnesses or in their carriers, the next step is to free the more passive cat from the harness or carrier. If all goes well, release the more aggressive cat during the next feeding while keeping the more passive cat confined in the carrier.

3. If you see no signs of trouble when one of the cats is free during meal time, try releasing both cats for side by side feeding. Begin to leave them alone together for gradually increasing amounts of time. One feeding station and one litterbox should be available for each cat and should be located in open areas so the cats can see each other and not be surprised by the approach of the other cat/s.

4. Once they are allowed to be together for longer periods of time, you should continue to praise them or provide treats whenever you see them together. If at any time you see one of the cats begin to avoid the other or see the aggressor staring or controlling the other cat’s movements or access to resources, it is time to return to an earlier phase of the reintroduction program where they are relaxed and begin again.

We understand that this process is tedious and it may take several months to achieve acceptable results. However, no matter how frustrating it may be, do not rush the reintroduction process as that will only exacerbate the problem.

You may wish to keep an “aggression diary” to help you document trends over time regarding the effectiveness of the therapeutic measures that you try.

We must advise you that the above techniques work well in some, but not all cases. Some cats will never be able to be

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left alone together, but they may be perfectly happy living separately in the same household. Leading separate lives is often more problematic for the owner than it is for the cats.

Sometimes the only recourse is to place one of the cats, usually the aggressor in a new home.

PATHOLOGIC AGGRESSION The most well known type of pathologic aggression in cats is that induced by hyperthyroidism. Hyperthyroid aggression shows a constellation of signs including increased appetite, unthriftiness (they become thin), hyperactivity, hypervocalization, and aggression. This condition is much more common in older cats and is treated medically, surgically, or by using radioactive iodine.

Another type of pathological aggression to bear in mind is that caused by disease of the central nervous system, including brain tumors, seizures, infections and parasitic conditions, like toxoplasmosis. Of these, aggression related to seizure activity seems to be the most common and is worth considering when a cat suddenly starts to display peculiar affect stalking and attacking an owner and becoming agitated at sounds. Sometimes the start of this aggression is reasonable and might fall into one of the categories above but its continuation in the odd circumstances mentioned provides a clue as to what is going on. Treatment with phenobarbital is often successful. A last type of paradoxic medical/pathologic aggression is associated with the feline hyperesthesia syndrome. Many people, including behaviorists at Tufts, regard feline hyperesthesia syndrome as being a seizure-based condition. Although the normal presentation is of frenetic, selfdirected bouts of grooming and agitation with dilated pupils and skin rippling; there are aggressive sequelae too which can occur in isolation or as part of the syndrome as a whole.

Treatment can be with phenobarbital as for more typical seizure based conditions or with SSRI’s.

OTHER TYPES OF AGGRESSION There are several types of aggression that occur in cats including sexual aggression, pain-induced aggression, and maternal aggression. Sexual aggression occurs at mating when male cats bite females in the back of the neck to pin them as they mate. Following the successful accomplishment of penetration by the male and ejaculation, the female will often swat at and attack the male and drive him away. The aggression of the male and of the female are termed sexual aggression. Pain induced aggression occurs when a cat is injured (e.g. someone steps on its tail and it turns around and attacks). Maternal aggression will occur when a cat protects as a cat is protecting its kittens. A bizarre antithesis of maternal protective aggression is male destructive aggression directed towards the kittens of another sire.

This infanticide, as it is called, occurs in wild and domestic cats alike.

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Feline fear-based conditions Ansia e marcatura con urina del gatto

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto Il gatto, come il cane, può essere spaventato da cause animate o inanimate e da particolari situazioni. Tuttavia, la reazione dei felini è abbastanza diversa da quella del cane. I gatti non manifestano l’immobilizzazione ed i tentativi di pacificazione, compresa la ipersottomissione, e, in realtà, mostrano una reazione molto comune a tutti i tipi di paura: la marcatura territoriale con l’urina. In questa relazione verranno trattati lo sviluppo e la manifestazione della paura dei gatti nei confronti degli estranei e di altri gatti e i timori derivanti da particolari situazioni come l’ansia da separazione; tuttavia, la relazione sarà focalizzata principalmente sull’eliminazione inappropriata, che rappresenta il più comune problema comportamentale del gatto. Verrà anche discussa l’influenza dei fattori genetici ed ambientali sulla genesi dei vari tipi di paura.

Cats, like dogs, can be frightened of animate, inanimate, and situational cues. Although their reaction is somewhat different to that of dogs. Freezing, and attempts at appeasement, including super-submission are not manifested by cats and, in fact, a very common reaction to all types of fear is territorial urine marking. In this lecture, the development and manifestation of cats’ fearfulness toward strangers and other cats will be discussed as will situational fears including separation anxiety, however, inappropriate elimination problems, the most common behavior problem in cats will be the focus of this lecture. The influence of genetics and environment in the genesis of the various types of fear will also be discussed.

FELINE FEAR-BASED CONDITIONS Cats can show fearfulness in response to the same challenges as dogs but their reaction is somewhat different.

When they are frightened of animate cues (e.g. people or other cats) their first response is to run and hide (flight) though they may show aggression, either directed at fear-inducing person or animal or redirected to one alongside.

Other possible responses to fear-inducing stimuli, such as freezing and appeasement, are not seen in cats. Of all the possible fearful reactions, aggression is the one most commonly presented as a behavior problem. Feline affective defense behavior was discussed earlier and includes all the usual signs of autonomic arousal, such as pupillary dilatation, increased heart rate and blood pressure, and piloerection. Fearful posturing of cats is designed to intimidate rather than to appease.

Cats that are frightened of inanimate cues, such as thunderstorms, are much less demonstrative than dogs tending to hide away cowering and shrinking from the problem at hand. Because of this inanimate fears of cats are very rarely reported to behaviorists.

Separation anxiety occurs in cats as it does in dogs though, once again, the signs are much subtler and are reported less frequently. Typically affected cats are extremely bonded to their owners and become distressed when they are left alone. Rather than pacing and panting and engaging in destructive behavior like dogs however cats tend to become depressed and reclusive may engage in anxiety-related urine marking behavior in their owner’s absence. Urine marking by a cat that occurs only in the owner’s absence is a cardinal sign of separation anxiety in this species. Treatment of fears is along the same lines as it is with dogs (i.e. systematic desensitization with counterconditioning). Essential features of the program include:

1) Identify the fear-inducing stimulus (including other associated cues) and isolate the cat from it.

2) Devise a method of controlling the intensity of the fearinducing stimulus for representation in a controlled manner.

3) Introduce the fear-inducing stimulus at a low intensity while counter conditioning the cat to a different expectation of the event.

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4) Gradually increase the intensity of the stimulus until it is at a previously fear-inducing level using a stepwise approach (systematic desensitization).

5) Once successfully treated, the cat must be periodically exposed (once a month) to the stimulus and rewarded for not acting fearfully.

Important factors to remember concerning treatment For fear inducing stimuli that are rarely encountered, anti-anxiety drugs are the treatment of choice. The owner must be able to anticipate the fear-inducing stimulus and the drug must be given such that the anxiolytic (anti-anxiety) effect is recognizable prior to the exposure to the fear. The correct drug and dosage differs between individuals. For frequently encountered fears it is inappropriate to use drugs alone. For more pervasive problems, pharmacological treatment should be combined with behavior modification.

How quickly a treatment regime works depends on the severity of the fear and the frequency of the treatment sessions. Moderate fears can take a few weeks to resolve while severe fears may take as much as three to four months. Even if treatment sessions are a week apart the fear can be successfully treated.

During treatment the cat must not be exposed to the fear except during the behavior modification procedure.

Other methods of treating fears 1) Flooding, for very mild fears or fears with several stimuli (e.g. fear of street noise). This method should be used with great care.

2) Pharmacological desensitization for fears when the intensity of the stimulus cannot be controlled or the fear-inducing stimulus is not known.

Inappropriate Elimination in Cats Although cats are quite fastidious about their elimination behavior, “inappropriate elimination” is their number one behavior problem. Inappropriate elimination can be either by spraying (marking), or squatting (marking or simple house soiling). Marking and simple house soiling (a litter box aversion problem) have different motivations and treatments.

Important Facts about Elimination Behavior in Cats a. Cats have an innate need to bury their excreta. Some cats do not cover feces as a territorial mark. b. Cats like to urinate on absorptive surfaces such as carpet & paper and are not so keen to use smooth non-absorbent surfaces, such as tile or linoleum. c. There is no cat litter type that is favored by all cats.

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Diagnostic Approach Inappropriate Urination 1. Diagnostic tests to rule-out underlying medical causes: Complete physical examination, CBC, profile, urinalysis, urine culture to exclude medical causes of urination problems. For fecal elimination problems, test for gastrointestinal parasitism, inflammatory bowl disease, malabsorption/maldigestion, and food allergies.

2. Deal with medical problems, but warn the owner that the inappropriate urination may persist, therefore behavior modification may be necessary.

3. Get an extensive history in order to diagnose the condition correctly and try to isolate any causative factors.

1. SPRAYING OR MARKING Feral cats have large overlapping home ranges but may defend a much smaller territory. Male cats have larger home ranges and mark more than females. Spraying is a normal marking behavior in intact cats. Spraying is used to inform other males and especially estrus females of the male’s presence.

Sprayed urine of toms has a different chemical make-up than normal urine and stimulates female estrus behavior.

Hereditary and learning play an important role in the expression of spraying behavior. Remember that female cats will also spray.

How to Recognize Spraying a. Urinating on vertical surfaces while standing with a quivering tail and treading with the paws is the most common posture in spraying. b. Some cats spray from a crouching position. c. With only one exception (see d.), small amounts of urine are released when a cat is spraying/marking. d. Larger amounts of urine are expelled when the stress is caused by a particular person. These puddles are possibly an attempt to cover up human pheromones and usually deposited on clothes, bed linen, hair brushes, etc. (anything that has a strong odor of the person).

Causes of Spraying Spraying is most often caused by anxiety or an environmental stress. a. A new person or pet (most commonly a new cat) in the household. b. A new cat in the yard, perhaps spraying on the owner’s window. c. The presence of an estrus female. d. Some female cats spray when in estrus (heat). e. Any change in routine, especially of a person the cat finds important (feline separation anxiety) or a move to a new environment.

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Treating a Spraying Problem Ideally, isolating the inciting cause and removing it would be the best method of dealing with the problem. Unfortunately this is not always possible, therefore anti-anxiety medication is the most effective way of handling this condition.

1. See diagnostic approach to inappropriate urination (earlier).

2. Neuter the cat- 80% of cats have a rapid decline in spraying. A further 10% will have a gradual decline in spraying. Approximately 10% of cats will continue to spray.

3. Cleaning the sprayed area is very important because cats have a need to refresh sprayed areas. Use an enzymatic odor eliminator.

4. If a neighborhood cat is spraying on basement windowstry to discourage this behavior by burying bloodmeal two inches below the soil around the windows.

5. Pheromone treatment of soiled areas (“Feliway”).

6. Drug therapy The drugs that can be used to treat inappropriate elimination resulting from anxiety are as follows:

Buspirone Studies have shown that buspirone has its greatest success in multi-cat households.

1) Buspirone, tradename BuSpar, is a “smart” drug that works specifically to treat anxiety. It works on 5HT1A receptors and to some extent on dopamine receptors (as an agonist of the former and an antagonist of the latter) to reduce anxiety and apprehension. It has virtually no organ toxicity, is not addictive and there is no withdrawal. Side effects in cats include increased affection to the owners, increased playfulness and kittenish behavior, occasional spats of aggression towards an aggressor (because of new found confidence) and occasionally (unfortunately) some paradoxical excitement about thirty to sixty minutes after administration. Buspirone is usually dosed at 5 mg twice a day for a cat though this can be increased to 10 mg twice a day especially for larger cats that have only partially responded at the lower dose.

Treatment is normally continued for two to three months and then the dose is tapered over two to three weeks.

Diazepam (Valium) Diazepam used to be the drug of choice and is about as efficacious as buspirone, successfully treating some 60% of anxiety related urine-marking cats.

1) The difference between diazepam and buspirone is that diazepam produces more side effects (increased appetite, lethargy, ataxia, weight gain), is addictive, precipitates a withdrawal syndrome when it is discontinued abruptly, and recently has been associated with a fatal syndrome of hepatotoxicity.

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2) In addition to the other drawbacks, cats treated with diazepam often relapse into their original state following the treatment. The recidivism rate has been reported at around 91% with diazepam (versus 50% following a two-month course with buspirone).

Various anti-depressants have been used to treat anxietyrelated urine marking behavior in cats, including older tricyclic antidepressants like amitriptyline and imipramine.

More recently clomipramine and fluoxetine have been efficacious.

Although most cats with anxiety related urine-marking behavior can now be controlled with anxiolytic medication there is a percentage that cannot be controlled in this way. It has been suggested that neutered male cats that are refractory to anxiolytic medication may continue spraying because of residual male mechanisms that operate without the need for testosterone. This is borne out to some extent by the successfulness of progestin therapy for these cats. Across the board, progestins are only efficacious in some 30% of cats that urine mark and the biological cost of such treatment is high. Treated cats can display any one of a number of untoward side effects such as increased appetite, weight gain, lethargy, diabetes, adrenal problems, etc., so the practitioner must question the validity of this treatment and carefully weigh the potential outcome of even successful treatment with the side effects.

2. HOUSE-SOILING How to Recognize House-Soiling a. Can be either urine or feces. b. If it is urine, always large amounts (puddles) are released. c. Litter box often avoided completely.

Causes of House-Soiling House soiling occurs because of a disruption of housetraining. a. Litter Aversion i) litter type -some cats do not like to use a particular type of litter. Many cats do not like scented litter. As a general rule, longhaired cats dislike clay litter because it sticks to their fur and between their toes. This is the most common reason that many longhaired cats do not bury their feces. ii) litter too dirty -many cats will avoid their litter if it is not cleaned often enough. iii) litter too clean -some cats require some odor of urine to stimulate urination. Many cats dislike the smell of soap in their litter pan. b. Litter pan-most cats prefer large open litter pans. Other cats prefer covered pans. c. New Substrate Preferences-some cats will find an absorbent material they favor over litter such as paper or carpet.

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d. Prevented Access i) a second cat or a dog in the household may not allow the cat to get to the litter. ii) locked door. e. Inappropriate Position of Litter Pan i) in an area that is too busy. ii) near food or water bowl. f. Inadequate cleanup of a previously soiled area- the smell of urine will stimulate a cat to continue to use an area. g. Superstitious learning-the cat may associate a negative event (such as a loud noise, something falling on them, painful urination, or punishment) with being in the litter.

As a result the cat will not re-enter the litter pan.

Several of the above causes can come into play at the same time. For example, access to the litter may be prevented; as a result, the cat urinates on the carpet and decides that he prefers the new substrate.

Treating Feline House-Soiling Because it is almost impossible to know the exact cause (or causes) for house soiling in, a multifactorial approach is employed. The objectives of the treatment of house soiling are to make the inappropriate site less desirable, to make the litter more attractive, and to remove the initial cause of the problem, if possible.

1. See diagnostic approach to inappropriate urination (earlier).

2. Making the inappropriate site less desirable i) The site can be made less appealing by thorough cleaning of the area with non-ammonia cleaner.

Clean tile with 1 part Detol to 4 parts water. Because it is almost impossible to get all of the odor out, the owner may need to mask the odor with a commercial product. ii) Clean other surfaces, rugs, etc., with professional odor neutralizer (e.g. Odorban, Nature’s Miracle) that

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has an enzymatic action. iii) The soiled site can be covered with foil or plastic.

Another alternative is to use crushed mothballs in the area. The odor of the mothballs should only be present at the level of the carpet. iv) Place the cat’s food bowl in the chosen site. v) For cats which are defecating or urinating in bath tubs, fill the tub with 2 inches of water.

3. Making the Litter More Attractive i) Remove feces from the litter daily and change the entire litter (except clumping litter) every 2-3 days.

Clumping litter should be changed completely every 2-3 weeks. Do not use soap to clean the litter pan (just warm water). ii) Each litter pan should have a different litter type of litter (e.g. clay, sand, clumping, compressed paper“Yesterday’s News” brand). Most cats like at least 2 inches of litter in a pan. The cat’s preference will become evident. iii) Try different types of litter pans (e.g. open topped, covered, one with high sides, etc.). iv) It may also be necessary to place a litter pan close to the inappropriately soiled site to provide an easily accessible alternative site. (The litter can be moved slowly to a desired position once the cat is using it regularly).

4. Removing the Inciting Cause i) Employ 1 litter pan for each cat in the household plus 1 extra pan (N+1). ii) Find a discrete location for a new litter pan away from traffic or out of reach of any dogs. iii) Have at least one litter pan on each level of the household. iv) Have at least litter pan on each level of the house.

5. Some cats that have had this problem for a number of years may need to be enclosed in a small space (e.g. bathroom) with a litter pan or 2). Once a new eliminative behavior is established, the cat can gradually be permitted access to the rest of the home.

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Feline compulsive behavior Disturbi ossessivo-compulsivi del gatto

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto Come nel cane, anche nei felini i comportamenti compulsivi sono basati su atteggiamenti naturali che sembrano essere in qualche modo frustrati dal modo in cui l’animale viene tenuto o dagli ambienti ristretti. In questa relazione i comportamenti compulsivi dei felini verranno illustrati facendo riferimento alle compulsioni più diffuse, come l’alopecia psicogena, il succhiare la lana/pica e l’iperestesia felina. I segni tipici di queste 3 compulsioni verranno discussi facendo riferimento anche alla sensibilità di razza, all’impatto degli stress ambientali ed alla modificazione comportamentale e all’arricchimento ambientale come terapia. Viene anche trattata brevemente la terapia farmacologica.

As with dogs, feline compulsive behaviors are based on natural behaviors that appear to be somehow frustrated by management practices or restricted environments. In this lecture feline compulsive behaviors will be illustrated with reference to the most prevalent of these compulsions including psychogenic alopecia, wool-sucking/pica, and feline hyperesthesia. Clinical signs of these three compulsions will be discussed including mention of breed susceptibility, the impact of environmental stresses, and behavior modification and environmental enrichment as therapy. Pharmacologic treatment will also be discussed briefly.

FELINE COMPULSIVE BEHAVIOR As with dogs, feline compulsive behaviors are based on natural behaviors that appear to be somehow frustrated by management practices and/or restrictive environments. Sometimes owners can predict a specific time or place when these behaviors will occur and eliciting stimuli can often be identified. As time goes by, a compulsive behavior may be shown more often or for longer periods of time anytime the cat is anxious. As previously mentioned, compulsive behavior initially may be performed as a displacement behavior.

For example, when a cat is torn between responding with aggression or running away, it may displace into a seemingly unrelated behavior, such as grooming, as a way to reduce emotional tension. If exposure to an anxiety-provoking stimulus continues, the cat may express the behavior repetitively and out of context. At this stage, even when the behavior appears to have adverse consequences for the cat (i.e. pain), the behavior may continue to be performed. The level of stimulation required to trigger the behavior may decrease over time so that the behavior occurs in response to any level of arousal. Because certain cat breeds are seen more often in the compulsive behavior case loads, genetic influences appear to be involved in determining which individuals will display compulsive behaviors and what the actual compulsions are.

The most common compulsive behaviors exhibited by cats include wool sucking or fabric eating, over-grooming/hair-barbering or hair-pulling behavior (psychogenic alopecia), and feline hyperesthesia. By far, oral behaviors such as wool sucking and psychogenic alopecia predominate in feline compulsive disorders.

Wool-Sucking “Wool-sucking” is expressed as repetitive and inappropriate sucking and chewing on fabric usually woolen, synthetics, or cotton substrates such as sweaters, blankets, or carpets. Some cats suck on or ingest plastic substrates. The condition resembles displaced nursing behavior and may be a feline equivalent of thumb sucking. Wool sucking may start as a nursing behavior directed toward the queen or other cats coat. Such misdirected nursing may subsequently generalize to other fuzzy substrates. As the cat matures, sucking may progress to pica (consumption of inedible material) and the range of materials ingested may broaden to include a wide variety of fabrics and other inappropriate items such as shower curtains, rubber bands, shoe laces, and plastic bags. Damage can be quite extensive and costly and can impose health risks including intestinal blockage. Consequently, wool-sucking can be dangerous to the cat as well as

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a nuisance to the owner. The onset of wool sucking is usually observed anytime after weaning, especially during the first year of life and frequently before 6 months of age.

Several predisposing factors have been suggested for this behavior including persistence of kitten oral behavior following early weaning, heredity, inadequate environmental or social stimulation (feline separation anxiety), or a malfunction of neural control of appetitive behavior. Medical conditions that can trigger abnormal ingestion of inappropriate material include hunger, nutritional deficiencies such as anemia or inadequate dietary fiber, diabetes, or tumors.

Wool-sucking is predominantly seen in oriental breeds, although other purebreds and cats of mixed origin as well as domestic long and short hairs exhibit this condition. Siamese cats appear to be particularly susceptible and account for ~ 50% of the affected population. Given the breed predilection, compulsive wool sucking is thought to have genetic underpinnings possibly related to the comparatively anxious and active temperaments of affected breeds.

Psychogenic Alopecia Cats normally groom as a displacement behavior when momentarily stressed, but in some cases the frequency and duration of grooming lasts longer than would be considered functional. In susceptible animals exposed to chronic stress, grooming may become maladaptive and be performed out of the normal context. Such grooming is repetitive, excessive, and inappropriate in frequency and intensity of occurrence.

Excessive self-licking and chewing result in areas where hair shafts have been sheared leaving stubble. Some cats may engage in the behavior more aggressively and actually bite and pull out patches of hair from their coat. Hair pulling and chewing may result in skin wounds and ulceration. Hair loss is typically noted on areas only accessible to the cat (abdomen, flank, back, chest, and legs). A stressful change in the environment often coincides with the onset and concurrent anxiety-associated behaviors such as hiding, anorexia, avoidance, and nervousness may be observed.

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Feline Hyperesthesia Feline hyperesthesia is a complicated behavioral condition with some features that appear compulsive and others that appear frankly neurological. It is characterized by compulsive self-directed grooming/aggression and affected cats episodically become abnormally sensitive to perceptual input. In some cases, the condition may progress to generalized seizures. Because of the overlap between symptoms, it is thought to possibly be a form of partial seizures with compulsive components.

Symptoms characteristic of feline hyperesthesia include dilation of pupils, excessive skin rippling, and frenetic selfdirected grooming which may result in hair loss. Grooming may be so intense it may manifest as self-directed aggression often focused on the tail, flank, or pelvis. Aggression may sometimes be explosive and directed at people. Affected cats may emit excessive and unusual vocalizations and appear to hallucinate (“act afraid of their tail”) and run away.

They may appear “manic” (excited look, frantic running, jumping) and are frequently extremely sensitivity to touch.

Sometimes aggressive bouts are preceded by attention seeking and enhanced affection to people. Affected cats are often anxious and restless, constantly wandering and pacing.

There is an apparent sensitivity to touch (episodes may be induced by stroking along the spine), which can trigger attacks and accounts for the name of this syndrome. Feline hyperesthesia is usually associated with heightened affect and aggression. Attacks appear to be more frequent in the evening or early morning. Aggression appears spontaneously and for no obvious reason and the bouts can end as quickly as they appear. Following an episode, the cat often looks confused. The behavioral manifestation varies between cats and milder forms of feline hyperesthesia may be confused with psychogenic alopecia because of the common symptoms of excessive grooming that may result in hair loss.

The onset usually occurs in young to middle age cats between one to five years of age. The signs may last a few seconds to a few minutes and may vary in incidence from month to month. Episodes may occur every few days or almost constantly all day. Medical ruleouts include fleabite dermatitis, food allergy, intervertebral disc disease, vertebral trauma, infection, toxins, or neoplasia.

The condition may have a genetic basis since it occurs predominantly, but not exclusively, in purebred cats, especially Siamese or Siamese crosses.

Medical rule-outs include allergies or hypersensitivity to parasites, food, dust, pollen, or mold. If a trial dose of steroids controls excess grooming, the condition is probably medical and not psychogenic in origin. Other medical conditions causing discomfort but not associated with skin conditions can cause excessive grooming (cystitis, inflammation of anal sacs, hyperthyroidism). Even if a medical condition triggers the onset and is subsequently resolved, a susceptible cat may continue to groom excessively.

TREATMENT FOR FELINE COMPULSIVE BEHAVIOR

In general females appear to be more commonly affected than males. The onset of psychogenic alopecia may occur at any age, but tends to occur around puberty. Psychogenic alopecia is thought to have a genetic basis because a) it appears to be a displaced grooming behavior which is hard-wired and b) the condition is seen predominantly, but not exclusively, in purebred cats of oriental breeding and is usually associated with cats with anxious temperaments.

1. Eliminate or reduce exposure to stressors or eliciting triggers – The first line of attack for treating anxietybased disorders is to remove or reduce the source of conflict or anxiety. If this is not possible, then counterconditioning (teaching the cat to perform a behavior that is incompatible with fearful behavior) and desensitization (gradually introducing the cat to the stimulus it fears and coupling this with a positive experience) techniques are the treatment of choice.

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Common Eliciting Triggers for Feline Compulsive Behaviors - Separation anxiety (owners absence, loss of companion animal) - New animal or person in household - New environment - Restricted access to outdoors - Inadequate social or environmental stimulation - Early weaning - Resolved medical condition - Stroking or petting cat on back - Loud or high pitched noises If the cat sucks on fabric, restrict its access by picking up clothing and preventing it from going in rooms where it may suck on bedspreads or curtains. If the cat chews specific items, make these items aversive by coating them with bitter tasting substances. Remember to provide acceptable alternative items for play and chewing and place them in the area where the cat normally would seek fabric.

If the cat suffers from feline hyperesthesia, advise the owners to avoid stroking their cat along its back as this can trigger attacks.

2. Environmental Enrichment to distract cat from compulsive behavior Climbing frames Many cats enjoy climbing frames that make their environment more three-dimensional and allow them to express their natural tendency to climb trees.

Bird feeders, fish tanks Placing a bird feeder near a window where the cat can observe the birds may help keep it entertained. Some cats will even watch bird videos. Fish tanks are also entertaining for cats just be sure to place a cover securely on top of the tank to protect the fish.

Prey facsimiles Toys attached to strings, feather wands, and fishing pole toys stimulate predatory behavior. Daily rotation of toys is recommended to keep the cat mentally stimulated.

Non-toxic grasses Some cats respond well to fresh catnip or cat grass grown especially for them. Along the same theme, some cats also enjoy lettuce or green beans. Other cats can be redirected onto pieces of thin rawhide coated lightly with fish oil or cheese spread. Owners should offer the rawhide chews only when they will be directly supervising their cat.

Novel feeding opportunities Have several different feeding stations so the cat will have to search for its food. Some cats respond very well to “food puzzles” that they must bat around in order to obtain food. Food puzzles can be purchased in pet supply stores or

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crafted at home by taking an empty toilet paper roll and punching a number of holes in the tube. Make the holes large enough to release the kibble. Fill the tube with kibble and securely tape the ends to contain the food. The owner may need to show the cat how to roll the tube in order to obtain food. Make several food puzzles, fill with the cat’s daily meal, and distribute them around the house. With this technique, the cat will have to hunt for its food. The goal is to keep the cat occupied and mentally stimulated for much of its active time.

3. Exercise –Daily aerobic exercise helps decrease arousal. We recommend that the owner spend 10-15 minutes twice a day engaged in aerobic, interactive play with their cat.

One way to accomplish this is to attach treats or furry toys to string and play “predator” games with the cat. Some cats prefer feather wands and will perform some amazing acrobatics while they try to catch their “avian prey”. Try several different types of toys and rotate them regularly so the cat does not tire of them.

4. Diet – Prolonging feeding behavior can be helpful.

For example, feeding a high fiber dry food ad-lib may help redirect the cat from sucking on fabric or over-grooming to eating. Putting large rocks in the food bowl can increase the difficulty of obtaining food and prolong the foraging effort.

As previously mentioned, food puzzles are a great way to increase a cat’s activity level and prolong feeding.

5. Predictable schedule – Having a set routine helps calm many cats. Regularly scheduled times for feeding, playtime, and attention are recommended.

6. Attention Seeking Behavior – Owners should be instructed to consistently ignore the cat’s repetitive behavior if there is any indication it is performed to get their attention.

If the behavior is ignored, the owners will ensure that they are not reinforcing the performance of the unwanted behavior. If there is an attention -seeking component to the behavior, the frequency of occurrence should decrease if it is not rewarded. The owner should be forewarned, however, that the frequency of the behavior may initially increase as the cat attempts to gain the owner’s attention. Owners should be warned to not incorrectly assume that the treatment is ineffective. Continued lack of reward (ignoring the behavior) will diminish the performance of the behavior if there is an attention-seeking component involved.

7. Restraint and punishment – Generally, treatment of over-grooming conditions by physical restraint (Elizabethan collars) is not recommended. Although it may prevent the cat from injuring itself, it does nothing to address the underlying anxiety issues that maintain the behavior. The cat should never be punished since punishment may actually contribute to the underlying conflict and increase the cat’s anxiety.

8. Pharmacological treatment – Once the behavior becomes engrained, the cat may continue to show compulsive behavior even when the initiating stressors are removed. At

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this stage, the behavior may become refractory to standard behavior modification techniques and management changes alone. Pharmacological intervention, in addition to management changes and behavior modification, is often required in the treatment of feline compulsive behaviors. This is especially true if the environmental triggers can not be identified and eliminated.

As mentioned in the introduction, compulsive behaviors appear to involve changes in brain neurotransmitters that may promote the continued expression of the behaviors. Serotonin involvement is suspected because drugs that inhibit the reuptake of serotonin in the brain are the most helpful for treating compulsive disorders. We currently favor the use of fluoxetine or clomipramine for the treatment of compulsive behavior in cats. The actual mechanism for the involvement of serotonin in compulsive behavior is unknown. However, from a practical viewpoint, medications that inhibit the reup-

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take of serotonin appear to normalize brain chemistry, minimize the impact of environmental stressors, and help stabilize the cat’s mood. A less anxious cat will be less driven to engage in compulsive behavior.

Although we can not always completely eliminate compulsive behavior, the treatment program outlined above for both dogs and cats is effective in reducing the incidence of compulsive behavior. To be effective, all phases of the program must be followed simultaneously and consistently. It is often helpful to have the owners keep a daily diary of their pet’s behavior. This helps them be more accurate in assessing the animal’s improvement and may help increase owner compliance. In addition, it will make your job easier in terms of having accurate information regarding which aspects of treatment are effective and which are not beneficial for each individual case. In difficult cases, weekly follow-up calls may also improve owner compliance and provide emotional support.

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Pharmacologic approaches to managing behavior problems Psicofarmacologia

Nicholas H. Dodman BVMS, MRCVS, DVA, MAPBC, Dipl ACVA, Dipl ACVB - Tufts University, Massachussets, USA

Riassunto A partire dalla metà degli anni ’80 del secolo scorso si è verificata una vera e propria esplosione delle conoscenze relative ai tipi di farmaci utilizzabili per la modificazione del comportamento in medicina veterinaria. Lo scopo di questa relazione è quello di fornire i presupposti razionali su cui basare la scelta dei principi attivi più appropriati per il trattamento dei vari tipi di problemi comportamentali negli animali domestici. Il lavoro sarà diviso in 3 sezioni, che tratteranno gli agenti utilizzati per la terapia dell’aggressività, quelli indicati per le paure e le fobie e quelli impiegati per i trattamenti compulsivi. L’approccio alla scelta dei farmaci sarà di tipo meccanicistico e, in una certa misura, riduzionistico, anche se verranno comunque trattati argomenti pratici come le posologie, le probabilità di successo del trattamento, la durata ottimale, gli effetti collaterali e la sicurezza.

Since the mid-1980’s there has been an explosion of knowledge in veterinary medicine about the types of drugs that are available for behavioral modification purposes. The purpose of this lecture will be to provide rationale as to the selection of appropriate pharmaceuticals to treat the various types of behavior problems in domestic animals. The lecture will be divided into three sections dealing with those drugs used to treat aggression, those that are used to treat fears and phobias, and those that are used to treat compulsive behaviors. The approach to the selection of drugs will be mechanistic and to some extent reductionist though practical issues such as dose rates, the likely successive treatment, optimum duration of treatment, side effects and safety will be discussed.

INTRODUCTION There is burgeoning interest in drug therapy for behavior disorders in human and veterinary medicine. The 1990’s, which has been described as the “decade of the brain”, portend an explosion in knowledge pertaining to psychopharmacologic therapy. This revolution in pharmacological treatment of behavior problems has been facilitated by rapidly expanding information about receptor pharmacology and recent advances in pharmacological therapy have derived from the use of receptor specific drugs. These new drugs, socalled “smart drugs” have relatively few side effects and have high therapeutic indices. They have a wide range of applications and may be used to treat a variety of behavioral problems. Veterinary practitioners may welcome the thought of treating behavioral problems medically, but some caveats apply. First, it is imperative to make an accurate behavioral diagnosis and to institute appropriate management and behavior modification strategies to complement pharmacologic therapy. Second, not all patients respond well to drug therapy, and some may develop unacceptable side effects. With these provisos and limitations in mind, pharmacologic ther-

apy can be used successfully to complement behavior modification therapy in a variety of animal behavior problems.

Dose rates of the most frequently prescribed drugs are listed in Tables 1 and 2. Table 3 classifies these drugs and indicates their site of action.

AGGRESSION Reis suggested that all forms of aggression could be classified into two main types, predatory or affective. This is a useful classification when designing pharmacologic treatment strategies. Predatory aggression is innate, reflexive behavior which is triggered by moving prey (or facsimile). It involves minimal mood change and seems automatic and preprogrammed. Affective aggression, on the other hand, involves significant mood change with activation of the autonomic nervous system resulting in signs such as pupillary dilatation and piloerection as well as the adoption of aggressive postures. The distinction between offensive and defensive aggressive modes of affective aggression is made with reference to the animal’s reaction to

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Table 1 - Drugs used to treat aggression

Dose Rate NEUROLEPTICS Acepromazine

1-2 mg/kg 0.05-0.1 mg/kg

Route of Administration

Dose Interval

Side Effects

PO IM or IV

TID

Sedation, reduced social and exploratory behavior, lowers seizure threshold

SERENICS Eltoprazine

0.5-1 mg/kg

PO

TID

Panting

AZAPIRONES Buspirone

0.5-2 mg/kg

PO

BID or TID

Paradoxical response in some animals

ANTIDEPRESSANTS Fluoxetine

1 mg/kg

PO

SID

Anxiety, reduced appetite

Clomipramine

0.5-1 mg/kg

PO

SID

Anticholinergic effects, sedation

BETA BLOCKERS Propranolol

0.5-2 mg/kg

PO

TID

Bradycardia, inactivated cardiovascular reserve mechanism

Pindolol

0.125-0.25 mg/kg

PO

BID

Anxiety (panting, inappropriate urination)

ANTI-EPILEPTIC DRUGS Phenobarbital 1-4 mg/kg

PO

BID

Sedation, hepatic dysfunction

Phenytoin

6-35 mg/kg

PO

TID

Progressive hepatic injury

Valproic Acid

undetermined

PO

undet.

Gastrointestinal disturbances, hepatic disorders

Diazepam

0.25-0.5 mg/kg

PO

PRN

Sedation and increased appetite

Sustained release diazepam (Valrelease)

0.5-1 mg/kg

PO

SID or BID

Sedation and increase in aggression, increased appetite

BENZODIAZAPINES Diazepam

0.5-1 mg/kg

PO

PRN

Sedation, paradoxical increase in aggression, increased appetite

Alprazolam

0.05-0.1 mg/kg

PO

TID

Sedation, paradoxical excitement

STIMULANTS Dextroamphetamine

0.5-1.0 mg/kg

PO

SID

Excitement, hyperactivity

PROGESTINS Medroxy-progesterone

5 mg/kg

IM

single

Endocrine admin. disturbances

Megestrol

2-5 mg/kg

PO

SID- 1 to Endocrine disturbances 2 weeks (then reduce frequency)

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Table 2 - Drugs used to treat anxiety, fears, and phobias

Dose Rate NEUROLEPTICS Fluphenazine signs,

Route of Administration

Dose Interval

Side Effects

PO

Undet.

Lower seizure thresh-hold, extrapyramidal

Undetermined

xerostomia, constipation Perphenazine signs,

0.88 mg/kg

PO

BID or TID

Lower seizure thresh-hold, extrapyramidal xerostomia, constipation

BENZODIAZAPINES Diazepam

0.5-1 mg/kg

PO

BID or TID

Sedation, paradoxical excitement, increased appetite

0.5-1 mg/kg

PO

SID or BID

Sedation, liver damage

AZAPIRONES Buspirone

0.5-2 mg/kg

PO

BID or TID

Paradoxical response in some animals

BETA BLOCKERS Propranolol

0.5-2 mg/kg

PO

TID

Bradycardia, inactivated cardiovascular reserve mechanism

Pindolol

0.125-0.25 mg/kg

PO

BID

Anxiety (panting, inappropriate urination)

ANTIDEPRESSANTS Amitriptyline

2-4 mg/kg

PO

SID or BID

Sedation, reduced appetite

Clomipramine

0.5-1 mg/kg

PO

SID

Anticholinergic affects, sedation

Clorazepate (dipotassium)

OPIOID ANTAGONISTS

Table 3 Drug

Class

General site

Specific site

Acepromazine

Dopamine blocker

7

D2 postsynaptic dopamine receptors

Clomipramine

Serotonin reuptake

5

Serotonergic neurons blocker

Fluoxetine

Serotonin agonist

5

Serotonergic neurons

Buspirone

Serotonin agonist

7

Activation of 5HT1A receptors

Naltrexone

Narcotic antagonist

7

Blockade of postsynaptic opioid receptors

d-amphetamine

Dopaminergic agonist

4

Presynaptic vesicles (release dopamine)

Pindolol

Adrenergic antagonist

7

Blocks Ă&#x;2 receptors and 5HT1A receptors

Alprazolam

Benzodiazepine

7

GABA - benzodiazepine chloride channel receptor complex

This table defines the site of action for some specific agents that are used to treat behavior disorders.

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the stimulus for aggression. Different types of aggression are the result of activation of different brain centers and neuromodulators coordinated in an integrated response. In predatory aggression, which is hypothathalmic in origin, acetylcholine plays a key role.

Affective aggression involves the frontal cortex/amygdala and utilizes serotonergic, catecholaminergic, cholinergic and possibly GABAergic systems. Using the Reis classification of aggression, an assessment can be made of which brain centers and neurotransmitter systems are likely to be involved in a particular case. This leads to logical design of pharmacologic treatment strategies.

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Azapirones These compounds are referred to as anxioselective agents because of their specific anxiolytic action, which is achieved with minimal or no side effects. Azapirones, like buspirone, also have useful anti-aggressive effects mediated by agonist activity at serotonin (5HT1A) receptors. Offensive aggression and predatory aggression are reduced by this group of compounds. We have had successful results using buspirone to treat offensive aggression in dogs and cats. Buspirone is extremely safe and has no significant sedative or muscle relaxant effects. Also, it is free from dependence-producing properties so that there are no withdrawal side effects.

Neuroleptics The primary mode of action of neuroleptics in the treatment of aggression is antagonism of dopamine. Dopamine regulates thought processes by its action in the mesolimbic area of the brain stem. It also facilitates motor function through its action in the nigrostriatal area of the brain and has a neurohumoral regulatory action. Most of the neuroleptics which have been used in the past are not specific for the treatment of aggression and cause parallel shifts in social and exploratory behavior.1 At levels which control aggression, drugs such as acepromazine, a low potency neuroleptic, will produce signs of sedation and a general indifference to surroundings. Prolonged use of neuroleptics can lead to the development of an extrapyramidal syndrome. This property alone limits the usefulness of this class of drugs. High potency neuroleptics, like haloperidol, fluphenazine and perphenazine, produce less sedation but are still nonspecific, reducing activity levels in parallel with their anti-aggressive effect. Furthermore, this latter group is even more likely to lead to extrapyramidal side effects with prolonged use.

Clozapine is an atypical neuroleptic which appears to have a rather specific anti-aggressive effect in experimental animals. This neuroleptic is associated with an extremely low incidence of extrapyramidal side effects in humans, possibly by a preferential action on mesolimbic rather than nigrostriatal dopaminergic structures. Clozapine offers some promise for the treatment of veterinary patients, although salivation and potentially seizures are worrying side effects.

Serenics This group of drugs, typified by eltoprazine, has a highly specific anti-aggressive profile. Offensive aggression is reduced in a dose-dependent fashion by eltoprazine in experimental animals, leaving defensive aggressive behaviors, social interactive behavior and exploratory behavior intact.

Eltoprazine and congeners are serotonin agonists, exerting their effect at the 5HT1A receptor. The pharmacokinetics of eltoprazine has been worked out in the dog, but none of the serenic compounds is currently available for routine veterinary use.

a

Miczek KA. Tufts University, Boston, MA. Personal communication, 1992.

Antidepressants In the laboratory, these drugs have been shown to suppress predatory aggressive behavior but they may be ineffective, or even enhance, affective aggressive behavior. Appropriate selection of the antidepressant is important in treating affective aggression. Modern antidepressants, such as clomipramine and fluoxetine, which preferentially inhibit the reuptake of serotonin, are most effective. There is substantial evidence in humans that increased irritability, hostility and impulsivity is associated with reduced central serotonergic functioning. Increasing central serotonin levels almost invariably reduces aggression. We have had good results using serotonin reuptake inhibitors to treat offensive aggression in dogs and cats.

Beta Blockers In human medicine, beta blockers are often prescribed to reduce anxiety. Stress, anxiety, and high arousal predispose to aggressive incidents, in part by increasing adrenergic activity. Beta blockers, like propranolol and pindolol, have been shown to possess anti-aggressive properties in animal models of aggression and in human clinical patients. There has been some debate over whether the mechanism of action is peripheral or central and whether the serotoninergic actions of these drugs also plays a role in their anti-aggressive effect. Recent studies demonstrating the successful treatment of aggression with nadolol, a beta blocker which does not cross the blood brain barrier, tends to confirm a substantial peripheral effect. It is thought that the beta blockers exert their peripheral anti-aggressive effect indirectly by antagonizing adrenergic receptors on muscle spindles. Decreases in muscle tension result, reducing somatic afferent bombardment of the central nervous system and, consequently, the level of arousal. We have had clinical success with the use of propranolol and pindolol in the treatment of affective defense behavior (fear aggression) in dogs.

Anti-epileptic Drugs Anti-epileptic drugs have been used successfully to treat aggression in human patients with extreme mood swings.

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The mechanism is thought to be due to a nonspecific mood stabilizing effect of the anticonvulsant, because these drugs can control affective aggression in humans who do not have epilepsy. Clearly, if aggression is related to seizure activity, anticonvulsants are specifically indicated. Drugs which may be used include phenobarbital, phenytoin, carbamazepine, and valproic acid. Benzodiazepines, such as diazepam and clonazepam, may also be effective in the treatment of seizure-related aggression, though they may have to be administered frequently, (perhaps q 2-3 hr) unless a sustained acting formulation is used. Tolerance develops rapidly to the anti-epileptic effects of benzodiazepines which are thus only useful for short term treatment.

Benzodiazepines The use of benzodiazepines for their anxiolytic effect in the treatment of aggression is logical when stress and anxiety are involved. Unfortunately, the anti-aggressive effects of most benzodiazepines are achieved only at the expense of reductions in locomotor activity and social behavior. In addition, paradoxical excitement or a paradoxical increase in aggression may occur in some animals. If benzodiazepines are to be used in the treatment of aggression, alprazolam would be the most logical choice, because it has powerful anti-aggressive effects at doses well below the level which causes alterations in other behaviors.

Stimulants Hyperactivity (or hyperkinesis) and associated aggression has been described in dogs. This condition, like its human counterpart, responds to treatment with low doses of stimulants, such as methylphenidate and dextroamphetamine. Hyperkinesis in dogs, with or without aggression, is best confirmed before embarking on a prolonged course of treatment with stimulants. Confirmation is by means of challenge with a low dose dextroamphetamine or a short clinical trial. A positive result is paradoxical calming of the hyperkinetic patient with reductions in heart rate and respiratory rate.

Progestins Synthetic progesterone-like substances, such as medroxyprogesterone and megestrol, have been used to treat canine and feline aggression for years. Their anti-aggressive effect can be attributed to anti-androgenergic or feminizing properties but nonspecific central nervous system depression also plays a role, especially at higher dose rates. Low dose progestin therapy may well have a place in the control of aggression, but high doses of progestins are associated with unacceptable levels of sedation, impaired cognition, and unacceptable endocrine side effects, such as diabetes mellitus, adrenocortical suppression, and acromegaly. Mammary hyperplasia and mammary tumors are also possible sequelae, and pyometra may result in intact bitches and queens.

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ANXIETY, FEARS AND PHOBIAS Anxiety is a nebulous condition comprising components of uncertainty and fear. It may be acute (e.g. separation anxiety) or chronic. Chronic anxiety is characterized by hypervigilance, apparent insecurity, changes in appetite and/or sleeping pattern and, in some cases, urine and/or fecal marking behavior. Fears are more specific than anxiety and the cause is clearly identifiable. Animals may be fearful of living things (e.g. people or other animals), sensory stimuli (e.g. sounds, sights, odors and touch) and/or situations (e.g. travelling in the car, going to the veterinarians office). Phobias are extreme and apparently irrational fears. There is some blurring of the boundaries between anxiety, fears and phobias. In the following section on pharmacologic treatment these conditions will be dealt with together. It is important to remember that when dealing with fear-based conditions, behavior modification by desensitization, with or without counterconditioning, is central to any successful treatment. Drug treatment should be designed to complement systematic desensitization. Careful selection of the drug and its dosage is necessary in order to avoid impairment of learning and memory.

Neuroleptics Low potency neuroleptics like acepromazine traditionally have been used to treat fear-based conditions such as separation anxiety and thunderstorm phobia. Dosages which prevent the untoward response are usually accompanied by marked sedation and changes in awareness. High potency neuroleptics like fluphenazine and perphenazine are more logical choices if neuroleptics are to be used but the same caveats apply as discussed earlier.

Benzodiazapines These drugs are by far the most popular anxiolytic medications prescribed today. Diazepam has been used successfully to prevent anxiety-induced urine marking behavior in cats and benzodiazepines have been described as the drugs of choice for the treatment of fear-related behaviors. Some caution must be exercised if benzodiazapines are to be used to treat fear aggression as disinhibition can lead to a paradoxical escalation in the level of aggression in certain animals. Theoretically, benzodiazapines are an excellent choice for the management of separation anxiety. Two disadvantages of benzodiazapines are their amnesic effect and dependence-producing property. 90% of cats successfully treated for anxiety-based inappropriate urine marking behavior relapse following the discontinuation of therapy. The relapses may, at least in part, be attributable to a withdrawal syndrome. On another negative note, diazepam has been associated with fulminant hepatic failure in cats and clorazepate has caused a similar syndrome in dogs, so that it is advisable to monitor hepatic function during treatment. Phobias in humans do not respond well to benzodiazapine treatment, but there is anecdotal information suggesting efficacy in canine thunderstorm phobias.

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Azapirones

REPETITIVE BEHAVIOR PROBLEMS

Azapirones, like buspirone, theoretically are ideal for the treatment of anxiety- related conditions. In support of this, it was recently found that buspirone is the most effective pharmacologic agent for the prevention of anxiety-related inappropriate urine marking and spraying in cats. The only side effects reported were increased attention seeking in some cats, and occasional spats of aggression from previously low ranking cats directed at conspecifics in multi-cat households. The relapse rate of these cats following buspirone treatment for two months was around 50%, considerably better than with diazepam. We have used buspirone effectively for animate phobias (including fear-induced aggression) in dogs and cats, and have found it effective in smoothing the transition of semi-feral animals into a social environment. Separation anxiety in dogs should respond well to treatment with buspirone but our experiences with buspirone in the treatment of this condition has been somewhat disappointing.

Thunderstorm phobia can be palliated by treatment with buspirone, but not prevented absolutely. Buspironeâ&#x20AC;&#x2122;s onset of action is gradual and the full effects may not be seen for up to three or four weeks. Expense may be a factor when high doses of buspirone are administered to larger patients over long periods of time and this is a serious limitation to its application.

Stereotypies (now more appropriately called compulsive behaviors) are repetitive behaviors which appear pointless and mindless to the onlooker. They arise from frustration and chronic conflict and probably provide some relief from stress. Once incorporated into the animalâ&#x20AC;&#x2122;s behavioral repertoire, stereotypies will be performed even if the initiating stressors are eliminated, making these conditions refractory to behavior modification strategies. Conflict behaviors, including displacement behavior and re-directed behavior, may become ritualized into stereotypies when they occur outside the context in which they develop. One suggested mechanism for the development of stereotypies is that stress releases endorphins which in turn act on nigrostriatal dopaminergic neurons resulting in motor activity. The movements generated are circumstance and species specific, and tend to involve aspects of eating, grooming, predation, or locomotion. In addition, endorphins may stimulate pleasure centers in the brain leading to reinforcement of the behavior.

Serotonin has an inhibitory effect on dopaminergic pathways. Facilitation of serotonergic activity in the central nervous system should reduce the frequency of stereotypic behavior. Because of the similarity of certain grooming stereotypies to human obsessive compulsive disorders (OCD) some investigators have considered these stereotypies animal equivalents of human OCD. Human anti-obsessional drugs have proved effective in canine acral lick dermatitis and a growing number of other stereotypies.

Beta-Blockers Propranolol and pindolol have proved effective in a range of fear-based conditions including fear of people, fear-induced aggression, sound phobias, and separation anxiety. Side effects of treatment with beta blockers are minimal, although these drugs are contraindicated if unimpaired activity of the sympathetic nervous system is necessary to maintain vital organ function (e.g. in shock and bronchospastic disease). Pindolol, which is a mixed beta agonist antagonist, may cause urinary incontinence in some dogs by an agonist effect on the internal sphincter of the bladder.

Antidepressants Amitriptyline, a tricyclic antidepressant, has been used successfully to treat anxiety related urine marking behavior in cats, urine marking (leg lifting) in dogs and separation anxiety in cats and dogs. Amitriptyline blocks the reuptake of catecholamines and serotonin in the central nervous system, elevating and stabilizing mood. A calming effect is often observed in treated animals suggesting a greater contribution of the serotonin reuptake blocking action of the drug, in dogs at least. Logically, specific serotonin reuptake inhibitors should be more effective. The authors have successfully treated a small number of urine marking cats with clomipramine and early results of another series suggest that clomipramine is effective in the treatment of thunderstorm phobia in dogs.

Opioid Antagonists Pure opioid antagonists, such as naloxone, naltrexone, and nalmefene, have been used successfully to treat self directed behaviors, including acral lick dermatitis in dogs. Self-mutilation, which sometimes accompanies stereotypic behavior may respond to treatment with pure opioid antagonists.

Neuroleptics Stereotypic disorders can be facilitated by dopamine agonists and prevented by dopamine antagonists. Curiously, neuroleptics, whose primary action is to block dopamine, have not been used to any great extent in the treatment of animal stereotypies. This may be because low potency neuroleptics are associated with unacceptable sedation, and high potency neuroleptics have never really achieved popularity in veterinary medicine. There are reports of apparently successful treatment of flank biting horses with fluphenazine, but there is no information available about the use of high potency neuroleptics in treatment of stereotypic behaviors in small animals.

Anti-depressants Anti-depressants which preferentially enhance the action of serotonin by blocking its reuptake would be expected to be effective in the treatment of stereotypies. Clomipramine,

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a preferential serotonin reuptake inhibitor, has been found to be effective in the treatment of canine acral lick dermatitis.

We have reported the successful treatment with clomipramine of compulsive wool-sucking in cats and tail chasing in dogs.

Recently, compulsive pacing in a captive polar bear was shown to respond to treatment with an SSRI (fluoxetine).

Feather picking in birds responds to treatment with clomipramine or fluoxetine. It is anticipated that in the future other successful reports will appear regarding the use of specific serotonin reuptake inhibitors in the treatment of stereotypies.

Hyperactivity Overactive dogs are best dealt with by a combination of altered management and behavior modification therapy. Hyperactivity (or hyperkinesis) may have to be managed pharmacologically but the condition should be diagnosed properly before instituting treatment. Confirmed hyperactivity may be successfully treated with low doses of psychostimulants, such as dextroamphetamine or methylphenidate. In adult humans, the addition of a beta blocker (nadolol) to psychostimulant therapy increases the efficacy of the stimulant, but this treatment has still to be tried in animals.

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Eating disorders Eating disorders fall into two main categories: those in which the appetite is reduced or absent; and those in which the appetite is increased to an excessive level. Psychogenic anorexia, representing the former category, is sometimes seen in kenneled cats, and is a feature of separation anxiety in dogs. When anorexia is due to anxiety, benzodiazepines may stimulate the animal to eat. Hyporexia that results from chronic anxiety and/or depression may also respond to benzodiazepines, but prolonged treatment with anti-depressants may be more appropriate in this situation. The direct effect of anti-depressants is to decrease appetite, but when reduced food intake is associated with depression, a paradoxical increase in appetite may be observed.

Psychogenic polyphagia, which has been reported in dogs, is probably best treated by behavioral management.

Coprophagia in dogs and pica, commonly seen in Siamese cats may respond to ad lib feeding of dry food with a high fiber content. The use of appetite suppressants in the treatment of overeating, indiscriminate eating or pica has not, to our knowledge, been tried in animals.

CONCLUSION Depression This condition has not been well documented in veterinary practice but most behaviorists agree that it occurs. Depression is sometimes seen following the death of a person or animal to which the subject was closely bonded. It is manifested by a lack of interest in events which would previously have aroused the animalâ&#x20AC;&#x2122;s attention, inactivity, and a decreased appetite. In such cases, treatment with an antidepressant is a logical strategy. 2% of beagles in one breeding colony appeared to be depressed, as evidenced by a withdrawn attitude, low levels of motor activity, little exploratory activity, decreased appetite and decreased sexual activity.

These dogs responded to treatment with anti-depressants and a benzodiazapine, but not to a neuroleptic or beta blocker.

A plethora of new drugs are available for the treatment of behavioral problems. To understand how a particular drug might help in dealing with a veterinary behavior problem, it is necessary to know how the drug exerts its effect and any reported side effects or adverse reactions. From this information, it is possible to project any likely beneficial effects versus risks of a particular treatment. These kind of projections can be corroborated by reference to published clinical case reports or case series. Subsequently, a logical treatment plan can be deduced. In general, new drugs represent improvements over existing drugs, and the current trend is for more specific agents with fewer side effects and fewer adverse reactions. With this in mind, we can be optimistic about the future of veterinary behavioral pharmacology in the years to come.

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Novità diagnostiche in dermatologia veterinaria Fabrizio Fabbrini Med. Vet., Dipl. CES Dermatologia - Libero Professionista - Milano

Riassunto Nell’ambito delle nuove metodiche diagnostiche, l’uso della PCR (Polymerase Chain Reaction) è da considerarsi tra le più importanti e rivoluzionarie. Applicata inizialmente nella ricerca (es. per clonare i geni deputati alla produzione delle IgE, nell’ambito di studi sulla immunopatogenesi dell’Atopia canina), attualmente è utilizzata per “amplificare”, rendendo velocemente identificabile, sequenze di DNA o di RNA-m di virus, batteri, funghi o protozoi presenti in svariati campioni biologici (tessuti organici, sangue, midollo osseo) rendendo la diagnosi delle malattie correlate, veloce (1-2 giorni) e sicura (la sensibilità e la specificità in alcuni casi raggiungono il 100%). L’uso di questa metodica per ora è limitato a pochi laboratori veterinari e centri di ricerca universitari ma probabilmente presto sarà di larga diffusione dato che esistono ditte come la Synbiotics Corporation (USA) che ne commercializzano i kit.

La PCR è stata impiegata con successo in medicina per identificare Leishmania spp, Borrelia burgdorferi, M. Tuberculosis, M. bovis, M. genavense, Nocardia spp, Microsporum gypseum, Microsporum nanum, Microsporum canis, Tricophyton mentagrophytes, C. albicans, Cryptococcus neoformans, Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum.

Nell’ambito della diagnosi delle dermatofitosi, è stato allestito un nuovo metodo per aumentare la sensibilità dell’esame microscopico del pelo. Si tratta di utilizzare, assieme a KOH al 20%, coloranti particolari (Calcafluor white F6239 e Evans blue E2129 della Sigma Chemical) capaci di legarsi in maniera specifica alla componente polissaccaridica della parete fungina rendendola facilmente evidenziabile quando esaminata con un microscopio a luce fluorescente.

Altre novità diagnostiche, riguardano l’uso di test ELISA (Heska ) per la diagnosi della rogna sarcoptica nel cane (sensibilità del 92% e specificità del 96%), l’uso di nuove diete commerciali (HA-Formula CNM Purina ed Exclude DVM Pharmaceuticals) per la diagnosi delle allergie alimentari, preparate con proteine modificate (NURISH1500) o a basso peso molecolare, teoricamente non immunogene (proteine idrolizzate), capaci d’indurre la remissione dei sintomi in 4 settimane.

Nella diagnostica dell’atopia del cane sono stati rivisti e modificati da Prélaud i “criteri diagnostici clinici” di Willemse ed è stato introdotto un test ELISA di nuova concezione (Allercept Heska) che, valutato in parallelo agli skintest, ha dimostrato sensibilità del 90% e specificità del 86% (non presenta falsi positivi in quanto capace di rilevare solo le IgE presenti nel campione).

L’augurio di ogni Clinico, da quando esiste la Medicina moderna, è di avere a disposizione esami di laboratorio capaci di rilevare, sin dal suo esordio e senza possibilità d’errore, la presenza di un processo patologico in atto. In realtà non esistono a tutt’oggi metodiche diagnostiche “infallibili”, piuttosto, si è consapevoli dei loro limiti (possibilità di esiti falsamente negativi o falsamente positivi, valore predittivo mediocre) e della necessità che ogni dato di laboratorio sia interpretato “alla luce della clinica”. Per tale motivo il Veterinario talvolta è obbligato a ripetere o ad eseguire più test in tempi successivi, prima di riuscire a documentare la presenza di una malattia sospetta, a scapito della compliance con il proprietario e del buon esito della terapia.

Nell’ambito delle nuove metodiche diagnostiche, l’uso della PCR (Polymerase Chain Reaction) è da considerarsi tra le più importanti e rivoluzionarie. Applicata inizialmente

nella ricerca (es. per clonare i geni deputati alla produzione delle IgE, nell’ambito di studi sulla immunopatogenesi dell’Atopia canina), attualmente è utilizzata per “amplificare”, rendendo velocemente identificabile, sequenze di DNA o di RNA-m di virus, batteri, funghi o protozoi presenti in svariati campioni biologici (tessuti organici, sangue, midollo osseo) rendendo la diagnosi delle malattie correlate, veloce (1-2 giorni) e sicura (la sensibilità e la specificità in alcuni casi raggiungono il 100%). L’uso di questa metodica per ora è limitato a pochi laboratori veterinari e centri di ricerca universitari ma probabilmente presto sarà di larga diffusione dato che esistono ditte come la Synbiotics Corporation (USA) che ne commercializzano i kit.

La PCR è stata impiegata con successo in medicina per identificare Leishmania spp, Borrelia burgdorferi, M. Tuberculosis, M. bovis, M. genavense, Nocardia spp, Microsporum

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gypseum, Microsporum nanum, Microsporum canis, Tricophyton mentagrophytes, C. albicans, Cryptococcus neoformans, Blastomyces dermatitidis, Coccidioides immitis, Histoplasma capsulatum.

Nell’ambito della diagnosi delle dermatofitosi, è stato allestito un nuovo metodo per aumentare la sensibilità dell’esame microscopico del pelo. Si tratta di utilizzare, assieme a KOH al 20%, coloranti particolari (Calcafluor white F6239 e Evans blue E2129 della Sigma Chemical) capaci di legarsi in maniera specifica alla componente polissaccaridica della parete fungina rendendola facilmente evidenziabile quando esaminata con un microscopio a luce fluorescente.

Altre novità diagnostiche, riguardano l’uso di test ELISA (Heska ) per la diagnosi della rogna sarcoptica nel cane (sensibilità del 92% e specificità del 96%), l’uso di nuove diete commerciali (HA-Formula CNM Purina ed Exclude DVM Pharmaceuticals) per la diagnosi delle allergie alimentari, preparate con proteine modificate (NURISH1500) o a basso peso molecolare, teoricamente non immunogene (proteine idrolizzate), capaci d’indurre la remissione dei sintomi in 4 settimane.

Nella diagnostica dell’atopia del cane sono stati rivisti e modificati da Prélaud i “criteri diagnostici clinici” di Willemse ed è stato introdotto un test ELISA di nuova concezione (Allercept Heska) che, valutato in parallelo agli skin-test, ha dimostrato sensibilità del 90% e specificità del 86% (non presenta falsi positivi in quanto capace di rilevare solo le IgE presenti nel campione).

Riferimenti bibliografici 1.

2.

Ashford DA, Bozza M, Freire M, Miranda JC, Sherlock I, Eulalio C, Lopes U, Fernandes O, Degrave W, Barker RH Jr, Badaro R, David JR, (1995), Comparison of the polymerase chain reaction and serology for detection of canine visceral leishmaniasis. Am J Trop Med Hyg, 53: 251-255.

Aranaz A, Liébana E, Pickering X, Novoa C, Mateos A, Domìnguez L, (1996), Use of polymerase chain reaction in the diagnosis of tuberculosis in cats and dogs. Vet Rec, 138: 12, 276-280.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

Bevier DE, Mondesire RL, et al., (1997), Fc_R1_-based ELISA technology for in vitro determination of allergen-specific IgE in a population of intradermal skin-tested normal and atopic dogs. Supplement Compend Contin Educ Pract Vet 19: 11, 10-16.

Böddinghaus B, Rogall T, Flohr T, Blöcker H, Böttger E C, (1990), Detection and identification of mycobacteria by amplification of rRNA . J Clinic Microbiol, 28: 1751-1759.

Bornstein S, Thebo P, Zakrisson G, (1996), Evaluation of an enzymelinked immunosorbent assay (ELISA) for the diagnosis of canine sarcoptic mange. Vet Derm, 7: 21-28.

Eisenstein BI, (1990), The polymerase chain reaction. A new method of using molecular genetics for medical diagnosis. New England J Med, 322: 178-183.

Groh M, Moser E, (1998), Diagnosis of food allergy in the non-seasonally symptomatic dog using a novel antigen, low molecular weight diet: a prospective study of 29 cases. Vet Aller Clinic Immunology, 6: 5-6.

Howell SA, Barnard RJM, Humphreys F, (1999), Application of molecular typing methods to dermatophyte species that cause skin and nail infection. J Med Microbiol, 48: 33-40.

Mayer J, Kovarika A, Vorlicek J, et al.,(1998), Efficacy of polymerase chain reaction for detection of deep mycotic infections: confirmation by autopsy. Mycoses, 41: 471-475.

Prélaud P, (1998), Diagnostic de la dermatite atopique canine: un diagnostic clinique. Prat Méd Chir Anim Comp 33: 331-342 .

Prélaud P, Guaguere E, (1998), Réévaluation des critères de diagnostic de la dermatite atopique. Revue Medecine Veterinaire 149: 11, 1057-1064.

Roura X, Sànchez A, Ferrer L, (1999), Diagnosis of canine leishmaniasis by a polymerase chain reaction technique. Vet Rec, 144: 262-264.

Roura X, Fondevilla D, Sànchez A, Ferrer L, (1999), Detection of Leishmania infection in paraffin-embedded skin biopsies of dogs using polymerase chain reaction. J Vet Diag investigation, 11: 385-387.

Sparkes A H, Werrett G, Stokes C R, Gruffydd-Jones T J, (1994), Improved sensitivity in the diagnosis of dermathophytosis by fluorescence microscopy with calcafluor white. Vet Rec, 134: 307-308.

Trevisan G, stinco G, Cinco M, (1997), Neonatal skin lesions due to a spirochetal infection: a case of congenital Lyme borreliosis. International Journal of Dermatology 36: 9, 677-680.

Wasson DL, Grieve RB, (1998), In vitro measurement of canine and feline IgE: a review of Fc_R1_-based assays for detection of allergen-reactive IgE. Vet Derm 9: 173-178.

Wilson RW, Steingrube VA, Brown BA, Wallace RJ Jr, (1998), Clinical application of PCR-restriction enzyme pattern analysis for rapid identification of aerobic actinomycete isolates. J Clinic Microb 36: 148-152.

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Risultati preliminari sull’uso di autovaccini nella piodermite ricorrente del cane Fabrizio Fabbrini Med. Vet., Dipl. CES Dermatologia - Libero Professionista - Milano

Le piodermiti recidivanti rappresentano un problema spesso frustrante a causa delle difficoltà incontrate nell’identificare malattie primarie sottostanti, o nel convincere i proprietari ad eseguire iter diagnostici e trial terapeutici adeguati. Esse sono trattate con la somministrazione ciclica d’antibiotici, ma come risultato si ha spesso miglioramento transitorio seguito da recidive di pari o maggiore gravità.

In letteratura sono segnalate diverse metodiche immunoterapiche, come aiuto collaterale nel trattamento delle piodermiti ricorrenti, tra queste, l’uso di autovaccini.

L’autovaccino è allestito con microrganismi isolati dal paziente nel quale sarà successivamente reinoculato; il principio sul quale si basa, è quello di indurre una risposta immunitaria, specifica e attiva, nei confronti del microrganismo stesso.

L’immunoterapia è utilizzata per prevenire ricadute una volta che la patologia iniziale è stata risolta da antibiotici.

In un precedente lavoro eseguito presso l’istituto di Microbiologia della Facoltà di Medicina Veterinaria dell’Università di Milano, è stata valutata, in via preliminare, l’efficacia a lungo termine (1 anno) di un trattamento con autovaccini, in cani affetti da piodermite e somministrati secondo un protocollo comune (inoculati per via I.M a giorni alterni e a dosi crescenti per sette dosi, seguiti da un ottavo inoculo di richiamo a distanza di 15 giorni). Si trattava di sedici cani di razza, sesso ed età diversi, con problemi di piodermite cronica (dodici presentavano una piodermite profonda e quattro una piodermite superficiale).

Nel 43,75% dei casi esaminati si è avuta una guarigione completa, 18,75% si è assistito a un miglioramento e nel rimanente 37,5%, si sono manifestate recidive di pari gravità.

Nel successivo lavoro, è stata valutata l’efficacia degli autovaccini somministrati a 13 cani con problemi di piodermiti ricorrenti (10 profonde e 3 superficiali), secondo posologia e via di somministrazione diverse. La razza prevalente era il Pastore Tedesco 7/13, il sesso quello maschile 11/13 mentre l’età media era di 7 anni.

Ogni cane è stato sottoposto a visita dermatologica, per valutare la presenza di malattie primarie sottostanti, la gravità e la distribuzione topografica del prurito e delle lesioni e la percentuale di superficie corporea interessata. Sono stati eseguiti 5 controlli clinici a 3-6-10-16 e 21 settimane di distanza dalla prima visita.

L’autovaccino è stato somministrato per via sottocutanea alla dose di 0,5 cc ai cani con un peso < 12 kg e alla dose di 1 cc ai cani con un peso > 12 kg. La terapia è durata 17 settimane e ha previsto la somministrazione di 13 dosi: le prime 5 sono state eseguite a giorni alterni quindi, sono state eseguite 3 dosi a distanza di 1 settimana l’una dall’altra; quindi 4 distanziate di 2 settimane ed infine, è stata eseguita un’ultima dose a 4 settimane dalla precedente. Durante il trattamento, tutti i soggetti sono stati sottoposti a terapia antibiotica per almeno 1 settimana (in caso di piodermite superficiale) o 2 settimane (in caso di piodermite profonda) oltre la risoluzione clinica della piodermite.

Nei vari controlli sono stati valutati gli stessi parametri iniziali ed è stata data una valutazione complessiva alle lesioni (punteggio da 0 a +++).

L’efficacia dell’autovaccino è stata determinata considerando l’evoluzione clinica della malattia. Sono state considerate le condizioni iniziali e finali valutando la gravità della piodermite, delle lesioni e del prurito, percentuale di superficie corporea interessata e tempo intercorso tra la sospensione della terapia antibiotica e l’eventuale comparsa di una recidiva. I risultati ottenuti possono essere così schematizzati: GUARIGIONE, la piodermite è guarita e non ci sono state recidive; MIGLIORAMENTO, la piodermite è di minor gravità (più superficiale, lesioni diminuite e limitate come estensione corporea) e/o la recidiva avviene in tempi più lunghi rispetto ai dati precedenti; ASSENZA DI MIGLIORAMENTO, la recidiva si è manifestata con le stesse caratteristiche cliniche iniziali e/o in tempo più breve.

Dei 13 casi considerati, 10 sono stati completati. Al 5° controllo 4 sono guariti e 6 migliorati, raggiungendo una guarigione apparente nei controlli intermedi e, manifestando solo tardivamente una recidiva di minor gravità rispetto alla forma iniziale (inoltre interessando una superficie corporea inferiore). Il tempo intercorso tra la sospensione dell’antibioticoterapia e la recidiva risultava aumentato rispetto al tempo medio rilevato in precedenza negli stessi soggetti.

In conclusione, il trattamento con autovaccini sembra rappresentare un valido ausilio terapeutico da affiancare alla terapia antibiotica in soggetti con piodermite ricorrente.

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Riferimenti bibliografici 1.

2.

3.

Agut M, Bayò M, et all.(1996), Autovacination: a study of fifteen cases in dog, Biomedical Letters 53: 185-189.

Curtis CF, Lamport AI, and Lloyd DH, (1999), Blinded, controlled study to investigate the efficacy of a staphylococcal autogenous bacterin for the control of canine idiophatic recurrent pyoderma, Proceedings 16th ESVD Meeting Helsinki.

DeBoer DJ, Moriello KA, (1990), Evaluation of a commercial staphylococcal bacterin for management of idiopathic recurrent superficial pyoderma in dogs, Am J Vet Res 51: 636-639.

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The essential fatty acids: ten years latter Acidi grassi essenziali: dieci anni dopo

Jacques Fontaine DMV, Dip ECVD - Bruxelles - Belgium

At the end of the eighties, several papers were published attesting the effects of the essential fatty acids (EFA) in the management of the atopic dermatitis. They were often only clinical reports without placebo controlled and standardized diet. Nevertheless, sometimes this treatment was very effective. So a lot of companies have developed EFA complements or have added EFA in diets.

During the last 10 years a lot of papers were written on this topic, not only in the field of dermatology but also for the management of cancer, cardio-vascular diseases, arthritis…

Despite of the abundant litterature, several questions remain: What is the best source of EFA? In the opinion of the author, for the management (as an adjuvant to other treatments) of the atopic dermatitis (with the words “atopic dermatitis” we exclude the food intolerance) an EFA complement is probably the best way because of: • good control of the amount of EFA; • better control of the source: ratio ω6 /ω3 controlled, choice of an ω6 enriched in GLA, complement well protected against the oxidation.

What is the best ω6/ω3 ratio? The optimum ω6/ω3 ratio between 5:1-10:1 was proposed by Vaughn et al in Vet Derm in 1994. But recently, Hwang et al in 1997 showed that the absolute amounts of ω3 is more important that the ratio.

What is the dosage needed? In men, the therapeutic effect of EFA complement is observed with doses 70-160 higher than those used in the dog! High doses of EFA do not promote the synthesis of pro-inflammatory substances. ω6 are the source of arachidonic acid (ARA, often consider as a pro-inflammatory fatty acid). Complementation with ω6 induces only mild increase of ARA. But some problems can arise due to a large amount of ω3. Actually, affinity of the δ-desaturases are more important for the ω3 than the ω6. So increase of ω3 intakes can push the pathways to the ω3 derivates. LA cannot be used.

Direct complementation with GLA avoids the limiting step of the δ-6 desaturase.

A other aspect of the EFA complementation is the cosmetic effect: 1) for reducing hair shedding; 2) to improve the coat quality.

Biochemistry of the EFA:

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Theory on the anti-inflammatory effects of EFA ω6 and ω3

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GDV, corpi estranei, torsione della milza, volvolo intestinale: diverse facce della stessa medaglia Luca Formaggini Med. Vet. - Libero Professionista - Dormelletto (NO)

Gabriel Lozano Osun˜ a Med. Vet. - Roma

Riassunto Vengono segnalati e discussi alcuni casi clinici in cui la GDV (Gastric Dilatation-Volvolus) ne rappresenta il denominatore comune. Gli eventi patologici segnalati precedentemente, in concomitanza o successivi ad un episodio acuto di GDV sono: corpi estranei gastrici, splenectomia per torsione della milza, volvolo intestinale.

GDV E CORPI ESTRANEI GASTRICI

Caso n° 4

Caso n° 1

Segnalamento: Meticcio, 15 anni, maschio intero Riscontri clinici: distensione addominale, dolore, dopo diverse ore di tentativi di vomito non produttivo Riscontri radiografici: stomaco ruotato Tipo di corpo estraneo: mutandine

Segnalamento: Pastore Tedesco, 11 anni, maschio intero Riscontri clinici: vomito non produttivo, addome disteso, paresi posteriore Riscontri radiografici: stomaco ruotato contenente diverso materiale radio-opaco Tipo di corpo estraneo: pezzi di osso

Caso n° 2 Segnalamento: Doberman, 9 anni, femmina intera Riscontri clinici: distensione addominale dopo il pasto Riscontri radiografici: stomaco ruotato contenente materiale a densità disomogenea Tipo di corpo estraneo: “palle” di erba

Caso n° 3 Segnalamento: Pastore Tedesco, 5 anni, maschio intero Riscontri clinici: distensione addominale dopo diverse ore di tentativi di vomito Riscontri radiografici: stomaco ruotato contenente materiale radio-opaco Tipo di corpo estraneo: sasso

DISCUSSIONE Qualsiasi veterinario che operi nel settore dei piccoli animali ricorderà almeno un caso di GDV associata alla presenza di corpi estranei gastrici, ma nonostante esista una prolifica letterarura sulle diverse ipotesi ezio-patogenetiche e sui fattori predisponenti, nella casistica internazionale non è presente alcun lavoro che metta in relazione GDV e corpi estranei gastrici.

Parte dei molteplici fattori descritti da numerosi autori come predisponenti alla GDV erano presenti nei casi presentati (conformazione del torace, razze grossa taglia, voracità, un solo pasto al giorno) e proprio per questo motivo non si pretende di ipotizzare una correlazione diretta tra GDV e corpi estranei, ma è possibile che questi ultimi si comportino come fattore precipitante in soggetti già di per se predisposti. Il possibile meccanismo patogenetico è rappresentato dall’aerofagia durante i tentativi di espellere il corpo estraneo con il vomito. Altre situazioni peraltro già descritte in letteratura potrebbero essere presenti come conseguen-

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za del corpo estraneo gastrico: ipergastrinemia (via gastrite), alterata motilità e funzione dello stomaco e dell’esofago, stress per il dolore. Ma, visto la tuttaltro che costante presenza di associazione GDV-corpi estranei gastrici, la dinamica dello sviluppo della torsione dello stomaco in questi casi risulta assolutamente difficile da stabilire.

La rilevanza clinica di queste segnalazioni è rappresentata nel fatto che la laparatomia in caso di GDV o di corpi estranei gastrici deve essere effettuata il più precocemente possibile; inoltre dal momento che nel caso numero quattro il corpo estraneo è stato rimosso attraverso la sonda oro-gastrica al momento della decompressione risulta efficace l’utilizzo di diametri delle sonde il più elevati possibile.

GDV E SPLENECTOMIA

dentemente alla torsione della milza; in questo caso si rafforza l’ipotesi che entrambe le patologie possano avere alla base una patogenesi comune, ma il “come e perchè” rimane per ora difficile da interpretare.

Alla luce anche delle precedenti segnalazioni, risulta opportuno effettuare regolarmente la gastropessi (in questo caso preventiva) nel caso in cui si dovesse ricorrere ad una splenectomia per torsione dell’organo sul proprio peduncolo. A questo proposito si ricorda che la gastropessi circumcostale non modifica in modo significativo le caratteristiche della motilità e del tempo di svuotamento gastrico su un organo che non ha ancora sofferto di un episodio acuto di GDV. Di conseguenza, il chirurgo esperto potrebbe prolungare l’intervento di splenectomia (se le condizioni del paziente lo permettono) ed effettuare la fissazione dell’antro pilorico alla parete addominale destra.

Caso n° 1 GDV E VOLVOLO INTESTINALE Segnalamento: Bobtail, 9 anni, femmina sterilizzata Prima presentazione: torsione della milza e splenectomia GDV dopo 3 mesi

Caso n° 2 Segnalamento: Pastore Tedesco, 7 anni, maschio intero Prima presentazione: torsione della milza e splenectomia GDV dopo 6 mesi

DISCUSSIONE I due casi sopra riportati, descrivono episodi di GDV in seguito ad interventi di splenectomia effettuati a causa della torsione dell’organo sul proprio peduncolo. In letteratura sono già stati descritti altri casi analoghi a quelli sopra riportati, ma risulta ancora difficile inquadrare le due patologie in un binomio “causa-effetto”. Anche se dal punto di vista epidemiologico la torsione isolata della milza è un evento meno comune rispetto alla GDV, entrambe le condizioni patologiche sono riscontrabili in cani di razza grande-gigante.

Questa analogia, unita alle evidenti correlazioni anatomiche tra i due organi indirizza le ipotesi patogenetiche verso una origine comune delle due patologie.

Nel caso in cui la GDV sia stata successiva alla splenectomia, si potrebbe supporre che la torsione della milza non sia stato un evento isolato, ma la conseguenza di ripetuti episodi di malposizionamento dello stomaco (torsione gastrica “cronica”). È stato dimostrato che in corso di torsione gastrica la milza assume un ruolo assolutamente passivo e viene solamente “trascinata” dalla rotazione dello stomaco: questo potrebbe spiegare la torsione splenica. Inoltre, dal momento che è stato anche dimostrato che la sola splenectomia in corso di torsione gastrica non è in grado di prevenire le recidive, ecco che i pazienti hanno continuato il loro processo patologico (anche se splenectomizzati) fino all’episodio acuto di GDV. La correlazione tra le due patologie è evidentemente presente anche nei casi in cui la GDV si sia verificata prece-

Caso n° 1 Segnalamento: Setter inglese, 6 anni, maschio intero Prima presentazione: GDV e gastropessi circumcostale modificata Volvolo intestinale 8 mesi dopo

Caso n° 2 Segnalamento: Alano, 3 anni, maschio intero Prima presentazione: GDV e gastropessi circumcostale modificata Volvolo intestinale 3 mesi dopo

Caso n° 3 Segnalamento: Pastore tedesco, 5 anni, maschio intero Prima presentazione: GDV e gastropessi circumcostale modificata Volvolo intestinale 1 anno dopo

DISCUSSIONE In tutti i casi descritti i pazienti avevano manifestato singoli episodi acuti di torsione gastrica, rispettivamente 8 mesi, 3 mesi e 1 anno prima. La GDV era stata risolta e i soggetti condussero una qualità di vita normale.

Da un lato ci troviamo di fronte alla GDV, una sindrome ad eziologia ancora incerta ma che trova nelle disfunzioni della motilità gastrica ed eofagea le teorie da più Autori invocate come possibili cause; dall’altro, il volvolo intestinale, entità patologica che porta al manifestarsi di sintomi e sequelae sovrapponobili alla GDV e che, come la precedente colpisce di regola cani di grossa taglia e non identifica nessun preciso fattore eziologico. Nell’ambito della Letteratura internazionale, la maggior parte delle segnalazioni riguardano casi di volvolo intestinale in soggetti sani, la cui anam-

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nesi non riporta notizie di precedenti disturbi gastrointestinali. Altre segnalazioni invece riportano la patologia come correlata a trattamenti per parassiti intestinali, enterite linfoplasmacitaria, carcinoma ileo-colico, insufficienza pancreatica del Pastore Tedesco. Un recente studio retrospettivo su sei casi di volvolo intestinale ha inoltre identificato in ogni paziente un antecedente disturbo gastrointestinale: 3 di questi soggetti avevano manifestato un episodio di torsione gastrica. È interessante notare come un altro lavoro riporta 23 casi di torsione gastrica in cui era concomitante la presenza di patologie infiammatorie intestinali (inflammatory bowel disease). È stato quindi riscontrato almeno un denominatore comune tra le due patologie.

Anche sulla base dei dati riportati in questi ultimi lavori è lecito concludere che sia il volvolo intestinale che la torsione gastrica sono situazioni che si possono verificare come conseguenza di altre patologie che alterano la motilità gastrointestinale e, nei casi clinici sopra descritti, la malattia precedentemente manifestata dai pazienti con volvolo intestinale era rappresentata dalla GDV. Dal punto di vista terapeutico e prognostico, la sindrome della dilatazione-torsione gastrica del cane è indubbiamente affrontabile con maggior sicurezza rispetto al volvolo intestinale e, proprio per le scarse possibilità terapeutiche, cercare di prevenire o di prevedere quest’ultima, risulta di fondamentale importanza al fine della sopravvivenza del paziente. Come citato in precedenza un possibile denominatore comune tra le due sindromi potrebbe essere quell’insieme di patologie intestinali che vengono raggruppate sotto il nome di Inflammmatory Bowel Disease; è importante quindi diagnosticare nel momento in cui un soggetto venisse presentato alla visita per dilatazione-torsione gastrica acuta o ricorrente, la presenza o meno di una concomitante patologia infiammatoria intestinale al fine di impostare una corretta terapia nei confronti di quest’ultima.

Questa presentazione di tre semplici casi clinici potrebbe essere il primo passo di una indagine più approfondita nei confronti delle procedure preventive da mettere in atto nei confronti del manifestarsi del volvolo intestinale nei soggetti che hanno manifestato e superato in precedenza un episodio di dilatazione-torsione gastrica.

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Letture consigliate EPIDEMIOLOGY PROGRAM RESEARCH TEAM: “Clues to Bloat Prevention Emerging from Case-Control Study”. Bloat Notes: News from the Canine Gastric Dilatation-Volvulus Research Program; Aprile 1996; School of Veterinary Medicine, Purdue University.

LAWRENCE T. GLICKMAN et al.: Analysis of risk factors for gastric dilatation and dilatation-volvulus in dogs. JAVMA 204: 9, p 1465 DARRYL L. MILLIS et al.: Gastric dilatation-volvulus after splenic torsion in two dogs. JAVMA 207: 3, p 314. 1995 P.J. NEATH et al.: Retrospective analiysis of 19 cases of isolated torsion of the splenic pedicle in dogs. JSAP 38, p 387. 1997 R.L. STICKLE: Radiographic signs of isolated splenic torsion in dogs: Eight cases (1980-1987). JAVMA, 194, 1, , p 103 1989 JOHN T. HATHCOCK: Radiographic View of Choice for the Diagnosis of Gastric Volvulus: The Right Lateral Recumbent View. JAAHA, 20, 1984 pp 967-969.

STEVEN M. FOX: Crisis Management: Dealing with the gastric dilatationvolvulus syndrome. Vet Medicine, Jan. 1987, pp 36-50.

JACQUELINE R. DAVIDSON: Acute gastric dilatation-volvulus in dogs: Surgical treatments. Vet. Medicine, Feb. 1992, pp 118-126 J. A. HALL et al.: Gastric emptying of nondigestible radiopaque markers after circumcostal gastropexy in clinically normal dogs and dogs with gastric dilatation-volvulus. Am J Vet Res, 53: 10, 1992 pp 1961-1965.

J.A. HALL et al.: Effect of circumcostal gastropexy on gastric myoelettric and motor activity in dogs. JSAP 38, 200-207 1997 SLATTER DH: Textbook of small animal surgery. 1st ed. Philadelphia: WB Saunders, 1985: 751.

STAMPLEY AR et al.: Gastric myoelettrical activity after experimental gastric dilatation-volvolus and tube gastrostomy in dogs. Vet Surg 1992; 21: 10-4 Van SLUIJS, FJ & WOLVEKAMP, WTC: Abnormal oesophageal motility in dogs with recurrent gastric dilatation-volvolus. Vet Surg 1993; 22: A250 JEAN A. NEMZEK et al.: Mesenteric Volvulus in the Dog: A Retrospective Study. JAAHA, 29, 1993 pp 357-362.

BRAUN, L et al: Gastric dilatation-volvolus in the dog with histological evidence of preexisting inflammatory bowel disease: a retrospective study of 23 cases. JAAHA, 32; 287 1996

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Blueprint for Transformational Change in the Practice of Veterinary Medicine Progetto per una nuova professione veterinaria

Steve D. Garner DVM, Dipl AVBP - Safari Animal Care Centers - League City, Texas, USA

Riassunto In questa relazione verrà illustrato il “modello operativo” per l’esercizio della professione veterinaria. La medicina veterinaria consiste nel trattare le malattie, eseguire gli interventi chirurgici e salvare delle vite, ma l’esercizio della professione comprende anche il servizio alla clientela, la motivazione dello staff e la gestione dell’impresa. Il successo o il fallimento di un “modello operativo” dipende dalla sua capacità di fornire in modo efficiente i servizi ai quali viene attribuito un valore (cure mediche), mantenendo al tempo stesso una struttura di gestione di impresa che consenta di sostenere tali servizi.

Il modello tradizionale delle strutture veterinarie private è inefficiente, può essere causa di notevoli attriti e richiede che il veterinario svolga molteplici funzioni che esulano dalla sua preparazione professionale specifica. Affrontando queste inefficienze, risulta evidente che è necessario sviluppare un nuovo modello di fornitura di cure mediche per assicurare il successo economico della professione.

La relazione esamina le differenze esistenti fra il cambiamento per incremento di un sistema esistente (che è il messaggio della maggior parte dei consulenti di gestione di impresa) e quello per trasformazione, che porta ad un nuovo modello di offerta di servizi veterinari. Il cambiamento per trasformazione è giustificato solo quando il nuovo modello può raggiungere livelli di efficienza che risulteranno di diversi ordini di grandezza al di sopra della norma. Ciò è dovuto al fatto che questo tipo di cambiamento modifica in modo fondamentale il modo in cui viene considerato ed offerto l’esercizio della medicina veterinaria.

Il Dr. Garner illustrerà i benefici ed i concetti basilari di un nuovo modello di professione veterinaria che incorpora concetti utilizzabili in ogni situazione, sia nelle strutture di piccole dimensioni che in quelle più grandi. Questo modello è potenzialmente in grado di trasformare l’intera industria veterinaria generando forti incentivi per il futuro sviluppo della professione.

This lecture examines the “operational model” for delivery of veterinary medicine. Veterinary medicine is about treating illnesses, performing surgeries, and saving lives but veterinary practice is also about serving customers, motivating staff, and running a business. Success or failure of an “operational model” is determined by its ability to efficiently perform the valued service (medical care) while maintaining an operational business structure that supports that service.

The traditional model for private veterinary practice delivery is inefficient and highly frictional, requiring the veterinarian to participate in many functions that are outside his or her medical training. By addressing these inefficiencies it becomes obvious that a new model for veterinary medical care delivery is in order to ensure the economic success of the profession.

This lecture examines the difference between incremental change of an existing system (which is the message of most practice management consultants) and transformational change to a new model of veterinary care delivery. Transformational change is only warranted when the new model can provide efficiencies that are orders of magnitude above the norm. This is because transformational change fundamentally changes the way that the practice of veterinary medicine is approached and delivered.

Dr. Garner will show the benefits and underlying concepts of a new model of veterinary practice that embodies concepts that can be used in any practice situation large to small. This practice model has the potential of transforming the entire veterinary industry creating strong incentives for the future growth of the profession.

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Veterinary practice today is undergoing tremendous change and development. Corporate interests both within the profession as well as outside the profession are targeting it for consolidation. As private practitioners, we will be competing with these corporate practices for not only our clients but also for our lay staff and associate veterinarians. It will be very difficult for private veterinary practice to match the benefit packages and compensation plans that can be offered by corporate America. To compete in this environment requires a change in the current model for veterinary practice.

There are two types of change. One type is “incremental change”. This change nudges your practice procedures into alignment with the currently accepted “Standard of Excel-

lence” practices. Using this type of process over time you may eventually reach or possibly exceed these standards set by the profession. The other type of change is “transformational change”. This change radically changes the way that you look at veterinary practice. This type of change comes about by setting new “standards of excellence” orders of magnitude above the norm and fundamentally changing operations to achieve these standards. The current economic environment of veterinary practice dictates “transformational change” to compete and thrive in the future.

Within these new “standards of excellence” it is possible for a practice to perform at atypical levels of growth and production.

Active Clients Per Veterinarian

Gross Sales Per Veterinarian Per Year

These charts represent national averages as published in the most recent AVMA study as well as information provided about the Veterinary Economics® “Practices of Excellence” (P of E) as compared to Safari Animal Care Centerssm.

The average veterinary practice serves between 800 and 1200 active clients per veterinarian. This number of clients served seems to reach a steady state after the initial rapid growth. The typical veterinary practice will continue to grow in active clients at the rate of about 10% per year.

This equates to about 10 new clients per veterinarian per month. The average new practice grows at the rate of about 60 new clients per veterinarian per month but then slows when the number of active clients reaches about 800. I do not feel that the demographics of the veterinary practice area dictate the rate of growth or the total number of active clients. I believe this is determined almost solely by the level of customer service a veterinary clinic can deliver.

Veterinary clients and pets require a certain minimum contact time to handle the entire transaction. If this contact time is primarily with the veterinarian then there becomes a

diminishing number of free contact minutes per day for that veterinarian to serve new customers. A trade-off occurs with either new clients or the existing clients and growth slows.

Therefore, the capacity for service will determine the rate of hospital growth and ultimately the total number of active clients per veterinarian. Increasing the number of active clients per veterinarian is the key to transformational growth of a veterinary practice.

The key to increasing the number of active clients per veterinarian is to empower the staff to handle a portion of the customer contact time. This can only come about by creating a culture of change and setting high standards that guide that change in the right direction.

Standards are the cornerstone and foundation upon which we build the transformed veterinary practice that can compete in the future.

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FIVE STEPS TO SUCCESSFUL TRANSFORMATION

2) Set goals to be accomplished within the standards

1) Set standards to act as guidelines for the transformation process

The goals that we must set involve how we handle our client transactions. Being able to handle more client transactions in a more effective manner is the ultimate goal of the transformative process. If we do this we will be rewarded with more clients and re-initiation of rapid practice growth.

Increased client transactions per veterinarian can only be accomplished by more effective dissemination of the veterinarians’ knowledge to the client. This is accomplished by a combination of setting standards for veterinary procedures and staff education regarding those procedures.

Standards are the key to the transformation process, without a standard there is no way to know where you are going or when you are there. Setting high standards of Care, Service, Conduct, Communication and Appearance throughout the practice will set the guidelines for the goals that we hope to achieve. Standards are the rails that the locomotive of our practice travels on the way to success. Standards for the veterinary procedures include formal attention to protocols for common conditions. These protocols include diagnostic plans, therapeutic plans, management considerations as well as client education. Standards of staff education are set and implemented by formal training on the “pillars of practice” (topics considered being the most important health issues for the practice’s clientele). This education process enhances the staff’s understanding of recommendations made by the veterinarian and enhances bonding of the client to the staff.

3) Staff training and development of an operation plan Each step of the communication process with the client is mapped and each member of the team is given a role to play to ensure all stages of the transaction are handled effectively and efficiently. Planning for client communications

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by preparing all documentation of the case and recommendations prior to the communication ensures success. Tools are developed to aid in the communication process to the client, which now includes the staff as well as the veterinarian. These tools can be in the form of handouts or automated and personalized for each case. Redesigning the workflow of a client or case to more involve the staff in the communication process is a key element in the transformation process. For the staff to become proficient in this role extensive training is necessary to teach the fundamentals of animal husbandry around the “Pillars of Practice” and “Standards of Care”.

4) Develop the culture A common vision is shared so the entire staff can see the part they play in the common goal. Every staff member is trained equally on the “standards” and “pillars” of the practice. They are shown that by mastering these concepts they can elevate themselves in the eyes of other employees and the doctors as well as the clients. The standards give the employees the guidelines to make decisions regarding the care of the pet and client. They feel a part of the team and can see

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their career pathway for success. The standards that are set help instill self-esteem in the staff and teach them to be effective communicators.

5) Celebrate Success This vision is reinforced in weekly customer service and training meetings. Customer service is one of the driving forces behind the successfully transformed practice. The humans that bring in the pets are the people who pay our salary and they must be kept happy at all costs. Stories of exemplary customer service are celebrated and the standards of care and service are reinforced.

The result of establishing standards, setting goals within those standards, and training to those standards combined with re-designing the work-flow and incorporating technology is the ability to effectively see and treat more animals.

By practicing with these higher standards, the pet is more likely to have an effective treatment, the client will wait less and will be happier by the professionalism exhibited by the hospital staff, and the clinic will most likely have increased revenues. These satisfied clients will refer additional clients and the clinic growth rate will continue to increase.

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The “Bond” as the Fuel for Success in Veterinary Communications “The Bond” ovvero “il legame” è il carburante per il successo nella comunicazione veterinaria

Steve D. Garner DVM, Dipl AVBP - Safari Animal Care Centers - League City, Texas, USA

Riassunto “The Bond” (“il legame”) è il termine utilizzato per identificare il rapporto uomo/animale da compagnia. Le strutture veterinarie che si basano sulla conoscenza di questo legame sottolineano in modo particolare l’unione che lega un proprietario al suo animale. Il riconoscimento di questo rapporto è il prerequisito per poter fornire prestazioni ottimali a quei clienti che considerano il loro compagno come un membro della famiglia.

Questi clienti sono più affezionati e più disposti ad impegnarsi perché il loro animale possa godere di cure ottimali e desiderano essere informati sulla prevenzione delle malattie e sulla possibile longevità oltre che sulla terapia delle malattie e delle lesioni traumatiche. Offrire queste informazioni e queste cure supplementari può rappresentare per la struttura veterinaria un’opportunità per differenziarsi all’interno della comunità. A differenza delle prestazioni di natura medica e chirurgica, le numerose esigenze di comunicazione che nascono dal “legame” possono essere soddisfatte tanto dai veterinari quanto dai loro collaboratori.

Una volta stabilire le linee guida di base, tutti i membri dello staff possono contribuire ad aiutare il proprietario a garantire al suo animale una vita più sana, più felice e più lunga. L’offerta di informazioni sulla medicina preventiva, sul benessere animale e sulle procedure diagnostiche di routine fondata sul “legame” sarà accolta positivamente dai clienti in grado di apprezzarla. Questa risposta instaurerà a sua volta un rapporto con i vari membri dello staff, permettendo un flusso di energia positiva che spingerà in alto la produttività e la redditività della struttura.

Il Dr. Garner delineerà come sia possibile sviluppare un sistema autoperpetuantesi per instaurare con il cliente una comunicazione basata sul “legame”. Questi sistemi incanalano attraverso i membri dello staff (veterinari e non) l’energia che nasce dal “legame”, portando ad apprezzare meglio il lavoro che svolgiamo nella nostra professione per aiutare la società nel suo complesso.

“The Bond” is the term that we use to identify the human/companion animal relationship. The “Bond Centered” veterinary practice or veterinary medical care places more emphasis on the relationship that the pet owner has with their pet. Appreciation of this relationship is the prerequisite for providing optimal care to those clients that consider their pet to be a part of the family.

These clients are more attached and more committed to optimal pet care and want information on disease prevention and longevity in addition to therapy for illnesses and injuries. Providing this additional information and care can be an opportunity for the veterinary practice to differentiate itself in the community. Unlike medicine and surgery the many of “Bond Centered” communications can be provided by non-veterinary as well as veterinary team members.

Once basic guidelines are set, all staff members can participate in helping the pet owner enjoy a healthier, happier and longer life with their pet. As staff members communicate information about preventative care, wellness and routine diagnostic procedures focused on the “Bond”, positive responses will be received from the appreciative client. This feedback will flow through the now empowered staff members creating positive energy that will drive practice productivity and profitability.

Dr. Garner will outline how a self-perpetuating system for development of “Bond Centered” client communications can be developed. These systems channel the energy created by the “Bond” through the staff members both veterinary and non-veterinary giving a higher level of appreciation for the work we do in our profession to help society as a whole.

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INTRODUCTION The development of a model for successful small animal veterinary practice has been in evolution since the 1950’s.

This evolutionary tree has at its roots a strong foundation of service and devoted care that has earned the respect and goodwill of the pet owning public. The cost for this respect has been paid in the past by the veterinarians willing to sacrifice their time, energy and home-life for the positive energy that is derived from practicing in the most honored profession on earth.

While this tree has a strong trunk and branches that have born fruit for these dedicated practitioners in the past, it is time for new growth to occur which will take the profession to new heights. The veterinary professional evolution is undergoing “transformational change”, which will herald a new paradigm for veterinary practice.

There is a need for different fruit to satisfy the new breed of veterinarian practicing in this evolving digital and socioeconomic environment.

The new breed of veterinary practitioner wants fewer work hours, more vacation, more compensation, and less responsibility as his or her fruit. The “transformed” veterinary tree will branch to provide for these needs, but what will be the fertilizer, the energy the strength for this growth?

Will this veterinary tree consist of a corporate practice on one branch, or a superstore branch, or perhaps a central hospital/satellite clinic branch. It is almost certain that the private veterinary practice as we know it today will not exist in the not too distant future.

VETERINARY CENTERED VERSUS CLIENT CENTERED PRACTICE The veterinarian is the center of the current practice paradigm providing everything from medicine and surgery to customer service and practice management. This model of practice, however, cannot generate the revenues to compete with the benefit packages and compensation plans that can be offered by corporate America.

A new model will develop that places the client in the center of the equation. This client-centered practice will enjoy the benefits of empowerment of the health care team to provide customer service, client education, and “bond” appreciation, while the veterinarian provides only the things that only a veterinarian can do. By distributing the customer service effort across the health care team and by expanding the members of the team, the knowledge of the veterinarian is leveraged to new heights.

The positive energy created by the human/companion animal bond is the fuel for the growth of this new branch of the veterinary evolutionary tree. This branch will bear more fruit, be bigger thicker and more robust that the other branches of the new millennium veterinary models because it is nurtured by the sharing of knowledge, celebrating the bond and empowerment of those who work with us in this great profession.

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FIVE STEPS TO SUCCESSFUL TRANSFORMATION Veterinary clients and pets require a certain minimum contact time to handle the entire transaction. If this contact time is primarily with the veterinarian there becomes a diminishing number of free contact minutes per day for that veterinarian to serve new customers.(veterinarian centered operations) A trade-off occurs with either new clients or the existing clients and growth slows. Therefore, this “capacity for service” determines the rate of hospital growth and ultimately the total number of active clients per veterinarian.

Increasing the number of active clients per veterinarian is the key to transformational growth of a veterinary practice.

The key to increasing the number of active clients per veterinarian is to empower the staff to handle a portion of the customer contact time. This can only come about by creating a culture of change and setting high standards that guide that change in the direction of customer service, and the human/companion animal bond. The “transformed” practice changes from a medicine and surgery center to customer service and “Bond” center. Standards are set in line with this new vision and become the cornerstone and foundation upon which we build the transformed veterinary practice that can compete in the future.

1) Set standards to act as guidelines for the transformation process Standards are the key to the transformation process, without a standard there is no way to know where you are going or when you are there. Setting high standards of Care, Service, Conduct, Communication and Appearance throughout the practice will set the guidelines for the goals that we hope to achieve. Standards for the veterinary procedures include formal attention to protocols for communicating to clients. These protocols include diagnostic plans, therapeutic plans, management considerations that are centered on the special relationship that people have with their pets. Standards of staff education are set and implemented by formal training on the “pillars of practice” (topics considered being the most important health issues for the practice’s clientele). This education process enhances the staff’s understanding of recommendations made by the veterinarian and enhances client communication with the staff empowered by a common appreciation of the “Bond”.

2) Set goals to be accomplished within the standards The goals that we must set involve how we handle our client transactions. Being able to handle more client transactions in a more effective and “bond centered” manner is the ultimate goal of the transformitive process. If we do this we will be rewarded with more clients and re-initiation of rapid practice growth. Increased client transactions per veterinarian can only be accomplished by more effective dissemination of the veterinarians’ knowledge to the client.

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This is accomplished through “trusted communications” by health care team members well founded in the “standards”.

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and client. They feel a part of the team and can see their career pathway for success. The standards that are set help instill self-esteem in the staff and teach them to be effective communicators.

3) Staff training and development of an operation plan 5) Celebrate Success Each step of the communication process with the client is mapped and each member of the team is given a role to play to ensure all stages of the transaction are handled effectively and efficiently. Planning for client communications by preparing all documentation of the case and recommendations prior to the communication ensures success.

Tools are developed to aid in the communication process to the client, which now includes the staff as well as the veterinarian. These tools can be in the form of handouts or automated and personalized for each case. Redesigning the work-flow of a client or case to more involve the health care team in the communication process is a key element in the transformation process. For the health care team member to become proficient in this role, extensive training is necessary to teach the fundamentals of animal husbandry around the “Pillars of Practice” and “Standards of Care” including appreciation for the human companion animal bond.

4) Develop the culture A common vision of a “Bond Centered Practice” is shared so the entire staff can see the part they play in the common goal. Every staff member is trained equally on the “standards” and “pillars” of the practice. By mastering these concepts they can elevate themselves in the eyes of other employees, the doctors as well as the clients to the position of “Care Giver”. The standards give the employees the guidelines to make decisions regarding the care of the pet

The vision is reinforced in weekly customer service and training meetings. Customer service is one of the driving forces behind the successfully transformed practice. The humans that bring in the pets are the people who pay our salary and they must be kept happy at all costs. Stories of exemplary customer service are celebrated and the standards of care, service and the “bond” are reinforced.

Summary By setting standards that embrace the human /companion animal bond and by using these standards as the foundation upon which “trusted communication” is fostered with the client elevates the health care team member to the position of “care giver”. The empowered veterinary health care team member can share in the power released by the socioeconomic powerhouse known as “the bond”. Health care team empowerment and leverage of the veterinarians knowledge and love for animals allows for increased capacity for service. This increased capacity facilitates a positive upward spiral of value being created in the eyes and hearts of the client, and the health care team. When surplus value is created, opportunities flourish for the profession. This model of veterinary practice will prove to be the superior evolutionary branch of the veterinary tree bearing the fruits, which will enable a veterinary renaissance in the new millennium.

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Situational Communications Dealing with Clients and Co-workers La comunicazione - trattare con i clienti ed i collaboratori

Steve D. Garner DVM, Dipl AVBP - Safari Animal Care Centers - League City, Texas, USA

Riassunto Fissare gli standard di comunicazione è il primo passo per la realizzazione del vero valore del bene rappresentato dalla vostra preparazione. Questi standard stabiliscono nei dettagli come si sviluppa la comunicazione, sia all’interno della struttura veterinaria che verso il mondo esterno.

Il valore finale di una struttura veterinaria è la somma di tutte le conoscenze racchiuse nelle menti delle persone che vi lavorano. Il suo valore percepito è invece il solo valore che un cliente apprezza. La struttura veterinaria che è in grado di diffondere nel modo più efficace le conoscenze di cui dispone induce nella clientela la massima percezione del proprio valore.

Le capacità di comunicazione interpersonale possono essere standardizzate, insegnate ed apprese da tutti coloro che lavorano nella struttura. Queste capacità costituiscono la base per la diffusione delle conoscenze; dapprima all’interno della struttura stessa e poi all’esterno, verso i clienti.

La verifica delle comunicazioni si ha quando insorgono delle situazioni difficili, che rappresentano dei “momenti della verità” da cui la vostra struttura può uscire vittoriosa o sconfitta. La pianificazione di questi momenti attraverso la messa a punto di standard e l’allenamento alla loro applicazione portano alla formazione di un team rafforzato e vincente. Questo, a sua volta, è in grado di suscitare l’apprezzamento e da parte della clientela e, attraverso una comunicazione efficace, renderla più consapevole e, quindi, più preparata.

E chi ha i clienti migliori vince!

Setting standards of communications is the first step in the realization of the true value of your knowledge asset. These standards detail how communications occur both within the practice as well as to the outside world.

The ultimate value of a veterinary practice is the sum total of the knowledge contained within the minds of the people who work within that practice. The perceived value of a veterinary practice is the only value that a client appreciates. The veterinary practice which is able to disseminate its knowledge asset most effectively will create the highest perceived value for the client.

Interpersonal communication skills can be standardized, taught and learned by all people within the practice. These skills will provide the foundation for knowledge dissemination; first within the practice, itself, then, outside the practice to the clients.

Communications are tested when difficult situations arise creating “moments of truth” during which your practice either wins or looses. Planning for these moments by setting standards and training to those standards creates an empowered team. The empowered practice team will develop client appreciation and knowledge through effective communications thereby creating an educated client.

And he who has the smartest client - wins!

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The veterinary team must deal with situations that are “moments of truth” for the veterinary clients. Learning how to handle communication situations such as: communication the cost for services, telephone communications, taking messages, how to handle distraught clients, and interpersonal communications are essential functions in the successful practice.

If the caller does not identify himself/herself, ask if you may say who is calling. For example: “Yes, he/she is in. May I tell her/him who’s calling?”

(Don’t say, “Who’s calling?”)

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TELEPHONE USE INSTRUCTIONS Placing a Call on Hold 1. Press the hold button 2. May place on “Double Hold” by pressing hold button twice. This prevents any one else from picking up the phone from another extension. Press the hold button twice to place on double hold.

3. Press the intercom (ITCM) button to place a caller on hold and to transfer calls.

4. Using the Intercom 5. Press “ITCM” and then the number for the station that you wish to contact (they are labeled on right-hand side of phone).

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GROOMING BOARDING PET SHOP CONFERENCE RM RECEPTIONIST RECEPTIONIST LABORATORY AREA OFFICE

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Assume a client can hear what you are saying over the intercom until the phone is picked-up.

You may respond to Intercom without picking the phone up.

When someone calls your work area on the Intercom please respond to the person immediately if you can in a very polite but firm tone so that they will hear you.

Always use a very pleasant voice on the Intercom or telephone and use extreme courtesy when communicating with your fellow staff members.

Always wait for a reply to make sure someone has heard you. If no one responds assume that they are either with a client and cannot respond or that they did not hear you.

Answering the Phones Answer the telephone promptly, on the first ring if possible.

Smile when you pick up the receiver. A pleasant look will help assure a pleasant voice.

Identify yourself and the our hospital name. Offer your assistance. For example: “Our Clinic Name,” Linda speaking. May I help you?”

After being greeted, the caller will usually tell you his/her name and what they want.

Acknowledge the caller’s name and request. For example: “Yes, Mrs. Smith, the doctor is in.

I’ll get him/her for you.”

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Transferring Calls When transferring a call to the another location in the hospital, tell the person receiving the call who you are transferring and why.

Giving them this information eliminates the need for the caller to repeat the information and it saves time. For example: “Wayne, I have Mr. Smith on the line and he has a question about...”

Putting a Caller on Hold Let the caller complete a statement before putting him/her on hold. Don’t interrupt or cut them off.

Although it is preferable to complete business in one call, if information is required and some delay will occur, ask the caller if he/she would like to call back, would he or she like us to call, or would they rather hold? For example: “It will take a few minutes to locate the information.

Would you like to wait, or may I call you back?”

If the caller chooses to wait, return to the line every 15 20 seconds to inform the caller of the progress being made. Check to see if the caller wants to continue holding.

For example: “Mr. Smith, I’m still checking on that. Would you like to continue holding or do you want me to call you back?”

Progress reports assure the caller that the call is receiving continued attention.

When you return to the line, address the caller by name (if known), and thank him/her for waiting. For example: “Mr. Jones, thank you for waiting.

I have that information now.”

When a call comes in and you are on another line, ask the first caller to hold the line while you answer the second call. For example: “Would you hold, please?”

Finish with the business of the second call immediately. If it cannot be done immediately, let the caller know you will be right back. Take his or her name and number. Return to the first caller and thank him/her for waiting, or apologize for the wait.

For example: “Thank you for waiting,” or “I’M sorry to keep you waiting.”

If the telephone rings, and you are with another customer, excuse yourself from that customer and say: “Excuse me. I’ll be right with you.”

Answer the phone by saying: “Our clinic name”. Could you hold, please?”

Wait for the caller to respond, thank them and put the call on hold and finish the business of the first customer.

Then, return to the caller and say: “Thank you for waiting. This is (your name).

How may I help you?”

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Taking Messages Take messages willingly. If you ask a person to call back, he/she may have to call several times before reaching their party.

• Include the following: 1. Client’s first and last name 2. Client’s telephone number 3. Time and date of message.

4. The complete message 5. Your initials • Take care to write legibly and record the message on a message pad so that there is a duplicate in the event the message gets lost or needs to be referred to in the future.

• Do not hesitate to ask the caller to spell his or her name, or to repeat the phone number. It shows you care about communicating an accurate message to the person being called.

• After taking the message, read it back to be sure the information you have is correct.

• To obtain information for a message, request the information. Don’t demand it. For example: “May I have your name. Please?”

(Don’t say, “What’s your name?”)

• If the person is not available or not in the clinic or pet shop, let the caller know. It is seldom necessary to tell the caller where the person is; only that they are out and that you expect them at (whatever time you expect them).

For example: “She is out of the clinic this morning. I expect her about two o’clock this afternoon. May I have her call you?”

“He’s not available at the moment.

May I take a message and have him call you?”

“She is on the other line. May I have her call you?”

“He/she is not available at this time, may I have him/her call you?” or, “May I let them know what your call is concerning?”

• Take messages promptly. There should never be an occasion where a caller has to ask, “Why didn’t you return my call?” Inform the person if one message is more important than another, and indicate which calls have been made more than once.

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Terminating Calls Leave an impression with the caller that you were glad to help. Ask if you can be of further help. Always thank them for making the call. For example: “Is there anything else I can help you with, Mrs. Jones?”

Then, “Thank you for calling Our Clinic Name”.”

• Let the caller hang up first so you can be sure he or she has finished the call. Sometimes the caller will have an afterthought or remember a question he/she wanted to ask.

Also, place the receiver gently into the phone cradle.

Don’t let it “bang” down. The “bang” will be the last thing the person remembers about your conversation.

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CLIENT RELATIONS AND THE TELEPHONE Every time you make or receive a call, you are representing the hospital. Our hospital is judged by the voice that speaks for it over the phone. You become the

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Hospital by what you say and how you say it.

What you say and your tone of voice create a picture in the mind of the caller. You can influence that image by the telephone personality you convey. Over the phone, the other person forms his/her impressions of you solely by your voice. He/she cannot see the expression on your face, the smile on your lips, or feel a warm hand clasp. The only thing that counts is what meets his/her ear: your voice.

Conveying a Positive Attitude To convey a positive attitude, we must see the telephone as an important tool, not a nuisance. Show a sincere desire to help people when they call. Care enough to follow through with their requests. Focus on what you can do for them, not what you cannot do.

If we want people to see our hospital as an organization that cares about people and their pets, we must never leave a caller with the feeling that he/she is intruding.

In fact, answering the phone and helping clients is one of the most important aspects of your job and it must be seen as a top priority.

Be Warm and Friendly Keep a smile in your voice. It is difficult to be harsh when you are smiling. Show that you are interested in being helpful. Warmth begins with truly caring about the caller and wanting to help. Personalize your conversation by using the caller’s name.

Be Courteous and Tactful Use phrases of courtesy such as “Please,” “Thank you,” and “You’re welcome.” Be a good listener.

Do not interrupt the caller while she/he is speaking.

Give the caller your full attention.

Treat Every Call as Important Be helpful and informative. Make the caller feel he/she is getting your personal attention. Be careful not to convey impatience. The caller doesn’t know it may have been a bad time to call.

Dealing with callers in a professional manner helps establish trust, respect, and confidence. Remember how you handle each call affects future good will that takes years to create but only a few seconds to destroy.

ANSWERING QUESTIONS AND GIVING INFORMATION ON THE TELEPHONE When a caller asks the price of a service, respond by telling them what the service includes, then cite a price. If you quote the amount first, the caller may decide he/she does not want the service before hearing what is involved.

For example: “A bath and dip includes (explain the service, for twenty-five.” (It is not necessary to say “dollars”).

May I make an appointment for you?”

“Did you want to come in today?

I’d be glad to make an appointment for you.”

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When a caller asks about hours or how late we are open, give the caller the complete information about our hours.

For example: “In the Animal Hospital we are open from 7:00 a.m. to 7:00 p.m. Monday through Friday.

On Saturday we are open from 7:30 a.m. until 3:00 p.m.

May I make an appointment for you?” or “In the Pet Shop we are open from 10:00 a.m. to 7:oo p.m.

Monday through Thursday, from 9:00 a.m. to 7:00 p.m. on Fridays, from 9:00 a.m. to 6:00 p.m. on Saturdays, and from 12 noon to 5:00 p.m. on Sundays.

If you would like to drop your pet off earlier for Boarding or Grooming you may come in as early as 7:00 a.m. to the Animal Hospital Monday through Friday and as early as 7:30 a.m. through the Animal Hospital on Saturdays.”

Many of the calls you will receive will be clients who have perceived a problem with their pet. Get as much information as possible about the condition of the animal. Get the client’s name and the pet’s name. Find out how critical the situation is and how long the symptoms have persisted.

Ask the following questions: 1. Species, Breed, Age, Sex 2. What seems to be the problem?

3. How long has this been going on?

4. Is the pet presently on Medications?

5. Are her/his Vaccinations current? Or, when was it last vaccinated?

6. Has the pet been tested for heartworm?

7. Does the pet stay inside or outside?

that needs correcting, do so immediately or refer the matter to someone who can correct it.

Get All the Information Necessary Ask questions until you have received the information you need to help the caller. Make note of the facts as you understand them. Give the caller feedback to make sure you do have the facts straight.

State What Action Will be Taken Express a sincere desire to help. Tell the caller exactly what you plan to do about the situation. Tell them how long it will take. If there is nothing you can do, explain that to the caller. If the caller is not satisfied with the action or inaction, and if they ask to speak to the veterinarian or pet shop manager, let them do so. Thank the person for calling and ask if they are in need of further help.

Follow Up Once you have assured the caller the situation will be taken care of, follow up to make sure it has been. If a problem will take longer than you thought, call the client back and tell them. Keep them updated. In some cases you may need to call the person to be sure they are satisfied with the action that has been taken. Inform the veterinarian or pet shop manager of any major or recurring problems or complaints.

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HANDLING A DISSATISFIED OR DISTRAUGHT CLIENT A call informing us of a complaint or problem can be a blessing in disguise. It is a way of identifying ways of improving our service or method of doing things. Even when we have not erred, we can leave the caller with the positive, helpful and caring impression of our hospital. The following are five steps to follow when handling a dissatisfied or distraught client: Listen Listen to the caller’s complaint. Do not interrupt. If you try to defend yourself or give explanations before the person has had their say, you may make matters worse.

Listening will have a therapeutic effect on the person. By letting the caller unwind, you allow them to release tension.

It makes the caller feel better having vented frustration to someone who seems to care.

Show Understanding Express genuine concern. Put yourself in the caller’s position. Offer sympathetic understanding by saying “I’m sorry about this,” or “I can sympathize with your concern.”

You are not agreeing or disagreeing with the caller. You are simply confirming that you have heard the concern. Even if the caller is wrong, let them know you understand how they feel and, that you regret the inconvenience. If it is a matter

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As we all know, the telephone can bring us hundreds of clients everyday. But, we can also lose that many clients per day if we don’t use the phone properly - because of phone shoppers!

We must learn how to convert shoppers into clients and to get appointments scheduled. These techniques are not only for the receptionists; everyone answers that telephone at one point or another. Potential clients can form powerful impressions based solely on the value and quality they perceive over the phone.

Remember, every call is a potential new client, worth plenty of our time A study conducted in 1988 revealed that the average client is willing to spend $529.00 per year on his or her dog.

Multiply this figure by the number of referrals we get from each caller-turned-client, and each of you will see how important proper telemarketing can be.

The key is to get the phone shopper through the door one time, and then work like crazy to keep them. Pamper them, cater to them, DO MORE THAN THEY EXPECT. It is up to us to bond clients to us.

We must learn to sell value over the phone. At the time of the call this “commodity” will be perceived value. After we schedule an appointment, we must make sure we provide received value when the client visits our hospital.

In today’s crowded market, clients look for uniqueness, convenience, and a notably better practice. We should all convey concisely why our hospital meets these three criteria.

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DIALOGUE: 1) Greet the client as usual, then listen to question.

2) Before answering the question, obtain information about the pet - especially the pet’s name.

3) Tell the caller what our hospital has to offer and describe why we are unique.

4) Tell the potential client why she/he needs our services and how we will help solve the problem at hand and help the pet in the long run.

5) Tell her/him an estimate of how much this will cost, but keep low emphasis here.

6) Allow the potential client to decide that “your clinic name” offers value.

7) Schedule the appointment.

8) Reinforce the value we offer by assuring the client she made a good choice, i.e.: “We’re looking forward to seeing you and Fluffy on _____ and repeat appointment time.”

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It is vitally important that everyone here understand this sequence must be done exactly and completely in this order.

If you tell the client only the price, or discuss price first, she/he will make her/his decisions based on fee alone, without considering benefits.

An excellent follow up for those few clients that will not schedule an appointment (those who have to “discuss it with their spouse”) - ask for the address and volunteer to put together some information on the subject discussed to mail to them. Include with this information a short note or card thanking them for the opportunity to discuss their pet’s health with them. This must be done immediately following the conversation in order to be effective.

Asking the potential client to schedule an appointment and offering one for the next day - conveys convenience.

Suddenly, the estimate quoted represents much more than a “shot” for her/his pet.

Follow through is very important. When this client comes in, she must be given the value promised. Remember – under-promise and over-deliver.

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Customer Service as the Focus of the Empowered Employee Il servizio clienti quale obiettivo per il veterinario di successo

Steve D. Garner DVM, Dipl AVBP - Safari Animal Care Centers - League City, Texas, USA

Riassunto La medicina veterinaria è la fornitura di servizi medici e chirurgici agli animali da compagnia. Nella nostra professione, noi partiamo dal presupposto che se ci concentriamo sull’animale – e lo salviamo – il cliente lo apprezzerà abbastanza da pagarci per i nostri servizi. Sfortunatamente, molti proprietari sono incapaci di determinare il vero valore dei nostri servizi medici e chirurgici. La loro percezione di tale valore può dipendere molto di più dal modo in cui li trattiamo.

La nascita del concetto di valore dipende quindi non solo dalla fornitura di servizi medici e chirurgici, ma anche dal prestare attenzione al modo in cui questi vengono offerti al cliente. I veterinari di successo, oltre a disporre di un’ottima preparazione professionale, sono capaci di indurre un enorme idea di valore nella loro clientela.

Sviluppare i sistemi che permettano ai professionisti di vedere come possono mettere in atto questi principi è l’argomento di questa relazione. Il suo scopo è quello di mettere a punto un sistema autoperpetuantesi per assicurare un eccellente servizio clienti da abbinare a prestazioni mediche eccellenti.

Veterinary medicine is the delivery of medical and surgical services to pets. In our profession we assume that if we focus on the pet - and save the pet - the client will be appreciative enough to pay us for our services. Unfortunately many clients are unable to determine the true value of our medical and surgical services. The clients perception of value may reside more in how they are treated as customers.

The creation of value therefore relies not only in providing medical and surgical services but also in paying attention to how those services are delivered to the client. Employees which are empowered to provide service to customers, while leveraging the knowledge asset of the veterinarian create huge value for the client.

Developing systems that enable the employee to see how they can perform these functions is the topic of this discussion. Developing a self-perpetuating system for ensuring both excellent customer service while providing excellent medicine is the goal of this lecture.

The practice of veterinary medicine is considered within the service sector of our economy. The customer and only the customer defines service. Being able to respond to the service needs of our customer is the rate-limiting factor in the growth and eventual size of our business. Empowerment of the staff to provide customer service through formal training and example is the key to re-kindling practice growth.

Maintaining this rate of growth while retaining existing customers is the formula for increasing the number of active clients per veterinarian. This is accomplished by increasing the capacity for customer contact through a motivated staff.

This article will detail the essence of creating a culture

within a veterinary facility that fosters this level of exemplary customer service.

Many things have been written on what defines exemplary customer service; however, the practice manager or veterinarian alone cannot provide exemplary customer service. For the client to experience this level of customer service, it is necessary for each member of the hospital team to strive for exceptional customer service. Essential to each client having an exceptional experience on a consistent basis is to develop a culture within your hospital that fosters and promotes exceptional customer service. The steps in developing this culture are:

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1) Celebrate Service - “Weekly Customer Service Meetings” 2) Hire for Service / Promote Staff Based on Service 3) Train for Service a) Develop the Guiding Principles b) Establish Standards c) Empower Staff for Service d) Develop Tools

CELEBRATE SERVICE “WEEKLY CUSTOMER SERVICE MEETING” The key element in establishing the culture is the “Weekly Customer Service Meeting”. Once the culture is established, the “Weekly Customer Service Meeting” serves to rejuvenate the culture on a routine basis. It serves as the well of communication from which we draw to satisfy our customers’ needs. Each and every employee is asked to bring incidents of either good or bad customer service from the previous week to the meeting. As these incidents are shared, we all learn how our customers are being treated. If the incident is a good one it reinforces the guiding principles of customer service and is rewarded by public recognition among peers (one of the highest rewards that a human can receive). If the incident is a bad one no repercussions are felt other than to learn how to prevent the incident in the future. Positive steps are made to implement permanent changes that will prevent this from happening again. This is a learning process in which seasoned staff members are the chief instructors. Staff members are taught how to listen to clients to gather important customer information, then they are taught how to act on that information to change their actions as well as those of their co-workers to better serve the customer.

The most powerful tool used in this process of education is storytelling. Throughout time storytelling has been used to keep the guiding principles of cultures alive. In this same sense, we use stories to help propagate and disseminate excellent customer service through the center. The power of telling stories resides in their symbolic nature and the ability to get a technical concept across to non-technical people. Each week stories of good service and bad service are used to make points about how a customer or situation should be handled. To give you some examples I offer these. The story about the pet that got loose from your clinic and how everyone chased it. The story about how one client’s dog bit another client’s dog because the employees walked them too close together. The story about the staff member who washed the client’s flea-infested bed sheets for them. Or the staff member who changed the light bulb in the dark kitchen for the elderly client so she could see to put her groceries away. The staff member who took a forgotten collar and leash to the client on their way home. The time the husband picked up the wrong Spitz from grooming.

The time the IV catheter was sent home in the pet’s leg. The time the thermometer was sent home in the rectum. The time that Mary told Mrs. Howell that her fat rabbit would look good in a stew as Mrs. Howell paid her $1000.00 bill. These stories and the lessons behind them live beyond the customer service meeting because anyone can tell and retell them thereby propagating the essence of the hospital culture.

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The logistics of an effective customer service meeting have been derived from thirteen years of modification and adaption. The sole focus of the meeting is the customer. This may be obvious, but many veterinary hospitals have “staff meetings” which do not talk anything about customer service. Attendance is mandatory by all staff members and is “on the clock”. The time selected is consistent for every week and is the slowest day, most likely a Wednesday. Early morning is best. All staff members pitch in to do morning treatments and duties prior to the meeting. Staff members rotate the responsibility of arranging for food, coffee and juice for the meeting. The staff sits in a circle so that everyone can see everyone else and there is no obvious hierarchy. The answering service is on and the hospital is closed, nevertheless drop-offs and emergencies are handled seamlessly by alternating staff members as necessary. The facilitator for the meeting has the primary function of moderating time and topics so that everyone has the opportunity to speak. It is mandatory that everyone speaks. Correspondence from the clients is read as well as the obituary list. All staff members sign sympathy cards for deceased pets while the meeting is in progress. Other cards such as thank you, get well and congratulations are signed at this time as well. The customer service items need not necessarily involve only the animal hospital but can also involve customer service that the staff has experienced elsewhere. Technical training is held later in the day, however, veterinarians provide technical clarification as it relates to customer service issues. As an initiation to the culture, new staff members are introduced to the entire staff at their first customer service meeting by the existing staff providing not only their name and position but also their definitions or examples of excellent customer service.

HIRE FOR SERVICE / PROMOTE STAFF BASED ON SERVICE The first step in creating the culture is to hire staff members who have a propensity to serve both people and pets. In the initial interview discussions, strong emphasis is placed on customer service to develop an understanding of the applicant’s desire to be service-oriented. During the workinginterview, the applicant is evaluated for their actions and communications that demonstrate a desire to serve. Developing these employees that desire to thrive within this culture is fundamental to success. This involves an investment in the employee’s development as a person and as an animal care giver. Formal training in etiquette is not easily found today and is greatly appreciated by those who receive it. The standards of communication, conduct, service and appearance act as a common bond that unites the employees within a defined and greatly appreciated set of rules under which they work. The education process involved in the animal husbandry training or “Pillars of Practice” gives them a set of professional communication tools that are not available anywhere else. This investment raises their self-esteem and self-worth as well as their worth to the practice. They will repay this investment many times over by their newly developed penchant for service to the customer. Their recommendations are made with such enthusiasm that the typical

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veterinary client is more than happy to comply. This process of development of employees culminates in a shared vision of pet and customer care. When this zenith is reached it becomes obvious that more energy is derived from serving the customer and the pet than goes into the process. This positive energy is contagious and drives the engines of success. In addition to the positive feedback which the staff member receives from clients and from the Customer Service Meeting, staff members are promoted based solely on their dedication and contribution to excellent customer service. This promotion supersedes that which might be earned by way of seniority or experience. In many practice situations where promotions are based on seniority or level of experience or education, staff members who have been with the practice longer may feel secure in their hierarchy and may not be compelled or motivated to provide excellent customer service.

Therefore it is important to emphasize that actions of superior customer service are the mechanism for recognition and promotion. Thus a new staff member can excel early in employment by demonstrating an appreciation of the guiding principles of superior customer service.

TRAIN FOR SERVICE Setting standards of care, service, conduct, communication and appearance are the first steps in the process. They are the foundation upon which the guiding principles of customer service are set. These principles along with the standards define the culture. Within the culture there is no tolerance for actions that are not within the standards or within the guiding principles of customer service. The culture therefore, uses the actions dictated by the standards and the guiding principles of service to satisfy the customer’s perceived needs. As soon as possible after being hired and going through the orientation process, new staff members receive six to eight hours in “Standards” training. The guiding principles of customer service are communicated at this time. Staff members receive “Standards” notebooks and are formally tested on the Standards with an associated raise upon scoring 90% or above on the Standards test. Initial training is then reinforced with weekly customer service meetings. Periodically the entire staff goes on a retreat that focuses on customer service. Usually these are centered around attending a practice management seminar with an emphasis on customer service such as “It’s What’s Up Front That Counts”. These serve to re-vitalize the group as a whole and cause the entire group to be intensely focused on customer service at the same time.

Once trained, staff members are empowered to provide excellent customer service. This means using the guidelines and standards to “make decisions on their own” regarding customer service. They are encouraged to be creative but they are also instructed as to limitations, i.e., when to give a refund, when to discount, when to acknowledge mistakes, when to involve senior staff members or a veterinarian, when and how to let the client know that we cannot accommodate their wishes, or, when to accommodate the client’s wishes outside of the normal procedures.

Additional infrastructure is developed to serve as the

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tools for the employees to use in this process. This involves development of procedures, forms, and handouts as well as other tools of communication and training. Once in place, a staff member has the tools, standards and guiding principles and empowerment necessary to completely satisfy customers’ needs.

GUIDING PRINCIPLES Our business is very complex and involves more facets than most other businesses. Employees must be multi-talented to cope with the customer service challenges poised in a veterinary hospital. These challenges require a person to become proficient at technical skills as well as communication skills. Even with these skills, situations will arise that are novel. These types of unpredictable situations in a complex environment can only be handled effectively by applying a few guiding principles to each situation. It is our challenge to develop and present those guiding principles to the staff members in a manner so they are internalized and used almost without notice as situations arise. This internalization process must be continuous with positive reinforcement for following these guiding principles. The successful principles of customer service have been proven over the years in many other businesses. Within the veterinary industry however, it seems that lack of application of these principles may be a rate-limiting factor in the size of a veterinarian’s client base. These Guiding Principles and their applications are as follows:

Show you care •

Express feelings and words of concern and understanding regarding both the pet and its human. Reflect your understanding of the client’s concerns, their situation, their fears, their financial limitations, and their love for their pet back to them. Restate what they have said in a manner that shows understanding and concern. Let the pet know that you are concerned about whether or not it feels scared or desires attention.

• Be an advocate for the pet in educating the pet owner about the needs of the pet and the services and products available to satisfy the pet’s needs.

• Let the client know that it is important to you whether they are happy and whether or not the pet is happy and well.

This principle teaches each staff member to take personal responsibility to educate the client to the best of their ability about the needs of the pet, thereby taking personal responsibility to market services and products and gain owner’s acceptance and compliance for the benefit of the pet.

The result of this personal commitment on the part of the staff member is a more educated client, healthier pet, and increased revenues for the hospital as well as a staff member who feels a sense of accomplishment in achieving the desired results.

During the Weekly Customer Service Meeting, staff members identify situations in which either the client reco-

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gnized that we “cared” about them and their pet, or, the client perceived that we did not care about them and their pet. If the client feels we care, then they are more accepting of a difficult situation or forgiving should a mistake occur.

Realizing this value reinforces the importance of letting the client know that we care.

Listen •

Listen to the client to develop an understanding of their wishes. Do not assume you know what they want. Based on the Standards of Care that have been established, educate the client about what is best for their pet and let the client make the decision about the course of action for their pet. Do not assume a client will respond in a certain manner or desire services based on a certain set of circumstances - always educate, ask, and Listen. Listen to the client’s feedback to ensure that we are doing what they think we should be doing.

• Listen to our clients with eyes as well as ears so that we can have an accurate perception of what the client is saying. Clients may be “mixed-message senders” and may say one thing but really mean another. Attention to the client’s body language may reveal a different message than they are verbalizing. Reflect to the client what they are saying using the phrase “I see that you feel …” and explain what emotion they are having about the situation. Express a verbalization of an emotion so that they will understand that you have heard them.

• Listen to the client to ensure that they have understood the information that we have relayed to them. Do not assume that because we have said something to the client or given them something to read that they understand what we are trying to communicate. Ask the client questions and listen to their response to ensure that they understand the information. Once the client has an understanding of all of the information, do not make the client feel bad if they choose a course of action that is different from the one you would have chosen.

By internalizing this principle, the staff member is trained that the objective is to understand what the client wants so that the staff member can satisfy the client or educate the client about why this may not be possible and what other choices are. The guiding principle is “seek first to understand, then to be understood”. Because the staff understands that the care the pet receives is ultimately the decision of the client, they feel a personal sense of responsibility to ensure by listening that they have given the client the information they need, including fee estimates, to make an educated decision about the care of their pet.

A primary component of the Weekly Customer Service Meeting is for the staff members to communicate comments that they have heard from the clients - both good and bad. This reinforces the “listening habit” and becomes almost peer pressure to bring to the meeting what the clients are saying.

Appreciate the Client •

Verbally express to a client that you are glad they chose

your animal care facility - “Thank you for coming in Mrs. Jones - it really means a lot to us that you let us help you take care of Fluffy”.

• Demonstrate through small actions that you are thinking about them - this demonstrates appreciation. “I knew you were coming in today so I have Fluffy’s favorite treats ready for him.

• Let the client know you appreciate their efforts for their pet. “We appreciate you bringing Fluffy in for his bloodwork”.

• Let the client know that you appreciate any inconvenience to them - even if you feel uncomfortable about the situation. “ I know your time is important Ms. Jones. We really appreciate you waiting. Is there anything I can do for you while you wait?”

• Appreciation can also be said non-verbally by making eye contact with a client and smiling.

Staff members are trained on the importance of letting clients know they appreciate them. They understand that clients in today’s market are not likely to return where they are not appreciated and may not return unless there is some demonstration of appreciation.

At the Weekly Customer Service Meeting, staff members get to express their creativity in letting clients know they appreciate them. Among the staff members there is almost a “competition” that evolves in who can be the most creative.

You are Empowered •

•

•

•

Once you understand the desires or needs of the client, offer information to let the client know that you have the knowledge or can take an action to satisfy their desires or needs. “ I understand you are calling about the price of a spay”. Let the client know what it is we have to offer - in great detail if necessary, differentiate our service, relay the fee, and offer to schedule an appointment or give them more information.

Many times a client may not be aware that the staff member has been empowered to meet their needs so that it may be necessary for the staff member to verbally express to the client that they perform the action, task or function that meets their needs. “Yes Mrs. Jones, I’ll be happy to have your food delivered to you.”

If a staff member does not know the answer to a question and more information is needed, he/she will be happy to get that information for them. When a staff member is new, there is no need to communicate this to the client.

The client is only concerned with getting the information that they need. The new staff member will respond “I’ll be happy to find that out for you.” They will then seek out the correct response and communicate that response back to the client.

Staff members are trained on how to disseminate information to the client. Many times clients do not expect that anyone other than the veterinarian can answer their questions so the staff members let the clients know that they can answer questions. They are taught that the client will not always know the questions to ask and it is their responsibility to offer information to the client. By going

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through this process, the client develops trust for the staff. The person who knew the correct information (the veterinarian) did not necessarily spend time communicating with the client, and, the new staff member learned how to respond such that the next time that specific question is asked they will not need to involve someone else.

At the Weekly Customer Service Meetings, staff members relay the positive responses that they received from clients when they meet the client’s needs. This positive feedback builds the staff member’s self-esteem and causes the staff member to feel important and a part of a team. As a result, the staff member will want to reproduce this feeling of self-worth by continuing to provide information and meet clients’ needs.

Solve Problems •

Once you have demonstrated concern for the client’s problem and have developed an understanding of the problem, let the client know that you can and will solve their problem. Clients might expect that you would pass the problem on to someone such as a manager or an owner. However, if the problem is within your capabilities, let the client know that you will solve their problem. It may be necessary for you to consult with others, but you will be the primary problem-solver.

• If you cannot immediately solve their problem, let the client know that you will take personal responsibility for following through to make sure the problem is taken to the person who can resolve the issue and that you will be an advocate for resolution.

• If a problem the client has occurred with another staff member or another department, let the client know that you accept the responsibility as your own for solving the problem. Do not say “that is not my problem”, or point out who made the mistake, just let the client know that you will accept the responsibility. The client is not necessarily concerned with who made the mistake, only that the problem is resolved to their satisfaction.

• When a problem is presented, take the opportunity to bond the client to the clinic even more than if the problem had never arisen. In the client’s mind, a “momentof-truth” has occurred and critical to the bonding process is that the staff member demonstrates concern and accepts responsibility for the problem, and, that the problem is resolved to the client’s satisfaction.

• Resist the tendency to become defensive and to be personally offended when a client presents a problem. Look at the problem from the client’s viewpoint and for ways to respond positively to them.

Staff members are empowered to solve problems. They are trained on what options and what resources are available to them. Staff members are given specific instructions on how to handle distraught clients. As the staff member involves others to solve problems they do not know how to solve, they learn how to solve those problems for the future. They are taught what problems require additional input from senior staff members, managers, veterinarians or the owner.

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As the staff member becomes an effective problem-solver they begin to free up more and more of the managers’ or veterinarians’ time and are able to provide a quicker response to client problem-solving, thereby making the clients happier.

At the Weekly Customer Service Meeting, the problems that have occurred throughout the week are discussed. The staff member states how the problem was handled and the status or disposition of the problem. This process allows everyone to know how we handle the problem and allows newer staff members to learn how to handle that problem should they encounter the problem in the future. In the event that the Practice Manager or veterinarian might have wanted the problem handled differently, the staff member is not scolded but rather it is discussed that we would prefer to handle the problem differently in the future with an explanation of why.

New procedures, forms, or protocols are established in this group setting. This has many benefits. It prevents future problems, lets everyone know how guidelines are developed – that there are reasons behind them, and reinforces why it is important to follow all Standards and Principles. During this process in a group setting, a staff member volunteers to be the person responsible for ultimate resolution although it may involve several people. This staff member will volunteer to make the follow-up phone call, research for more information as well as send a written note about the resolution to the client. When we have resolved a problem and the client has expressed their appreciation - this is a time to celebrate. This positive feedback causes the staff member to want to solve more client problems and even look for problems to solve. The staff understands that by solving client problems we prompt more client visits. If the staff members don’t listen for the problems they will never have the chance to solve problems before the client is gone. If we discover a problem and resolve it in a manner that causes a closer bond to the client, then they will tell others about how happy they are and the practice will continue to grow.

Always Use Courtesy • • • • •

Use verbal expressions that convey respect and appreciation Use eye contact, facial expressions and body language that express respect and appreciation Use personal names whenever possible – last names only of clients Always use formal communications, never casual Use expressions of warmth and elegance

Exceed Client’s Expectations • • •

Clients expect the facility to smell like a veterinary hospital. Make it so clean that it has no smell at all.

Clients do not expect type written release instructions and examination forms personalized for their pet.

Clients do not expect to be invited into the back area or on a tour.

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• • • • •

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Clients do not expect to be offered a beverage.

Clients do not expect to be treated like ladies and gentlemen when entering a veterinary hospital.

Clients do not expect highly-trained professional, competent staff.

Clients do not expect their pet to have a bandana and to be groomed after every visit.

Whenever possible, go beyond what the client has requested.

The rate-limiting step to the growth of a practice is the

ability to provide consistent exemplary customer service.

Practice growth is determined by the number of happy clients and pets that are out in the community marketing your business for you. Most veterinary facilities reach a steady state of practice growth at about 800 to 1200 active clients per veterinarian. This process of developing and rewarding staff for providing excellent customer service is effective at multiplying this statistic. A large investment in time and energy as well as trust by the veterinarian is necessary, but the development of a culture that fosters exemplary customer service will repay the practice many times over.

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Novità terapeutiche in dermatologia veterinaria Giovanni Ghibaudo Med. Vet. - Libero Professionista - Samarate (Va)

Riassunto In questi ultimi anni diverse nuove molecole sono state studiate ed utilizzate nell’ambito della terapia clinica dermatologica nei piccoli animali. Durante questa relazione, alcune molecole saranno solo accennate, come l’utilizzo della formulazione iniettabile del lufenuron nel gatto per la lotta alle pulci; l’utilizzo del L-Deprenil nell’iperadrenocorticismo pituitario-dipendente o della melatonina nelle alopecie ricorrenti del fianco e nella cosiddetta “pattern baldness” del cane.

In corso di demodicosi generalizzata, oltre ai protocolli classici a base di amitraz, è stata utilizzata l’ivermectina (lattone macrociclico, anti GABA) al dosaggio di 0,3-0,6 mg/kg una volta al giorno per bocca per 2-7 mesi con una buona percentuale di successo (48-83%). La milbemicina (lattone macrociclico e anti GABA) al dosaggio di 2 mg/kg SID per OS e la moxidectina, un’altra avermectina, a 0,2-0,4 mg/kg SID per OS sono state testate per la demodicosi generalizzata con buoni risultati e senza effetti collaterali. Nella demodicosi felina localizzata, autori francesi, utilizzano una crema a base di crotamitone ad azione acaricida ed antipruriginosa giornalmente per 6-8 settimane con buoni risultati.

In corso di dermatofitosi il farmaco per la terapia sistemica tuttora normalmente usato è la griseofulvina micronizzata (fungistatico). Altre molecole sono negli ultimi anni state utilizzate come l’itraconazolo, utilizzato a dosaggi di 5 mg/kg SID per OS nel cane e 10 mg/kg SID per OS nel gatto, e più recentemente la terbinafine nella dermatofitosi felina a 30 mg/kg SID per OS. Nelle dermatiti immunomediate oltre ai corticosteroidi vengono utilizzati altri chemioterapici quali l’azatioprina nel cane e il clorambucile nel pemfigo foliaceo e nel complesso granuloma eosinofilico felino. L’associazione tetraciclina e niacinamide dimostra una discreta efficacia in corso di lupus eritematoso discoide e nel pemfigo eritematoso del cane; mentre la pentoxifillina, è stata trovata utile, in alcuni casi, nel trattamento della dermatomiosite e di altre dermatopatie infiammatorie. La ciclosporina, polipeptide ciclico liposolubile, con attività immunosoppressiva ed antinfiammatoria, è stata utilizzata recentemente in corso di fistole perianali e dermatite atopica. Al dosaggio di 10-20 mg/kg per OS SID. Infine gli AGE (acidi grassi essenziali) sono utilizzati come antinfiammatori in corso di dermatite atopiche. Recentemente, questi acidi grassi insaturi, sono stati testati anche in corso di linfomi cutanei con successo e senza effetti

In questi ultimi anni diverse nuove molecole sono state studiate ed utilizzate nell’ambito della terapia clinica dermatologica nei piccoli animali. Durante questa relazione, alcune molecole saranno solo accennate, come l’utilizzo della formulazione iniettabile del lufenuron (IGR inibitore della crescita) (SC due volte l’anno) nel gatto per la lotta alle pulci1; o come l’utilizzo del L-Deprenil (inibitore delle MAO) 1 mg/kg SID per OS nell’iperadrenocorticismo pituitario-dipendente2,3. L’ efficacia di quest’ultima molecola è stata però riscontrata solo in pochi casi molto selezionati. Nelle alopecie ricorrenti del fianco e nella cosiddetta “pattern baldness” - calvizia da settore del cane è stata utilizzata la melatonina sintetica (sostanza normalmente sintetizzata dalla ghiandola pineale) con risultati incoraggianti. Questo presidio sembra agire, in generale, come promotore aspecifico della crescita di pelo invernale. La somministrazione avviene attraverso iniezioni o impianti sottocutanei di melatonina o per OS con dosaggi di 5-6 mg ogni 8-24 ore4,5. Considerata la sua breve

emivita, l’intervallo più corretto sembra essere di una somministrazione ogni 8 ore. Un ciclo di somministrazione di 1,5-2 mesi sembra sufficiente ad indurre il rientro dei peli in fase anagena. Per prevenire un nuovo episodio dell’alopecia stagionale dei fianchi, si consiglia di somministrare un ciclo terapeutico di melatonina a partire da 2 mesi prima della data abituale di comparsa.

DEMODICOSI In corso di demodicosi generalizzata, oltre ai protocolli classici a base di amitraz, è stata utilizzata l’ivermectina (lattone macrociclico, anti GABA) al dosaggio di 0,3-0,6 mg/kg una volta al giorno per bocca per 2-7 mesi con una buona percentuale di successo (48-83%)6,7; viene consigliato un dosaggio iniziale di 0,1 mg/kg per ridurre la possibilità di effetti collaterali aumentando poi giornalmente la dose fi-

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no al raggiungimento di quello desiderato. Il suo uso è controindicato nei cani di razza Pastore Scozzese, Shetland, Bearded Collie, Bobtail e Berger Australiano. Per questo motivo è stata sperimentata in diversi studi8,9 la milbemicina (lattone macrociclico e anti GABA) al dosaggio di 2 mg/kg SID per OS. Questa molecola sembra essere ben tollerata anche nelle razze a rischio. Ancora più recentemente la moxidectina, un’altra avermectina, è stata testata per la demodicosi generalizzata a 0,2-0,4 mg/kg SID per OS con buoni risultati e senza effetti collaterali10. L’ulteriore vantaggio nell’utilizzo di questa molecola risiede nel fatto d’essere più economica rispetto alla milbemicina. Nella demodicosi felina localizzata, autori francesi utilizzano una crema a base di crotamitone ad azione acaricida ed antipruriginosa giornalmente per 6-8 settimane con buoni risultati11.

DERMATOFITOSI In corso di dermatofitosi il farmaco per la terapia sistemica tuttora normalmente usato è la griseofulvina micronizzata (fungistatico)12. La posologia consigliata è di 50 mg/kg SID attraverso una somministrazione orale insieme ad un pasto grasso per rendere ottimale l’assorbimento intestinale.

La durata della terapia è in genere di 2-4 mesi. Anoressia, nausea e vomito sono gli effetti collaterali più comuni. La durata della terapia e gli effetti collaterali di questa molecola hanno indotto a cercare altre molecole altrettanto efficaci ma meno tossiche: l’itraconazolo, derivato triazolico, ha queste caratteristiche. Utilizzato a dosaggi di 5 mg/kg SID per OS nel cane e 10 mg/kg SID per OS nel gatto, è ben tollerato e necessita di un tempo terapeutico lievemente minore13,14. La somministrazione deve avvenire a stomaco pieno in quanto la sua biodisponibilità è ottimale in un ambiente acido. Il fluconazolo, altro derivato azolico, è indicato nelle criptococcosi sistemiche a 50 mg/gatto SID per OS15. Questa antifungino non sembra avere, invece, una reale efficacia in corso di dermatofitosi; questo perché il fluconazolo è idrosolubile e non raggiunge gli strati cutanei in concentrazioni adeguate. In alcuni lavori è stata testata l’efficacia della terbinafine nella dermatofitosi felina16,17. Questa molecola appartenente alla classe delle allilamine, sembra avere, a differenza delle molecole sopracitate, proprietà fungicide.

La sua efficacia è stata confermata in uno studio clinico ad un dosaggio di 30 mg/kg SID per OS. Sembrerebbe agire a dosaggi inferiori ma non è stato ancora definito un dosaggio ottimale.

DERMATITI ATOPICHE E IMMUNOMEDIATE Una serie di molecole con proprietà antinfiammatorie e/o immunosopressive sono continuamente al centro dell’attenzione in campo dermatologico.In particolare nelle dermatiti immunomediate oltre ai corticosteroidi vengono utilizzati altri chemioterapici quali la ciclofosfamide e l’azatioprina nel cane (pemfigo fogliaceo, pemfigoide bolloso e in corso di lupus eritematoso sistemico e discoide). L’azatioprina inizia a manifestare la sua efficacia 3-6 settimane dopo l’inizio della somministrazione è quindi consigliabile l’utilizzo ab-

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binato di corticosteroidi: una volta raggiunta la remissione delle lesioni si deve diminuire il dosaggio di entrambi, iniziando, se non ci sono problemi di effetti collaterali, con la diminuzione dei cortisonici mirando a raggiungere la dose di 1 mg/kg ogni 48 ore; nella fase di attacco il dosaggio dell’azatioprina nel cane è di 1,0-2,5 mg/kg SID per OS una volta diminuita la dose dei cortisonici si punta anche alla diminuzione dell’azatioprina a giorni alterni, se non si hanno ricadute si cerca di diminuire la dose fino a trovare quella minima sufficiente a mantenere il controllo della patologia. I principali effetti collaterali dell’azatioprina sono la trombocitopenia e la leucopenia, questo nella fase d’induzione rende essenziale il monitoraggio bisettimanale dei principali parametri dell’emocromocitometrico. Questa sostanza immunosopressiva non deve essere utilizzata nel gatto in quanto risulta essere altamente tossica e a volte letale. La sostanza immunosopressiva che permette di risparmiare sulla dose dei corticosteroidi nel gatto è il clorambucile 0,1-0,2 mg/kg SID o BID per OS. Sono stati riscontrati buoni risultati nel pemfigo foliaceo e nelle lesioni da complesso granuloma eosinofilico particolarmente gravi. Anche per questa molecola è essenziale il monitoraggio delle variazioni emocromocitometriche. L’associazione tetraciclina e niacinamide ha dimostrato una discreta efficacia in corso di lupus eritematoso discoide e nel pemfigo eritematoso del cane, il dosaggio indicato è di 500 mg per entrambe le molecole ogni 8 ore per OS in soggetti maggiori di 10 kg in seguito, in caso di risposta terapeutica, si può passare a somministrazioni meno frequenti (ogni 12 o 24 ore). Un altro presidio con azione immunomodulatoria è la pentoxifillina, utile, in alcuni casi, nel trattamento della dermatomiosite, vasculite e dermatite allergica da contatto. È indicato un dosaggio di 10-15 mg/kg per OS BID18. La ciclosporina è un polipeptide ciclico liposolubile, con attività immunosoppressiva ed antinfiammatoria. Usato in veterinaria, soprattutto in medicina interna, come trattamento per le malattie immunomediate. Di recente è stata accertata la sua efficacia nel controllo di alcune forme di fistole perianali19 come pure di dermatiti atopiche particolarmente gravi. Il dosaggio della ciclosporina usato è stato di 10-20 mg/kg per OS SID (nel gatto diviso in due somministrazioni)20,21. In corso di atopia una volta ottenuto il controllo della forma si riduce gradualmente fino al raggiungimento della dose minima sufficiente a tenere in remissione il soggetto. Effetti collaterali segnalati nel cane sono vomito e mielosoppressione. Gli AGE (acidi grassi essenziali) sono utilizzati come antinfiammatori in corso di dermatite atopiche. Alcuni lavori clinici su cani atopici hanno confermato queste tesi22,23. Una integrazione alimentare di acidi grassi essenziali con un rapporto compreso tra 5:1 a 10:1 tra omega 6 e omega 3 è stato accertato essere quello in grado di dominare meglio la risposta infiammatoria. La loro azione in combinazione con corticosteroidi o antistaminici risulta essere sinergica24.

LINFOMA CUTANEO In corso di linfoma cutaneo sono stati utilizzati prodotti topici alla carmustina, o sistemici quali retinoidi (isotretinoidi 1-3 mg/kg SID per OS) e chemioterapici come i corti-

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costeroidi, L-asparaginasi e la dacarbazina tutti con scarsi risultati. Recentemente sono stati riportati casi di linfomi sia multicentrici sia cutanei che hanno risposto ad una terapia solo a base d’integrazione d’acidi grassi25,26. Nell’uomo è ormai provato l’efficacia terapeutica e preventiva degli omega 3 nei confronti di diverse neoplasie quali carcinomi mammari, prostatici e melanomi; e quella degli omega 6 nei confronti dei linfomi27,28. Il meccanismo d’azione risiederebbe nella formazione di superossidi e di radicali liberi aventi effetti citotossici.

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Bibliografia 18.

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L’anestesia del paziente in GDV Oscar Grazioli Med. Vet. - Libero Professionista - Reggio Emilia

NOTA: Attraverso una sessione interattiva l’autore intende mettere in risalto i concetti espressi nella seguente relazione.

Il paziente affetto da GDV può presentarsi con uno stato del sensorio depresso, fino allo stato di shock acuto, a causa delle profonde alterazioni che ne compromettono l’equilibrio emodinamico e acido basico. Questa è la situazione più frequente, almeno per quanto concerne l’esperienza pratica dell’autore. Talvolta, soprattutto quando il proprietario si accorge precocemente della patologia in atto, può accadere che il cane si presenti con uno stato del sensorio ansioso e agitato. È evidente che il comportamento da tenere nei due casi sarà molto diverso. Dal momento che la prima fase di trattamento della GDV prevede la decompressione, attraverso l’inserimento di una sonda orogastrica di diametro adeguato, se il cane di presenta in stato di grave prostrazione a causa delle turbe emodinamiche e dello shock sarà necessaria semplicemente una blanda sedazione, utilizzando farmaci che abbiano il minore impatto possibile sul cardiovascolare. A tal proposito se il cane, come spesso capita in questi casi, tollera una maschera ad ossigeno sarà opportuna una preossigenazione con O2 ad alti flussi. Per quanto riguarda i farmaci, essendo la manovra di inserimento della sonda orogastrica poco dolorosa, si darà la precedenza ai tranquillanti minori, quali il diazepam o il midazolam, tenendo conto che il primo andrà iniettato endovena lentamente perché, essendo veicolato in glicole propilenico, l’iniezione rapida può causare ipotensione, mentre il secondo può causare depressione respiratoria, seppur di modesta entità. Talvolta è sufficiente la sola benzodiazepina per poter inserire la sonda in un cane che, seppur prostrato, non permetta tale intervento, se non a seguito di una pur blanda sedazione. Nel caso la benzodiazepina non fosse sufficiente si può aggiungere una bassa dose di fentanil (1 mcgr/kg) o remifentanil (0.5 mcgr/kg). Personalmente l’autore preferisce quest’ultimo farmaco che fa parte di una nuova classe di 4-anilidopiperidine ultrabrevi in grado di stimolare i recettori µ degli oppioidi ed è dotato di una clearance estremamente veloce e indipendente dalla funzionalità epatica e renale. Contemporaneamente, o prima ancora , di iniziare le manovre di sedazione è bene andare alla ricerca di eventuali aritmie cardiache, in quanto, come è noto, queste rappresentano la più temuta complicazione sia in corso di GDV che nelle ore successive.

Se l’aritmia è emodinamicamente significativa andrà trattata senza indugio con un bolo endovenoso di lidocaina alla

dose di 2-4 mg/kg seguito, in caso di successo e di ricomparsa dell’aritmia, da una perfusione continua dello stesso farmaco al dosaggio di 40-80 mcgr/kg/min. ad effetto. In caso di insuccesso si procederà alla somministrazione di procainamide, da sola o in combinazione con la lidocaina, alla dose di 0.5-2 mg/kg/EV seguita da una perfusione continua di 20-40 mcgr/kg/min. Si suggerisce molta cautela e uno stretto monitoraggio, nell’impiego di farmaci antiaritmici in associazione. Qualora l’aritmia non fosse emodinamicamente sigificativa (Es: rari VPC monofocali) o non comparisse per niente, l’autore non utilizza la lidocaina o altri antiaritmici, in quanto possono causare, specie ai dosaggi più elevati, ipotensione (lidocaina) e diminuzione della portata cardiaca (procainamide) Nel caso il cane si presenti agitato, per quanto controversa, è ammessa (e dall’autore auspicata) una sedazione con bassi dosaggi di acetilpromazina (20-40 mcgr/kg) eventualmente associata ad un oppiaceo a breve o ultrabreve durata (fentanil, remifentanil). Si consideri che l’acetilpromazina è un antiemetico e aiuta a prevenire l’insorgenza di aritmie. Il basso dosaggio non deve fare temere una marcata ipotensione.

Nel caso fosse necessario un farmaco anestetico per l’induzione la preferenza dell’autore va sicuramente all’etomidat che offre ampi margini di garanzia per quanto riguarda l’impatto sul sistema cardiovascolare, superiori a qualsiasi altro farmaco d’induzione. Purtroppo l’etomidat non è ancora registrato in Italia, ma lo è in alcuni paesi europei, nonché transoceanici quali gli Stati Uniti. Certamente sconsigliati, soprattutto a dosaggio pieno, sono i farmaci potenzialmente in grado di scatenare aritmie (tiopentale). Controverso è il ruolo del propofol (potente ipotensivo) generalmente accettato ai dosaggi più bassi, mentre l’associazione ketamina-diazepam si può impiegare con discreta sicurezza a patto che non vi siano aritmie in atto o rilevanti scompensi cardiaci. Controversa è anche l’induzione in maschera mediante anestetici volatili che l’autore personalmente non usa e sconsiglia.

Per quanto riguarda il mantenimento dell’anestesia, nei rari casi in cui il cane dovesse subire un intervento immediato, la scelta dell’autore va a favore dell’anestesia bilanciata con l’utilizzo di benzodiazepine, oppiacei a breve o ultrabreve emivita (fentanil, remifentanil) e facilmente antagonizzabili, associati all’uso di un bloccante neuromuscolare che non liberi istamina (cis-atracurium) e ad un anestetico volatile, quale l’isoflurano o il sevoflurano settando il vaporizzatore ad una MAC pari a 1 e non oltre.

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In qualsiasi caso è sempre necessario avere la possibilità di effettuare una ventilazione assistita manualmente o una ventilazione meccanica tramite respiratore automatico. Il monitoraggio dovrà essere il più completo possibile anche nelle ore successive ad una decompressione che abbia avuto rapida risoluzione, soprattutto se il cane è stato trattato per aritmie emodinamicamente significative.

L’autore ha lasciato per ultimo l’uso del protossido d’azoto il cui impiego è stato, per anni, controindicato durante la GDV a causa del suo noto potere diffusivo all’interno di cavità ripiene di gas, nonché per la sua capacità di distendere ulteriormente gli organi cavi. In realtà quest’ultimo effetto si rende evidente a seguito di un uso continuativo per almeno due ore e il suo utilizzo potrebbe avere una indicazione, in quanto consente di abbassare la concentrazione degli anestetici volatili. Si sconsiglia comunque vivamente di impiegarlo prima della decompressione avvenuta e sempre quando la saturimetria subisca cedimenti di rilievo.

Va da sé infine che, a decompressione avvenuta, una volta che il paziente sia stato opportunamente stabilizzato, l’eventuale intervento chirurgico andrà programmato possibilmente entro e non oltre le dodici ore successive, quando comunque l’organismo abbia recuperato sufficientemente la sua stabilità cardiovascolare e la sua omeostasi metabolica.

In tale situazione l’anestesista non dovrà far altro che seguire le corrette procedure di una qualsivoglia anestesia generale condotta su di un paziente che non versa più in una si-

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tuazione “di vita o di morte”. Dal momento che le alterazioni cardiache, quali le aritmie, possono comunque insorgere anche nelle ore successive alla decompressione, a dispetto di una apparente perfetta “ripresa” del paziente, è necessario utilizzare farmaci con minimo impatto sul sistema cardiovascolare e soprattutto non aritmogenici. Ancora una volta l’autore ritiene che l’anestesia bilanciata costituisca la miglior scelta se contempla l’utilizzo di farmaci quali benzodiazepine, oppiacei ultrabrevi, etomidat. bloccanti neuromuscolari e isoflurano o sevoflurano alla minima MAC possibile. Se il paziente ha avuto un buon recupero, valide alternative possono essere una premedicazione con basse dosi di acetilpromazina (20 mcgr/kg), associata ad un oppiaceo come il fentanil o il remifentanil, seguita dall’induzione con etomidat, propofol, o ketamina/diazepam e dal mantenimento con isoflurano o sevoflurano alla minima MAC possibile.

L’uso di un oppiaceo intraoperatorio, in boli o in perfusione continua, agevolerà l’uso di una bassa concentrazione di anestetico volatile, garantendo l’adeguata analgesia al paziente. In tale situazione è concesso l’uso del protossido d’azoto, sempre al fine di abbassare il più possibile il settaggio del vaporizzatore.

Gli oppiacei possono diminuire la motilità intestinale, ma questo problema è, di solito, clinicamente poco rilevante. E comunque buona norma, come già si è ribadito, affidarsi a farmaci con clearance molto elevata, come il remifentanil e il più comune e collaudato fentanil.

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Diagnosi e trattamento delle neoplasie gastrointestinali del cane e del gatto Massimo Gualtieri Med. Vet., PhD - Istituto di Clinica Chirurgica e Radiologia Veterinaria - Università di Milano

Riassunto Le neoplasie gastrointestinali costituiscono il 2% circa di tutte le neoplasie del cane e del gatto e le forme maligne ne rappresentano il 75%. Il tratto maggiormente colpito risulta essere l’intestino ed il tipo istologico più frequente è l’adenocarcinoma, seguito dal linfoma. Le neoplasie esofagee sono rare e sono costituite prevalentemente da sarcomi nel cane e carcinoma squamoso nel gatto. La diagnosi definitiva si basa principalmente sull’esame endoscopico dell’esofago, che consente la visualizzazione diretta e il prelievo bioptico della lesione. Il trattamento prevede la resezione chirurgica con ampio margine del tumore, tuttavia le difficoltà che caratterizzano la chirurgia esofagea associate all’invasività di queste forme neoplastiche e alla generale tardività della diagnosi comportano una prognosi infausta. Le neoplasie gastriche, anch’esse non frequenti, colpiscono più comunemente il cane rispetto al gatto. Tra i tumori maligni dello stomaco del cane, il carcinoma è il tipo neoplastico più comune, seguito dal linfoma. Nel gatto invece, la maggior parte dei tumori gastrici sono linfomi. La gastroscopia con prelievo di campioni bioptici conduce in gran parte dei casi ad una diagnosi definitiva, anche se in alcuni casi è necessario ricorrere ad una laparotomia esplorativa per ottenere una biopsia a tutto spessore e per una definitiva stadiazione del tumore. Il solo trattamento potenzialmente curativo del tumore gastrico localizzato è quello chirurgico. La chemioterapia è invece indicata per i linfomi, in associazione o meno alla chirurgia. La prognosi dei tumori gastrici maligni è comunque riservata o infausta.

Nel cane e nel gatto la maggior parte delle neoplasie intestinali sono maligne e gli adenocarcinomi ne costituiscono la forma più frequente, seguiti dai linfosarcomi. A seconda del tratto intestinale interessato, la diagnosi definitiva può avvalersi dell’esame endoscopico con prelievo bioptico oppure della biopsia per via laparotomica. Il trattamento di scelta delle neoplasie intestinali non linfoidi è costituito dall’asportazione chirurgica del tumore. Il trattamento del linfoma intestinale si basa invece primariamente sulla chemioterapia e sull’associazione tra chirurgia e chemioterapia. La prognosi è buona per gli adenocarcinomi e i linfomi intestinali localizzati asportati in maniera completa, mentre è riservata o infausta per le forme avanzate o metastatiche.

INTRODUZIONE Il tumore costituisce la principale causa di morte negli animali da affezione.

Da uno studio condotto su 2.000 autopsie canine è emerso che il 23% dei soggetti esaminati era deceduto per tumore, mentre la percentuale saliva al 45% se si consideravano solo i soggetti di età ≥ a 10 anni. Relativamente alle neoplasie gastrointestinali, queste costituiscono il 2% circa di tutte le neoplasie del cane e del gatto e le forme maligne ne rappresentano il 75%. Il tratto maggiormente colpito risulta essere l’intestino ed il tipo istologico più frequente è l’adenocarcinoma, seguito dal linfoma. I soggetti colpiti sono generalmente di età adulta o anziani (da 7 a 10 anni) ed il sesso maggiormente rappresentato, relativamente alla specie canina, è quello maschile, specialmente per quanto concerne adenocarcinomi e linfomi. Nel cane non è stata dimostrata una predisposizione di razza per i tumori GI nel loro complesso, mentre si riconoscono alcune razze maggiormante colpite se si considerano i singoli organi. Nel gatto, la razza

Siamese sembra maggiormente esposta alle forme adenomatose ed adenocarcinomatose intestinali.

I presidi terapeutici che possono essere utilizzati nella lotta contro i tumori sono numerosi tuttavia, per le neoplasie GI, la chirurgia costituisce lo strumento terapeutico essenziale, poichè l’efficacia di chemioterapia (fatta eccezione per i linfomi) e radioterapia per le neoplasie gastrointestinali è scarsa e attualmente poco documentata. Purtroppo la diagnosi di neoplasia GI viene nella maggioranza dei casi posta quando il tumore è in uno stadio avanzato o quando ha già manifestato i suoi effetti sull’ospite; tuttavia la principale causa di insuccesso della terapia chirurgica non è rappresentato da ciò, ma più spesso dalla presenza di metastasi non evidenziabili presenti da prima della diagnosi del tumore primario.

Prima di aggredire chirurgicamente un paziente oncologico è necessario fare delle considerazioni pre-operatorie che riguardano lo stato generale del paziente, il comportamento biologico del tumore, la sua localizzazione ed estensione, la presenza/assenza di metastasi, la qualità della vita e

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l’aspetto dell’animale dopo l’intervento nonchè le implicazioni emotive del proprietario. I pazienti affetti da neoplasia sono spesso soggetti anziani e in scadenti condizioni generali nei quali si possono rilevare alterazioni funzionali a carico di più apparati che possono influire profondamente sull’esito dell’intervento. I principali apparati che influenzano l’incidenza di rischio sono l’apparato cardiovascolare, respiratorio, urinario e digerente (porzione ghiandolare) per cui è sempre d’obbligo ricorrere ad esami collaterali (radiografie di torace e addome, ecografia, elettrocardiogramma, es. emocromocitometrico, es. ematochimici) che forniscano indicazioni sulla loro funzionalità e/o sul loro coinvolgimento al processo neoplastico. Le alterazioni concomitanti, infatti, possono non essere in relazione con la malattia neoplastica (insufficienza renale, epatica o cardiaca), o esserne una conseguenza (disidratazione secondaria al vomito per tumore digestivo, tumori pancreatici, epatici). L’esistenza di una di queste alterazioni concomitanti può aumentare il rischio chirurgico, limitare o escludere il trattamento chirurgico, controindicare una eventuale chemioterapia complementare. Alcuni tumori, inoltre, sono in grado di produrre delle sostanze attive (polipeptidi, ormoni) in grado di causare disordini sistemici non in relazione con il tumore primario o metastatico. Questa condizione, ad oggi ancora poco conosciuta, è nota con il termine di sindrome paraneoplastica e, anche se poche sono le neoplasie GI che la producono (insulinoma, carcinoma epatocellulare ecc.), questa deve essere obbligatoriamente trattata prima dell’intervento chirurgico.

ESOFAGO Le neoplasie esofagee sono rare nel cane e nel gatto, costituendo meno dell’ 1% di tutte le neoplasie maligne e meno del 5% dei tumori maligni dell’apparato gastroenterico.

Le neoplasie metastatiche sono più frequenti rispetto a quelle primarie in questa sede e originano in massima parte per diffusione linfatica di carcinomi gastrici, tiroidei, mammari e broncogenici, oppure da carcinomi squamosi e linfosarcomi. I tumori esofagei del cane più frequentemente osservati sono i sarcomi, in particolare fibrosarcomi e sarcomi osteogenetici secondari a granulomi da Spirocerca lupi, seguiti da carcinomi squamosi, leiomiosarcomi e, raramente, tumori benigni come leiomiomi e papillomi. Nel gatto, il tipo istologico più comune è il carcinoma squamoso, mentre i sarcomi sono estremamente rari. Il carcinoma squamoso colpisce in genere gatti adulti o anziani e non è stata osservata alcuna predisposizione di razza nè di sesso. Il tumore si localizza più frequentemente nel terzo medio dell’esofago, subito caudalmente all’ingresso del torace e nella maggior parte dei casi appare come una proliferazione stenosante della mucosa che circonda il lume esofageo ad anello, a volte con aspetto nodulare ed ulcerato. È una neoplasia localmente invasiva e può metastatizzare ai linfonodi regionali o per via ematogena (polmone, reni, tiroide, milza). Istologicamente è riconoscibile il tipico aspetto del carcinoma a cellule squamose.

I segni clinici associati a tumore esofageo possono insorgere in maniera insidiosa e progredire lentamente e sono in genere rappresentati da rigurgito di materiale solido poco

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dopo l’assunzione del cibo, anoressia, disfagia, dimagramento, alitosi, depressione ed ematemesi. In genere sono segni riconducibili ad ostruzione esofagea e può essere presente anche broncopolmonite ab ingestis. All’eame clinico le neoplasie a carico dell’esofago cervicale possono essere in alcuni casi palpabili e la compressione del collo può provocare deglutizioni ripetute ed eccessive. Gli animali con neoplasie primarie possono essere asintomatici fino a quando la massa diventa sufficientemente voluminosa da produrre segni di ostruzione esofagea.

L’esame radiografico diretto può rivelarsi significativo solo in caso di neoplasia in stadio avanzato. Questa può essere apprezzata sottoforma di area più o meno estesa, talora sporgente nel lume, con radiopacità variabile e non sempre omogenea accompagnata, nei casi più gravi, da ritenzione di aria a monte della neoformazione medesima, con distensione e dilatazione del viscere. Accanto a questi reperti principali possono coesistere alterazioni del decorso della trachea, dell’esofago e possono essere presenti segni di megaesofago. L’esofagografia opaca evidenzia in genere un difetto di riempimento di aspetto polimorfo, a seconda della sede, dell’estensione e del tipo di tumore. Possono essere apprezzate aree di stenosi circoscritte, segmentarie, di aspetto anulare, ispessimenti della parete, formazioni nodulari, alterazioni della mucosa a carattere ulcerativo, turbe della motilità.

Gli studi fluoroscopici possono mostrare anomalie della motilità. I cani con infestazioni da S. lupi sono comunemente affetti da spondilosi deformante accompagnata o meno da osteopatia ipertrofica.

All’esame endoscopico si evidenzia in genere una lesione rilevata, spesso ad anello stenotico, rivestita da mucosa di aspetto nodulare, irregolare e con erosioni ed ulcerazioni più o meno profonde (Fig. 1); più raramente l’infiltrazione può essere diffusa. In questa sede è possibile eseguire prelievi citologici e tissutali della lesione. Occasionalmente è possibile identificare un adulto di S. lupi protrudere nel lume dalla massa esofagea.

I valori ottenuti da esami di laboratorio possono indicare una patologia cronica o una sindrome paraneoplastica. Si possono identificare le uova di S. lupi negli esami del sedimento fecale, ma di solito non sono facili da reperire.

Le opzioni terapeutiche per le neoplasie maligne dell’esofago sono rappresentate dal resezione chirurgica della neoplasia (esofagectomia parziale) ed anastomosi termino-terminale, radioterapia, chemioterapia e misure palliative come dilatazione della stenosi neoplastica e applicazione di protesi esofagee.

Sono state descritte inoltre tecniche di sostituzione esofagea con innesti di digiuno e di colon e muscolo striato.

Idelamente, il tumore dovrebbe essere asportato con ampio margine e il difetto dovrebbe essere riparato con un’anastomosi termimo-terminale. Tuttavia, nella maggior parte dei casi l’avanzato stadio del tumore non consente tale operazione. Inoltre, la chirurgia esofagea è caratterizzata da ben note difficoltà quali la difficile esposizione dell’organo, la sua limitata elasticità longitudinale, la mancanza di uno strato di rivestimento sieroso e la tensione esercitata dal diaframma durante la normale respirazione. Le tecniche di sostituzione esofagea hanno ad oggi unicamente valore sperimentale. Radioterapia e chemioterapia sono raramente state applicate, mentre le misure palliative sono improbabili per

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Gatto, c.e., M, 8a: carcinoma squamoso esofageo

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Gatto, c.e., F(i), 6a: linfosarcoma gastrico

Figura 1

Figura 2

queste forme neoplastiche.

A causa della natura aggressiva di questi tipi neoplastici e delle limitate possibilità terapeutiche disponibili, la prognosi delle neoplasie maligne esofagee è infausta.

all’estensione a livello gastrico di un linfoma multicentrico.

Non sembra esistere una predisposizione di razza o sesso per questo tipo neoplastico. L’età di insorgenza è assai variabile, essendo compresa tra 7 mesi e 14 anni. In linea generale, il linfoma gastrico colpisce cani più giovani rispetto al più frequente carcinoma.

I segni clinici sono in genere costituiti da vomito, accompagnato da diarrea nelle forme diffuse di linfoma, dimagramento, anoressia, letargia. La perforazione del tumore si verifica più frequentemente nel linfoma che nel carcinoma e può causare segni di peritonite ed addome acuto.

L’esame clinico può rilevare un soggetto con segni di debilitazione cronica oppure in condizioni discrete. La palpazione dell’addome spesso non è rilevante, ma in caso di linfoma alimentare è possibile palpare la presenza di una o più masse riferibili al tumore gastrico o più facilmente al coinvolgimento neoplastico dell’intestino o dei linfonodi addominali. Il pallore delle mucose può essere secondario ad emorragia gastrica o ad anemia conseguente ad interessamento del midollo osseo da parte del linfoma.

Gli esami emocromocitometrico ed ematochimico possono riflettere le alterazioni secondarie al vomito e all’eventuale emorragia gastrica oppure la diffusione sistemica del linfoma. L’esame radiografico diretto può evidenziare la presenza di masse in uno o più tratti dell’apparato gastroenterico, l’aumento di volume dei linfonodi addominali e l’eventuale interessamento metastatico di altri organi (fegato, rene, ecc.). L’esame contrastografico ha un maggiore sensibilità diagnostica nell’evidenziare la localizzazione intraluminale delle lesioni neoplastiche gastrointestinali.

L’esame endoscopico è fondamentale per la diagnosi di neoplasie dell’apparato gastroenterico superiore, consentendo la visualizzazione diretta della sede e dell’estensione del tumore (Fig. 2) ed il prelievo di campioni citologici e bioptici: questi ultimi devono essere multipli e profondi, poiché il linfoma alimentare in stadio iniziale ha in genere una localizzazione sottomucosa ed è spesso accompagnato da intensa flogosi linfocitico-plasmacitica.

Il prelievo di campioni citologici o bioptici può essere effettuato anche mediante ago-aspirazione percutanea “alla cieca” o ecoguidata delle masse addominali palpabili, oppu-

STOMACO Tra gli animali domestici, il cane è la specie che più comunemente sviluppa tumori gastrici spontanei, anche se in misura minore rispetto all’uomo. Nel gatto, le neoplasie gastriche sono estremamente rare.

Nel cane, le neoplasie benigne sono più frequenti di quelle maligne e tra le prime, le più comuni sono i leiomiomi, seguite dai polipi e assai raramente da lipomi e fibromi. I leiomiomi sono tumori che originano dallo strato muscolare liscio della parete gastrica originando masse sottomucose che possono causare, se localizzate in corrispondenza dell’antro o del piloro, ritardato svuotamento gastrico. Si riscontrano nei cani molto anziani (età media = 15 anni) e spesso sono asintomatici. I polipi gastrici sono in gran parte costituiti da polipi iperplastici o adenomatosi e costituiscono spesso reperto occasionale in sede endoscopica o necroscopica.

A volte invece, soprattutto quando localizzati in sede antro-pliorica, possono divenire sintomatici. La trasformazione maligna dei polipi, che è stata suggerita per i polipi rettali, non è provata per quelli gastrici.

L’incidenza dei tumori gastrici maligni, in accordo con quanto descritto da Head nel 1990, è inferiore all’ 1% di tutti i tumori del cane.

Tra i tumori maligni dello stomaco del cane, il carcinoma è il tipo neoplastico più comune (47-76%), seguito dal linfoma (5-7%) e, in misura assai minore, da leiomiosarcoma e fibrosarcoma. Nel gatto invece, la maggior parte dei tumori gastrici sono linfomi e raramente sono confinati al solo stomaco.

Il linfoma gastrico nel cane può apparire come forma gastrica solitaria oppure essere parte di una forma di linfoma alimentare multifocale o diffuso, con estensione ad altri tratti dell’apparato gastroenterico. Può inoltre essere secondario

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re per via laparotomica o laparoscopica.

Anche per il linfoma alimentare, come per gli altri tipi di linfoma, la stadiazione del tumore è importante a fini prognostici e terapeutici.

Il trattamento del linfoma gastrico differisce per le forme localizzate e per quelle diffuse. Nel primo caso infatti è in genere consigliabile effettuare l’escissione chirurgica del tumore seguita da chemioterapia. Nelle forme diffuse o con diffusione metastatica a più linfonodi o visceri e nelle forme divenute sistemiche, il trattamento è principalmente chemioterapico. Numerosi sono i protocolli chemioterapici disponibili, anche se è segnalata una sensibilità minore alla chemioterapia del linfoma alimentare rispetto ad altre forme di linfoma.

La prognosi è migliore per le forme localizzate di linfoma trattate con escissione chirurgica seguita da chemioterapia.

Il carcinoma gastrico colpisce soggetti di età compresa tra 3 e i 15 anni, con un incidenza massima a 9 anni e un rapporto maschi/femmine di 3:1. Sono state segnalate predisposizioni di razza per il Cairn Terrier e il West Highland White Terrier, per il Rough Collie e lo Stafford Shire Terrier e per il Pastore Belga. Da un punto di vista anatomopatologico, i quattro principali tipi di carcinoma gastrico sono, in ordine di frequenza, il tipo ulcerativo, quello infiltrativo, il tipo vegetante e la forma polipoide.

I tumori ulcerativi sono i più frequenti e di solito si localizzano a livello dell’antro o della piccola curva dello stomaco; sono caratterizzati da margini irregolari con bordi rilevati e il tessuto circostante è di consistenza aumentata, irregolare ed infiltrato. L’ulcera ha un fondo necrotico, rugoso e spesso nodulare; le pliche mucose che si dipartono dal cratere dell’ulcera, non hanno un aspetto regolare come nell’ulcera peptica. Le ulcere neoplastiche tendono ad essere più estese di quelle non neoplastiche.

Nella forma infiltrativa, la diffusione del tumore interessa di solito l’intero spessore della parete dello stomaco, frequentemente a partenza da un’area limitata della regione pilorica.

Le forme vegetante e polipoide si riscontrano più raramente. La prima è caratterizzata da una proliferazione irregolare della mucosa, a margini non definiti e aggettante nel lume gastrico. La seconda è rappresentata da forme sessili a larga base di impianto, rivestite da mucosa adesa ai piani sottostanti e di aspetto irregolare o morulato.

Sebbene il tumore sia in genere esteso al momento della diagnosi, in gran parte dei casi è localizzato ai due terzi distali dello stomaco. La più comune localizzazione è quella antro-pilorica con estensione al corpo, di solito lungo la piccola curva. La seconda localizzazione è quella primaria a livello di corpo gastrico, più frequentemente a livello di piccola piuttosto che di grande curva; raramente il tumore è localizzato presso la regione cardiale. L’interessamento di tutto lo stomaco è possibile, ma si riscontra raramente.

I carcinomi gastrici possono metastatizzare per diffusione locale oppure attraverso la via linfatica, ematica o per disseminazione transperitoneale.

Dal punto di vista istologico e secondo la classificazione redatta dal WHO, i tumori epiteliali maligni dello stomaco comprendono adenocarcinomi di tipo papillare, tubulare, mucinoso, con cellule ad anello con castone e carcinomi indifferenziati.

Come per altri tumori, anche per il carcinoma gastrico è

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essenziale effettuare un’accurata stadiazione del tumore, al fine di emettere un giudizio prognostico e stimare la possibile risposta al trattamento.

I segni clinici di carcinoma gastrico nel cane come nell’uomo, non sono specifici ed è per questa ragione che in molti pazienti la diagnosi è tardiva, cioè ad uno stadio avanzato di malattia. Tuttavia, i sintomi più frequentemente osservabili sono riferibili ad una progressiva alterazione della funzionalità gastrica, quali vomito variabilmente associato a ematemesi o a melena in caso di ulcerazione del tumore, ed altri segni meno specifici come perdita di peso, anoressia, anemia, dolore addominale, disidratazione. Occasionalmente possono essere evidenti sintomi associati alla diffusione di metastasi a livello epatico, come ittero, ascite e masse addominali.

L’anamnesi più comune in un paziente con tumore gastrico evidenzia l’insorgenza di vomito intermittente incoercibile, in genere non associato all’assunzione di alimento, contenente spesso sangue parzialmente digerito di aspetto simile al fondo di caffè. I segni clinici insorgono improvvisamente, a volte in modo drammatico e sono spesso associati ad anoressia.

In alcuni pazienti i sintomi possono suggerire la presenza di lesioni in zone ben precise. Un’anamnesi di disfagia può indicare un tumore localizzato al cardias che si estende attraverso la giunzione gatroesofagea. Il vomito di materiale alimentare parzialmente indigerito a distanza di alcune ore dal pasto (3-12) può essere compatibile con un carcinoma antrale che ostruisce il piloro. La presenza di melena può indicare l’ulcerazione del tumore.

All’esame clinico il paziente può mostrarsi mediamente letargico, disidratato, dimagrito e con pelo opaco e/o furfuraceo. La palpazione addominale spesso non è significativa ma in alcuni casi è possibile evocare dolore addominale nel comparto craniale o apprezzare una massa a livello gastrico.

Ascite, ittero o disturbi respiratori possono essere la conseguenza di metastasi in altri organi.

I dati di laboratorio non sono generalmente diagnostici; il reperto di leucocitosi e anemia ipocromica microcitica è comune in caso di forme ulcerative. È possibile osservare alterazioni dei valori biochimici del siero in caso di metastasi sistemiche.

L’esame delle feci può essere utile per valutare la presenza di sangue occulto in caso di anemia inspiegabile.

In seguito ad esame clinico, l’indagine radiografica costituisce il primo passo per la diagnosi di tumore gastrico.

L’esame radiografico diretto normalmente non è diagnostico, tuttavia nel caso di una forma molto estesa può mettere in evidenza una massa o l’ispessimento della parete gastrica.

Lo studio contrastografico è invece molto utile per la diagnosi di lesioni gastriche. I caratteri che devono essere indagati in radiogrammi multipli sono l’ispessimento e la rigidità della parete gastrica, la distorsione del lume gastrico e il sovvertimento delle pliche mucose, difetti di riempimento, ulcere e marcato ritardo di svuotamento gastrico con ritenzione di mezzo di contrasto.

L’esame radiografico è anche utile nella ricerca di metastasi sistemiche e deve comprendere uno studio del torace.

Altra tecnica d’indagine utile per l’identificazione dei tumori gastrici è l’ultrasonografia, che consente di evidenziare in maniera non invasiva una massa o un aumento di spessore della parete gastrica e l’estensione o metastatizzazione

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Cane, siberian husky, M, 8a: AC gastrico (p.c.)

Figura 3

a livello linfonodale, mesenterico, peritoneale e epatico.

La tomografia assiale, quando disponibile, permette un accurata stadiazione del grado di estensione del tumore primario e una completa valutazione dello stato dei linfonodi nonché l’identificazione di metastasi sistemiche.

L’endoscopia è la metodica diagnostica non invasiva di elezione per la diagnosi di tumore gastrico. Essa consente infatti la visualizzazione diretta delle lesioni che, ad un occhio esperto, sono spesso suggestive di malignità. È possibile inoltre valutare dimensioni, localizzazione e morfologia del tumore, inclusa l’estensione in senso prossimale e/o distale (di rilevante valore prognostico), nonchè eventuali alterazioni della mucosa associate (Fig. 3). Fondamentale è comunque effettuare biopsie multiple mirate o prelievi citologici mediante spazzolamento della lesione. L’esame istologico dei campioni bioptici perendoscopici è uno degli strumenti più attendibili per confermare la diagnosi di carcinoma gastrico. È tuttavia possibile incorrere in falsi negativi quando il tumore gastrico si sviluppa negli strati più profondi della parete gastrica, con scarso interessamento della mucosa; in questo caso la biopsia endoscopica può rivelarsi troppo superficiale per consentire una diagnosi di tumore gastrico.

In accordo con la classificazione usata in endoscopia umana, i tumori gastrici possono essere raggruppati in cinque principali tipi: tumore polipoide, ulcerativo, esofiticoulcerativo, infiltrativo e avanzato non classificabile.

Forma polipoide: tumore proliferativo di forma irregolare, a volte con aspetto polipoide.

Forma ulcerativa: ulcera neoplastica caratterizzata da margini indistinti rilevati nodulari e irregolari con mucosa friabile e sanguinante e una base necrotica.

Forma esofitico-ulcerativa: tumore ulcerato con margini non definiti a causa dell’ infiltrazione delle zone circostanti.

Forma infiltrativa: in questo caso il tumore interessa tutto lo stomaco, alterando il lume e la forma dell’organo. La consistenza della parete gastrica è notevolmente aumentata e l’organo appare rigido e ligneo. La plicatura gastrica è ridot-

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ta ed irregolare, la mucosa perde la sua normale lucentezza e diventa friabile e facilmente sanguinante.

Forma avanzata non classificabile: l’architettura dello stomaco è gravemente compromessa, la mucosa gastrica appare biancastra, proliferante e irregolare con aree emorragiche e necrotiche frammiste. Sono anche presenti erosioni e ulcere di diversa dimensione e profondità.

Il solo trattamento potenzialmente curativo del tumore gastrico localizzato e in assenza di metastasi a distanza è quello chirurgico, che può prolungare il tempo di sopravvivenza di mesi. In alcuni casi può essere giustificabile anche il trattamento chirurgico palliativo, finalizzato alla temporanea risoluzione dell’ostruzione gastrica indotta dal tumore.

Un tumore gastrico dovrebbe essere asportato mediante una resezione gastrica ampia che includa margini di tessuto sano di almeno 1-2 cm, ovvero tramite resezioni segmentarie o gastrectomia parziale. In molti casi ciò è reso impossibile dall’estensione e dalla sede del tumore. Poichè la maggior parte dei tumori coinvolge la regione antro-pilorica, la chirurgia comporta spesso l’asportazione del piloro, seguita da una anastomosi gastro-intestinale.

La chemioterapia trova applicazione soprattutto per il trattamento dei linfomi. Sebbene ci siano numerose segnalazioni di risposte positive alla chemioterapia del carcinoma gastrico dell’uomo, nel cane non sembra tuttavia essere efficace per questo tipo neoplastico.

La radioterapia trova scarsa applicazione perchè i tessuti sani viciniori, come il fegato e l’intestino, poco tollerano gli effetti dannosi dell’irradiazione.

La prognosi per i tumori gastrici maligni è estremamente riservata. L’esito poco favorevole riflette lo stadio avanzato del tumore al momento della diagnosi, la difficoltà di garantire un ampio margine di resezione chirurgica, nonché l’elevato potenziale metastatico di questi tumori.

A fronte di numerose descrizioni di lunghe sopravvivenze in singoli soggetti dopo trattamento chirurgico, esistono pochi studi che considerano la sopravvivenza a lungo termine. L’intervento palliativo di ricanalizzazione può consentire sopravvivenze comprese tra uno e sei mesi di vita. In caso di chirurgia curativa, il tempo di sopravvivenza totale è compreso tra sei mesi e cinque anni.

INTESTINO Nel cane e nel gatto la maggior parte delle neoplasie intestinali sono maligne e gli adenocarcinomi ne costituiscono la forma più frequente, seguiti dai linfosarcomi. Neoplasie meno frequenti sono leiomiosarcomi, leiomiomi fibrosarcomi, mastocitomi, emangiosarcomi, sarcomi anaplastici, carcinoidi, plasmocitomi, neurolennomi. Tra i tumori benigni, i polipi adenomatosi si riscontrano soprattutto nel duodeno del gatto e nel retto del cane. I soggetti colpiti sono in genere anziani con età media che varia tra gli 11 e i 12 anni, anche se quelli colpiti da linfoma sono più giovani. Non è stata segnalata una predisposizione di razza, anche se nel gatto la razza siamese sembra maggiormente esposta a sviluppare adenocarcinomi intestinali. Nel cane il sesso maschile sembra maggiormente predisposto per lo sviluppo di adenocarcinomi e linfomi mentre nel gatto questa predisposizione non sembra evidente. Nel ca-

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Cane, PT, M, 9a: AC retto con infiltrazione della sierosa

Gatto, persiano, M(c), 6a: linfosarcoma retto

Figura 5 Figura 4

ne i tumori intestinali sono più frequenti nel colon e nel retto, mentre nel gatto compaiono più spesso nell’intestino tenue.

I tumori intestinali possono causare ostruzione meccanica intramurale o endoluminale poiché invadono più comunemente lo strato muscolare della parete intestinale dove compromettono il diametro del lume e ne riducono la capacità di distensione. La porzione di intestino prossimale si può dilatare per accumulo di fluidi e gas con compromissione della sua funzionalità tale da simulare un’occlusione da corpo estraneo. Spesso, al momento della diagnosi la neoplasia si trova già in stadio avanzato ed ha prodotto delle lesioni metastatiche.

Gli adenocarcinomi sono localmente invasivi e a lenta crescita. Insorgono prevalentemente nel duodeno e nel colon nel cane e nel digiuno distale e ileo nel gatto. Si possono distinguere tre varietà morfologiche: - adenocarcinomi infiltranti che si manifestano come un’area stenotica ispessita che ostruisce il lume intestinale; - adenocarcinomi ulcerativi che producono ulcere della mucosa profonde e indurite con margini rilevati; - adenocarcinomi proliferativi che sono masse endoluminali espansive e lobulate.

L’ulcerazione della mucosa può provocare melena e anemia da carenza di ferro. Questi tumori si diffondono alle adiacenti superfici sierose (Fig. 4), al mesentere, all’omento e ai linfonodi regionali per invasione locale e possono metastatizzare a distanza (polmoni, fegato).

Il linfosarcoma gastrointestinale del cane e del gatto può colpire primariamente questa sede oppure essere parte della forma multicentrica di linfoma. Nel gatto può essere causato dal virus FeLV o FIV, anche se il 20-30% dei gatti colpiti da linfoma GI risultano negativi al test ELISA per la leucemia felina. La neoplasia può presentarsi in forma diffusa o nodulare. Nella prima l’infiltrazione diffusa della lamina propria e della sottomucosa da parte dei linfociti neoplastici provoca malassorbimento e occasionalmente ulcerazioni profonde. La forma nodulare è caratterizzata invece da una massa intestinale espansiva che determina occlusione e che

si verifica spesso nella regione ileocolica. È comune l’interessamento dei linfonodi regionali e di altri organi.

I segni clinici sono incostanti ed aspecifici e rendono spesso questi tumori difficili da differenziare da affezioni non neoplastiche. Essi sono rappresentati da depressione, anoressia, letargia, diarrea e/o vomito, perdita di peso progressiva. I sintomi possono in alcuni casi indirizzare il clinico verso una sede specifica del tratto intestinale. Per esempio, il vomito è più frequentemente associato a tumori del duodeno o del digiuno, mentre dimagramento e diarrea si osservano più spesso qunado sono coinvolti digiuno e ileo. Tenesmo e ematochezia sono più frequenti in presenza di tumori del colon e retto. Altri segni clinici possono comprendere disidratazione, melena, ematemesi, anemia, febbre, ittero e/o versamento addominale. Possono anche comparire segni di occlusione intestinale, di ascessualizzazione e di malassorbimento. L’ostruzione dei vasi linfatici può provocare steatorrea dovuta a linfangectasia. Secondariamente a diffusione metastatica si possono sviluppare segni che interessano altri organi.

La diagnosi, oltre che sull’esame clinico, si basa sull’esame radiografico, endoscopico, ecografico e sull’esplorazione chirurgica della cavità addominale. La palpazione addominale può rivelare la presenza di una massa dura, soprattutto quando la neoplasia colpisce le porzioni prossimali del piccolo intestino, di anse intestinali ispessite o di linfoadenopatia meseraica. L’esplorazione del retto può rivelare la presenza di una massa spesso peduncolata, di una stenosi o di irregolarità della parete rettale. Gli esami ematologici ed ematochimici sono in genere poco significativi e possono evidenziare anemia, leucocitosi neutrofila con spostamento a sinistra della formula, trombocitopenia, ipoalbuminemia o concentrazioni elevate di enzimi epatici. In alcune forme di linfosarcoma sono evidenti disordini linfoproliferativi. L’esame radiografico diretto dell’addome può evidenziare delle masse, un’anomala distribuzione del comparto gas/fluido, dislocazione di visceri e la presenza di liquido addominale. I radiogrammi con mezzo di contrasto sono utili per delineare aree di irregolarità della mucosa intestinale, restringimenti del lume, infiltrazioni intramurali, ispessimenti o noduli. L’esame ecografico addominale spesso mette in evidenzia la massa, facilitandone inoltre il prelievo

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Cane, PT, M, 10a: AC retto-colico

Gatto, meticcio, M, 8a: AC polipoide retto

Figura 6

Figura 7

bioptico percutaneo. I tumori intestinali producono un’ampia varietà di quadri ecografici. Si possono riconoscere ispessimenti della parete e perdita della distinzione tra i diversi strati parietali, oppure l’intestino può apparire normale. Sono inoltre osservabili ileo, accumulo di liquido e linfoadenopatie. L’ultrasonografia è inoltre il presidio diagnostico elettivo per la stadiazione dei tumori intestinale del cane.

Endoscopicamente si possono identificare masse (Fig. 5), irregolarità della mucosa (Fig. 6), infiammazione, ulcerazioni, restringimento del lume, presenza di polipi (Fig. 7).

L’esecuzione di prelievi bioptici endoscopici della mucosa e della parete o di una polipectomia sono fondamentali ai fini diagnostici, con l’accorgimento di eseguire prelievi multipli e profondi per ridurre il rischio di esiti falsi negativi in presenza di lesioni sottomucosali o accompagnate da intensa flogosi. La diagnosi delle neoplasie del piccolo intestino spesso richiede una biopsia per via laparotomica.

Il trattamento di scelta delle neoplasie intestinali non linfoidi è costituito dall’asportazione chirurgica del tumore.

La chemioterapia, sia come trattamento primario che come adiuvante alla chiurgia, ha dato risposte incostanti e di scarso significato clinico per questi tipi neoplastici. Spesso la resezione completa è impedita dall’avanzato stadio di diffusione del tumore o dalla presenza di metastasi; in quest’ultimo caso la resezione chirurgica può essere palliativa.

Il trattamento del linfoma intestinale si basa invece primariamente sulla chemioterapia e sull’associazione tra chirurgia e chemioterapia, in base alla forma anatomica (nodulare vs. diffuso) e alla diffusione del tumore.

I protocolli chemioterapici esistenti sono numerosi; tra i più noti sono il COAP, il CHOP e l’LMP. La terapia radiante è stata utilizzata primariamente per gli adenocarcinomi rettali con risultati incoraggianti.

La prognosi è in genere eccellente per le forme benigne e per i polipi adenomatosi asportati in maniera completa.

Nei pazienti in cui è possibile la resezione completa di un adenocarcinoma intestinale localizzato la prognosi è buona, mentre è riservata o infausta per le forme avanzate o metastatiche data la scarsa o nulla efficacia dei presidi terapeutici adiuvanti (chemioterapia e radioterapia). I gatti con adenocarcinoma intestinale possono sopravvivere più di 2 anni dopo l’intervento chirurgico. Indicativamente, gli adenocarcinomi polipoidi peduncolati sono caratterizzati da una prognosi migliore rispetto alle forme diffuse o anulari. Anche i linfomi localizzati del piccolo intestino presentano una prognosi migliore rispetto alle forme diffuse. Le lesioni linfomatose a carico del colon e del retto sembrano invece essere caratterizzate da un carattere biologico più benigno, sia in termini di risposta alla chemioterapia che in termini di tempi di sopravvivenza.

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Gualtieri M, Monzeglio M.G., Scanziani E.: Gastric Neoplasia. In Progress in Gastroenterology Vet. Clin.of North Am. S.A.P. 29:2, 415-440, 1999.

Fonda D.; Gualtieri M.; Scanziani E.: Gastric carcinoma in the dog: A clinicopathological study of 11 cases. Jour. of Small Anim. Pract.

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Scanziani E.; Giusti A.; Gualtieri M.; Fonda D.: Gastric carcinoma in the belgian shepherd dog. Jour. of Small Anim. Prac. 32, 465-469, 1991.

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Physical Examination of the Cardiopulmonary Systems Esame fisico dell’apparato cardiovascolare

Robert L. Hamlin DVM, The Ohio State University - Columbus - Ohio, USA

Riassunto L’esame clinico del cuore e dei polmoni, effettuato mediante ispezione, auscultazione, percussione e palpazione del torace, delle arterie e delle vene periferiche può, nella maggior parte dei casi, consentire la formulazione di una diagnosi corretta o, almeno, lo sviluppo di un ragionevole elenco di possibili diagnosi differenziali. Per apprendere queste tecniche è necessario seguire per un adeguato periodo di tempo qualcuno già esperto nell’impiego di questi metodi, ma si tratta di un impegno che ricompenserà ampiamente il veterinario, i suoi clienti ed i suoi pazienti. Vengono riassunte le possibili diagnosi differenziali delle più comuni ed importanti alterazioni cardiopolmonari: versamento pleurico: dispnea, murmure vescicolare attutito o assente, suono ottuso alla percussione; pneumotorace: dispnea, murmure vescicolare attutito o assente, suono iper-risonante alla percussione; edema polmonare: dispnea, murmure vescicolare più forte del normale, suono ottuso alla percussione, rantoli alla fine dell’espirazione e nella fase intermedia dell’inspirazione, cianosi di breve durata; fibrosi polmonare/pneumopatia cronica ostruttiva (COPD): dispnea, rantoli eccezionalmente forti, cianosi cronica; pneumopatia cronica: peso corporeo normale o aumentato, frequenza cardiaca normale o esagerata aritmia sinusale respiratoria, polso arterioso normale, riflusso epato-giugulare, cardiomegalia destra, epatomegalia; insufficienza cardiaca: peso corporeo diminuito, aritmia sinusale ridotta, polso arterioso debole o vibrante, cardiomegalia sinistra, ritmo di galoppo.

Physical examination of the heart and lungs, using inspection, auscultation, percussion and palpation of the thorax, peripheral arteries and peripheral veins, can most often permit a correct diagnosis or at least to develop a reasonable list for differential diagnosis. It requires that the veterinarian devote time under the tutelage of a person experienced in these methods, but the rewards to the veterinarian, client and patient are rich. The differential diagnosis for common and important cardiopulmonary defects is summarized: pleural effusion: dyspnea, soft or absent vesicular breath sounds, dull note of percussion, pneumothorax: dyspnea, soft or absent vesicular breath sounds, hyper-resonant note of percussion, pulmonary edema: dyspnea, louder than normal vesicular breath sounds, dull note of percussion, end-expiratory and mid-inspiratory crackles, short-lived cyanosis, pulmonary fibrosis/COPD:dyspnea, exceptionally loud crackles, chronic cyanosis, chronic pulmonary disease: normal to increased body weight, normal heart rate to exaggerated respiratory sinus arrhythmia, normal arterial pulses, hepato-jugular reflux, right-sided cardiomegaly, hepatomegaly, heart failure: reduced body weight, reduced sinus arrhythmia, feeble or sharp-tapping arterial pulses, left-sided cardiomegaly, gallop sound

Introduction: This session will discuss how inspection, auscultation, percussion and palpation can result in a correct diagnosis, and selection of appropriate therapy, in the majority of cardiopulmonary diseases of dogs and cats. This methodology is accurate, inexpensive, repeatable, noninvasive and enjoyable; but it requires considerable experience.

Because of time constraints, examples of a few specific, common cardiopulmonary diseases will be presented. All patients will be presented with shortness-of-breath, hereafter called dyspnea. They may have pleural effusion, pulmonary edema, pneumothorax, or chronic obstructive pulmonary disease (COPD) with pulmonary fibrosis. Differentiation

will be based upon amplitude and distribution of vesicular breath sounds, types and distribution of adventitious breath sounds (i.e. rales and rhonchi), notes of percussion and their distributions, heart rate and rhythm, and character of arterial and venous pressure pulses.

Pleural effusion: This entity consists of fluid—usually a modified transudate—occupying space between the visceral and parietal pleura. It occurs most often in cats with cardiomyopathy, but may be neoplastic in origin. Patients with pleural effusion are usually tachypneic (i.e. breath too rapidly) in addition to being dyspneic. Rapidity of respiration is

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determined with difficulty in the veterinarian’s office, because most animals are excited and therefore breath more rapidly than normal. Dogs, cats and humans—at rest—usually breath fewer than 20 times per minute. The client, in the the peace and quiet of his/her home—can usually obtain a more correct respiratory rate by counting them while the pet sleeps or rests comfortably. Inspiratory vesicular breath sounds produced by air tumbling through the large airways (e.g. larynx, trachea, mainstem bronchi) are usually softer than normal over the region affected by the effusion. This attenuation of the vesicular breath sound occurs for two reasons. First the lung into which the turbulent air flows is displaced from where auscultation is performed, and secondly the sound transmitted through the lungs is reflected (i.e. not transmitted) by the air-water interface. A rule of thumb is: Always put a needle into the thorax—that is perform a pleurocentesis—where there is an absence of vesicular breath sounds. In addition, a note of percussion over a pleural effusion is usually duller than normal, since a dense structure resounds with a rather short, highpitched note interpreted as dullness.

Pneumothorax: This entity consists of air occupying space between the visceral and parietal pleura. It occurs most commonly from trauma, but may occur because of lung disease. As with pleural effusion the patient breaths rapidly and with dyspnea. As with pleural effusion patients with pneumothorax have diminished vesicular breath sounds over regions of the afflicted pleural space. This occurs for two reasons. First the lung is collapsed away from the region of auscultation, and second the vesicular breath sound transmitted through the lung is not transmitted well through the air-filled pleural space. Of course the same rule of thumb is applied, that is, put a needle into the thorax where there is an absence of a vesicular breath sound. But contrary to the note of percussion for pleural effusion, the note of percussion over the air-filled pleural cavity is hyper-resonant, that is it sounds like a tympani drum, because an air-filled structure resounds for a relatively long time at at a low frequency.

Thus, although both pleural effusion and pneumothorax have have absence of vesicular breath sounds and the patients are tachypneic, they may be separated easily by notes of percussion.

Pulmonary edema: This entity occurs when fluid oozes from the pulmonary capillaries into the interstices of the lungs faster than the pulmonary lymphatics can return it to the blood. It occurs most commonly with left-sided congestive heart failure, but occurs rarely with electric shock or head trauma. Like pleural effusion and pneumothorax the patient with pulmonary edema is usually tachypneic. However because a wet, dense lung transmits sound better than a normal lung, the vesicular breath sounds are louder than expected. They are termed bronchial or bronchovesicular breath sounds when they are louder than expected. How do you know what is louder than expected? Answer...by auscultating and percussing every possible normal dog or cat! A second rule of thumb is, under no circumstances should as needle be put into the chest of a patient with louder than expected vesicular breath sounds. They are usually caused by engorgement of pulmonary vessels which, if stuck with a

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needle, will cause hemorrhage into the thorax. The breath sounds of pneumonia are identical with those of pulmonary edema, but of course is observed much less commonly than edema. It usually occurs in younger patients without previous indication of heart disease. In addition to the bronchial breath sounds and tachypnea, patients with pulmonary edema also have dull notes of percussion due to the wet, dense lung; and most often have crackles (rales) caused by airways “scrunching” closed at end expiration and popping open during mid-inspiration. Crackles are not caused by bubbles exploding, rather they are caused by airways closing and opening. The crackles of edema and pneumonia are usually soft and quiet, in contradistinction to the loud, “ugly” crackles of COPD/pulmonary fibrosis. If the edema and airways closure are severe, patients may have cyanosis. Cyanosis is caused by too little oxygenated hemoglobin in the arterial blood, because the pulmonary blood flows through poorly ventilated regions of the lung and therefore pick-up little or no oxygen.

COPD/pulmonary fibrosis: Patients afflicted with this pulmonary disease may be just as dyspneic—or more so—as the patients discussed previously. However these patients will most often be of normal weight or obese, they usually have long-standing cyanosis, and their crackles are loud and “ugly”. Their crackles arise from fibrotic, emphysematous, bronchitic regions of the lung being “scrunched” closed during expiration and then popping open during inspiration.

Whereas crackles or pulmonary edema may be mimicked by auscultating am unwrapped loaf of white bread as you squeeze it, crackles of COPD/fibrosis may be mimicked by auscultating the wrapper of the bread as you squeeze it. Most patients ill from heart disease will have rapid heart rates, absence of respiratory sinus arrhythmia (speeding of the heart rate during inspiration and slowing during expiration), and feeble arterial pulses; whereas patients with COPD/fibrosis will most often have exaggerated respiratory sinus arrhythmias and strong arterial pulses. The cyanosis in animals with COPD/fibrosis persists because regions of the lung remain poorly ventilated since there is no method for expanding them. Patients with cyanosis from heart failure either improve with diuretics or die—therefore the cyanosis is shortlived.

Differentiating a patient ill from heart disease from one ill from pulmonary disease— This differentiation may be difficult since patients with diseases of either organ system share many symptoms and signs. They are dyspneic, they may be cyanotic, and they may have murmurs. However patients ill from lung disease usually have abundant fat, rightsided enlargement, flat diaphragms, small lungs, and pulmonary retraction (a caving in of the thoracic wall near the diaphragm) of thoracic radiographs, and their electrocardiograms have peak P-waves and often deep S-waves in leads I and aVF. Patients ill from heart disease are usually skinny, have left-sided cardiomegaly and large lungs on thoracic radiographs, and their electrocardiograms have broad P-waves and high voltage R-waves in leads II and aVF. Definitive diagnosis often requires X-ray and ECHO, but the physical examination, alone, will often generate a clinical outcome little different from that generated by more elaborate, expen-

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sive and invasive methods.

HEART SOUNDS AND MURMURS Most cardiovascular diseases can be diagnosed by auscultation of heart sounds and murmurs. Sounds and murmurs occur when structures in the chest oscillate at a frequency (between 60 and 500 cycles/second [Hz]) and intensity (greater than 15 decibels) which can be heard by the human ear. Sounds, rather short periods of oscillations, are produced either by rapid deceleration of volumes of blood either in the ventricles (as with the 1st heart sound) or in the aorta and pulmonary trunk (as with the 2nd heart sound).

Murmurs are relatively long sounds—actually pseudosound—that are transmitted in the direction blood flows; and murmurs are usually produced by blood flow in turbulence because of high velocity. Heart sounds are channeled best with a stethoscope which has a chest piece placed on the thorax, two tubes conducting sound from the chest piece, and ear pieces that fit snugly into the external ear canal.

The bell chest piece transmits all cardiac sounds with only minimal attenuation. The diaphragm attenuates low pitched sounds, therefore it appears that high frequency sounds are amplified—which they are not. Most murmurs and the 2nd heart sound are comprised of high-pitched sounds, therefore they may be heard best using the diaphragm. The 1st heart sound and gallops (the 3rd and 4th heart sounds) are low pitched and are usually heard best with the bell chest piece.

In general heart sounds are heard best closest to the chamber whose oscillations produces them, but murmurs are heard best either in the direction of high velocity, turbulent blood flow or close to a relatively dense structure (e.g. bone) that might couple the murmur to the place on the thorax where the stethoscope is placed. For example, the 1st heart sound (Lub) is produced predominantly by oscillations of the left ventricle when the blood within is suddenly prevented from reentering the left atrium by closure of the leaflets of the mitral valve. Since the left ventricle almost touches the thoracic wall at the left 5th or 6th intercostal space near the sternum (at the left apex), the 1st heart sound is heard best at that point. The 2nd heart sound

(dup) is produced predominantly by oscillations of the ascending aorta when the blood within is suddenly prevented from reentering the left ventricle by closure of the leaflets of the aortic valve. It is heard best at the left base—at the 2nd or 3rd intecostal space 1/3 of the ventrodorsal distance from the sternum.

The period between the Lub and the dup is termed systole—the period of ventricular contraction; while the period between dup and the next Lub is termed diastole—the period of ventricular relaxation. Whenever the ventricles are stiffer than normal—as is caused by chronic stretch, hypertrophy, or oxygen deprivation—there is often a 3rd heart sound (uh) that appears slightly after the 2nd, and a 4th heart sound (ba) that appears just before the 1st. The 3rd and 4th sounds occur in diastole, and they are termed gallops in the presence of disease. When all 4 heart sounds are heard it sounds like: ba-Lub dup-uh, ba-Lub dup-uh. The 3rd heart sound occurs in early diastole in the wake of rapid ventricular filling immediately after the aortic and pulmonic valves close. These valves will close more rapidly when blood enters the ventricle more rapidly due to high venous pressure seen with heart failure. Since the 4th heart sound occurs in the wake of atrial contraction, unless the atria contract vigorously, the 4th heart sound will not be heard. Of course with atrial fibrillation when the atria do not beat, there can be no 4th heart sound.

During inspiration, the heart rate speeds, and during expiration the heart rate slows. Although difficult to hear, during inspiration the 2nd heart sound actually splits (du-dup).

This is caused by the aortic valve closing before the pulmonic valve closes. Thus one might hear: ba-Lub da-dup-uh There are 7 murmurs—or combinations—that are important. They are classified (1) by when they occur (i.e. systole, diastole, both systole and diastole, continuously), (2) by how long they occur (e.g. ejection type are relatively short and build-up and fall-down in intensity, regurgitant type are relatively long and uniform in intensity), (3) by how intense they are (i.e. I/vi is the softest, vi/vi is the loudest), and (4) by their character (i.e. harsh, blowing). Below are found 7 murmurs and 2 gallops typical of common and important

heart diseases: Lesion

Heard Best

When

Length

Intensity

pulmonic stenosis

left base

systole

ejection

iv/vi

aortic stenosis

left and right base

systole

ejection

ii-iv/vi

mitral regurgitation

left apex

systole

regurgitant

I-vi/vi

tricuspid regurgitation

right apex

systole

regurgitant

I-iii/vi

ventricular septal defect

right apex

systole

regurgitant

iii-v/vi

aortic regurgitation

right sternal border

diastole

regurgitant

I-iii/vi

patent ductus arteriosus

left base

both

continuous

iii-v/vi

hypertrophic cardiomyopathy

left apex

late diast.

short

soft

heart failure

left apex

early diast.

longer

soft

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Clinical Physiology Essential for the Diagnosis and Treatment of Cardiopulmonary Diseases in Small Animals I principi di fisiologia clinica necessari per la diagnosi ed il trattamento delle malattie cardiopolmonari

Robert L. Hamlin DVM, The Ohio State University - Columbus - Ohio, USA

Riassunto La frequenza cardiaca è importante sia per mantenere la gittata che per determinare la quantità di ossigeno presente nel cuore e necessario alla produzione di ATP, che rappresenta la fonte energetica utilizzata per la contrazione ed il rilassamento del miocardio. La frequenza cardiaca è data dall’equilibrio fra il tono parasimpatico (vagale) e quello simpatico (β-adrenergico) che agiscono sul nodo senoatriale. Inoltre, è influenzata dalla temperatura e dal grado di stiramento dell’atrio destro e della parete arteriosa a livello del nodo senoatriale. Uno degli scopi importanti della terapia è quello di minimizzare la frequenza cardiaca; in questo senso, possono essere indicati la digitale e gli agenti di blocco β-adrenergico. Se il battito cardiaco è troppo rapido, troppo lento o troppo irregolare per mantenere una gittata adeguata, lo scopo della terapia può essere quello di regolare la frequenza cardiaca con gli antiaritmici.

La forza della contrazione ventricolare è determinata dalla contrattilità miocardica (lo stato inotropo), dal volume del sangue presente all’interno del ventricolo immediatamente prima della contrazione (il precarico) e dalle forze che si oppongono all’eiezione del sangue all’interno e lungo l’albero arterioso (il postcarico). Uno scopo importante della terapia è quello di ridurre al minimo il postcarico e mantenere un precarico adeguato perché il ventricolo generi una forte contrazione. Si possono utilizzare gli ACE-inibitori e/o l’idralazina per ridurre il postcarico e la digitale per aumentare la forza contrattile e si deve cercare di raggiungere un equilibrio fra la somministrazione di diuretici e l’infusione di fluidi, in modo da mantenere adeguato il precarico.

Molti segni clinici (come la tachipnea e l’intolleranza all’esercizio fisico) sono dovuti alla ritenzione idrica (sotto forma di congestione e/o edema) a livello polmonare. Questa ritenzione è dovuta al fatto che il cuore sinistro non è in grado di smaltire adeguatamente il flusso venoso che giunge dai polmoni, per cui la pressione nelle vene e nei capillari polmonari aumenta. Quando l’incremento della pressione capillare supera un certo livello, il siero filtra negli spazi interstiziali dei polmoni più rapidamente di quanto i vasi linfatici polmonare possano reimmetterlo in circolo, per cui si sviluppa un edema locale. Ciò rende i polmoni umidi, pesanti e rigidi ed è causa di una dispnea che si manifesta con una tachipnea. Inoltre, poiché alcune regioni del polmone non sono ventilate adeguatamente perché risultano più rigide di altre, il sangue che fluisce attraverso di esse possiede un’emoglobina meno ossigenata, con conseguente comparsa di cianosi. Quindi, uno scopo importante della terapia è quello di spostare il sangue dai polmoni ad altri distretti dove risulti meno pericoloso. A tal fine, possono essere indicati i diuretici ed i vasodilatatori venosi.

La rigidità del miocardio ventricolare interferisce con lo riempimento delle camere cardiache, portando ad una riduzione del precarico e ad un calo della forza contrattile. L’aumento della rigidità può essere dovuto all’inadeguato apporto di energia (ATP) per il rilassamento, all’ipertrofia concentrica, alla dilatazione o alle alterazioni della struttura istologica come la fibrosi. Naturalmente, lo riempimento ventricolare può anche essere ostacolato dalla presenza di una pericardite o di un versamento pericardico. Uno degli scopi della terapia è quello di migliorare la funzione diastolica (riempimento) ventricolare. A tal fine, è possibile utilizzare i calcio-bloccanti, rallentando la frequenza cardiaca, migliorando la sistole atriale e, naturalmente, rimuovendo le restrizioni o i versamenti pericardici.

Heat rate is important to sustain cardiac output, and it is an important determinant of the amount of oxygen present in the heart— the oxygen necessary to produce ATP which is the source of energy for both muscle contraction and relaxation. Heart rate is a balance between parasympathetic (vagal) and sympathetic (beta adrenergic) tone to the sinoatrial node. It is affected also by temperature and the degrees of stretch on the right atrium and SA nodal artery. An important goal of therapy is to minimize heart rate; and digitalis and beta adrenergic blockers may be indicated. If the heart beats too rapidly, too slowly or too irregularly to sustain an adequate cardiac output, then a goal of therapy may be to regulate the heart rate with antiarrhythmics.

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The force of ventricular contraction is determined by myocardial contractility (the inotropic state), the volume of blood within the ventricle just before it contracts (the preload), and the interference to the ejection of blood into and through the arterial tree (the afterload). An important goal of therapy is to minimize afterload and to sustain a preload adequate for the ventricle to generate a forceful contraction. ACE inhibitors and/or hydralazine may reduce the afterload, digitalis may increase the force of contraction, and a balance between diuretics and fluid administration must be sought to sustain proper preload.

Many signs (e.g. tachypnea) and symptoms (e.g. exercise incapacity) result from fluid retention (as congestion and/or edema) in the lungs. This fluid retention occurs because the left side of the heart cannot adequately remove the pulmonary venous effluent from the lung, and pulmonary venous and capillary pressures elevate. When capillary pressure increases to a certain level, serum weeps from the capillaries into the interstices of the lungs faster than pulmonary lymphatics can pump it back into the circulation, and pulmonary edema develops. This makes the lung wet, heavy and stiff, and this leads to dyspnea manifested as tachypnea. Furthermore because some regions of the lung do not ventilate adequately because they are stiffer than other regions, blood flowing through these inadequately ventilated regions posseses more unoxygenated hemoglobin, manifested as cyanosis. Therefore one important goal of therapy should be directed at shifting the dammed-up blood from the lungs to places where it does less harm. Thus diuretics and venodilators may be indicated.

Stiffness of the ventricular myocardium interferes with filling of the chamber leading to decreased preload and decreased force of contraction. Increased stiffness may result from inadequate ATP to fuel relaxation, from concentric hypertrophy, from dilatation, or from histological structural changes like fibrosis. Of course restriction of ventricular filling can result from either pericarditis or pericardial effusion. One goal of therapy is to improve ventricular diastolic (filling) function. This can be done by calcium channel blockers. By slowing the heart, by improving atrial systole, and of course by removing either a restricting pericardium or pericardial effusion.

Introduction: Identifying the origins and symptoms of, and the basis of selecting drugs to treat, cardiopulmonary disorders is based upon the understanding of certain essentials of structure (anatomy) and function (physiology) of the cardiopulmonary and neuroendocrine systems. Rather than memorizing lists of signs, symptoms and drugs relating to specific diseases, it is much simpler—and more fun—to learn a few principles, which when applied to specific diseases, permits ready knowledge of signs, symptoms and therapy. This discussion shall include the four general topics: heart rate, force of contraction/interference to blood flow, stiffness of the ventricle, the amount of oxygen present in the myocardium for energy.

Heart rate (HR) refers to how many times per minute the heart beats or the arteries pulsate. Normally the HR for dogs varies between 45 and 80 beats/minute at rest, to over 220 beats/minute during maximal exertion or excitement.

Equivalent values for healthy cats are 100 to 140 beats/minute during rest, to over 240 beats/minute during excitement. The heart beats because the SA node in the right atrium discharges a wave of depolarization which traverses the atria, generating the P-wave of the ECG and “shocking” the atria into contraction. This wave is picked-up by the AV node located in the right atrium near the ventricles, travels slowly through the AV node, and then bursts through the ventricles. As it travels through the ventricles it produces the QRS-complex of the ECG, and “shocks” the ventricles into contraction. Normally the P-waves is <60 ms in duration, the QRS-complex is <65 ms in duration, and the PQ interval—from onset of P-wave to onset of QRS-complex— is approximately 120 ms for dogs and 80 ms for cats.

The rate with which the SA node discharges, and the velocity with which the AV node conducts, is determined by a balance between the parasympathetic nerves (the vagus)

which decrease both, and the sympathetic nerves which increase both. The parasympathetic receptors in the heart are stimulated by acetyl choline but may be blocked with atropine, while the sympathetic receptors are stimulated by norepinephrine but may be blocked by a drug ending in olol (e.g. atenolol).

The force of ventricular contraction is determined by 3 factors: preload (PL), myocardial contractility (the inotropic state denoted by the sign, Vm), afterload (AL). The PL refers to the volume of blood (in ml) within the ventricle just before it contracts—the end-diastolic volume (EDV).

The EDV is determined by the ratio of the pressure of blood within the venous portion of the lungs to the stiffness (i.e. ability to resist stretching) of the ventricle. The pressure of blood within the venous portion of the lungs is determined by how much blood is there; and that, in turn, is determined by how much blood is not in the peripheral veins (where most of the blood is stored) and how well the left ventricle removes blood from the lungs and pumps it into and through the arterial tree. A venodilator (e.g. nitroglycerine, iv furosemide, or enalapril) which relaxes the smooth muscle in the venous walls, allows the veins to dilate, and they “steal” blood from the lungs therefore decreasing PL. Conversely, if the left ventricle fails to move blood adequately, blood dams-up in the veins, exerts greater pressure, and increases PL. In general, the greater the PL, the greater the force of myocardial contraction.

You may remember this as the Frank-Starling law-of-theheart. If PL is too small, force of contraction falls, cardiac output falls, blood pressure falls, and the patient may fall.

That is why dogs with blood volume depletion due to Addison’s disease are weak.

Myocardial contractility (Vm) is an intrinsic property of the contractile machinery. It is determined by the velocity

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with which the cross-bridges of the contractile machinery cycle, once activated by Ca++. Sympathetic activity (e.g. epinephrine, norepinephrine, dobutamine) increases Vm when neurotransmitters bind to B-receptors in the muscle, therefore increase force of contraction. In heart failure, Vm is decreased, cardiac output and arterial pressure may fall, unless PL increases, and the patient may fall. Digitalis increases Vm.Vm is determined by the rate of liberation of energy from the hydrolysis of ATP. Remember that the force of contraction—assuming constant afterload—is the product of preload and contractility.

No matter how great the PL and Vm are, the ventricle still cannot develop much force unless it contracts against an interference. This interference is termed the afterload (AL).

The AL depends upon the degree of constriction (increases AL) or relaxation (decreases AL) of the smooth muscle in the aorta and arterioles. The interference to ejection of blood by the left ventricle into and through the arterial tree is expressed as the AL. The AL imparted by the relative stiffness of the aorta is termed the impedance, while that imparted by the systemic arterioles is termed the systemic vascular resistance (svr). It is important that the afterload is great enough to sustain arterial pressure adequate to perfuse the organs, but not so great as to tax the ventricle which must generate that pressure. The degree of contraction or relaxation of arterial smooth muscle is influenced by many neural (e.g. sympathetic), endocrine (e.g. vasopressin, angiotensin) and local factors (e.g. endothelin, nitric oxide, adenosine). For any given pressure generated by the ventricle, the AL also depends upon the PL and wall thickness (WT). In fact AL is actually the peak tension generated by the wall of the ventricle; and the peak tension is the peak value of the product of ventricular pressure times preload divided by wall thickness. It is interesting to note that the peak value always occurs at the instant the aortic valve opens and the ventricle

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just begins to eject blood into the aorta. That pressure in the aorta is termed the diastolic arterial pressure.

The ease of filling of the ventricles is termed lusitropy or compliance. Lusitropy is determined by the rate with which Ca++ is driven off of the contractile machinery and back either out of the cell or into storage sites (sarcoplasmic reticulum) within the cell. This activity requires energy, also from the hydrolysis of ATP; thus an energy-starved heart is one that neither relaxes nor contracts well. Lusitropy may also be reduced if the myocardium is riddled with scar tissue (myocardial fibrosis), if the wall is very thick, if the ventricle is stiff due to being dilated, or if the filling of the heart is restricted by the pericardium or its contents (tamponade).

Cats with hypertrophic cardiomyopathy have a stiff left ventricle, it does not fill well, therefore the force of contraction is reduced. Of course even a stiff ventricle may be filled if the venous pressure—the filling pressure—is increased; but that means that the capillary pressure may be elevated enough to produce pulmonary edema.

Since oxygen is essential to the production of ATP—the source of energy for everything— adequate amounts of oxygen must be in the muscle at all times. The amount present is a balance between the amount delivered minus the among consumed. The amount delivered depends upon lung function, the amount of hemoglobin in the blood, and the coronary blood flow. The coronary blood flow depends upon the force driving that flow—the pressure difference between the aorta and right atrium. The forces interfering with coronary blood flow are the coronary vascular resistance and how much time the heart spends contracting (i.e. the HR) and cutting-off its blood supply by squeezing on the coronary vessels within the muscle. Oxygen demand is related to HR, Vm and AL. Since HR increases oxygen demand and decreases oxygen delivery, it is essential to control HR in patients with heart disease.

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Electrocardiography Using 2-leads Elettrocardiografia con 2 derivazioni

Robert L. Hamlin DVM, The Ohio State University - Columbus - Ohio, USA

Riassunto L’interpretazione degli ECG in II derivazione o aVF, o in I derivazione ed aVF o II consente nella maggior parte dei casi di ottenere le stesse informazioni che si potrebbero avere con un maggior numero di derivazioni. Anche se non fornisce dati sulla forza di contrazione degli atri e dei ventricoli, l’ECG è utile per acquisire informazioni su: (1) frequenza di depolarizzazione degli atri e dei ventricoli (che normalmente si verifica lo stesso numero di volte per minuto e varia da 45 durante il sonno a 240 durante la massima attività fisica) (2) sequenza di attivazione (normalmente, gli atri precedono i ventricoli di 100 ms) e tempo necessario per la depolarizzazione degli atri (normalmente, meno di 60 ms) e dei ventricoli (normalmente meno di 70 ms) (3) tempo necessario per la depolarizzazione e ripolarizzazione dei ventricoli (normalmente 200 ms, ma varia in modo inversamente proporzionale alla frequenza cardiaca) (4) presenza di un aumento dell’irritabilità indicato da battiti prematuri (extrasistoli) atriali e/o ventricolari che si verificano singolarmente, in brevi sequenze (parossismi) o in periodi di tachicardia prolungata.

L’ECG rappresenta un metodo sensibile e specifico per rilevare l’aumento di dimensioni del ventricolo destro, ma possiede una sensibilità limitata per l’ingrossamento del ventricolo sinistro, dell’atrio sinistro o dell’atrio destro. Ciò è probabilmente dovuto più ai nostri limiti ed alla nostra scarsa abilità nell’interpretare l’ECG che a vincoli intrinseci dell’elettrocardiografia.

Interpretation of ECG lead II or aVF, or of leads I and aVF or II, will most often provide as much useful clinical information as might be obtained from a greater number of leads. While the ECG gives no information about force of contraction of atria or ventricles, it is useful for providing information on: (1) the rate with which both atria and ventricles are depolarized (normally the same number of times per minute and varying between 45 during sleep to over 240 during peak exertion), (2) the sequence of activation (normally atria 100 ms before ventricles), the duration required for atrial (normally less than 60 ms) and ventricular (normally less than 70 ms) depolarization, (3) the duration required for both ventricular depolarization and repolarization (normally 200 ms but varying inversely with heart rate), (4) the presence of increased irritability as indicated by atrial and/or ventricular premature beats occurring singly, in short bursts (paroxysms) or sustained in a tachycardia.

The ECG is both sensitive and specific for detecting right ventricular enlargement, but has limited sensitivity to detect left ventricular, left atrial or right atrial enlargement. The limitations probably arise more from our limitations and lack of cleverness at interpreting the ECGs rather than in intrinsic limitations to electrocardiography.

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Basis of Selection of Drugs to Treat Common Cardiopulmonary Disorders in Dogs Approccio diagnostico e criteri terapeutici delle più comuni malattie cardiovascolari nel cane

Robert L. Hamlin DVM, The Ohio State University - Columbus - Ohio, USA

Riassunto Dal momento che la gran parte delle cardiopatie del cane è rappresentata dal rigurgito della valvola mitrale o dalla miocardiopatia dilatativa, prenderemo in considerazione in modo particolare gli scopi della terapia di queste due entità patologiche; tuttavia, poiché la miocardiopatia “aritmica” si riscontra piuttosto frequentemente nel boxer, nel pastore tedesco e nei cani di grossa taglia dopo un trauma e può portare a morte improvvisa, sarà necessario illustrare anche le basi della scelta dei farmaci per il trattamento delle aritmie. Va sottolineato che i vari cardiologi non concordano molto sulle modalità precise con cui selezionare i diversi agenti ed utilizzarli per il trattamento delle cardiopatie. È possibile minimizzare lo stiramento cronico dell’atrio sinistro – identificato mediante radiografia o ecografia – servendosi di agenti che riducono il postcarico (come gli ACE-inibitori). Questi farmaci permettono al ventricolo sinistro di spostare – con maggior facilità – una maggior quantità di sangue, che viene immessa e fatta progredire lungo l’albero arterioso sistemico. Quindi, il sangue viene drenato meglio dalla circolazione polmonare – e dall’atrio sinistro –, riducendo al minimo lo stiramento dell’atrio sinistro.

Se l’ipertensione venosa polmonare è significativa, la pressione del sangue nella circolazione polmonare aumenta il precarico del ventricolo sinistro e può determinare uno stiramento cronico delle sue fibre. Questo stiramento cronico – identificato mediante esami radiografici o ecografici – può essere ridotto utilizzando gli agenti che diminuiscono il postcarico ed eventualmente rafforzando la funzione ventricolare sistolica mediante farmaci inotropi positivi (come la digitale).

La broncocostrizione – identificabile attraverso la percezione di sibili – determinata da un riflesso innescato dalla distensione delle vene polmonari deve essere ridotta con la somministrazione di broncodilatatori (come la teofillina).

Naturalmente, l’edema – identificato mediante auscultazione, tachipnea, radiografie – va trattato con diuretici (come la furosemide) che aumentano la produzione di urina e/o con vasodilatatori venosi (come la nitroglicerina) che spostano il sangue dai polmoni congesti alle vene dell’addome. Se la palpazione del polso femorale o – meglio – l’ECG rivelano che il cuore batte troppo lentamente, è possibile ottenere una cardioaccelerazione attraverso la somministrazione di un agente vagolitico, l’atropina; se è presente una bradicardia e il cuore si contrae troppo debolmente, si deve prendere in considerazione l’impiego dell’adrenalina o della dopamina. Se la frequenza ventricolare è troppo rapida (come avviene nella maggior parte dei casi a causa della fibrillazione atriale e come si può identificare meglio attraverso l’elettrocardiografia) bisogna rallentare la frequenza ventricolare con un calcio-antagonista, il diltiazem. Prima di utilizzare ognuno di questi farmaci, il veterinario dovrà stabilire uno scopo specifico della terapia, un risultato terminale altrettanto specifico, i rischi di tossicità e le modalità con cui identificare l’insorgenza delle manifestazioni tossiche e le potenziali interazioni fra farmaci.

Since the vast majority of heart disease in dogs is either mitral regurgitation or dilated cardiomyopathy, we should focus on goals of therapy for these two entitities; but, because “arrhythmic” cardiomyopathy occurs rather frequently in boxers, German shepherds and large dogs following trauma and may lead to sudden death, basis for selection of drugs to treat arrhythmias must also be discussed. It should be emphasized that there is little agreement among cardiologists on precisely how to select drugs and use them to treat heart disease.

Minimizing chronic stretch of the left atrium— identified by x-ray or ECHO— can be achieved by use of afterload reducers (e.g. ACE inhibitors). These compounds allow the left ventricle to move more blood— and more easily— into and through the systemic arterial tree. Thus blood is drained more optimally from the pulmonary circulation— and left atrium— leading to minimizing of left atrial stretch.

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If pulmonary venous hypertension is significant, then the pressure of blood in the pulmonary circulation will increase left ventricular preload and may produce chronic stretch on left ventricular fibers. This chronic stretch— identified by x-ray or ECHO— may be reduced by use of afterload reducers and possibly by strengthening systolic ventricular function with positive inotropes (e.g. digitalis).

Bronchoconstriction— identified by wheezing— produced by a reflex initiated by distension of pulmonary veins should be reduced by bronchodilators (e.g. theophylline).

Of course edema— identified by auscultation, tachypnea, x-ray— should be treated with diuretics (e.g. furosemide) which increase urine production and/or with venodilators (e.g. nitroglycerine) which shift blood from the congested lungs to veins in the abdomen. If the heart is beating too slowly as indicated by palpation of the femoral pulses or— best— by ECG, cardioacceleration may be produced by the vagolytic, atropine; or if there is bradycardia and a feebly-contracting heart, epinephrine or dopamine should be considered. If the ventricular rate is too rapid— as is caused most often by atrial fibrillation and as may be identified best by electrocardiography— then the ventricular rate should be slowed with the calcium channel antagonist, diltiazem.

Before using each drug, the veterinarian should identify a specific goal for the therapy, specific end-points of the therapy, risk for toxicity and how to identify toxicity, and the potential of drug interactions.

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Diagnosis and Selection of Drugs to Treat the Three “Hypers” in Cats: Hypertrophic Cardiomyopathy, Hyperthyroidism, Hypertension Diagnosi e principi di scelta terapeutica delle tre “IPER” del gatto: miocardiopatia IPERtrofica, IPERtiroidismo ed IPERtensione

Robert L. Hamlin DVM, The Ohio State University - Columbus - Ohio, USA

Riassunto Le 3 “iper” rappresentano la grande maggioranza delle cardiopatie del gatto, ma la miocardiopatia ipertrofica costituisce probabilmente l’85% o più della totalità delle malattie cardiache dei felini. Negli animali colpiti, si osserva un ispessimento di entità variabile del ventricolo sinistro e del setto interventricolare e le fibre miocardiche possono subire delle alterazioni di orientamento e venire inframmezzate da fibrosi derivante da sclerosi arteriolare. Ciò induce l’alterazione dello riempimento ventricolare (malfunzionamento diastolico) e la diminuzione del precarico. L’ipertrofia del setto impone una restrizione del flusso di sangue che fuoriesce dal ventricolo (ostruzione del cono arterioso o dinamica) e, a causa dell’abnorme posizione assunta dal lembo anteriore della valvola mitrale (movimento sistolico anteriore) si può avere l’insorgenza di un rigurgito mitralico. Il malfunzionamento sistolico e/o quello diastolico portano alla distensione dell’atrio sinistro, che può esitare in edema polmonare e/o versamento pleurico, e/o nel tromboembolismo arterioso. Molti dei gatti colpiti dalla malattia – probabilmente la maggior parte – restano asintomatici, ma di solito presentano un ritmo di galoppo S4 (4° tono cardiaco) e/o un soffio sistolico. Il metodo più sensibile e specifico per diagnosticare la condizione e quantificarne la gravità è probabilmente rappresentato dall’ecocardiografia, ma è necessaria una notevole abilità sia per ottenere che per interpretare le immagini ecocardiografiche. È raro che un gatto con miocardiopatia ipertrofica non presenti ritmo di galoppo e soffio e la gravità della condizione può essere valutata in modo semiquantitativo con l’esame radiografico del torace (ombra cardiaca “a forma di cuore di carta da gioco”). La terapia della miocardiopatia ipertrofica è volta a promuovere il miglioramento della funzione diastolica rallentando la frequenza cardiaca (con i β-bloccanti), migliorando la funzione atriale (con la digitale), rendendo il ventricolo meno rigido (con il diltiazem) e prevenendo il tromboembolismo (con il warfarin) ed eventualmente riducendo il livello di ipertrofia cellulare, sclerosi arteriolare e fibrosi miocardica (con gli ACE-inibitori). Attualmente, si sta cercando di tracciare le basi genetiche della malattia. Per ora, l’impiego degli ACE-inibitori e della digitale è controverso.

The 3 “hypers” constitute the vast majority of heart diseases in cats, but hypertrophic cardiomyopathy (hCMy) constitutes probably 85% or more of all feline heart disease. In this disease the left ventricle and interventricular septum are thickened to a variable degree, and the myocardial fibers may be in disarray and interspersed with fibrosis resulting from artiolarsclerosis. This promotes abnormal ventricular filling (diastolic malfunction) and decreased preload. Hypertrophy of the septum imposes a restriction to the flow of blood exiting the ventricle (outflow tract or dynamic obstruction), and because of abnormal position of the anterior leaflet of the mitral valve (systolic anterior motion) mitral regurgitation may occur. Systolic and/or diastolic malfunction leads to left atrial distension, which may lead to pulmonary edema and/or pleural effusion, and/or to arterial thromboembolism. Many— possibly most— cats afflicted with this disease are asymptomatic, but usually manifest an S4-gallop (a 4th heart sound) and/or a systolic murmur. Echocardiography is probably the most sensitive and specific method for diagnosis and quantitation of the severity; but a great deal of skill is required to both obtain and interpret the echocardiograms. It is rare that a cat with hCMy does not have a gallop and murmur; and the severity may be semiquantified by thoracic radiology (i.e. the valentine-shaped heart). Therapy for hCMy is directed at promoting better diastolic function by slowing the heart (using beta blockers) and improving atrial function (using digitalis), at rendering the ventricle less stiff (using diltiazem), at preventing thromboembolism (using coumadin), and possibly at decreasing the rate of cellular hypertrophy, arteriolarsclerosis and myocardial fibrosis (using ACE inhibitors). Currently there are efforts to track the genetic basis for this disease. The use of ACE inhibitors and digitalis is controversial at this time.

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As many as 11% of the feline population has heart disease. Most of these cats are asymptomatic, a small percentage is symptomatic and is referred to the veterinarian because of the symptoms, and a rare number of asymptomatic cats either die or become deathly ill after stress such anesthesia and elective surgery. By far the most prevalent heart disease in cats is hypertrophic cardiomyopathy of one form or another, whereas systemic arterial hypertension is observed commonly in cats with azotemia, and many older cats may have hyperthyroidism. Thus it may be said the cats have 3 hypers: hypertrophic cardiomyopathy, hypertension, hyperthyroidism. Hypertrophic cardiomyopathy is almost certainly a genetic disease, while hyperthyroidism and hypertension may be, or the diseases (e.g. renal disease, prostatic neoplasia) promoting them may be familial.

Most cats afflicted with heart disease are depressed, dyspneic (tachypnia at rest, often mouth-breathing), hypothermic and anorectic. The more severe any of the diseases, the more pronounced the symptoms. They usually have high heart rates (normal during examination usually less than 220 beats/minute), but some may have normal heart rates or even may be bradycardic, particularly if they are hypothermic. Although not “fool proof”, hyperthyroidism should be expected in very old cats, hypertension should be expected in cats with azotemia and in particular with pathologicallydilated pupils or retinal hemorrhages, and hypertrophic cardiomyopathy should be expected in cats with tachycardia, arrhythmia, gallop heart sounds, and—for certain—in cats with acute posterior paralysis and cool pelvic limbs.

Cats with cardiomyopathy are usually afflicted with the hypertrophic form which is characterized, functionally, with abnormal filling of the left ventricle and subsequent distension of the left atrium. A less-commonly observed form of cardiomyopathy in cats is termed restrictive. Cats with restrictive cardiomyopathy have pathophysiology very similar to that of hypertrophic cardiomyopathy, the prime difference being that in the restrictive form neither left ventricular free wall not ventricular septum septum need be hypertrophied.

Dilated cardiomyopathy is observed rarely in cats today, because it was found to be caused by deficiency of the amino acid taurine; and taurine is now supplemented in commercial feline diets. Anatomically hypertrophic cardiomyopathy is characterized by a grossly thickened interventricular septum and usually left ventricular free-wall. The flow of blood out of the left ventricle into the aorta is usually obstructed partially due to both hypertrophy of the interventricular septum (a “muscle-bound” state) and sometimes by so-called anterior displacement of the septal leaflet of the mitral valve. The precise mechanism for this anterior displacement is not known, but it is thought by many to result from the high velocity of blood traversing the subaortic valvular region. In addition to subvalvular aortic stenosis producing a soft ejection murmur manifested on Doppler interrogation of the orifice as a high velocity jet, there may be a murmur of mitral regurgitation.

While hyperthyroidism can be identified, occasionally by palpable enlargement of the thyroid(s) and by symptoms typical of hyperthyroidism (e.g. tachycardia, weight loss, hyperactivity), the most definitive diagnosis may be made through analysis of thyroid hormones in the blood.

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It is reasonable to believe that hypertension—suggested by eye changes and azotemia—could be detected easily by measurement of systemic arterial blood pressure. Unfortunately, however, blood pressure may be quite difficult to measure in cats, normal values have not been established, and a cat may have highly labile blood pressure—particularly depending upon the person and the method measuring. Indirect sphygmomanometry—similar to that used for measuring blood pressure with an arm cuff in human beings—often produces highly variable and erratic measurements, and the “white coat” elevations occurring in anxious humans may be even more distorting due to the volatile nature of cats.

Goals of therapy for hypertrophic cardiomyopathy in cats are directed at: (1) reducing pulmonary edema and/or pleural effusion, (2) controlling heart rate and rhythm, (3) improving left ventricular filling, (4) reducing the likelihood of thromboembolism, (5) improving ventilation.

Whereas pleural effusion which restricts motion of the lung is treated best by thoracentesis followed by diuretics, diuretics are the drugs of choice for treating pulmonary edema. It is important that the veterinarian be able to determine whether a dyspneic cat is dyspneic predominantly because of effusion or edema (see the section of the physical examination). The loop diuretic, furosemide, should be given orally–at a dose of 1 mg/kg bid . Diuresis may be sustained or increased by adding a second diuretic which exerts its effect on the distal convoluted tubule. Enalapril (0.25 mg/kg, qd), chlorothiazide (5 mg/kg, bid), and spironolactone (1 mg/kg, bid) all work synergistically with furosemide, however the thiazide is likely to aggravate hypokalemia whereas both the angiotensin converting enzyme inhibitor and spironolactone are potassium-sparing diuretics. Caution must be exercised, when using combinations of diuretics, that the cat does not become volume-depleted, since much of the ability of the cat to conserve water is blocked when reabsorption of provisional urine from both the loop of Henle and distal convoluted tubule is prevented. Volume depletion is particularly adverse in a cardiomyopathic cat, since it is thought that dehydration increases the likelihood of thromboembolism.

Heart rate is most often rapid in cats with heart disease.

This not only increases myocardial oxygen consumption and decreases myocardial oxygen delivery, but it also impairs ventricular filling by shortening the period of diastole when filling occurs. Two methods are used to reduce heart rate, one of which also reduces the likelihood of arrhythmia. Beta adrenergic blocking agents (e.g. atenolol, metoprolol, propranolol) both slow heart rate and reduce myocardial irritability. Atenolol is often used at a dose of 6.25 mg/cat qd to bid. In addition to slowing the heart, beta blockers also reduce the force of ventricular contraction. This reduces the velocity of blood exiting the left ventricle into the aorta, and tends to reduce the dynamic obstruction to the outflow tract of the ventricle caused by septal hypertrophy and anterior motion of the anterior leaflet of the mitral valve. The calcium channel blocker, diltiazem, not only slows the heart, but also is thought to make the ventricle less stiff. If the cat has tachycardia predominantly, many prefer a beat blocker; but if the cat has minimal tachycardia and a loud S4 gallop indicating a stiff left ventricle, many prefer to use diltiazem.

And, of course, there are some that administer both beta

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blockers and diltiazem. Many cardiologists prefer to use the sustained release form of diltiazem, Dilacor, at a dose of 15 to 30 mg/cat bid.

The likelihood of thromboembolism, resulting from clots forming in the dilated left atrium and being shed into the aorta, may be minimized by aspirin (1/4 of a 5 gr/cat, q3d), or coumadin (0.25 to 0.5 mg/cat, qd). If a clot has already been shed and the pulses to the pelvic quarters are reduced or absent, 750 units of heparin may be given SQ, tid. It is thought that collateral channels circumventing the obstruction can be sustained by the alpha blocker/tranquilizer, ace-

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promazine (1 to 2 mg, SQ, bid). It is difficult ult to predict which cats will shed emboli, but it is though by some that those cats with the largest left atrial to aortic dimensions or that have shed clots previously should be treated, prophylactically, with coumadin. Of course, in the rare instance when clots can be visualized echocardiographically, it is wise to administer coumadin prophylactically.

Unfortunately there is little objective information based upon placebo-controlled clinical trials supporting efficacy that any specific therapy for hypertrophic cardiomyopathy is efficacious.

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Emergency Management of Cardiopulmonary Disorders Management delle emergenze cardiopolmonari

Robert L. Hamlin DVM, The Ohio State University - Columbus - Ohio, USA

Riassunto La maggior parte delle emergenze cardiopolmonari si manifesta con una riduzione improvvisa dell’apporto di ossigeno ai tessuti. Ciò determina una deplezione delle fonti di energia (ATP) per lo svolgimento delle funzioni organiche, o un’asfissia dovuta ad un’inadeguata ventilazione. I più comuni disordini cardiovascolari sono riferibili a emergenze ed emorragie, insufficienza cardiaca congestizia sinistra da rigurgito mitralico o miocardiopatia dilatativa, tachicardia/fibrillazione ventricolare, asistolia ventricolare, tromboembolismo arterioso. Anche la distensione gastrica acuta (meteorismo) costituisce un’emergenza cardiovascolare.

Le emergenze cardiovascolari evolvono di solito in edema polmonare/versamento pleurico (che porta ad asfissia) o inadeguata perfusione dell’encefalo o dei reni. Le malattie polmonari che portano alla comparsa delle emergenze sono nella maggior parte dei casi dovute a grave fibrosi polmonare e bronchite cronica, con conseguente riduzione del movimento del polmone.

Le emergenze cardiopolmonari possono essere riconosciute precocemente mediante osservazione (ad es., cianosi, sincope, pallore delle mucose), elettrocardiografia (ad es., arresto sinusale, blocco cardiaco, tachicardia/fibrillazione ventricolare), ossimetria (ad es., riduzione della saturazione arteriosa) o esame del polso arterioso (ad es., assente o troppo debole) e/o venoso (ad es., troppo “pieno” o troppo “vuoto”).

La terapia deve essere volta a correggere l’emorragia, adeguare la ventilazione e migliorare l’ossigenazione del sangue, incrementare la gittata cardiaca, regolare la frequenza ed il ritmo cardiaci, diminuire la pressione capillare polmonare, minimizzare l’estensione del trombo arterioso e promuovere lo sviluppo di canali collaterali intorno all’ostruzione, e ridurre la distensione gastrica.

Most cardiopulmonary emergencies are manifested by sudden reduction in delivery of oxygen to the tissues. This results in depletion of sources of energy (ATP) for organ function, or in asphyxia due to inadequate ventilation. The most common cardiovascular disorders leading to emergencies are hemorrhage, left-sided congestive heart failure as caused by mitral regurgitation or dilated cardiomyopathy, ventricular tachycardia/fibrillation, ventricular asystole, arterial thromboembolism. Acute gastric distension (i.e. bloat) also constitutes a cardiovascular emergency. The cardiovascular emergencies are usually resolved to pulmonary edema/ pleural effusion (leading to asphyxia), or to inadequate perfusion of the brain or kidneys. Pulmonary diseases leading to emergencies are most often due to severe pulmonary fibrosis and chronic bronchitis leading to restriction of lung motion.

Early recognition of cardiopulmonary emergencies may be made by observation (e.g. cyanosis, syncope, pale mucous membranes), electrocardiography (e.g. sinus arrest, heart block, ventricular tachycardia/fibrillation), oximetry (e.g. reduction in arterial saturation), or by examination of the arterial (e.g. absent or too feeble) and/or venous pulses (e.g. too “full” or too “empty”).

Therapy should be directed at correcting hemorrhage, adequate ventilation and improving oxygenation of the blood, improving cardiac output, regulating the heart rate and rhythm, lowering pulmonary capillary pressure, minimizing extension of arterial thrombus and promoting collateral channels around the obstruction, decreasing gastric distension.

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Diagnosis and clinical management of dogs with mitral regurgitation Introduction: Mitral regurgitation occurs when the leaflets of the mitral valve fail to coapt (i.e. come together appropriately) and regurgitates from the left ventricle into the left atrium. This is the most common form of heart disease, occurs mainly in small, older aged, chondrodystrophic breeds (e.g. Cocker Spaniels, Dachshunds), and occurs most commonly and in an aggravated form in Cavalier King Charles Spaniels. It is caused by endocardiosis in which the leaflets of the mitral—and less so the tricuspid—valve are thickened and gnarled due to infiltration with abnormal glycosaminoglycans (acid mucopolysaccharides). The etiology is unknown, but it obviously has a genetic component.

History: Most commonly dogs with mitral regurgitation (MR) are asymptomatic, although they have a murmur.

When symptomatic, they usually manifest a hacking cough caused by compression of the left mainstem bronchus by an enlarged left atrium (LA), in later stages they may become dyspneic (tachypneic) and possibly cyanotic due to pulmonary congestion and/or edema, and they may faint due either to reduced cardiac output or to activation of mechanoreceptors located within the vigorously-moving left ventricle (LV). The LV moves so vigorously because it ejects more blood than usual—a nearly normal amount into the arteries and the regurgitant volume into the LA. Dogs with MR may also have reduced exercise capacity due both to pulmonary congestion and possibly low cardiac output.

Physical Examination: Dogs with MR almost always have a systolic murmur heard best at the left apex beat (5th intercostal space at the costochondral juncture). The murmur is caused by blood leaking through the mitral orifice from LV into LA during systole—between and often obfuscating the the first (S1) and second (S2) heart sounds. When MR first appears no doubt the murmur is soft, and the murmur becomes louder as the regurgitation increases. However when the regurgitant orifice becomes very large (due to the valves becoming more gnarled or the AV annulus dilating) or the LV weakens, the murmur may actually become softer.

There is little relationship between the murmur intensity and the selection of drugs or the prognosis; but the murmur tells—for certain—that there is mitral regurgitation and the patient should be explored in greater depth by x-ray to help is selection of drugs. It should be emphasized that although the patient may be asymptomatic, the ventricle is still probably failing as evaluated by clinical physiology. With pulmonary congestion the lung is stiff and the patient tachypneic, with pulmonary edema there may be crackles, bronchial breath sounds, dull note of percussion, and possibly cyanosis. Both HR and rate of femoral arterial pulsations increase with increasing severity of MR. The intensity of the femoral pulses may be normal with mild MR, reduced with more severe MR, or sharp and tapping with more severe heart failure. If the patient is in atrial fibrillation, of course the heart rate will be rapid and irregularly-irregular, an there will be a marked pulse deficit, i.e. many fewer pressure pulses than heart beats. Commonly patients with MR will have lenticular sclerosis, graying under the chin, arthritis, polyuria, gastritis and

anorexia. But these signs may merely indicate ageing or a common etiology rather than MR. The severity and the actual amount of blood regurgitating through the mitral orifice can be estimated quite accurately by ECHO/Doppler; however whether or not this impacts on the outcome of the case is equivocal.

Therapy: Therapy should be directed at specific goals.

These are, in general in common to all heart diseases: adjust the heart rate, reduce chronic stretch of myocardial fibers, decrease regurgitant fraction, improve forward cardiac output, reduce pulmonary congestion and/or edema, improve oxygenation. With early MR, the LA becomes enlarged becomes of the regurgitation. Enlargement of the LA may be detected quite accurately—but not with as great a sensitivity as with ECHO—by thoracic radiography. This enlargement may be quantified by the bulge in the cardiac silhouette from 1 to 3 o’clock on the DV radiograph. When present, an afterload reducer such as enalapril (or any other of the prils) is thought to reduce the regurgitant fraction and to retard the rate with which the LA continues to enlarge. With more severe MR, enough blood regurgitates so that the pressure in the lungs is great enough to increase LV preload. Increased LV preload can also be identified on thoracic radiographs as a bulge on the DV film from 3 to 7 o’clock, and by dorsal displacement of the trachea. Sometimes compression of the left mainstem bronchus can be observed. It is thought that digitalis (most often used as digoxin) can retard the rate with which the LV continues to enlarge, as well as digoxin slowing the heart rate, strengthening the diaphragm, and reestablishing baroreceptor function in heart failure. As MR worsens, the pulmonary veins become engorged, leading to tachypnea due to stiffening of the lungs and wheezes elicited by a bronchoconstrictory reflex. Pulmonary venous engorgement can be identified on lateral radiographs, but can be inferred by enlargement of both LA and LV. It is thought that theophylline both strengthens the muscles of ventilation and inhibits the bronchoconstriction, thus improving ventilation. If pulmonary edema is observed by worsening of the dyspnea, by crackles and bronchial breath sounds, and by cyanosis, and is confirmed by thoracic radiographs, then diuretics—including the potassium-sparing spironolactone— should be given. If the patient has developed atrial fibrillation due to chronic stretch of the left atrium, the rapid ventricular rate can be slowed with the AV blocking, Ca++ blocking agent, diltiazem. Although there is no value for certain, a ventricular rate slower than 130 beats per minute should be sought. Digitalis and possibly the B-blocker, atenolol or carvedilol, also help to reduce the ventricular in patients with atrial fibrillation. If the patient shows many multiform premature ventricular beats or periods (paroxysms) of rapid ventricular tachycardia, then it is thought that an antiarrhythmic—either procainamide or sotalol— should be used to control the ectopic (misplaced) ventricular activity.

With heart failure, it is thought that patients with severe MR have too few B adrenergic receptors and possibly deranged high pressure baroreceptors. “Up-regulation” of Breceptors can be achieved with low dose non-specific B-

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blockers, while baroreceptors can be adjusted using digitalis, enalapril or spironolactone—all compounds that reduce the toxic activity of Na-K ATPase within the baroreceptors.

The veterinarian might consider either measuring blood or myocardial levels of taurine and carnitine, or presuming they are deficient and adding them to the diet. It is thought that deficiencies of these amino acids is probably rare in heart failure caused by MR. A frequent concomitant with MR is myocardial fibrosis resulting from arteriolar sclerosis. Arteriolar sclerosis refers to narrowing of the lumena of small, intramural coronary ar-

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teries or arterioles due to myointimal proliferation. With reduced coronary blood flow and delivery of oxygen to myocardium down stream from the narrowed vessel, the myocardium first becomes injured (and may serve as as focus for arrhythmias), and then may die if oxygen debt is severe and prolonged. Myocardial fibrosis can often be identified by prolongation (or “sloppiness”) of the down slope of the R wave in lead aVF or II ECG, and again, dogs so afflicted are pron to develop arrhythmia. The fibrotic myocardium not only does not contract normally, but it is usually too stiff and the ventricles fills abnormally.

Dilated cardiomyopathy and more specifics about therapy Introduction: Dilated cardiomyopathy is a disease primarily of large breed dogs, in particular Doberman pinchers.

It is observed most commonly in dogs from middle age on.

There is no known etiology in most cases, however a small—but as of yet unknown—number may be caused by deficiency of l-carnitine. Dilated cardiomyopathy use to be a common disease in cats, but since supplementation of diets with taurine, it occurs extremely rarely in cats. It may be caused by the antineoplastic compound doxorubicin (Adriamycin). There is a slight genetic predisposition since it is observed more prevalently in certain breeds and in certain families. The term dilated cardiomyopathy comes from the fact that all four chambers of the heart are dilated, but the disease also involves skeletal muscle. The muscle fibers are elongated and have reduced contractility. Frequently there is myocardial fibrosis and arteriolar sclerosis, and dogs with cardiomyopathy commonly die suddenly from ventricular tachycardia leading to ventricular fibrillation or from cardiac arrest due to suppression of discharge of the SA node.

History: Dogs with dilated cardiomyopathy are usually referred for anorexia, weight loss, labored breathing, exercise intolerance, fainting and cough. There is characteristically a “wasting” of skeletal muscles over the vertebrae, dogs are dehydrated but may have ascites, and eyes are frequently “sunken into” the orbits.

Physical Examination: Dogs with dilated cardiomyopathy are often short-of-breath and may have “deep” guttural coughs. They frequently have systolic murmurs—most often grades ii/vi to iii/vi due probably to mitral and/or tricuspid regurgitation resulting not from diseased leaflets but from either abnormal mode of ventricular contraction or such dilatation of the annuli that the normal leaflets cannot coapt (come together) during systole. Third heart sounds— termed S3 gallops—are heard often at the left apex, and these gallops arise from a relatively stiff ventricle and elevated pulmonary venous pressure. Dogs with dilated cardiomyopathy almost always have elevated heart rates; and many with atrial fibrillation have extremely elevated heart rates that are irregularly-irregular and produce arterial pulse deficits. It is common to auscultate wheezes—sibilant rhonchi— in dogs with pulmonary venous engorgement due to this cardiomyopathy. If pulmonary edema or severe congestion is

present, the dogs will be tachypneic, and may have both bronchial breath sounds and crackles. Often dogs with dilated cardiomyopathy will manifest reduced exercise capacity and/or syncope. Radiographically dogs will usually have four-chamber cardiomegaly, engorged pulmonary vessels, often hepatomegaly, and signs of pulmonary edema and/or ascites. Echocardiographically the left ventricle is usually dilated, the free-wall is thin to normal (but the ratio of lumen to wall thickness is great), and there is a large distance between the opened anterior leaflet of the mitral valve and the left ventricular face of the interventricular septum. The ratio of the time the aortic valve remains open during systole (termed the ejection time) to the duration between the onset of the QRS and the time the aortic valve opens (termed the pre-ejection period) is relatively small.

Therapy: Therapy for dilated cardiomyopathy is very similar to that for mitral regurgitation. The goals are to regulate the heart rate and rhythm, minimize chronic stretch of myocardial fibers, decrease the interference to the ejection of blood from the left ventricle into and through the arterial tree, reduce edema, improve ventilation/oxygenation, up-regulate beta adrenergic receptors. Heart rate should be reduced to less than 120 to 130 beats/minute during rest, therefore the clients should be trained to measure it while their pets rests. In fact the precise heart rate that should be sought is not known, and may vary depending upon the pathological state. If the heart is accelerated because of a rapid sinus discharge, digoxin (starting approximately 0.00125 mg/kg, po bid) may be useful at slowing it; however, since digitalis exerts its cardiodecelleration via a vagal mechanism, it only slows the heart when the patient is sleeping or quiet. For additional cardiodecelleration—in particular during daily activity and excitement—beta blockers (e.g. drugs ending in an olol) may work synergistically with digoxin. Beta blockers have the additional value of reducing ventricular irritability and “up-regulating” beta receptors; however they may also weaken the already failing myocardium and worsen the heart failure. Atenolol is a cardiospecific beta blocker that is less likely to produce bronchoconstriction than beta blockers that are less cardiospecific (e.g. propranolol), and a dose of approximately 0.25 mg/kg, po, bid is unusually safe and effective. If the heart rate is rapid because of atrial fibrillation, the calcium channel blocker, diltiazem, can slow the ventricular rate to any value desired. Again the precise value sou-

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ght is not known, and may depend upon the pathophysiological state. A ventricular rate between 120 and 130 during the examination is probably appropriate. Recent data in humans with heart failure suggests that the beta blocker, carvedilol, may be of greatest value. This compound is not only a beta blocker, but also blocks alpha adrenergic receptors (thus decreases afterload), and is a potent scavenger of free radicals of oxygen thought to participate in the pathogenesis of heart failure. If ventricular arrhythmias appear to produce symptoms (e.g. syncope, periodic weakness), they may be suppressed by more aggressive use of beta blockers (in particular sotalol, 1.5 mg/kg po bid), or a class IA antiarrhythmic such as procainamide (10 mg/kg, po, tid). Theophylline, 10 mg/kg po bid) may be useful to both bronchodilate and strengthen muscle of ventilation, thus to improve ventilation. Of course afterload reducers, in particular angiotensin converting enzyme inhibitors (ACEi) (.... pril) appear to be the mainstay in treating dilated cardiomyopathy, and they should be started earlier rather than later. Most ACEi (e.g. enalapril, benazepril) are given po, qd to bid, at a dose of approximately 0.25 mg/kg. These compounds are extraordinarily safe, and they not only reduce afterload, but they also reduce heart rate, improve renal function for most renal diseases, and work synergistically with diuretics. There is evidence, also, that they prevent adverse myocardial remodeling and ventricular arrhythmias, and firm evidence that they normalize barore-

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ceptor function thought to provoke many of the neuroendocrine abnormalities. A variable percentageâ&#x20AC;&#x201D;from 5% to 20%â&#x20AC;&#x201D;of dogs afflicted with dilated cardiomyopathy suffer from deficiency of l-carnitine. This aminoacid is necessary to supply the mitochondrion with substrate for production of ATP; thus, with l-carnitine deficiency, there will be energy deficiency with stiffening of the myocardium and reduced force of contraction. Unfortunately blood levels of l-carnitine do not necessarily predict myocardial levels, and it is myocardial levels that appear to be important in this form of cardiomyopathy. Whether or not l-carnitine deficiency can be proven, some believe in supplementing the canine diet with this aminoacid. A commercially-available canine diet is supplemented with l-carnitine. In the rare instances when l-carnitine deficiency is the cause of dilated cardiomyopathy, recovery from the disease is striking and rewarding with l-carnitine supplementation.

Almost all clinical and experimental studies of dilated cardiomyopathy demonstrate a decreased number (down-regulation) of beta adrenergic receptor density, with reduced ability for cardiovascular adjustment to physiological stress.

It is though that this down-regulation results from sustained elevation of circulating levels of norepinephrine. Paradoxically, low dose of non-cardiospecific beat blockers, in particular carvedilol, can increase (up regulate) the number of beta receptors. A dose of approximately 0.05 mg/kg of carvedilol given po, bid appears to be safe and effective.

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How, why and for what Diagnostic ultrasound in the Small Animal Diagnostica ultrasonografica: quando, come, perché e per che cosa impiegarla nella clinica degli animali d’affezione

Kerstin Hansson Med. Vet. - School of Veterinary Medicine - University of Uppsala, Svezia

Riassunto Introduzione Durante gli ultimi 15 anni, l’ecografia è diventata sempre più comune. Alcuni ritengono che niente abbia fatto di più del miglioramento di questa tecnica per cambiare gli standard della professione. Si tratta di una metodica molto sensibile che può rivelare le strutture interne di un organo e differenziare i tessuti molli dai liquidi. Nel corso di un esame ecografico, si possono monitorare i vari organi in tempo reale e ciò ha rivoluzionato le possibilità di diagnosi delle cardiopatie. Oggi è possibile effettuare il prelievo di aspirati con ago sottile e campioni bioptici di tessuto attraverso la visualizzazione diretta dell’ago e del suo percorso nell’organismo. Un altro importante fattore da tenere in considerazione è che l’ecografia non utilizza radiazioni ionizzanti.

A cosa pensare quando si intende acquistare un apparecchio ecografico e quando farlo Bisogna valutare accuratamente alcuni aspetti importanti, come le caratteristiche tecniche, e dare una risposta alla domanda “perché sto comprando un ecografo”. Ciò vale specialmente quando l’apparecchio che si intende acquistare dovrà essere destinato a molteplici impieghi e utilizzato per molte indicazioni differenti.

Come e per che cosa si può utilizzare l’ecografia Le indicazioni per l’impiego della diagnostica ecografica sono in costante espansione e la tecnica viene ora utilizzata per individuare la presenza di alterazioni in molte aree differenti dell’organismo. Prima di effettuare l’esame, bisogna preparare adeguatamente il paziente. Dopo aver tosato il mantello, si deve applicare un gel acustico per migliorare il contatto con la cute. Il transducer va scelto tenendo presenti le dimensioni dell’animale e l’organo/la regione da valutare.

Nella cavità toracica è possibile esaminare ecograficamente diverse aree. Tra l’altro, è possibile rilevare ogni processo patologico a carico di cuore, pericardio, mediastino e cavo pleurico.

Tutte le parti e gli organi della cavità addominale possono essere visualizzati ecograficamente. Uno dei metodi abitualmente suggeriti prevede di applicare inizialmente il transducer caudalmente al processo xifoideo dello sterno e cominciare ad effettuare la scansione proiettando il fascio ecografico in modo da farlo procedere lungo il fegato. Da qui, ci si sposta con un movimento in senso orario e si passa alla milza, al rene sinistro, alla vescica, al tratto genitale ed al rene destro per poi tornare al fegato. A seconda dell’esperienza e delle apparecchiature di cui si dispone, questa prima esplorazione circolare in senso orario, che comprende gli organi addominali di base, può essere seguita dall’esame di surreni, tratto gastroenterico (compreso il pancreas) e linfonodi mesenterici.

Introduction During the last 15 years ultrasound has become more and more common. Some people think that nothing has done more to change the standard of practice than the refinement of ultrasonography. The technique is very sensitive and can reveal the internal structures of an organ and differentiate soft tissue structures from fluid. During an ultrasound examination the organs can be monitored in real time which has revolutionised the possibility for diagnosing cardiac disease.

Fine-needle aspirates and tissue biopsies can be taken with direct visualisation of the needle and the needle tract. Another important factor is that ultrasound do not use ionising radiation.

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What to think about and when buying an Ultrasound machine Important issues like technical considerations and the question “Why am I buying an ultrasound equipment “ needs to be carefully evaluated. Especially as it is often that one ultrasound machine must suffice as a multipurpose system and is used for many different indications.

How and for What can ultrasound be used The indications for using Diagnostic Ultrasound are constantly expanding and the technique is now used for diagnosing changes in many different areas of the body. Before the examination the patient must be well prepared. The hair coat should be clipped and acoustic gel shall be used in order to improve skin contact. Transducer is chosen according to size of the animal and organ/area to be evaluated. In the thoracic cavity several areas can be evaluated with ultrasound. Among these are disease processes in the heart, pericardium, mediastinum and pleural cavity.

Any part and organ in the abdominal cavity may be imaged ultrasonographically. One suggested routine is to initially place the transducer caudal to the xiphisternum and start the scan by sweeping through the liver. From the liver continue in a clockwise movement and go on to the spleen, left kidney, bladder, genital tract, right kidney and back to the liver. Depending on experience and equipment this first clockwise circle including the basic abdominal organs can be followed by examination of the adrenals, gastro-intestinal tract including the pancreas and the mesenteric lymphnodes.

INTRODUCTION

BUYING AN ULTRASOUND MACHINE

As we all know, it started with the animals. They developed ultrasound some million years ago and today lots of animals including man benefit from this technique. In veterinary medicine, ultrasound has been used since the beginning of 1960s and one of the first applications was to diagnose pregnancies in sheep. During the last 15 years ultrasound has become more and more common and the use of ultrasound in every day clinical life have exploded. Some people think that nothing has done more to change the standard of practice than the refinement of ultrasonography. What was initially mostly used for scanning the heart and the urinary and the genital tract, has become a valuable tool for evaluation of the entire abdomen, thorax and an abundance of other areas of the body. The curiosity and the inventiveness of the ultrasonographer have become the limiting factor.

When you are planning to buy an ultrasound machine it is very important to spend some time on evaluating your needs and your reasons for buying ultrasound equipment.

You should ask yourself some questions.

– Why am I buying an Ultrasound machine?

– What is it I want to achieve in a long-term goal?

– What kind of and how many cases am I going to do per week/month?

– Am I going to perform both cardiac and abdominal scans?

– Am I expecting to finance the machine with income from ultrasound studies?

– Do I have a proper room where I can get easy access to the machine?

– How am I going to get training?

– Is time set aside for learning the technique?

PHYSICAL PRINCIPLES Ultrasound is defined as sound above the audible level of the human ear, which is 20,000 kHz. In Diagnostic Ultrasound frequencies of 2-10 MHz are often used. The ultrasound beam is produced by crystals caused to vibrate after being hit by electrical impulses. There may be multiple crystals, as in the linear and phased array systems, or single crystals as in many mechanical sector scanners.

When the transducer containing the vibrating crystal is placed in contact with the skin, the sound beam is transmitted through the soft tissues. The presented image will be rectangular or pie-shaped depending on what kind of transducer that is being used.

The depth of penetration and the image resolution are ruled by the transducer frequency. Lower frequency sound beams penetrate further than beams of higher frequency.

High frequency transducers on the other hand provide better resolution when compared with low frequency transducers.

One of the most important facts to remember is the time that needs to be spent for practising the technique. Ultrasound differs dramatically from radiology in the way that it is extremely operator dependent. You can increase the diagnostic usefulness of the machine in a dramatic way if you set aside enough time for learning and practising ultrasound.

A specific problem when it comes to maintenance on ultrasound machines used in veterinary medicine is the environment. Hair, dust etc from the animals can gain entrance to the machine through the control panel or fan system. If possible the best solution is to have a room designated for ultrasonographic examinations.

TECHNICAL CONSIDERATIONS In the academic setting we often have the luxury of having more than one ultrasound system and several transducer types to use for different applications. However, in private

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practice, one ultrasound machine must suffice as a multipurpose system. Small animal practitioners are often scanning both hearts and abdomens of various sized dogs and cats, which means that a sector transducer is most suitable. Mechanical sector scanners are because of the lower cost more widely used than phased-array systems. Cats and small dogs are preferably scanned with a 7,5 MHz transducer, middle size to large dogs with 5 - 3 MHz. For echocardiography the minimum requirements are 2DE, M-mode and electrocardiographic capabilities. The system should allow a high frame-rate, as it is essential for cardiac imaging of especially cats that commonly have heart frequencies around 200 bpm. The size of the footprint is very important due to the fact that all routine cardiac scan planes are done using an intercostal window. A small footprint is also useful for abdominal examinations. One example is scanning of the liver, which is done both from an intercostal position and from the area around the xiphisternum.

For evaluation of cardiac murmurs it is very useful if the system is equipped with pulsed (PW) and continuos (CW) wave Doppler.

Below are some guidelines to think about when you are planning to buy an ultrasound machine. The notes are for a more advanced machine.

MACHINE REQUIREMENTS IN THE ACADEMIC SETTING • Sector transducers with small footprint, 2 - 10 MHz • T-shaped 7,5 MHz linear array transducer with maximum footprint of 4x1cm, detachable standoff.

• Curvilinear transducer, 3 - 5 MHz. • All transducers connected to the system.

• Preselected user programs.

• User friendly keyboard.

• Depth between 2 - 30 cm.

• Zoom function, selected by the user not preselected.

• Documentation on VCR, printer, discs.

• VCR functions on control panel.

• Cine loop/image memory on all modes.

• Simultaneous 2DE and M-mode.

• ECG with indications for M-mode measurements.

• Area, distance and cardiac calculations package for real time and from VCR. • CW and PW Doppler.

• Simultaneous 2DE and CW/PW Doppler.

• Colour Doppler with high temporal and spatial resolution.

• Different frequencies for 2DE and colour Doppler.

• Physiologic unit for phonocardiogram etc.

• Biopsy guide line and biopsy device.

– Upgradable machine and transducers.

– Good technical and user support from the company.

Additional advantages – Split screen with zoom and normal 2DE. – Zoom function in real time and frozen image.

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– Triplex presentation with 2DE, colour and PW Doppler.

– Patient register on VCR. – Cine loop in slow motion for 2DE and colour.

– B-colour.

– Digital technique and digital image storage.

– Harmonic imaging.

APPLICATIONS Thorax – – – – – –

Congenital and required heart disease.

Pericardial disease.

Pleural disease such as free fluid and neoplasias.

Mediastinal changes Diaphragmatic hernias.

Superficial pulmonary lesions.

Abdomen – Lesions in parenchymatous organs such as liver and spleen.

– Gastro-intestinal disease.

– Uro-genital disease.

– Lesion in endocrine organs such as pancreas and adrenals.

– Abdominal lymphnodes.

– Abdominal masses.

– General abdominal changes such as free fluid and peritonitis – Vascular anomalies such as porto-systemic shunts and aortic trombembolisms.

Miscellaneous – – – – – – – – –

Tendinous and ligamentous lesions.

Orbital and periorbital lesions.

Hydrocephalus.

Salivary glands.

Retropharyngeal lesions, larynx and the thyroid and parathyroid gland.

Hernias, inguinal and abdominal.

Miscellaneous soft tissue swellings and masses.

Fistulous tracts/foreign bodies.

Guided fine needle aspirates and tissue biopsies

ULTRATALK Like for all areas of veterinary medicine, ultrasound has its own language. Black areas are called anechoic as no sound is being reflected from the structure. Fluidfilled areas like the urinary bladder and vascular structures are usually anechoic. Hyperechoic areas on the other hand are white due to that the investigated structures are echo-rich. Highly reflecting interfaces and areas con-

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taining fibrous or calcified tissue are hyperechoic. Tissues with various shades of grey are called hypoechoic. Many parenchymal organs like the liver, spleen and kidneys show various hypoechoic patterns.

To describe image texture terms like fine or coarse are used. These terms reflects the size of the dots (small or large dots) in for instance the liver. With the term uniform texture one often means that the produced image of a tissue shows similar size dots that are evenly distributed.

The words uniform and non-uniform shall be used for echogenicity and texture separately as all sorts of combinations is possible.

The major factors involved in how a tissue will look on an ultrasonographic examination is the amount of fat, water and collagen fibres together with the arrangement of tissue elements and cells.

The resulting image will thus be composed of black, white and grey areas just like the radiograph and one could ask – what have we gained in comparison to plain radiography?

Ultrasound has many advantages specially when it comes to diagnostic procedures involving soft tissue structures. It is a very sensitive technique that can reveal the internal structures of an organ and it can differentiate soft tissue structures from fluid. During an ultrasound examination the organs can be monitored in real time which has revolutionised the possibility for diagnosing cardiac disease. It is also very useful for monitoring moving organs in the abdomen like the GI-tract.

Fine-needle aspirates and tissue biopsies can be taken with direct visualisation of the needle and the needle tract.

Another important factor is that ultrasound do not use ionising radiation which is a fact for many other diagnostic imaging modalities. Many radiation and time consuming examinations like gastro-intestinal contrast studies can now be replaced by ultrasound. It must be remember though that there is no competition between radiology and ultrasound but often a synergistic effect if the two techniques are combined.

Artefacts As in all imaging modalities artefacts are produced and found. Two of the more important artefacts are useful for the ultrasonographer as they help to identify the composition of the investigated structure. One is called acoustic shadowing and is created by structures of high attenuation.

Shadowing occurs as a result of nearly complete reflection and/or absorption of the sound. This artefact can be produced by gas or bone.

Bone, caliculi and barium create a black or “clean” shadow while an echoic or “dirty” shadow is seen in conjunction with gas.

Edge shadowing is seen at the edges of rounded structures such as the urinary bladder. The other useful artefact is called distant enhancement or through transmission and is seen as an increase of echo amplitude distal to an anechoic structure. This artefact helps to differentiate a hypoechoic fluid-filled structure from a solid mass.

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ULTRASONOGRAPHIC EXAMINATION OF THE ABDOMEN Patient Preparation The patients can be scanned standing or in dorsal or lateral recumbency. No sedation is needed in the majority of cases. To avoid disturbing gas it is preferred if food can be withdrawn 12-24 hours prior to the examination and that the colon do not contain faecal material. This is the same type of preparation that is used for abdominal radiography. If both a radiographic and an ultrasonographic examination are planned it is often best to start with radiography. The films can give you information about organ size, amount of gas/faecal material etc. If you start with the ultrasound you must make sure that there are no gel left in the hair coat. Gel or a wet hair coat creates disturbing shadows on the radiograph. Another factor to remember is that barium contrast is highly reflecting and will cause a lot of disturbing shadows and reverberations. The ultrasonographic examination must therefore be done either before contrast is given or after it has passed the GI-tract.

The hair coat should be clipped and acoustic gel shall be used in order to get good contact between the transducer and the skin. In animals with an irregular skin alcohol can be applied before the gel, in order to further improve skin contact.

Sometimes alcohol can be used alone as contact medium. If you are going to look at a small area and if the animal has a long hair coat it is often possible to just part the hair to the side and wet the skin with alcohol.

Performing the scan Transducer is chosen according to size of the animal and organ/area to be evaluated.

Any part and organ in the abdominal cavity may be imaged ultrasonographically. The image site is selected to overly the area of interest, but to avoid as far as possible skeletal or gas filled structures. Maximum reflection and thus the best image are gained if the examined structure is perpendicular to the ultrasound beam.

During the scan the image should be oriented with the cranial portion of the animal to the viewers left on sagittal scans and the right side of the animal to the viewers left on transverse scans.

There are many different ways to perform an abdominal ultrasound examination. The most important issue is to create a routine that works well for the practise. One suggested routine is to initially place the transducer caudal to the xiphisternum and start the scan by sweeping through the liver. From the liver continue in a clockwise movement and go on to the spleen, left kidney, bladder, genital tract, right kidney and back to the liver. Depending on experience and equipment this first clockwise circle including the basic abdominal organs can be followed by examination of the gastro-intestinal tract including the pancreas and the mesenteric lymphnodes. The adrenals can be scanned either in conjunction with examination of the kidneys or at a later stage in your routine.

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Normal findings The abdominal organs have different echogenicity and they are often compared to each other in order to evaluate if a structure is more or less echogenic than normal. The most echogenic organs are the prostate in an intact male and the spleen. The liver is equal or slightly more echogenic when compared to the cortex of the kidneys. The pancreas has almost the same echogenicity as the surrounding hyperechoic fat and is more echogenic than the closely related duodenum. The gastro-intestinal tract has a layered appearance.

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Using a high frequency transducer it is possible to distinguish five different wall layers. The central hyperechoic layer represents the interface between the intestinal lumen and the mucosa. The mucosa is often the most prominent layer and it is anechoic. Next layer is hyperechoic and represents the submucosa, which is followed by an anechoic muscle layer. The most peripheral layer is the hyperechoic serosa.

The uterus is hypoechoic and the ovaries have a variable echogenicity depending on changes in the reproductive cycle.

Fluid containing organs like the urinary bladder, the gallbladder and vascular structures are anechoic.

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Imaging of thoracic trauma Diagnostica per immagini del trauma toracico

Kerstin Hansson Med. Vet. - School of Veterinary Medicine - University of Uppsala, Svezia

Riassunto La radiologia è una delle tecniche diagnostiche più importanti per la valutazione del trauma toracico. Di solito, fornisce informazioni più specifiche di quelle ottenibili con l’esame clinico e può essere effettuata in modo relativamente economico e rapido. Risulta estremamente importante il posizionamento dell’animale, che nei soggetti traumatizzati richiede particolare cura. Se il paziente è dispnoico, spesso è possibile effettuare una prima ripresa in proiezione dorsoventrale, riservandosi di completare l’esame quando le condizioni del soggetto siano state stabilizzate. È importante ricordare che il trauma toracico non può essere valutato con una sola radiografia in proiezione laterolaterale. La decisione diagnostica più fondamentale è quella di stabilire se il torace dell’animale è normale oppure no. Lo stadio della respirazione e l’entità del volume ematico circolante influenzano l’apparente radiopacità della regione.

IL TORACE ANORMALE Le emergenze dell’apparato respiratorio possono essere suddivise facendo riferimento alla loro localizzazione anatomica: extratoracice, della parete toracica, del diaframma, dello spazio pleurico, del cuore e dei polmoni. Va ricordato che nei pazienti traumatizzati è spesso presente il coinvolgimento di molteplici settori dell’organismo.

Il riscontro di un’eccessiva radiotrasparenza dei polmoni e di una riduzione delle dimensioni delle arterie e delle vene è frequente nei pazienti traumatizzati come segno di ipoperfusione secondaria ad ipovolemia o shock.

Le fratture costali complicano spesso altre lesioni traumatiche, anche se non sono potenzialmente letali di per sé. Si osservano meglio nelle immagini in proiezione ventrodorsale o dorsoventrale.

La lesione più comune del diaframma è la rottura. La condizione può essere potenzialmente letale se una parte del tratto gastroenterico fa ernia attraverso la breccia e viene incarcerata.

Le lesioni dello spazio pleurico si manifestano spesso con una difficoltà respiratoria ad insorgenza acuta dovuta ad un collasso polmonare. La diagnosi va basata su segni clinici e riscontri fisici e solo dopo aver stabilizzato le condizioni dell’animale si deve ricorrere ad altre procedure diagnostiche come le indagini radiografiche. Nel cosiddetto pneumotorace “iperteso” è presente una pressione intratoracica positiva, che costituisce una situazione pericolosa che deve essere affrontata immediatamente. Il liquido pleurico nei pazienti traumatizzati è spesso rappresentato da sangue o trasudati modificati (chilotorace, torsione di un lobo polmonare).

Nei pazienti traumatizzati si riscontrano comunemente contusioni ed ematomi polmonari. Le forze di taglio che lacerano i tessuti polmonari sono causa di cisti traumatiche o pneumatocele. Occasionalmente, nei cani che hanno subito un trauma grave si può riscontrare il “polmone da shock” o la sindrome da difficoltà respiratoria acquisita (SARD), sotto forma di infiltrato diffuso non strutturato. Qualsiasi infiltrato traumatico che non regredisca o diventi più diffuso dopo alcuni giorni deve essere considerato una possibile SARD.

Radiology is one of the most important diagnostic tests in the investigation of thoracic trauma. It usually provides more specific information than the physical examination and can be performed relatively cheaply and quickly. Positioning of the animal is very important and special care shall be taken in a traumatised animal. If the animal is dyspneic it is often possible to initially take a dorso-ventral film and complete the examination when the animal has been stabilised.

It is important to remember that thoracic trauma cannot be assessed with only one lateral view. The most fundamental diagnostic decision is to determine if the animal has a normal or abnormal thorax. Stage of respiration and amount of circulating blood volume will influence the apparent opacity in the thorax.

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THE ABNORMAL THORAX Respiratory system emergencies may be classified in terms of anatomical location: extrathoracic, chest wall, diaphragm, pleural space, heart and lung. It must be remembered that there is often an involvement of multiple areas in trauma patients.

Hyperlucent lungs together with small arteries and veins are often seen in trauma patients as a sign of underperfusion secondary to hypovolemia or shock.

Rib fractures frequently complicate other traumatic injuries even if they are not life threatening themselves. They are best seen on ventro-dorsal or dorso-ventral views.

The most common injury of the diaphragm is a rupture. A life threatening condition can occur if parts of the gastrointestinal tract are herniated and become incarcerated.

Lesions of the pleural space often present with signs of acute onset of respiratory difficulty due to lung collapse. Diagnosis should be based on clinical signs and physical findings and only after the animal is stabilised should other diagnostic procedures such as radiography be performed. In so called “tension” pneumothorax there is a positive intrathoracic pressure, which is a dangerous situation that must be dealt with immediately. Pleural fluid in trauma patients often consists of blood or modified transudates (chylothorax, lung lobe torsion).

In trauma patients lung contusion and hematomas are common changes. Shearing forces tearing the lung tissue apart cause traumatic cysts or pneumatocoele.

“Shock lung” or acquired respiratory distress syndrome (ARDS) can occasionally be seen in dogs after severe trauma as a widespread unstructured infiltrate. Any traumatic infiltrate that does not regress or becomes more widespread after a few days must be considered as possible ARDS.

Introduction Radiology is one of the most important diagnostic tests in the investigation of thoracic diseases. It usually provides more specific information than the physical examination and can be performed relatively cheaply and quickly thus providing rapid results that can be used as a guideline for the next set of decisions. The radiographs can give information about organ systems that otherwise would be very difficult to asses. Before taking the radiographs you should have formulated questions that you want the examination to answer. You should also know the limitations of the technique. Radiographs reveal not only the shadows of gross lesions but also often the physiologic effects of and the organ systems compensation for the disease. Paradoxically, the clarity of thoracic films can lead to erroneous diagnoses.

One example is images of the lungs where many different lesions can have the same appearance and the same disease can show many different patterns.

The radiographic procedure Positioning of the animal is very important and special care shall be taken when positioning a traumatised animal.

That does not mean that poor positioning is accepted. With patience and careful handling it is possible to achieve good quality radiographs of trauma patients. If the animal is dyspneic one can often start by taking a dorso-ventral (DV) film and complete the examination when the condition of the animal has been stabilised. It must be remembered that when a patient has been lying on its side for some time, the lower lung becomes poorly inflated. The poorly aerated lung provides so little contrast that lesions may be entirely invisible

if they are in the lower lung. On the other hand an underinflated lung can be falsely diagnosed as a pathologic change.

To avoid this, the position of the animal shall be shifted and the animal shall be given sufficient time to aerate the lower lung before radiographs are taken. Thoracic trauma cannot be assessed with only a lateral view. To be sure of detecting lesions you may have to take both lateral views (left and right) and either a ventro-dorsal (VD) or DV view or both.

In cats it is often possible to take “whole-body” films that includes both the thoracic and the abdominal cavity to get base line information about the extent of suspected lesions. It must be remembered though that these films are to be regarded as screening films and repeated views of specific areas of interest shall be taken to provide more accurate information.

THE NORMAL THORAX The most fundamental diagnostic decision is to determine if the radiographed animal has a normal or abnormal thorax. The canine thorax is highly variable and even the feline thorax can show some variability. Puppies, kittens, mature animals and old animals have different characteristics.

Many degenerative changes of no clinical significance resemble lesions.

Normal physiologic changes contribute to the resulting image. Stage of respiration and amount of circulating blood volume will influence the apparent opacity in the thorax.

The lungs can have a hyperlucent appearance in the normal thin and deep chested dog or if the lungs are hyperinflated secondary to the animal taking a deep breath. The lungs may also be pathologically hyperlucent if they are underperfused like in shock or hypovolemia.

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THE ABNORMAL THORAX Respiratory system emergencies may be classified in terms of anatomical location: extrathoracic, chest wall, diaphragm, pleural space, heart and lung. It must be remembered that there is often an involvement of multiple areas in trauma patients.

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a mediastinal shift away from the affected side as they push on the heart and mediastinum. A life threatening condition can occur if parts of the gastro-intestinal tract are herniated and become incarcerated. Ultrasound can be helpful in diagnosing suspected diaphragmatic hernias.

Pleural Space Disorders Extrathoracic emergencies The most common emergencies of the upper airways are various kinds of obstruction and haemorrhage. If a satisfactory explanation in a dyspneic animal cannot be found in the thorax it is mandatory to extend the examination into also include the oronasal cavity, the pharynx/larynx and the cervical part of the trachea.

Chest wall emergencies The thoracic wall tends to be forgotten when looking at the contents of the thorax. Lesions of importance can be missed, particularly in trauma cases. Dyspnea can be related to injuries in the thoracic wall just as well as to the more dramatic lesions like pneumothorax. Check for symmetry in the DV/VD view. Trauma to one side can restrict inflation on the affected side and cause compensatory overinflation on the other side. On the other hand unilateral lesions like diaphragmatic hernias can cause expansion of the thoracic wall on the affected side.

Rib fractures are commonly located dorsally near the spine and they are usually seen best on VD or DV views.

Traumatic rib fractures are rarely life threatening themselves but frequently complicate traumatic injuries to the chest wall. Fractured ribs may puncture the pleura and cause pneumothorax or lung contusion. Laceration of lung or chest wall arteries may cause substantial haemorrhage.

Flail chest occurs when a section of the chest wall is mobilised by dorsal and ventral fractures of adjacent ribs allowing paradoxical movement during respiration. If the flail segment is large enough, severe respiratory distress may result from loss of negative pleural pressure and from lung damage.

Trauma to the spine shall be evaluated carefully on thoracic films. If you suspect spinal lesions from the thoracic films or the clinical examination you shall continue the radiographic procedure and take collimated films exposed for bone.

Depending on the extent of the condition, lesions of the pleural space often present with signs of acute onset of respiratory difficulty due to lung collapse. Diagnosis should initially be based on clinical signs and physical findings and only after the animal is stabilised should other diagnostic procedures such as radiography be performed.

Pneumothorax may be associated with traumatic rupture of lung or chest wall, spontaneous rupture of a lung bulla, and neoplastic or inflammatory erosion of lung tissue. The radiological signs of a pneumothorax on a lateral view are that the ventral parts of the lungs and the cardiac shadow are retracted and displaced away from the sternum and the resulting space between the lungs and the sternum becomes black.

A clear radiolucent band will also appear between the lung and the diaphragm and spine. On VD/DV views the lungs are retracted from the thoracic wall with a radiolucent area appearing along the thoracic wall. On all views the lungs will have a sharp edge and the lung opacity becomes slightly increased, as the lung-tissue is less aerated then in normal situations.

In so called “tension” pneumothorax there is a positive intrathoracic pressure, which is a dangerous situation that must be dealt with immediately. The diaphragm becomes flattened and the edges become scalloped in the VD/DV view as it is pulled away from the intercostal muscles.

Pleural fluid in trauma patients often consists of blood or modified transudates (chylothorax, lung lobe torsion). Fluid lying along the thoracic wall, mediastinum, the diaphragm and the lung allows the lung to retract from the adjacent structure by its normal elasticity. On a radiograph fluid can be seen as an opacity obliterating the borders of these structures. In the lateral view the lungs has a ”scalloped” ventral border as the thinner parts are recoiling and becomes rounded. Fluid is also seen between the lung-lobes as interlobar fissures on both lateral and VD/DV views. The costodiaphragmatic angles become rounded and the mediastinum appears widened secondary to fluid accumulation.

Pulmonary lesions Diaphragmatic changes The two most common changes seen in the diaphragm in trauma cases are a flat caudally pushed diaphragm secondary to tension pneumothorax and a “missing” diaphragm. The latter is often caused by either fluid opacity in the lung or in thoracic cavity obscuring the diaphragm or by a diaphragmatic hernia. The appearance of a diaphragmatic hernia is depending on what abdominal organs that are herniated into the thorax. The organs themselves are rarely seen clearly because fluid often surrounds them. They often cause

The terminology used for describing abnormal changes in the lungs could be made on the basis of pathologic terms, anatomic terms or purely descriptive terms.

For interpretation of radiological changes descriptive terms are probably the best. Typical terms are diffuse or focal, lobar, alveolar or interstitial, bronchial or peribronchial, perihilar or peripheral, patchy or scattered and ventral or dorsal. These terms are not specific but can give information that can be useful in trying to classify the disease process and its seriousness.

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The alveolar pattern is seen when the alveoli are flooded with fluid and/or cells that have replaced the air. It is defined as an opacity that obscures the vascular markings accompanied by an air bronchogram sign. The interstitial pattern differs from the alveolar pattern in that it is not as opaque and the vascular shadows are not totally obscured. This division into patterns is descriptive rather than diagnostic, as many conditions will cause the same pattern. More important for the diagnosis is the distribution of the opacities.

In trauma patients lung contusion and hematomas are common changes. These lesions may be located anywhere in the lung. Hematoma has a solid appearance, while contusion and haemorrhage may appear as patchy or diffuse alveolar type lesions.

Shearing forces tearing the lung tissue apart cause traumatic cysts or pneumatocoele. They are seen as radiolucent focal lesions usually surrounded by an opaque lung contusion. They usually reabsorb spontaneously along with the contusion. If filled with blood they are opaque and have the appearance of pulmonary hematomas.

Pulmonary oedema is defined as an increase in lung water content. Causes include congestive heart failure, respiratory distress syndrome, smoke inhalation, electric shock and neurogenic oedema. Oedema usually causes an unstructured infiltrate that when its severe appears as an alveolar opacity.

If the location is bilateral, symmetrical and dorsal in distribution it is strongly suggestive of a cardiogenic pulmonary oedema. Neurogenic oedema that can be seen secondary to trauma to the central nervous system commonly has a caudodorsal patchy and often peripheral location.

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“Shock lung” or acquired respiratory distress syndrome (ARDS) can occasionally be seen in dogs after severe trauma as a widespread unstructured infiltrate. It is associated with poor gas exchange and dyspnea and is often irreversible. Any traumatic infiltrate that does not regress or becomes more widespread after a few days must be considered as possible ARDS. The rate of progression and regression is important in differentiating diseases and “time” shall be regarded as an important dimension in the diagnostic procedure.

Hyperlucent lungs together with small arteries and veins are often seen in trauma patients as a sign of underperfusion secondary to hypovolemia or shock.

Cardiac changes The most common change in trauma patients is that the heart and pulmonary vessels becomes smaller than normal secondary to hypovolemia.

In rare cases traumatic changes in the heart and the pericardial sac can be seen. In the classic case of cardiac tamponade the cardiac silhouette becomes enlarged with a rounded appearance. In cases of rapid fluid accumulation like in traumatic haemorrhage the pericardium has not had the time to adapt and stretch and the heart is small and hypovolemic.

As a result the cardiac shadow might erroneously have a normal appearance. Ultrasound can help to reveal the presence of a hemopericardium.

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Ultrasonography of the genital tract Ecografia dell’apparato riproduttore maschile e femminile nel cane

Kerstin Hansson Med. Vet. - School of Veterinary Medicine - University of Uppsala, Svezia

Riassunto Tecniche di esame ed aspetto normale Per effettuare l’esame dell’apparato riproduttore maschile e femminile è meglio utilizzare un transducer ad alta frequenza, preferibilmente da 7,5-10 MHz. L’animale va posto in decubito dorsale o laterale.

L’utero è situato fra la vescica ed il colon e può essere individuato sia nelle scansioni trasversali che in quelle longitudinali. Le ovaie sono situate in posizione sorprendentemente superficiale. L’aspetto normale dell’utero e delle ovaie e la posizione della cervice variano durante il ciclo riproduttivo. In estro, le corna uterine sono più ampie, più lunghe e più ipoecogene che in anestro.

Il punto di repere per l’identificazione della prostata è la vescica. La scansione viene progressivamente spostata in direzione caudale lungo il collo vescicale e l’uretra fino a trovare la ghiandola. Quest’ultima è iperecogena e presenta una forma bilobata e simmetrica.

Alterazioni patologiche L’alterazione patologica più comunemente diagnosticata nelle vie genitali femminili è la piometra. Il lume dell’organo contiene fluidi di ecogenicità variabile e la parete può risultare di 1-10 mm. Nelle pareti ispessite dei soggetti con piometra si riscontrano spesso molteplici lesioni cistiche anecogene che indicano un’iperplasia endometriale cistica.

Nelle ovaie è possibile diagnosticare le alterazioni cistiche abbastanza grandi da essere rilevabili. Occasionalmente si possono identificare delle neoplasie ovariche, ma, come sempre, non è possibile caratterizzare in alcun modo il tessuto basandosi solo sull’aspetto della massa.

Le alterazioni patologiche della prostata hanno un aspetto aspecifico. Come linea guida, si dice spesso che quanto più la prostata appare eterogenea, tanto più è probabile che sia colpita da una malattia a carattere aggressivo. Per la diagnosi specifica si raccomanda la biopsia tissutale.

Diagnosi di gravidanza L’ecografia viene utilizzata da molti anni per la diagnosi di gravidanza ed è considerata sicura sia per l’operatore che per il paziente. In letteratura sono stati pubblicati molti lavori sulla diagnosi ecografica di gravidanza. In generale, si consiglia di attendere fino al 25° giorno successivo all’accoppiamento prima di effettuare questo tipo di valutazione.

Nel corso di un normale esame per la diagnosi di gravidanza non è raro osservare la presenza sia di sacchi fetali normalmente sviluppati che di altri in vari stadi di regressione.

L’aspetto post-partum dell’utero è variabile. Come semplice indicazione generale, si può tenere presente che occorrono circa 2 mesi all’utero per tornare alla normalità dopo una gravidanza.

Scanning technique and normal appearance The male and female genital tract is best evaluated using a high frequency transducer preferably 7,5 – 10 MHz. The animal is placed in dorsal or lateral recumbency.

The uterus is situated between the bladder and the colon and can be found using either transverse or longitudinal sweeps. The ovaries are situated surprisingly superficial. The normal appearance of the uterus and the ovaries and the position of the cervix are variable during the reproductive cycle. During oestrus the uterine horns are wider, longer and

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more hypoechoic than in anoestrus The landmark for finding the prostate is the urinary bladder. Sweep caudally along the bladder neck and the urethra to find the prostate. It is hyperechoic and has a bi-lobed symmetrical shape.

Pathologic changes The most commonly diagnosed pathologic change in the female genital tract is pyometra. The lumen contains fluid of variable echogenicity and the wall can be 1 - 10 mm. In the thick walled pyometras there is often multiple anechoic cystic lesions indicating cystic endometrial hyperplasia.

In the ovaries it is possible to diagnose cystic changes if they are large enough. Occasionally ovarian neoplasias can be detected but as always no tissue characterisation can be made only on the appearance of the mass.

Pathologic changes in the prostate have a non-specific appearance. As guide line it is often said that the more heterogeneous the prostate appears the more likely it is to contain an aggressive disease. Tissue biopsy is recommended for specific diagnosis.

Pregnancy diagnosis Ultrasound has been used for many years to diagnose pregnancies and is consider safe for both the operator and the patient. Multiple studies concerning pregnancy diagnosis using ultrasound has been published. In general it is recommended to wait until 25 days after mating before a pregnancy evaluation is done.

In a normal pregnancy examination it is not uncommon to see both normally developed foetal sacs and foetal sacs undergoing various stages of regression.

The post partum appearance of the uterus is variable. As a simple guide it takes approximately 2 months for the uterus

Scanning technique The female genital tract is best evaluated using a high frequency transducer preferably 7,5 â&#x20AC;&#x201C; 10 MHz. The animal can be placed in dorsal or lateral recumbency. It is also possible to do the scan with the animal standing as the genital tract then falls towards the transducer and this might facilitate the examination in some animals.

Preparation is done according to standard routines. When clipping the hair coat it is important to include the area of the ovaries. They are located surprisingly dorsal and very superficial and can easily be missed if the prepared area is too small. Some ultrasonographers prefer that the animal have a well-filled bladder to use as an acoustic window. That is true for the caudal parts of the uterus and for the cervix but has no beneficial effects for scanning the uterine horns. In fact an overfilled bladder may cause such a displacement of the uterine horns that they become difficult to trace.

The easiest way to find the uterus is to locate the body of the uterus or the cervix. They are situated between the bladder and the colon and can be found using either transverse or longitudinal sweeps. After locating the body of the uterus, each uterine horn can be followed by use of small movements and gentle pressure. If the transducer is pressed to hard against the skin the superficially located uterine horn and ovary will be dislocated and impossible to find. Scanning the draining lymphnodes is included in the procedure.

Normal appearance The normal appearance of the uterus and the ovaries and the position of the cervix are variable during the reproductive cycle. In anoestrus it might be difficult to find

the normal uterus, as it is often no more than 3-4 mm in diameter. During oestrus the uterine horns become longer and wider and the entire uterus can often be follow. The walls are hypoechoic and even in echotexture. The peripheral part is often seen as a hyperechoic layer. The lumen can sometimes be distinguished as centrally located hyperechoic lines. The cervix are located more cranially during oestrus and becomes wider and more prominent often with a layered of folded appearance sometimes resembling the flower of a tulip.

The ovaries are situated surprisingly superficial. During anoestrus they are located adjacent to the caudal pole of the kidney. In oestrus they are more variable in position and can often be more caudal and ventrally located. The normal appearance of the ovaries depends on the hormonal influence during the reproductive cycle. In anoestrus they are usually oval in shape and around one centimetre large with a hypoechoic texture. During the period around oestrus the ovaries contains various amount of fluid filled anechoic follicles and after ovulation anechoic cavitated corpora lutea can be seen.

Pathologic changes The most commonly diagnosed pathologic change of the uterus is pyometra. The lumen can be seen containing fluid of variable echogenicity. The wall can be 1-2 mm or up to around 10 mm. In the thick walled pyometras there is often multiple anechoic cystic lesion of variable sizes indicating a cystic endometrial hyperplasia. The involvement of the uterus is also variable. Often the entire uterus is dilated and fluid-filled but occasionally there is only a segmental involvement with an ampulla like dilation. Other differentials to consider if a fluid-filled uterus is detected are hydrometra

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or mucometra. If medical treatment of the pyometra is chosen ultrasound can be used to monitor the effect of treatment. Postoperative complications like stump granuloma formation can be difficult to evaluate. If an anechoic cavity is seen it is often possible to aspirate fluid for cytology and bacterial culture. In cases with local peritonitis the surrounding fat tissue becomes hyperechoic and sometimes fluid-filled pockets can be seen in the caudal part of the abdominal cavity.

In the ovaries it is possible to diagnose cystic changes if they are large enough. Care should be taken when it comes to concluding that it is a pathologic cystic change and not a cavitary corpora lutea. Occasionally ovarian neoplasias can be detected but as always no tissue characterisation can be made only on the appearance of the mass. Differentials are other abdominal masses in the area and lymphadenopathy.

PREGNANCY DIAGNOSIS Ultrasound has been used for many years to diagnose pregnancies and is consider safe for both the operator and the patient. Multiple studies concerning pregnancy diagnosis using ultrasound has been published. In the dog the conceptuses may be imaged for the first time around 15 days post mating. It is then only about 2 mm in diameter so a high frequency transducer is mandatory in order to detect such a small structure.

At 20 days after mating the foetal sac is oval and measures approximately 15 mm in length. In general it is recommended to wait until 25 days after mating before a pregnancy evaluation is done. At that time an embryo with distinct cardiac activity can be seen in the spherical foetal sac.

If the examination is done earlier it might be difficult to differentiate a foetal sac from small amounts of free fluid in the uterus and other fluid-filled structures like cysts in the ovaries and cross sections of vascular structures. Around day 30, foetal movements are first detected and clear differentiation into a head, trunk and abdomen can be visualised. At the same time mineralisation of the mandible can become apparent as a small hyperechioc structure causing acoustic shadowing. The most rapid growth of the foetus occurs between days 32 and 55. At day 38 â&#x20AC;&#x201C; 40 the anechoic fluidfilled stomach and urinary bladder can be seen and at day 43 - 45 it becomes possible to separate the thoracic and abdominal cavities as the lungs and the liver develops into having different echogenicities.

In a normal pregnancy examination it is not uncommon to see both normally developed foetal sacs and foetal sacs undergoing various stages of regression. If this resorbtion takes place during early pregnancy no clinical signs are present in the bitch.

The post partum appearance of the uterus is variable.

During the first 48 hours there is a rapid decrease in size of the uterus. Fluid can often be seen in the lumen until 3 weeks post partum and the diameter varies between 5 â&#x20AC;&#x201C; 15 mm depending if the measurements are done at placental or inter-placental areas. As a simple guide it takes approximately 2 months for the uterus to become normalised after a pregnancy.

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ULTRASOUND OF THE MALE GENITAL TRACT Scanning technique The prostate is relatively easy to localise unless it is situated in the pelvic canal or has undergone atrophy secondary to castration. The landmark is the urinary bladder that is oval and anechoic. The prostate can be found by sweeping caudally along the bladder neck and the urethra in longitudinal and transverse scan planes. It is recommended that the testes are included as a routine part of the scanning procedure of the prostate to include the entire male genital tract. Scanning the draining lymphnodes should be included.

Normal appearance The prostate is localised directly caudal to the urinary bladder and the position is variable with age. In the young puppy the prostate is localised entirely in the abdominal cavity until the regression of the urachus when the position is shifted caudally and the prostate is situated in the pelvic canal. If the male is intact the prostate usually undergoes hyperplasia when the dog reaches middle age. It is then shifted cranially towards and partly into the abdominal cavity. The prostate has a bi-lobed symmetrical shape. There are no reliable criteria for judgement of normal prostatic size due to breed and age variability. The texture is even and the echogenicity is hypoechoic in the young and castrated male and hyperechoic in the middle age and older dogs. The urethra is situated in the middle of the prostate in the cranial and central parts. In the caudal part the urethra is more dorsally located and surrounded by a diffuse hypoechoic zone.

The testes has an even texture and echogenicity. They are hypoechoic with a centrally located hyperechoic testicular mediastinum. The epidymidis are slightly less echogenic in comparison to the testes.

Pathologic changes Pathologic changes in the prostate have a non-specific appearance and it is not possible to distinguish between benign hyperplasia and diffuse chronic prostatitis. In many dogs these two disease processes goes on simultaneously. The most common appearance of benign hyperplasia is a symmetric prostatomegaly often accompanied by few or numerous small anechoic cysts.

Larger anechoic areas can be prostatic cysts, abscesses or cavitary neoplasias. It is recommended that a fine needle aspirate be taken from the fluid filled areas to add to the information of disease process. Ultrasound guided aspiration of fluid filled cavities can also add to treatment of the disease. Neoplastic processes in the prostate are rare and have a very variable appearance. As guide line it is often said that the more heterogeneous the prostate appears the more likely it is to contain an aggressive disease. Tissue biopsy is recommended for specific diagnosis.

Changes in the testes are readily visualised by use of ultrasound. Non palpable masses can easily be detected. Diffuse or localised changes can be separated and testicular versus scrotal disease can be differentiated.

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Imaging of the animal with haematuria Impiego della diagnostica per immagini nel paziente con ematuria

Kerstin Hansson Med. Vet. - School of Veterinary Medicine - University of Uppsala, Svezia

Riassunto Esame radiografico o ecografico?

La questione relativa all’impiego delle tecniche radiografiche o ecografiche per la valutazione del tratto urinario sta diventando sempre più importante. Con queste metodiche è possibile caratterizzare morfologicamente i vari organi rilevandone, ad esempio, la posizione, le dimensioni, la forma, il profilo e la radiopacità (nel caso della radiografia) e l’ecogenicità (nell’ecografia). Le indagini ecografiche forniscono un maggior numero di informazioni regionali, mentre le radiografie consentono di valutare le strutture addominali sulla base di una prospettiva più geografica. L’ecografia è ideale per la valutazione degli organi formati da tessuti molli e delle strutture piene di liquidi e, come tale, risulta molto adatta all’esame delle vie urinarie. Si tratta di un metodo non invasivo, che non prevede l’uso di radiazioni ionizzanti e si è dimostrato sicuro e molto utile sia per l’operatore che per il paziente. Altri fattori in suo favore sono la convenienza in termini di tempo e di costo.

Tuttavia, non bisogna mai dimenticare che per la corretta interpretazione dei riscontri radiografici ed ecografici sono ancora essenziali le tradizionali indagini cliniche e di laboratorio. Associando tutte queste metodiche è spesso possibile arrivare ad una diagnosi corretta.

Indicazioni per l’impiego della diagnostica per immagini negli animali con ematuria Le cause più comuni di ematuria nel cane e nel gatto sono i calcoli urinari, la cistite, i polipi vescicali e le alterazioni neoplastiche. Nella maggior parte dei casi, il processo patologico responsabile dell’ematuria può essere localizzato nelle basse vie urinarie. In alcuni pazienti, il problema può invece essere localizzato nel tratto superiore dell’apparato. Sono esempi di nefropatie in grado di causare ematuria le neoplasie e la malattia del rene policistico del gatto. Non tutti i casi di ematuria saranno sottoposti ad un’ulteriore valutazione con le varie tecniche di diagnostica per immagini. Per selezionare i casi in cui è necessario ricorrere agli esami radiografici ed ecografici si possono utilizzare i seguenti criteri: • riscontri clinici anomali, come la percezione alla palpazione di un ispessimento della parete vescicale o della presenza di calcoli • malattie ricorrenti • malattie che non rispondono alla terapia • malattie di vecchia data Nel corso della relazione verranno illustrate le comuni cause di ematuria, confrontando l’impiego della radiografia e dell’ecografia in queste entità patologiche.

Radiography or ultrasonography?

The question of whether to use radiography or ultrasonographic techniques for assessment of the urinary tract has become increasingly important. Morphologic characterisations like organ position, size, shape, contour and density for radiographic procedures and echogenicity for ultrasonographic procedures can be gathered. Ultrasound provides more regional information while the radiograph produces a more geographic perspective of the abdominal structures. Ultrasound is ideally suited for evaluating soft tissue organs and fluid filled structures and as such is well suited for the urinary tract. It is non-invasive, does not involve the use of ionising radiation and has been proven to be a safe and very useful technique both for the operator and for the patient. Other factors in favour of ultrasound is that it is time and costeffective.

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One must always remember though that traditional physical and laboratory methods are still essential for proper interpretation of the radiographic and sonographic findings. By combining these methods a correct diagnosis can often be achieved.

Indications for imaging the animal with haematuria The most common causes of haematuria in the dog and the cat are urinary tract calculi, cystitis, bladder polyps and neoplastic changes. In the majority of cases the pathologic process responsible for causing the haematuria can be localised to the lower urinary tract. In some patients the problem can be found in the upper urinary tract. Examples of renal disease causing haematuria are neoplastic changes and feline polycystic kidney disease. Not all cases of haematuria shall be subjected to further examination with various imaging techniques. The following criteria can be used for selection of the patient to be examined radiographically or ultrasonographically; • Abnormal physical findings like palpation of bladder wall thickening or calculi • Recurrent disease • Non-responsive disease • Long-standing disease Common causes for haematuria will be covered during the session. The use of radiography and ultrasound for these disease entities will be compared.

Radiography or ultrasonography?

The question of whether to use radiographic or ultrasonographic techniques for assessment of the urinary tract has become increasingly important. In all imaging procedures there are various types of information that can be gathered. Morphologic characterisations like organ position, size, shape, contour and density for radiographic procedures and echogenicity for ultrasonographic procedures can be gathered.

Ultrasound provides more regional information while the radiograph produces a more geographic perspective of the abdominal structures. Ultrasound is ideally suited for evaluating soft tissue organs and fluid filled structures and as such is well suited for the urinary tract.

The next consideration in the choice of imaging technique is the safety of the procedure for the patient and the feasibility of performing the procedure in that specific patient. The excretory urography includes the potential hazard associated with systemic contrast medium administration.

Although a systemic hypotensive or anaphylatic reaction is always possible, these are rare if the patient is adequately hydrated.

Cystography on the other hand does not include systemic injection of a contrast medium but it needs the use of an urethral catherisation.

Ultrasound is non-invasive and does not involve the use of ionising radiation. It has been proven to be a safe and very useful technique both for the operator and for the patient.

Other factors in favour of ultrasound is that it is both time and cost-effective.

One must always remember though that traditional physical and laboratory methods are still essential for proper interpretation of the radiographic and sonographic findings.

By combining these methods a correct diagnosis can often be achieved.

Indications for imaging the animal with haematuria The most common causes of haematuria in the dog and the cat are urinary tract calculi, cystitis, bladder polyps and neoplastic changes. In the majority of cases the pathologic process responsible for causing the haematuria can be localised to the lower urinary tract. In some patients the problem can be found in the upper urinary tract. Examples of renal disease causing haematuria are neoplastic changes and feline polycystic kidney disease.

Not all cases of haematuria shall be subjected to further examination with various imaging techniques. The following criteria can be used for selection of the patient to be examined radiographically or ultrasonographically; • Abnormal physical findings like palpation of bladder wall thickening or calculi • Recurrent disease • Non-responsive disease • Long-standing disease

RADIOGRAPHY OF THE URINARY TRACT For evaluation of the urinary system the entire abdomen from the diaphragm caudally to the pelvic canal must be included on both lateral and ventro-dorsal radiographs. The stomach and the colon should be empty as the presence of food and/or faecal material will interfere with evaluation of the radiographs.

Non-contrast radiographs provide information about the position, size, shape, contour and opacity of the urinary tract. The normal kidneys are bean-shaped and localised in the cranial and mid-dorsal abdomen. The right kidney of the dog is often difficult to identify, as it is more cranially located and difficult to separate from the dorsal parts of the

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liver. It is also often obscured by parts of the gastro-intestinal tract.

The normal bladder is ovoid with a cranial blunt apex. In the female dog and in the cat the bladder neck is longer with a gradually tapering shape in comparison to the male dog.

Excretory urogram provides good anatomic and some functional information about the kidneys, ureters and the bladder. The cystogram is very useful for evaluation of the bladder and can be performed as a positive (using iodinecontaining contrast medium), negative (using air) or double contrast study.

ULTRASONOGRAPHY OF THE URINARY TRACT Imaging of the urinary system can often be performed using a high frequency transducer preferably 7,5 â&#x20AC;&#x201C; 10 MHz. The animal can be examined in dorsal or lateral recumbency. Hair is clipped and ultrasound gel is applied according to standard procedure.

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COMMON CAUSES OF HAEMATURIA Bladder calculi and blood clots Many bladder calculi have a size and opacity that makes them possible to be detected on plain film radiography.

Small stones, mineralised sediment and calculi consisting of non-radiopaque material may not reveal themselves unless high quality cystography is performed and even then, some still remains undetected.

Ultrasound can easily identify intraluminal bladder abnormalities like blood clots and calculi. Calculi are seen as curvilinear hyperechoic structures that causing a clear acoustic shadow if they are large enough in comparison to the beam width. Calculi are moveable and shift position as the position of the patient is shifted. Blood clots are usually hyperechoic but without acoustic shadowing. They can either be freely moving in the bladder lumen or they can be attached to the mucosa.

Cystitis Ultrasound of the normal urinary bladder The urinary bladder is best evaluated when it is filled but not overfilled with urine. With an over-distended bladder small mucosal and mural lesions may be missed due to bladder wall stretching. The normal bladder is anechoic and has a smooth well-defined wall. Acoustic enhancement is seen deep to the urinary bladder. The normal bladder wall has three distinct layers.

The outer serosa and the inner mucosa/lumen interface are hyperechoic. Between these two layers the hypoechoic smooth muscle layer can be seen. Care should be taken when evaluating bladder wall-thickness as the wall becomes thicker in a nearly empty bladder. The normal bladder wall should be no more than 1-2 mm. The oval shape is also lost in an empty bladder.

Ultrasound is superior to radiography in diagnosing several bladder diseases as it allows imaging of the wall and the content of the urinary bladder in great detail without the use of catherisation and ionising radiation.

Ultrasound of the normal kidney The normal kidney is smooth and well defined. The renal capsule can be seen as a thin echogenic line. The cortex is moderately hypoechoic and the medulla is hypoechoic and almost anechoic. The renal pelvis is seen as two hyperechoic lines surrounded by hyperechoic fatty tissue. The left kidney is often easy to visualise as it is situated more caudal than the right kidney. In many cases the right kidney needs to be scanned through an intercostal approach and sometimes it is difficult to image the whole kidney because of rib shadows.

Scanning of especially the right kidney needs the use of distinct pressure on the transducer to get good skin contact and to displace parts of the intestinal tract that might be overlying the kidney.

Bladder wall and mucosal lesions can be detected with both cystography and ultrasound. Ultrasound produces more specific information about the extent and appearance of the lesion. Involvement of the different wall layers can be identified and the disease process can be monitored in great detail during and after treatment. The most typical appearance in cystitis is a localised irregularity or thickening often with loss of normal layering in the cranioventral part of the bladder. One must be aware of that cystitis and tumours can produce a similar pattern. Both lesions can be either localised or involve the entire bladder circumference and in both instances intraluminal blood clots can be seen.

Bladder neoplasi As mentioned above there is an overlap in the appearance of cystitis and bladder neoplasias both on cystography and ultrasonography. Transitional cell carcinoma is the most common neoplasm of the urinary bladder and it is often localised in the trigone area. Localised tumour masses are seen as hypoechoic, hyperechoic or mixed echoic masses bulging into the bladder lumen. Thickening of the bladder wall at the site of attachment can often be seen. A tumour and a blood clot can both be attached to the mucosal surface and are as such impossible to differentiate from each other. Tissue biopsy is recommended for specific diagnosis. The iliac lymph nodes should always be evaluated in cases of suspected neoplasi of the bladder.

Polyps Polyps may be seen as distinct echogenic structures projecting into the bladder lumen. They are often pendulous masses with a more narrow base in comparison to neoplastic changes but histology is needed for a proper diagnosis.

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Polycystic Kidney Disease in the Persian Cat The most common cause for heamturia to occur due to changes in the upper urinary tract is renal neoplasia and polycystic kidney disease (PKD). The latter has become a problem in the Persian cat as it is inherited according to an autosomal dominant trait.

Survey abdominal radiographs are normal in early stages of the disease. As the changes progress the kidneys become enlarged and irregular renal contours may be observed. Excretory urography can be helpful in the diagnosis of the disease. During the nephrogram stage the cysts can be seen as numerous sharply marginated radiolucencies throughout the parenchyma of the kidneys. Ultrasound has been found to be an excellent non-invasive technique for early diagnosis of PKD. Cysts as small as 1-2 mm can be seen with a high frequency transducer. Ultrasonographically cysts appear as round, smooth anechoic structures that demonstrate distant enhancement.

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neoplasias can have a normal appearance on both radiography and ultrasound. Mass lesions are easier to identify but have a variable appearance. They are often seen as irregularly enlarged kidneys often accompanied by distortion and invasion of the renal pelvis. The ultrasonographic appearance is highly variable with a mixed echogenicity and it can be impossible to distinguish between neoplasms, heamatomas and abscess. Renal biopsy is recommended for specific diagnosis.

Renal calculi Renal calculi can be seen on survey radiographs as opaque structures located in the central area of the kidney.

On ultrasound renal calculi appear as hyperechoic structures causing a clear acoustic shadow. Dilation of the renal pelvis can be seen as a central anechoic “hole” within the kidney.

Prostatic disease Renal neoplasia Renal neoplasias can be either diffusely infiltrating the kidney or be presented as localised mass lesions. Diffuse

Prostatic disease must be taken into account when making a list of differential diagnosis causing haematuria in the male dog. The subject will be covered in a following session presented by Dr. Borgarelli.

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Whatâ&#x20AC;&#x2122;s new in reptile virology Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Francesco Origgi Med. Vet., Departments of Small Animal Clinical Sciences and Pathobiology College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto Inclusion body disease of boid snakes - This disease has been seen in a variety of boid snakes including boa constrictor (Constrictor constrictor), anaconda (Eunectes murinus), Haitian boa (Epicrates striatus), Burmese python (Python molurus bivittatus), Indian python (P. m. molurus), reticulated python (P. reticulatus), and ball python (P. regius).

In boa constrictors, the first clinical sign manifested is regurgitation of a prey item within several days of feeding. While some snakes die within several weeks of first manifesting illness, others may survive for months. Some of these snakes may eventually show signs of central nervous system (CNS) disease, exhibiting disorientation, head tilting, and opisthotonus. In Burmese pythons the disease is more chronic with primary signs of CNS disease; several snakes with flaccid paralysis of the CNS have been seen. Regurgitation is seldom seen in Burmese pythons. The major histologic finding, which appears characteristic of this disease, is the presence of eosinophilic intracytoplasmic inclusions within hematoxylin and eosin stained sections of multiple tissues. In boa constrictors the inclusions are most prominent in the kidney, pancreas and liver and also brain, while in Burmese pythons the inclusions are mostly found within neurons in the CNS. Additionally, snakes with signs of CNS disease often have a significant encephalitis. However, the encephalitis is more severe in pythons compared to boa constrictors. Several retroviruses been isolated in tissue culture from affected boa constrictors and the same agent has been identified in tissue section. This viruses are presently being characterized.

History: For over 20 years in private and zoological collections of boas and pythons in the United States, Africa and Europe a naturally occurring disease characterized by the formation of intracytoplasmic inclusions in epidermal cells, visceral epithelial cells, and neurons in the central nervous system (CNS), has been recognized and named inclusion body disease (IBD).1 Recently, IBD was seen in Australia in two captive native pythons (Morelia spilota variegata and Morelia spilota spilota)2 and in captive boa constrictors in the Canary Islands, Spain.3 In addition, the disease has been diagnosed by one of us (ERJ) in an eastern king snake (Lampropeltis getulus, family Colubridae) which was housed with boa constrictors (Boa constrictor). Starting in the late 1970s and extending into the mid-1980s, Burmese pythons (Python molurus bivittatus) were the most common boid snakes seen with IBD, with signs of CNS disease as the most common clinical sign.

Host: All boid snakes should be considered susceptible.

Characteristic inclusions also have been seen in an eastern king snake that was housed with boa constrictors. The primary host of this virus has not been identified.

Distribution: Worldwide in captive boid snakes. Its occurrence in the wild is unknown. Several cases have recently been seen in captive pythons in Australia, Canary Islands, and Italy. The transport of captive snakes in the pet trade and transport between different zoologic institutions probably account for the spread around the world.

Ages Affected: Has been identified primarily in adult snakes. However, all age groups should be considered susceptible. There are anecdotal reports of infection in neonates.

Etiologic Agent: A retro-like virus has been incriminated as the causative agent of IBD. Tissues and blood from two boa constrictors (Boa constrictor constrictor and B.c. occidentalis) diagnosed with IBD and one Madagascan ground boa (Acranthophis dumerili) that had a littermate in which IBD was diagnosed were submitted for viral isolation attempts. Three viruses (RV-1, RV-2, and RV-3) were isolated either from buffy coat cells cocultivated with viper heart cells or primary kidney cells of boid snakes with IBD. Using electron microscopy, the three isolates were compatible morphologically with members of the family Retroviridae.

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This was supported by demonstration of reverse transcriptase activity in those sucrose gradient fractions which were rich in virus. Polyclonal antibody raised in rabbits against RV-1 was used to compare viral proteins by Western blot analysis. Both RV-1 and RV-2 had proteins with similar migration patterns. Major bands occurred at corresponding molecular weight markers of 20 and 30 kd. Using electron microscopy and immunogold labeling, polyclonal antibody against RV-1 recognized virions of both RV-1 and RV-2.

Whether this virus(es) represents the causative agent of IBD is yet to be determined. An endogenous retrovirus is known to be present in VH2 cells, a cell line that is commercially available and commonly used in the isolation of reptile viruses. This is extremely important to realize when using these cells to isolate reptile viruses. However, we have no evidence of replication of this endogenous virus in any of the VH2 cells examined by electron microscopy. Future transmission studies will be necessary to esatblsih a causal relationship.

ine transmission to developing embryos in viviparous species and eggs in oviparaous species; 3) veneral transmission. The snake mite, Ophionyssus natricis has been implicated as a vector for the virus since mite intestations are commonly seen in epizootics of IBD.

Clinical Signs: Clinical signs are quite variable. Regurgitation and signs of central nervous system disease are commonly seen in boa constrictors. Stomatitis, pneumonia, undifferentiated cutaneous sarcomas, lymphoproliferative disorders, and leukemia have all been seen. Burmese pythons generally show signs of central nervous system disease without manifesting any other clincal signs; regurgitation is not seen in Burmese pythons.

Control: Identify infected snakes and euthanatize. All new snakes should be quarantined for minimally 90 days before introduction into an established collection. Recommendations for boas is 6 month quarantine period. Mite control and elimination is essential. Fibroglass cages of infected snakes should be cleaned with chlorox and left out in the sun to dry before being used for other snakes. Wooden cages, unless sealed with urethane or some other sealeant should be discarded.

Pathology: By light microscopy, in hematoxlin and eosin stained tissues sections of a wide variety of epithelial and neuronal cells, characteristic intracytoplasmic inclusions are seen. Several snakes have been seen with proliferative pneumonia. While inclusions are commonly seen in the liver, kidney, and pancreas, we have seen cases where there are very few inclusions. In a few snakes with signs of central nervous sytem disease, and with a severe encephalitis, no inclusions have been seen in any cells. While the presence of characteristic inclusions is diagnostic for the disease, the absence of inclusions does not necessarily mean the snake is disease or IBD virus free. While cells having inclusions may show mild degeneratve changes, inflammation is rarely seen in visceral tissues. In the brain, mild to severe encephalitis, with lymphocytic perivascular cuffing may be seen. Several snakes with lymphoproliferative disorders have been identified with lymphoid infiltrates in multiple organs.

Transmission: The exact route of transmission has not been identified. Possibly by: 1) direct contact; 2) intrauter-

Diagnosis: Currently there is no serologic assay available for determining exposure. If one of the retroviruses we have isolated is found to be the causative agent, we will be able to start developing a serological test. Boa constrictor immunoglobulin has been purified and a mice have been inoculated to produce a polyclonal against this immunoglobulin. At the University of Florida College of Veterinary Medicine, we perform complete blood counts on suspect snakes.

Infected snakes commonly have white blood cells counts >30,000/ul. Intracytoplasmic inclusions are occasionally seen in peripheral lymphocytes. We also take esophageal, gastric, and liver bopsies. If inclusions are identified in any cells, euthanasia is recommended.

Current and Future Research: The major lines of research involve identification and isolation of the causative agent and then development of a serodiagnostic test. At this point in time it is unrealistic to consider development of a vaccine. A serologic test will be used to identify exposed/ibfected snakes that can be eliminated from breeding collectioms.

Given the number of snakes that have died of this disease over the last few years, IBD should be considered the most important health problem of captive snakes in the world today.

References 1.

2.

3.

Schumacher J, Jacobson E R, Homer B L and Gaskin JM. 1994. Inclusion body disease in boid snakes. J Zoo Wildl Med 25: 511-524.

Carlisle-Nowak MS, Sullivan N, Carrigan M, Knight C, Ryan C, and Jacobson ER. 1998. Inclusion body disease in two captive Australian pythons (Morelia spilota variegata and Morelia spilota spilota).

Aust Vet J 76: 98-100.

Oros J., Tucker S., and Jacobson E.R. 1998. Inclusion body disease in two captive boas in the Canary islands. Vet. Rec. 143: 283-285.

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Mycoplasma Infection in Tortoises Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto The most significant bacterial disease in free-ranging and captive desert and gopher tortoises in the United States is mycoplasmosis. In 1988, desert tortoises with upper respiratory tract disease (URTD) were seen in the Desert Tortoise Natural Area (DTNA), Kern County, California. In 1989, a detailed survey of the DTNA and nearby areas in the Rand Mountains and Freemont Valley indicated that 43% of 468 live desert tortoises encountered on the sections surveyed showed signs of this disease. Desert tortoises with URTD have also been seen in the Las Vegas Valley, Nevada, the Beaver Dam Slope, Utah/Arizona, and the Sonoran Desert, Arizona, USA. Pathologic studies of 17 ill desert tortoises from the DTNA and one ill desert tortoise from Utah indicated that major microscopic lesions were confined to the upper respiratory tract (URT). Electron microscopic studies revealed small (350 to 900 nm), pleomorphic organisms resembling Mycoplasma in close association with the surface epithelium of the URT of ill tortoises. Mycoplasma was cultured from the nasal passageways of ill tortoises, and at the time, represented only the second report of isolation of a mycoplasma from a reptile. Mycoplasma testudinis was previously isolated from the cloaca of a spur-thighed tortoise. However, the pathogenicity of this organism is unknown. The mycoplasma isolated from the desert tortoise was named Mycoplasma agassizii, with strain PS6 the type strain. In a recent transmission study, that organism was demonstrated to be the cause of URTD in the desert tortoise. Mycoplasma agassizii has been isolated from wild gopher tortoises in Florida with rhinitis, and transmission studies also have confirmed it as the causative agent. An ELISA has been developed to determine exposure of desert and gopher tortoises to that bacteria.

History: Rhinitis and upper respiratory tract disease (URTD) have been reported in a variety of species of wild and captive tortoises in the United States1 and Europe.2 While hypovitaminosis A was considered a predisposing problem in certain tortoises, Fowler3 discussed the differences between URTD and hypovitaminosis A. Several agents have been hypothesized to cause respiratory tract disease in tortoises, including viruses,4 Mycoplasma sp.,3,5 and Pasteurella sp.6 In Europe, Sendai virus was considered a possible cause of rhinitis in captive spur-thighed (Testudo graeca ) and Hermann’s tortoises (T. hermanni),4 but a later study5 found no increase in antibody titers against Sendai virus over a 3 month period. A herpesviruslike infection was associated with rhinitis, anorexia, and death in Argentine tortoises (Geochelone chilensis) imported into south Florida.7 Apparent herpesviruses8 and iridoviruses9 have been associated with rhinitis, glossitis, pharyngitis, pneumonia, and death in spur-thighed, Hermann’s and Russian (T. horsfieldii) tortoises. Recent attempts to isolate and cultivate the herpesvirus have been successful, and show promise for developing a diagnostic test for determining exposure.10 Recently, an iridovirus was identified in a gopher tortoise with clinical signs of URTD. In the 1980s, major declines (33-76% over 10 yr) of desert tortoises (Gopherus agassizii) were documented at

several sites in the western Mojave Desert of California, USA, and at one site in the eastern Mojave.12 Tortoises with clinical signs of URTD were observed among affected populations at several sites.13 As a result of the declines, in 1990, desert tortoises in the Mojave Desert north and west of the Colorado River were declared threatened by the U.S. Fish and Wildlife Service.

Beginning in 1989, efforts were undertaken to determine the etiology of URTD in desert tortoises.1 By electron microscopy, pleomorphic organisms resembling Mycoplasma sp. were seen on cell surfaces and tightly adhered to cell membranes of ill tortoises, and Mycoplasma sp. were isolated from ill tortoises. The mycoplasma was determined to be a new species, provisionally named Mycoplasma agassizii.14 An enzyme-linked immunosorbent assay (ELISA) to detect antibodies against the mycoplasma in plasma and serum samples was developed,15 and experiments were undertaken to fulfill Koch’s Postulates. The disease was induced by inoculation of tortoises with pure cultures of the mycoplasma, but not Pasteurella testudinus (Brown et al., 1994).16 Histologically, the lesions were consistent with those seen in the previously examined naturally infected tortoises. A polymerase chain reaction (PCR) was developed to detect nucleotide sequences of the 16s rRNA gene of the bacteria in nasal flush and swab samples.14

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Although URTD has been seen in captive gopher tortoises, the first documentation of the disease in wild gopher tortoises was in 1989, when an epizootic of URTD was documented on Sanibel Island, Lee County, Florida, USA, during the course of an ecological study. When tested by ELISA, >80% of the adult tortoises from Sanibel Island were seropositive for antibodies against M. agassizii. Due to the 1979 listing by the Florida game and Fresh Water Fish Commission of the gopher tortoise as a species of special concern, and the subsequent permitting of over 450 relocations involving more than 8000 tortoises, particular attention has been focused on the dynamics and persistence of both natural and relocated populations.17 The observation of URTD on Sanibel Island and the association of mycoplasmosis with declines of certain desert tortoise populations in the Mojave Desert elicited concerns regarding declining and isolated populations of gopher tortoises. Because an understanding of the effects of URTD on both individuals and populations is essential for proper management of remaining populations, a study was begun in 1993 on the etiology, pathology, and diagnosis of URTD in gopher tortoises.

Host Range: Of the 40 species of tortoises, mycoplasmosis has been identified in desert tortoises, gopher tortoises, leopard tortoises (G. pardalis), Indian star tortoises (G. elegans) , Asian tortoises (Indotestudo spp.), spurthighed tortoises and box turtles (Terrapene carolina bauri). Unless proven otherwise, all species of tortoises should be considered susceptible.

Distribution: Known to occur in wild gopher tortoises in Florida, USA, and in wild desert tortoises in California, Nevada, Utah, Arizona, USA and Testudo graeca in France.

Mycoplasmosis is primarily seen in adult tortoises in the wild, but under experimental conditions all age groups are susceptible.

Clinical Signs: Major clinical signs include palpebral edema, conjunctivitis, and rhinitis. Clear serous to tenacious mucous may be seen bubbling from nares. Mycoplasmosis can occur as a subclinical infection.18 We have seen an annual cycle of convalescence and recrudescence of clinical signs in some captive desert and gopher tortoises. Other mycoplasmal diseases also can exist as chronic, subclinical infections, with recurrence of clinical signs and increases in transmission potential when the host is stressed.

Environmental Factors: Although data are lacking, we suspect that various environmental changes may influence the periodicity of outbreaks. Annual fluctuations in temperature, rainfall, and forage availability may be sufficient to cause detectable outbreaks in an infected population. Increased morbidity and mortality may occur in times of unusually severe environmental stress, such as prolonged drought, hurricanes, excessive rainfall with flooding of burrows, or very cold winters. Human impacts on tortoises and their habitat, whether through disruption of normal behavior patterns, degradation of habitat through

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agriculture, silviculture, mining or development operations, or pollution, may cause sufficient physiological stress to trigger proliferation of the mycoplasma and recurrence of signs. Capturing and transporting of tortoises during relocation, restocking and repatriation efforts also may be significant sources of stress that result in overt disease. The release of ill captive tortoises may be a significant factor accounting for the presence of URTD in certain populations.

Transmission: The results of the experimental challenge studies support the hypothesis that M. agassizii was horizontally transmitted between adult tortoises, and between adult and hatchling tortoises. Direct contact is the most likely route. If aerosol transmission occurs, it is probably over short distances (<0.5 m). Sentinel and control animals housed in pen sections that also housed ill tortoises did not become ill or seroconvert, which indicated that aerosolized bacteria did not travel even relatively short distances over low (0.7 m) barriers. Based on the environmental transmission study, fomites are unlikely to play a major role in URTD transmission. Although horizontal transmission of M. agassizii has been documented, there is no evidence of vertical transmission. It appears that tortoises with clinical signs of URTD can produce URTD free eggs.

Control: Ill tortoises need to be isolated from healthy tortoises. Do not release ill tortoises back to the wild.

Healthy tortoises need to be thoroughly evaluated if they are to be released to the wild. In affected tortoises, mycoplasmosis is a chronic upper respiratory disease. While certain antibiotics such as enrofloxacin (5 mg/kg of total body weight, i.m., s.i.d for 10 treatments) have been utilized by injection and infused into the nasal cavity (0.5 cc of injectable enrofloxacin diluted 1:10 )in most cases the organism will not be eliminated. While clinical signs of illness may abate following treatment, relapses commonly occur.

Diagnosis: Mycoplasma can be cultured directly from the nasal cavity of infected tortoises. However, these organisms are difficult to isolate and a mycoplasmologist needs to be consulted. An Enzyme Linked Immunosorbent Assay (ELISA) has been developed to measure plasma/serum antibodies which are specific for mycoplasma (Schumacher et al, 1993). A PCR assay has been developed to determine presence of specific nucleotide sequences in mycoplasma DNA. Ideally, culture, ELISA and PCR all should be used in making a diagnosis of exposure and infection.

References 1.

2.

Jacobson, E.R., Gaskin, J.M., Brown, M.B., Harris R.K. Gardiner, C.H., LaPoint, J.L., Adams, H.P. and Reggiardo, C. 1991. Chronic upper respiratory tract disease of freeranging desert tortoises, Xerobates agassizii. J. Wildlife Disease. 27:296-316.

Jackson, O.F. 1980. The sick chelonian. proceedings of the European Herpetology Symposium, pp. 1-4.

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3.

4.

5.

6.

7.

8.

9.

10.

11.

Fowler, M.E. 1980. Differential diagnosis of pneumonia in reptiles, in: J.B. Murphy and J.T. Collins (eds.) Reproductive Biology and Diseases of Captive Reptiles. Society for the Study of Amphibians and Reptiles, Lawrence, KS. Pp. 227-233.

Jackson, O.F., and J.R. Needham. 1983. Rhinitis and virus antibody titers in chelonians. J. of Small Animal Practice 24: 31-36.

Lawrence, K., and J.R. Needham. 1985. Rhinitis in long-term captive Mediterranean tortoises (Testudo graeca and T. hermanni). Veterinary record 117: 662-664.

Snipes, K.P., and E.L. Biberstein, and M.E. Fowler. 1980. A Pasteurella sp. associated with respiratory disease in captive desert tortoises.

J.A.V.M.A. 177: 804-807.

Jacobson, E.R., S. Clubb J.M. Gaskin, and C.H. Gardiner. 1985. Herpes-like infection in Argentine Tortoises. J.A.V.M.A., 187: 12271229.

Lange H, Herbest W, Wiechert JM, and Schlieber TH: Elektronen mikoskopischer nachweis von herpesviren bei einem massessterben von griechischen landschildkroten(Testudo hermanni) und vierzehenschildkroten (Agrionemys horsfieldi). Tieraztl Prax 17:319-321, 1989.

Muller M, Sachsse W, and Zangger N. 1990. Herpesvirus-Epidemie beider griechischen (Testudo hermanni) und der maurischen Landschildkrote (Testudo graeca) in der Schweiz. Schweiz Arch Tierhelk 32:199-203.

Kabisch D, and Frost JW. 1994. Isolation of herpesvirus from Testudo hermanni and Agrionemys horsfieldii. Verh ber Erkrg Zootiere 36:241-245.

Westhouse, R.A. , E.R. Jacobson, R.K. Harris, K.R. Winter, and B.L. Homer. 1996. Respiratory and pharyngo-esophageal iridovirus infection in a gopher tortoise (Gopherus polyphemus). J. of Wildlife Diseases 32: 682-686.

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12.

13.

14.

15.

16.

17.

18.

Corn, P.S. 1994. Recent trends of desert tortoises populations in the Mojave Desert. Pp 85-94 in R.B. Bury and D.J. Germano (eds.). Biology of North American tortoises. National Biological Survey, Fish and Wildlife Research Report 13.

Knowles, C. 1989. A survey for diseased desert tortoises in and near the Desert Tortoise Natural Area, Spring 1989. report prepared for the Bureau of Land Management, Riverside, California, Contract No. CA 950-(t9-23), 26 pp.

Brown, D.R., Crenshaw, B.C., McLaughlin, G.S., Schumacher, I.M., McKenna, C.E., Klein, P.A., Jacobson, E.R., and Brown, M.B. 1995.

Taxonomic analysis of the tortoise mycoplasmas Mycoplasma agassizii and Mycoplasma testudinis by 16S RNA gene sequence comparison. Int. J. Syst. Bact. 45: 348-350.

Schumacher, I.M., M.B. Brown, E.R. Jacobson, B. R. Collins, and P.A. Klein. 1993. Detection of antibodies to a pathogenic mycoplasma in desert tortoises (Gopherus agassizii) with upper respiratory tract disease. J. of Clinical Microbiology, 31: 1454-1460.

Brown, M.B., Schumacher, I.M., Klein, P.A., Harris, D., Corell, T., Jacobson, E.R. 1994 Mycoplasma agassizii causes upper respiratory tract disease in the desert tortoise. Inf. Immun. 62:45804586.

Cox, J. 1989. Survival characteristics of small gopher tortoise populations and their possible influence on relocation efforts. Pp. 7-14 in: J.E. Diemer, D.R. Jackson, J.L. Landers, J.N. Layne, and D.A. Wood.

Gopher tortoise relocation symposium proceedings. Florida Game and Fresh Water Fish Commission, Nongame Wildlife Program Technical Report #5, Tallahassee, FL. Jacobson, E.R., Brown, M.B., Schumacher, I.M., Collins, B.R., Harris R.K., and Klein, P.A. 1995. Mycoplasmosis and the Desert Tortoise (Gopherus agassizii) in Las Vegas Valley, Nevada. Chelonian Conservation and Biology. 1(4):279-284.

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Mycotic infections of reptiles: Diagnosis and treatment Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto Various fungal diseases have been reported in collections of turtles and tortoises. In a review of over 200 necropsies and the published literature of the chelonians necropsied, 3% of the deaths were due to mycotic pulmonary disease with terrestrial species more commonly affected than those that were aquatic. Scutes and dermal bone of the shell were also colonized with fungi. Colonization of the keratin layer of the shell of turtles by fungi often follows previous trauma and in many situations may not represent primary invasion. An epizootic of fungal pneumonia was described in mariculture reared juvenile green turtles at Cayman Turtle Farm, Grand Cayman, BWI. There are several reports of mycotic disease in Galapagos and Aldabra tortoises (Geochelone gigantea). Fatal pneumonitis due to Aspergillus amstelodami was reported in a Galapagos tortoise that lived at the Chicago Zoological Park for over 30 years. In that study, both Geotrichum candidum and A. amstelodami were isolated from another Galapagos tortoise with pulmonary disease. Another fungus, Beauvaria, was isolated from a Galapagos tortoise with pulmonary abscesses. A severe generalized case of penicilliosis was described in a Galapagos tortoise, with multiple lesions found in the lungs, stomach, liver, and pancreas from which Penicillium was cultured. Paecilomyces fumoso-roseus was cultured from pulmonary abscesses in an Aldabra tortoise that had been in captivity at the Chicago Zoological Park for about five months prior to death. At the Copenhagen Zoo a fatal case of aspergillosis of the lungs was seen in an Aldabra tortoise that had been ill for over one year. Microscopically, all lesions consisted of granulomatous inflammation with branching, septate, fungal hyphae. Penicillium lilacinum was isolated from the lung of a yellow-footed tortoise (Geochelone denticulata) dying of pneumonia at the Rotterdam Zoo. Mycotic diseases have been reported in variety of lizards, including members of Iguanidae, Agamidae, Chamaeleontidae, Teiidae, and Lacertidae. Chrysosporium keratinophilum has been isolated from visceral lesions in Iguana iguana. Several Anolis carolinesis submitted from a research colony were found to have nuchal hematomas from which the fungus Trichosporon cutaneum, the causative agent of white piedra of man, and the bacterium Pseudomonas aeruginosa were isolated. A Mucor sp. has been isolated from multiple cutaneous lesions in a bearded lizard. Organisms resembling Candida albicans have been identified from multiple necrotic areas of the liver in a two-banded chameleon (Chamaeleo bitoeniatus) and Shaley reported a mycotic enteritis in an adult Jackson’s chameleon (Chamaeleo jacksoni). The enteritis was associated with an intussusception of the posterior portion of the colon. Aspergillosis has been identified in a black tegui (Tupinambis nigropunctatus).

There are several reports of mycotic infections of snakes, with mycotic dermatitis being the most common. Oral candidiasis may be involved in infectious stomatitis. Clinical signs of systemic disease preceding death are often subtle and so go unrecorded. Mycotic dermatitis is easily diagnosed by culture correlated with the histopathologic appearance of a skin biopsy. Skin lesions commence as discolored necrotic scales that may spread in a circular fashion; ventral scales appear to be more common involved. Geotrichum candidum, Trichoderma spp., and Fusarium spp. have been isolated. As in higher vertebrates, mycotic dermatitis may be associated with predisposing factors such as high humidity, malnutrition, overcrowding, and debris buildup in the animal’s environment.

Mycotic infections are also commonly seen in all major groups of captive reptiles, with the integumentary and respiratory system most often involved.1,2 The dermatomycoses of mammals caused by Microsporum and Trichophyton are rarely reported in reptiles. However, fusariosis, geotrichosis, phycomycosis and chromomycosis appear to be relatively

common. Predisposing factors such as suboptimal cage temperatures and filthy environmental conditions are often involved. Based upon the literature, most cases of mycotic disease in reptiles are diagnosed at necropsy. As a result, there are relatively few reports which discuss medical management.3-5

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CHELONIA (Turtles and Tortoises) Various fungal diseases have been reported in collections of turtles and tortoises. In a review of over 200 necropsies and the published literature of the chelonians necropsied, 3% of the deaths were due to mycotic pulmonary disease with terrestrial species more commonly affected than those that were aquatic.6 Scutes and dermal bone of the shell were also colonized with fungi. Colonization of the keratin layer of the shell of turtles by fungi often follows previous trauma and in many situations may not represent primary invasion.

An epizootic of fungal pneumonia was described in mariculture reared juvenile green turtles (Chelonia mydas) at Cayman Turtle Farm, Grand Cayman, BWI.7 There are several reports of mycotic disease in Galapagos (Geochelone elephantopus) and Aldabra tortoises (G. gigantea). Fatal pneumonitis due to Aspergillus amstelodami was reported in a Galapagos tortoise that lived at the Chicago Zoological Park for over 30 years.8 In that study, both Geotrichum candidum and A. amstelodami were isolated from another Galapagos tortoise with pulmonary disease. Another fungus, Beauvaria, was isolated from a Galapagos tortoise with pulmonary abscesses. A severe generalized case of penicilliosis was described in a Galapagos tortoise, with multiple lesions found in the lungs, stomach, liver, and pancreas from which Penicillium was cultured.9 Paecilomyces fumoso-roseus was cultured from pulmonary abscesses in an Aldabra tortoise that had been in captivity at the Chicago Zoological Park for about five months prior to death.8 At the Copenhagen Zoo a fatal case of aspergillosis of the lungs was seen in an Aldabra tortoise that had been ill for over one year.10 Microscopically, all lesions consisted of granulomatous inflammation with branching, septate, fungal hyphae. Penicillium lilacinum was isolated from the lung of a yellow-footed tortoise (G. denticulata) dying of pneumonia at the Rotterdam Zoo.11

CROCODILIA (Crocodiles. Alligators, Caiman) Candida albicans has been identified as the agent responsible for pneumonia in unspecified species of crocodile and caiman.12 Aspergillus fumigatus and A. ustus have been cultured from pneumonic lesions in several captive American alligators 2 to 6 weeks of age.13 Trevino described a fatal diffuse granulomatous pneumonia and hepatitis due to Cephalosporium in three Caiman sclerops.14 Poor adaptation to their captive environment was considered a predisposing factor. Three species of crocodilians in a zoologic park, including a Morelet’s crocodile (C. moroleti), an American crocodile (C. acutus), and a Nile crocodile (C. niloticus) developed a respiratory infection with lung lesions from which Mucor was isolated.15 Overcrowding of animals in pools and buildup of debris in the exhibit were considered contributing factors. Several American alligators (Alligator mississippiensis) have been submitted from local alligator farms with multiple granulomatous inflammatory lesions on the foot pads and granulomatous lesions in the lungs from which a variety of fungi have been identified. Long-term housing in

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cement tanks results in abrasions on ventral body surfaces and invasion of opportunistic fungi. Poor diet and poor water quality are often associated and are contributing factors.

LACERTILIA (Lizards) Mycotic diseases have been reported in variety of lizards, including members of Iguanidae, Agamidae, Chamaeleontidae, Teiidae, and Lacertidae. Chrysosporium keratinophilum has been isolated from visceral lesions in Iguana iguana.16 Several Anolis carolinesis submitted from a research colony were found to have nuchal hematomas from which the fungus Trichsporon cutaneum, the causative agent of white piedra of man, and the bacterium Pseudomonas aeruginosa were isolated. A Mucor sp. has been isolated from multiple cutaneous lesions in a bearded lizard.17 Organisms resembling Candida albicans have been identified18 from multiple necrotic areas of the liver in a two-banded chameleon (Chamaeleo bitaeniatus) and Shalev reported a mycotic enteritis in an adult Jackson’s chameleon (Chameleo jacksoni).19 The enteritis was associated with an intussusception of the posterior portion of the colon. Aspergillosis9 and candidiasis18 have been identified for a black tegu (Tupinambis nigropunctatus) and a crocodile lizard (Crocodilurus lacertinus), respectively.

OPHIDIA (Snakes) Mycotic dermatitis is commonly seen in captive snakes.20 Skin lesions commence as discolored necrotic scales that may spread in a circular fashion; ventral scales appear to be more common involved. Geotrichum candidum, Trichoderma spp., and Fusarium spp. have been isolated. As in higher vertebrates, mycotic dermatitis may be associated with predisposing factors such as high humidity, malnutrition, overcrowding, and debris buildup in the animal’s environment. Mycotic dermatitis is easily diagnosed by culture correlated with the histopathologic appearance of a skin biopsy.

Therapy Ketoconazole. There is only a single study concerning blood concentrations and pharmacokinetics of this antifungal drug in a reptile. In a multiple dose study in gopher tortoises, Gopherus polyphemus, the administration of ketoconazole, given orally at 15 and 30 mg/kg of body weight, resulted in concentrations of drug in plasma that were considered therapeutic.21 Itraconazole. There is a single pharmacokinetic study of itraconazole in a reptile. Itraconazole (23.5 mg/kg) was administered PO with a food bolus to spiny lizards (Sceloporus sp.) for 3 consecutive days.22 Blood and tissue samples were then collected up to 18 days following administration. A peak concentration of 2.48 µg/kg was obtained and it was expected that a steady state of 3.1 µg/kg would be achieved

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in 10 days. With this dosing regimen, plasma and liver concentrations would persist within reported MICs for many fungal pathogens for 6 days beyond peak concentration.

Nystatin. Though there are no pharmacokinetic studies of nystatin in the literature, this drug has been administered orally to reptiles with Candida infections of the oral cavity and gastrointestinal tract. The recommended dose is 100,000 IU/kg every 24 hr.23

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11.

12.

13.

14.

References 1.

2.

3.

4.

5.

6.

7.

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Austwick PKC, Keymer IF. 1981. Fungi and actinomycetes. In Cooper JE, and Jackson OF (eds): Diseases of the Reptilia, Vol. I.London, Academic Press, pp. 192-231 Migaki G, Jacobson ER, Casey HW 1984. Fungal diseases of reptiles. In Hoff GL, Frye FL, Jacobson ER (eds): Diseases of Amphibians and Reptiles, New York, Plenum Press, pp. 183-204.

Jacobson ER. 1980. Necrotizing mycotic dermatitis in snakes: clinical and pathologic features. J Amer Vet Med Assoc 177: 838-841.

Jacobson ER. 1980. Infectious diseases of reptiles. In Kirk RW (ed): Current Therapy, Vol. 7. Philadelphia, WB Saunders, pp. 625-633.

Jacobson ER, Calderwood MB, Clubb SL. 1980. Mucormycosis in hatchling Florida softshell turtles. J Amer Vet Med Assoc 177:835837, 1980.

Hunt TJ. 1957. Notes on diseases and mortality in testudines. Herpetologica, 13:19-23.

Jacobson ER, Calderwood MB, Clubb SL. 1980. Mucormycosis in hatchling Florida softshell turtles. JAVMA 177:835-837.

George LE, Wiiliamson W M, Tilden EB, Getty RE. 1962. Mycotic pulmonary disease of captive giant tortoises due to Beauvaria bassiana and Paecilomyces fumoso-roseus. Sabouraudi 2:80-86.

Hamerton AE. 1934. Report on the deaths occurring in the Societyâ&#x20AC;&#x2122;s garden during tbe year 1933. Proc. Zool. Soc. London, 104:389-403.

Andersen S, Eriksen E. 1968. Aspergillose bei einer Elephantenschildkrote (Testudo gigantea elephantina). In X Internationalen

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Symposiums uber die Erkrankungen der Zootiere, Akademie der Wissenschaften der DDR, Berlin.

Bemmel AC, Van Peters JC , Zwart P. 1960. Report on births and deaths occurring in the Gardens of the Royal Rotterdam Zoo during the year 1958. Tijdschr. Diergeneesk. 85:1203-1213.

Zwart P. 1968. Parasitare und mykotische Lungenaffektionen bei Reptilien. In X. International Symposium Erkr. Zootiere (Salzburg) Berlin, Akademie Verlag, p. 45.

Jasmin AM, Carroll JM, Baucom JN. 1968. Pulmonary aspergillosis of the American alligator (Alligator mississippiensis). Am. J. Vet. Clin. Path., 2:93-95.

Trevino G S. 1972. Cephalosporiosis in three caimans. J. Wildl. Dis., 8 :384-388.

Silberman MS, Blue J, Mahaffey E. 1977. Phycomycoses resulting inthe death of crocodilians in a common pool. In Annual Proceedings of the American Association of Zoo Veterinarians, pp. 100-101.

Zwart P. 1968. Parasitare und mykotische Lungenaffektionen bei Reptilien. X International Symposium Erkr. Zootiere (Salzburg). Berlin, Akademie Verlag, pp. 45-48.

Frank W. 1966. Multiple hypkeratose bei einer Bartagame, Amphibolurus barbatus (Reptilia, Agamidae), hervorgeruten durch eine Pilzinfektion, zugleich ein Bertrag zur Problematik von Mykosen bei Reptilien. Salamandra 2:6-12.

Reichenbach-Klinke, H., and Elkan, E. 1965. The Principal Diseases of Lower vertebrates. Academic Press, New York.

Shalev M, Murphy JC, Fox JG. 1977. Mycotic enteritis in a chameleon and a brief review of phycomycoses of animals. J. Am. Vet. Med. Assoc. 171:872-875.

Jacobson, E.R. 1980. Necrotizing Mycotic Dermatitis in Snakes: Clinical and Pathologic Features. J.A.V.M.A. 177:838-841 Page CD, Mautino M, Derendorf H, et al: Multiple dose pharmacokinetics of ketoconazole administered to gopher tortoises (Gopherus polyphemus). J Zoo Wildlf Med 22:191-198,1991.

Gamble K, Alvarado T, and Bennett C (1996): Plasma itraconazole phamacokinetics in spiny lizards (Sceloporus spp.) from once-daily dosing, in Proceedings of the American Association of Zoo Veterinarians, pp. 245.

Jacobson ER (1995): Use of antimicrobial therapy in reptiles, (eds): Antimicrobial Therapy in Caged Birds and Exotic Pets, An International Symposium. Trenton, NJ, Veterinary Learning Systems, pp. 28-37.

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Diagnostic Techniques in Reptile Medicine Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto As in birds and mammals, evaluating the health status and diagnosing disease problems in captive reptiles often requires the collection of appropriate biological samples for laboratory investigations. While some samples can be collected using manual restraint alone, others will require use of sedation, local or general anaesthetics. Blood samples can be obtained from a variety of sites. Complete blood counts (CBCs) should be routinely performed on ill reptiles. In performance of CBCs, analyses include: 1) red blood cell counts; 2) white blood cell counts; 3) differential white blood cell counts; 4) packed cell volumes (PCV); and 5) hemoglobin concentrations. Biochemical evaluations of blood generally involve analysis of plasma or serum samples for the following inorganic and organic constituents: sodium, potassium, chloride, calcium, phosphorus, glucose, urea, uric acid, creatinine, cholesterol, aspartate aminotransferase activity (AST; formerly GOT), alanine aminotransferase activity (ALT; formerly GPT), alkaline phosphatase activity (ALP), and total protein. Very few serological tests have been developed and are available for diagnosing disease problems in captive reptiles. The collection of biopsies often is necessary to diagnose disease problems in reptiles. These samples can provide invaluable information necessary to successfully manage and treat the patient. Biopsies can be evaluated by light and electron microscopical techniques. Examination of touch impressions and wet mounts of various lesions is extremely helpful in diagnosing disease problems in reptiles.

Depending upon the suspected disease or presence of pathogenic organisms, a variety of staining techniques can be used in evaluating smears. Swab specimens, aspirates, and biopsy specimens can be collected and submitted for microbial isolation attempts including those for: 1) viruses; 2) aerobic bacteria; 3) anaerobic bacteria; 4) special bacterial organisms such as Chlamydia and Mycoplasma; and 5) fungi. Proper collection technique is a prerequisite for successful recovery of microorganisms responsible for an infectious disease. Of all the biological samples collected from reptiles, fecal samples are generally the easiest to obtain. If a fecal sample is not available and the reptile has not defecated recently, a colonic wash can be obtained. Few normal data are available for urine and spinal fluid of reptiles. Samples of both of these fluids are not easy to obtain and without many published data, interpretations are difficult.

INTRODUCTION As in birds and mammals, evaluating the health status and diagnosing disease problems in captive reptiles often requires the collection of appropriate biological samples for laboratory investigations. While some samples can be collected using manual restraint alone, others will require use of sedation, local or general anaesthetics. Anaesthesia has been addressed in another chapter (17) and will not be discussed here.

The information gleaned from any of the samples collected will only be as good as the techniques used in collecting, handling, and processing these samples. It goes without saying that the ultimate usefulness of these samples will depend upon the clinician’s ability to interpret the results and use them for developing a medical management programme.

In this chapter, methods for obtaining and processing various biomedical samples for diagnosing disease prob-

lems in reptiles will be discussed. The emphasis is on samples from clinical cases. Post-mortem techniques are discussed elsewhere (see Chapter 20). The most commonly collected samples include: 1) blood for haematological, biochemical, and serological evaluations; 2) biopsies for: cytology, histopathology, electron microscopy, microbial isolation attempts, and heavy metal, toxicological, mineral, and vitamin analyses; 3) scrapings, washings, and exudates for microbiological and cytological evaluations; 4) fluids and faeces for negative-staining electron microscopy; 5) faecal samples for parasitological investigations, and 6) urine and spinal fluid for analysis.

BLOOD EVALUATIONS COLLECTION The total amount of blood which can be safely withdrawn from a reptile depends upon the reptile’s size and

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health status. The total blood volume of reptiles varies between species but as a generalization is approximately 5 to 8% of total body weight (Lillywhite and Smits, 1984; Smits and Kozubowski, 1985). Thus, a 100 g snake has an estimated blood volume of 5 to 8 ml. Since clinically healthy reptiles can acutely lose 10% of their blood volume without any detrimental consequences, from a snake weighing 100 g, 0.7-ml of blood can be withdrawn safely. Much larger volume percentages of blood can chronically be removed over an extended period of time (Lillywhite et al, 1983). However, this practice is limited to experimental animals under controlled laboratory conditions.

Chelonians (turtles and tortoises) Several sites can be used in obtaining blood from chelonians, each having advantages and disadvantages. Sites include the heart, jugular vein, brachial vein, ventral coccygeal vein, orbital sinus, and trimmed toenails (Avery and Vitt, 1984; Dessauer, 1970; Gandal, 1958; Jacobson, 1987; Maxwell, 1979; McDonald 1976; Nagy and Medica, 1986; Rosskopf, 1982; Stephens and Creekmore, 1983; Taylor and Jacobson, 1981).

Cardiac sampling, although not recommended, has been utilized. In young chelonians, before the shell has calcified, a needle can be passed through the plastron into the heart.

Older tortoises with calcified shells requires either drilling a hole through the plastron over the heart, or using a spinal needle for percutaneous sampling through soft tissue in the axillary region at the base of the forelimbs. In all situations, a sterile technique is necessary since contamination of the pericardial sac with bacteria and other potential pathogens can lead to pericarditis and death of the turtle. A sterile drill bit should be used to create a hole, and the hole should be sealed with an appropriate sealant such as bone wax (Johnson and Johnson Co., Somerville, N.J., USA) and a methacrylate resin (Cyanoveneer, Ellman International Mfg., Inc., Hewlett, N.Y. USA).

In turtles and tortoises orbital sinus sampling can be used for collecting small volumes of blood in capillary tubes (Nagy and Medica, 1986). However, in order to prevent damage to periocular tissues and possible trauma to the cornea a moderate amount of care must be taken when using this technique.

The end of the capillary tube is placed into the lateral canthus of the orbit and utilizing a gentle twisting motion blood can be collected. A further problem with this technique is that dilution of the blood sample with extravascular fluids and secretions may alter composition of plasma and effect volume percentages of cellular components. Blood samples are also commonly obtained from the scapular vein, brachial vein and brachial artery of chelonians (Avery and Vitt, 1984; Rosskopf, 1982). However, vessels associated with limbs can rarely be visualized through the skin, and sampling is usually blind. In addition, since lymphatics are well developed in chelonian forelimbs (Ottaviani and Tazzi, 1977), obtaining blood samples from these vessels may result in hemodilution with lymph. At times pure lymph may be obtained.

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The author has found that the only peripheral blood vessels which can be consistently visualized in many small and moderate sized tortoises is the jugular vein and carotid artery (Jacobson et al, 1991). The major problem encountered when sampling from these vessels is that manual extension and restraint of the head of the tortoise beyond the margins of the plastron is required, which at times may be difficult or impossible. One method is to push in or lightly touch the rear limbs, which usually causes the tortoise to extend its head from the shell, and allows the sampler to restrain the tortoise’s head. Once grasped, the head is pulled out with one hand, and while sitting, the sampler positions the tortoise between the knees, with the tortoise’s head pointing toward the sampler’s body. The jugular vein and carotid artery are well-developed on both right and left sides of the neck. Once the head is extended, the jugular can often be seen as a bulge through the cervical skin, coarsing caudal from the level of the tympanic membrane to the base of the neck. The carotid artery is deeper and more difficult to visualize and is located ventral and parallel to the jugular vein. Once either vessel is identified, the skin over the puncture site should be cleaned with 70% ethanol and a 23 or 25 gauge butterfly catheter can be used for obtaining the sample. With the cap removed from the end of the tube, blood will flow down the tube once the needle is inserted into the vessel. The technique described above can be used in Mediterranean tortoises (Testudo spp.), but is not always successful.

Crocodilians (crocodiles, alligators, gharial) Blood samples can be obtained from the supravertebral vessel located caudal to the occiput and immediately dorsal to the spinal cord (Olson et al, 1975). The skin behind the occiput is cleansed with an organic iodine solution and 70% ethanol. A 3.75-cm, 22- or 23-gauge needle is inserted through the skin in the midline directly behind the occiput and is slowly advanced in a perpendicular direction.

As the needle is advanced, gentle pressure is placed on the plunger. If the needle is passed too deep, the spinal cord will be pithed. Other sites of blood collection which are commonly used include the heart (via cardiocentesis) and ventral coccygeal vein (Jacobson, 1984). The heart is located in the ventral midline, approximately 11 scale rows behind the forelimbs. In collecting blood from the coccygeal vein, the crocodilian is placed in dorsal recumbency and the needle is inserted through the skin toward the caudal vertebrae.

Lizards Blood samples can be obtained from several sites. In large lizards, blood is easily obtained from the ventral tail vein (Esra et al, 1975). Toe nails can be clipped, and blood can be obtained in a microcapillary tube (Samour et al, 1984). Microcapillary tubes also can be used to obtain blood samples from the orbital sinus (LaPointe and Jacobson, 1974), in a similar fashion for collecting blood from mice.

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Snakes

BIOCHEMICAL EVALUATIONS

Blood samples can be obtained from a variety of sites, including the palatine veins, ventral tail vein, and via cardiocentesis (Olson et al, 1975; Samour et al, 1984). The author prefers heart puncture to other methods, and as long as the heart is not excessively traumatized with multiple attempts at sampling, the procedure is safe and effective. This method should be limited to those snakes over 300 grams (Jackson, 1981). Essentially, the heart is located either directly by seeing it beating through ventral scales or by palpation. The heart is relatively moveable within the coelomic cavity and is easy to move manually several scale rows both cranially and caudally.

Once the heart is located, it is stabilized by placing a thumb at its apex and forefinger at its base. A 23- or 25gauge needle attached to a 3- to 6-ml syringe is advanced under a ventral scale, starting at the apex and aiming toward the base.

With gentle suction, a sample can be obtained. Sometimes a clear fluid is withdrawn, representing the pericardial fluid. In such cases, the needle should be withdrawn, a new syringe and needle secured, and the procedure repeated.

Sometimes in obtaining a sample from the heart, the clinician will note that blood can be withdrawn with each beat of the heart.

Biochemical evaluations of blood generally involve analysis of plasma or serum samples for the following inorganic and organic constituents: sodium, potassium, chloride, calcium, phosphorus, glucose, urea, uric acid, creatinine, cholesterol, aspartate aminotransferase activity (AST; formerly GOT), alanine aminotransferase activity (ALT; formerly GPT), alkaline phosphatase activity (ALP), and total protein. The author prefers to use plasma rather than serum since a greater volume of plasma can be collected per unit volume of blood compared with serum. Also, it is more common for clots to occur in serum than plasma. Serum removed from the blood sample following centrifugation may suddenly clot into a gelatinous mass. Although the causes of this phenomenon are unknown, clotting is more common in glass tubes and possibly the electric charge on the glass is an initiating factor.

Plasma samples are collected from blood placed into 2 microtainer lithium heparin tubes. The tubes should be centrifuged immediately following collection and the plasma removed and submitted for evaluation. Since plasma potassium values will increase over the time period plasma is in contact with blood, it should be removed and frozen immediately following centrifugation (Jacobson et al, 1991). In performance of field work on blood biochemical values of free-ranging reptiles, plasma can be placed in cryotubes and frozen in liquid nitrogen. If the samples need to be sent to a laboratory, the samples should be transported frozen on dry ice.

To date, no information appears to have been published on the accuracy of different methodologies used in determining various plasma biochemical analytes in reptiles. A variety of automated machines have been developed for use in determination of plasma/serum biochemical profiles of humans. The veterinary profession also uses these machines for determination of blood biochemical values of both domestic and non-domestic animals. Although it is quite simple to submit a sample and have it analyzed on an automated machine, it is difficult to determine the accuracy of these values. In studies the author has conducted on replicate plasma samples submitted from the same sample of blood and analyzed on different machines, flame photometry appear to be more accurate for determination of sodium and potassium values than machines utilizing ion-exchange electrodes.

With automated machines, procedures for determining total protein values are often based on the Biuret method (Kingsley, 1972) and the author has found results by this method significantly different from values for the same samples determined by refractometry. The Biuret method appears to be more accurate and should be the preferred method. Albumen values are generally determined utilizing various dyes such as bromcresol green (BCG) and globulin values by subtracting albumen from total protein. When doing studies on blood proteins of reptile plasma, the author has found significant differences when comparing albumen and globulin values determined by electrophoresis with those determined utilizing BCG. Based on the authorâ&#x20AC;&#x2122;s experience, it is likely that albumen values determined by dye techniques are inaccurate and methods utilizing these chem-

HAEMATOLOGIC EVALUATIONS Complete blood counts (CBCs) should be routinely performed on ill reptiles. The author prefers using microtainer tubes containing lithium heparin (Fisher Scientific Co., Orlando, Florida, USA). Immediately following collection of the sample, 0.6-ml of blood is added to a tube and the tube is inverted several times to prevent clotting. Other anticoagulants which can be used for CBCs include sodium heparin and ammonium heparin. Since potassium ethylenediaminetetraacetic acid (EDTA) results in haemolysis of chelonian red blood cells, this anticoagulant is not recommended (Jacobson, 1987).

In performance of CBCs, analyses include: 1) red blood cell counts; 2) white blood cell counts; 3) differential white blood cell counts; 4) packed cell volumes (PCV); and 5) haemoglobin concentrations. Red blood cell counts are determined using an automated coulter counter. White blood cell counts can be determined either manually utilizing a haemocytometer (Schermer, 1967) or as an estimated count from a blood film, similar to that used in birds (Campbell and Coles, 1986). Packed cell volumes are determined following centrifugation of a sample in a microhaematocrit tube. Haemoglobin values are determined utilizing a haemoglobinometer.

Although total protein values are often determined utilizing a refractometer, the authorâ&#x20AC;&#x2122;s experience suggests that accuracy of this method with reptile blood is questionable.

Proper methods for determining total protein of reptile blood will be discussed under biochemical evaluations of blood.

Normal haematological values can be found elsewhere (Jacobson, 1987).

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icals should be avoided. Serum/plasma protein electrophoresis is more costly to perform but is more accurate.

The most important points to remember when submitting plasma/serum samples for biochemical evaluations are: 1) Try and utilize the same blood collection technique at all times.

2) Handle the blood in a consistent fashion. Use the same anticoagulant and try and add the same volume of blood to the collection tube.

3) Centrifuge the blood immediately following collection and remove the plasma immediately following centrifugation. The warmer the ambient temperature, the quicker potassium will move out of red blood cells into surrounding fluid, resulting in falsely elevated values.

4) Freeze the sample following collection, preferably on dry ice, in liquid nitrogen, or in an ultracold freezer at -70째C. 5) The sample should be transported frozen to the laboratory, preferably on dry ice.

6) Try and use the same clinical pathology laboratory utilizing the same machine. Make sure the samples are handled similarly prior to analysis. For instance, small plasma volumes which have to be diluted in order to reach a minimum volume necessary for the machine will have a dilution error superimposed upon other technique errors.

Normal biochemical values of reptile blood can be found elsewhere (Jacobson, 1987).

SEROLOGY Very few serological tests have been developed and are available for diagnosing disease problems in captive reptiles. Serological studies have been performed on free-ranging reptiles and reptiles used in experimental studies to determine presence of antibodies to various togaviruses (Jacobson, 1986a). However, infections with these viruses do not appear to be clinically important in reptiles. A haemagglutination inhibition test has been developed for determining presence of antibody to viperid paramyxovirus (Jacobson and Gaskin, 1990) and has been used for monitoring exposure to this pathogen in zoological and private collections of snakes. However, the only laboratory currently performing this test is that of Dr. Jack Gaskin, Department of Infectious Diseases, University of Florida, Gainesville, Florida, USA. Serum banks on healthy and ill reptiles need to be established and maintained for retrospective studies as more tests and laboratories performing these tests become available.

BIOPSIES The collection of biopsies often is necessary to diagnose disease problems in reptiles. These samples can provide invaluable information necessary to successfully manage and treat the patient.

In collecting biopsy specimens, multiple samples should

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be obtained for: 1) histopathology; 2) electron microscopy; 3) cytology; and 4) microbiology. Biopsies are commonly obtained from the integumentary and digestive system and the author will focus on these. Similar techniques can be used for collecting samples from other systems.

COLLECTION Integumentary System Reptiles are often presented with skin disease (see Chapter 9), and a great variety of infectious and noninfectious disease problems can result in pathological changes in the integument. The clinician needs to determine if the changes are due to local infection or are a manifestation of systemic illness. Many systemic diseases will result in pathological changes in the integumentary system.

The key to evaluating skin lesions of reptiles is collecting and properly evaluating a good biopsy specimen for both histopathology and microbial culture. Microbial culture by itself is often misleading because many microbes often secondarily colonize skin lesions.

Chelonians Of all the reptiles, chelonians present the greatest challenge for biopsy, especially when lesions involve the shell.

The reptile shell is a very hard biological structure that makes biopsy somewhat difficult. While under anaesthesia (see Chapter 17), a rotary power saw (Dremel Mototool, Dremel Mfg. Co., Racine, Wisconsin, USA) or bone trephine can be used to cut a wedge out of the shell. Ideally, the biopsy should include normal tissue along with the diseased component. A piece should be fixed in neutral buffered 10 per cent formalin for histopathological evaluation and a piece (with the most superficial contaminated portion removed) submitted for microbial culture. For initial attempts at isolation, the author often uses a broth such as tryptic soy broth.

The defect created in the shell should be filled with calcium hydroxide dental paste (Root-Cal, Ellman International Mfg., Inc., Hewlett, New York, USA) and covered over with a methacrylate resin (Cyanoveneer, Ellman International Mfg., Inc., Hewlett, New York, USA). This technique is routinely used in repair of the chelonian shell.

For biopsy of soft tissue, a 2 per cent xylocaine block is satisfactory and can be infiltrated around the biopsy site and the skin cleaned with 70% ethanol and allowed to dry. If the sample is to be cultured, sterile saline is used instead of ethanol. If there is epidermal involvement, a biopsy punch can be used for collecting the sample. Following punch biopsy, the skin may require a single suture for closure.

Monofilament nylon is routinely used. If a subcutaneous mass is present, fine-needle aspiration can be performed.

This is a rapid method, resulting in minimal trauma to the patient. A 22-gauge needle is inserted into the mass and using a 6 to 12 ml syringe, full negative pressure is developed by quickly pulling back on the plunger. While maintaining negative pressure on the syringe, the needle is moved throughout the mass in multiple planes. After several passes

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through the mass, the plunger is released and the needle removed from the mass. Pressure should not be applied to the plunger while removing the needle from the mass since this will cause the sample to be aspirated into the syringe barrel.

The preparation of the specimen will be discussed later.

Crocodilians and Lizards A full-thickness biopsy may be difficult in those areas of the crocodilian integument having osteoderms (see Chapter 2). Small crocodilians and most lizards can be manually restrained, whereas large crocodilians and large monitors must be chemically immobilized. The area around the biopsy site should be infiltrated with 2 per cent xylocaine and a fullthickness skin incision taken with a biopsy punch. As with chelonians, a minimum of two biopsies should be taken, one for histopathology and one for microbiology. For microbial culture, the lesions can be ground in a sterile tissue grinder and samples applied to appropriate media. This appears to be particularly important for isolation of fungi from reptile skin lesions. The author has had more success in isolating fungi when the skin is ground prior to attempts at isolation.

Snakes Snakes are ideally suited for skin biopsy. Harmless species can be manually restrained, and poisonous species can be guided into a plexiglass tube for restraint or anaesthesia. Affected scales can be removed with a scalpel blade, or a sterilized one-hole paper punch can be utilized for biopsies of individual scales. In such cases, the area around the lesion should be infiltrated with 2 per cent xylocaine hydrochloride. In certain skin diseases, such as vesiculating skin lesions, larger samples may be needed. Similarly, for sampling subcutaneous masses, 2 per cent xylocaine can be infiltrated subcutaneously around the mass. Once removed, the mass should be split into several portions for various diagnostic evaluations (see later).

DIGESTIVE SYSTEM Numerous reptiles are submitted with clinical signs of regurgitation, anorexia, or passing loose stools (faeces) that appears to be abnormal. A regurgitation syndrome is commonly seen in wild emerald tree boas (Corallus canina) imported into the U.S.A., and the cause of this syndrome has not been completely elucidated.

For problems of the upper gastrointestinal tract, endoscopic examination for purposes of direct visualization of the oesophageal and gastric mucosa and collection of biopsy specimens for histopathology and culture are routine. For those clinicians without such equipment, a sterile nasogastric tube can be placed via the oesophagus into the stomach.

Stomach washings can be obtained for preparation of wet mounts, cytological evaluation, and microbial culture. Radiographic evaluation using normal films followed by contrast techniques should be utilized in diagnosing cases of regurgi-

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tation (see Chapter 6).

For persistent cases of regurgitation in which upper gastrointestinal involvement has been ruled out, the next approach would be examination of the lower gastrointestinal tract. The reptile should be anaesthetized, and a vaginal speculum utilized to dilate the cloaca and locate the colonic opening. A flexible scope will allow the clinician to observe the colonic mucosa directly, and biopsy samples can be secured for histopathology and microbial culture.

PATHOLOGIC EVALUATIONS Biopsies can be evaluated by light and electron microscopical techniques. For histopathology, neutral buffered 10% formalin (NBF) is the most commonly used fixative (see Chapter 20). The NBF volume to tissue ratio should be at least 10:1. For best penetration, tissue should not exceed 6-mm in thickness. A fixative which the author routinely uses for doing light and electron microscopy is Trumpâ&#x20AC;&#x2122;s solution (McDowell and Trump, 1976) which is a combination of 4% formaldehyde and 1% glutaraldehyde. This solution needs to be refrigerated prior to use and is stable at refrigeration temperatures for several months.

Following light microscopical examination of a paraffin embedded sample, the pathologist can determine whether or not to follow with an electron microscopical evaluation.

Electron microscopy is costly and labour intensive and is only performed on selected specimens. Electron microscopy also can be performed on paraffin embedded tissue samples.

A small piece of the paraffin embedded tissue can be removed from the block and processed for electron microscopy. In diagnostic reptile medicine, electron microscopy is invaluable in determining the nature of various intracytoplasmic and intranuclear inclusions and the presence of viruses as well as unusual bacterial organisms such as Mycoplasma and Chlamydia.

CYTODIAGNOSTICS Examination of touch impressions and wet mounts of various lesions is extremely helpful in diagnosing disease problems in reptiles. Because of the ease and rapidity of processing these samples, much information can be gathered in a short time. For external lesions, samples can be collected with relative ease. Depending upon the size and nature of the patient, manual restraint alone may be all that is needed. In larger more fractious reptiles, or in those patients with internal masses, sedation or anaesthesia will be required.

Collection and Preparation The collection method used will depend upon the nature and consistency of the lesion being sampled. Prior to collection of the sample, the distribution, colour, morphological description, size, and odour (if present) of the lesion should be noted. For cutaneous lesions, scrapings can be collected from keratinized structures such as shell lesions of cheloni-

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ans or hyperkeratotic surfaces. A sample can be suspended in a small quantity of saline and a coverslip placed over the sample. Next, a “squash-prep” can be made by applying gentle pressure with a fingertip (in a twisting motion) to the coverslip. This will help in detecting pathogens contained within keratinized material. Potassium hydroxide can be used for digesting keratinized material and improving examination for pathogens.

Lesions containing fluid or purulent material can easily be sampled with a needle. If the lesion is cutaneous, it should be cleaned with a small amount of 70% ethanol and allowed to dry prior to sampling. As discussed earlier, fineneedle aspiration biopsy specimens also can be collected from firm masses.

Aspirates should be examined first as a wet mount. This will give the clinician an idea of what additional preparations should be made. Some organisms such as protozoa and nematode larvae are better appreciated in a wet mount than in a stained preparation. Aspirates having good cellularity can be used to prepare direct smears using the conventional wedge method or the method used for preparing blood films on coverslips. Aspirates containing tenacious material with thick cellular fragments should be prepared using a squash technique. After the sample is placed on a microscopic slide, another slide is used to flatten the material and both slides are quickly pulled apart.

Not uncommonly, snakes and those lizards with spectacles (see Chapter 2) will develop accumulations of clear or purulent fluid in the subspectacular space (Millichamp et al, 1983). The spectacle should be cleansed with sterile saline, a fine-gauge needle (25 to 27 gauge) inserted under the spectacle, and an aspirate collected. Since the spectacle is an extremely vascular structure, it is not uncommon to have blood cells collected with the aspirate. In reptiles having intraerythrocytic parasites such as Hepatozoon, at times red cells may rupture releasing these parasites into the surrounding fluid. The clinician should be aware of this and if protozoan parasites are seen in the aspirate, their possible origin from red blood cells should be considered.

Lung washes should be routinely collected from reptiles with respiratory disease. While samples can be collected from some reptiles using manual restraint, other patients will have to be sedated or anaesthetised. The jaws of the reptile are held apart and a sterile catheter guided through the glottis into the lung field. The location of the lung field will vary between each major group of reptiles, and with snakes will differ even between members of the same family. The clinician needs to know the location of the lung(s) before collecting a lung wash. With a syringe attached to the catheter, sterile saline (1 ml for a 200 gram snake) can be introduced into the lung field and aspirated several times. Material collected can be used for both cytological evaluation and microbiological culture.

If the reptile is large enough, samples can be collected via bronchoscopy. Bronchoscopy has an added advantage of permitting the lower respiratory tract to be examined directly. The author prefers the patient to be anaesthetised when performing bronchoscopy with the flexible fiberoptic bronchoscope passed through the endotracheal tube. A t-tube connected to the endotracheal tube can be used to allow the

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technique to be performed while the patient remains connected to the gas anaesthesia machine. Utilizing this technique, the tracheobronchial system can be methodically examined and sampling procedures such as lavage, culture, brushing, and transbronchial biopsy can be performed on specific areas of the respiratory tract. For collecting samples for culture, the plugged telescoping catheter brush system is the method of choice (Schaer et al, 1989).

Aspirates and lung washes of low cellularity can be concentrated utilizing a number of techniques. Using the conventional wedge method, cells can be marginated by lifting the spreader slide from the smear slide just prior to reaching the end of the smear. Cells also can be concentrated by simple centrifugation in a plastic capped tube followed by examination of the pelleted sediment. If samples are sent to a clinical pathology laboratory, cells can be concentrated on a microscopic slide using a cytocentrifuge.

The collection of biopsy specimens has already been discussed and in addition to histopathology, biopsy specimens can be evaluated cytologically. The cut surface of a specimen can either be scraped with a sterile scalpel blade or touched several times by a microscopic slide to make impression smears. If the surface of the specimen contains a moderate amount of blood or clots of blood, this can be removed by gently cleaning the surface with sterile saline via a syringe and needle or gently rolling a saline moistened cotton swab across the surface. A swab also can be used for collecting cellular samples for examination on a microscopic slide.

STAINING Depending upon the suspected disease or presence of pathogenic organisms, a variety of staining techniques can be used in evaluating smears. The method of fixation of the smear to the slide will depend upon the staining procedure used.

The most common method used for initial evaluation of smears is the Wright’s-Giemsa stain. Prior to staining, the smear is fixed in absolute methanol for approximately 10 seconds. Quick staining techniques are commercially available and allow staining of smears in a few seconds. Other stains which are commonly used in evaluating smears of lesions from reptiles include Gram’s stain for bacteria, acidfast stain for mycobacteria, and new methylene blue for fungi.

NEGATIVE STAINING ELECTRON MICROSCOPY Negative staining in conjunction with transmission electron microscopy (TEM) is a useful and rapid method of examining clinical specimens. The principle of negative staining is that there is no reaction between the stain and the specimen. The most commonly used negative stains are uranyl acetate (0.5-1.0%) and potassium phosphotungstate (PTA) (0.5-3.0%). In cases where a viral agent is suspected, this technique may be used in a variety of specimens. De-

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pending on the nature of the tissue, different ways of processing the sample are required to detect viral particles. Fluid from vesicles can be obtained with a sterile pipette and may be placed directly on a Formvar-coated 200-mesh copper grid, while large amounts of fluid (serum, urine, liquor) require centrifugation for clarification. In these cases the supernatant after low speed centrifugation (1,500 g) or the diluted pellet after high speed centrifugation (15,000 g) is placed on the grid for staining. Faecal material requires suspension and concentration and will be placed in distilled water or phosphate buffered saline (PBS). A very useful method is to mix faecal material with PBS to give a 20% suspension in 5 ml. After centrifugation a drop of the supernatant is placed on a grid and negatively stained. Alternatively one drop of a 1:1 mixture of supernatant and stain is placed directly on a grid for examination. If needed, bacitracin as a wetting agent may be added. If the grids will be stored or cannot be examined immediately, the stain of choice is uranyl acetate because it will not have adverse effects.

Tissues such as liver, kidney, spleen, etc., require grinding to obtain a homogenate which will be processed in the same way as the above samples. In general the method used for processing specimens depends on the concentration of viruses suspected in the sample.

MICROBIOLOGY Swab specimens, aspirates, and biopsy specimens can be collected and submitted for microbial isolation attempts including those for: 1) viruses; 2) aerobic bacteria; 3) anaerobic bacteria; 4) special bacterial organisms such as Chlamydia and Mycoplasma; and 5) fungi. Proper collection technique is a prerequisite for successful recovery of microorganisms responsible for an infectious disease. The recovery of contaminants may result in improper or even harmful treatment. While isolation of aerobic organisms is relatively inexpensive and fairly rapid to do, isolation of the other groups of pathogens listed above, requires special techniques and is far more costly. Viruses, Chlamydia and Mycoplasma require special media and conditions for isolation and most human and veterinary diagnostic laboratories have little experience with these pathogens in reptiles. The clinician will need to establish a special rapport with either a university research laboratory or diagnostic laboratory in order to culture these organisms. The author of this chapter will rarely culture for viruses, Mycoplasma, Chlamydia, or fungi unless histopathology or cytology supports or suggests their presence. Fluids, aspirates, and biopsy specimens can be frozen on dry ice or in an ultrafreezer at -70°C until a decision is made as to specific isolations that will be attempted.

Most diagnostic laboratories have ultrafreezers for storage of biological samples.

The author has rarely attempted viral isolation attempts on ante-mortem cases. For the most part, viral isolation attempts are generally made following histopathological evaluation of a necropsy case. Where a viral disease is suspected, representative portions of major organs such as liver, spleen, kidney, and heart are frozen for future isolation. In the author’s experience, most reptile viruses are best isolat-

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ed in reptile cell cultures and in the U.S.A. several reptile cell lines are commercially available (American Type Culture, Bethesda, Maryland, USA). In some cases, cell cultures from the species being evaluated need to be established. If a laboratory is available to attempt viral isolation, samples should be submitted either: 1) as fresh tissue samples in a sterile container on wet ice; 2) as minced pieces in a transport media such as Eagle’s minimal essential medium; or 3) as fresh frozen samples transported on dry ice or in liquid nitrogen. In an ante-mortem case if a viral disease is suspected, aspirates, washings, or biopsy specimens can be handled and transported similarly.

For isolation of aerobic bacteria, a variety of sterile swabs with associated transport media are commercially available.

The size of the swab may be important. Once the sample is collected, the swab should be returned to its protective holder, placed in a plastic zip-lock bag, and sent to the laboratory on ice as rapidly as possible. Some private practitioners have established their own microbiology laboratories and in such cases, swab specimens can be immediately streaked onto appropriate agar plates.

Samples taken in the field from reptiles can be placed in a cryotube containing tryptic soy broth and frozen in a tank containing liquid nitrogen. Once frozen, the cryotubes can be transported on dry ice to the laboratory for culture.

It is only recently that anaerobic bacteria have been appreciated as potential pathogens in reptiles (Stewart, 1990).

Samples submitted for anaerobic culture require special collection techniques to improve the success of recovery. For obligate anaerobes, anaerobic swab culturettes are available and for biopsy specimens the samples should be delivered to the clinical pathology laboratory in an anaerobic pack system. These are available through various microbial and scientific supply companies. It is important that the specimen is placed in the anaerobic transport system as soon after collection as possible.

Samples of blood for culture should be collected from reptiles suspected of being septicaemic. Depending on the reptile being sampled prior to the collection, the skin needs to be thoroughly cleaned with three applications of both an organic iodine solution and 70% ethanol. As large a volume of blood as is safe to collect is obtained in a sterile syringe and quickly added to the blood culture bottle containing the appropriate culture media. The top of the blood culture bottle needs to be cleaned several times with swabs of 70% ethanol prior to insertion of the needle. Sterile technique must be used at all steps in the collection process. Both aerobic and anaerobic bottles need to be used. Blood culture bottles are commercially available from most microbiology or medical supply companies.

Fastidious microbial organisms such as Chlamydia and Mycoplasma are only recently being appreciated as causes of illness and death of reptiles. While Chlamydia has been seen in tissue section of puff adders (Bitis arietans) dying of pericarditis and hepatitis (Jacobson et al, 1989) and in monocytes and spleen of a flap-necked chameleon (Chameleo dilepis) in Tanzania (Jacobson and Telford, 1990) as yet this organism does not appear to have been isolated from a reptile. If Chlamydia is suspected, biopsy specimens should be submitted in an appropriate transport medium such as that rou-

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tinely used for samples collected from pet birds or cats.

It is only recently that Mycoplasma is being appreciated as a potential pathogen in reptiles. The only described mycoplasma from a reptile is M. testudinis which was isolated from the cloaca of a Greek tortoise (Testudo graeca) (Hill, 1985). Multiple isolates of Mycoplasma have been obtained from nasal exudate of desert tortoises (Xerobates agassizii) and other tortoises (Geochelone spp.) with chronic upper respiratory tract disease (Jacobson et al, 1990b). This organism appears to be an important pathogen in this complex disease. A special enrichment media, SP4 media, is used both as a broth and agar in culturing for this organism in chelonians (Jacobson et al, 1990b). A tom-cat catheter attached to a syringe containing tryptic soy broth is inserted through the external nares of an ill tortoise and an aspirate obtained. The aspirate can be either placed in a cryotube containing tryptic soy broth, frozen on dry ice and shipped to a diagnostic laboratory or placed immediately in SP4 media if it is available.

In the U.S.A., SP4 media is commercially available (Remel, Lenexa, Kansas, USA).

Fungal diseases are commonly encountered in reptiles, particularly in cutaneous or subcutaneous lesions in lizards and snakes (Jacobson, 1980; Austwick and Keymer, 1981; Migaki et al, 1984). Biopsies of suspected mycotic disease are preferable to swab specimens or scrapings. Biopsy specimens can be minced or if the sample is heavily keratinized, gently ground in a sterile tissue grinder containing sterile saline and antibiotics such as gentamicin or amikacin.

Minced or ground samples can be cultured on an appropriate mycotic media such as Sabouraud’s agar containing antibiotics to suppress bacterial growth. Fungi will also readily grow in tissue culture media such as Eagle’s minimal essential media. New, previously unreported, fungal organisms are constantly being cultured from reptiles (Austwick and Keymer, 1981) and for identification require a mycologist familiar with the particular family of fungus isolated. It may take well over one year to have an isolate identified. Often a new species will need to be described.

FAECAL EXAMINATIONS AND COLONIC WASHES Of all the biological samples collected from reptiles, faecal samples are generally the easiest to obtain. If a faecal sample is not available and the reptile has not defecated recently, a colonic wash can be obtained. For most reptiles this is fairly easy to do using manual restraint. Some tortoises will have to be anaesthetised to collect a sample. A lubricated French-catheter filled with sterile saline, and attached to a syringe containing saline, is passed into the colon via the cloaca. The catheter should slide in fairly easy and should not be forced. The cloaca and colon are relatively thin and if the clinician is not careful the tip of the catheter can penetrate the walls of these structures resulting in rupture and subsequent peritonitis. Once the catheter has been inserted into the colon, several millilitres of saline are flushed into the colon, followed by aspiration. This can be repeated several times. Once a sample has been collected the following can be examined: 1) a direct wet mount for

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protozoa and helminth ova; 2) sediment following centrifugation for protozoa and trematode ova; 3) a flotation specimen using similar techniques to those in domestic animals for identification of nematode ova. Faecal samples can be evaluated similarly.

A few papers with photomicrographs of gastrointestinal parasites and helminth ova of reptiles are available (Jacobson, 1986b; Barnard, 1986) and should be used as guides for proper identification. The clinician needs to become familiar with parasites and parasite ova of prey species fed to carnivorous reptiles since these may also be encountered in the faeces. For instance, eggs of lice found on mice are commonly found in the faeces of snakes being fed rodents. There is no reason for the clinician to treat a reptile because of the presence of noninfectious prey parasites which are simply passing through the intestinal tract.

In the author’s opinion, Gram staining of faeces is of limited value. However, culturing can provide useful information.

URINE AND SPINAL FLUID COLLECTION Few normal data are available for urine and spinal fluid of reptiles. Samples of both of these fluids are not easy to obtain and without many published data, interpretations are difficult.

In those reptile species such as crocodilians and snakes which do not have bladders, collection of a pure urine sample is almost impossible unless the ureters can be catheterized. In these reptiles, urine enters the terminal colon via the cloaca, and when the animals “urinate”, urine is mixed with faeces. The urinary papillae can be visualized under anaesthesia, in the cloaca of these reptiles. The paired urinary openings are located on the dorsal aspect of the cloaca near the orifices to the reproductive tract. While the author has collected urine samples by this method, the procedure is not easy to do and may have more academic than practical value.

Urine samples are fairly easy to collect from chelonians, particularly tortoises. Many times when a tortoise is examined and manipulated it will spontaneously urinate. The clinician needs to be ready with a cup to collect these samples.

Another method commonly used is cystocentesis. The skin around the right hind-limb is cleaned with several alternating applications of an organic iodine solution and 70% ethanol, the tortoise placed in a vertical position with the lateral side of the left margins of the shell up, and the right hind limb pulled back away from the skin. Utilizing a 22 or 23 gauge needle a percutaneous sample can be collected from the bladder. Because tortoises have large bladders, cystocentesis is fairly easy to perform. Some normal data are available for tortoise urine (Dantzler and Schmidt-Nielsen, 1966; Nagy and Medica, 1986). In the wild, tortoises are seen to go through rather complex changes in urine composition dependent upon the amount of available water and food, and the season of the year (Nagy and Medica, 1986).

Diseases of the central nervous system are commonly seen in snakes. Unfortunately, the author has found it extremely difficult to collect spinal fluid from snakes, because

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of the vertebral anatomy of these animals. Spinal fluid samples are also difficult to collect in lizards for the same reason. However, samples can be collected from crocodilians and chelonians. The site for collecting these samples is in the midline, immediately beyond the occiput of the skull.

However, a large supravertebral vessel is present in this location and the needle needs to be passed through this vessel to be able to collect a spinal fluid sample. Contamination of the sample with blood will make evaluation difficult and because of this a “clean” spinal fluid sample is difficult to obtain.

Acknowledgements The author would like to thank Dr. Juergen Schumacher for information provided on negative-staining techniques.

References Austwick, P.K.C., and Keymer, I.F. (1981) Fungi and actinomycetes. In: Diseases of the Reptilia. Eds. J.E. Cooper and O.F. Jackson, Vol. 1. Academic Press, London. pp. 193-231.

Avery, H.W., and Vitt, L.J. (1984) How to get blood from a turtle. Copeia.

1984, 209-210.

Barnard, S.M. (1986) An annotated outline of commonly occurring reptilian parasites. In: Maintenance and Reproduction of Reptiles in Captivity. Eds V.L. Bels, and P.V. Den Sande. Acta Zoologica et Pathologica Antvenpiensia II, 39-72.

Campbell, T.N. and Coles, E.H. (1986) Avian clinical pathology. In: Veterinary Clinical Pathology. Ed. E.H. Coles. W.B. Saunders Co., Philadelphia. pp. 279-301.

Dantzler, W.H., and Schmidt-Nielsen, B. (1966) Excretion in fresh-water turtle (Pseudemys scripta) and desert tortoise (Gopherus agasszii).

American Journal of Physiology 210, 198-210.

Dessauer, H. (1970) Blood chemistry of reptiles: Physiological and evolutionary aspects. In: Biology of the Reptilia. Eds. C. Gans and T.S. Parsons, Vol. 3, Morphology C. Academic Press, New York. pp. 1-72.

Esra, G.N., Benirschke, K. and Griner, L.A. (1975) Blood collecting techniques in lizards. Journal of the American Veterinary Medical Association 167, 555-556.

Gandal, C.P. (1958) Cardiac punctures in anesthetized turtles. Zoologica 43, 93-94.

Hill, A.C. (1985) Mycoplasma testudinis, a new species isolated from a tortoise. International Journal of Systematic Bacteriology 35, 489-492.

Jackson, O.F. (1981) Clinical aspects of diagnosis and treatment. In: Diseases of the Reptilia, Vol 2. Eds. J.E. Cooper and O.F. Jackson. Academic Press, London. pp. 507-534.

Jacobson, E.R. (1980) Necrotizing mycotic dermatitis in snakes: Clinical and pathologic features. Journal of the American Veterinary Medical Association 177, 838-841.

Jacobson, E.R. (1984) Immobilization, blood sampling, necropsy techniques and diseases of crocodilians a review. Journal of Zoo Animal Medicine 15, 38-45.

Jacobson, E.R. (1986a) Viruses and viral associated diseases of reptiles. In: Maintenance and Reproduction of Reptiles in Captivity. Eds. V.L. Bels and P.V. Den Sande. Acta Zoologica et Pathologica Antverpiensia 2, 73-90.

Jacobson, E.R. (1986b) Parasitic disease of reptiles. In: Zoo and Wild Animal Medicine, 2nd ed. Ed. M.E. Fowler. W.B. Saunders Co., Philadelphia. pp. 162-181.

Jacobson, E.R. (1987) Reptiles. In: Veterinary Clinics of North America: Small Animal Practice. Ed. J. Harkness. Saunders, Philadelphia. pp.

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1203-1225.

Jacobson, E.R. and Telford, S.R. (1990) Chlamydial and poxvirus infections of circulating monocytes of a flap-necked chameleon (Chamaeleo dilepis). Journal of Wildlife Disease 26, 572-577.

Jacobson, E.R. and Gaskin, J.M. (1990) Paramyxovirus infection of viperid snakes. In: The Biology of Pitvipers. Ed. J.A. Campbell. In Press.

Jacobson, E.R., Gaskin, J.M. and Mansell, J. (1989) Chlamydial infection in puff adders (Bitis arietans). Journal of Zoo and Wildlife Medicine 20, 364-369.

Jacobson, E.R., Schumacher, J. and Green, M.E. (1991) Techniques for sampling and handling blood for hematologic and plasma biochemical determinations in the desert tortoise, Xerobates agassizii. Copeia.

Submitted for publication.

Kingsley, G.R. (1972) Procedure for serum protein determinations. In: Standard Methods of Clinical Chemistry, Vol. 7. Ed. G.R. Cooper.

Academic Press, New York. p. 199.

LaPointe, J.L. and Jacobson, E.R. (1974) Hyperglycemic effect of neurohypophysial hormones in the lizard, Klauberina reversiana. General and Comparative Endocrinology 22, 135-136.

Lillywhite, H.B., and Smits, A.N. (1984) Journal of Experimental Biology 110, 267-274.

Lillywhite, H.B. Ackerman, R.A. and Palacios, L. (1983) Journal of Comparative Physiology 152, 59-65.

Maxwell, J.H. (1979) Anesthesia and surgery. In: Turtles: Perspectives and Research. Eds. M. Harless and H. Morlock. John Wiley and Sons, Inc., New York. pp. 127-152.

McDonald, H.S. (1976) Methods for the physiological study of reptiles. In: Biology of the Reptilia. Eds. C. Gans and W.R. Dawson, Vol. 5, Physiology A. Academic Press, New York. pp. 19-125.

McDowell, E.M. and Trump, B.F. (1976) Historical fixatives suitable for diagnostic light and electron microscopy. Archives of Pathology and Laboratory Medicine 100, 405-414.

Migaki, G., Jacobson, E.R. and Casey, H.W. (1984) Fungal diseases in reptiles. In: Diseases of Amphibians and Reptiles. Eds. G. Hoff, F.L. Frye, and E.R. Jacobson, Plenum Press, New York. pp. 183-204.

Millichamp, N., Jacobson, E.R., and Wolf, E.D. (1983) Diseases of the eye and ocular adnexa in reptiles. Journal of the American Veterinary Medicine Association 183, 1205-1212.

Nagy, K., and Medica, P.A. (1986) Physiological ecology of desert tortoises in southern Nevada. Herpetologica 42, 73-92.

Olson, G.A., Hessler, J.R., and Faith, R.E. (1975) Techniques for blood collection and intravascular infusions of reptiles. Laboratory Animal Science 25, 783-786.

Ottaviani, G., and Tazzi, A. (1977) The lymphatic system. In: Biology of the Reptilia. Eds. E. Gans and T.S. Parsons, Vol. 6. Morphology E. Academic Press, New York. pp. 315-462.

Rosskopf, W.J. (1982) Normal hemogram and blood chemistry values for California desert tortoises. Veterinary Medicine/Small Animal Clinician 77, 85-87.

Samour, H.J., Risley, D., March, T., Savage, B., Nieva, O., and Jones, D.M. (1984) Blood sampling techniques in reptiles. Veterinary Record 114, 472-478.

Schaer, M., Ackerman, N., and King, R.R. (1989) Clinical approach to the patient with respiratory disease. In: Textbook of Veterinary Internal Medicine, Vol. I. Ed. S.J. Ettinger. W.B. Saunders Co., Philadelphia. pp. 747-767.

Schermer, S. (1967) The Blood Morphology of Laboratory Animals, 3rd ed.

F.A. Davis, Philadelphia. pp. 137-169.

Smits, A.W., and Kozubowski, M.M. (1985) Partitioning of body fluids and cardiovascular responses to circulatory hypovolemia in the turtle Pseudemys scripta elegans. Journal of Experimental Biology 116, 237-250.

Stephens, G.A., and Creekmore, J.S. (1983) Blood collection by cardiac puncture in conscious turtles. Copeia. 1983, 522-523.

Stewart, J.S. (1990) Anaerobic bacterial infections in reptiles. J. Zoo Wild.

Med. 21, 180-184.

Taylor, R.W., and Jacobson, E.R. (1981) Hematology and serum chemistry of the gopher Tortoise, Gopherus polyphemus. Comparative Biochemistry and Physiology 72A, 425-428.

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Development of a Serodiagnostic Test for the Detection of Herpesvirus Infection in Tortoises Francesco Origgi Med. Vet., Departments of Small Animal Clinical Sciences and Pathobiology College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto Beginning in the mid 1970s, herpesviruses have been reported as pathogens associated with different diseases in several species of chelonians. More recently herpesvirus infection has been identified as a significant health problem in Mediterranean tortoises (Testudo graeca and hermanni). A variety of clinical signs, including stomatitis rhinitis, conjunctivitis, pneumonia and signs of central nervous system disease can be observed in ill tortoises. The disease seems to target more aggressively the upper respiratory tract of the tortoise, but involvement of the lower respiratory tract has also been reported.

The transmission route is totally unknown in the wild. Captive tortoises are commonly exchanged between different collectors, resulting in spreading of the disease. No specific therapy is currently available. An early diagnosis is the most effective preventive measure for reducing the risk of infection. A new enzyme-linked immunosorbent assay (ELISA) has been recently developed at the University of Florida. This assay is currently been validated through a transmission study conducted in Mediterranean tortoises. This serodiagnostic assay will allow rapid screening of tortoises in wild, private, breeding and zoo populations.

Aknowledgments: This study was supported by a contract from the Department of the Army, Corps of Engineers.

Beginning in the mid 1970s, herpesviruses have been reported as pathogens associated with different diseases in several species of chelonians (Cox et al 1980; Drury et al 1998/1999; Frye et al., 1977; Harper et al., 1982; Heldstab and Bestetti, 1989; Jacobson et al., 1982/1985/1986/1991; Kabish and Frost 1994; Marschang et al., 1997/1998/1999; Muro et al., 1998; Rebel et al., 1975). More recently herpesvirus infection has been identified as a significant health problem in Mediterranean tortoises (Testudo graeca and hermanni) (Drury et al 1998/1999; Heldstab and Bestetti, 1989; Kabish and Frost 1994; Marschang et al., 1997/1998/1999; Muro et al., 1998). Several herpesvirus strains have been isolated from pet Mediterranean tortoise in Europe and in the US, thereby showing a worldwide distribution of these viruses. Two isolates have been recently purified in our laboratory. A variety of clinical signs, including stomatitis rhinitis, conjunctivitis, pneumonia and signs of central nervous system disease can be observed in ill tortoises (Heldstab and Bestetti, 1989). Glossitis can be severe and diphteritic plaques on the tongue as well on the

hard palate of the tortoises in the advanced stages of the disease are a common finding. The disease seems to target more aggressively the upper respiratory tract of the tortoise, but involvement of the lower respiratory tract has also been reported. Using light microscopy, intranuclear eosinophilic inclusions have been detected in multiple epithelial tissues and in the brain. Electron microscopy has shown inclusions to consist of virions that are morphologically compatible with herpesvirus.

The transmission route is totally unknown in the wild.

Captive tortoises are commonly exchanged between different collectors, resulting in spreading of the disease. A six month quarantine is necessary to reduce the risk of transmission of the pathogen from infectious to naive tortoises. In naive collections the mortality can be as high as the 100% (Drury et al., 1998).

No specific therapy is currently available. An in vitro study with acyclovir and gancyclovir has shown the ability of these chemotherapeutics in reducing viral replication (Marschang et al., 1997).

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An early diagnosis is the most effective preventive measure for reducing the risk of infection. The most definitive diagnostic test for herpesvirus infection in Mediterranean tortoises is virus isolation. Unfortunately virus isolation is not always achievable. In tortoises in early stages of the disease, relatively little or no virus at all is shed.

Of serological tests serum-neutralization is considered the “gold standard” for detection of exposure to herpesvirus in tortoises. This test detects the presence of serum-neutralizing antibodies and 11-14 days are needed for a diagnosis to be made (Frost and Shmidt, 1997). A new enzyme-linked immunosorbent assay (ELISA) has been recently developed at the University of Florida (Origgi and Jacobson, 1999).

Preliminary unpublished data shows a high sensitivity and specificity of the test compared to SNT. In a survey conducted on 175 plasma samples obtained from Mediterranean tortoises in a rehabilitation facility in France, 35 samples were positive for the presence of SN antibodies while 38 were positive using the ELISA test. All the samples positive by SN were positive also by ELISA. This assay is currently been validated through a transmission study conducted in Mediterranean tortoises. Furthermore we are currently screening a total of 31 recombinant DNA fragments obtained from the cloning of an America herpesvirus isolate (HV1976).

Partial sequencing of several recombinants has already been accomplished. The ultimate goal is the cloning of one of the surface viral glycoproteins and polypetide expression using a bacterial system. This recombinant protein would provide a low cost, standardizible antigen for use in the ELISA test. This serodiagnostic assay will allow rapid screening of tortoises in wild, private, breeding and zoo populations.

Aknowledgments This study was supported by a contract from the Department of the Army, Corps of Engineers.

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References Cox WR, Rapley WA, Barker IK: Herpesvirus like Infection in a painted turtle (Chrysemys picta). J Wild Dis 16:445, 1980 Drury SEN, Gough RE, McArthur S, et al: Detection of herpesvirus-like and papillomavirus associated with diseases of tortoises. Vet Rec 143:639, 1998 Drury SEN, Gough RE, McArthur S: Isolation and identification of herpesvirus and papillomavirus from tortoises in Great Britain. In Proceedings of the 6th ARAV Conference. Columbus, 1999, p 69 Frye FL, Oshiro SL, Dutra FR, et al: Herpesvirus like Infection in two pacific pond turtles. J Am Vet Med Assoc 171:882, 1977 Frost JW, Schmidt A: Serological evidence of susceptibility of various species of tortoises to infection by herpesviruses. Verh Ber Erkrg Zootiere, 38: 29, 1997 Harper PAW, Hammond DC, and Heuschele WP: A Herpesvirus-like agent associated with a pharyngeal abscess in a desert tortoise. J Wild Dis.18: 491, 1982 Heldstab A, Bestetti G: Herpesviridae causing glossitis and meningoencephalitis in land tortoises (Testudo hermanni). Herpetopathologia. 1: 5, 1989 Jacobson ER, Gaskin JM, Wahlquist H: Herpesvirus like infection in map turtles. J Am Vet Med Assoc 181: 1322,1982 Jacobson ER, Clubb S, Gaskin JG, et al: Herpesvirus like infection in Argentine tortoises. J Am Vet Med Assoc 187:1227, 1985 Jacobson ER, Gaskin JM, Roelke M, et al: Conjunctivitis, tracheitis, and pneumonia associated with herpesvirus infection in green sea turtles. J Am Vet Med Assoc 189:1220, 1986 Jacobson ER, Buergelt C, Williams B: Herpesvirus in cutaneous fibropapillomas of the green turtle (Chelonia mydas). Dis Aquat Org 12: 1, 1991 Kabish D, Frost JW: Isolation of herpesvirus from Testudo hermanni and Agrionemys horsfieldii. Verh Ber Erkrg Zootiere 36: 241, 1994 Marschang RE, Gravendyck M, Kaleta EF: Investigation into virus isolation and the treatment of viral stomatitis in T. hermanni and T. graeca. J Vet Med. Series B. 44: 385, 1997 Marschang RE, Posthaus H, Gravendyck, et al: Isolation of Viruses from Land Tortoises in Switzerland In Proceedings of the AAZV and AAWV Joint conference. Omaha, 1998, p 281 Marschang RE: Evidence for a new herpesvirus serotype associated with stomatitis in Afghan Tortoises, Testudo horsfieldi. In Proceedings of the 6th ARAV Conference. Columbus, 1999, p 77.

Muro J, Ramis A, Pastor J, Velarde L, Tarres J, Lavin S. Chronic rhinitis associated with Herpesviral Infection in captive spur-thighed tortoise from Spain. J Wild Dis, 34:487, 1998 Origgi F and Jacobson ER: Development of an ELISA and an Immunoperoxidase based test for herpesvirus exposure detection in tortoises. In Proceedings of the 6th ARAV Conference. Columbus,1999, p 65.

Rebell H, Rywlin A, and Haines H: A herpesvirus-type agent associated with skin lesions of green turtles in aquaculture. Am J Vet Res 36:1221, 1975.

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Medical Problems of Bearded Dragons, Chameleons and Iguanid Lizards Problemi medici di Bearded Dragon, camaleonti e lucertole iguanidi

Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto L’iguana verde (Iguana iguana), i camaleonti (Chamaeleo, Bradypodion, Furcifer spp.) e di Bearded Dragon (Pogona spp) sono diventati popolari come animali da compagnia negli Stati Uniti o in Europa. Negli USA, la domanda di Bearded Dragon e camaleonti come animali da compagnia ha portato ad una loro diffusione in cattività su piccola e vasta scala. Per quanto riguarda l’iguana verde, la maggior parte dei neonati/giovani immessi nel circuito commerciale degli animali da compagnia proviene da allevamenti situati in America Centrale e Sud America.

Con l’aumentare del loro numero, in queste lucertole è stata descritta una gran varietà di malattie infettive e problemi medici. Mentre sono stati identificati parecchi virus nelle iguane, nei Bearded Dragon e nei camaleonti, non è stato condotto alcuno studio sulla trasmissione di questi agenti per stabilire una relazione causale. Le epizoozie batteriche sono poco comuni fra le lucertole tenute in cattive condizioni e gran parte delle infezioni segnalate sono riferibili a traumi. In diverse specie di camaleonti in cattività è stato osservato un attinomicete, Dermathophilus. Le infezioni micotiche nelle lucertole sono sporadiche e derivano anch’esse da cattive condizioni di allevamento e traumi pregressi. Infestazioni da acari e zecche sono state osservate nelle iguane importate, ma le malattie causate da questi parassiti sono minime. È stata descritta l’infestazione da parte di protozoi (Cryptosporidium e Microsporidium) in associazione con problemi clinici, rispettivamente, in iguane e Bearded Dragon. Mentre in entrambe queste specie sono comuni le infestazioni da ossiuridi, il loro ruolo nella malattia non è stato dimostrato. Fra le malattie non infettive, le osteopatie metaboliche si continuano ad osservare in molte iguane e camaleonti. I problemi riproduttivi in questi animali sono comunemente rappresentati da distocia o stasi follicolare.

The green iguana (Iguana iguana), chameleons (Chamaeleo, Bradypodion, Furcifer spp.), and bearded dragons (Pogona spp.) have become popular pets in the United States and Europe. In the United States, the demand for bearded dragons and chameleons as pets has resulted in both small and large-scale captive propagation. Regarding the green iguana, most neonates/juveniles entering the pet trade originate from farming operations in Central and South America. With large numbers in the pet trade, a wide variety of infectious diseases and medical problems have been reported in these lizards. While several viruses has been identified in iguanas, bearded dragons and chameleons, no transmission studies have beeen done with these agents to establish a causal relationship. Bacterial epizootics are uncommon in lizards with poor husbandry and trauma accounting for many of the reported infections. The actinomycete, Dermatophilus, has been seen in several species of captive chameleons. Fungal infections in lizards are sporadic and also result from poor husbandry and prior trauma. While mite and tick infestations have been seen in imported iguanas, diseases caused by these parasites are minimal.

The protozoan parasites Cryptosporidum and Microsporidum have been reported to be associated with disease problems in iguanas and bearded dragons respectively. While oxyurid infections are common in iguanas and bearded dragons, their role in disease has not been demonstrated. Of noninfectious diseases, metabolic bone disease continues to be seen in many iguanas and chameloens. Reproductive problems in iguanas and chameleons commonly include dystocia or follicular stasis.

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The green iguana (Iguana iguana), chameleons (Chameleo, Bradypodion, and Furcifer spp.), and bearded dragons (Pogona spp.) have become popular pets in the United States and Europe. In the US, the demand for bearded dragons and chameleons as pets has resulted in both small and large-scale captive propagation. Regarding the green iguana, most neonates/juveniles entering the pet trade originate from farming operations in Central and South America. With the increased numbers of these lizards being captive bred and entering the pet trade, a wide variety of infectious diseases and medical problems have been seen. Here I will review the most important infectious agents and diseases of these lizards.

Viruses. Intracytoplasmic inclusions are commonly seen in red blood cells of wild chameleons. In one study, of blood films examined from 170 specimens of 15 Chalmaeleo spp. in Tanzania, 3 of 50 flap-necked chameleons (C. dilepis), were found to have intracytoplasmic inclusions (IN1) within circulating monocytes.1 One of the chameleons was maintained in captivity and was sequentially bled. At 46 days, a second type of inclusion (IN2) was occasionally seen within monocytes. The lizard became ill and was euthanatized on day 55. All circulating monocytes were found to have either one or both types of inclusions. By electron microscopy, IN1 was seen to be composed of poxvirus and IN2 contained developmental stages of the genus Chlamydia.

Giemsa-stained blood films from 9 of 50 flap-necked chameleons, Chamaeleo dilepis, and 1 of 18 Fischer’s chameleons, Bradypodion fischeri, collected in Tanzania had intraerythroctic inclusions.2 Using electron microscopy, the inclusions consisted of aggregations of viral particles consistent with the family Iridoviridae. This group of viruses is referred to as Lizard Erythrocytic Virus. No mortality was attributed to this virus.

A 6-month-old, 15 gram captive born Jackson’s chameleon (Chamaeleo jacksoni) became anorexic and died 3 days later.3 A necropsy was performed and histopathology revealed a proliferation of the mucosal epithelial lining of the esophagus and trachea. In hematoxylin and eosin stained tissue sections, eosinophilic intranuclear inclusions were seen within many of the epithelial cells of both the esophagus and trachea. Based upon size, morphologic characteristics, and location, the viral particles seen were most compatible with those of adenovirus.

There are several reports of bearded dragons dying with adenovirus infection. Adenoviruses have been described from a captive bearded dragon (Amphibolurus barbatus) in New Zealand4 and in captive-bred Rankin’s dragons (Pogona henrylawsoni) in the United States.5 In four neonate bearded dragons (Pagona vitticeps) from two collections in the United States, one lizard had intranuclear inclusions in hepatocytes and three had inclusions in enterocytes in the small intestine.6 Two different sized particles could be visualized by electron microscopy. Larger particles were consistent with an adenovirus while smaller particles were consistent with members of the genus Dependovirus.

A herpes-like virus has been recovered from the liver, spleen, kidney, heart, and lung of apparently normal green iguanas.7 Cytopathic effects and intranuclear eosinophilic inclusions were observed in iguana cell cultures of the above

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organs incubated at 30EC and 36EC. Despite the in vitro cytopathic effects, the pathogenicity of this virus was inconclusive based upon in vivo transmission studies. While it has been suggested that a form of lymphocytic leukemia may be related to herpes virus infection in green iguanas,8,9 a causal relationship has not been demonstrated.

A reovirus has reportedly been isolated from multiple organs of an anorectic green iguana.10 Little information is available about the prevalence and pathogenicity of this virus in iguanas.

Bacteria. As in other reptiles, bacterial diseases are a common problem in green iguanas and chameleons. Bacterial infections in bearded dragons are sporadic. Primary infections can often be attributed to a compromised host immune system as a consequence of inappropriate husbandry leading to stress. Poor nutrition can also compromise the host and allow secondary bacterial infections.

While both gram-positive and gram-negative bacteria have been implicated in disease, gram-negative bacteria seem to be most often involved. The most common bacteria isolated from lesions of reptiles are Aeromonas hydrophila, Serratia marcescens, Corynebacterium, Pseudomonas spp., Salmonella spp., Proteus spp., and Edwardsiella spp. A newly described Neisseria has been isolated from the oral cavity and bite wounds of iguanas.11 The presence of anaerobic bacteria, either alone or mixed with aerobic bacteria, may frequently occur in reptile infections. Anaerobic bacteria of the genera Bacteroides, Fusobacterium, Clostridium, and Peptostreptococcus may be underdiagnosed in reptilian infections.

In a epizootic of imported neonate green iguanas, evaluation of the intestine by electron microscopy an organism with developmental stages consistent with chlamydia has been seen by the author of this paper. It was not determined if the chlamydia was the causative agent of the epizootic.

There has been much publicity about green iguanas and Salmonella. Salmonella can be intermittently shed by healthy reptiles and presents a major zoonotic concern.12,13 Owners of iguanas and other reptile pets should be very aware of this problem and use appropriate hygiene to curtail infection. Despite the increased media attention that reptileassociated salmonellosis has received, some pet owners may still fail to recognize the zoonotic potential of reptile contact.

Skin infections caused by Dermatophilus have been reported in chameleons.14,15 Members of this genus are unique in forming filamentous structures that segment transversely and longitudinally. The lesions are seen as raised brown multifocal encrustations.

Fungi. Relatively few fungi have been identified in lesions in green iguanas, chameleons or bearded dragons. Trichosporon beigelii has been isolated from a fungal urolith from a green iguana.16 A necrotizing pneumonia associated with branching, septated hyphae resembling Aspergillus spp. was seen on histopathological examination of a green iguana.17 Candidiasis has been associated with stomatitis in a green iguana.18 An iguana with a fistulous tract leading from one naris was treated for 1.5 years before death and necrop-

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sy.19 On necropsy, numerous fungal granulomas were found in the lung and viscera combined with mycotic osteomyelitis of the nasal septum. Biopsies from a series of imported green iguana hatchlings with cutaneous small to large black raised plaques revealed hyperkeratosis associated with yeast-like organisms.20 The common saprophyte Geotrichum candidum was cultured from these lesions. An adult Jackson’s chameleon which developed a rectal prolapse was found to have an intussusception of the terminal portion of the colon.21 A mycotic enteritis was daignosed.

Parasites. Protozoans. Many protozoans have been found in the gastrointestinal tract and circulatory system of lizards. Most of these organisms do not seem to cause disease and may be a normal constituent of the lizard’s fauna.

In general, iguanas seem less susceptible to disease from gastrointestinal protozoans than do carnivorous reptiles.

Some of the flagellates commonly encountered include Monocercomonoides, Monocercomonas, Proteromonas, and Tritrichomonas. While the amoeba, Entamoeba invadens, is a well-known reptilian pathogen, herbivorous lizards such as green iguanas seem to be less susceptible to amoebiasis than are carnivorous reptiles and may serve as asymptomatic carriers. However, there are reports of systemic amoebiasis in green iguanas.22-25 While coccidia are commonly encountered in lizards, relatively few diseases have been seen. Aberrant cryptosporidian infections have been reported in the outer ear canal of green iguanas.26 Coccidiosis is the most common parasitic disease seen in bearded dragons, with Isospora amphiboluri identified as the causative agent.27 In a recent report, systemic microsporidiosis was reported in bearded dragons.28 These are obligate intracellular protozoa that are in the Phylum Microspora.

Nematodes. Oxyurid nematodes are common in the colon of iguanas and bearded dragons. As many as nine oxyuroid species have been described in the green iguana, including those of the genera Alaeruis, Ozolaimus, Pseudalaeuris, and Tachygonetria.29,30 In iguanids, each species may inhabit a different region of the large intestine and may serve to mechanically break up ingesta and prevent cellulose impactions. Despite the common occurrence of this nematode, only one report exists of associated pathology in iguanids. A Fiji Island iguana, Brachylophus fasciatus, that had a large intestinal impaction comprised of a mass of Alaeruis brachylophi, a species not reported in green iguanas.31 The filariid Oswaldofilaria brevicaudata has been identified in green iguanas.32 The viviparous adults reside in extraintestinal sites while the microfilariae are found in the circulatory system. Transmission is by arthropod vectors. The role of this filarid in disease is unknown. In an Oustalet’s chameleon (C. oustaleti) with fluctuant enlargement of the right superior eyelid, five live, yellow-orange filarid nematodes that ranged from 3 to 6 cm in length were removed from the lesion and identified as Foleyella.33 The lesion healed without complications.

Mites. The snake mite, Ophionyssus natricis, is the most important mite in reptiles.34 Red, pterygosmid mites of the genus Hirstiella may be present in recently imported juve-

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nile iguanas with hyperpigmented, patchy skin necrosis.35 Ticks. Amblyomma dissimile, the iguana tick, is probably the most common species parasitizing imported iguanas.36 Ticks can cause anemia and focal ulceration in reptiles. However, tick infestations in captivity are rarely severe. Ticks may also serve as vectors in transmission of viral, rickettsial, or filarial pathogens, although little is known about this association in reptiles.

Masses/Swellings. Subcutaneous masses/swellings are common in green iguanas and chameleons. While bacteria are most often recovered from abscesses, fungi, foreign bodies, neoplasia, and metazoan parasites are other possible causes. Subcutaneous abscesses are frequently seen and may represent a single bacterial species or a mixed infection. In chameleons, abscesses in the angle of the jaw, oral cavity, periorbital tissue and joint spaces are common. Orbital abscesses also have been reported in the green iguana.37 Agents that have been isolated from the abscesses of iguanas include Neisseria iguanae, Corynebacterium spp., Morganella morgani, Salmonella Marina, Serratia marcescens, Micrococcus spp., and Fusobacterium necrophorum.

In iguanas, bite-wound inoculation of bacteria is probably an important source of infection. In one group of green iguanas and a rhinoceros iguana, Cyclura cornuta, the gramnegative diplococcus, Neisseria iguanae, was isolated from abscesses of the oral cavities of healthy and infected cagemates, indicating inoculation by intraspecific aggression.11,38 Several of these animals developed chronic abscesses and septicemia that responded poorly to treatment.

Infectious Arthritis. Joints infections are common in iguanas and chameleons. The interphalangeal joints are most often affected. Fractures, penetrating wounds, nail bed injury, and hematogenous spread from localized or systemic infections can result in arthritis. In iguanas, husbandry conditions often contribute to septic arthritis as inappropriate caging or relocation can induce an iguana to dig at its cage in attempts to escape. Fine gauge or bare wire will hook the lizard’s nails and can result in loss of the nail and possibly arthritis. The nail may regrow after several months or be lost permanently. Septicemia, abscessation, and bites from cagemates are other predisposing factors in infectious arthritis.

Correction of underlying problems is essential.

Dystocia and Follicular Stasis. Female green iguanas and chameleons seem to be particularly prone to certain reproductive problems in captivity. In dystocia, or egg retention, the female fails to pass some or all the shelled eggs from the reproductive tract. Dystocias may be obstructive, in which the ova are mechanically unable to pass through the reproductive tract due to malformation of ova or anatomical abnormalities in the female, or they may be non-obstructive, where the female fails to oviposit due to lack of suitable nesting sites, stress, or abnormal hormonal stimulation. In follicular stasis, vitellogenesis occurs but ovulation does not.

The failure of some iguanas to ovulate may be related to the solitary status of many pet iguanas. Although follicular stasis can occur, as seen in iguanas that develop caseous follicles, female iguanas may normally experience prolonged

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follicular development. The presence of large pre-ovulatory follicles can warrant intervention as ovariosalpingectomy will prevent future reproductive cycling, which can be stressful for both iguanas and owners. However, treatment may not be necessary in most iguanas with pre-ovulatory ova as the iguana may either be entering a normal phase of reproduction or may resorb the follicles.

Metabolic Bone Disease. Metabolic bone disease (MBD) refers to a variety of diseases that result from dietary imbalances of calcium and phosphorus and/or from a lack of appropriate wavelengths of light. MBD is also known as fibrous osteodystrophy or nutritional secondary hyperparathyroidism. It is very common in small to mid-sized, juvenile iguanas and chameleons A common factor in MBD in iguanas is inadequate exposure to ultraviolet light, primarily of the UV-B wavelength range of 290-315 nm, necessary for the presumed synthesis in iguanas of vitamin D3 (1, 25-dihydroxycholecalciferol). Preliminary data indicated that vitamin D3 is not absorbed from the gastrointestinal tract of green iguanas in significant amounts.39 MBD can also result from an inversion of the desired dietary Ca:P ratio of 1-2:1.40 Inadequate calcium intake alone can contribute to this condition. Renal disease and primary hyperparathyroidism are also potential causes of MBD. MBD results in deposition of fibrous tissue in and around bone, especially in the long bones and mandible. A swollen, “rubbery” appearance and feel of the mandible and alterations in posture are early signs. As the mandible loses density, it can be pulled caudally by the constant tension of the musculature, resulting in brachygnathism. Swelling around the femur with pathologic fractures of the long bones are common as the condition progresses.

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Frye FL, Munn RK, Gardner M, Barten SL and Hadfy LB. 1994. Adenovirus-like hepatitis in a group of related Rankin’s dragon lizards (Pogona henrylawsoni). J. Zoo Wildl. Med. 25:167-171.

Jacobson ER, Kopit W, Kennedy FA, and Funk RS. 1996. Coinfection of a bearded dragon, Pogona vitticeps, with adenovirus- and dependovirus-like Viruses. Vet. Pathol. 33:343-346.

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Bacterial infections and antimicrobial treatment in reptiles Panoramica delle più comuni infezioni batteriche nei rettili e dei relativi trattamenti antimicrobici

Elliot R. Jacobson DVM, Phd - College of Veterinary Medicine - University of Florida - Gainesville - Florida, USA

Riassunto L’importanza degli agenti infettivi come causa di malattia e mortalità nei rettili in cattività è ben documentata. Come agenti patogeni primari o secondari è stata indicata una gran varietà di batteri, ma sembra che le infezioni causate dai microrganismi Gram-negativi siano più comuni di quelle sostenute dai Gram-positivi. Pseudomonas aeruginosa, Aeromonas hydrophila, Providencia rettgeri, Morganella morganii, Salmonella arizonae e Klebsiella oxytoca sono stati frequentemente isolati da rettili in cattività, sia sani che malati; questi microrganismi diventavano invasivi in presenza di condizioni tali da modificare la resistenza dell’ospite o selezionare ceppi patogeni; lo stesso effetto si è osservato in seguito ad una malattia virale primaria, come la polmonite da paramyxovirus negli ofidi.

Anche le infezioni micotiche si osservano comunemente in tutti i principali gruppi di rettili in cattività; nella maggior parte dei casi, risultano colpiti l’apparato tegumentario e quello respiratorio. Le dermatomicosi dei mammiferi causate da Microsporum e Trichophyton sono segnalate raramente nei rettili, mentre la fusariosi, la geotricosi, la ficomicosi e la cromomicosi sembrano essere più comuni. Spesso sono coinvolti fattori predisponenti come la temperatura subottimale del terrario e la sporcizia delle condizioni ambientali. Secondo quanto pubblicato in letteratura, nella maggior parte dei casi le malattie micotiche dei rettili vengono diagnosticate alla necroscopia. Di conseguenza, il numero delle segnalazioni che trattano della terapia medica è relativamente scarso.

La somministrazione di agenti antimicrobici è una parte importante della terapia medica dei rettili malati con infezioni batteriche o micotiche; a questo proposito, occorre tenere presente che la scelta dei chemioterapici specifici è più difficile che nei mammiferi, a causa dell’ampia gamma di peculiarità comportamentali, anatomiche e fisiologiche delle varie specie della classe Reptilia. Oltre a ciò, sono stati condotti solo pochi studi farmacocinetici su un numero molto scarso di specie. Quindi, al momento attuale, la scelta dei chemioterapici appropriati è spesso più un’arte che una scienza. Per determinare i dosaggi dei farmaci nei rettili per i quali non sono disponibili dati farmacocinetici spesso si ricorre all’estrapolazione dalle specie più prossime ed alle nozioni relative alle caratteristiche metaboliche degli antibiotici.

The importance of infectious diseases as causes of illness and mortality in captive reptiles is well documented. While a variety of bacteria have been incriminated as either primary or secondary pathogens, it appears that infections caused

by Gram-negative bacteria are more common than those caused by Gram-positive bacteria. Pseudomonas aeruginosa, Aeromonas hydrophila, Providencia rettgeri, Morganella morganii, Salmonella arizonae, and Klebsiella oxytoca have frequently been isolated from healthy and ill captive reptiles, becoming invasive when conditions either change the resistance of the host or select for pathogenic organisms. These organisms may also become invasive following a primary viral disease such as ophidian paramyxovirus pneumonia.

Mycotic infections are also commonly seen in all major groups of captive reptiles, with the integumentary and respiratory system most often involved. While the dermatomycoses of mammals caused by Microsporum and Trichophyton are rarely reported in reptiles, fusariosis, geotrichosis, phycomycosis and chromomycosis appear to be more common. Predisposing factors such as suboptimal cage temperatures and filthy environmental conditions are often involved. Based upon the literature, most cases of mycotic disease in reptiles are diagnosed at necropsy. As a result, there are relatively few reports which discuss medical management.

Antimicrobial therapy is an important part of medically managing reptiles ill with bacterial and mycotic disease, with selection of specific chemotherapeutics made more difficult than with mammals because of the broad range of behavioral, anatomic and physiological peculiarities of the various species within the class Reptilia. Added upon this, relatively few pharmacokinetic studies have been performed in a handful of species. Thus, at times, the selection of appropriate chemotherapeutics is often more of an art than a science. Extrapolation from one species to the next and metabolic scaling of antibiotics are often used when determining drug dosages in a species for which no pharmacokinetic data are available.

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The importance of infectious diseases as causes of illness and mortality in captive reptiles is well documented. While a variety of bacteria have been incriminated as either primary or secondary pathogens, it appears that infections caused

by Gram-negative bacteria are more common than those caused by Gram-positive bacteria. Pseudomonas aeruginosa, Aeromonas hydrophila, Providencia rettgeri, Morganella morganii, Salmonella arizonae, and Klebsiella oxytoca have frequently been isolated from healthy and ill captive reptiles, becoming invasive when conditions either change the resistance of the host or select for pathogenic organisms. These organisms may also become invasive following a primary viral disease such as ophidian paramyxovirus pneumonia.

Some groups of reptiles seem particularly prone to infection with specific types of bacteria. For instance, the American alligator, Alligator mississippiensis, is susceptible to Aeromonas hydrophila infections. A new Neisseria, N. iguanae, has been isolated from the oral cavity and bite wounds of the green iguana, Iguana iguana. A chronic upper respiratory disease has been seen in the desert tortoise (Gopherus agassizii) and other tortoises and a new mycoplasma, Mycoplasma agassizii, has been identified as the causative agent of this disease. A new mycoplasma also has been identified as the cause of arthritis and pneumonia in Nile crocodiles (Crocodylus niloticus) and the American alligator.

While Infections with chlamydia have been reported in reptiles, it is unknown whether the scarcity of reports is because they have been missed or whether infections with chlamydia are uncommon in reptiles.

Mycotic infections are also commonly seen in all major groups of captive reptiles, with the integumentary and respiratory system most often involved. While the dermatomycoses of mammals caused by Microsporum and Trichophyton are rarely reported in reptiles, fusariosis, geotrichosis, phycomycosis and chromomycosis appear to be more common. Predisposing factors such as suboptimal cage temperatures and filthy environmental conditions are often involved. Based upon the literature, most cases of mycotic disease in reptiles are diagnosed at necropsy. As a result, there are relatively few reports which discuss medical management.

Antimicrobial therapy is an important part of medically managing reptiles ill with bacterial and mycotic disease, with selection of specific chemotherapeutics made more difficult than with mammals because of the broad range of behavioral, anatomic and physiological peculiarities of the various species within the class Reptilia. Added upon this, relatively few pharmacokinetic studies have been performed in a handful of species. Thus, at times, the selection of appropriate chemotherapeutics is often more of an art than a science. Extrapolation from one species to the next and metabolic scaling of antibiotics are often used when determining drug dosages in a species for which no pharmacokinetic data are available.

There are a number of considerations when selecting the most appropriate antimicrobial to be used in treating a reptile ill with an infectious disease. Primary is identification of the causative agent. If a lesion is present, in addition to collecting a swab specimen for culture, a biopsy specimen should be collected for cytologic and histologic evaluation.

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This is essential when interpreting the significance of cultured microbes. In reptiles suspected of being septic, blood samples should be obtained for culture.

As mentioned above, identifying the causative agent is primary. Following isolation and identification of the causative agent(s), for bacteria, minimum inhibitory concentrations (MICs) of antibiotics should be determined. Once MICs are known, selection of the most appropriate antibiotic will depend upon the following: 1)system affected and type of lesion, 2) antibiotic pharmacodynamics and pharmacokinetics, and 3)size, clinical condition, temperament and immune status of the host.

In selecting an antibiotic, the clinician should choose a drug that will reach therapeutic concentrations in the affected tissue. While this approach is similar to that used in mammals, there are several special biological features of reptiles that will influence treatment and requires some discussion.

First, reptiles often produce granulomatous inflammation in response to a variety of pathogens. Since most antibiotics do not readily penetrate well developed granulomas, the list of affective drugs may be quite short. In those cases where mature granulomas are located subcutaneously, concurrently with use of appropriate antimicrobials, most of these lesions should be removed surgically. Another special feature of some reptiles is the spectacle. The spectacle embryologically represents a fusion of the upper and lower eyelids which have become transparent. It is present over the cornea in all snakes with eyes and in some lizards. Infections of the subspectacular space have been reported and topical antibiotics do not appear to move across this barrier. In treating reptiles with such infections, a wedge needs to be removed from the spectacle and then appropriate topicals applied directly onto the globe and within the space.

Pharmacologic properties of antibiotics need to be considered. As mentioned above, the clinician needs to select a drug that will penetrate the affected tissue and lesion. Further, potential side-effects and toxicities of the drugs need to be considered. For instance, in treating a reptile ill with severe renal disease, the use of nephrotoxic antibiotics such as gentamicin would be contraindicated.

As already discussed, there are relatively few scientifically derived antibiotic and antifungal drug dosages in reptiles. This information is critical when administering drugs that are potentially toxic. For instance, gentamicin associated visceral gout has been reported in reptiles when this antibiotic was administered at mammalian therapeutic dosages. The half-lives of a number of antibiotics appears to be considerably longer in reptiles compared to mammals.

Since reptiles are a highly diverse group, both anatomically and physiologically, it may not be scientifically correct to extrapolate from one species to the next. For instance, while enrofloxacin was found to have prolonged blood concentrations following an intramuscular injection of 5 mg/kg of body weight in box turtles, in Hermannâ&#x20AC;&#x2122;s tortoise the therapeutic blood concentrations lasted only 24 hr following an intramuscular injection of 10 mg/kg. Differences more than likely also exist within a species, varying with age and size.

As an example, a hatchling Burmese python, Python molurus, weighing 125 grams would probably require a higher dose of antibiotic per kg of body weight compared to an

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adult weighing over 100 kg. Antimicrobial dosage regimens have been determined by metabolic scaling, utilizing the daily minimum energy cost rather than live body weight.

Obviously, a great deal of work needs to be conducted on blood concentrations of antibiotics in reptiles.

The immune status of the ill reptile will also be important in selecting the most suitable antimicrobial drug. Since many ill reptiles, especially those with chronic infections, appear to be immunocompromised, the use of bacteriocidal antibiotics is often recommended. Further, since the immune system of reptiles is affected by body temperature, maintaining the ill reptile under optimum environmental conditions is imperative. Snakes ill with respiratory disease have been successfully treated only by maintenance at elevated environmental temperatures, without concurrent antibiotic administration. This has been termed thermotherapy.

Size and temperament of the patient may also influence the drug being selected, including the route of administration. Most species of reptiles are under 100 g and many are under 30 g. There are species of lizards which as adults weigh only a few grams. Dosing drugs to these animals can be extremely difficult. The clinician may be limited to those antibiotics which can easily be diluted to a concentration that can be precisely and safely injected. At the other end of the spectrum are those reptiles which are quite large in size and dangerous to approach. In such cases the clinician may have to choose a drug that can be administered in a relatively small volume via an injection dart. In those dangerous reptiles such as venomous snakes, a drug that can be administered every few days rather than daily would be preferred. Some reptiles are extremely timid and nervous, and may not be suitable for injection. In such cases the antibiotic will have to be administered orally, preferentially in food if the animal is still feeding. Thus, the route of administration will also influence the choice of antibiotics to be administered.

In most cases, antimicrobials will be given by injection, either SC or IM. The author generally administers oral antimicrobials only in those cases where there is primary infection of the gastrointestinal tract, in those species that do not tolerate injections and have to be medicated in their feed, and in those disease conditions requiring a drug that is only available in an oral form. In farming operations of reptiles such as with crocodilians and sea turtles, when large numbers of reptiles are ill and have to be treated, it may not be practical to administer drugs by injection. In such cases, oral medication is generally the preferred route of administration.

Several problems exist with oral medication of reptiles. First, very few pharmacokinetic studies have been performed on drugs administered orally to reptiles. Thus, for the vast majority of antimicrobials the dose selected will not be based on science. The gastrointestinal transit time varies greatly between the various groups and species of reptiles, being the slowest in the large herbivorous reptiles. Even in some carnivorous reptiles the transit time may be quite prolonged. Thus, in these animals it may be difficult to achieve optimum therapeutic concentrations of antimicrobials in blood following administration of oral medicants.

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While many oral medicants can be administered in the food of ill reptiles that are feeding, orally medicating reptiles that are not feeding may not be a simple task in all cases. Venomous snakes and large crocodilians are dangerous to handle and manipulate for administration of oral drugs. It may be impossible to extricate the head beyond the shell margins and force open the mouths of many species of turtles and tortoises. The keratinized epidermal hard parts over the mandibles and dentary bones are easily traumatized, and extreme care must be taken in trying to force the mouth open. The giant tortoises are particularly difficult to administer oral medicants.

These reptiles will have to be anesthetized and a pharyngostomy tube inserted for oral medication.

As a generalization, snakes are the easiest group of reptiles to orally medicate. The mouths of most snakes are simple to open and because the glottis is in an extremely cranial position, is easily avoided. A lubricated French catheter or nasogastric tube can be passed down the esophagus of the snake with minimal resistance. Catheters that are very rigid should be avoided. It is important to have the snake relatively straight when passing the catheter. Since the cranial esophagus is extremely thin in most species, the end of the catheter should be round and smooth. While the stomach of most snakes is from one-third to half way down the distance from the head to cloaca, it is not necessary to pass a catheter as far as this organ. In most situations passing the catheter half way between the stomach and oral cavity is satisfactory.

Most of the antibiotics commonly used in reptile medicine are administered either IM or SQ. The problem with IV administration of antibiotics is that except in tortoises, peripheral vessels cannot be visualized. While blood can be collected from a number of sites in different species of reptiles, most of this sampling is â&#x20AC;&#x153;blindâ&#x20AC;? and may not be suitable for repetitive infusions. With SQ and IM drug administrations, the author tends to avoid administering drugs that require large volumes per kg of body weight, especially if the drug is irritating to surrounding tissues. For instance, the author has had several snakes develop necrotizing skin lesions following injection of more than 1 cc of enrofloxacin at a single site.

Since most species of reptiles have a renal portal system, with blood from the caudal half of the body going to the kidneys before reaching systemic circulation, it has been recommended that SQ and IM injections be given in the cranial half of the body. However, there are few studies which have looked at this potential problem scientifically. In a study in red-eared sliders, Trachemys scripta elegans, blood from the caudal region of the body did not necessarily flow through the kidney via the renal portal system. Blood draining the caudal portion of the body in the red-eared slider perfuses the liver in addition to, or instead of, the kidneys. Thus hepatic metabolism also must be considered. When red-eared sliders received either gentamicin (10mg/kg) or carbenicillin (200 mg/kg) in a forelimb or hindlimb no significant differences were found in any of the pharmacokinetic determinants in turtles treated with gentamicin while those that received carbenicillin in a hindlimb had significantly lower blood levels for the first 12 hr post-injection than those that received it in a forelimb. However, since blood levels for

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both injection sites were still well above the MIC for organisms generally treated with carbenicillin, this difference was not considered clinically significant. Still, the renal portal system varies in development between various groups of reptiles and further work is needed before broad generalizations can be made. This is particularly important when injecting drugs that are potentially nephrotoxic and those that are eliminated primarily through the renal system.

Snakes are the easiest reptiles to inject because of the large dorsal muscle masses associated with the ribs and vertebrae. In lizards, the muscle masses associated with the forelimbs are not very substantial and small volumes of drug will be needed in these animals. Tortoises, especially the large tortoises, have extremely thick epidermal hard parts on the cranial aspect of their forelimbs, therefore injections are generally made through the thinner skin on the caudal (posterior) aspect of the forelimbs.

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Bush M, Smeller JM, Charache P, et al. 1976b. Biological half-life of gentamicin in gopher snakes. Am J Vet Res 39:171-173.

Bush M, Custer R, Smeller JM, et al. 1977. Preliminary study of gentamicin in turtles. Am Assoc Zoo Vet Annu Proc, Honolulu. pp. 711978.

Caligiuri, RL, Kollias, GV, Jacobson, ER, et al. 1990. The effects of ambient temperature on amikacin pharmacokinetics in gopher tortoises. Vet. Pharmacol. Therap. 13:287-291.

Clark CH, Rogers ED, Milton SL. 1985. Plasma concentrations of chloramphenicol in snakes. Am J Vet Res 46:2654-2657.

Gamble KC, Alvarado TP, and Bennett CL. 1997. Itraconazole plasma and tissue concentrations in the spiny lizard (Sceloporus sp.) following once daily dosing. 28: 89-93.

Helmick KE, Papich MG, Vliet KA, et al. 1997. Preliminary kinetics of single-dose intravenously administered enrofloxacin and oxytetracycline in the American alligator (Alligator missippiensis). Ann Proc Amer Assoc Zoo Vet, October 26-30, Houston, TX, pp27-28.

Hilf M, Swanson D, Wagner R, et al. 1991. Pharmacokinetics of piperacillin in blood pythons (Python curtus) and in vitro evaluation of efficacy against aerobic gram-negative bacteria. J Zoo Wildlf Med 22:199-203.

Hungerford C, Spelman L, and Papich M. 1997. Pharmcokinetics of enrofloxacin after oral and intramuscular administration in savanna monitors (Varanus exanthematicus). Ann Proc Amer Assoc Zoo Vet, October 26-30, Houston, Texas. pp. 89-92.

Jacobson ER, Brown MP, Chung M, et al. 1988. Serum concentration and disposition kinetics of gentamicin and amikacin in juvenile American alligators. J Zoo Anim Med 19:188-194.

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Klingenberg RJ, and Backner B. 1991. The use of ciprofloxacin, a new antibiotic, in snakes. In Proceeding of the 15th International Sympo-sium on Captive Propagation and Husbandry of Reptiles and Amphibi-ans, Seattle, Washington, pp. 127-140.

Klingenberg RJ: Therapeutics. 1996. In Mader DR (ed): Reptile Medicine and Surgery, Philadelphia, WB Saunders Co, pp. 299321.

Kolmstetter CM, Frazier, D, Cox S, et al. 1997. Metronidazole pharmacolkintetics in yellow ratsnakes (Elaphe obsoleta quadrivitatta).

Ann Proc Amer Assoc Zoo Vet, Houston, TX, Oct 26-30, pp.26 Lawrence K. 1984. Preliminary study on the use of ceftazidime, a broad spectrum cephalosporin antibiotic, in snakes. Res Vet Sci 36:16-20.

Lawrence K, Needham JR, Palmer GH, et al. 1984. A preliminary study on the use of carbencillin in snakes. J Vet pharmacol Ther 7:119-124.

Lawrence K, Palmer GH, Needham JR. 1986. Use of carbenicillin in 2 species of tortoise (Testudo graeca and T hermanni). Res Vet Sci 40:413-415.

Mader DR, Conzelman GM, Baggot JD. 1985. Effects of ambient temperature on the half-life and dosage regimen of amikacin in the gopher snake. J Am Vet Med Assoc 187:1134-1136.

Maxwell LK, and Jacobson ER. 1997. Preliminary single-dose pharmcokinetics of enrofloxacin after oral and intramuscular administration in green iguanas (Iguana iguana). Proceedings of the American Association of Zoo Veterinarians, October 26030, Houston, Texas. pp. 25.

Page CD, Mautino M, Derendorf H, et al. 1991. Multiple dose pharmacokinetics of ketoconazole administered to gopher tortoises (Gopherus polyphemus). J Zoo Wildlf Med 22:191-198.

Prezant RM, Isaza I, and Jacobson ER. 1994. Plasma concentrations and dipsosition kinetics of enrofloxacin in gopher tortoises(Gopherus polyphemus). J Zoo Wildl Med 25:82-87.

Raphael B, Clark CH, Hudson R. 1985. Plasma concentrations of gentamicin in turtles. J Zoo Anim Med 16:138-139.

Raphael BL, Papich M, and Cook RA. 1994. Pharmcokinetics of enrofloxacin after a single intramuscular injection in Indian star tortoises (Geochelone elegans). J Zoo Wildl Med 25:88-94.

Sp_rle H, G_bel T, Schildger B. 1991. Blood-levels of some anti-infectives in the Hermannâ&#x20AC;&#x2122;s tortoise (Testudo hermanni). In 4th International Colloquium on Pathology and Medicine of Reptiles and Amphibians. Abstract.

Stamper MA, Papich M, Lewbart G, et al. 1997. Single dose pharmacokintetics of ceftazidime in loggerhead sea turtles (Caretta caretta). Ann Proc Amer Assoc Zoo Vet, Houston, TX, Oct. 26-30, pp.16.

Young LA, Schumacher J, Papich MG, et al. 1997. Disposition of enrofloxacin and its metabolite ciprofloxacin after IM injection in juvenile Burmese pythons (Python molurus bivittatus) J. Zoo Wildl Med. 28: 71-79.

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Approach to the clinically ill psittacine Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto Clinically ill psittacine birds that do not present as an emergency allow a more thorough initial approach to diagnostics and treatment. These birds will still be perching and will respond to your entrance into the exam room by looking alert, with smooth feathers. Within a short time however, they may begin to fluff their feathers, and even return to a sleeping stance (a more severe clinical sign). If tame, when they step onto your hand, their grip may be weaker than normal and their feet may feel warm. Almost any illness can present with these clinical signs. This presentation is the basic “sick bird” that is still able to temporarily mask its signs of illness, but is unable to maintain this appearance due to underlying disease. As usual, thorough veterinary medicine begins with client communication: • Explain to the owner the myriad of conditions that can cause the general “sick bird” presentation.

• Collect a thorough anamnesis to help direct diagnostics and therapeutics.

• Assuming the bird remains stable, gather the diagnostic samples (bloodwork, gram stains, radiographs, etc.) necessary to narrow the diagnosis.

• Initiate preliminary therapy as indicated.

• In formulating your differential diagnoses, the species and age of the patient together with the history obtained from the client will direct you to the most likely etiologies.

• Extensive client communication at the onset will allow the owner to understand the potential severity of the situation, and hopefully gain their permission for the necessary diagnostics to proceed in a specific treatment direction.

• Remember to give the owner a guarded prognosis until the underlying cause, and the bird’s response to treatment, are known. Very thin birds always warrant a more guarded prognosis.

Treatment while awaiting laboratory results may consist of: 1. Oxygen and humidified warmth.

2. Fluids (route as determined by condition and experience).

3. Antibiotic(s) such as enrofloxacin @ 10-15 mg/kg, or pipracillin (100 mg/kg IM TID) Other useful avian antibiotics include the cephalosporins, such as cefitofur , ceftazidime.

4. Crop feeding if/when hydration is improved and bird is sufficiently stable to avoid aspiration.

5. Metoclopramide @ 0.5 mg/kg IM if regurgitation or g.i. stasis is involved. (Caution with macaws - an occasional macaw will become hyper-excitable with metoclopramide. We generally use 50% of this dose with macaws, especially the miniature macaw species).

6. Ca EDTA if suspicious of heavy metal toxicity (20 - 40 mg/kg, IM, BID - TID).

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Chelonian Shell Repair Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto Turtle shell fractures are common in exotic practice and occur in both free-ranging and pet chelonians. These fractures are often the result of trauma from automobiles, dogs, lawn mowers, boats or humans. Fractures may involve the carapace and/or the plastron and may range from mild cracks to severe shell damage and displacement of shell fragments. Often there is internal injury accompanying the visible external damage.

Injuries that are less than a few hours old are contaminated but not yet infected and may be flushed with sterile saline, cleaned, debrided and repaired immediately if the patient is in a stable condition. Wounds more than a few hours old will be infected. Topical and parenteral antibiotics will be necessary. These shells can not be repaired until a healthy bed of granulation tissue appears, which may take weeks. During this time it is important to maintain proper hydration and caloric intake. Semi-aquatic turtles should be allowed to swim for one hour twice a day, again avoiding contamination of the coelomic cavity.

Once the patient is chemically or physically restrained, the wound must be cleaned and debrided. The surrounding area also needs to be cleaned and gently scrubbed free of algae and debris. Surfaces must be dried well to allow adhesion of epoxy. Pieces of shell that are devascularized should be removed. Any large pieces should be saved in case they are needed later for autologous bone/shell grafts.

Acetone is used to clean the borders of the injury, taking care not to get any of the substance into the wound. Pieces of sterilized fiberglass mesh that are 2 to 3 cm greater in diameter than the area to be covered are prepared. The edges are cut in a curved line to prevent unraveling of the material. A thin coat of epoxy is applied around the defect extending about 2 cm out from the injury and taking care not to get epoxy into the wound. The fiberglass mesh is placed over the defect and imbedded into the epoxy. One to three layers of fiberglass mesh and epoxy may be needed depending on the size of the repair and the strength desired.

In aquatic turtles, a coat of marine resin should be applied over the epoxy 1 to 2 days after the initial repair. This material may be obtained from marine supply stores. It is slower to dry but is more durable in water than the quick drying epoxy. The patch may be left indefinitely on adult chelonians and those with defects that are too large to fill. If the turtle is a free-ranging animal, you will probably not see it after release. A business card may be placed under the final epoxy layer in case they are re-injured or otherwise recaptured. Maintaining large, free-ranging aquatic turtles during shell healing is usually difficult unless the proper facilities are available.

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Emergency presentation in birds Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto Numerous factors such as the bird’s ability to mask clinical signs until the late stages of disease and their high metabolic rate can lead to oxygen deprivation and death during diagnostic sampling or treatment. We must be vigilant in avian medicine not to cause nor accelerate a bird’s demise with over-aggressive intervention. The motto I use for this is “A tentatively diagnosed pet bird that lives is far preferable to a confirmed diagnosis at necropsy”. The following is an outline of differential diagnoses for several common categories of emergency presentation. The lecture and long proceedings will also contain diagnostic and therapeutic protocols for these syndromes.

1) Respiratory Impairment: a. Tracheal/syringeal obstruction - Severe. Usually two presentations.

1. Cockatiels - often seed hull aspiration.

2. Larger birds (macaws, cockatoos, A. Grays). More often due to chronic malnutrition, squamous metaplasia, and secondary tracheal or syringeal infection. b. Tracheal/syringeal - Partial Obstructions. With these one can see increased respiratory effort, but bird is still alert, able to ambulate, and tracheal outflow is noisy but still moving. c. Lower respiratory clinical signs: Hand-feeding young bird - The possible etiologies include: a. Aspiration pneumonia b. Air saculitis/pneumonia (other): Chlamydia, bacterial septicemia, fungal, Sarcocystosis c. Hepatic lipidosis or Hepatic hematoma d. Anemia (Polyoma virus - other) Adult bird - possible etiologies a. Air sacculitis/pneumonia - multiple etiologies as above b. Chronic malnutrition (Vitamin A deficiency) squamous metaplasia, with subsequent fungal etiology very likely, bacterial also common. c. Sarcocystosis d. Abdominal organomegaly: ⇒ Hepatic • Infectious • Neoplastic • Lipidosis • Iron storage (mynahs and Toucans) • Cirrhosis with ascites ⇒ Reproductive Egg bound Ovarian infection Ovarian/Testicular Neoplasia Egg peritonitis Cystic ovaries ⇒ Gastrointestinal G.I. Stasis (PDD, ileus from any illness) ⇒ Abdominal Granuloma ⇒ Miscellaneous e. Cardiac - ascites f. Anemia

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2) Hemorrhage: Traumatic etiologies are the most common. Numerous other conditions can occasionally be the source of hemorrhage. When an owner presents a bird with a “bleeding emergency”, it is important to first distinguish between: a. Frank hemorrhage occurring from an external site on bird (i.e. wing, beak, foot). b. Blood on cage and on bird, but no active bleeding (no fresh blood) noted from any location on bird. c. Frank hemorrhage from vent.

3)

Neurologic Presentations - Possible Etiologies a. Heavy metal (Zn/Pb) b. Trauma c. Neoplasia - pituitary (common in budgies and cockatiels) d. Toxic - (organophosphate - other) e. Seizures - epileptiform 1. Idiopathic - (Red-lored Amazons, others) 2. Other - (Vibration induced, traumatic, neoplastic) 3. Metabolic (hypocalcemia, hypoglycemia, atherosclerosis, hepatic encephalopathy) f. Egg-Yolk Stroke (egg yolk protein occluding vasculature) g. CNS infection (variation of PBFD, PDD, Sarcocystosis, bacterial, fungal, or viral infection). h. Nutritional (Vitamin E/Selenium deficiency, Vitamin B deficiency) i. Terminal stage of any disease

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Gastrointestinal presentations in ferrets Patologie gastroenteriche del furetto (Mustela putorius furo)

Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto I furetti sono colpiti da numerose affezioni gastroenteriche. La differenziazione fra l’infezione da Helicobacter, l’enterite proliferativa, l’enterite eosinofilica, l’ingestione di corpi estranei e la forma di diarrea rapidamente contagiosa comunemente indicata col nome di enterite catarrale epizootica (ECE) non è sempre facile.

ECE (Enterite catarrale epizootica) Anche se la patogenesi di questa condizione è fortemente indicativa di un’eziologia virale, non è ancora stato possibile isolare alcun microrganismo. In molti furetti ricoverati è stato stabilito un apparente stato di portatore latente, che persiste per un periodo di tempo indefinito. I segni clinici generalmente sono rappresentati da una grave diarrea verde fluorescente, in genere successiva ad una recente esposizione ad un nuovo furetto asintomatico.

Ingestione di corpi estranei I furetti giovani vengono portati alla visita per una moltitudine di problemi, fra i quali è piuttosto frequente l’ingestione di corpi estranei. Tuttavia, la presenza di corpi estranei a livello gastroenterico non è costantemente associata a vomito proiettile, né a qualsiasi altra forma di vomito. I segni clinici più comuni sono rappresentati da diarrea, anoressia e letargia.

Enterite eosinofilica A questa condizione è spesso associata un’eosinofilia periferica. Le anse intestinali sono di solito ispessite alla palpazione e, secondo l’esperienza dell’autrice, gli animali sottoposti a questo tipo di indagine mostrano un certo disagio, ma non un dolore acuto. L’eziologia della sindrome non è nota, ma la maggior parte dei casi risponde ai corticosteroidi.

Enteropatia proliferativa L’enteropatia proliferativa (PDB, proliferative bowel disease) è una malattia a carattere diarroico del tratto intermedio e distale dell’apparato digerente che provoca la comparsa di ispessimento delle regioni interessate e tenesmo ed è spesso accompagnata da prolasso rettale, perdita di peso e disidratazione. Gli animali più colpiti sono i giovani.

Helicobacter musteliade Le ulcerazioni e le emorragie che si verificano in presenza di una gastrite da Helicobacter possono determinare l’insorgenza di vomito o la comparsa di sangue digerito nelle feci. I furetti colpiti mostrano in genere un intenso dolore in risposta alla palpazione dello stomaco. Inoltre, sembrano essere sottoposti ad un notevole stress e possono manifestare degli “spasmi” della regione facciale e delle orecchie e toccarsi la bocca con le zampe. Ai fini del trattamento risultano efficaci le associazioni di metronidazolo (20 mg/kg BID), amoxicillina (10 mg/kg BID) e salicilato basico di bismuto (circa 1 ml/kg BID-TID).

I segni clinici di diarrea, anoressia, nausea e, occasionalmente, vomito possono essere dovuti anche a sindromi non gastroenteriche, come l’insufficienza renale, le epatopatie (comprese la lipidosi epatica ed il linfoma) e varie condizioni neoplastiche.

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Numerous gastrointestinal conditions occur in ferrets. The differentiation between Helicobacter, proliferative enteritis, eosinophilic enteritis, foreign body ingestion and the rapidly contagious diarrhea currently referred to as epizootic catarrhal enteritis (E.C.E.), is not always easy.

E.C.E. (Epizootic catarrhal enteritis) While the pathogenesis is strongly suggestive of a viral etiology, no organism has yet been isolated. An apparent latent carrier state is established in many recovered ferrets, that persists for an indefinite period of time. Clinical signs generally include severe, fluorescent green diarrhea, generally after recent exposure to a new, but asymptomatic ferret.

Foreign body ingestion Young ferrets present with a multitude of problems, including frequent foreign body ingestion. However, the occurrence of projectile vomition, or any vomiting, with gastro-intestinal foreign bodies is not consistently found. Diarrhea, anorexia, and lethargy are the most common presenting signs.

Eosinophilic enteritis Peripheral eosinophilia is often associated with eosinophilic enteritis. The bowel loops are generally palpably thickened, and in this author’s experience, uncomfortable but not acutely painful on palpation. The etiology of this syndrome is not known, but most cases are responsive to glucocorticoids.

Proliferative Bowel Disease Proliferative bowel disease (PBD) is a diarrheal disease of the middle and lower gastrointestinal tract causing thickening of these regions, tenesmus, and is often accompanied by rectal prolaspe, weight loss and dehydration. Most affected animals are young.

Helicobacter mustelidae With Helicobacter gastritis, gastric ulceration and hemorrhage may cause either the vomitus or the stool to contain denatured blood. These ferrets are generally very painful upon gastric palpation. These ferrets seem to be in considerable distress and may exhibit facial and ear “twitching” and pawing at the mouth. Effective antibiotic combinations include Flagyl (metronidazole) @ 20 mg/kg BID, amoxicillin 10 mg/kg BID and Pepto-Bismol(bismuth subsalicylate) @ about 1 ml/kg B-TID. Non-gastrointestinal syndromes may cause clinical signs of diarrhea, anorexia, nausea, and occasionally vomiting. These include renal failure, liver disease (including hepatic lipidosis and lymphoma) and various neoplastic conditions.

Numerous gastrointestinal conditions occur in ferrets.

The differentiation between Helicobacter, proliferative enteritis, eosinophilic enteritis, foreign body ingestion and the rapidly contagious diarrhea currently referred to as epizootic catarrhal enteritis (E.C.E.), is not always easy.

E.C.E. (Epizootic catarrhal enteritis) Note: Hopefully, both the name and the acronym E.C.E. will be changed to reflect a more accurate description of the disease, since it is neither epizootic nor primarily catarrhal in nature. While the pathogenesis is strongly suggestive of a viral etiology, no organism has yet been isolated. An apparent latent carrier state is established in many recovered ferrets, that persists for an indefinite period of time. Clinical signs generally include severe, fluorescent green diarrhea, generally after recent exposure to a new, but asymptomatic ferret. In young, healthy ferrets, very little treatment other than supportive care is required. Older ferrets with concurrent problems are the ones at risk for sequelae, including severe dehydration, emaciation, and death. The incubation pe-

riod is extremely short, and the etiologic agent appears highly contagious.

Foreign body ingestion Young ferrets present with a multitude of problems, including frequent foreign body ingestion. However, the occurrence of projectile vomition, or any vomiting, with gastro-intestinal foreign bodies is not consistently found. Diarrhea, anorexia, and lethargy are the most common presenting signs. 1,2,7,15,16,18,19 Luckily, the abdomen of ferrets is amenable to palpation and detection can often be made in this manner. Both plain film and contrast radiography may be utilized to help confirm the diagnosis.

Eosinophilic enteritis Peripheral eosinophilia is often associated with eosinophilic enteritis. The bowel loops are generally palpably thickened, and in this author’s experience, uncomfort-

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able but not acutely painful on palpation. Multi-systemic eosinophilic disease also occurs, which may involve the liver, respiratory tract, lymphatic system, and isolated eosinophilic infiltrates. 14,18 The etiology of this syndrome is not known, but most cases are responsive to glucocorticoids.

Some ferrets will recur with eosinophilic enteritis when the glucocorticoid therapy is discontinued, while others may be successfully tapered off of therapy.

Proliferative Bowel Disease Proliferative bowel disease (PBD) is a diarrheal disease of the middle and lower gastrointestinal tract causing thickening of these regions, tenesmus, and is often accompanied by rectal prolaspe, weight loss and dehydration. Most affected animals are young, (less than 19 months of age) so the differential must also include gastro-intestinal foreign bodies. Confirmative diagnosis of PBD is not possible without biopsy, but the response to treatment (cholamphenicol @ 50 mg/kg BID, PO or parenteral), along with supportive care, is usually dramatic. This syndrome, while extremely serious, is not being noted in the U.S. with the same frequency as it was in previous years. The name of the causative organism has been changed several times. It is currently relegated to the scientific name Lawsonia intracellularis. This organism is not amenable to culture, and diagnosis on biopsy requires special staining.5,7,8,15,16,18

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The technique of scruffing and slowly infusing the medication into the mouth while the ferret is in the “frozen” mental state may be the most successful). Most ferrets enjoy the taste of pediatric amoxicillin suspension. Additional medications that have been found useful include sulcrafate (Carafate, 25 mg/kg q 8 hrs.) and H2 receptor blockers such as cimetidine (Tagamet, 5-10 mg/kg q 8 hrs.).

Non-gastrointestinal syndromes may cause clinical signs of diarrhea, anorexia, nausea, and occasionally vomiting.

These include renal failure, liver disease (including hepatic lipidosis and lymphoma) and various neoplastic conditions.

References 1)

2) 3) 4) 5) 6)

7) 8)

Helicobacter mustelidae 9)

With Helicobacter gastritis, gastric ulceration and hemorrhage may cause either the vomitus or the stool to contain denatured blood. These ferrets are generally very painful upon gastric palpation. The prevalence of Helicobacter m. enteritis seems to be rising, though that impression may be skewed by an increased awareness of its existence, (partially due to the pathophysiology of the same genus in gastric ulcers of people) and an increase in histopathology submissions. Affected ferrets are often adults, although the syndrome is also reported in juveniles. Often the stress of a concurrent syndrome, such as an insulinoma or adrenal disease, may precipitate the clinical manifestation of an infection.

These ferrets seem to be in considerable distress, and may exhibit facial and ear “twitching” and pawing at the mouth.

Effective antibiotic combinations include Flagyl (metronidazole) @ 20 mg/kg BID, amoxicillin 10 mg/kg BID and Pepto-Bismol(bismuth subsalicylate) @ about 1 ml/kg BTID5,7,8,15,16,18 (Note: Forewarn the owners that both the Pepto-Bismol and the Flagyl will not be palatable to the ferret.

10) 11) 12) 13) 14) 15) 16) 17) 18) 19)

Rosenthal, K. Ferrets. In The Veterinary Clinics of North America Small Animal Practice Exotic Pet medicine II, WB Saunders January, 1994: (24) 1: 1 - 23.

Brown, SA. Ferrets. In A Practitioner’s Guide to Rabbits and Ferrets, The Professional Library Series, AAHA, 1993, 43-100.

Fox, JG. Biology and Diseases of the Ferret. Lea & Febiger, Philadelphia, 1988.

Bartlett, LW. Unpublished data, 1998.

Williams BH. Infectious Diseases of Ferrets. In The North American Veterinary Conference Proceedings, 1995, 584-585.

Rosenthal, KA. Hyperadrenocorticism associated with adrenocortical tumor or nodular hyperplasia of the adrenal gland in ferrets: 50 cases (1987-1991), Journal of the AVMA, July 15, 1993 Vol 203 (2) 271-275.

Hoefer, HL. Gastrointestinal Diseases of Ferrets. In TNAVC Proceedings, 1995, 579 - 580.

Bell, J. Infectious Diseases of Ferrets. In The North American Veterinary Conference (TNAVC) Proceedings, 1993. 721- 723.

Brown, SA Adrenal and Pancreatic Neoplasia in TNAVC Proceedings, 1993, Rosenthal, K, How We Treat An Insulinoma in the Ferret, In TNAVC Proceedings, 1994, 822.

Rosenthal, K, Adrenal Disease in the Ferret. In TNAVC Proceedings 1994, 823 - 824.

Miller, MS, Ferret Cardiology, In TNAVC Proceedings 1993, 735736.

Brown, SA Clinical Management of Lymphoma in the Ferret, In TNAVC Proceedings, 1993. 730-732 Lightfoot TL, J. of Exotic Animal Medicine, “Multi-systemic Eosinophilic Complex in a Ferret”, Quesenberry, K, Gastrointestinal Disorders of Ferrets. In TNAVC Proceedings, 1996, 870-871.

Johnson-Delaney, CA, Harrison, LR. Exotic Companion Medicine Handbook. Wingers Publishing , Lake Worth, FL. 1996, 30 - 40.

Stamoulis, ME. Cardiac Disease in Ferrets. In Seminars in Avian and Exotic Pet Medicine Vol 4 (1) January 1995 43 - 48.

Hillyer EV, Quesenberry KE, Ferrets, Rabbits, and Rodents - Clinical Medicine and Surgery, 1997, W.B. Saunders Pub. Co. Bartlett LW, Lightfoot TL, Harrison GJ, Manarino R. Exotic Companion Animal Surgery CD-ROM, Wingers Publishing Company, Lake Worth, FL, In Press (Copyright 1998 – Exotic Veterinary Seminars, Inc.)

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Ferret neoplasia Neoplasie del furetto e relativi protocolli terapeutici

Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto Nei furetti degli USA si riscontra un’elevata incidenza di neoplasie, come i tumori delle cellule surrenali, gli insulinomi (adenocarcinomi delle cellule β del pancreas) ed i linfomi. Sono anche comuni le neoplasie cutanee, che comprendono, senza essere limitati ad essi, i mastocitomi, gli adenocarcinomi e gli adenomi basocellulari.

Neoplasie cutanee In linea generale, si può affermare che le neoplasie cutanee possono essere rappresentate da masse ricorrenti, multifocali o isolate, ma non tendono a dare origine a metastasi ad organi distanti. Di solito, il trattamento consigliato è la resezione chirurgica. I furetti sono in genere eccellenti pazienti da operare e tollerano estremamente bene l’anestesia con isofluorano.

Linfoma In modo molto simile a quanto avviene nel gatto, il linfoma si riscontra comunemente in due gruppi di età. I furetti giovani sono spesso colpiti dal linfoma mediastinico e possono essere portati alla visita perché presentano dispnea, letargia e tosse. Negli animali di questo gruppo di solito non si nota una linfoadenopatia periferica. Nei furetti più anziani con linfoma si osservano quadri più variabili. La linfoadenopatia periferica in questo caso è presente, ma è necessario effettuare con attenzione la palpazione dei linfonodi periferici per differenziarli dall’accentuato accumulo di grasso che in genere li circonda.

Neoplasie e malattie delle surreni L’alopecia ed il prurito che si possono riscontrare nei furetti con malattie delle surreni sembrano clinicamente simili all’atopia e ad altre affezioni dermatologiche primarie, allergiche o infettive, del cane. La teoria prevalente è che l’orchiectomia o l’ovaristerectomia precoci che vengono eseguite sulla maggior parte dei furetti domestici allevati negli Stati Uniti spingano le surreni a compensare la carenza di estrogeni e/o androgeni circolanti. Anche la mancanza di un fotoperiodo normale può avere un ruolo nel determinare questa sindrome. La successiva metaplasia delle cellule endocrine delle ghiandole surrenali in questi giovani furetti porta alla produzione di ormoni delle gonadi. La rimozione chirurgica delle surreni colpite è in genere risolutiva, anche se, a meno che non vengano rimosse completamente le due ghiandole (come è indicato nel caso in cui siano entrambe colpite), i segni clinici possono recidivare in seguito allo sviluppo di altro tessuto surrenalico patologico. Recenti studi hanno indicato che il Depo-Lupron®, un agonista del GnRH, è in grado di sopprimere la produzione ectopica di ormoni delle gonadi da parte delle surreni e viene utilizzato in associazione o in luogo della resezione chirurgica delle ghiandole colpite.

Insulinomi (carcinomi delle cellule β del pancreas) Gli insulinomi dei furetti anziani (di età superiore a tre-quattro anni) sono un riscontro comune negli Stati Uniti. La presenza di un insulinoma attivo ed in stadio avanzato determina la comparsa di ipoglicemia, che si può presentare sotto forma di debolezza, letargia, anoressia (dovuta principalmente alla nausea) o stupore. Anche se di solito si nota una risposta positiva alla chirurgia, bisogna tenere presente che la neoplasia ha generalmente già dato origine a micrometastasi in altre parti del pancreas prima dell’insorgenza dei segni clinici. Il trattamento con prednisone (alla dose di 0,5-4,0 mg/kg suddivisi in due somministrazioni al giorno) consente spesso di migliorare la qualità della vita e prolungare la sopravvivenza.

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Ferrets in the U. S. have a high incidence of neoplasia, including adrenal cell tumors, insulinomas (Beta-cell pancreatic adenocarcinomas) and lymphoma. Cutaneous neoplasia is also common, including but not limited to mast cell tumors, basal cell adenomas and adenocarcinomas.

Cutaneous Neoplasias As a generalization, cutaneous neoplasias may be recurrent, multi-focal or isolated masses but they do not tend to metastasize to distant organs. Surgical resection is usually the recommended treatment. Ferrets are generally excellent surgical patients, and tolerate Isoflurane anesthesia extremely well.

Lymphoma Lymphoma is common in two age groups, much as in cats. The young ferret is often affected with mediastinal lymphoma and may present with dyspnea, lethargy, and coughing. Peripheral lymphadenopathy is not usually noted in this group. Older ferrets with lymphoma have more variable presentations. Peripheral lymphadenopathy does occur, but the practitioner should be cautious when palpating peripheral lymph nodes to differentiate between the pronounced accumulation of fat that commonly surrounds these lymph nodes and the actual node itself located within the fat.

Adrenal Disease and Neoplasia The alopecia and pruitis that may occur with adrenal disease in ferrets appears clinically similar to atopy and other primary allergic or infectious dermatologic diseases in dogs. The prevalent theory is that very early orchiectomy or ovariohysterectomy as is performed on the majority of domestically raised ferrets in the United States causes the adrenal glands to compensate for the lack of circulating estrogens and/or androgens. Lack of a normal photoperiod may also be involved in this syndrome. The subsequent metaplasia of endocrine cells in the adrenal gland of these young ferrets then leads to the production of gonadal hormones. Surgical removal of the affected adrenal gland(s) is generally curative, although unless both glands are completely removed (which is indicated if both are pathologic), recurrence of clinical signs may occur when more pathologic adrenal tissue develops. Recent studies have indicated that Depo-LupronR, a GnRH agonist, may suppress ectopic adrenal production of gonadal hormones and be used in conjunction with or in lieu of surgical resection of the affected gland(s).

Insulinomas (Beta cell carcinomas of the pancreas) Insulinomas of older ferrets are common clinical findings in the U. S. after a ferret reaches three to four years of age.

Hypoglycemia is the result of an active and advanced insulinoma and may present as weakness, lethargy, anorexia (due most likely to nausea) or stupor. Although a positive clinical response to surgery is usually noted, the neoplasia has generally micro-metastasized to other parts of the pancreas prior to the onset of clinical signs. The use of prednisone (at 0.5 â&#x20AC;&#x201C; 4.0 mg/kg divided BID) will often increase the quality and length of life.

Ferrets in the U. S. have a high incidence of neoplasia, including adrenal cell tumors, insulinomas (Beta-cell pancreatic adenocarcinomas) and lymphoma. Cutaneous neoplasia is also common, including but not limited to mast cell tumors, basal cell adenomas and adenocarcinomas.13,16,18

CUTANEOUS NEOPLASIAS As a generalization, cutaneous neoplasias may be recurrent, multi-focal or isolated masses and they do not tend to metastasize to distant organs. Surgical resection is usually the recommended course of treatment. Ferrets are generally excellent surgical patients, and tolerate Isoflurane anesthesia extremely well.

Lymphoma Lymphoma is common in two age groups, much as in cats. The young ferret is often affected with mediastinal

lymphoma, and may present with dyspnea, lethargy, and coughing. Peripheral lymphadenopathy is not usually noted in this group. Response to chemotherapy is variable in young ferrets with lymphoma. One case of a nine month old ferret with a pronounced mediastinal mass underwent the following chemotherapy, and is still clinical disease free over 14 months later. A regime of prednisone, Vincristine and cyclophosphamide was used over a seven week period.

Prednisone was administered at 1 mg/kg orally twice daily for the entire seven weeks. Cyclophosphamide was given at 10 mg/kg orally on Day 3, ???Day 24, and Day 45. (once every 3 weeks for three treatments) Vincristine was administered IV @ 0.12 mg/kg starting on Day one, and then repeated once weekly for a series of four injections. Other protocols are listed in reference eighteen.

Older ferrets with lymphoma have more variable presentations. Peripheral lymphadenopathy does occur, but the practitioner should be cautious when palpating peripheral lymph nodes to differentiate between the pronounced accumulation of fat that commonly surrounds these lymph nodes and the actual node itself lying within the fat. Lymph node

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excision is usually conclusive, whereas aspirates are difficult due to the surrounding fat and the relatively small size of even enlarged nodes. The popliteal lymph node in ferrets is easily accessible for resection and not as vascular as in dogs and cats. Splenic lymphoma may occur, but without biopsy and histopathology it is difficult to diagnose due to the nearly universal splenic enlargement (usually benign extra-medullary hematopoesis) that occurs as ferrets of the U.S. gene pool as they age. Cardiac (hilar) lymphadenopathy occurs with some frequency, and is often noted in conjunction with cardiomyopathy on radiographs. Peripheral lymphocytosis may or may not occur, and the finding of peripheral lymphoma cells on a blood smear is rare. Hepatic involvement is also common, requiring biopsy for diagnosis.

The finding of enlarged lymph nodes in the intestinal mesentery, often encountered during a routine adrenalectomy, warrants a biopsy, since lymphoma is often demonstrated in these nodes.1,2,13,14,18 Protocols for chemotherapy have been used, and the option of treatment with prednisone alone exists, with generally the same positive and negative indications as in the treatment for lymphoma in dogs and cats.13,16,18 Unlike cats, no viral etiology has been discovered.

Occasionally a middle-aged (2-3 year old) ferret will present with lymphoma. This is often a very acute onset, with bone marrow involvement and severe secondary infection. In this author’s experience, these cases are usually not amenable to treatment and often the diagnosis is made postmortem.

Adrenal Disease and Neoplasia The alopecia and pruitis that may occur with adrenal disease in ferrets appears clinically similar to atopy and other primary allergic or infectious dermatologic diseases in dogs.

Even when veterinarians are aware of the prevalence of this adrenal syndrome in ferrets, the tendency is to think of this as a “Cushings”, or pituitary based disease. Another assumption is that the primary hormone produced in excess is a glucocorticoid, when in actuality estrogen, testosterone, or progesterone derivatives are elevated.

The prevalent theory is that very early orchiectomy or ovariohysterectomy as is performed on the majority of domestically raised ferrets in the United States causes the adrenal glands to compensate for the lack of circulating estrogens and/or androgens.1,2,6,9,11,18,19 Lack of a normal photoperiod may also be involved in this syndrome. The subsequent metaplasia of endocrine cells in the adrenal gland of these young ferrets then leads to the production of gonadal hormones. Therefore, clinical signs may vary according to the particular hormone(s) that are being produced. The University of Tennessee currently has a commercially available assay for these hormones. Preliminary data shows a correlation between the elevation of serum estrogen levels and the occurrence of vulvar swelling in female ferrets. A similar parallel has been noted in male ferrets with an increase in serum testosterone levels that exhibit aggression, sexual behavior, and prostatic enlargement (often leading to dysuria).

These clinical signs in the male ferret may occur with or without the more common finding of progressive alopecia.

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The link between elevated progesterone and specific clinical signs is still being investigated. Interestingly, the glucocorticoid levels in these ferrets are generally normal to low, indicating that the diseased adrenal glands are not producing this hormone in significant amounts. Surgical removal of the affected adrenal gland(s) is generally curative, although unless both glands are completely removed (which is indicated if both are pathologic), recurrence of clinical signs may occur when more pathologic adrenal tissue develops. Mineralocorticoid deprivation does not seem to affect most ferrets, even with total resection of both glands.1,6,9,11,16,18,19 In this author’s experience, only two of dozens of ferrets have required fludrocortisone (Florinef) therapy following bilateral adrenalectomy.

The prevalence of left adrenal gland disease over right adrenal disease is no longer being noted, and bilateral disease is more commonly reported than in previous years. It is doubtful that this is due to a true change in distribution, but rather to the increased ability of practitioners and surgeons to locate the cranially placed right adrenal gland. The right adrenal gland is easily overlooked, being located cranial to the right kidney, abutting the vena cava, and lying below (dorsal to) the right caudate lobe of the liver. Unless the ligament connecting the caudate liver lobe to the kidney and vena cava is severed, the gland is not visible.9,18,19 However, palpation can be accomplished without transection of this ligament. The potential for laceration of the caudal vena cava is great if the right adrenal gland is totally resected. The use of a Savinsky neonatal vascular clamp (Avery Bennett, personal communication, Jan, 1998) greatly reduces this risk. Without this device, the right gland is often debulked rather than totally resected. Although recurrence of clinical signs is possible if affected adrenal gland tissue remains, several factors should be considered prior to attempting total resection of the right gland.

1) If the left gland is also removed, leaving a small portion of right adrenal gland may maintain some normal glucocorticoid production.

2) If the equipment or expertise to resect the entire gland is not present, without risking significant laceration of the vena cava and requiring its ligation, then the procedure should not be undertaken. Although anecdotal reports of ligation of the vena cava and successful recovery have been reported, these ferrets may shortly thereafter suffer from vascular compromise of the renal or hepatic systems.

3) Although a percentage (reports vary from 10 – 75%) of the adrenal masses are histologically adrenal adenocarcinomas, metastasis to other organs is rare. The risk of potential destruction of the caudal vena cava in the absence of the proper equipment and/or ability to remove the entire gland would therefore not be warranted, and de-bulking may be an acceptable alternative.

Mitotane (Lysodren) therapy in lieu of surgery is not a reliable alternative. Some ferrets with tolerate the medication (although those with insulinomas should not be given this drug, due to the potential for developing a severe hypoglycemic episode). The clinical signs, however, are usually only partially and temporarily improved. Owners may note

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some decrease in vulvar swelling and some re-growth of hair, but the effect seems to be short-lived, and even if the owners continue therapy the clinical signs often recur within several months. Ketaconazole is not an effective treatment for adrenal disease in ferrets. To date, there is no published information on the use of Metyrapone nor Deprenyl for the treatment of ferret adrenal disease. Due to the pituitary action of these medications, they are not likely to be efficacious in ferrets.

Recent studies have indicated that Depo-LupronR, a GnRH agonist, may suppress ectopic adrenal production of gonadal hormones, and be used in conjunction with or in lieu of surgical resection of the affected gland(s). Dosages of 100 ug/kg are being used by many practitioners. Another researcher is currently using 800ug/kg. Most empirical evidence now suggets that the injection should be repeated in four to eight weeks.Another useful medication in male ferrets with concurrent prostatic cystic disease is ProscarR (finasteride), a medication designed for prostatic hypertrophy in human males. A daily dose of 0.5 – 1.0 mg/kg can be used. It prevents the conversion of testosterone to the active form of testosterone. These two medications are currently being used by many practitioners. The long-term benefits are yet to be determined but preliminary information is encouraging.

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(which raises the blood glucose) perpetuates the belief that the problem was musculoskeletal.

Treatment consists of surgical resection of visibly affected portions of the pancreas. These may be discrete pancreatic nodules, or generalized areas of abnormal tissue. Although a positive clinical response to surgery is usually noted, the neoplasia has generally micro-metastasized to other parts of the pancreas prior to the onset of clinical signs. The use of prednisone (at 0.5 – 4.0 mg/kg divided BID) as either the initial treatment, or as the treatment subsequent to surgical resection if and when hypoglycemia recurs, will often increase the quality and length of life.2,10,16,18 Diazoxide (Proglycem - @ 5-25 mg/kg B-TID) can be added to aid in maintaining blood glucose, but it is expensive and in some practitioners’ experience, minimally effective. It may allow the reduction of the prednisone dose, but it will not substitute for prednisone therapy.

References 1)

2) 3)

Insulinomas (Beta cell carcinomas of the pancreas)

4) 5) 6)

Insulinomas of older ferrets are common clinical finding in the U. S. after a ferret reaches three to four years of age.

Hypoglycemia is the result of an active and advanced insulinoma, and may present as weakness, lethargy, anorexia (due most likely to nausea), or stupor.1,2,10,16,18,19 A blood glucose is often diagnostic, even without fasting. Generally, clinically affected ferrets will display blood glucose levels of 20 - 60 g/dl, and at these levels this is diagnostic. Ferrets brought in earlier in the course of the disease may have blood glucose levels in the high 70’s and require a four hour fast to confirm the diagnosis. Interestingly, several young ferrets (less than three years of age) have had insulinomas discovered during exploratory surgery for gastrointestinal foreign bodies. The blood glucose levels of these ferrets were still within the normal range. The actual age of onset of the formation of these tumors is not known, but it is likely that they exist asymptomatically in many ferrets for prolonged periods. Insulin/glucose ratios are available and useful diagnostically when performed by a laboratory that has verified their accuracy in ferrets. Initial treatment of the acute, laterally recumbent, hypoglycemic, hypothermic ferret is I.V. dextrose, and the results are usually dramatic.

Ferrets with insulinomas may also present with a hypoglycemia-induced weakness, reported as rear end paresis or ataxia, and this may be confused with spinal or disc trauma.

The positive clinical response to a glucocorticoid injection

7) 8) 9) 10) 11) 12) 13) 14) 15) 16) 17) 18) 19)

Rosenthal, K. Ferrets. In The Veterinary Clinics of North America Small Animal Practice Exotic Pet medicine II, WB Saunders January, 1994: (24) 1: 1 - 23.

Brown, SA. Ferrets. In A Practitioner’s Guide to Rabbits and Ferrets, The Professional Library Series, AAHA, 1993, 43-100.

Fox, JG. Biology and Diseases of the Ferret. Lea & Febiger, Philadelphia, 1988.

Bartlett, LW. Unpublished data, 1998.

Williams BH. Infectious Diseases of Ferrets. In The North American Veterinary Conference Proceedings, 1995, 584-585.

Rosenthal, KA. Hyperadrenocorticism associated with adrenocortical tumor or nodular hyperplasia of the adrenal gland in ferrets: 50 cases (1987-1991), Journal of the AVMA, July 15, 1993 Vol 203 (2) 271-275.

Hoefer, HL. Gastrointestinal Diseases of Ferrets. In TNAVC Proceedings, 1995, 579 - 580.

Bell, J. Infectious Diseases of Ferrets. In The North American Veterinary Conference (TNAVC) Proceedings, 1993. 721- 723.

Brown, SA Adrenal and Pancreatic Neoplasia in TNAVC Proceedings, 1993, Rosenthal, K, How We Treat An Insulinoma in the Ferret, In TNAVC Proceedings, 1994, 822.

Rosenthal, K, Adrenal Disease in the Ferret. In TNAVC Proceedings 1994, 823 - 824.

Miller, MS, Ferret Cardiology, In TNAVC Proceedings 1993, 735736.

Brown, SA Clinical Management of Lymphoma in the Ferret, In TNAVC Proceedings, 1993. 730-732 Lightfoot TL, J. of Exotic Animal Medicine, “Multi-systemic Eosinophilic Complex in a Ferret”, Quesenberry, K, Gastrointestinal Disorders of Ferrets. In TNAVC Proceedings, 1996, 870-871.

Johnson-Delaney, CA, Harrison, LR. Exotic Companion Medicine Handbook. Wingers Publishing , Lake Worth, FL. 1996, 30 - 40.

Stamoulis, ME. Cardiac Disease in Ferrets. In Seminars in Avian and Exotic Pet Medicine Vol 4 (1) January 1995 43 - 48.

Hillyer EV, Quesenberry KE, Ferrets, Rabbits, and Rodents - Clinical Medicine and Surgery, 1997, W.B. Saunders Pub. Co. Bartlett LW, Lightfoot TL, Harrison GJ, Manarino R. Exotic Companion Animal Surgery CD-ROM, Wingers Publishing Company, Lake Worth, FL, In Press (Copyright 1998 – Exotic Veterinary Seminars, Inc.)

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Clinical Techniques of Selected Exotic Species: Chinchilla, Prairie dog, & Hedgehog Tecniche cliniche in alcuni piccoli mammiferi esotici: cincillà, cani della prateria e ricci africani

Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto Cincillà (Chinchilla laniger) In natura, i cincillà sono animali notturni o crepuscolari, che vivono nei climi freddi e asciutti delle montagne delle Ande. NON tollerano il calore, né l’umidità elevata. Partoriscono una “prole atta”, per cui la gestazione è prolungata (circa 110 giorni). Sono dotati di un ceco molto simile a quello del coniglio (anche se più piccolo quanto a capacità rispetto alle dimensioni) e molti dei fabbisogni e dei problemi digestivi delle due specie risultano correlati.

Fra questi, rientra il fabbisogno di elevate quantità di fibra (come il fieno di coda di topo) nella dieta, sia per quanto riguarda la digestione che per contribuire a prevenire l’eccessiva crescita dei molari ed il conseguente sviluppo di difetti di occlusione.

La perdita di pelo è un problema clinico comune. Le possibili eziologie sono rappresentate da autotraumatismo (tonsura), traumi inferti dai compagni di gabbia (nella maggior parte dei casi, da parte della femmina ai danni del maschio, più piccolo), dermatofitosi, pulci o mancanza di un “bagno di polvere” in cui effettuare la propria toelettatura.

Cani della prateria (Cyonomys ludovicianus) Si tratta di una delle specie più frustranti fra quelle che possono essere presentate ad un veterinario che si occupi di animali esotici. Attualmente, si hanno a disposizione pochissimi dati sul modo di allevare questi animali. La dieta è simile a quella del cincillà, anche se i cani della prateria tollerano e gradiscono una percentuale più elevata di erba. In natura, infatti, si alimentano con le varie erbe che circondano le loro tane.

Indipendentemente dalla presenza o meno di una grave obesità, i problemi respiratori sono non solo un evento comune, ma la regola nei cani della prateria tenuti in cattività. La dispnea, che si può manifestare con respirazione a bocca aperta e/o respirazione addominale e letargia può essere indicativa di un’affezione respiratoria allergica, batterica, micotica o neoplastica, oppure di una cardiopatia; spesso le due malattie vengono diagnosticate in associazione.

I cani della prateria sono dotati di una pronunciata triade di papille di ghiandole olfattive che spesso appaiono distese quando l’animale viene contenuto. Sino ad oggi, l’autrice non ha riscontrato problemi clinici connessi a queste strutture anali. Nota: i cani della prateria selvatici catturati sono potenziali serbatoi di Yersinia pseudotuberculosis e Yersinia pestis. Dato il potenziale zoonosico di questi animali, bisogna scoraggiare i clienti che manifestino l’intenzione di tenerne uno come soggetto da compagnia.

Ricci africani I “ricci africani”, come vengono comunemente chiamati, sono di solito rappresentati da Atalerix albiventris, ma in Africa esistono diverse specie di ricci, il cui temperamento varia notevolmente. I ricci selvatici sono principalmente insettivori, ma consumano anche alcune radici, erbe e bacche. Per queste specie animali non sono stati stabiliti i fabbisogni nutrizionali. L’obesità è un problema comune ed alcuni ricci possono arrivare quasi a raddoppiare il peso normale.

Per effettuare un esame clinico accurato e completo è necessario ricorrere all’anestesia. L’isofluorano è ben tollerato.

Gli acari sono estremamente comuni in questi animali. Bisogna verificare sempre l’eventuale presenza di neoplasie orali, che sono abbastanza comuni nei ricci. Le unghie delle dita si incurvano secondo un’angolazione estremamente accentuata. Si riscontrano comunemente unghie incarnite e/o la presenza intorno alle punte delle dita o alle zampe di fibre che causano zoppia.

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Chinchilla (Chinchilla laniger) Chinchillas are nocturnal to crepuscular in nature, and live in the cool dry climate of the Andes mountains. They do NOT tolerate heat nor high humidity. Their young are born precocious, so gestation is prolonged (about 110 days).

Possessing a cecum much like a rabbit, (though smaller in capacity relative to size) many of the digestive requirements and problems of rabbits correlate with those seen in chinchillas. This includes the need for fiber, such as Timothy hay, in the diet in ample quantities both for digestion and to help prevent overgrowth of molars and subsequent malocclusion.

Hair loss is a common clinical problem. Possible etiologies include self trauma (barbering), cage mate trauma (more often the female picking on the smaller male), dermatophytosis, fleas, or lack of a dust bath in which to keep themselves groomed.

Prairie Dogs (Cyonomys ludovicianus) This is one of the more frustrating species presented to the exotic practitioner. Very little concrete data is present on the proper husbandry of prairie dogs. Diet is similar to that of the chinchilla, with a higher percentage of greens tolerated and enjoyed by this species. In nature, prairie dogs forage for various grasses surrounding their burrows.

With or without severe obesity, respiratory problems are not only common, but are the rule in prairie dogs kept in captivity. Dyspnea, including open mouth and/or abdominal breathing and lethargy can be indicative of allergic, bacterial, fungal, or neoplastic respiratory disease, or cardiac disease, and these are often diagnosed in combination.

Prairie dogs possess a pronounced trio of scent gland papilla that often appear distended when the animal is restrained. To date, this author has experienced no clinical problems with these anal structures. Note:. Wild caught prairie dogs are potential reservoirs of Yersinia pseudotuberculosis, and Yersinia pestis. With the zoonotic potential of wild prairie dogs, clients should be discouraged from keeping these as pets.

Hedgehogs The African hedgehog, as it is generically labeled, is usually Atalerix albiventris, but several species of hedgehogs occur in Africa and their temperaments vary widely.

Hedgehogs are mainly insectivorous in the wild, with some roots, grasses and berries also consumed. Nutritional requirements have not been determined in this species. Obesity is common in hedgehogs, and some may approach double their normal body weight. To accomplish a thorough physical examination, anesthesia must be used. Isoflurane is well tolerated. Mites are extremely common in hedgehogs. Be sure to check for oral neoplasia, which is fairly common in hedgehogs. The toe nails curve at an extremely abrupt angle. It is common to find both ingrown toenails, and/or fibers around toes or feet causing lameness.

The plurality of species seen in the small animal/exotic practice today is extraordinary. Often there are crucial differences in these patients in either handling, diagnostic sampling, or common clinical presentations. This article is not comprehensive either in its listing of species, nor in the clinical techniques that are described. It is designed to give a brief description of some peculiarities of several of these species to aid the practitioner in their safe and effective diagnosis and treatment.

CHINCHILLA (Chinchilla laniger) Chinchillas are nocturnal to crepuscular in nature, and live in the cool dry climate of the Andes mountains. They do NOT tolerate heat nor high humidity. Their young are born precocious, so gestation is prolonged (about 110 days). In captivity, they are not particular about where they deposit their fecal droppings (much like guinea pigs), though they do tend to urinate in the same location, and may use a litter box for this purpose if it is provided.

Possessing a cecum much like a rabbit, (though smaller in capacity relative to size) many of the digestive require-

ments and problems of rabbits correlate with those seen in chinchillas. This includes the need for fiber, such as Timothy hay, in the diet in ample quantities both for digestion and to help prevent overgrowth of molars and subsequent malocclusion.1 Chinchilla bones are very delicate, especially the elongated and thin tibia and vestigial fibula, and fractures can occur easily if the animal is frightened and jumps from the arms of the owner or hospital personnel. Refer to the “Restraint” section of the Rabbit article in this issue for several tips that are applicable in handling the chinchilla. Some people advocate the restraint of chinchillas by the base of the tail.

Few chinchillas (or clients) appreciate this technique, though it can be used to subtly grasp the base of the tail, then sliding the other hand under the body to support the animal from the ventrum. Most chinchillas that are nervous seem to prefer to be held close to the body, with their head tucked in the holder’s axilla. In addition, chinchillas can undergo “fur slip”, where excessive restraint leads to the loss of fur over the area being grasped - an effective mechanism in the wild for escaping predators, but not conductive to instilling client confidence.

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Clinical techniques: Dentition and malocclusion problems: Chinchillas have open rooted teeth, and both incisor and molar trimming may be necessary. Clinical signs indicative of potential occlusion problems are the same as those in the rabbit, including “slobbers”, anorexia, and grinding of the teeth. The oral cavity is extremely small, and visualization is much more difficult than in the rabbit. Multiple speculum wielding assistants, an excellent light source, small rongeurs or hemostats (DremmelR type tools rarely fit inside the oral cavity) and anesthesia are needed to attempt this procedure.1,2 Venipuncture: Generally in debilitated or tame chinchillas the cephalic vein can be utilized for collection of samples of small amounts of blood (such as for a CBC or blood glucose). Use a 26 or 27 gauge needle for venipuncture in this location. Debilitated or calm chinchillas may allow jugular venipuncture while awake. With Isoflurane anesthesia, which is well tolerated, the jugular is readily accessible. Considerable alcohol may be needed to sufficiently wet the copious fur, allowing visualization of the vein.

Reproductive syndromes and techniques: Though reproductive problems in well kept breeding facilities seem to be minimal, this author has seen an inordinate number of uterine infections and prolapses in female chinchillas. This may be due to poor husbandry techniques (poor hygiene), and the propensity for bacterial and fungal growth, especially in Florida’s warm, humid climate. Cesarean sections can be successfully performed, though this author would encourage concurrent ovariohysterectomy for female chinchillas demonstrating gross uterine pathology at the time of surgery. Ovariohysterectomy can be performed in the pet female chinchilla under Isoflurane with relative ease. As with rabbits, the rapid return to calorie intake is critical, and the analgesics administered post-operatively to rabbits (see “Analgesia” in Rabbit article) generally work well in the chinchilla. This author has the most experience with butorphanol (Torbutrol) @ 0.05 - 0.1 mg/kg SC or IM.3,4 Male chinchillas may develop loops of hair around the penile sheath that prevent its retraction. When detected early, this paraphimosis usually resolves with the removal of the hair (“fur ring”) accomplished while under inhalation anesthetic.1,2, Dermatology: Hair loss is a common clinical problem.1,2,5 Possible etiologies include self trauma (barbering), cage mate trauma (more often the female picking on the smaller male), dermatophytosis, fleas, or lack of a dust bath in which to keep themselves groomed.6 A fungal culture is generally indicted to rule out dermatophytosis, since Trichophyton mentagrophytes can occur. Except for fleas, ectoparasites are not common in chinchillas.

PRAIRIE DOGS (Cyonomys ludovicianus) This is one of the more frustrating species presented to the exotic practitioner. Very little concrete data is present on the proper husbandry of prairie dogs. Diet is similar to that

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of the chinchilla, with a higher percentage of greens tolerated and enjoyed by this species. In nature, prairie dogs forage for various grasses surrounding their burrows.7 Respiratory disease: With or without severe obesity, respiratory problems are not only common, but are the rule in prairie dogs kept in captivity. Whether humidity has a causative role in the multiple respiratory syndromes is not documented. In nature, prairie dogs are diurnal desert dwellers, so they are exposed to a dry daily environment.5,7 However, their extensive burrows contain a higher moisture content. This has led to disagreement between practitioners as to whether keeping the humidity either high or low are potentially causative factors. Cardiomyopathy is also noted in a high percentage of captive prairie dogs after two to three years of age (Crispen Spencer, DVM, ACVR, personal communication), and the possibility of a nutritional origin for this condition has been postulated, but not identified. Cardiomyopathy will present with clinical signs similar to primary respiratory disease. Dyspnea, including open mouth and/or abdominal breathing, and lethargy can be indicative of allergic, bacterial, fungal, or neoplastic respiratory disease, or cardiac disease, and these are often diagnosed in combination.

If the diet of a prairie dog is not limited and exercise not encouraged, obesity is inevitable. This may either cause or add to respiratory impairment.5 Prairie dogs need material in which to burrow, substituting for their dens in the wild.5,7 Avoid any shavings or materials that produce dust, as this may add to the potential for respiratory disease.

Clinical techniques: Physical examination: Some prairie dogs remain tame with frequent handling, and can be thoroughly examined awake. However, they are able to inflict a painful bite, so choose your candidates for handling carefully. Stroking of the gums and cheeks is enjoyed by tame prairie dogs, but once again, it would not be advisable if the temperament of the animal is questionable. A thorough oral examination should be performed, especially if respiratory signs are present, since oral, pharyngeal, and hard palate neoplasias are common.1 Radiographs of the thorax will often aid in determining whether respiratory impairment is due to pulmonary or cardiac disease, or a combination of these systems. Tracheal washes are often helpful in differentiating between pulmonary infection (bacterial or fungal), allergic, inflammatory or neoplastic syndromes. This is accomplished in the same manner as in the dog, generally under sedation with either Ketamine @ 20 - 50 mg/kg IM, 4,5 or a light plane of Isoflurane inhalation anesthesia. Bacterial culture and sensitivity should be performed. It is not unusual to get cytology from these washes with combinations of increased eosinophils, PMNs, bacteria , and occasionally yeast or fungal hyphae.

Multiple etiologies make treatment more difficult. Although the initial response to therapy is often good in many of these respiratory cases, recurrence is the norm. Long term prognosis in this author’s experience is poor.

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Venipuncture: Even tame prairie dogs are reticent to allow venipuncture while awake. They tolerate Isoflurane masking or chamber induction well, and jugular sticks are usually best, though the excessive fat on the neck can make this procedure more difficult than in other species. While the prairie dog is under sedation, be sure to check the toenails, which can overgrow quite severely. Hepatic problems are common, including hepatic lipidosis and hepatic adenocarcinoma.1,2,5 Serum chemistries and CBCs can be utilized to aid in determining any underlying disease.4,5 Hepatic biopsies are often indicated following either radiographic evidence of hepatomegaly, or hepatic enzyme elevation. As in chinchillas and guinea pigs, the thoracic cavity is relatively small compared to the abdominal cavity.2,5 Be cautious with obese patients, and elevate the head and thorax to aid in respiration while under anesthesia. Malocclusion can occur in this species, but does not seem to be as common as in rabbits and chinchillas.5 Anal Sac Triad: Prairie dogs possess a pronounced trio of scent gland papilla that often appear distended when the animal is restrained. To date, this author has experienced no clinical problems with these anal structures.

Note: This article relates to captive prairie dogs. Wild caught prairie dogs are potential reservoirs of Yersinia pseudotuberculosis, and Yersinia pestis. With the zoonotic potential of wild prairie dogs, clients should be discouraged from keeping these as pets.

HEDGEHOGS The African hedgehog, as it is generically labeled, is usually Atalerix albiventris, but several species of hedgehogs occur in Africa and their temperaments vary widely.2,7,8 The long eared Egyptian hedgehog is noted for a generally nasty disposition. African hedgehogs are not the same genus as the larger European hedgehog, and do not hibernate.

Despite being cute as babies, and often initially tame at a young age, most hedgehogs resent handling as adults and will ball up when approached. Hedgehogs are mainly insectivorous in the wild, with some roots, grasses and berries also consumed. Nutritional requirements have not been determined in this species. Several selections of successful diets used in captivity are listed in reference five. Generally, a combination of cat or kitten food, gut-loaded insects, and fruits and vegetables are supplied.5 Obesity is common in hedgehogs, and some may approach double their normal body weight.

Clinical Techniques: Physical Examination: To accomplish a thorough physical examination, anesthesia must be used. Once again, Isoflurane is well tolerated. We often administer atropine, since the odor of the Isoflurane often causes hypersalivation.

This may be related to the “anting” behavior these animals perform when they encounter an unfamiliar or unpleasant taste.1,2,5,7,8

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Anesthesia is accomplished by removing the diaphragm from a large dog anesthetic mask, and placing the entire mask over the balled-up hedgehog, using it as a small chamber.

When the hedgehog is anesthetized and uncurls, a small anesthetic mask may be placed over the face. With the animal in lateral recumbency, the spines can be retracted with the underlying skin to the dorsum of the animal so the abdomen can be palpated, and the heart and lungs auscultated. Tartar buildup may occur in older hedgehogs, but malocclusion is uncommon. Be sure to check for oral neoplasia, which is fairly common in hedgehogs. The toe nails curve at an extremely abrupt angle.5,9 It is common to find both ingrown toenails, and/or fibers around toes or feet causing lameness. As in most species, when detected early, trimming of the nails or removal of the foreign material and treatment of any subsequent infection may be sufficient for recovery. However, amputation of a digit or an entire foot, is sometimes necessary.

Dermatology: Mites are extremely common in hedgehogs. Two major types are generally seen in practice. The macroscopically visible mite, possibly the same species as the European hedgehog mite (Caparinia tripilis) is usually distributed over a large portion of the body. As a practitioner, one may suddenly notice that the entire hedgehog looks like it is moving. These mites may be associated with pruritus and quill loss, and cause or accompany debilitation. Ivermectin (as dosed below) may decrease the number of mites, but a pyrthrin based shampoo used weekly for several weeks is often necessary. The second type of mite is Sarcoptiform in nature (probably Chorioptic sp.)9 - occurring mostly on the face and ears, and causing moderate to severe skin irritation. This can be diagnosed by a skin scraping, however, if mites are suspected but not visualized, treatment is still warranted. For this type of mite, Ivermectin (0.2mg/kg SC), repeated in two to three weeks, is generally effective.3,4,5 Injections while under Iso can be given subcutaneously in a non-quilled area.

Venipuncture: Blood collection is best accomplished via the jugular vein. Hedgehogs are prone toward obesity in captivity and the jugular may have to be a “blind stick”. It is located anatomically in the same thoracic inlet orientation as in dogs and cats.5,9 Medicating: If medication such as an antibiotic needs to be given daily to an anorexic hedgehog , oral formulas will be nearly impossible for the owner to administer. Hedgehogs can be given SC injections while awake and balled up, inserting the needle between the quills over the back into the subcutaneous space. Have an assistant with a towel or gloves gently but firmly hold the “ball” in place. When the needle is inserted the hedgehog may startled or hiss, but it will seldom unroll, and the injection can be accomplished.

Hedgehogs that are obese often contain a thick layer of subcutaneous fat under the quills, so injections given here have the potential of being absorbed more slowly if the needle is not inserted to a sufficient depth.

Reproduction: Seldom is ovariohysterectomy or castration requested in this species. One often repeated “fact” in the literature is that male hedgehogs have abdominal testes.

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It is not possible to determine the “natural” location of a male hedgehogs testes, since attempts at palpation of these in an awake hedgehog are anything but natural. However, under Isoflurane anesthesia, adult male hedgehogs have palpable testicles subcutaneously, though with no scrotal sac.

This author has performed numerous castrations on male hedgehogs and their recovery was routine.

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2) 3) 4)

5) 6)

References 1)

Hoefer HL: Clinical Approach to the Chinchilla, in: 1995 Proceedings, The North American Veterinary Conference (TNAVC). Gainesville, FL, Eastern States Veterinary Association (ESVA), 1995, pp 672- 673.

7) 8) 9)

Hoefer HL: Chinchillas. Vet Clin North Am (Sm Anim Pract) Exotic Pet Medicine 24:1, 103 - 112., Jan. 1994.

Carpenter JW, Mashima TY, Rupiper DJ: Exotic Animal Formulary, Manhattan, Kansas, Greyston Publications, 1996.

Marx, KL, Roston, MA: The Exotic Animal Drug Compendium - An International Formulary. Trenton, NJ, Veterinary Learning Systems, 1996.

Johnson-Delaney CA: Exotic Companion Medicine Handbook for Veterinarians. Lake Worth, FL, Winger’s Publishing, 1996.

Coulton JC: Practical Chinchilla Keeping. Alton Hanks, GU34 1 DL, Nimrod Press LTD, 1989.

Nowak, RM, (ed): Walker’s Mammals of the World - Volume 1, (ed 3). Baltimore, MD, Johns Hopkins University Press, 1991.

Stocker L: The Complete Hedgehog. London, England, Chatto & Windus LTD, 1987.

Smith AJ: Medicine of the African Hedgehog, in: 1994 TNAVC Proceedings, Gainesville, FL, ESVA, 1994, pp 935-936.

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Rabbit medicine, surgery and pasturella Conigli: problemi medici e pasteurellosi

Theresa L. Lightfoot DVM, Diplomate ABVP (Avian Practice) - Largo, Florida USA

Riassunto Il coniglio domestico (Oryctolagus cuniculus) mantiene la fisiologia ed il comportamento di una specie che, in natura, rappresenta una preda. La liberazione di adrenalina e dei composti ad essa correlati in risposta a stress o dolore può causare un’ischemia renale, con conseguente endotossiemia e morte. Il fatto, comunemente noto, della scarsa percentuale di risveglio di questi animali dall’anestesia è spesso da riferire al dolore e l’impiego degli analgesici (illustrato nella sezione dedicata a questo argomento) ha notevolmente aumentato le percentuali di successo degli interventi chirurgici in questa specie animale.

DIFETTI DI OCCLUSIONE: Uno dei principali fattori da tenere presenti è che, benché possa avvenire in modo indipendente, l’eccessiva crescita degli incisivi è spesso la conseguenza di un difetto di occlusione e di un mancato consumo dovuti ad un malallineamento primario dei molari. Questi ultimi possono presentare una considerevole crescita abnorme, causando ulcerazioni orali e linguali, incapacità di masticare e, perfino, l’occlusione parziale della faringe. I conigli tollerano molto bene l’isofluorano, per cui, se si è abituati ad utilizzare questo anestetico, ma non si ha un’adeguata esperienza nel contenimento di questi animali, può essere preferibile ricorrere all’anestesia gassosa mediante maschera piuttosto che impegnarsi in una lotta con un coniglio sveglio.

CONSIDERAZIONI OPERATORIE: l’analgesia postoperatoria ha notevolmente aumentato la velocità degli interventi e la percentuale di sopravvivenza. Lo stesso farmaco può essere utilizzato anche quando viene portato alla visita un coniglio colpito da un intenso dolore, prima dell’intervento chirurgico (ad esempio, in caso di frattura della tibia, lacerazioni, ecc.). Allo scopo, sono stati utilizzati diversi agenti, ma, a parere dell’autrice, il più sicuro, efficace e facilmente reperibile è il butorfanolo tartrato (0,05-0,5 mg/kg IV, SC, IM ogni 4-6 ore). Di solito, immediatamente e poi dopo l’intervento, si somministra una dose di 0,1 mg/kg per via sottocutanea, da ripetere o aumentare a seconda delle necessità. Non è necessario tenere i conigli a digiuno prima dell’anestesia, dal momento che non rigurgitano. Fanno eccezione gli interventi sul tratto gastroenterico, per i quali può essere utile un digiuno di 6-8 ore per ridurre la quantità del contenuto dell’apparato digerente. Durante l’anestesia, date le ridotte dimensioni del torace (come nei cani della prateria) è necessario tenere sollevata la parte craniale dell’animale, per ridurre la pressione sul torace ed aumentare il volume tidalico. L’intubazione dei conigli può essere difficile ed è comune il laringospasmo. Se la natura dell’intervento è tale da rendere necessaria l’intubazione, bisogna servirsi di un laringoscopio ed applicare un anestetico locale sulla glottide prima di effettuare l’operazione. In generale, in questi animali è preferibile mantenere l’anestesia con una maschera. Le aderenze addominali sono più comuni nei conigli che nelle altre specie. Per prevenirle, può essere utile allontanare le polveri in eccesso dai guanti chirurgici e manipolare con molta delicatezza i tessuti.

Ovaristerectomia: L’adenocarcinoma uterino è la neoplasia più comune nelle coniglie. Poiché l’incidenza di questi tumori è così elevata, di solito si raccomanda di sterilizzare tutte le coniglie da compagnia prima del secondo anno di vita.

Pasteurella multocida: ascessi, epifora, infezioni respiratorie e testa piegata sono tutte condizioni che possono riconoscere molteplici eziologie, ma nel coniglio nella maggior parte dei casi si osservano in conseguenza di un’infezione da Pasteurella multocida.

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The domestic rabbit (Oryctolagus cuniculus) maintains the physiology and behavior of a prey species. The release of epinephrine and its related compounds in response to stress or pain can cause renal ischemia, with subsequent endotoxemia and death. The notoriously poor recovery rate from anesthesia in rabbits is often due to pain, and the use of analgesics (as in discussed in the section on this subject) has greatly increased the success rate of surgical procedures in rabbit patients MALOCCLUSSION: A major point is that although overgrown incisors can happen independently they are often the result of malocclusion and lack of wear due to a primary molar malalignment. The molars can overgrown considerably, causing oral and lingual ulcerations, inability to masticate and even partial occlusion of the pharynx. Rabbits tolerate Isofluorane very well, so if you are comfortable with this anesthetic, but not experienced with rabbit restraint, it may be wise to mask the rabbit with Isoflurane rather than struggling with an awake rabbit.

SURGICAL CONSIDERATIONS: Post surgical analgesia has greatly increased the speed and percentage of survival. The same medication can be used on presentation of a rabbit in pain prior to surgical intervention (i.e. a fractured tibia, lacerations). Several medications have been utilized, but in this author’s opinion the safest, most effective and readily available is butorphanol tartrate (TorbutrolR @ 0.05-0.5 mg/kg IV, SC, IM q 4-6 hours). A dose of 0.1 mg/kg subcutaneously is usually given initially immediately post-operatively and repeated or increased if needed. It is not necessary to fast rabbits prior to anesthesia since they do not regurgitate. The exception would be gastrointestinal surgery, when a fast of 6-8 hours may be useful in decreasing the quantity of gastrointestinal contents. During anesthesia, due to the small size of the thorax (as in prairie dogs) the cranial aspect of the animal should be elevated to reduce pressure on the chest and increase tidal volume. Intubation of rabbits can be difficult, and laryngospasm is common. If intubation is necessary due to the nature of the surgery, then a laryngoscope, and a topical anesthetic should be applied to the glottis prior to intubation. Generally, maintaining the rabbit with a cone (mask) is preferable. Abdominal adhesions are more common in rabbits that in most other animals. Removing excess powder from the gloves and being gentle with tissue handling may prevent adhesions.

Ovariohysterectomy: Uterine adenocarcinoma is the most common neoplasia of female rabbits. Because the incidence of uterine cancer is so high, it is usually recommended that all female pet rabbits be “spayed” before they are two years of age.

Pasteurella multocida: Abscesses, epiphora, respiratory infections and head tilts can all have multiple etiologies, but are most commonly encountered in rabbits subsequent to Pasteurella multocida infection.

The domestic rabbit (Oryctolagus cuniculus) maintains the physiology and behavior of a prey species. The release of epinephrine and its related compounds in response to stress or pain can cause renal ischemia, with subsequent endotoxemia and death. The notoriously poor recovery rate from anesthesia in rabbits is often due to pain, and the use of analgesics (as in discussed in the section on this subject) has greatly increased the success rate of surgical procedures in rabbit patients. In addition to analgesia, we must recognize that rabbits are very susceptible to stress in the form of excessive stimulation or handling, and the scent, sight or sound of potential predators (i.e. dogs, cats, ferrets). The avoidance of these debilitating factors in the hospital environment can make a great difference in recovery.

Rabbits that are well acclimated to their captive environment generally have better recovery rates from illness that their more wild counterparts. Unfortunately, we cannot choose our patient’s temperament. Observation of the rabbit’s behavior will help identify those that are “adrenaline rushing” and therefore warrant not only a more careful approach but also a guarded prognosis, regardless of the underlying disease. Frightened rabbits have more rapid respiratory rates, and sit motionless in a crouched, ready to jump position with wide unblinking eyes. Rabbits that are relaxed

will usually move around the exam table or floor, sniffing at the surface and blinking their eyes in a normal manner.

When in the cage, these acclimated rabbits may recline in a semi-recumbent position, with the rear end extended (this can also happen with severely ill, or rear end paralysis rabbits, but these are usually obvious to the veterinarian).

It is best to examine frightened rabbits while seated on the floor (you, and the rabbit). If the rabbit struggles it can be released, or if it escapes it will not have a long way to fall, therefore avoiding spinal trauma or leg fractures. Covering the eyes of a rabbit whether with a towel, or by tucking its head into your axilla (polite way of saying armpit..) will have a calming effect by removing visual stimulation.

Occasionally, you will have an aggressive rabbit that will thump its feet at you when you approach, or actually attack and attempt to bite. Once again, due to the propensity for these rabbits to move/jump quickly and risk skeletal damage, handling them on the floor in a closed room is the safest method.

Rabbits can be picked up a variety of ways. Dr. Susan Brown has an excellent synopsis on various methods of restraint in the article “Clinical Techniques in the Rabbit” in Seminars in Avian and Exotic Pet Medicine - Clinical Techniques - April 1997, Vol. 6, No.2. In summary, these methods all involve the idea of either scruffing the rabbit, while

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supporting the hindquarters to prevent kicking, or hiding the rabbit’s head to decrease stimulation, while once again supporting the hind quarters. This article also contains a detailed explanation of the method she advocates for toe nail trims, both in the office and for owners to practice at home.

PHYSICAL EXAMINATION Performing a complete physical examination on an awake fractious rabbit can be a challenge. The most difficult aspect is examination of the oral cavity, since rabbits often violently object to having their heads elevated, much less their mouths opened. Generally, with an assistant seated, the rabbit can be held like a child sitting in the lap, and either an otoscope with a regular large size cone attached, or a special modified speculum for the otoscope head can be utilized. This author has found that a pediatric laryngoscope can also be used to visualize molars and perform molar trims on both rabbits and chinchillas. A major point is that although overgrown incisors can happen independently they are often the result of malocclusion and lack of wear due to a primary molar malalignment. The molars can overgrown considerably, causing oral and lingual ulcerations, inability to masticate and even partial occlusion of the pharynx. Rabbits tolerate Isofluorane very well, so if you are comfortable with this anesthetic, but not experienced with rabbit restraint, it may be wise to mask the rabbit with Isoflurane and get a quick look, rather than struggling with an awake rabbit.

ANALGESIA / SEDATION As mentioned, the success of treatment can be decreased in rabbits that are severely stressed by pain or fear. In a prey species such as the rabbit signs of discomfort or pain may include grinding of their teeth, anorexia, hiding, and being slow to respond to stimuli.

Post surgical analgesia, as stated in the section on surgery, has greatly increased the speed and percentage of survival. The same medication can be used on presentation of a rabbit in pain prior to surgical intervention (i.e. a fractured tibia, lacerations). Several medications have been utilized, but in this author’s opinion the safest, most effective and readily available is butorphanol tartrate (TorbutrolR @ 0.05-0.5 mg/kg IV, SC, IM q 4-6 hours). A dose of 0.1 mg/kg subcutaneously is usually given initially immediately post-op, and repeated or increased if needed.

For more chronic or inflammatory conditions such as arthritis and perineal dermatitis, flunixin meglumine (BanamineR 1.0 mg/kg SC q 8 hours) is often effective. For a more comprehensive list of non-steroidal anti-inflammatories utilized in rabbits, see item number four on the recommended reading list following this article.

Injections: Rabbits tolerate subcutaneous injections extremely well.

Many owners find injectable antibiotics easier to administer

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at home than oral medications. See the section on “Venipuncture” for a discussion of accessible veins for I.V. injections. One note of caution is that although collecting blood from the central auricular artery can work well when obtaining small quantities, injection of medications INTO this artery, especially medications with tendencies for perivascular irritation, can cause sloughing of the delicate tissue of the pinna. (This author has had a permanent “pierced ear” appear in response to extravasated I.V. ketamine).

VENIPUNCTURE The rabbit’s blood volume is approximately 6 - 7% of the body weight.

Therefore a 1500gm (approximately 3 lb.) rabbit has a blood volume of about 90 - 100 ml. On a healthy rabbit, 10% of this (about 9 ml) can be collected safely at one time.

Generally, 27 - 25 gauge needles are a good size for blood collection. The cephalic vein can be visualized readily and utilized as in a dog or a cat for small volumes of blood (such as for a CBC or a blood glucose). The central auricular artery is the favorite site of collection for many veterinarians dealing with rabbits. The major drawback to this artery is that hematoma formation is common, so be certain to apply digital pressure for a sufficient period after venipuncture. The marginal ear veins, in all but the largest rabbits, often collapse during venipuncture. The lateral saphenous vein as in a dog, is a good site for collection, though the person restraining must be careful to hold the rear end firmly, yet without causing spinal trauma. Scruffing the rabbit, as with a cat in lateral recumbency is often helpful.

As in most species, the jugular vein will give the fastest and most consistent blood draw. However, on an awake rabbit, the experience of the person performing venipuncture and person restraining, along with the temperament of the rabbit, gives variable success with this technique. If the rabbit is under anesthesia the jugular should certainly be utilized.

(Note: the major variation in rabbit serum chemistries is that the calcium is normally higher than that of other mammals. This is not always stated as such in the literature, where the normal range is reported to be 5.6 12.5mg/dl. In this author’s experience, values above 10 mg/dl are the norm).

FLUID ADMINISTRATION I.V. catheters, and I.O. catheters can be used successfully in debilitated rabbits. Rabbits that are still responsive and able to chew, however, are difficult candidates both for placement and maintenance of these devices. The veins generally utilized are the cephalic, jugular, and lateral saphenous. In this author’s experience, subcutaneous fluids, with the addition of hyaluronidase (WydaseR) at 150 Units/liter of fluids, greatly speeds absorption of the fluid from under the skin. This makes it unnecessary to use I.V. of I.O. fluid therapy in all but the most debilitated (and therefore, most complacent) rabbits.

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SURGICAL CONSIDERATIONS As stated previously, it is not necessary to fast rabbits prior to anesthesia, since they do not regurgitate. The exception would be gastrointestinal surgery, when a fast of 6-8 hours may be useful in decreasing the quantity of g.i. contents.

During anesthesia, due to the small size of the thorax (as in prairie dogs) the cranial aspect of the animal should be elevated, to reduce pressure on the chest and increase tidal volume.

Intubation of rabbits can be difficult, and laryngospasm is common. If intubation is necessary due to the nature of the surgery, then a laryngoscope, and a topical anesthetic should be applied to the glottis prior to intubation. Generally, maintaining the rabbit with a cone (mask) is preferable.

Abdominal adhesions are more common in rabbits that in most other animals. Removing excess powder from the gloves, and being gentle with tissue handling may prevent adhesions.

Closure, as with most animals prone to chewing at external sutures, is best accompanied with a subcuticular pattern.

Ovariohysterectomy: Uterine adenocarcinoma is the most common neoplasia of female rabbits. Because the incidence of uterine cancer is so high, it is usually recommended that all female pet rabbits be “spayed” before they are two years of age. Endometrial hyperplasia, uterine polyps, pyometra and endometritis are also known to occur in rabbits.

Signs of disease of the female rabbit’s reproductive tract may include hematuria serosanguineous vaginal discharge, decreased fertility, cystic mammary glands and an enlarged uterus on palpation.

Rabbits have delicate skin and very thick fur which makes the clipping required for surgery a challenge. Rabbits will often get a post-surgical dry skin flakiness that is quite pronounced within a week or so post-operatively. The use of Chlorhexidine in lieu of iodine as a surgical scrub may decrease this occurrence.

A ventral midline incision through the skin is begun about half way between the umbilicus and the cranial rim of the pubis. Be careful not to penetrate the linea which is often thin and slightly transparent. Carefully incise the linea in a routine manner. The bladder may be directly underlying the incision. Locate the uterine horns dorsal to the cranial pole of the bladder. The uterus is bicornuate and there is no uterine body. Each of the uterine cornua possess a cervix.

The mesometrium is a site of fat storage making identification of vessels difficult. The oviduct is much longer than in a dog or cat and coils around in a loop. For a complete step by step description of this and many other routine exotic surgeries, see reference # five.

Post-operative Considerations: It is critical to get rabbits eating soon after surgery. Since they often become anorectic when uncomfortable, anal-

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gesics are highly recommended following painful procedures (see section on analgesia). Anorectic rabbits may be syringe fed as needed for 24 - 48 hours to prevent hepatic lipidosis and gut stasis if they refuse food after surgery. Hospitalized rabbits should be provided with their usual diet and protected from stress related to the noise, sight, or odor of dogs, cats, snakes, ferrets or other potential predators.

Castration: Male rabbits that are not castrated usually have an objectionable odor, as well as a tendency toward aggressive behavior. Castration is well tolerated by male rabbits, with a few precautions. The skin around the perineum and scrotal area tears very easily, and extreme care must be taken while clipping for surgery. Generally, the scrotum must have an incision made over (and slightly laterally) to each testicle. A closed castration will avoid the danger of herniation from the open inguinal rings. Double ligate, and observe the spermatic cord once it has been returned to the abdomen to be certain that the ligatures are secure. Post -operative butorphanol is indicated not only for discomfort and rapid return to eating, but also to minimize activity, thereby avoid hemorrhage. Closure is routine: subcuticular, tissue glue, or leaving the incision open and manually opposing the tissue.

Generally, especially in younger rabbits with less developed testes, the tissue will adhere to itself and heal much like in a cat. This author feels safer however, with a subcuticular closure that also opposes the fascia over the inguinal canal. Be certain that the rabbit’s testicles are readily palpable prior to surgery. Young rabbits (under 8-20 weeks, depending on the individual and the breed) may have either undescended testicles, or testes that retract readily into the inguinal canal.

Incisor removal: Overgrowth of both the incisors and the molars of rabbits may occur. Generally, congenital malocclusion is presented in young rabbits, with obvious overgrowth of the incisors.

Older rabbits are more likely to have gradual overgrowth of molars, with subsequent inability to masticate the food, and secondary incisor overgrowth from the molar malalignment and lack of incisor wear. Every rabbit should have both the incisors and molars checked as part of the routine physical examination.

The young rabbit that presents for abnormal incisor occlusion has historically been destined to have its teeth trimmed on a very regular basis for its entire life. The alternative to this is the extraction of all six incisors (two lower, and four upper). This has been shown to be well tolerated in most rabbits, with the most common side effect in my experience being mild lip fold dermatitis. The procedure is not difficult, but the length of the roots of the upper incisors make it critical that all ligaments, especially those on the medial aspects, be completely severed prior to attempting extraction. The position of the teeth within the oral cavity should be visualized as the direction in which to extract the

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incisors is determined, so as not to fracture them. If a fracture does occur, and the vestige of the tooth is not accessible, the remainder of the incisors can be extracted and the rabbit can be rescheduled to have the fractured tooth extracted when it grows out to an accessible length - usually about 6 weeks. Post operative analgesia, and supportive care with syringe feeding are critical for the first 24-48 hours or until the rabbit is eating on its own.

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cluded naso lacrimal duct. Excessive pressure should NOT be applied. The naso-lacrimal duct can rupture, and the effect will be an immediately noticeable periorbital swelling as the saline infuses into the surrounding tissue. This swelling will be absorbed in a matter of hours, but the integrity of the nasolacrimal duct will then be questionable. If you find it difficult to determine if the duct is patent, Fluorescin stain in the eye can be used, and a Woods lamp to check for the appearance of the dye in the nare.

COMMON DISEASE SYNDROMES Respiratory infections: Abscesses: Rabbits tend to develop large abscesses with purulent material the consistency of cream cheese (nice image, huh?) Though it is tempting to culture a big wad of this lovely material, it is generally old WBCs and dead bacteria. The wall, or capsule, of the abscess should be used for culture. Be forewarned (and forewarn the owners) that negative cultures are common despite the obvious presence of bacteria. Therefore, a gram stain taken at the same time as the culture will allow you to start on an antibiotic chosen with the class of bacteria present in mind, and will allow you to continue that treatment should the culture prove non-productive.

Besides systemic antibiotics (both enrofloxacin at 10 mg/kg S - BID and Procaine penicillin G at 50,000 u/kg subcutaneously or intramuscularly, once weekly for two weeks) are commonly utilized. The implantation of acrylic antibiotic impregnated beads, or umbilical tape soaked in an antibiotic as both a drain and a source of antibiotic release, show promise in treatment of these abscesses. Extensive surgical excision is ideal, however, the location, extensive nature, and heavy vasculature of many of these abscesses make this impossible.

Three major bacteria are commonly isolated from respiratory infections of rabbits; Pasteurella multocida, Staphylococcus aureus and Bordetella bronchiseptica. Of these, the first two are also the most common in cutaneous abscesses.

A mini-tip culturette introduced into the medial aspect of the sinus (quickly in and out as far as it will go) may yield a positive culture. Most rabbits donâ&#x20AC;&#x2122;t appreciate this procedure, and will jump. A small amount of blood may appear on the culturette or on the rabbits nare. Allow the rabbit to sit quietly for a few moments and when its blood pressure drops, the bleeding will stop.

Pasteurella titers are also available to evaluate exposure to this organism. Since a high percentage of rabbits may be latently infected, the titer should be interpreted accordingly.

A very high titer, a rising paired titer, or a titer that decreases after treatment and an improvement of clinical signs gives a presumptive diagnosis of Pasteurellosis. Pasteurella can be difficult to isolate from both abscesses and nasal cultures, but a positive culture is confirmatory. A gram stain will also give you a reasonable idea of the presence of Pasteurella.

Urinary/Reproductive Infections: Epiphora: Dacryocystitis presents with unilateral epiphora and may be accompanied by facial irritation or dermatitis. Bilateral epiphora can also be caused by dacryocystitis, but in the presence of bilateral epiphora, especially if the discharge is not clear, an infectious primary cause, such as Pasteurellosis, should be investigated..

When dacryocystitis is suspected, the naso-lacrimal duct should be cannulated and flushed. This can be accomplished either with topical ocular anesthetic, or with general anesthesia. The puncta is quite large and prominent, but can be difficult to visualize if the peri-orbital tissue is inflamed and swollen. Although the time of cannulation is the opportune moment to obtain cultures, on occasion we have to treat the eye with a combination antibiotic/corticosteroid drop for 3-5 days in order to decrease the swelling and visualize the puncta.

When cannulating the duct, any cannula that will fit in the opening, and with which the practitioner is comfortable will work - from regular naso-lacrimal cannulas to tom cat catheters. Often the first few attempts at flushing will result in a back flow of whitish purulent discharge into the peri-orbital area. Subsequent flushing will hopefully clear the oc-

Rabbits often present for either discolored urine, odiferous urine, or vaginal discharge. The porphyrin pigment that occurs in rabbit urine as an orange tinge is normal. Uterine infection and uterine adeno-carcinoma are common, as are cystitis and cystic calculi. A urinalysis is often helpful, preferably obtained via cystocentesis since a clean cysto sample can aid in differentiating these syndromes.

Head Tilt Presentations: The most common presentation of torticollis in a rabbit is the acute onset in the absence of external signs. Obvious trauma or acute otitis externa may cause a head tilt, but these would be readily visible on the physical examination. The usual cause of a sudden onset of a head tilt and other signs of vestibular disease is an inner ear infection - usually Pasteurella. These rabbits may have nystagmus, and may roll uncontrollably injuring themselves in the subsequent panic.

Valium or acepromazine is often helpful initially to decrease the stress and trauma of this acute presentation. To attempt to confirm the presence of Pasteurella, titers are available (see the section on Pasteurella) since the inner ear is not ac-

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cessible for culture. Many practitioners have had excellent results with the use of enrofloxacin , with the head tilt resolving partially or completely. However, after the cessation of antibiotic therapy, the head tilt may recur. Many rabbits require long term antibiotic therapy to control this disease.

There is controversy as to whether the organism Encephalitozoon cuniculi can cause head tilt in rabbits. This microsporidian organism invades the CNS, and can cause granuloma formation. Titers are available to check for the presence of antibodies to E. cuniculi. However, many rabbits have positive titers, and no clinical signs. There is no treatment currently for E. cuniculi.

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Recommended Reading 1) 2) 3) 4) 5) 6)

Hillyer EV , Quesenberry KE : Ferrets, Rabbits, and Rodents. Philadelphia, PA, W.B. Sanders Co. 1997 Harkness JE, Wagner JE : The Biology and Medicine of Rabbits and Rodents 3rd Ed. Philadelphia, PA, Lea & Febiger Johnson-Delaney CA : Exotic Companion Medicine Handbook for Veterinarians. Lake Worth, FL, Wingers Publishing Inc. Brown SA, Clinical Techniques in Rabbits, in Seminars in Avian and Exotic Pet Medicine Vol. 6, No. 2 April 1997: p 86- 95.

Bartlett LW, Exotic Companion Animal Surgeries, (CD-ROM) Wingerâ&#x20AC;&#x2122;s Publishing Co., Lake Worth, Florida, March 1999.

Bennett Avery, Proceedings of International Conference on Exotics, 1999, Delray Beach, Florida, USA.

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Polipi del rinofaringe, dell’orecchio medio e dell’orecchio esterno del gatto: prendi tre e paghi uno Carlo Maria Mortellaro* Med. Vet., Istituto di Clinica Chirurgica e Radiologia Veterinaria - Università degli Studi di Milano

* in collaborazione con: C. Alfieri, P. Pasini, D.A. Mussi, A. Di Donato

Riassunto I polipi rinofaringei ed auricolari sono neoformazioni benigne, a superficie liscia, più o meno peduncolate in rapporto alla sede, costituiti da connettivo fibroso lasso rivestito da epitelio cilindrico cigliato. Originano dalla tuba uditiva o dalla zona della cavità timpanica circostante l’ostio della tuba stessa, all’interno quindi del comparto dorso-laterale della bolla timpanica; sono considerati lesioni secondarie a fenomeni infettivo-infiammatori cronici delle alte vie respiratorie e dell’orecchio medio. A seconda del percorso anatomico seguito da tali neoformazioni durante l’accrescimento, si distinguono in: polipi dell’orecchio medio (si espandono esclusivamente nella bolla timpanica), polipi dell’orecchio esterno (si accrescono verso il canale auricolare esterno dopo rottura della membrana timpanica) e polipi del rinofaringe (si espandono lungo la tuba di Eustachio attraverso un sottile peduncolo per poi accrescersi nel rinofaringe).

La presenza di un polipo nell’orecchio medio può essere accompagnata da quadri sintomatologici diversi che variano dall’assenza di segni-sintomi, alla presenza di sintomi sovrapponibili ad un’otite esterna (otorrea ceruminosa o purulenta, prurito auricolare e scuotimento del capo) o ad un’otite media (sindrome di horner) fino a casi ben più rari in cui compaiono segni di otite interna (nistagmo, atassia vestibolare, vomito); l’“head tilt” è sintomo frequente più spesso correlato all’intenso dolore da otite media piuttosto che ad un coinvolgimento dell’orecchio interno. La poliposi dell’orecchio esterno determina costantemente un’otite esterna cronica con sintomi generalmente aspecifici. Sintomi legati alla presenza di un polipo rinofaringeo sono riferibili ad un quadro di patologia cronica, prevalentemente ostruttiva, delle vie aeree superiori unitamente ad una disfagia più o meno grave fino all’anoressia.

Ogni qualvolta si sospetti o si accerti la presenza di una lesione polipoide in una delle tre possibili localizzazioni caratteristiche è indispensabile indagare anche le due rimanenti sedi; l’iter diagnostico è perciò standard: esame clinico con palpazione ed ispezione del rinofaringe, radiografie delle bolle timpaniche ed accurato esame otoscopico. TAC e miringotomia/centesi possono rendersi talora indispensabili. La bullectomia ventrale viene attualmente considerata terapia d’elezione nel trattamento dei polipi dell’orecchio (medio ed esterno) ed è consigliabile eseguirla anche dopo trazione transorale di polipi rinofaringei. Una valida alternativa per i polipi dell’orecchio esterno, soprattutto in assenza di importanti alterazioni radiografiche della bolla timpanica ed in assenza di sintomi di otite media e/o interna potrebbe essere una tecnica mininvasiva da noi sperimentata in 8 casi: la trazione perendoscopica transtimpanica.

INTRODUZIONE I polipi rinofaringei ed auricolari sono neoformazioni benigne riscontrabili a livello di rinofaringe, orecchio medio ed orecchio esterno 1,2,3.

La sede di origine di tali polipi è stata a lungo materia controversa : in studi relativamente recenti è stata prospettata l’ipotesi che prendano origine dalla tuba uditiva o dalla zona della cavità timpanica circostante l’ostio della tuba stessa, quindi all’interno del comparto dorso-laterale della bolla timpanica 1,2.

Per quanto riguarda l’eziopatogenesi dei polipi auricolari e rinofaringei nel gatto l’ipotesi più accreditata appare quella che li considera lesioni secondarie a fenomeni infettivo-infiammatori cronici delle prime vie respiratorie e dell’orecchio medio.

Gli aspetti clinici, diagnostici e le scelte terapeutiche risultano diverse a seconda del percorso anatomico seguito da tali neoformazioni durante l’accrescimento perciò distinguiamo: polipi dell’orecchio medio (si espandono esclusivamente nella bolla timpanica), polipi dell’orecchio esterno (si accrescono verso il canale auricolare esterno dopo rot-

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tura della membrana timpanica) e polipi del rinofaringe (si espandono lungo la tuba di Eustachio attraverso un sottile peduncolo per poi accrescersi nel rinofaringe) 2.

La presenza di un polipo nell’orecchio medio può essere accompagnata da quadri sintomatologici diversi che variano dall’assenza di segni-sintomi 4, alla presenza di sintomi sovrapponibili ad un’otite esterna o ad un’otite media (sindrome di Horner) fino a casi ben più rari in cui compaiono segni riferibili ad otite interna (nistagmo, atassia vestibolare, vomito); l’head tilt è sintomo frequente, il più delle volte correlato all’intenso dolore provocato dall’otite media piuttosto che ad un coinvolgimento dell’orecchio interno 5,6,7.

L’iter diagnostico deve includere l’indagine radiografica delle bolle timpaniche ed un accurato esame otoscopico 5.

L’assenza di segni radiografici ed una normale membrana timpanica all’esame otoscopico non possono tuttavia far totalmente escludere una patologia dell’orecchio medio (l’incidenza di radiografie falsamente negative in alcuni studi raggiunge il 25%); per tale motivo potrebbe essere indicata una bullectomia esplorativa 8. Possibili alternative non invasive potrebbero essere costituite dalle Tomografia Assiale Computerizzata (TAC), Risonanza Magnetica Nucleare (RMN) e forse anche da miringotomia/centesi.

L’unica opzione terapeutica in caso di poliposi dell’orecchio medio consiste nell’esplorazione chirurgica della bolla timpanica; la bullectomia con accesso ventrale rappresenta, in tal senso, la tecnica d’elezione. La massa asportata deve essere sottoposta mandatoriamente ad esame istologico per la conferma diagnostica poichè la diagnosi differenziale si pone quasi esclusivamente nei confronti di lesioni occupanti spazio di tipo neoplastico 1,9,10.

La poliposi dell’orecchio esterno determina costantemente un’otite esterna cronica spesso monolaterale (!!) con sintomi generalmente aspecifici 1,2,5; l’esame otoscopico permette costantemente di evidenziare la neoformazione. Ogni qualvolta si sospetti o si accerti la presenza di una lesione polipoide in una delle tre possibili localizzazioni caratteristiche è indispensabile indagare anche le due rimanenti sedi; in caso quindi di diagnosi, ancorchè presuntiva, di poliposi auricolare esterna, oltre ad eseguire un accurato esame otoscopico di entrambi i condotti uditivi ed indagini radiografiche di entrambe le bolle (proiezioni oblique sia destra che sinistra), sarà mandatorio ispezionare accuratamente il rinofaringe per escludere la contemporanea presenza di un polipo rinofaringeo 1,5,9,10. La diagnosi definitiva pre-operatoria può essere raggiunta mediante biopsia incisionale ed, in presenza di polipi voluminosi (talvolta protundenti dal condotto uditivo), anche per mezzo di ago aspirato.

La bullectomia ventrale viene attualmente considerata terapia d’elezione anche nel trattamento dei polipi dell’orecchio esterno poiché la semplice trazione si è dimostrata possedere un elevato rischio di recidiva (valutato tra il 50 ed il 100%) e l’approccio laterale alla bolla timpanica per contro è caratterizzato da una non trascurabile incidenza di complicanze neurologiche 1,2,5,10.

In accordo con quanto riportato in letteratura si può ancora affermare che i polipi rinofaringei, rispetto a quelli auricolari (range 3 mesi – 15 anni) e rispetto ad altre lesioni occupanti spazio del rinofaringe, sono di più frequente riscon-

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tro nei soggetti giovani (range 2-3 mesi – 7 anni) 12,13.

Sintomi legati alla presenza di un polipo rinofaringeo sono riferibili ad un quadro di patologia cronica, prevalentemente ostruttiva, delle vie aeree superiori unitamente ad una disfagia più o meno grave fino all’anoressia 1,2,3,10,13. Possono essere presenti contemporaneamente segni di otite media.

Un accurato protocollo diagnostico nei confronti della poliposi rinofaringea deve comprendere innanzitutto un esame clinico con palpazione transpalatina del rinofaringe nel soggetto vigile e successivamente accurata ispezione dello stesso nel soggetto in anestesia generale, previo ribaltamento dell’estremità libera del palato molle 1,2; dovrebbe successivamente prevedere l’esame radiografico delle bolle timpaniche e, soprattutto in caso di positività radiografica ma anche in assenza di questa (per quanto sopra ricordato), un esame otoscopico per escludere la contemporanea presenza di polipi nelle altre due sedi caratteristiche 1,6,14. L’opzione terapeutica che garantisce un’immediata risoluzione dei sintomi è l’asportazione del polipo mediante trazione perorale, previo ribaltamento cranio ventrale dell’estremità libera del palato molle; a causa della relativamente alta frequenza di recidive correlate a tale intervento, e per scongiurare lo sviluppo di una poliposi dell’orecchio medio, è tuttavia consigliabile eseguire un’esplorazione chirurgica della bolla timpanica ipsilaterale mediante bullectomia ventrale, anche in assenza di alterazioni radiografiche della stessa 1,2.

ESPERIENZE PERSONALI La nostra casistica comprende 23 gatti afferiti all’Istituto di Clinica Chirurgica e Radiologia Veterinaria dell’Università di Milano portatori di poliposi auricolare (esterna e/o media) e/o rinofaringea nel periodo compreso tra Marzo 1995 e Dicembre 1999.

Tutti i pazienti sono stati sottoposti al protocollo diagnostico standard, come sopra specificato, utilizzando per l’esame otoscopico un artroscopio a visione frontale del diametro di 2.7 mm.

In 3 gatti è stato diagnosticato unicamente un polipo rinofaringeo; un gatto presentava poliposi rinofaringea bilaterale e polipo dell’orecchio medio a destra (positività radiografica a destra e quindi bullectomia ventrale destra); in un gatto sono state diagnosticate tutte e tre le tipologie di polipo (rinofaringeo destro, dell’orecchio medio a sinistra e dell’orecchio esterno a destra) ed infine un gatto era portatore di polipo rinofaringeo a sinistra e polipo auricolare esterno sempre a sinistra; gli altri 17 gatti presentavano esclusivamente polipi dell’orecchio esterno.

Una volta emessa la diagnosi presuntiva di poliposi rinofaringea si è immediatamente eseguita, a motivo della gravità dei sintomi, la rimozione del polipo mediante trazione (in totale 7 interventi di trazione); a ciò ha fatto seguito l’esame istopatologico della neoformazione per la conferma diagnostica. Nel caso di poliposi rinofaringea la bullectomia ventrale è stata eseguita solo in caso di positività radiografica delle bolle timpaniche (2 casi); in un caso non è stata eseguita per mancato consenso del proprietario.

Nei casi di presuntiva poliposi auricolare, in corso di esame endoscopico, si è proceduto a biopsia incisionale/escis-

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sionale; confermata mediante esame istopatologico la sospetta diagnosi solo in un secondo momento si è attuata la bullectomia ventrale (in totale 14 interventi, in due casi bilaterale).

L’esplorazione chirurgica della bolla ha consentito di diagnosticare la presenza, in due casi, di poliposi dell’orecchio medio.

In 8 gatti con polipi dell’orecchio esterno e senza sintomi di otite media è stata sperimentata una nuova tecnica: la trazione perendoscopica transtimpanica (in un caso associata ad otostomia di Zepp per eccessiva stenosi del condotto auricolare).

La principale complicanza sia per la trazione di polipi rinofaringei (2 casi su 6) che per la bullectomia ventrale (6 casi su 12) è risultata essere la sindrome di Horner; tuttavia in 7 casi tale complicanza è stata solo temporanea (durata massima di 4 mesi); un caso è stato perso al follow-up. Il gatto in cui si sono diagnosticate tutte e tre le tipologie di polipi è deceduto dopo l’intervento di bullectomia ventrale bilaterale (solo in questo caso si è intervenuti contemporaneamente su entrambe le bolle).

Nessuno degli 8 casi su cui è stata eseguita la trazione perendoscopica ha presentato sindrome di Horner; in due casi si è verificata recidiva rispettivamente a distanza di 1 e 4 mesi ed è stato necessario un secondo intervento sempre di trazione con tecnica perendoscopica.

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re i rischi di recidive. Tale intervento è inoltre relativamente scevro da gravi complicanze. Una valida alternativa, soprattutto in assenza di importanti alterazioni radiografiche della bolla timpanica ed in assenza di sintomi di otite media e/o interna (sindrome di Horner e sindrome vestibolare periferica), potrebbe essere rappresentata dalla rimozione perendoscopica transtimpanica del polipo.

Ulteriore casistica e follow-up più lunghi sono necessari al fine di una valutazione definitiva di questa tecnica “minimally invasive”.

Bibliografia 1-

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3-

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DISCUSSIONE E CONCLUSIONI Ci preme sottolineare l’importanza di un protocollo diagnostico standard per tutti e tre i polipi comprendente l’esame radiografico delle bolle timpaniche (proiezione craniocaudale a bocca aperta ed oblique soprattutto), l’esame otoscopico accurato, se è possibile mediante artroscopio, e l’ispezione del rinofaringe.

In corso di poliposi rinofaringea la terapia meno invasiva e comunque in grado di garantire un rapido miglioramento dei sintomi (tanto da essere eseguita nei casi più gravi prima di indagare altre possibili sedi di poliposi) è sicuramente rappresentata dalla trazione perorale previo ribaltamento del palato molle.

In caso di poliposi auricolare, sulla scorta della nostra esperienza e dai dati della letteratura 1-2-5-9-10 emerge inequivocabilmente che solo un iter terapeutico completo, comprensivo cioè di esplorazione e curettage della bolla timpanica mediante bullectomia ventrale è in grado di minimizza-

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Kapatkin AS, Matthiesen DT, Noone KE, Church EM, Scavelli TE, Patnaik AK, (1990), Results of surgery and long term follow up in 31 cats with nasopharyngeal polyps, J Am Anim Hosp Assoc, 26: 387392.

Lane JG, (1995), Poliposi rinofaringea del gatto: diagnosi e trattamento, Atti del 29° Congresso Scivac: Medicina e chirurgia di naso, gola e orecchio, 55-65.

Seitz SE, Losonsky JM, Marretta SM, (1996), Computed tomographic appearance of inflammatory polyps in three cats, Vet Rad Ultras, 37: 99-104.

Parker NR, Binnington AG, (1985), Nasopharyngeal polyps in cats: three case reports and review of literature, J Am Anim Hosp Assoc, 21: 473-478.

Pope ER, (1995), Feline inflammatory polyps, Sem Vet Med Surg (Sm An), 10: 87-93.

Shell L (1988), Otitis media and otitis interna, Vet Clin North Am Small Anim Pract, 18: 885-899.

Bruyette DS, Lorenz MD (1993), Otitis externa and otitis media: diagnostic and medical aspects”; Sem Vet Med Surg (Sm An), 8: 3-9.

Remedios AM, Fowler JD, Pharr JW, (1991), A comparison of radiographic versus surgical diagnosis of otitis media, J Am Anim Hosp Assoc, 27: 183-188.

Faulkner JE., Budsberg SC, (1990), Results of ventral bulla osteotomy for treatment of middle ear polyps in cats, J Am Anim Hosp Assoc, 26: 496-499.

Trevor PB, Martin RA, (1993), Tympanic bulla osteotomy for treatment of middle ear disease in cats: 19 cases (1984-1991), J Am Vet Med Assoc, 202: 123-128.

Barreau P, (1989), Polype lymphoide de l’oreille moyenne chez un chat: traitement chirurgical, Pratique Medicale et Chirurgicale de l’animal de compagnie, 24: 661-670.

Lane JG, Orr CM, Lucke VM, Gruffy DD, Jones TJ, (1981), Nasopharyngeal polyps arising in the middle ear of the cat, J Small Anim Pract, 22: 511-522.

Allen HS, Broussard J, Noone K, (1999), Nasopharyngeal Diseases in cats: a retrospective study of 53 cases (1991-1998), J Am Anim Hosp Assoc, 35: 457-461.

Schmidt JF, Kapatkin A, (1990), Nasopharyngeal and ear canal polyps in the cat, Feline pract, 18: 16-19.

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Otite terminale nel cane e nel gatto Indicazioni e limiti della TECALBO (Total Ear Canal Ablation and Lateral Bulla Osteotomy)

Carlo Maria Mortellaro* Med. Vet., Istituto di Clinica Chirurgica e Radiologia Veterinaria - Università degli Studi di Milano

* in collaborazione con: S. De Dominici

Riassunto L’otite terminale del cane e del gatto, o “end stage otitis” (ESO) degli AA. Anglosassoni, definisce un processo flogistico cronico, in particolare del tratto orizzontale del condotto uditivo, caratterizzato da impervietà parziale o totale del lume stesso. Il processo è complicato generalmente da concomitante otite media. Stenosi del condotto in esito a fibrosi cicatriziale, suo “collasso”, sua occlusione ad opera di imponenti processi proliferativi dell’epitelio di rivestimento, ossificazione e/o calcificazione delle cartilagini auricolare e anulare, sono all’origine della non pervietà (“deficient horizontal ear canal”) che contraddistingue una ESO. L’ablazione totale del condotto uditivo esterno associata a ostectomia laterale della bolla timpanica (in sigla TECALBO dall’inglese “Total Ear Canal Ablation and Lateral Bulla Osteotomy”) rappresenta l’intervento di elezione nel controllo dell’otite cronica di cui sopra. La metodica, inoltre, trova indicazione nelle neoplasie del tratto orizzontale del condotto uditivo, nelle neoplasie primitive dell’orecchio medio, malformazioni, affezioni para-auricolari, neoplastiche e non, gravi traumatismi dell’orecchio esterno, insuccessi di altre procedure di resezione; l’iperplasia delle ghiandole ceruminose, polipi dell’orecchio esterno particolarmente invasivi ed il carcinoma squamoso della pinna costituiscono ulteriori indicazioni, peculiari della specie felina. TECALBO è una procedura chirurgica che prevede l’escissione della cartilagine auricolare verticale ed orizzontale e con contemporanea rimozione di porzioni della parete laterale della bolla timpanica al fine di realizzare un meticoloso curettage del suo epitelio di rivestimento. In sede operatoria la complicanza maggiore è rappresentata dall’emorragia dovuta a recisione di grossi vasi (arteria carotide esterna, vena retroglenoidea). Le complicanze del periodo post-operatorio immediato comprendono paresi/paralisi del nervo facciale, nervo ipoglosso, sindrome vestibolare, eventualmente ipoacusia, deiscenza della sutura e suppurazione superficiale. Una ascessualizzazione periauricolare con creazione di tragitti fistolosi costituisce infine temibile e tardiva complicanza. Per tali motivi la procedura dovrebbe essere affrontata da chirurghi con adeguata competenza tecnica, ma soprattutto con solida conoscenza dell’anatomia della regione, spesso distorta. La nostra esperienza basata su circa 40 interventi (di cui 35 nel cane) conferma che la TECALBO è un efficace metodo di trattamento dell’otite terminale con risultati a lungo termine buoni o eccellenti. L’alta incidenza di complicanze, peraltro in gran parte evitabili con adeguato training e non pregiudicanti la vita del soggetto non deve scoraggiare il chirurgo dall’affrontare l’intervento in questione.

INTRODUZIONE L’otite terminale del cane e del gatto, o “end stage otitis” (ESO) degli AA. Anglosassoni, definisce un processo flogistico cronico, in particolare del tratto orizzontale del condotto uditivo, caratterizzato da impervietà parziale o totale del lume stesso1. Il processo è complicato generalmente da concomitante otite media. Stenosi del condotto in esito a fibrosi cicatriziale, suo “collasso” o sua occlusione ad opera di imponenti processi proliferativi dell’epitelio di rivestimento, ossificazione e/o calcificazione ossea delle cartilagini auricolare e

anulare, sono all’origine della non pervietà (“deficient horizontal ear canal“) che contraddistingue una ESO. Per tale motivo e soprattutto a causa della concomitante non diagnosticata otite media, la resezione laterale del condotto uditivo, come pure la resezione totale del suo tratto verticale, esitano quasi costantemente in insuccesso se attuate in un paziente canino o felino portatore di otite terminale 2. La non conoscenza o la sottovalutazione dei gravi processi patologici irreversibili che una ESO sottende, o peggio ancora una sua misdiagnosi, costituiscono dunque i presupposti per l’inefficacia terapeutica delle due metodiche chirurgiche testè ricordate.

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L’ablazione totale del condotto uditivo esterno associata a ostectomia laterale della bolla timpanica (in sigla TECALBO dall’inglese “Total Ear Canal Ablation and Lateral Bulla Osteotomy”) rappresenta, per contro, l’intervento di elezione nel controllo dell’otite cronica di cui sopra. La metodica, inoltre, trova indicazione nelle neoplasie del tratto orizzontale del condotto uditivo, nelle neoplasie primitive dell’orecchio medio, con o senza evidente estensione al canale orizzontale, otiti medie refrattarie, malformazioni, affezioni para-auricolari, neoplastiche e non e, da ultimo, gravi traumatismi dell’orecchio esterno. È tecnica d’elezione, infine, per il trattamento degli insuccessi sequela di altre procedure di resezione (otostomia secondo Zepp, ablazione del condotto uditivo).

L’iperplasia delle ghiandole ceruminose, il carcinoma squamoso della pinna e talora i polipi dell’orecchio medio estesi al condotto uditivo esterno costituiscono ulteriori indicazioni, peculiari della specie felina.

TECNICA CHIRURGICA TECALBO è una procedura chirurgica che prevede l’escissione della cartilagine auricolare verticale ed orizzontale e del sovrastante epitelio con contemporanea rimozione di porzioni della parete laterale della bolla timpanica al fine di asportare il contenuto della bolla stessa, ma soprattutto di realizzare un meticoloso curettage del suo epitelio di rivestimento4. La rimozione minuziosa di tale epitelio, spesso in condizione di iperplasia, metaplasia e cheratinizzazione è il fattore decisivo per il raggiungimento del risultato sperato: la cura definitiva, in assenza di gravi complicazioni, dell’otite terminale. La tecnica operatoria descritta originariamente da Cechner5 nel 1982, è oggi dettagliatamente riportata in numerosi trattati di chirurgia veterinaria 6,7,8,9ed in alcune pubblicazioni specifiche1,4,10,11,12,13. Tali fonti bibliografiche sono provviste di ricca iconografia che facilità la comprensione di una non facile metodica e ad esse per tanto si rimanda. Le tappe fondamentali della TECALBO, che tuttavia sinteticamente riportiamo, comprendono in successione: incisione cutanea a “T” con tratto orizzontale parallelo alla cartilagine del trago e tratto verticale in corrispondenza della relativa porzione del canale auricolare; dieresi della cute e della cartilagine della superficie mediale della conca, ad andamento curvilineo ed in posizione dorsale rispetto alla precedente incisione orizzontale; (tale dieresi deve congiungersi tanto cranialmente quanto caudalmente con il tratto orizzontale della T in modo da delimitare circolarmente un cono cartilagineo); dissezione, per via smussa o mediante incisione, del tessuto lasso pericartilagineo fino a completa scheletrizzazione del cono cartilagineo in precedenza delimitato, ovverossia il condotto uditivo verticale : al fine di preservare quanto più possibile le strutture neurovascolari adiacenti alla cartilagine auricolare, soprattutto la componente vascolare, è importante mantenersi strettamente a ridosso del pericondrio; estensione della scheletrizzazione al condotto uditivo orizzontale fino a livello della cartilagine anulare; identificazione ed isolamento del nervo facciale e sua eventuale retrazione ventrale; amputazione del cono cartilagineo (canale uditivo verticale ed orizzontale) a livello del meato acu-

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stico osseo; rimozione mediante scollaperiostio e curettes di adeguate dimensioni dello strato epiteliale del succitato meato; ostectomia della rima ventrale del meato stesso con conseguente visualizzazione della bolla timpanica (previo scollamento tissutale e periostale) e della cavità timpanica; prelievo di materiale dall’orecchio medio per allestimento di esame colturale e/o istologico; ampliamento del meato acustico lungo la sua circonferenza, mediante piccola pinza ossivora o fresa pneumatica da ossa, con estensione dell’ostectomia, variabile da caso a caso, alla porzione ventrale di tale meato, corrispondente alla parete laterale della bolla timpanica; minuziosa toelettatura chirurgica dell’orecchio medio da detriti, tessuto patologico o, più spesso, mucosa iperplastica (al fine di evitare complicazioni neurologiche quali la sindrome vestibolare, si eviti tuttavia il curettage del recesso epitimpanico che alloggia le finestre ovale e rotonda nonché la catena degli ossicini); lavaggio copioso con soluzione salina o ringer lattato (taluni autori suggeriscono l’impiego di soluzione di ioduro di povidone 1%); posizionamento di un drenaggio di Penrose all’interno della bolla ed infine sutura cutanea. A margine di quanto sopra esposto va ricordato che alcune varianti sono state apportate negli anni alla tecnica originariamente descritta. Tra queste menzioniamo la possibilità (materia di preferenza del chirurgo!) di optare per una dieresi cutanea circolare10anziché a T. Tale modifica contribuisce a minimizzare i rischi di danno alla ghiandola parotide posta profondamente in corrispondenza del tratto verticale della T. La scelta è tuttavia ininfluente ai fini del successo: ciò che più conta è semmai una “generosa” (in senso di estensione dorsale) dieresi/exeresi della cartilagine della porzione mediale della conca che possa includere tutto il tessuto patologico. Specie in quest’ultima evenienza i pazienti canini ad orecchie erette ed i gatti soffriranno di una evidente menomazione estetica: per quanto il portamento corretto dell’orecchio costituisca legittima aspettativa per il proprietario e per il chirurgo, l’escissione di tutta l’area patologica, ancorché di natura benigna, rimane di prioritaria importanza per il successo definitivo.

Variazioni importanti sono state introdotte anche nel modo di effettuare l’ostectomia della bolla: da una tecnica da alcuni definita “key hole” (“buco della serratura”) si è passati oggi (e chi scrive si è perfettamente adeguato) ad una ostectomia di tipo “conservativo”.

Ciò sta ad indicare che se l’ampliamento circonferenziale del meato acustico esterno, previa rimozione della porzione ossea del canale auricolare, consente l’accesso visivo e strumentale all’orecchio medio, l’ulteriore ostectomia della parete laterale e ventrale della bolla timpanica, qualora non sussistano motivazioni specifiche (osteomielite, tumore), diviene un inutile esercizio chirurgico potenzialmente pericoloso. Non concordiamo quindi con chi scrive che un “adequate removal of the lateral wall of bulla is mandatory to allow proper drainage of the middle ear”10. Una tecnica osteotomica minimamente invasiva mette al riparo dal danno iatrogeno a strutture vascolari importanti quale la vena retroglenoidea, l’arteria stilomastoidea ed altre ancora la cui scontinuazione genera emorragie forse non fatali (un decesso è tuttavia riportato in letteratura da danno alla carotide esterna1) ma sempre difficili e tediose da arrestare.

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COMPLICANZE Numerose e frequenti sono le complicazioni associate alla TECALBO: alcune di queste appannaggio della fase intraoperatoria, altre, le più numerose, caratteristiche della fase post-operatoria. In sede operatoria la complicanza maggiore è rappresentata dall’emorragia dovuta a recisione di grossi vasi (arteria carotide esterna), potenzialmente fatale; meno drammatica nei suoi effetti, ma pur sempre preoccupante, è la scontinuazione della vena retroglenoidea. Tale vaso, che emerge dal forame retroglenoideo subito cranialmente alla bolla timpanica, si retrae immediatamente all’interno del forame stesso (porzione petrosa dell’osso temporale) dopo scontinuazione accidentale, vanificando le normali procedure emostatiche (pinzamento e legatura, elettrocoagulazione etc); solo l’applicazione di cera da ossa sul forame menzionato o in assenza di questa, un generoso zaffamento con tamponi assorbibili (spugna di gelatina, di fibrina) si dimostrano efficaci in tale circostanza. La esecuzione di ostectomie della bolla minimanente invasive (evitare l’uso dell’osteotomo!!) confinate, se possibile, lungo il perimetro del meato acustico, riduce notevolmente il rischio di danno alla vena retroglenoidea. L’infezione post-operatoria è una non infrequente complicanza connessa alla TECALBO e può manifestarsi nell’immediato periodo post-operatorio, come drenaggio prolungato dalla ferita, sua deiscenza e cellulite superficiale, o a distanza di settimane o mesi dall’intervento con la creazione di ascessi para-auricolari associati o meno a fistolizzazioni. Mentre le complicanze infettive acute riflettono una possibile contaminazione batterica intraoperatoria da manipolazione di tessuti costantemente infetti (impossibile è ottenere l’asepsi), l’ascessualizzazione tardiva rappresenta l’inevitabile sequela di una incompleta rimozione dell’epitelio della bolla e/o del canale osseo, potenzialmente infetto, ma pur sempre dotato di proprietà secretive.

In presenza di tale frustrante complicazione è mandatorio effettuare una seconda chirurgia con approccio ventrale o laterale alla bolla, da noi preferito, volta ad asportare definitivamente frustoli di cartilagine o più spesso di epitelio. A nulla valgono terapie antibiotiche pur mirate e protratte nel tempo.

La paralisi parziale o completa del nervo facciale, temporanea o permanente, costituisce ulteriore complicanza associata alla TECALBO. Tale disfunzione nervosa, la cui incidenza varia dal 5 al 58% nelle differenti casistiche, deriva da neuropraxia o assonotmesi del nervo facciale o,più raramente, da neuroassonotmesi (frequente in caso di intrappolamento del nervo da parte di tessuto metaplastico). Segni clinici associati al danno del nervo facciale comprendono la riduzione/assenza del riflesso palpebrale e la ptosi labiale o auricolare.

La spesso paventata cheratocongiuntivite secca è rarissima a verificarsi e presuppone il danno della porzione parasimpatica del nervo facciale che fornisce l’innervazione alla ghiandola lacrimale. La maggior parte dei pazienti con deficit neurologico del 7°nervo cranico,tuttavia,non manifesta alcun segno/sintomo importante: una secrezione lacrimale ancora adeguata, la retrazione del globo oculare mediata dal nervo abducente e la conseguente procidenza della terza palpebra sono in grado,infatti,di garantire una efficace lubrificazione dell’occhio prevenendo l’ulcerazione corneale. Più

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serie e spesso permanenti sono le conseguenze associate a danno del recesso epitimpanico e conseguentemente delle finestre ovale e rotonda. Questa complicanza, che si verifica nel 5-10% dei soggetti trattati,è forse la più grave tra quelle riferibili a TECALBO essendo responsabile di “head tilt”, nistagmo e anomalie posturali conseguenza di danno ai recettori vestibolari posti nel labirinto membranoso di danno alla porzione vestibolare dell’8° nervo cranico. Per quanto riguarda,infine,la residua capacità uditiva dei pazienti sottoposti a TECALBO, la questione permane controversa. L’effetto di questa “invasiva” procedura chirurgica sulla funzione acustica è difficile da valutare oggettivamente: mentre molti pazienti manifestano ipocusia/anacusia dopo TECALBO bilaterale, valutazioni soggettive di alcuni proprietari indicano,per contro, un miglioramento dell’udito.

CONCLUSIONI L’ablazione totale del condotto uditivo esterno associata ad ostectomia della bolla timpanica è procedura chirurgica tecnicamente non facile e potenziale causa di danni neurovascolari talora irreversibili. Per tale motivo dovrebbe essere confinata a casi gravi di ESO ed affrontata da chirurghi con adeguata competenza tecnica, ma soprattutto con solida conoscenza dell’anatomia della regione. Anatomia che spesso è macroscopicamente distorta da imponenti processi distrofico-metaplastici della cartilagine auricolare, da tumori, estese ascessualizzazioni periauricolari o “mascherata” da gravi emorragie; tutto ciò, unitamente ad una relativa inesperienza del chirurgo, è stata ed è all’origine delle complicanze connesse alla TECALBO. Pur tuttavia è procedura di salvataggio irrinunciabile, contrassegnata da prognosi ottimisticamente favorevole in un elevato numero di pazienti canini; in medicina felina, per contro, l’alta prevalenza di neoplasie del condotto orizzontale associate ad un’ESO suggerisce l’emissione di un prognostico riservato 3. La nostra esperienza relativa al quinquennio 1994-1999, basata su circa 40 interventi (di cui 35 nel cane), conferma che la TECALBO è un efficace metodo di trattamento dell’otite terminale, con risultati a lungo termine buoni o eccellenti. Se si escludono le patologie neoplastiche comunque trattate con tale tecnica ,il tasso di successo è stato di circa il 90%. L’alta incidenza di complicanze connesse con l’esecuzione della TECALBO, riportate in alcune casistiche e verificatesi nel 75% dei casi accorsi alla nostra attenzione, non deve inoltre scoraggiare il chirurgo dall’affrontare (con le premesse di cui sopra) tale procedura chirurgica di salvataggio. Una quota rilevante di tali complicanze (sieroma, deiscenza della sutura, suppurazioni superficiali) risulta di facile e relativamente breve risoluzione; altre (paresi, paralisi del nervo facciale, sindrome di Horner) pregiudicano minimamente la qualità di vita del soggetto; le più gravi (sindrome vestibolare, infezione profonda con fistolizzazione) sono sicuramente frustranti ma altrettanto sicuramente minimizzabili ricorrendo, come ebbero occasione di scrivere Williams e White3 , ad una “more meticulous dissection, gentle tissue handling and taking care not to be overzealous with curettage of the medial aspect of the bulla”.

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Bibliografia 1.

2.

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Mason KL, Harvey CE, Orsher RJ, (1988), Total ear canal ablation combined with lateral bulla osteotomy for end-stage-otits in dogs.Results in thirty dogs , Vet Surg, 17: 263-268.

Smeak DD, DeHoff WD, (1986), Total ear canal ablation: clinical results in the dog and cat, Vet Surg, 15: 161-170.

Williams JM, White RAS, (1992), Total ear canal ablation combined with lateral bulla osteotomy in the cat,J Small Anim Pract, 33: 225-227.

Beckman SL, Henry WB, Cechner P, (1990), Total ear canal ablation combined with lateral bulla osteotomy and curettage in dogs with chronic otitis externa and media, J Am Vet Med Assoc, 196: 84-90.

Cechner P, (1982), Combined ear canal ablation and lateral bulla osteotomy in the dogs,quoted by Harvey CE in: Slatter DH, ed. Textbook of Small Animal Surgery, WB Saunders CO, Philadelphia, 1985.

Smeak DD, (1990), Total ear canal ablation, in Bojrab MJ, ed. Current Techniques in Small Animal Surgery 3rd ed., Lea & Febiger, Philadelphia, 140-147.

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Smeak DD, (1998), Total ear canal ablation and lateral bulla osteotomy,in Bojrab MJ, et al. eds. Current Techniques in Small Animal Surgery, 4th ed., Williams & Wilkins, Baltimora, 102-109.

Fossum TW, (1997), Surgery of the ear, in Fossum TW, ed., Small Animal Surgery, Mosby, S. Louis, 153-161.

Krahwinkel DJ, (1993), External ear canal,in Slatter D, ed., Textbook of Small Animal Surgery, 2nd ed.,WB Saunders Company, Philadelphia, 1560-1567.

Henderson JH, Radasch RM, (1995), Total ear canal ablation with lateral bulla osteotomy for the management of end-stage otitis in dogs, Compend Contin Educ Pract Vet, 17: 157-164.

White RAS, Pomeroy CJ, (1990), Total ear canal ablation and lateral bulla osteotomy (TECA/LBO) in the dog: indications, complications, and long term results in 100 procedures,Vet Surg, 19:81-88.

White RAS, Pomeroy CJ, (1990),Total ear canal ablation and lateral bulla osteotomy in the dog, J Small Anim Pract, 547-553.

Matthiesen DT, Scavelli T, (1990), Total ear canal ablation and lateral bulla osteotomy in 38 dogs, J Am An Hosp Assoc, 26: 257-267.

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Malattie di recente descrizione in dermatologia veterinaria Chiara Noli Med. Vet., Dipl. ECVD - Libero Professionista - Milano

Riassunto La piodermite delle giunzioni mucocutanee si manifesta con lesioni crostose, erosive e, depigmentazione, che le rendono spesso indistinguibili clinicamente da alcune malattie autoimmuni.

La sovraccrescita batterica si manifesta con lesioni cliniche conclamate, bensì sono con prurito, e occasionale untuosità, eritema o iperidrosi cutanea, e può aggravare il prurito nei soggetti allergici.

Sono state descritte piodermiti superficiali e profonde causate da S. aureus meticillino-resistente, un batterio nosocomiale multiresistente, in cani per lo più di proprietà di personale ospedaliero.

La fasciite streptococcica è una infezione della cute e dei tessuti sottostanti, sostenuta da streptococchi spp, in grado di prudurre tossine istolesive.

Una infezione dermatofitica dello strato corneo, sostenuta da Trichophyton mentagrophytes, M persicolor o M. gypseum è stata recentemente riconosciuta come importante diagnosi differenziale del penfigo foliaceo e del penfigo eritematoso. È stata recentemente proposta una nuova classificazione delle malattie immunomediate eritema multiforme, sindrome di Steven Johnson e necrosi epidermolitica tossica. Queste forme rappresenterebbero manifestazioni di gravità crescente di uno stesso processo patologico. È stata formulata l’ipotesi che la necrosi epidermolitica tossica sia associata più frequentemente dell’eritema multiforme a somministrazione di farmaci e che l’eritema multiforme e la sindrome di Steven Johnson siano invece manifestazioni di infezioni virali, di origine per ora sconosciuta.

Sindromi paraneoplastiche feline: nel gatto sono state recentemente riconosciute tre malattie cutanee di probabile origine paraneoplastica: la dermatite esfoliativa legata a timoma, l’ alopecia non infiammatoria legata a tumore pancreatico e la follicolite murale linfocitaria/sebadenite, a volte fase iniziale del linfoma epiteliotropo.

INTRODUZIONE La dermatologia veterinaria ha compiuto enormi progressi negli ultimi vent’anni, tuttavia le malattie di recente descrizione sono sempre di meno. Queste riguardano soprattutto le malattie infettive batteriche e fungine, e quelle immunomediate.

Malattie batteriche Fra le malattie batteriche del cane sono state descritte recentemente tre nuove entità: la piodermite delle giunzioni mucocutanee, la sovraccrescita batterica, la piodermite da stafilococco meticillino resistente e la fasciite streptococcica.

Piodermite delle giunzioni mucocutanee La piodermite delle giunzioni mucocutanee si manifesta con lesioni crostose ed erosive localizzate nelle giunzioni mucocutanee (labbra, narici, palpebre, ano, prepuzio, vulva).

A volte si osservano anche depigmentazione e ulcerazioni, che le rendono spesso indistinguibili clinicamente da alcune malattie autoimmuni (ad esempio lupus discoide). La diagnosi si ottiene con la somministrazione di prova di antibiotici per 3-4 settimane e/o con una biopsia cutanea. In caso di piodermite mucocutanea la terapia antibiotica determina la risoluzione completa delle lesioni, mentre l’esame istologico testimonia la presenza di granulociti neutrofili, tipici di una infezione batterica. La causa di questa piodermite è sconosciuta, non si conosce predisposizione di razza, sesso o età.

Sovraccrescita batterica La sovraccrescita batterica è stata recentemente ipotizzata come concausa di prurito nei cai con dermatite atopica.

Essa non si manifesta con lesioni cliniche conclamate, bensì sono con prurito, e occasionale untuosità, eritema o iperidrosi cutanea. È stato riportato che nei soggetti atopici i batteri sono maggiormente in grado di aderire ai corneociti di superficie e quindi moltiplicarsi in sovrannumero. I prodotti metabolici di questi microorganismi in eccesso (ad esempio

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proteina A) sono in grado, anche in assenza di lesioni clinicamente manifeste, di penetrare l’epidermide e causare prurito. Per questo motivo spesso gli antibiotici sono capaci di alleviare il prurito in animali allergici senza lesioni tipiche di piodermite. Per determinare la presenza di sovraccrescita batterica in uno studio (S. Colombo, dati non pubblicati) è stato contato il numero di batteri per unità di superficie, ottenuti con la metodica citologica per apposizione di Tzank ed osservati al microscopio ad immersione, da animali sani e da animali sospetti. Negli animali malati il numero di batteri è signicativamente superiore che negli animali sani. Con una semplice terapia antibiotica per 3 settimane si può diagnosticare con facilità la sovraccrescita batterica. È però importante ricordare che, se non si identifica e corregge la malattia allergica sottostante, il prurito legato alla sovraccrescita batterica è destinato a recidivare al termine della terapia antibiotica.

Piodermite da stafilococchi meticillino-resistenti In medicina umana negli ultimi anni si è osservata con grande proccupazione l’emergenza di ceppi batterici, per lo più Staphylococcus aureus, di origine nosocomiale, resistenti alla maggior parte degli antibiotici. Fra questi è molto importante lo S. aureus meticillino-resistente (MRSA), insensibile a tutte le penicilline e cefalosporine (è infatti oxacillino-resistente) e sensibile solo alla vancomicina. È di pochi mesi fa, inoltre, l’isolamento di uno S. aureus anche vancomicino-resistente (VISA). Negli ultimi anni sono state descritte nel cane, per fortuna in maniera sporadica, piodermiti superficiali e profonde causate da S. aureus multiresistenti e in particolare da MRSA. La peculiarità di questi casi è che, la maggior parte degli aimali colpiti erano di proprietà di personale medico o paramedico ospedaliero, il che suggerisce un contagio uomo (portatore sano)animale. Le infezioni con tali germi nel cane possono essere a loro volte fonte di infezione per altre persone, magari debilitate o immunodepresse, e vanno quindi prontamente riconosciute e trattate radicalmente con terapia antibiotica efficace.

Fasciite streptococcica È stata recentemente occasionalmente descritta una infezione della cute e dei tessuti sottostanti, sino ai piani muscolari sottostanti, sostenuta da streptococchi spp, in grado di prudurre tossine istolesive. Le lesioni sono profonde e devastanti in maniera inconsueta per una piodermite, e a volte il decorso della malattia può essere rapidamente fatale.

MALATTIE FUNGINE Una infezione dermatofitica dello strato corneo, sostenuta da Trichophyton mentagrophytes, M persicolor o M. gypseum è stata recentemente riconosciuta come importante diagnosi differenziale del penfigo foliaceo e del penfigo eri-

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tematoso. La prima segnalazione descrite due casi nel cane, dove l’infezione fungina aveva colpito la canna nasale e le zone perioculari con formazione di croste e esfoliazione e lesioni parzialmente essudative. Gli esami citologici ed istologici erano fortemente suggestivi di penfigo foliaceo, tuttavia l’animale trattato con terapia immunosoppressiva mostrava peggioramenti. Un più accurato esame delle sezioni istologiche colorate con acido periodico di Schiff (PAS) rivelò la presenza di una infezione dermatofitica dello stato corneo, che mimava clinicamente le lesioni di penfigo. Le lesioni si risolsero completamente con terapia antifungina. Si consiglia pertanto di richiedere l’esame delle sezioni sitologiche colorate con PAS in ogni caso di sospetto penfigo foliaceo o eritematoso.

MALATTIE IMMUNOMEDIATE È stata recentemente proposta una nuova classificazione delle malattie immunomediate eritema multiforme, sindrome di Steven Johnson e necrosi epidermolitica tossica5. In questo studio l’eritema multiforme viene descritto come una malattia nella quale le lesioni non ulcerative (papule, macule, eritema) si estendono per meno del 50% della superficie corporea e quelle ulcerative per meno del 10%. Nell’eritema multiforme variante minor è coinvolta al massimo una mucosa, in quello variante major più di una mucosa. La sindrome di Steven Johnson è caratterizzata dalla presenza di lesioni non ulcerative su più del 50% della superficie corporea con ulcerazioni al di sotto del 10% di quest’ultima, e dalcoinvolgimento di più mucose. Nella necrosi epidermolitica tossica le lesioni si estendono a più del 50% della superficie corporea, di cui ulcerazioni in più del 30% del corpo, con coinvolgimento di molte mucose. Queste forme rappresentano così probabilmente manifestazioni di gravità crescente, in un continuum di uno stesso processo patologico. Gli autori di questo articolo hanno anche analizzato l’associazione di queste manifestazioni cutanee con altre malattie o con somministrazione di farmaci, per poterne determinare una causa scatenante. Essi formulano l’interessante ipotesi, che la necrosi epidermolitica tossica sia associata più frequentemente dell’eritema multiforme a somministrazione di farmaci (e possa quindi rappresentare una reazione da farmaco) e che l’eritema multiforme e la sindrome di Steven Johnson siano invece manifestazioni di infezioni virali, di origine per ora sconosciuta.

SINDROMI PARANEOPLASTICHE FELINE Nel gatto sono state recentemente riconosciute tre malattie cutanee di probabile natura immunomediata e forse di origine paraneoplastica.

Dermatite esfoliativa legata a timoma. I gatti affetti da questa malattia mostrano una dermatite desquamativa diffusa, e occasionalmente aree di alopecia, dove i peli sono facili da eradicare con una semplice trazione. L’esame istologico mostra un’ipercheratosi lamellare e una esocitosi linfocitaria con apoptosi simile al “graft versus host disease”.

Questo tipo particolare di dermatite è associata a timoma e

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può risolversi se il tumore viene riconosciuto e escisso in fase precoce.

Alopecia totale non infiammatoria legata a tumore pancreatico. Questa forma di alopecia non infiammatoria lascia la cute completamente glabra e lucida. Istologicamente i follicoli sono completamente atrofizzati, mentre l’epidermide e il derma sono normali. I gatti affetti da questa malattia sono inizialmente asintomatici, e solo successivamente mostrano disturbi gastroenterici, anche se non sempre i valori biochimici ematici sono alterati. In genere questi animali muoiono a causa di un tumore pancreatico maligno.

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Follicolite murale linfocitaria/sebadenite. I gatti affetti da questa malattia mostrano desquamazione, seborrea da secca a untuosa, con formazione di tappi follicolari con gradi variabili di alopecia. Istologicamente si osserva un infiltrato murale linfocitario nell’infundibolo e nell’istmo dei follicoli piliferi associato a volte a adenite sebacea linfocitaria. In alcuni casi questa malattia rappresenta il primo stadio di un linfoma epiteliotropo, in altri casi i gatti sopravvivono a lungo senza sviluppare il tumore. Tuttavia, in genere molti muoiono per lo più per cause ancora sconosciute.

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Efficacia dell’olio di semi di ribes nero nella dermatite atopica del cane: uno studio controllato randomizzato in doppio cieco Chiara Noli Med. Vet., Dipl. ECVD - Libero Professionista - Milano

INTRODUZIONE È stato osservato recentemente che acidi grassi essenziali della serie omega-3 e omega-6 hanno notevoli attività antiinfiammatorie in corso di dermatite atopica del cane1. In particolare è stato riportato che prodotti contenenti un rapporto quantitativo tra omega-3 e omega-6 pari o inferiore a uno a cinque2, o contenenti alte percentuali di acido gammalinolenico sono probabilmente i più efficaci3. L’olio di semi ribes nero (Ribespet®, N.B.F. Lanes, Milano) ha queste prerogative.

0 e il giorno 30 gli sperimentatori hanno valutato il prurito, l’eritema e le lesioni cutanee secondo una scala numerica e ne hanno comparato i risultati. Obiettivo dello studio è di valutare la relazione dose-risposta mediante un modello di regressione lineare.

RISULTATI I risultati verranno presentati durante la tavola rotonda.

Qualora la relazione dose risposta non fosse evidente i dati verranno analizzati con un modello di ANOVA seguito da confronti multipli fra i gruppi di trattamento.

MATERIALI E METODI Ventuno cani atopici, rispondenti ai criteri proposti da Willemse4 e non trattati altrimenti sono stati inclusi nello studio e divisi in modo randomizzato in tre gruppi di 7 cani ciascuno. Al primo gruppo è stato somministrato il prodotto testato secondo i dosaggi proposti dalla ditta produttrice (7 gocce ogni 10 kg p.v BID), al secondo il prodotto al doppio della dose e al terzo al triplo della dose.

Tutti gli animali sono stati trattati per 30 giorni. Il giorno

Referenze 1.

2.

3.

Campbell KL, (1993), Clinical use of fatty acid supplements in dogs, Vet Derm, 4: 167-173.

Vaughn DM et al., (1994), Evaluation of effects of dietary n-6 to n-3 fatty acids ratios on leukotriene B synthesis in dog skin and neutrophils, Vet Derm 5: 163-173.

Horrobin DF, (1992), Nutritional and medical importance of gammalinolenic acid, Progr Lip Res, 163-194.

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Workshop sulla terapia delle malattie batteriche Note introduttive e problemi potenziali Chiara Noli Med. Vet., Dipl. ECVD - Libero Professionista - Milano

INTRODUZIONE: LE PIODERMITI E LA LORO TERAPIA Le infezioni batteriche del cane e del gatto sono per lo più sostenute da stafilococchi, e più raramente da streptococchi, Pseudomonas, Proteus o altri batteri. Si riconoscono piodermiti della superficie, come l’intertrigine e l’hot spot, piodermiti superficiali, come la follicolite, l’impetigine, la piodermite mucocutanea e la piodermite superficiale diffusiva, e quelle profonde, come l’acne del mento, la foruncolosi (secondaria a infestazione da demodex o la pododermatite), la piodermite dei calli, i granulomi da leccamento e la piodermite del Pastore Tedesco.

In tutti i casi la terapia si basa sul trattamento antibiotico (secondo antibiogramma per le forme profonde o recidivanti) con cefalosporine di prima generazione (cefadroxil, cefalessina), amoxicillina-acido clavulanico, macrolidi e lincosamidi, o fluorochinolonici. La terapia deve venire protratta per un minimo di 3 settimane nelle forme superficiali (una settimana oltre la guarigione clinica) e di 6 settimane per quelle profonde (2 settimane oltre la guarigione clinica). La terapia locale con shampoo, spray o creme può coadiuvare quella sistemica, e la può occasionalmente sostituire nelle forme dette “della superficie”. In tutti i casi di piodermite è importantissimo, per una buona riuscita della terapia e per evitare le recidive, identificare e correggere una eventuale causa sottostante.

I PROBLEMI LEGATI ALLE PIODERMITI E ALLA LORO TERAPIA Mentre in genere non è un problema riconoscere la piodermite (si eseguono preparati citologici in cui si osserva la presenza di cocchi intracellulari in neutrofili degenerati), esse pongono dei problemi terapeutici a volte difficili da risolvere.

Compliance: Il problema principale è la compliance del proprietario, che tende a interrompere prematuramente la te-

rapia e mettere a repentaglio la riuscita del trattamento. I motivi principali sono: la buona riuscita del trattamento, il costo, la lunghezza eccessiva della terapia e la paura che possa nuovere all’animale, la scomodità della somministrazione bi- o trigiornaliera, la difficoltà a somministrare terapie per os, e gli effetti collaterali (inappetenza e vomito).

Mancata individuazione causa sottostante, con ricaduta della piodermite, dovuta a limitazione di mezzi economici ed esami per ottenere la diagnosi o, nonostante che venga attuato un approccio corretto e gli esami vengano effettuati, mancanza di ottenimento di una diagnosi. Nelle razze a pelo corto si parla di una follicolite idiopatica ricorrente, nel Pastore Tedesco della piodermite profonda del Pastore Tedesco. È possibile che queste malattie siano veramente primarie e associate forse a carenze di difesa sistemiche o focali dei follicoli piliferi. Questi animali sono condannati a terapia intermittente o continua per tutta la vita.

Insufficiente conoscenza dei meccanismi immunologici e/o delle carenze immunitarie, degli squilibri della flora di superficie e dell’ecosistema cutaneo alla base dello sviluppo delle piodermiti, soprattutto quella del Pastore Tedesco, e insufficiente conoscenza di altri meccanismi immunitari, quali ad esempio l’ipersensibilità batterica (se esiste), la presenza di superantigeni batterici (proteina A) e il meccanismo di funzionamento degli autovaccini o di altri farmaci immunostimolatori.

Emergenza resistenza batterica, soprattutto negli animali con piodermiti croniche e recidivanti, in cui a causa dei ripetuti cicli antibiotici vengano selezionati i ceppi batterici più resistenti.

Piodermiti da germi multiresistenti vedi meticillino resistenti sono state descritte in animali di proprietà di personale ospedaliero. Si tratta di germi nosocomiali sensibili solo alla vancomicina trasmessi dal proprietario all’animale, che può a sua volta essere fonte di gravi infezioni in persone deboli o immunodepresse.

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Risultati di uno studio controllato multicentrico sull’effetto del Cefadroxil a dosaggio monogiornaliero nelle piodermiti superficiali e profonde del cane Angelo Oseliero Med. Vet., Libero Professionista - Milano

Le piodermiti del cane, sia superficiali che profonde, sono malattie molto frequenti nella pratica clinica; generalmente l’infezione batterica è sostenuta da Staphilococcus intermedius o da altri batteri beta lattamasi produttori.

Scopo del lavoro è dimostrare l’efficacia del Cefadroxil (Cefa Cure Tabs) in un’unica somministrazione giornaliera comparandola ad una associazione Amoxicillina - Ac. Clavulanico (Synulox) notoriamente efficace per questa patologia.

Nello studio sono stati inclusi 63 cani di razza diversa, 4 soggetti sono stati esclusi, successivamente, per inosservanza del protocollo. Nei 59 cani valutabili, 34 erano maschi e 25 femmine, l’età era compresa fra 9 mesi e 14 anni.

I cani trattati non avevano ricevuto antibiotici, antistaminici, antinfiammatori o cortisonici da almeno 14 giorni; nessuna terapia topica o sistemica era permessa per tutta la durata del trattamento, con la sola esclusione di shampoo terapia (Sebolac - Virbac), antiparassitari e iposensibilizzazione.

I cani sono stati divisi in due gruppi ai quali veniva somministrato, col metodo delle buste chiuse, Cefadroxil alla dose di 20 mg/kg/sid o Amoxicillina - Ac. Clavulanico alla dose di 12.5 mg/kg/bid. Tutti i soggetti venivano valutati al momento dell’ammissione e, successivamente, dopo 7 e 21 giorni (durata minima del trattamento).

In caso di trattamento più prolungato i soggetti venivano rivalutati ogni 14 giorni, per una durata massima del trattamento di 91 giorni.

La risposta alla terapia è stata altresì valutata dopo 7 e 28 giorni dalla fine del trattamento.

In occasione della visita di ammissione veniva prelevato direttamente dalle lesioni, e inviato entro 24 ore in laboratorio, un campione con tamponi sterili e terreno di trasporto per l’esame batteriologico.

RISULTATI Trentaquattro animali affetti da piodermite, superficiale o profonda, sono stati trattati con Cefadroxil e 25 con Amoxicillina - Ac. Clavulanico.

Trentasette cani (63%) mostravano lesioni cliniche compatibili con piodermite superficiale e 22 cani (37%) con piodermite profonda.

Dei cani con piodermite superficiale, 22 sono stati trattati con Cefadroxil e 15 con Amoxicillina - Ac Clavulanico.

Dei cani con piodermite profonda, 12 sono stati trattati con Cefadroxil e 10 co Amocillina - Ac. Clavulanico.

La durata media del trattamento è stata di 30 giorni per entrambi i gruppi; 4 animali (2 per ogni gruppo) sono stati trattati per meno di 21 giorni (14 giorni), 15 animali in ciascun gruppo (Cefadroxil 44%, Amoxicillina - Ac, Clavulanico 60%) non hanno ricevuto alcun trattamento concomitante.

Staphilococcus intermedius è stato isolato, solo o con altri microrganismi, dal 73% dei campioni ottenuti dai soggetti trattati con Cefadroxil e dal 76% dei campioni ottenuti dai soggetti trattati con Amoxicillina - Ac. Clavulanico.

Complessivamente, alla visita di controllo 7 giorni dopo la sospensione del trattamento, il 97% dei soggetti trattati con Cefadroxil è risultato rispondente , con guarigione clinica completa.

Il 96% dei soggetti trattatio con Amoxicillina - Ac. Clavulanico è risultato rispondente, con il 92% di guarigione completa, e il 4% che ha mostrato miglioramento.

Un cane in ciascun gruppo di trattamento è stato classificato come non rispondente.

Ventotto giorni dopo la sospensione del trattamento non ci sono state recidive tra i soggetti trattati con Cefadroxil, mentre 2 soggetti trattati con Amoxicillina - Ac. Clavulanico hanno mostrato ricadute.

DISCUSSIONE Precedenti studi avevano già confermato l’efficacia del Cefadroxil, in corso di infezioni cutanee, al dosaggio di 22-35 mg/kg/bid con percentuale di successo del 90-100%.

La somministrazione monogiornaliera al dosaggio di 22 mg/kg si era già dimostrata efficace con risoluzione del 90% dei casi trattati.

Il presente lavoro conferma i risultati positivi precedentemente ottenuti; la somministrazione monogiornaliera può risultare vantaggiosa per il proprietario ed inoltre ne deriva la possibilità di somministrare il farmaco sempre a stomaco pieno (anche per cani che mangiano una volta al giorno) riducendo i rischi di effetti collaterali di natura gastroenterica.

Il Cefadroxil, in somministrazione monogiornaliera, ha dimostrato un’efficacia paragonabile a quella dell’associazione Amoxicillina - Ac. Clavulanico somministrato ogni 12 ore.

Le cefalosporine sono, pertanto, antibiotici adatti alla terapia delle piodermiti, soprattutto se recidivanti.

Nel presente studio, infatti, si conferma che Cefadroxil somministrato alla dose di 20 mg/kg/24 ore è un trattamento efficace e sicuro nella piodermiti superficiali e profonde, anche ricorrenti, del cane.

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Epidemiologia dell’ansia da separazione in italia Risultati di un’indagine nazionale Maria Cristina Osella Med. Vet. - Dottore di Ricerca in Medicina Interna - Chivasso (Italia)

Riassunto L’ansia da separazione è un disturbo comportamentale del cane di frequente riscontro nella pratica professionale, segnalato in Europa, Stati Uniti e Canada. Alcuni studiosi del settore, rappresentanti di diverse scuole di pensiero, hanno identificato questa patologia definendone le caratteristiche essenziali (manifestazioni, cause, fattori predisponenti).

Obiettivo del presente lavoro è di rilevare alcuni aspetti dell’ansia da separazione in relazione al contesto italiano, a seguito di un’accurata ricerca in campo.

L’indagine è stata svolta utilizzando il Servizio Fax Verde in collaborazione con la Novartis Animal Health Spa, offrendo un servizio di consulenza comportamentale gratuito concernente l’ansia da separazione, attivo dall’1/4/99 al 30/9/99 con esclusione del mese di Agosto. Sono state messe a disposizione dei colleghi una cartella informativa sull’argomento, una scheda di rilievo dati appositamente predisposta, oltre ad alcune indicazioni operative. Nell’ambito di tale iniziativa, sono pervenute da tutta Italia 104 schede di rilievo dati, inviate da 66 colleghi, riguardanti casi di sospetto di ansia da separazione, in cui si richiedeva il parere di un consulente comportamentale in riferimento alla diagnosi (13%), alla terapia (21%) o entrambe (66%). L’ansia da separazione, in seguito alla valutazione comportamentale del cane attraverso l’analisi della scheda, è stata confermata in 69 casi sul totale di 104 casi segnalati (66%), in 20 dei quali (29%) si rileva la presenza di altre manifestazioni tipiche del disturbo oltre alla distruttività, all’inadeguato comportamento eliminatorio ed alle vocalizzazioni. In 35 casi dei 104 complessivi (37%), invece, il sospetto iniziale di ansia da separazione ha poi rivelato la diagnosi di altri disturbi comportamentali. A completamento del consulto, personalizzato per ciascun caso, e su richiesta dei colleghi, sono inoltre state inviate 47 schede di approfondimento sulla terapia comportamentale, 33 sulla terapia farmacologica, 41 sulle possibili complicanze. Nei 69 casi di ansia da separazione, sono quindi stati valutati alcuni fattori ritenuti punti chiave nell’espressione della patologia, in rapporto a quanto segnalato in bibliografia. L’autore sottolinea la necessità di incrementare indagini di questo tipo, al fine di contribuire in modo concreto alla realizzazione di una Clinica Comportamentale italiana, da proporre in un contesto internazionale.

INTRODUZIONE L’ansia da separazione è un disturbo comportamentale del cane di frequente riscontro nella pratica professionale, segnalato in Europa, Stati Uniti e Canada. Si fa riferimento ad una particolare condizione nella quale il cane esprime eccessivo disagio quando avverte la separazione dalle persone cui è affettivamente legato. La separazione può corrispondere ad una reale assenza dei proprietari, che escono effettivamente da casa, o essere avvertita come tale dall’animale, ad esempio perché si lascia il cane in giardino da solo, si va a fare la doccia o ci si corica per il riposo notturno.

Le vocalizzazioni, il comportamento distruttivo rivolto a mobili, vestiti, giocattoli e suppellettili varie, l’eliminazione inappropriata di feci e/o urina sono solo i segni più evidenti dello stato emotivo vissuto dall’animale, che può presentare tremori, tachipnea, tachicardia, ipersalivazione, diarrea e vomito come diretta conseguenza dell’attività del Sistema Ner-

voso Autonomo (SNA), di più difficile rilievo anamnestico (evidenziati mediante riprese con videocamere). Possono comparire episodi di autotraumatismo, quali lesioni da granuloma da leccamento, stereotipie ed altre componenti di sindromi ossessivo-compulsive.

Il termine stesso “ansia da separazione” è universalmente accettato dagli studiosi del settore, perché i comportamenti che ne sono caratteristici, unitamente ai segni ed ai sintomi clinici, riconducono al concetto di ansia, ripreso dalla psichiatria ed adattato alla dimensione veterinaria. In umana, l’ansia può essere definita come l’anticipazione apprensiva di un futuro pericolo o disgrazia, accompagnato da un senso di disforia e/o sintomi somatici di tensione, quali vigilanza e controllo, iperattività del SNA, aumentata attività motoria; il focus ansiogeno può essere insito nell’individuo o esterno ad esso1. Dodman e Mertens classificano l’ansia da separazione nel settore paure e fobie2, e nel dettaglio la considerano una paura legata a particolari situazioni,

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riconducendo il concetto di ansia ad uno stato di paura diffuso e persistente che esiste senza una causa o una minaccia evidenti. Pageat, che propone una diversa classificazione dei disturbi comportamentali rispetto agli autori precedentemente citati, nel caso dell’ansia da separazione conserva la stessa terminologia, definendola come un disturbo estremamente stabile nel tempo; i sintomi, espressione comunque di uno stato ansioso, possono evolvere, con un passaggio da un’ansia di tipo intermittente (caratterizzata da aggressività da paura o da irritazione accompagnata da disturbi neurovegetativi che compaiono in modo intermittente su uno sfondo di ipervigilanza) ad una forma di ansia permanente (che altera in modo continuo il comportamento del soggetto e si manifesta con uno stato di inibizione associato alla comparsa di attività di sostituzione)3.

Tra le possibili cause che originano l’ansia da separazione si annovera : predisposizione ereditaria, carenza di esperienze precoci, eventi traumatizzanti, cambiamenti improvvisi nella composizione del nucleo familiare, stimoli provenienti dall’ambiente esterno e circostanze ambientali non ottimali; inoltre, si devono sempre considerare eventuali problemi nella relazione cane- proprietario di tipo gerarchico, gli effetti del rinforzo anche involontario del comportamento del cane, gli effetti emotivi condizionati4. Infine, costituiscono una categoria a rischio i cani adottati dopo l’abbandono o che sono stati ospitati nei canili1.

Riguardo al concetto di attaccamento, i comportamenti che da questo derivano sono essenziali per gli animali che, come il cane, conducono una vita sociale5, poiché contribuiscono a mantenere compatto il branco, rinsaldando i legami tra i cuccioli e gli adulti da un lato e tra gli individui adulti dall’altro. Nel cane ciò si verifica anche quando animali adulti sono separati dagli individui verso i quali provano attaccamento; nel nostro caso, l’uomo. Infatti, l’attaccamento alle persone, che è positivo per il cucciolo e gli consente un corretto sviluppo, se mantenuto oltre la pubertà e quindi non associato al concetto del distacco, predispone all’iperattaccamento che è alla base dell’ansia da separazione3.

Partendo dai presupposti sopra esposti, sulla base di quanto riportato in letteratura, si presentano i risultati di un’indagine effettuata in Italia per rilevare informazioni sull’incidenza e sulla natura di questa patologia in Italia.

MATERIALI E METODI L’indagine è stata svolta utilizzando il Servizio Fax Verde in collaborazione con la Novartis Animal Health Spa, offrendo un servizio di consulenza comportamentale gratuito concernente l’ansia da separazione, attivo dall’1/4/99 al 30/9/99 con esclusione del mese di Agosto. Ai colleghi libero professionisti è stata inviata una cartella informativa sull’argomento, una scheda di rilievo dati appositamente predisposta, oltre alle indicazioni operative. Sulla base delle risposte del questionario, è stato possibile predisporre un consulto personalizzato, a livello di diagnosi e/o terapia dell’ansia da separazione, eventualmente integrato dal contenuto di schede di approfondimento sul trattamento, comportamentale e farmacologico del disturbo o su questioni di particolari rilievo che possano complicare la risoluzione del problema.

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Successivamente, parte del contenuto delle schede è stato sottoposto ad elaborazione statistica.

RISULTATI E DISCUSSIONE Nell’ambito dell’iniziativa citata, sono pervenute da tutta Italia 104 schede di rilievo dati, inviate da 66 colleghi, riguardanti casi di sospetto di ansia da separazione, in cui si richiedeva il parere di un consulente comportamentale in riferimento alla diagnosi (13%), alla terapia (21%) o entrambe (66%). L’ansia da separazione, in seguito alla valutazione comportamentale del cane attraverso l’analisi della scheda, è stata confermata in 69 casi sul totale di 104 casi segnalati (66%), in 20 dei quali (29%) si rileva la concomitante presenza di alterazioni comportamentali non riferibili a distruttività, inadeguato comportamento eliminatorio e vocalizzazioni (in 11 casi si evidenziano segni di aggressività da dominanza ed in 5 componenti di sindromi ossessivo-compulsive). In 35 casi dei 104 complessivi (37%), invece, il sospetto iniziale di ansia da separazione ha poi rivelato la diagnosi di altri disturbi comportamentali. A completamento del consulto, personalizzato per ciascun caso, e su richiesta dei colleghi, sono inoltre state inviate 47 schede di approfondimento sulla terapia comportamentale, 33 sulla terapia farmacologica, 41 sulle possibili complicanze.

Nei 69 casi di ansia da separazione, sono quindi stati valutati alcuni fattori ritenuti punti chiave nell’espressione della patologia. Da una prima elaborazione dei dati attraverso l’analisi delle frequenze di risposta alle varie domande del questionario, si evidenzia che l’ansia da separazione è presente sia in cani di razza pura (60%) che meticci (40%), interessando soggetti di piccola, media e grossa taglia; un dato preliminare interessante è che si tratta di maschi nel 74% dei casi contro il 26% di femmine.

Valutando l’età dei soggetti del campione, l’8% è < ai 6 mesi, il 26% è di età compresa tra i 6 e i 12 mesi, il 28% tra i 12 e i 24 mesi, il 31 % tra i 2 e gli 8 anni ed il 7% supera gli 8 anni di età; l’età di comparsa del disturbo, considerando che solo attualmente i veterinari sono sensibilizzati al riconoscimento della patologia, è in relazione alle diverse possibili cause che determinano l’insorgenza dell’ansia da separazione4.

Sul rapporto esistente tra le condizioni cliniche del soggetto e l’ansia da separazione, sono state segnalate patologie in atto nel 24% dei cani, di cui 4 casi di autotraumatismo alla coda e/o agli arti, 4 di disturbi gastroenterici (vomito e/o diarrea) e 5 casi di ipersensibilità verso componenti varie (3 alimentari, 1 morso delle pulci, 1 atopia). Tra le patologie pregresse, 24%, si segnalano 4 forme infettive con interessamento del SNC, che potrebbero originare alterazioni comportamentali, e 4 traumi determinanti interventi chirurgici in ambito ortopedico; in tal caso, le cure e l’attenzione dispensate all’animale per necessità contingenti dal proprietario potrebbero costituire un fattore predisponente di iperattaccamento. Interessante osservare che riguardo la provenienza la maggior parte dei cani è stata acquisita da privati (46%), mentre 2 soggetti sono nati da femmine già presenti nel nucleo familiare; il 17% proviene da allevamenti, il 13% da ne-

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gozi, l’11% da strutture rifugio; infine, l’11% dei cani è stato raccolto dalla strada. Questi dati suggeriscono che, non solo sarebbe opportuno predisporre programmi di prevenzione dell’ansia da separazione nel caso degli animali abbandonati, che costituiscono una categoria a rischio per questo disturbo, ma che occorrerebbe maggior attenzione alle modalità di gestione del cane nelle sue prime fasi di vita, soprattutto nelle delicate fasi del distacco dalla madre e dal resto della cucciolata e dell’inserimento del soggetto nel nuovo nucleo familiare. L’età di acquisizione offre altri spunti di riflessione: al momento dell’adozione, il 24% dei cani esaminati ha 2 mesi, il 20% è nella classe compresa tra 1 e 2 mesi, l’8% ha meno di 1 mese di età; il 31% ha un’età inclusa tra 2 e 6 mesi, il 5% tra 6 mesi e 1 anno ed infine il 9% supera l’anno di età; ciò implica che, nel rispetto delle diverse fasi di sviluppo del cucciolo, altri fattori sono importanti nell’insorgenza della patologia.

L’esame della composizione del nucleo familiare (1 persona: 14%, 2 persone: 26% e >2 persone: 60%) ed il fatto che in 10 casi sono presenti almeno un altro cane ed in 14 altri animali, per la maggior parte gatti, suggerisce che non sono solitudine e noia il nocciolo del problema dell’ansia da separazione.

In 12 casi il cane ha seguito un corso di addestramento definito di base, in 3 dei quali la finalità è stata la correzione dei segni dell’ansia da separazione; ciò evidenzia come l’addestramento non sia l’equivalente dell’intervento comportamentale in sede terapeutica e come non possa evitare l’insorgenza del disturbo, che non è una carenza educativa ma un fenomeno ansioso5 . In tutti i casi esaminati, la frequenza e/o la durata delle uscite del cane nell’arco della giornata risultano compatibili con una buona gestione dell’animale, così come non si registrano casi in cui il cane viene lasciato da solo per periodi di tempo obiettivamente inaccettabili.

Probabilmente in ambito urbano le conseguenze dell’ansia da separazione sono meno tollerate (ad esempio le vocalizzazioni), ma dalla ricerca effettuata non sono contemplate solo le grandi città (34%), ma anche città medie (32%) e piccole (24%), nonché contesti rurali (10%); se da un lato il 70% dei casi fa riferimento ad una soluzione abitativa di tipo condominiale, il 30% dei cani con ansia da separazione vive in una casa singola con spazi in esterno. Ciò sembra evidenziare che quelli che possono essere considerati elementi indispensabili per un buon rapporto cane-proprietario dal punto di vista umano non impediscono ad un soggetto ansioso di sviluppare la patologia.

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Infine, è stata analizzata la presenza di aggressività verso i familiari (cane che ha morsicato e/o minacciato di morsicare un membro della famiglia), di risposte riferite a paura (di rumori forti, botti o spari, temporali, folla, traffico) e di entrambe le componenti in uno stesso soggetto. Il risultato è del 17% per l’aggressività, del 33% per la paura e del 23% per entrambe, offrendo nuovi spunti di riflessione .

CONCLUSIONI Sulla base dei risultati emersi dall’indagine si possono trarre alcune considerazioni conclusive.

Innanzitutto, appare evidente che la problematica dei disturbi comportamentali del cane interessa non solo medici veterinari che hanno un interesse particolare per l’argomento, ma è ormai avvertita come una reale esigenza professionale; l’approccio ai disturbi comportamentali, a livello di diagnosi e terapia, sta acquistando una sua dimensione nell’ambito della clinica intesa in senso tradizionale e trova una suo valido riscontro nella pratica ambulatoriale per chi si occupa di animali d’affezione.

Secondariamente, se da un lato è opportuno seguire in modo scrupoloso l’aggiornamento scientifico sull’argomento grazie al contributo dei ricercatori, esponenti di diverse scuole di pensiero, che stanno attivamente operando nel settore, dall’altro si devono approfondire le conoscenze della realtà in cui si opera, e cioè del contesto italiano, al fine di elaborare i presupposti di una clinica comportamentale da proporre nel panorama culturale internazionale.

Bibliografia 1.

2.

3.

4.

5.

Overall KL, (1997), Clinical Behavioral Medicine for Small Animals, Mosby, St.louis, 209-250.

Dodman NH, Shuster (eds), (1998), Psychopharmacology of Animal Behavior Disorders, Blackwall Science, 122-140.

Pageat P, (1999), Patologia Comportamentale del cane, Le Point Vétérinaire Italie srl, Milano, 282-289.

Askew HR, (1996), Treatment of behavior problems in dogs and cats, Blackwall Science, Oxford, 216-227.

Voith VL, Borchelt PL, (1985), Separation Anxiety in dogs, Compend Contin Educ Pract Vet (1):42-52.

Si desidera ringraziare la Novartis Animal Health Spa per la disponibilità alla collaborazione ed i colleghi che hanno aderito all’iniziativa per il loro inestimabile contributo.

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Vet applications of the internet Internet utile per il medico veterinario

Yannick Poubanne Med. Vet., MS - Versailles - FRANCIA

Riassunto Alla fine del ’99, 200 milioni di persone sono correntemente connesse ad Internet, ma che si può dire dei veterinari?

In realtà, si sta affacciando all’orizzonte una nuova ed attiva comunità di “vetnauti”, che sta allargando il campo della nostra comunicazione. Ma cosa stanno davvero facendo? Si tratta di un lavoro utile ed economicamente conveniente? E che livello tecnico è realmente necessario? Per dare una risposta a queste domande, passeremo in rassegna, on line ed in modo interattivo, come effettuare la prima connessione e che cosa possiamo trovare su Internet. Quindi, illustreremo le possibilità di comunicazione con altre persone e la ricerca di specifiche informazioni, come un articolo scientifico. Infine, ultimo ma non ultimo, mostreremo come realizzare, da Internet nel nostro computer, un database bibliografico utilizzabile nel nostro word processor.

End of 99, 200 millions people are currently connected to the internet, but what about the vets? Actually, a new and active community of vetnautes is appearing, enlarging the field of our communication. But what are they really doing?

Is it useful and cost effective? And which technical level is really required? To answer these questions, we will review on lineand interactively, how to first get connected and what we can find on the internet. Then the communication with people and the search for a specific information like an scientific article will be demonstrated. Last but not least, we will present how to create from the internet into our computer, a bibliographic data base available in our word processor.

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Lesioni neoplastiche in piccoli roditori, lagomorfi e furetti: aspetti clinici e quadri microscopici a confronto Paola Roccabianca* & Co.§ * Med. Vet., Istituto di Patologia e Igiene Veterinaria, Facoltà di Medicina Veterinaria, Agripolis, Legnaro (PD) § Liberi professionisti (iscritti SIVAE e non)

Riassunto Sono stati esaminati 25 campioni di lesioni neoplastiche pervenute all’Istituto di Patologia e Igiene Veterinaria nell’arco del biennio 1998-1999 ed inviati da liberi professionisti per la maggior parte membri SIVAE. I campioni provenivano da 14 criceti, 3 scoiattoli, 2 conigli ed un furetto. Le biopsie fissate in formalina sono state incluse in paraffina e tagliate in sezioni di 5 µm colorate con ematossilina ed eosina. La descrizione e la diagnosi istologica preliminare sono state descritte secondo il modello di refertazione codificato dall’A.F.I.P. (Armed Forces Institute of Pathology). In alcuni casi la colorazione immunoistochimica è stata affiancata all’esame istologico. Il pannello di reagenti utilizzato è illustrato in tabella n.1. L’identificazione di molecole proteiche specifiche ha permesso una diagnosi precisa di linfoma in 4 casi e di definire il citotipo di origine in casi di neoplasia indifferenziata (3 casi). I tumori più comuni osservati nel criceto si sono rivelati quelli di origine epiteliale follicolare (6 casi) seguiti da adenomi/adenocarcinomi di origine apocrina (3 casi) e linfomi (2 casi). Nei casi esaminati, la serie di anticorpi applicata ha dimostrato una reattività sovrapponibile a quella codificata nei piccoli animali e nell’uomo e si è dimostrata di utile ausilio nella diagnostica oncologica di piccoli roditori, furetti e lagomorfi.

Tabella 1 - Pannello di anticorpi Ac Primario*

Ag Riconosciuto

Cellule Identificate

Vimentina

Vimentina

Cellule Mesenchimali

Citocheratina A1/A3

A1-cheratine acide A3- chreatine basiche

Cellule Epiteliali cheratinizzate e non

Fattore VIII

Fattore di Von Wilebrand

Endoteli Vasali Piastrine

GFAP

Proteina Acida Fibrillare della Glia

Astrociti Cellule Ependimali

SMA

α-Actina Muscolare Liscia

Fibrocellule Muscolari Lisce

A452

CD3-ε

Linfociti T

Hm57

CD79-a

Linfociti B

Filamenti Intermedi

Antigeni Leucocitari

* Tutti gli anticorpi sono prodotti della Compagnia Dako (Glostrup, Danimarca)

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INTRODUZIONE La casistica oggetto della presente relazione raccoglie 25 campioni di lesioni neoplastiche pervenute all’Istituto di Patologia e Igiene Veterinaria nell’arco del biennio 19981999 ed inviati da liberi professionisti per la maggior parte membri SIVAE. I casi provengono da 14 criceti, 3 scoiattoli, 2 conigli ed un furetto. La presentazione clinica verrà illustrata dai rispettivi veterinari ed affiancata ai relativi quadri istologici.

Il materiale bioptico pervenuto fissato in formalina è stato incluso in paraffina e tagliato in sezioni di 5 micron colorate con ematossilina ed eosina. La descrizione e la diagnosi istologica sono state refertate secondo il metodo codificato dall’A.F.I.P. (Armed Forces Institute of Pathology). Tale schema di refertazione impone una “Descrizione Istologica” del campione, seguita da una “Diagnosi Morfologica” che definisce il tipo di neoplasia.

In alcuni casi la colorazione immunoistochimica è stata affiancata all’esame istologico. L’immunoistochimica per-

mette di identificare la presenza di molecole proteiche specifiche espresse dalle cellule neoplastiche. L’identificazione di questi antigeni permette una diagnosi più precisa della neoplasia (es. linfoma di tipo B o T) o definisce il citotipo di origine in casi di neoplasia indifferenziata. Tuttavia, per essere di ausilio nella diagnostica oncologica è importante che l’indagine immunoistochimica sia condotta con un numero sufficientemente ampio di anticorpi (pannello) che permetta la distinzione tra i diversi tipi cellulari (cellule muscolari, cellule epiteliali, fibroblasti, ecc.). Il pannello di reagenti utilizzato è riassunto in tabella n.1 e comprende un totale di sette anticorpi in grado di identificare filamenti intermedi citoplasmatici ed antigeni della membrana linfocitaria. Nei casi esaminati, la serie di anticorpi applicata ha dimostrato una reattività sovrapponibile a quella codificata nei piccoli animali e nell’uomo ed si è dimostrata come utile ausilio per la diagnosi di linfoma B e T così come nell’identificazione del citotipo di origine nei casi di lesioni indifferenziate. I dati clinici, diagnostici e di follow-up potranno fornire utili indicazioni prognostiche nelle specie esaminate.

Tabella 1 - Pannello di anticorpi Ac Primario*

Ag Riconosciuto

Cellule Identificate

Vimentina

Vimentina

Cellule Mesenchimali

Citocheratina A1/A3

A1-cheratine acide A3- chreatine basiche

Cellule Epiteliali cheratinizzate e non

Fattore VIII

Fattore di Von Wilebrand

Endoteli Vasali Piastrine

GFAP

Proteina Acida Fibrillare della Glia

Astrociti Cellule Ependimali

SMA

α-Actina Muscolare Liscia

Fibrocellule Muscolari Lisce

A452

CD3-ε

Linfociti T

Hm57

CD79-a

Linfociti B

Filamenti Intermedi

Antigeni Leucocitari

* Tutti gli anticorpi sono prodotti della Compagnia Dako (Glostrup, Danimarca)

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SCHEDE DEI CASI Ciascun caso è descritto in una scheda che comprende: 1) il numero di riferimento 2)

il libero professionista responsabile

3)

una breve descrizione clinica

4)

una descrizione istologica

5)

la tabella di reattività immunoistochimica (se applicata)

6)

la diagnosi morfologica

7)

un eventuale commento

BE 1/99 Veterinario: Dr Fabrizio Benini Segnalamento: Scoiattolo giapponese (Eutamias sibiricus), F, 7 anni

Descrizione Clinica Lesione alla base dell’orecchio destro a rapido accrescimento, asportata chirurgicamente e recidivata nei successivi 30 giorni. La lesione si presenta di 3 X 3 cm, verrucosa, alopecica. La lesione si estende fino al periostio dell’osso temporale.

Al taglio il nodulo era caratterizzato da una superficie bianca, omogenea.

Descrizione Istologica Cute e cartilagine auricolare: La lesione è composta da un nodulo dermico non capsulato composto da elementi cellulari che infiltrano i tessuti circostanti compresa la cartilagine auricolare invasa in più punti. La neoplasia è composta da una diffusa e densa popolazione di cellule a volte organizzata in lobuli delimitati da un fine stroma vascolare. Gli elementi neoplastici si presentano di forma rotondocellulare e caratterizzati da anisocariosi ed anisocitosi. Le cellule hanno margini distinti, citoplasma abbondante, debolmente eosinofilo, granulare. I nuclei sono voluminosi, da rotondi ad ovali, occasionalmente indentati con cromatina finemente addensata. I nucleoli sono raramente evidenti. Sono presenti cellule multinucleate atipiche di 25-50 micron, che contengono da due a otto nuclei e che variano da una a 25 per campo.

Le figure mitotiche, per lo più metafasi tipiche ed atipiche, variano da 2 a 5 per campo 400X. Comprese nella neoplasia si osservano aree multifocali di necrosi coagulativa.

Sono presenti emboli intravascolari di cellule neoplastiche atipiche.

Colorazione IHC: Diagnostica Vimentina Citocheratina Actina CD3 CD79a

+ +

Diagnosi Morfologica: Cute Auricolare, cartilagine e piani ossei: Linfoma di tipo B

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BE 2/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Criceto Russo (Phodopus sungours), F, 7 mesi

Descrizione Clinica Voluminoso nodulo cutaneo in regione toracica con estesa area di ulcerazione superficiale. Il centro della lesione è cistico e contiene materiale giallastro friabile (detrito necrotico).

Descrizione Istologica Cute: Il campione è costituito da un voluminoso nodulo di 2,5 X 2 cm, non capsulato, con estesa area necrotica centrale. La lesione è localizzata nel derma e si estende al sottocute ed i piani muscolari profondi. La superficie cutanea appare estesamente ulcerata. Attorno alla zona necrotica centrale si osserva una popolazione di cellule che si espandono centripetamente e che sono irregolarmente organizzate in fasci o aggregati immersi in stroma fibroso sia denso che di tipo mixoide. In alcune aree è possibile mettere in evidenza cellule atipiche di forma cuboidale in singolo strato che si organizzano a formare strutture tubulari o papillari con un lume centrale. Le cellule neoplastiche sono caratterizzate da elevato pleomorfismo, di forma da fusata a stellata, occasionalmente poligonale con margini indistinti ed hanno una moderata quantità di citoplasma eosinofilo. I nuclei sono da rotondi ad irregolari, vescicolosi, con cromatina granulare marginata ed uno o due nucleoli eosinofili assai voluminosi. Sono presenti numerose figure mitotiche tipiche ed atipiche (in media 3 per campo a 400X).

Si osservano inoltre aree multifocali di necrosi ed emorragie.

Colorazione IHC: Diagnostica Vimentina Citocheratina Actina F VIII GFAP

+ -

Diagnosi Morfologica: Cute torace: Carcinoma anaplastico a cellule fusate

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BE 4/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Scoiattolo Giapponese (Eutamias sibiricus), F

Descrizione Clinica Fegato: lesione nodulare biancastra sulla superficie di 0.3 mm.

Cute: Massa bilobata a livello di cute ascellare associata a necrosi e dermatite. Il nodulo più voluminoso ha dimensioni di 3,5 X 2,5 cm con superficie necrotica. Al taglio il nodulo presenta aspetto variegato con aree giallastre di necrosi coagulativa e spazi cistici.

Descrizione Istologica Cute: Lesione bilobata che si estende dal derma sottoepidermico ai piani muscolari e delimitata da una sottile capsula che in numerose aree appare infiltrata da cellule neoplastiche. Le cellule che compongono la neoplasia sono organizzate in lobuli che sono occasionalmente caratterizzati da un’area necrotica centrale e sembrano essere circondate da cellule fusate di tipo mioepiteliale.

Le cellule che compongono il tumore hanno un elevato rapporto nucleo-citoplasmatico, sono voluminose (20-30 micron), poligonali, a margini indistinti, citoplasma abbondante, omogeneo, debolmente eosinofilo. In alcuni casi si osserva metaplasia squamosa. I nuclei sono ovali od irregolari con cromatina granulare o finemente dispersa ed un evidente, singolo nucleolo centrale rotondo o triangolare. Rare le figure mitotiche.

Numerosi emboli di cellule neoplastiche sono presenti nei lumi vascolari.

Fegato: Formazioni nodulari multiple non demarcate, non capsulate e che infiltrano il parenchima epatico. I noduli sono composti da cellule poligonali, voluminose (20-45 micron), con margini netti e citoplasma eosinofilo. I nuclei hanno forma variabile, cromatina diffusa e nucleoli eosinofili rotondi evidenti. Al centro del nodulo più voluminoso è presente una estesa area di necrosi.

Colorazione IHC: Utile conferma Vimentina Citocheratina Actina F VIII GFAP

+ -

Diagnosi Morfologica: Cute ascellare: Carcinoma mammario solido del tipo comedocarcinoma Fegato: Epatocarcinoma

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BE 5/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Criceto Dorato (Mesocricetus auratus) F, 2 anni

Descrizione Clinica Lesione ulcerata cutanea a livello di arto posteriore

Descrizione Istologica Cute: La superficie epidermica è ulcerata e caratterizzata da aree di colonizzazione batterica.

La lesione principale è organizzata in strutture lobulari che infiltrano il pannicolo adiposo ed i piani muscolari. La neoplasia è composta da cellule epiteliali ben differenziate, organizzate a formare strutture nodulari composte da epitelio pluristratificato con un evidente strato granulare e con n raccolta di cheratina lamellare centrale.

Nelle porzioni più basali dell’epitelio si osservano occasionali mitosi con morfologia normale.

In alcune aree il tumore acquista caratteristiche morfologiche di sdifferenziazione ed è composto da strutture epiteliali organizzate in cordoni radiali di cellule epiteliali cuboidali con elevato rapporto nucleo-citoplasmatico ed immerse in materiale mixoide.

Colorazione IHC: Non effettuata

Diagnosi Morfologica: Cute: tumore epiteliale di origine follicolare con due tipi di differenziazione: A) Tricolemmoma di tipo istmale invasivo B) Tricoblastoma “ribbon type”

Commento: L’aspetto istologico delle lesioni potrebbero essere riferibili ad una eziologia virale da Papovavirus.

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BE18/99 Veterinario: Dr.ssa Marta Avanzi Campione: Criceto Dorato (Mesocricetus auratus) F, 14 mesi

Descrizione Clinica Lesione di 1,5 X 0.5 cm di diametro a carico della regione fronto-nasale che invade i piani ossei sottostanti.

Lesioni nodulari multifocali di aspetto biancastro a livello del parenchima epatico.

Descrizione Istologica Cutane: Lesione nodulare a sede sottocutanea non ben demarcata che si estende ed invade i piani ossei frontali. Il tumore è composto da strutture epiteliali di aspetto cistico contenenti abbondante quantità di cheratina lamellare. La parete è costituita da epitelio pluristratificato cheratinizzato con un evidente strato granuloso. Due formazioni presentano una parete in diretta continuazione con l’epidermide a formare un poro (cheratoacantoma). Le cellule epiteliali che compongono il tumore sono di forma irregolare, presentano elevato rapporto nucleo-citoplasmatico ed evidenti reperti di anisocitosi ed anisocariosi. I nuclei sono da rotondi ad ovali, con cromatina finemente reticolare e sono spesso distorti soprattutto negli strati basali a causa della perdita di inibizione da contatto (nuclear molding). Sono presenti numerose cellule epiteliali apoptotiche e discheratotiche.

Alcuni piccoli gruppi di cellule di aspetto meno differenziato (basalioide) formano piccoli lobuli che si distaccano dalla parete delle strutture principali.

Il tumore è associato ad intesa desmoplasia e alla presenza di iperemia ed emorragie stromali.

Fegato: Infiltrati di linfoblasti sono presenti nella maggior parte degli spazi portali.

Milza: Imponente ematopoiesi extramidollare in assenza di una distinzione della polpa bianca in strutture follicolari. A livello perivascolare si osserva una popolazione monomorfa di linfoblasti.

Colorazione IHC: Non eseguita

Diagnosi Morfologica: Cutane fronto nasale: Cheratoacantoma invasivo Fegato e Milza: Lesioni compatibili con iniziale Linfoma

Commento: Nel criceto sia i linfomi che i tumori follicolari sembrano avere una eziologia virale riferibile a Papovavirus

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BE 21/99 Veterinario: Dr. Fabrizio Benini Soggetto: Criceto Dorato (Mesocricetus auratus), M

Descrizione Clinica Neoformazione cutanea a sede parascrotale. Il tumore è recidivato nella sede di asportazione 5 mesi dopo l’intervento.

L’animale ha sviluppato una lesione di 0,4 cm di diametro nella regione del fianco caratterizzata da centro necrotico.

All’esame autoptico si evidenzia una lesione epatica nodulare.

Descrizione Istologica Cute e derma (Prima asportazione): l’epidermide è caratterizzata da croste siero-cellulari superficiali, ipercheratosi ed acantosi in associazione alla presenza di Demodex criceti negli strati cheratinici superficiali.

Derma intermedio e profondo sono completamente sostituiti da una densa popolazione di cellule fusate organizzate in fasci irregolari o perpendicolari. Le cellule atipiche sono caratterizzate da margini indistinti, abbondante citoplasma eosinofilo, occasionalmente vacuolizzato e nuclei singoli o multipli, ovali, caratterizzati da indentature e ripiegature. La cromatina è finemente granulare e i nucleoli sono multipli, poco evidenti. Comprese nella popolazione neoplastica si osservano occcasionali cellule multinucleate con nuclei organizzati in fila indiana. Sono presenti numerose cellule apoptotiche e mitosi tipiche e atipiche che variano da 0 a 6 per campo a 400 ingrandimenti.

Cute cicatrice (5 mesi dopo): la recidiva presenta caratteristiche sovrapponibili a quelle della lesione iniziale.

Cute Fianco (5 mesi dopo): lesione sovrapponibile alle precedenti e riferibile ad una metastasi a distanza.

Fegato: compresa nel parenchima epatico si osserva una lesione focale ben delimitata composta da strutture irregolari di aspetto tubulare rivestite da un epitelio in singolo stato di tipo cilindrico ciliato con nuclei polarizzati alla base. Le cellule non presentano reperti di anaplasia. Il lume contiene del materiale eosinofilo e concrezioni brunastre (materiale biliare calcificato?)

Colorazione IHC: Diagnostica Vimentina Citocheratina Actina F VIII GFAP

+ + -

Diagnosi Morfologica: Cute: Tumore a cellule fusate riferibile a Leiomiosarcoma recidivante e metastatizzante Dermatite perivascolare con acantosi epidermica irregolare associate a Demodex criceti Fegato: Colangioma

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BE 22/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Scoiattolo giapponese (Eutamias sibiricus), M, 5 anni

Descrizione Clinica Neoformazione regione paranale

Descrizione Istologica Cute: Nodulo non capsulato, infiltrante composto da lobuli contenenti strutture ghiandolari caratterizzate da un lume centrale in cui si raccoglie materiale eosinofilo amorfo e cheratinico. Il tumore si estende dal derma superficiale ai piani muscolari profondi.

Le strutture ghiandolari sono composte da due popolazioni cellulari, la prima caratterizzata da cellule poligonali, voluminose (30-40 micron) con abbondante citoplasma chiaro, finemente vacuolizzato. Il nucleo è rotondo, centrale, con un evidente nucleolo, basofilo. Questa popolazione è caratterizzata da moderati reperti di anisocitosi ed anisocariosi. Una seconda e più numerosa componente del tumore è caratterizzata da cellule cuboidali, di piccole dimensioni (10-15 micron), con elevato rapporto nucleo citoplasmatico, margini indistinti e citoplasma basofilo, nucleo rotondo caratterizzato da cromatina addensata. All’interno di questa seconda popolazione oltre ad anisocariosi ed anisocitosi si osservano numerose mitosi tipiche ed atipiche. Sono inoltre presenti numerose figure apoptotiche, vasi neoformati, e flogosi neutrofilica che in alcuni lumi si presenta associata a colonie batteriche.

Colorazione IHC: Non eseguita

Diagnosi Morfologica: Cute/Mucosa paranale: Adenocarcinoma delle ghiandole epatoidi

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BE 23/99 Veterinario: Dr. Fabrizio Benini Segnalamento: Criceto Dorato (Mesocricetus auratus), M, 1 anno

Descrizione Clinica Noduli cutanei dorsali multipli

Descrizione Istologica Cute: Vengono esaminati tre noduli con caratteristiche morfologiche sovrapponibili. I noduli sono localizzati a livello del derma ed invadono il pannicolo adiposo ed i muscoli pellicciai.

I noduli sono composti da lobuli spesso con un centro necrotico o da strutture con un lume centrale contenente cheratina lamellare. Le cellule che compongono la neoplasia hanno un elevato rapporto nucleo citoplasmatico e si organizzano in strutture di aspetto rotondeggiante o conico con un abbozzo di papilla indicative di una differenziazione verso la formazione di bulbi piliferi (pilomatricioma).

Le strutture follicolari più differenziate che compongono il tumore presentano una parete di epitelio pluristratificato in cui uno degli strati contiene cellule con granuli di tricoialina corrispondenti alla lamina fibrosa esterna del follicolo (tricolemmoma istmale).

I follicoli più differenziati infiltrano il derma ed il pannicolo adiposo mentre la maggior parte delle strutture meno differenziate si organizza attorno ad una formazione cistica centrale contenente lamelle di cheratina e con una parete di epitelio pluristratificato cheratinizzato (cisti cheratinica infundibolare).

In un nodulo sono presenti strutture follicolari atipiche composte da strati di cellule chiare (ricche di glicogeno), con granuli di cheratoialina e circondate da una membrana basale riferibili a ticolemmoma di tipo inferiore.

Colorazione IHC: Utile conferma Vimentina Citocheratina Actina F VIII GFAP

+, positività variabile in base alla differenziazione cellulare.

-

Diagnosi Morfologica: Cute dorso: Tricoepiteliomi multipli, variante di tipo cistico

Commento: L’aspetto istologico delle lesioni, lo sviluppo in animale giovane e la presenza di lesioni multiple progressive potrebbero essere riferibili ad una eziologia virale da Papovavirus

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BE 24/99 Veterinario: Dr. Gabriele Ghisleni Segnalamento: Criceto Dorato (Mesocricetus Auratus), M, 1 anno,

Descrizione Clinica Noduli cutanei multipli in sede dorsale

Descrizione Istologica 1) Uno dei noduli a sede dermica è ben delimitato, non capsulato e composto da lobuli densamente cellulari delimitati da una membrana basale. I lobuli sono fromati da cellule epiteliali con elevato rapporto nucleo-citoplasmatico ed organizzate in strati concentrici a palizzata. I margini delle cellule sono indistinti con scarsa quantità di citoplasma debolmente acidofilo, e nuclei voluminosi, ovali, spesso deformati (nuclear molding) a causa della perdita di inibizione da contato, di aspetto vescicoloso e cromatina finemente granulare. Sono presenti occasionali figure mitotiche di aspetto atipico.

2) Un nodulo in sede dermo-epidermica è di tipo cistico a contenuto cheratinico. La parete della struttura cistica è in continuazione con l’epidermide a formare un poro. L’epitelio si presenta pluristratificato con uno spesso strato superficiale di cellule paracheratotiche, e numerosi strati di cellule di aspetto basale, a margini indistinti, citoplasma eosinofilo, nucleo da rotondo ad ovale ed un evidente nucleolo o piccoli nucleoli multipli. Negli strati meno differenziati sono presenti occasionali figure mitotiche corrispondenti a metafasi normali che variano da 0-4 per campo a 400 ingrandimenti Dalla parete della lesione principale si dipartono centrifugamente lobuli che presentano differenziazione in senso follicolare.

Il tumore è accompagnato da desmoplasia e flogosi neutrofilica.

Colorazione IHC: Non eseguita.

Diagnosi Morfologica: Cute dorso: 1) Tricoepiteliomi multipli, variante di tipo inferiore 2) Cheratoacantoma

Commento: L’aspetto istologico delle lesioni, lo sviluppo in animale giovane e la presenza di lesioni multiple progressive potrebbero essere riferibili ad una eziologia virale da Papovavirus

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BE 26/99 Veterinario: Dr.ssa Marta Avanzi Soggetto: Criceto Dorato (Mesocricetus auratus), M, 2 anni

Descrizione Clinica Organi vari

Descrizione Istologica Cuore, orecchietta sinistra: La parete ed il lume dell’orecchietta sono completamente sostituiti da un’infiltrato densamente cellulare. Le cellule sono pleomorfe, da rotonde a poligonali, di 25-30 micron di diametro, con margini indistinti ed una moderata quantità di citoplasma schiumoso. I nuclei sono centrali o paracentrali di forma da rotonda ad irregolare, spesso trifogliati od indentati, vescicolosi con cromatina marginata ed uno o più nucleoli di forma irregolare.

Le figure mitotiche variano da 1 a 6 per campo a 400 ingrandimenti, e sono occasionalmente atipiche. Sono presenti numerose aree di necrosi, infiltrati di neutrofili e cellule apoptotiche Rene: iperemia, microemorragie ed un’area infartuale di vecchia data con fibrosi e macrofagi attivati Fegato: lieve dilatazione dei sinusoidi epatici e delle vene centrolobulari con stasi ematica.

Polmone: aree di iperemia e di enfisema Milza: lieve iperplasia della polpa bianca

Colorazione IHC: Diagnostica Vimentina Citocheratina CD3 CD79a

variabile positività, debole +

Diagnosi Morfologica: Cuore: Linfoma di tipo B

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BE 28/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Criceto Dorato (Mesocricetus auratus), M, 2 anni

Descrizione Clinica Cute ispessita e presenza di una massa toracica.

Descrizione Istologica Cute: Il derma ed il pannicolo adiposo sono sostituiti da un infiltrato densamente cellulare composto da elementi rotondocellulari caratterizzati da spiccato pleomorfismo ed una quantità di citoplasma variabile, debolmente eosinofilo, finemente granulare. I nuclei sono rotondi od ovali, con indentature, cromatina marginata ed uno o due evidenti nucleoli eosinofili, rotondi ed occasionalmente di forma triangolare. Le mitosi, spesso atipiche, variano da 4 a 8 per campo a 400 ingrandimenti. Sono presenti numerose cellule apoptotiche.

Massa Toracica: associata al grasso bruno è presente una popolazione di cellule rotonde dalla morfologia sovrapponibile a quella della cute.

Colorazione IHC: Diagnostica Vimentina Citocheratina CD3 CD79a

variabile positività, debole + -

Diagnosi Morfologica: Cute e Massa Toracica: Linfoma di tipo T

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BE 30/99 Veterinario: Dr. Alessandro Bellese Soggetto: Coniglio (Oryctolagus cuniculus), Mc, 7 anni

Descrizione Clinica Massa cutanea in regione toracica destra delle dimensioni di 5 cm di diametro

Descrizione Istologica Cute: La lesione si estende dal sottocute al pannicolo adiposo ed infiltra i piani muscolari. Il tumore è organizzato in fasci paralleli o irregolarmente orientati composti da una popolazione pleomorfa di cellule fusate con margini indistinti, abbondante citoplasma eosinofilo, occasionalmente fibrillare. I nuclei sono ovali, vescicolosi, spesso caratterizzati da indentature e restringimenti multipli. La cromatina è marginata e si osservano uno o due nucleoli poco evidenti. Sono presenti cellule multinucleate con nuclei organizzati in fila indiana ed aree in cui le cellule hanno aspetto rotondeggiante con vacuoli perinucleari.

Le mitosi variano da 2 a 4 per campo a 400 ingrandimenti e sono spesso atipiche.

Colorazione IHC: Diagnostica Vimentina Citocheratina Actina F VIII GFAP

+ -

Diagnosi Morfologica: Cute: Leiomiosarcoma indifferenziato

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BE 31/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Criceto Russo (Phodopus sungorus), F

Descrizione Clinica Massa ascellare

Descrizione Istologica Cute: la neoformazione di 2 X 1,5 cm di diametro si estende dal derma ai piani muscolari. La lesione è composta da numerose strutture cistiche delimitate da una parete epiteliale composta da epitelio pluristratificato. Queste lesioni formano strutture trabecolari sostenute da una moderata quantità di stroma fibrovascolare spesso di aspetto mixoide e ricco di cellule da fusate a stellate che ricordano cellula mioepiteliali. Le cellule che compongono la parete delle lesioni sono da cubiche a colonnari, organizzate in più strati, con margini indistinti, citoplasma eosinofilo, vacuolizzato.

Nella porzione apicale che si affaccia nel lume il citoplasma è caratterizzato da proiezioni citoplasmatiche che si staccano dalla superficie cellulare e compongono parte del materiale contenuto nel lume dei tubuli. Si osserva la presenza di vescicole pinocitotiche e ciglia. I nuclei sono rotondi, spesso impaccati e deformati a causa della perdita di inibizione da contatto (nuclear molding), con cromatina marginata e nucleolo singolo, centrale, raramente evidente.

Il lume delle cisti contiene materiale eosinofilo amorfo.

Incluse nello stroma si osservano inoltre strutture tubulari atipiche.

Colorazione IHC: Vimentina Citocheratina Actina F VIII GFAP

+, più intensamente le cellule apicali -, + le cellule mioepiteliali -

Diagnosi Morfologica: Cute: Adenocarcinoma tubulare di tipo apocrino. Le origini più probabili sono sudoripara o mammaria)

Commento: I tumori di origine mammaria sono considerati assai rari nel Criceto a differenza del topo e del ratto. I tumori delle ghiandole sudoripare apocrine non sono stati segnalati in letteratura.

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BE 33/99 Veterinario: Dr.ssa Marta Avanzi Segnalamento: Criceto Dorato (Mesocricetus auratus), F, 1 anno

Descrizione Clinica Noduli multipli sottocutanei di 1-4 mm, alcuni con un punto nero al centro.

Descrizione Istologica Cute e sottocute: Il campione è costituito da noduli dermici multipli organizzati in lobuli. I lobuli sono composti da cellule che formano strutture follicolari riferibili a diverse porzioni del follicolo pilifero. Si riconoscono lobuli solidi composti da cellule basofile caratterizzate da elevato rapporto nucleo-citopaslmatico che tendono a formare bulbi piliferi (pilomatricioma). In altre aree si osservano formazioni composte da epitelio pluristratificato composto da cellule epiteliali con citoplasma chiaro (ricco di glicogeno) e contenenti granuli di cheratoialina assimilabili ai cheratinociti della porzione infundibolare del follicolo (Tricolemmoma inferiore).

La maggior parte delle strutture neoplastiche si organizza attorno ad una formazione cistica centrale contenente cheratina lamellare e composta da una parete di epitelio pluristratificato cheratinizzato (tricolemmoma istmale e cisti cheratiniche infundibolari).

Colorazione IHC: Utile conferma Vimentina Citocheratina Actina F VIII GFAP

+ -

Diagnosi Morfologica: Cute: Tricoepiteliomi multipli, variante di tipo cistico

Commento: Lâ&#x20AC;&#x2122;aspetto istologico delle lesioni, lo sviluppo in animale giovane e la presenza di lesioni multiple progressive potrebbero essere riferibili ad una eziologia virale da Papovavirus

40° Congresso Nazionale SCIVAC

BE36/99 Veterinario: Dr. Massimo Millefanti Segnalamento: Furetto (Mustela putorius furo), Femmina, 20 mesi

Descrizione Clinica Linfonodi mediastinici, reni, milza aumentati di volume. Sospetto di linfoma

Descrizione Istologica Gli organi inviati non sono identificabili, il parenchima è completamente sostituito da una densa popolazione monomorfa di cellule atipiche, rotonde con margini distinti ed elevato rapporto nucleo citoplasmatico.

Le cellule sono di piccole dimensioni (8-15 micron) con scarso citoplasma basofilo. Il nucleo è rotondo, centrale, con cromatina addensata, spesso marginata con nucleoli singoli paracentrali o multipli periferici. Le figure mitotiche sono rare ma il tumore è caratterizzato da un elevato indice apoptotico.

Sono presenti numerosi macrofagi in attiva fagocitosi di residui cellulari soprattutto di materiale nucleare (cellule di Flemming) e che danno al linfoma un aspetto a cielo stellato (Burkitt type). Sono inoltre presenti aree multifocali di necrosi.

Colorazione IHC: Utile ausilio Vimentina Citocheratina CD3 CD79a

+/-

Diagnosi Morfologica: Organi Linfoidi: Linfoma multicentrico diffuso, di tipo B

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BE37/99 Veterinario: Dr. Gabriele Ghisleni Segnalamento: Coniglio (Oryctolagus cuniculus), nano, M, 1 anno, vasectomizzato

Descrizione Clinica Il soggetto ha presentato ad un anno di età un nodulo cutaneo di 0,6 per 0,4 cm nella regione toracica dorsale. Il nodulo è stato rimosso. All’età di 6 anni l’animale ha sviluppato aumento di volume del testicolo sinistro. Veniva effettuata la castrazione dell’animale.

Descrizione Istologica Cute: La lesione di forma nodulare è localizzata al derma, non incapsulata ma ben delimitata e composta da lobuli densamente cellulari circondati da una minima quantità di stroma fibroso. In alcune aree si osservano cordoni composti da 2-6 strati di cellule incluse in stroma da fibroso a mixoide. Le cellule hanno un elevato rapporto nuclo-citoplasmatico, sono di forma cubica a margini indistinti con scarso citoplasma lievemente eosinofilo. I nuclei sono rotondi od ovali con cromatina addensata ed uno o due nucleoli. Le figure mitotiche variano da 0-1 per campo a 400 ingrandimenti.

Il tumore contiene infiltrati multifocali di linfociti maturi.

Testicolo Sinistro: Il testicolo appare completamente sostituito da una lesione di forma nodulare, non capsulata, composta da cellule rotonde caratterizzate da spiccato pleomorfismo. Le cellule infiltrano l’albuginea ed occasionalmente si osservano come emboli neoplastici nei vasi.

Le cellule hanno dimensioni variabili da 10 a 50 micron di diametro, rotonde o poligonali con quantità di citoplasma variabile omogeneo o finemente granulare, debolmente basofilo. I nuclei sono rotondi, con cromatina reticolare ed un nucleolo singolo, piccolo, centrale. Sono presenti occasionali cellule mutlinucleate atipiche. Le figure mitotiche variano da 0 a 4 per campo a 400 ingrandimenti.

All’interno della neoplasia sono presenti aggregati di linfociti maturi.

Testicolo Destro: Il testicolo destro appare completamente sostituito da una densa popolazione di cellule voluminose, poligonali. La neoplasia presenta numerosi capillari. Le cellule neoplastiche hanno bordi distinti, abbondante citoplasma granulare, eosinofilo. I nuclei sono da rotondi ad ovali, con cromatina finemente addensata ed un piccolo nucleolo centrale. I tubuli seminiferi localizzati alla periferia della lesione sono atrofici e non presentano cellule delle linea seminale.

Colorazione IHC: Non eseguita

Diagnosi Morfologica: Cute: Aree di Basalioma ed aree di tricoblastoma cordoniforme (ribbon type) Testicolo sinistro: Seminoma diffuso con emboli neoplastici vascolari Testicolo destro: Interstizioma diffuso

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BE 41/99 Veterinario: Dr. Fabrizio Benini Segnalamento: Criceto Dorato (Mesocricetus auratus), M, 20 mesi

Descrizione Clinica Lesione cistica a livello del fianco.

Descrizione Istologica Cute fianco: Voluminosa massa subepidermica, non delimitata e composta da numerosi spazi cistici a contenuto di cheratina lamellare. La parete di queste strutture è composta da un epitelio pluristratificato che contiene uno strato granuloso. Una delle più voluminose è caratterizzata da un poro a contatto con la superficie epidermica.

Nello spessore della parete di alcune formazioni cistiche e nel derma adiacente sono presenti strutture follicolari neoformate di aspetto differenziato che presentano una parete di epitelio pluristratificato in cui uno degli strati contiene cellule con granuli di tricoialina corrispondenti alla lamina fibrosa esterna del follicolo (tricolemmoma istmale).

Nella cheratina accumulata in grande quantità nel lume del cheratoacantoma sono evidenziabili numerosissime colonie batteriche di cocchi, numerose formazioni rotondeggianti da cui si diparte spesso una ifa (miceti) e numerosi aggregati di neutrofili degenerati.

Colorazione IHC: Non eseguita

Diagnosi Morfologica: Cute Fianco: Cheratoacantoma, cisti cheratiniche follicolari istmali e aree multiple di tricolemmoma istmale Complicati da irruzione secondaria di batteri e miceti.

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BE42/99 A e B Veterinario: Dr. Fabrizio Benini Segnalamento: Due soggetti A e B di Criceto Dorato (Mesocricetus auratus), F, 18 mesi (sorelle)

Descrizione Clinica Entrambi i soggetti hanno sviluppato contemporaneamente una neoformazione sottocutanea a sede ascellare. A) tra ascella sinistra e sterno e B) tra collo e sterno, ripiena di liquido.

Descrizione Istologica Le lesioni presentano reperti istologici sovrapponibili.

Cute: Lesioni irregolarmente nodulari a sede dermica, ben demarcate ma non incapsulate. Entrambe sono composte da tubuli ed occasionali lobuli immersi in una moderata quantità di stroma fibrovascolare che in A) si presenta mixoide ed in B) più fibroso. Il lume dei tubuli contiene materiale proteinaceo ed occasionali neutrofili e macrofagi.

Le strutture tubulari sono composte da cellule epiteliali da cilincriche a cubiche organizzate in uno o più strati. Le cellule epiteliali hanno una moderata quantità di citoplasma eosinofilo e quelle apicali sono caratterizzate da proiezioni citoplasmatiche che si staccano dalla superficie cellulare e compongono parte del materiale contenuto nel lume dei tubuli.

I nuclei sono da rotondi ad ovali, spesso polarizzati alla base, con cromatina reticolare ed un singolo nucleolo centrale basofilo. Non evidenti figure mitotiche.

Colorazione IHC: Non eseguita

Diagnosi Morfologica: A) Cute ascella: Adenoma tubulare apocrino B) Cute collo: Adenoma tubulare apocrino L’aspetto delle cellule indica una possibile origine da ghiandole sudoripare o ghiandola mammaria

Commento: L’aspetto istologico identico delle lesioni, il simultaneo sviluppo, la giovane età e la parentela potrebbero indicare una base genetica (mutazioni di oncogeni od oncosoppressori) o virale delle neoplasie.

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1) Tabella Casi Tumori Follicolari a Probabile base virale in Criceti Caso

Soggetto

Sede/Distribuzione

Diagnosi

BE5

Criceto Dorato, F, 2 anni

Cute arto posteriore

Tricolemmoma di tipo istmale invasivo Tricoblastoma “ribbon type”

BE18

Criceto Dorato, F, 14 mesi

Cute fronto nasale

Cheratoacantoma

BE23

Criceto Dorato, M, 1 anno

Cute Dorso, les. multiple

Tricoepitelioma variante di tipo cistico

BE24

Criceto Dorato, M, giovane

Cute Dorso, les. multiple

Tricolemmoma di tipo inferiore Cheratoacantoma

BE33

Criceto Dorato, F, 1 anno

Cute dorso, les. multiple

Tricoepitelioma variante di tipo cistico

BE41

Criceto Dorato, F, 1 anno

Cute fianco

Cheratoacantoma Tricolemmoma istmale Cisti cheratiniche

Sede/Distribuzione

Diagnosi

2) Tabella di Casi di Neoplasie in Criceti Caso

Soggetto

Tumori epiteliali BE2

Criceto Russo, F, 7 mesi

Cute Torace

Carcinoma anaplastico a cellule fusate

BE31

Criceto Russo, F

Cute ascellare

Adenocarcinoma tubulare apocrino

BE42 A

Criceto Dorato, F, 18 mesi

Cute Ascellare

Adenoma tubulare apocrino

BE42 B

Criceto Dorato, F, 18 mesi

Cute Cute Ventro-laterale

Adenoma tubulare apocrino

BE5

Criceto Dorato, F, 2 anni

Fegato e milza

Linfoma (non tipizzato)

BE26

Criceto Dorato, M, 2 anni

Orecchietta Dx Cuore

Linfoma di tipo B

BE28

Criceto Dorato, M, 2 anni

Cute e Massa Toracica

Linfoma di tipo T

BE21

Criceto Dorato, M

Cute

Leiomiosarcoma / Metastasi

BE21

Criceto Dorato, M

Fegato

Colangioma

Linfomi

Altro

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3) Tabella di Casi di Neoplasie in altre specie Caso

Soggetto

Sede/Distribuzione

Diagnosi

Scoiattolo giapponese, f, 7 anni Scoiattolo giapponese, F Scoiattolo giapponese, M, 5 anni

Padiglione auricolare Cute ascellare Cute paranale

Linfoma di tipo B Comedocarcinoma mammario Adenocarcinoma ghiandole paranali

Coniglio, Mc, 7 anni Coniglio nano M, 1 anno

Cute torace Cute torace Testicolo sinistro Testicolo destro

Leiomiosarcoma Basalioma Tricoblastoma cordoniforme Seminoma diffuso metastatizzante Interstizioma diffuso

Organi linfoidi multipli

Linfoma multicentrico di tipo B

Scoiattoli BE1 BE4 BE22 Conigli BE30 BE37

Furetti BE36

Furetto, F, 20 mesi

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Sarcomi indotti da trauma Giorgio Romanelli Med. Vet., Dipl. ECVS - Libero Professionista - Milano

Riassunto INTRODUZIONE La possibilità di trasformazione sarcomatosa di lesioni ossee benigne in seguito a reazione infiammatoria cronica è nota. Sono stati infatti segnalati tumori mesenchimali in corrispondenza di impianti metallici posizionati per il trattamento di fratture, di osso precedentemente irradiato, di protesi totale d’anca, di trapianti corticali, e in seguito a biotrasformazione di esostosi cartilaginee multiple.

L’incidenza di sarcomi è stata stimata in un numero variabile da 5 a 10 per 10.000 fratture o da 10 a 30 ogni 10.000 fratture trattate con mezzi di sintesi interna. Sono colpiti generalmente cani di grossa taglia e i segmenti ossei più comunemente interessati sono il femore, la tibia e l’omero, cosa che li differenzia dai tumori ossei spontanei.

EZIOLOGIA E PATOGENESI Nel tentativo di spiegare la formazione di sarcomi secondari ad impianti, sono state prese in considerazione varie ipotesi, accentrate sulla possibilità o meno dell’impianto metallico di essere direttamente responsabile della carcinogenesi locale.

Seguendo il processo dall’inizio si nota che già al momento del trauma si può verificare un’anossia più o meno lunga di alcuni tessuti. L’osteosintesi apporta normalmente una piccola carica batterica che si nasconde in prossimità dell’impianto come infezione criptica o con la conseguenza di un vero e proprio processo di osteomielite, mantenuta in attività dal mezzo di sintesi, soprattutto se instabile.

A questo si aggiungano una possibile eliminazione di ioni metallici come conseguenza del processo di corrosione e il tentativo di incapsulamento da parte dell’organismo, responsabile della componente infiammatoria presente istologicamente in questi tumori.

Se la consolidazione non avviene normalmente si evidenziano inoltre una minore tensione di ossigeno tessutale e un continuo turnover cellulare nel tentativo di portare il focolaio a guarigione. Tutte queste complicanze possono condurre ad un ulteriore processo di danno cellulare fino ad arrivare alla neoplasia.

DIAGNOSI In tutti i casi in cui ci sia anche solo il sospetto di un sarcoma secondario è necessario ottenere 2 radiogrammi ortogonali del raggio osseo interessato ed eseguire una biopsia ossea con un ago di Jamshidi o con piccolo trapano di Michelle.

L’interpretazione dei preparati istologici può essere complicata dalla necrosi e dall’ infiltrato infiammatorio normalmente presente.

Se la diagnosi è confermata istologicamente, prima del trattamento definitivo è necessario ottenere tre radiografie toraciche in proiezione laterale destra, sinistra e dorsoventrale.

TRATTAMENTO Il trattamento non differisce da quello standard per gli osteosarcomi spontanei e consiste nell’amputazione seguita da 3-6 trattamenti con un sale di platino (cisplatino o carboplatino).

PROGNOSI La prognosi ricalca quella degli osteosarcomi spontanei ed è normalmente infausta con una sopravvivenza ad un anno di meno del 10% dei soggetti in caso di amputazione senza chemioterapia adiuvante.

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INTRODUZIONE La possibilità di trasformazione sarcomatosa di lesioni benigne in seguito a reazione infiammatoria cronica è nota.

Sono stati infatti segnalati tumori mesenchimali secondari a trauma a carico del globo oculare nel gatto 1, in corrispondenza di una garza lasciata accidentalmente in cavità addominale 2, nel punto di inserimento di un pace-maker cardiaco 3, in caso di granulomi provocati dal parassita Spirocerca Lupi, in seguito alla penetrazione di corpi estranei e, per quanto riguarda le lesioni ossee, in corrispondenza di impianti metallici posizionati per il trattamento di fratture 4,5,6,7,8,9,10 , di osso precedentemente irradiato 11, di protesi totale d’anca 12,13, di trapianti corticali 14, e in seguito a biotrasformazione di esostosi cartilaginee multiple 15.

L’incidenza di sarcomi è stata stimata in un numero variabile da 5 a 10 per 10.000 fratture o da 10 a 30 ogni 10.000 fratture trattate con mezzi di sintesi interna., sono colpiti generalmente cani di grossa taglia e i segmenti ossei più comunemente interessati sono il femore la tibia e l’omero, cosa che li differenzia dai tumori ossei spontanei.

(Tabella 1)

EZIOLOGIA E PATOGENESI Nel tentativo di spiegare la formazione di sarcomi secondari ad impianti, sono state prese in considerazione varie ipotesi, accentrate sulla possibilità o meno dell’impianto metallico di essere direttamente responsabile della carcinogenesi locale Più precisamente, i fattori inizianti considerati sono stati: 1. L’impianto metallico 2. La corrosione metallica e i suoi bioprodotti 3. La reazione elettrolitica fra impianti di diverse marche

4. Il danno tessutale legato al trauma e all’intervento 5. L’alterazione cellulare secondaria ad una consolidazione non corretta 6. L’osteomielite Nei primi 3 casi l’impianto deve essere considerata la vera causa mentre nei secondi 3 agisce solo mantenendo e amplificando l’effetto tessutale. Alcuni sali metallici, quali quelli di cromo, nickel e cobalto sono effettivamente carcinogenetici, ma sembra improbabile che, in assenza di corrosione, l’impianto possa liberarne una quantità pericolosa così come è vero che due metalli diversi usati assieme in ambiente acido possono effettivamente generare una reazione galvanica con la liberazione di sali, ma questo è improbabile se vengono usati impianti che pur non appartenendo alla stessa marca siano composti dallo stesso metallo, generalmente acciaio 316L o titanio.

L’importanza dell’alterazione cellulare secondaria ad una consolidazione non corretta e dall’osteomielite giocano sicuramente un ruolo importante. È noto che, perlomeno nell’uomo, la possibilità di sviluppare un’osteosarcoma nei soggetti adulti è maggiore in ossa già colpite da altre malattie, soprattutto il morbo di Paget, nelle quale si assiste ad un continuo rimaneggiamento.

L’osteomielite non può che incitare un turnover cellulare ancora più tumultuoso per cercare di arrivare comunque alla consolidazione anche in presenza di infezione ed effettivamente in una buona parte dei casi riportati si è assistito ad un guarigione ossea complicata da componente settica.

L’ipotesi più probabile è la compartecipazione di fattori che hanno comunque in comune la derivazione da una guarigione ossea disturbata.

Seguendo il processo dall’inizio si nota che già al momento del trauma si può verificare un’anossia più o meno lunga di alcuni tessuti.

Tabella 1 Tumore osseo primitivo

Sarcoma da impianto

Alano, San Bernardo, Levriero Irlandese, Terranova

Nessuna identificata

Taglia

Grossa

Grossa

Sesso

Prevalentemente maschi

Prevalentemente maschi

Età media d’ insorgenza

7 anni

7 anni

Punto d’insorgenza

Metafis

Diafisi

Segmenti ossei

Radio, omero, tibia e femore

Femore, omero, tibia e radio

Tipo di tumore più comune

Osteosarcoma

Osteosarcoma

Infiammazione

No

Si

Necrosi

No o scarsa

Si

Razza

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L’osteosintesi apporta normalmente una piccola carica batterica che si nasconde in prossimità dell’impianto come infezione criptica o con la conseguenza di un vero e proprio processo di osteomielite , mantenuta in attività del mezzo di sintesi, soprattutto se instabile.

A questo si aggiungano una possibile eliminazione di ioni metallici come conseguenza del processo di corrosione e il tentativo di incapsulamento da parte dell’organismo, responsabile della componente infiammatoria presente istologicamente in questi tumori.

Se la consolidazione non avviene normalmente si evidenziano inoltre una minore tensione di ossigeno tessutale e un continuo turnover cellulare nel tentativo di portare il focolaio a guarigione.

Tutte queste complicanze possono condurre ad un ulteriore processo di danno cellulare fino ad arrivare alla neoplasia.

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PROGNOSI La prognosi ricalca quella degli osteosarcomi spontanei ed è normalmente infausta con una sopravvivenza ad un anno di meno del 10% dei soggetti in caso di amputazione senza chemioterapia adiuvante.

Bibliografia 1 2

3 4 5

DIAGNOSI In tutti i casi in cui ci sia anche solo il sospetto di un sarcoma secondario è necessario ottenere 2 radiogrammi ortogonali del raggio osseo interessato ed eseguire una biopsia ossea con un ago di Jamshidi o con piccolo trapano di Michelle.

L’interpretazione dei preparati istologici può essere complicata dalla necrosi e dall’ infiltrato infiammatorio normalmente presente.

Se la diagnosi è confermata istologicamente, prima del trattamento definitivo è necessario ottenere tre radiografie toraciche in proiezione laterale destra, sinistra e dorsoventrale.

6

7

8

9 10

11

12

TRATTAMENTO 13

Il trattamento non differisce da quello standard per gli osteosarcomi spontanei e consiste nell’amputazione seguita da 3-6 trattamenti con un sale di platino (cisplatino o carboplatino).

14 15

Dubielzig R.R. Ocular sarcoma following trauma in three cats. JAVMA, 1984, vol. 184, n°5, 3.

Pardo A.D., Adams W.H., McCracken M.D. et al. Primary jejunal osteosarcoma associated with a surgical sponge in a dog. JAVMA, 1990, vol 196, n°6, 3.

Rowland P.H., Moise S.N., Severson D. Myxoma at the site of subcutaneous pace-maker in a dog. JAAHA, 1991, vol. 27, n°6, 649-651.

Fry P.D., Jukes H.F. Fracture associated sarcoma in the cat. JSAP, 1995, 36, 124-126.

Stevenson S., Hohn R.B., Pohler O.E.M. et al. Fracture associated sarcoma in the dog. JAVMA, 1982, vol.180, n° 10, 5 Banks W.C., Morris E., Herron M.R., Green R.W. Osteogenic sarcoma associated with internal fixation in two dogs. JAVMA, 1975, vol.

167, n° 2, 7, Madewell B.R., Pool R.R., Leughton R.L. Osteogenic sarcoma at the site of a cronic nonunion fracture and internal fixation device in a dog. JAVMA, vol.171, n° 2, 1977 Sinibaldi K.R., Pugh J., Rosen H., Liu S.K. Osteomyelitis and neoplasia associated with use of the Jonas intramedullary splint in small animals. JAVMA, 1982, vol 181, n°9, 11 Bennet D., Campbell J.R., Brown P. Osteosarcoma associated with healed fractures. JSAP, 1979, 20, 13-18 Herring M.E., Smith G.K., Nunamaker D.M. Eight cases of implant associated osteosarcoma in the dog. ACVS Meeting 1986 in Veterinary Surgery, vol. 15, 196, 123 Thrall D.E., Goldshmidt M.H., Evans S.M., Dubielzig R.R. et al. Bone sarcoma following orthovoltage rdiotherapy in two dogs. Veterinary Radiology, 1983, vol. 24, n°4, 169-173 Marcellin-Little D.J., DeYoung D.J., Thrall D.E., Merril C.L. Osteosarcoma at the site of bone infarction associated with total hip arthroplasty in a dog. Veterinary Surgery, 1999, vol. 28, 54-60 Roe S.C., DeYoung D.J., Weinstock D., Kyles A. Osteosarcoma eight years after total hip arthroplasty. Veterinary Surgery, 1996, vol. 25, 70-74 Vasseur P.B., Stevenson S. Osteosarcoma at the site of a cortical bone allograft in a dog. Veterinary Surgery, 1987, vol. 16, 70-74 Doige C.E., Pharr J.W., Withrow S.J. Chondrosarcoma arising in multiple cartilagineous exostoses in a dog. JAAHA, 1978, vol. 14, 605-611

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Ruolo dell’ecografia nella diagnosi dell’ipercalcemia Roberto Santilli Med. Vet., Dipl. E.C.V.I.M.-C.A. (Cardiology) - Samarate (Varese)

Riassunto L’esame ecografico delle paratiroidi unitamente ai rilievi emato-chimici, quali calcio totale, calcio ionizzato, fosforo, cloro, Cl/P, paratormone (PTH), proteine simili al PTH (PTHrP), vitamina D e frazione d’escrezione del fosforo urinario, spesso permette di differenziare le diverse cause di ipercalcemia nel cane. Queste ultime includono: iperparatiroidismo primario, ipercalcemia da malignità, ipervitaminosi D, insufficienza renale cronica (iperparatiroidismo secondario e terziario), ipoadrenocorticismo, insufficienza renale acuta, iperparatiroidismo secondario nutrizionale, ipercalcemia da malattie sistemiche, osteoporosi generalizzata, disidratazione e ipotermia.

L’esame ecografico delle paratiroidi viene effettuato con sonde ad elevata frequenza (7,5 - 10 MHz), previa tricotomia e applicazione del gel conduttore di ultrasuoni. In primo luogo viene identificata l’arteria carotide comune attraverso una scansione longitudinale del collo, con un’angolatura di 45 gradi tra il piano parasaggitale e quello dorsale.

Inclinando successivamente la sonda medio-ventralmente, in posizione mediale rispetto all’arteria carotide comune appare la ghiandola tiroidea con un ecogenicità minore dell’avventizia ma maggiore rispetto ai muscoli circostanti. In condizioni normali le paratiroidi non vengono solitamente visualizzate avendo un diametro longitudinale ≤ 2 mm.

Nelle situazioni ipercalcemiche dove il PTH è basso, le paratiroidi sono ipoplasiche e quindi non visibili (ipervitaminosi D, ipercalcemia indotta da neoplasie maligne o patologie granulomatose sistemiche). Nell’insufficienza renale cronica con iperparatiroidismo secondario le paratiroidi sono solitamente tutte iperplastiche (tra 2 e i 4 mm), mentre nell’iperparatiroidismo primario da adenoma o adenocarcinoma secernente PTH, viene solitamente isolata una sola ghiandola con diametro longitudinale maggiore di 4 mm. Solo in rari casi più ghiandole iperplastiche possono essere evidenti come nel caso dell’iperparatiroidismo primario in corso di neoplasie endocrine multiple (MEN) tipo I e IIa o iperparatiroidismo terziario renale.

Sfortunatamente l’esame delle paratiroidi risulta complesso e correlato all’abilità dell’operatore, perciò il mancato ritrovamento di una o più ghiandole non esclude un’eventuale iperplasia o neoplasia secernente.

INTRODUZIONE Le più comuni cause d’ipercalcemia nel cane includono: l’iperparatiroidismo primario, l’ipercalcemia da malignità, l’ipervitaminosi D (avvelenamento da rodenticida), l’insufficienza renale cronica (iperparatiroidismo secondario e terziario), l’ipoadrenocorticismo, l’insufficienza renale acuta, l’iperparatiroidismo secondario nutrizionale, l’ipercalcemia da malattie sistemiche, l’osteoporosi generalizzata, la disidratazione e l’ipotermia. 2-4,7,9,12-16,18 L’ipercalcemia da neoplasie maligne è indotta da un’azione osteolitica locale (mieloma multiplo e disturbi mieloproliferativi), da metastasi a distanza (adenocarcinoma mammario, tiroideo, squamocellulare e liposarcoma), o mediata da sostanze umorali sistemiche quali le proteine simili al PTH (PTHrP) come nel caso del linfoma, delle masse mediastiniche, del mieloma multiplo, dell’adenocarcinoma dei sacchi anali, delle neoplasie delle cellule interstiziali testicolari, del timoma, del colangiocarcinoma, dell’adenocarcinoma nasale, del fibrosarcoma e del carcinoma epidermoide

polmonare. 4,9,13-14,16 L’aumento del PTHrP similmente a quello del PTH induce attività osteoclastica generalizzata, riassorbimento di calcio a livello renale con riduzione del riassorbimento di fosforo, ma a differenza del PTH riduce l’attività osteoblastica, inibisce l’escrezione di bicarbonato a livello renale e non stimola la formazione di calcitriolo mancando di un’attività sulla 1-alpha-idrossilasi. L’ipervitamonosi D è solitamente secondaria ad un sovradosaggio del farmaco nel trattamento dell’ipoparatiroidismo o all’ingestione di rodenticida contenente colecalciferolo, ne consegue un aumento del riassorbimento del calcio e del fosforo intestinale e renale, un intensa azione osteoclastica con iperfosfatemia, ipercalcemia e gravi calcificazioni distrofiche.7,12 L’ipoadrenocorticismo è una causa relativamente frequente d’ipercalcemia nel cane e nel gatto ed è causata dell’iperprotidemia secondaria alla disidratazione e all’emoconcentrazione, alla ritenzione renale di calcio, alla riduzione del tasso di filtrazione glomerulare (GFR) e alla riduzione dell’effetto anti-vitamina D dei corticosteroidi. Oltre all’ipercalcemia presente nel 33 % dei casi di Addison, le altre alte-

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razioni caratteristiche di ipoadrenocorticismo primario sono iperfosfatemia, iponatriemia, ipocloremia e ipercaliemia. 15 Ipercalcemia può essere presente durante la fase diuretica dell’insufficienza renale acuta per mobilizzazione dai tessuti di calcio e fosforo. Solo l’11 – 14% dei casi d’insufficienza renale cronica presentano ipercalcemia, nella restante parte diversi gradi d’iperparatiroidismo secondario inducono normocalcemia con riduzione della frazione ionizzata e iperfosfatemia. Diverse ipotesi sono state postulate per spiegare l’incremento di PTH in corso d’insufficienza renale cronica quali la riduzione della degradazione dell’ormone da parte del tubulo, la riduzione del GFR che comporta un aumento del fosforo, una contemporanea discesa dei livelli plasmatici di calcio con stimolazione delle paratiroidi a produrre PTH, una deficienza di calcitriolo con resistenza dello scheletro al PTH ed elevazione della concentrazione di calcitriolo necessaria a bloccare lo stimolo alla produzione di PTH. 4,12 I rari casi d’ipercalcemia presenti in corso d’insufficienza renale cronica possono essere causati da un’elevata sensibilità dei tessuti al calcitriolo rimanente, disidratazione, acidosi metabolica con passaggio del calcio dalla forma legata a quella ionizzata, aumento dei fosfati e citrati mediato dal PTH o dalla secrezione autonoma di PTH da parte di un adenoma paratiroideo (iperparatiroidismo terziario). 4,12 Nell’iperparatiroidismo primario l’eccesso di PTH e causato dalla presenza di un adenoma, adenocarcinoma o iperplasia di una o più ghiandole paratiroidee (MEN I e IIa).16 La forma più comune è l’adenoma o l’iperplasia delle cellule principali paratiroidee con solo il 4 % d’incidenza di neoplasie maligne. 2,4,12,18 Nel cane è stata descritta la presenza di adenomi ectopici paratiroidei 14 ma non di neoplasie non paratiroidee secernenti PTH. L’eccesso di PTH promuove l’attività osteoclastica, aumenta il riassorbimento renale di calcio, riduce il riassorbimento tubulare di fosforo, stimola la produzione renale di calcitriolo con maggior riassorbimento di calcio e fosforo intestinale e ulteriore attività osteoclastica. Un’ultima causa poco comune di ipercalcemia è quella secondaria a malattie sistemiche batteriche o fungine 3, ed è causata da un incremento dei livelli e dell’attività della vitamina D. I pazienti con ipercalcemia persistente vanno divisi in due gruppi secondo la presenza di azotemia. Il primo gruppo include pazienti con ipercalcemia, normo o ipofosfatemia e non-azotemici (ipercalcemia da malignità, iperparatiroidismo primario, ipervitaminosi D iniziale). Il secondo gruppo include invece pazienti ipercalcemici, iperfosfatemici e azotemici (ipercalcemia da malignità, iperparatiroidismo primario, ipervitaminosi D avanzata, insufficienza renale cronica primaria). L’ipercalcemia sostenuta induce calcinosi diffuse particolarmente a livello renale dove il calcio si deposita a livello di giunzione corticomidollare, spazio interstiziale, membrana basale periglomerulare e parete vasale con grave deterioramento della funzione renale. 10-12 La presenza di azotemia in corso d’ipercalcemia comporta, quindi, un grosso dilemma nel diagnosticare la patologia primaria.

Attraverso il segnalamento e l’anamnesi raramente viene identifica l’eziologia dell’ipercalcemia, mentre i rilievi emato-chimici e l’esame ecografico possono aiutare nel discriminare le diverse cause.

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RILIEVI EMATO-CHIMICI Il profilo biochimico, la concentrazione ormonale e l’esame delle urine risultano di particolare interesse nello studio delle cause d’ipercalcemia. Il calcio sierico è composto per il 50 % dalla forma legata alle proteine, per il 44 – 50 % dalla forma ionizzata biologicamente attiva e da una rimanente parte complessa. Il calcio ionizzato e il calcitriolo sono i più importanti inibitori del rilascio di PTH da parte delle paratiroidi. Il fosforo possiede un effetto diretto positivo sulla secrezione di PTH con iperplasia delle paratiroidi ed indiretto attraverso la riduzione del calcio ionizzato (equazione legge della massa). Il calcio ionizzato è, per cui, direttamente correlato alla titolazione del PTH fatta eccezione in presenza di acidosi metabolica che riduce l’affinità del calcio per le proteine. La contemporanea presenza di azotemia eleva la concentrazione plasmatica del fosforo per riduzione del GFR ed altera la fosfaturia (frazione di escrezione del fosforo urinario) impedendo l’analisi di questi parametri che, in assenza d’insufficienza renale, sono strettamente correlati alle variazioni del PTH o delle PTHrP. 5-6,18 La titolazione del PTH viene effettuata attraverso l’esame della forma intatta dell’ormone (iPTH) perché subisce meno gli effetti dell’azotemia. In condizioni normali un aumento del calcio ionizzato deve essere accompagnata da una riduzione del iPTH a testimonianza di una normale funzionalità paratiroidea.17 La misurazione delle PTHrP plasmatiche nella loro forma intatta o frammentaria può permettere di svelare la presenza di neoplasie causanti ipercalcemia, queste proteine possono essere in minima parte presenti anche in condizioni normali perché prodotte dalle paratiroidi, possono aumentare in caso di azotemia (PTHrP frammenti) ed essere assenti in caso di neoplasie non secernenti PTHrP. 12 Recentemente è possibile titolare la concentrazione plasmatica della 25-idrossivitamina D e 1-25-idrossivitamina D. Un aumento del colecalciferolo indica un probabile avvelenamento da rodenticidi, mentre un aumento del calcitriolo e strettamente correlato con un eccesso di PTH ma non di PTHrP, quindi in condizioni quali iperparatiroidismo primario, alcune neoplasie come il linfoma, ipervitaminosi D e malattie granulomatose, una sua riduzione è invece caratteristica dell’insufficienza renale cronica e altre neoplasie maligne.

Aumenti dell’urea e della creatinina possono essere il problema primario o causati dall’ipercalcemia con riduzione del GFR per la disidratazione o la vasocostrizione renale. L’incidenza di azotemia è minima in corso di iperparatiroidismo primario, mentre è frequente in caso di ipercalcemia da neoplasie, ipoadrenocorticismo, ipervitaminosi D e insufficienza renale cronica. Il cloro può risultare aumentato in corso di iperparatiroidismo primario per la riduzione del riassorbimento di bicarbonati mediato dal PTH a livello di tubulo renale ed una conseguente ritenzione di cloro con sviluppo di acidosi tubulare ipercloremica e Cl/P > 33. L’esame delle urine mostra spesso urine diluite per l’interferenza mediata dal PTH sulla vasopressina o per la presenza d’insufficienza renale cronica e cristalluria di ossalato o fosfato di calcio.

Le classiche anomalie in corso d’ipercalcemia indotta da neoplasie maligne sono un aumento della concentrazione

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plasmatica del calcio totale e ionizzato, il fosforo è solitamente normale o basso ad eccezione sia presente insufficienza renale secondaria, iPTH ridotto, PTHrP elevate, colecalciferolo normale, mentre calcitriolo basso, normale o elevato a seconda della produzione da parte del tumore. 6,9-12 In caso d’intossicazione da rodenticida il calcio totale, ionizzato e il fosforo sono elevati, iPTH e PTHrP sono ridotti, mentre il calcitriolo può essere normale o ridotto a seconda del grado d’insufficienza renale secondaria presente. 7 Durante l’ipoadrenocorticismo si sviluppa un’ipercalcemia con calcio ionizzato normale, il fosforo varia a seconda del GFR, iPTH e la vitamina D sono normali, le PTHrP possono essere aumentate per la contemporanea presenza d’insufficienza pre-renale, altre alterazioni presenti includono iperazotemia, ipercaliemia, iponatriemia, ipocloremia. 15 In corso d’insufficienza renale cronica primaria il calcio totale è normale, basso (10 %), o alto (20 %), mentre la forma ionizzata è bassa nel 40 % dei casi. In presenza di azotemia il fosforo, il iPTH e le PTHrP risultano aumentate, il colecalciferolo è normale mentre il calcitriolo è ridotto. 10-12 L’iperparatiroidismo primario in assenza d’iperazotemia è caratterizzato da un aumento del calcio totale e ionico, fosforo normale o ridotto, colecalciferolo normale e calcitriolo aumentato. 2,18 Nelle malattie granulomatose sistemiche la produzione extrarenale di calcitriolo induce un aumento del calcio totale e ionizzato, del fosforo con una riduzione del iPTH e delle PTHrP. 3

ESAME ECOGRAFICO L’ecografia può assumere un valore diagnostico in corso di ipercalcemia attraverso la valutazione delle paratiroidi e l’esame qualitativo dei reni.

L’esame ecografico delle paratiroidi viene effettuato con sonde ad elevata frequenza (7,5 – 10 MHz), previa tricotomia e applicazione del gel conduttore di ultrasuoni. In primo luogo viene identificata l’arteria carotide comune attraverso una scansione longitudinale del collo, con un’angolatura di 45 gradi tra il piano parasaggitale e quello dorsale. Inclinando successivamente la sonda medio-ventralmente, in posizione mediale rispetto all’arteria carotide comune appare la ghiandola tiroidea con un ecogenicità minore dell’avventizia ma maggiore rispetto ai muscoli circostanti.

In condizioni normali le paratiroidi sono presenti all’interno del tessuto tiroideo (interne) o adagiate lungo la sua superficie (esterne) e vengono visualizzate raramente come formazioni ipoecogene con un diametro longitudinale ≤ 2 mm.19 Nelle situazioni ipercalcemiche dove il PTH è basso, le paratiroidi sono ipoplasiche e quindi non visibili (ipervitaminosi D, ipercalcemia indotta da neoplasie maligne o patologie granulomatose sistemiche). Nell’insufficienza renale cronica con iperparatiroidismo secondario le paratiroidi sono solitamente tutte iperplastiche (tra 2 e i 4 mm), mentre nell’iperparatiroidismo primario da adenoma o adenocarcinoma secernente PTH, viene solitamente isolata una sola ghiandola con diametro longitudinale maggiore di 4 mm.

Solo in rari casi più ghiandole iperplastiche possono essere evidenti come nel caso dell’iperparatiroidismo primario in

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corso di neoplasie endocrine multiple (MEN) tipo I e IIa o iperparatiroidismo terziario renale. 16,19-23 Le paratiroidi ingrossate appaiono come formazioni ovalari ipoecogene con marcata differenza acustica rispetto al tessuto tiroideo circostante, con margini definiti e posizione solitamente sottocapsulare. Sono in prevalenza poste a livello craniale o caudale del lobo tiroideo e solo raramente centrale, in letteratura è riportata una predominanza di adenomi lobari destri craniali. 23 Il ritrovamento di masse isolate con diametro maggiore di 4 mm è molto sospetto di adenoma o adenocarcinoma secernente PTH, and se alcuni casi hanno dimostrato iperplasie tanto spinte. 22 Sfortunatamente l’esame delle paratiroidi risulta complesso e correlato all’abilità dell’operatore, perciò il mancato ritrovamento di una o più ghiandole non esclude un’eventuale iperplasia o neoplasia secernente. L’alta percentuale di falsi negativi oltre ad essere legata all’operatore e al tipo di macchinario utilizzato, può essere causata dalla scarsa ipoecogenicità di alcune varianti di adenoma che non risultano differenziabili dal parenchima circostante. Da ultimo la presenza di paratiroidi ectopiche può diminuire la sensibilità dell’esame, tali ghiandole sono solitamente presenti nella regione del collo, lungo il fascio neurovascolare, e raramente nel mediastino craniale.

L’apparizione ecografica della nefropatia ipercalcemica è variabile in base alla durata della patologia ed include inizialmente nefrocalcinosi con reni normali o modicamente ridotti, marcato aumento dell’ecogenicità corticale e presenza di una linea iperecogena a livello di giunzione corticomidollare. Stadi avanzati d’ipercalcemia provocano gravi danni tubulari e interstiziali con alterazioni dell’ecostruttura renale difficilmente differenziabile da altre patologie primarie croniche. 1,10-12

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Dow SW, Legendre AM et al.(1986): Hypercalcemia associated with blatomycosis in dogs. J Am Vet Med Assoc 188(7):706.

Druner FH (1981): Hypercalcemia in the dog and cat. J Am Vet Med Assoc 178(2):1252.

Feldman EC, et al.(1997): Comparison of results of hormonal analysis of samples obtained from selected venous sites versus cervical ultrasonography for localizing parathyroid masses in dogs. J Am Vet Med Assoc 211:54.

Finco DR (1983): Interpretations of serum calcium concentration in the dog. Comp Cont Ed Pract Vet 5(9):778.

Garlock SM, Matz ME et al.: Vitamin D, rodenticide toxicity in a dog. J Am Anim Hosp Assoc 27:356,1991.

Gooding GAW (1993): Sonography of the thyroid and parathyroid.

Radiol Clin North Amer 31:967, 1993.

Harris CL, Klausner JS et al.(1991): Hypercalcelcemia in a dog with thymoma. J Am Anim Hosp Assoc 27:281.

Kruger JM, Osborne CA (1994): Canine and feline hypercalcemic nephropathy. Part I Causes and consequences. Comp Cont Ed Vet Pract 16:1299.

Kruger JM, Osborne CA (1994): Canine and feline hypercalcemic nephropathy. Part II Detection, cure and control. Comp Cont Ed Vet Pract 16:1445.

Kruger JM, Osborne CA, Nachreiner RF, et al. (1996). Hypercalcemia and renal failure. Vet Clin North Am 26:1417.

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Meuten DJ, Cooper BJ et al.(1981): Hypercalcemia associated with an adenocarcinoma derived from the apocrine glands of the anal sac.

Vet Pathol 18:454.

Patnaik AK, MacEwen EG et al.(1978): Mediastinal parathyroid adenocarcinoma in a dog. Vet Pathol 15:55, 1978.

Peterson ME , Feldman JM (1982): Hypercalcemia associated with hypoadrenocorticism in sixteen dogs. J Am Vet Med Assoc 181(8):802.

Petemon ME, Randoiph JF et al.(1982): Multiple endocrine neoplasia in a dog. J Am Vet Med Assoc 180(12):1476.

Torrance AG, Nachreiner R (1989): Intact parathyroid hormone assay and total calcium concentration in the diagnosis of disorders of calcium metabolism in dogs. J Vet Intern Med 3(2):86.

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chemical, bone histomorphometric, and pathologic findings. J Am Vet Med Assoc. 189:1471.

Wisner ER, Mattoon JS et al.(1991): Normal ultrasonographic anatomy of the canine neck. Vet Rad 32(4):185.

Wisner ER, et al(1993): Ultrasonographic evaluation of the parathyroid glands in hypercalcemic dogs. Vet Radiol & Ultrasound 34:108.

Wisner ER. Nyland TG.(1994) Localization of a parathyroid carcinoma using high-resolution ultrasonography in a dog. J Vet Inter Med 8: 244.

Wisner ER, Pennick D, et al.(1997): High-resolution parathyroid sonography. Vet Radiol & Ultrasound 38:462.

Wisner ER, Nyland TG. (1998): Ultrasonography of the thyroid and parathyroid glands. Vet Clin North Am 28:973.

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Principi di scintigrafia negli animali da compagnia Roberto Santilli Med. Vet., Dipl. E.C.V.I.M.-C.A. (Cardiology) - Samarate (Varese)

GianMarco Gerboni Med. Vet. - Samarate (Varese)

Riassunto Tra le tecniche di diagnostica per immagine del cane e del gatto, la scintigrafia ha un ruolo minoritario e spesso complementare alla radiologia, ma propone nuovi campi applicativi e possibilità diagnostiche. Oltre alla ripresa d’immagini statiche simili a quelle radiografiche adatte alle valutazioni anatomiche, la scintigrafia fornisce immagini dinamiche per lo studio funzionale di organi ed apparati. Con lo studio dinamico si valuta qualitativamente e quantitativamente un tessuto normale, patologico o trapiantato. Lo studio dinamico viene effettuato attraverso l’analisi della velocità di accumulo e di eliminazione del radiofarmaco dall’organo indagato. Le radiazioni gamma, liberate dal radiofarmaco introdotto nel corpo dell’animale, producono l’immagine scintigrafica e sono captate e lette dal rilevatore di radiazioni, la gamma camera. Il radioisotopo ideale per la diagnostica clinica veterinaria è il 99mTecnezio che ha emivita di sei ore ed emette solo radiazioni gamma di 140 KeV. Vi sono delle applicazioni ormai comuni in medicina nucleare veterinaria, tra cui la scintigrafia ossea. Tecnica che offre notevoli vantaggi, come la precocità diagnostica, o la facilità di esaminare lo scheletro in corso di patologie che provocano alterazioni del flusso ematico e dell’attività osteogenica (osteoblastica). Anche la scintigrafia della ghiandola tiroidea, in corso di ipertiroidismo felino, ipotiroidismo canino, neoplasie tiroidee o masse cervicali di eziologia ed origine sconosciute è una metodica applicata frequentemente. La scintigrafia renale suddivisa in morfologica, per l’esame anatomico delle lesioni parenchimatose, e funzionale, indicata per lo studio dinamico quantitativo del tasso di filtrazione glomerulare (GFR). La scintigrafia epatica dinamica in corso di shunt portosistemici, permette di quantificare l’ampiezza del flusso anomalo e di ricavare la frazione di shunt, o di verificare l’efficacia di un intervento di chiusura. Sono state descritte numerose altre applicazioni della scintigrafia nei piccoli animali: del cervello, cardiaca, polmonare, la linfoscintigrafia, la scintigrafia in corso di insulinoma, feocromocitoma, adenoma paratiroideo e del tratto gastroenterico.

La scintigrafia è stata utilizzata a scopo diagnostico negli animali a partire dagli anni settanta negli Stati Uniti, mentre in Europa e nel Regno Unito la tecnica fu sviluppata più tardi. Nell’ambito della diagnostica per immagini del cane e del gatto, la scintigrafia ha un ruolo minoritario e sicuramente complementare alla radiologia, ma con ulteriori campi applicativi. Oltre alla ripresa d’immagini statiche simili a quelle radiografiche ed adatte alle valutazioni anatomiche, la scintigrafia fornisce immagini dinamiche per lo studio funzionale d’organi ed apparati. Con gli studi dinamici si ottengono valutazioni qualitative e quantitative di tessuti normali, patologici o trapiantati. Lo studio dinamico viene effettuato attraverso l’analisi della velocità di accumulo e di eliminazione del radiofarmaco dall’organo indagato.

La scintigrafia produce immagini mediante l’emissione di radiazioni gamma liberate dal radiofarmaco introdotto nel corpo dell’animale. Il radiofarmaco è una sostanza chimica

che contiene un atomo radioattivo (radionuclide) che può essere utilizzato a scopi diagnostici e terapeutici; è costituito da un radioisotopo associato ad un legante. Esistono diverse particelle leganti con differenti tropismi per i tessuti o per gli organi che si vogliono indagare. Una volta localizzato nell’organo bersaglio, il radiofarmaco emette radiazioni gamma. Queste captate e lette dal rilevatore di radiazioni, la gamma camera, sono tradotte in immagine da un computer appositamente destinato a tale scopo.

Il tempo di decadimento radioattivo di un radionuclide ci indica la sua radioattività, (numero di disintegrazioni per unità di tempo) ed è direttamente proporzionale al numero di atomi radioattivi. L’unità di misura della radioattività è il millicurie (mCi) negli Stati Uniti, che è uguale a 3,7 x 1010 disintegrazioni per secondo, o il Becquerel (Bq) Unità Internazionale che è uguale ad una disintegrazione per secondo (1 mCi = 37 MBq).

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Il decadimento radioattivo di nuclei instabili, con rapporto neutroni/protoni non bilanciato, avviene attraverso l’emissione di particelle alfa, beta o di radiazioni gamma. I principali tipi di decadimento radioattivo sono: 1) il decadimento alfa, che non trova applicazioni in medicina; 2) il decadimento attraverso negatroni caratteristico dei radionuclidi che emettono o solo particelle beta (32Fosforo), o particelle beta associate a radiazioni gamma (131Iodio); 3) il decadimento attraverso positroni, usato nella tomografia a emissione di positroni (PET); 4) il decadimento attraverso cattura di elettroni, caratteristico del 201Tallio. Un particolare tipo di decadimento, che riveste maggior interesse in medicina nucleare veterinaria, è la transazione isomerica attraverso la decantazione di un radionuclide metastabile. Un esempio è rappresentato dal decadimento beta del 99Molibdeno a 99m Tecnezio e la successiva transazione isomerica dal 99mTecnezio a 99Tecnezio con emissione di radiazioni gamma.

Il radiofarmaco ideale ai fini diagnostici è un radionuclide con bassissima emivita fisica, bassa dose radiante ( quantità di radiazioni assorbite dai tessuti ) capace di emettere solo radiazioni gamma a bassa energia. Il 99mTecnezio avendo emivita di sei ore ed emettendo solo radiazioni gamma di 140 KeV, risulta il radioisotopo di prima scelta.

Per ottenere tale molecola si utilizza un generatore di 99m Tecnezio, composto da una colonna cromatografica di ossido di Alluminio alla quale è legato il 99Molibdeno. Il 99m Tecnezio viene separato dal 99Molibdeno facendo attraversare la colonna da una soluzione salina allo 0,9%. Il risultato finale è una soluzione contenente il 99mTecnezio sodio pertechnetato (Na 99mTcO4), che è la forma ossidata del 99m Tecnezio. Il Na99mTcO4 possiede uno spiccato tropismo per la ghiandola tiroidea, le ghiandole salivari e la mucosa gastrica. Fissandosi a tali strutture, viene utilizzato tale quale per la diagnostica delle stesse. Per lo studio, invece, di altri organi e tessuti viene ridotto ad una forma carica positivamente attraverso l’utilizzo di un agente riducente a base di ione stagno e successivamente legato a sostanze chimiche non radioattive. Le radiazioni gamma emesse dai tessuti e dagli organi vengono captate dal rivelatore di radiazioni.

Esistono due diversi tipi di rilevatori: 1) a gas, come il contatore Geiger-Mueller, usato per valutare le radiazioni residue nell’animale; 2) rilevatori a scintillazione di sodio iodato quali la gamma camera. Quest’ultima rileva le radiazioni gamma permettendo sia la quantificazione che il posizionamento dalla fonte radiante. È composta da un collimatore-rilevatore, un circuito posizionale, un’unità per l’analisi dell’altezza dell’impulso, ed un’unità per la messa in sede e registrazione del segnale.

APPLICAZIONI CLINICHE Scintigrafia ossea La scintigrafia scheletrica è una delle applicazioni più comuni in medicina nucleare veterinaria. Tra i vantaggi della scintigrafia ossea ritroviamo la precocità nella diagnosi e la facilità di esaminare lo scheletro nella sua interezza. L’assorbimento del radiofarmaco dipende dal flusso ematico e dall’attività osteogenica (osteoblastica). 19

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L’esame scintigrafico dello scheletro può essere suddiviso in tre fasi. La fase vascolare o angiogramma nucleare (fase 1), utile nella diagnosi delle perdite di vascolarizzazione, come le patologie ischemiche e gli infarti. La fase extracellulare o dei tessuti molli (fase 2), in cui si possono valutare patologie infiammatorie quali: patologie tendinee o legamentose, sinoviti, miositi ed osteomieliti. La fase ossea (fase 3), per l’indagine e la valutazione di patologie ossee acute e croniche che coinvolgono o aumentano il turnover osseo, quali fratture non scomposte, osteoartriti, reazioni periostali e tumori, nonché la valutazione dei sequestri con morte tissutale in seguito a traumi o infarti. 19 In medicina nucleare veterinaria la scintigrafia ossea viene utilizzata in fase 3 per lo studio di metastasi 8, mentre l’esame completo è effettuato in campo ortopedico.

I radiofarmaci utilizzati sono il Na 99mTcO4 per la fase 1 e 2 ed il 99mTecnezio Difosfonato per la fase 3. Il radiofarmaco viene iniettato nel circolo sistemico e la capacità di assorbimento è determinata dal grado di rimodellamento del tessuto osseo nel segmento esaminato. Il risultato della fase ossea è un’immagine capace di fotografare l’attività metabolica ossea nel tempo di azione del radiofarmaco. La lettura ottimale per la fase ossea viene effettuata due o tre ore dopo l’iniezione. Il tessuto osseo fissa il 50% della dose iniettata, in modo dipendente dalla clearance renale. Le immagini scintigrafiche vengono raccolte come “total body” per gatti e cani di piccola taglia, oppure come regioni o segmenti ossei per gli animali di maggiore dimensione. Porzioni scheletriche che presentano un’anormale attività metabolica hanno la capacità di fissare una quantità maggiore di radiofarmaco.

Scintigrafia Tiroidea La scintigrafia tiroidea è tra le più comuni applicazioni della medicina nucleare. La tiroide capta sia lo 131Iodio 2 che il 99mTecnezio, ma in medicina veterinaria è il Na 99mTcO4 il più utilizzato, per la maggiore disponibilità, il basso costo e la sicurezza delle radiazioni gamma. 1,4,15,25 Le applicazioni cliniche della scintigrafia della ghiandola tiroidea sono in corso di ipertiroidismo felino 2,33, ipotiroidismo canino 4, neoplasie tiroidee 11 o masse cervicali di eziologia ed origine sconosciute. Attraverso la scintigrafia dei gatti ipertiroidei, è possibile determinare lo stato funzionale di uno o entrambi i lobi tiroidei, valutare l’eventuale presenza di tessuto tiroideo ectopico e stimare l’efficacia delle terapie. Il Na 99m TcO4 viene captato dalla ghiandola tiroidea, dalle ghiandole salivari e dalla mucosa gastrica. In entrambe le specie, l’esame viene effettuato mediante iniezione endovenosa di sodio Na 99mTcO4 ad una dose di 1-3 mCi (gatto) o 2-6 mCi (cane). La lettura viene solitamente effettuata 20 minuti dopo l’iniezione del mezzo con l’animale in decubito sternale.

Nel gatto sano i lobi tiroidei appaiono come due aree focali tondeggianti avide di tecnezio, localizzate cranialmente al terzo medio della regione cervicale. L’immagine scintigrafica dei due lobi viene poi confrontata con quella delle ghiandole salivari ipsilaterali. Nell’animale eutiroideo il grado di captazione presenta un rapporto di 1:1. In corso di ipertiroidismo felino è possibile ritrovare iperplasia o adenomi bila-

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terali nel 75% dei casi, monolaterali 25% e focolai ectopici mediastinici nel 3-5 %. 33 In queste condizioni il tessuto patologico ha un grado di attività maggiore e una maggiore capacità di captazione del radiofarmaco. Avremo cosi due aree enormemente attive nell’iperplasia bilaterale, una sola area ad alta attività che sopprime la captazione nel restante tessuto tiroideo sano, nel monolaterale, ed infine aree di attività localizzate nel torace nei focolai ectopici.

della tecnica scintigrafica, poiché l’esame è falsato dalla scarsa capacità di filtrazione e captazione dei reni. È intuitivo che il valore della scintigrafia è maggiore in animali con capacità di filtrazione glomerulare ancora compensata e non in caso di insufficienza renale cronica terminale.

Scintigrafia Renale

Gli shunts portosistemici (SPS) sono una comune patologia congenita di cani e gatti. In questa patologia la scintigrafia viene comunemente usata poiché risulta meno invasiva e apporta un numero di informazioni maggiore rispetto alle altre indagini disponibili. 9,16-18,22,28 Se confrontata, infatti, alla venografia mesenterica intraoperatoria, l’arteriografia mesenterica craniale selettiva e la venografia splenica con 99m Tecnezio-albumina macroaggregata23, è sicuramente più facile da eseguire e relativamente più economica.

La scintigrafia epatica dinamica permette di quantificare l’ampiezza della anomalia di flusso e di ricavare la frazione di shunt, verificare l’efficacia di un intervento di chiusura chirurgico calcolando la frazione di shunt pre e post-operatoria.9,16-18,22,32 Per l’esecuzione dell’esame l’animale viene messo in decubito laterale sinistro, e la gamma camera viene posta sopra la regione cardiaca ed epatica. Attraverso un catetere introdotto nel colon discendente si inietta il Na 99mTcO4 ad una dose di 1 – 2 mCi/kg. Immediatamente dopo l’iniezione comincia l’acquisizione delle immagini che dura 2-3 minuti con intervalli di 5 secondi. Il Na 99mTcO4 è rapidamente assorbito dalla mucosa del colon ed arriva attraverso la vena mesenterica alla vena porta. Lo studio che ne risulta è un porto-angiogramma nucleare, che permette di valutare il percorso del sangue portale attraverso il fegato, in condizioni normali, o diretto al cuore baypassando il fegato, in caso di SPS. 9,16-18,22 In un animale normale, il radiofarmaco arriva nel fegato dopo 8-10 secondi dalla somministrazione rettale e con un ritardo di 6-12 secondi al cuore. Le immagini raccolte dalla gamma camera vengono sommate e viene calcolata sia per l’area cardiaca che epatica la curva di attività in funzione del tempo. In un soggetto normale l’attività si manifesta prima a livello epatico e poi cardiaco, mentre in soggetti con SPS simultaneamente o addirittura prima a livello cardiaco. Attraverso lo studio ed il confronto delle due curve si calcola la frazione di shunt. Questa rappresenta la quota di sangue che passa attraverso lo shunt dalla porta alla cava senza entrare nel fegato. In condizioni di normalità la frazione di shunt varia da 5% a 15%.

La scintigrafia del rene si divide in funzionale e morfologica. L’uso di complessi formati da 99mTecnezio ed altri agenti radiofarmaceutici consente di studiare l’anatomia e la capacità di filtrazione del glomerulo. Il 99mTecnezio acido dietilentriaminopentacetico (DTPA) 3,30 ha la caratteristica di essere escreto rapidamente mediante filtrazione glomerulare ed è utilizzato sia per gli studi dinamici della perfusione renale che per quelli morfologici. Il radiofarmaco di prima scelta nella scintigrafia renale morfologica è invece il 99m Tecnezio acido 2,3-dimercaptosuccinico (DMSA), che capace di fissarsi alla corticale per diverse ore e di consentire un esame anatomico dettagliato delle lesioni parenchimatose.

La scintigrafia renale funzionale con 99mTecnezio-DTPA è indicata per lo studio dinamico quantitativo del tasso di filtrazione glomerulare (GFR). 3,13,30 Conoscere il tasso di filtrazione glomerulare globale e dei singoli reni, consente di valutare: il grado e la progressione delle patologie renali, la gravità di una patologia renale sub-clinica o non ancora clinicamente manifesta, i danni causati da agenti nefrotossici e la funzionalità di un rene, prima di asportare chirurgicamente il controlaterale.10 La scintigrafia morfologica con 99mTecnezio-DMSA è indicata nella valutazione della forma, l’anatomia e la topografia dei singoli reni. Esistono comunque tecniche diagnostiche alternative, quali l’ecografia, che permettono valutazioni approfondite a costi e rischi minori. La tecnica prevede l’iniezione endovenosa a bolo del radiofarmaco. La dose del 99mTecnezio-DTPA è di 1mCi nel gatto e da 1 a 3 mCi nel cane.

L’acquisizione delle immagini, nello studio dinamico, comincia simultaneamente all’iniezione con intervalli di 515 secondi, per un tempo totale di 3 minuti. L’animale è posto in decubito laterale sinistro e la gamma camera è posizionata dorsalmente alla regione craniale dell’addome. L’animale è sveglio e cosciente poiché l’uso di agenti anestetici potrebbe abbassare la pressione sistemica e il flusso ematico renale, una pressione media sotto gli 80 mmHg riduce la capacità di filtrazione glomerulare. 24,27 Il 99mTecnezio-DTPA è rimosso dal circolo per filtrazione glomerulare e non è riassorbito dai tubuli renali. Pertanto la clearance plasmatica e la capacita di filtrazione renale riflettono il GFR. Nel cane è considerato normale un GFR di 3 ml/min/kg. Nel gatto è considerato normale un valore di 2,5 ml/min/kg. Animali con insufficienza renale sub-clinica hanno un GFR totale compreso tra 1,2 e 2,5 ml/min/kg. Quando l’insufficienza renale diviene clinicamente manifesta, con Bun e creatinina elevate, il GFR ha valori di 1,0- 1,3 ml/min/kg. Per valori inferiori a 0,25 ml/min/kg di GFR diminuisce la precisione

Scintigrafia Epatica in corso di shunt porto-sistemici

Linfoscintigrafia La facilità d’applicazione unita alla non invasività rendono la linfoscintigrafia una tecnica che trova applicazione in medicina veterinaria per lo studio dell’anatomia e della funzionalità delle vie linfatiche.13 Per questo esame vengono utilizzati colloidi uniti al 99mTc (99mTc – albumina nanocolloide) iniettati nello spazio interstiziale e poi drenati dal sistema linfatico. La linfoscintigrafia consente lo studio del

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drenaggio linfatico delle estremità in corso di linfedema, o fenomeni ostruttivi, del dotto toracico in caso di chilotorace e della parete addominale e toracica per la ricerca di metastasi.

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Altre applicazioni Sono state descritte numerose altre applicazioni della scintigrafia nei piccoli animali, come la diagnosi delle lesioni e dei tumori cerebrali con 99mTc- acido dietilentriaminopentacetico (DTPA), ormai abbandonata per lo sviluppo della TAC e della risonanza magnetica. La valutazione della morfologia e della funzionalità epatobiliare con l’uso del 99m Tc -zolfo colloidale 26 o i derivati dell’acido iminodiacetico.14,31 Per quanto riguarda l’apparato cardiocircolatorio, esiste l’angiografia radionucleare, con 99mTc-sestamibi per quantificare gli shunt intra o extra-cardiaci, e lo studio della funzione ventricolare con il 99mTc legato ai globuli rossi in vivo. 7 Altre indicazioni riguardano l’utilizzo del 99mTc-zolfo colloidale per la valutazione della vitalità della mucosa gastrica, delle emorragie gastroenteriche, dello svuotamento gastrico, 29 del reflusso gastroesofageo, del 99mTc-sestamibi in corso di iperparatiroidismo 21, lo 111Indium-pentetreotide in corso d’insulinoma 20, 123Iodio metaiodobenzylguanidina per la diagnosi di feocromocitoma 6 e il 99mTc- acido dietilentriaminopentacetico (DTPA) per lo studio delle regioni . polmonari 5.

Tutte queste ultime tecniche sono risultate valide nella risoluzione di singoli casi, ma hanno ancora un’applicazione occasionale in medicina nucleare veterinaria.

Bibliografia 1.

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5.

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10.

Adams WH, Daniel GB, Petersen MG, et al. (1997). Quantitative 99m Tc-pertechnectate thyroid scintigraphy in normal beagles. Vet Radiol & Ultrasound 38:323-328.

Adams WH, Walker MA, Daniel GB, et al. (1995). Treatment of differentiated thyroid carcinoma in 7 dogs utilizing 131 I. Vet Radiol & Ultrasound 36:417-424.

Barthez PY, Hornof WJ, Cowgill LD, et al. (1998). Comparison between the scintigraphic uptake and plasma clearance of 99mTCdiethylenetriaminepentacetic acid (DTPA) for the evaluation of the glomerular filtration rate in dogs. Vet Radiol & Ultrasound 39:470-474.

Bernard P, Regnier A. (1989). Scintigraphie thyroidienne chez le chien. Revue de Med Vet 140 :193-198.

Berry CR, Ackerman N, Monce K. (1994). Pulmonary mineralization in four dogs with Cushing’s syndrome. Vet Radiol & Ultrasound 35:10-16.

Berry CR, Wright KN, Breitschwerdt BE, et al. (1993). Use of 131Iodine metaiodobenzylguanidine scintigraphy for the diagnosis of a pheochromocytoma in a dog. Vet Radiol & Ultrasound 34:52-55.

Daniel GB, Tucker RL, Bright JM, et al. (1993). Utilization of instantaneous ejection volume images to produce ventricular volume curves from an equilibrium radionuclide ventriculogram. Vet Radiol & Ultrasound 34:276-286.

Forrest LJ, Thrall DE. (1994). Bone scintigraphy for metastasis detection in canine osteosarcoma. Vet Radiol & Ultrasound 35:124-130.

Forster-van Hijfte MA, Mc Envoy FJ, White RN, et al. (1996). Per rectal portal scintigraphy in the diagnosis and management of feline congenital portosystemic shunts. J Small Animal Pract 37: 7- 11.

Gookin JL, Stone EA, Spaulding KA, et al. (1996). Unilateral nephrectomy in dogs with renal disease: 30 cases (1985- 1994). J Am Vet Med Assoc 208:2020-2026.

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31.

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Harari J, Patterson JR, Rosenthal RC. (1986). Clinical and pathologic features of thyroid tumors in 26 dogs. J Am Vet Med Assoc 188:11601164.

Hodges CC, Fossum TW, Komkov A, et al. (1992). Lymphoscintigraphy in healthy dogs and dogs with experimentally created thoracic duct abnormalities. Am J Vet Res 53:1048-1053.

Itkin RJ, Krawiec KR, Twardock AR, et al. (1994). Quantitative renal scintigraphic determination of effective renal plasma flow in dogs with normal and abnormal renal function, using 99m Tc- mercaptoacetyltriglycine. Am J Vet Res 55:1660-1665.

Kerr LY, Hornof WJ. (1986). Quantitative hepatobiliary scintigraphy using 99mTc-disida in the dog. Vet Radiol & Ultrasound 27:173177.

Kintzer PP, Peterson ME. (1994). Nuclear medicine of the thyroid gland. Vet Clin North Am: Small Animal Practice 24:587-605.

Koblik PD, Hornof WJ, Breznock EM, et al. (1983). Quantitative hepatic scintigraphy in the dog. Vet Radiol & Ultrasound 24:226-231.

Koblik PD, Hornof WJ, Breznock EM, et al. (1983). Use of quantitative hepatic scintigraphy to evaluate spontaneous portosystemic shunts in 12 dogs. Vet Radiol & Ultrasound 24:232-236.

Koblik PD, Komtebedde J, Yen CK, et al. (1990). Use of transcolonic 99m Tc-pertechnetate as a screening test for portosystemic shunts in dogs. J Am Vet Med Assoc 196:925-930.

Lamb CR. (1991). The principles and practice of bone scintigraphy in small animals. Seminars in Vet Med and Surg Small Animal 6:140153.

Lester NV, Newell SM, Hill RC et al. (1999) Scintigraphic diagnosis of insulinoma in a dog. Vet Radiol & Ultrasound 40: 174-178.

Matwichuk CL, Taylor SM, Wilkinson A.A. et al. (1996). Use of Technetium 99mTc sestamibi for detection of parathyroid adenoma in a dog with primary hyperparathyroidism. J Am Vet Med Assoc 209,1733-1736.

Mc Evoy FJ, Forster-van Hijfte MA, White RN, et al. (1998). Detection of portal blood flow using per- rectal 99m Tc- pertechnectate scintigraphy in normal cats.

Vet Radiol & Ultrasound 39:234-237.

Meyer MP, Rothuizen J, Van den Brom WE, et al. (1994). Quantitation of portosystemic shunting in dogs by ultrasound-guided injection of 99m Tc- macroaggregates into a splenic vein. Res in Vet Sci 57:5862.

Mitchell SK, Toal RL, Daniel GB, et al. (1998). Evaluation of renal hemodynamics in awake and isoflurane- anesthetized cats with pulsed-wave Doppler and quantitative renal scintigraphy. Vet Radiol & Ultrasound 39:451-458.

Napam P, Pollak YW, Van den Brom WE, et al. (1994). Quantitative aspects of thyroid scintigraphy with pertechnectate (Na 99mTcO4) in cats. J Vet Intern Med 8:302-303.

Newel SM, Selcer BA, Roberts RE, et al. (1996). Hepatobiliary scintigraphy in the evaluation of feline liver disease. J Vet Intern Med 10:308-315.

Newell SM, Ko JC, Ginn PE, et al. (1997). Effects of three sedative protocols on glomerular filtration rate in clinically normal dogs. Am J Vet Res 58:446-450.

Newell SM, Selcer BA, Roberts R, et al. (1994). Use of hepatobiliary scintigraphy in clinically normal cats. Am J Vet Res 55:762-768.

Steyn PF, Twedt D, Toombs W. (1995). The scintigraphic evaluation of solid phase gastric emptying in normal cats. Vet Radiol & Ultrasound 36:327-331.

Uribe D, Krawiec DR, Twardock R, et al. (1992). Quantitative renal scintigraphic determination of glomerular filtration rate in cats with normal and abnormal kidney function, using 99m Tc-diethylenetriaminepentaacetic acid. Am J Vet Res 53:1101-1107.

Van den Brom E, Rothuizen J. (1990). Quantitation of the hepatobiliary dynamics in clinically normal dogs by use of 99m Tc- iminodiacetate excretory scintigraphy. Am J Vet Res 51:249-252.

Van Vechten BJ, Komtebedde J, Koblik D. (1994). Use of transcolonic portal scintigraphy to monitor blood flow and progressive postoperative attenuation of partially ligated single extrahepatic portosystemic shunts in dogs. J Am Vet Med Assoc 204:1770-1774.

Wisner ER, Théon AP, Nyland TG, et al. (1994). Ultrasonographic examination of the thyroid gland of hyperthyroid cats: comparison to Na 99mTcO4 scintigraphy. Vet Radiol & Ultrasound 35:53-58.

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Valutazione clinica ed istologica di PLR 120 (Palmidrol Inn comicronizzato) in gatti con granuloma eosinofilico e con placca eosinofilica - uno studio pilota Fabia Scarampella Med. Vet. - Libero Professionista - Milano

Francesca Abramo Med. Vet., Dip. Patologia Animale, Università di Pisa

Chiara Noli Med. Vet., Dipl. ECVD - Libero Professionista - Milano

Questo studio è stato gentilmente sponsorizzato dall’ESVD Grant 1998 e da Innovet, Milano.

INTRODUZIONE Il granuloma eosinofilico (GE) e la placca eosinfilica (PE) del gatto, sono caratterizzati dalla presenza di numerosi mastociti nel derma che, degranulando, rilasciano sostanze importanti nel provocare il processo infiammatorio. Palmidrol è un N-acilamide (palmitoiletanolamide), che ha una funzione anti infiammatoria autacoide locale (meccanismo ALIA), inibendo la degranulazione dei mastociti grazie ad un legame specifico sui recettori CB2 1,2.

In questo studio pilota descriveremo i miglioramenti delle lesioni ottenuti con PLR 120 in gatti con GE e PE.

MATERIALI E METODI Otto gatti con GE e sette con PE di entrambi i sessi sono stati inclusi in questo studio (età media: 34 mesi, range 7134 mesi). I soggetti erano risultati negativi agli esami colturali per dermatofiti e non erano stati trattati con cortisonici a breve azione, con antistaminici o con acidi grassi essenziali nel corso delle due settimane che hanno preceduto l’inclusione, né avevano ricevuto iniezioni di steroidi deposito da almeno due mesi. Gli animali che migliorarono grazie alla profilassi antipulci o alla terapia con ivermectina (0,3 mg/kg SC due iniezioni a 14 gg. di intervallo) non vennero inclusi nello studio. PLR 120 è stato somministrato per 30 giorni per via orale (10 mg/kg/BID). I gatti sono stati valutati clinicamente impiegando una scala numerica per il prurito, l’eritema, l’alopecia e le lesioni prima e dopo il trattamento col farmaco. Sono state eseguite biopsie delle lesioni cutanee prima e dopo il trattamento, fissate in formalina al 10%, processate per l’istologia di routine e colorate con blu di Toluidina. Il numero di mastociti/mm2 è stato determinato su sezioni colorate con blu di Toluidina utilizzando Quantimet 400 Analyser System (Laica) in 56 campi di 1,2 mm2

per ciascuna sezione. Le aree occupate dai follicoli piliferi o dalla collagenolisi non venivano considerate durante i conteggi. È stata eseguita l’analisi densitometrica di 21 mastociti colorati con blu di toluidina provenienti da sette campi diversi di una stessa sezione. La valutazione clinica e il conteggio dei mastociti sono stati analizzati con il test della t di Student, con l’analisi di covarianza per misure ripetute, e tramite il test di correlazione lineare di Pearson.

RISULTATI L’analisi statistica dei dati clinici ha dimostrato un miglioramento significativo dei sintomi (prurito, eritema, alopecia) e della gravità delle lesioni nel 67% degli animali. Come supposto, non sono state riscontrate variazioni nel numero di mastociti presenti tra le biopsie pre- e post trattamento, mentre i valori densitometrici hanno dimostrato un incremento significativo nelle biopsie post trattamento (p= 0.009).

DISCUSSIONE Questi risultati confermano la capacità del Palmiodrol di inibire la degranulazione dei mastociti senza peraltro alterarne il numero, a differenza dei corticosteroidi, che riducono drasticamente i mastociti, mettendo a rischio l’equilibrio omeostatico dei tessuti periferici, inclusa la cute. Questo studio suggerisce che PLR 120 può rappresentare un alternativa possibile all’uso dei corticosteroidi nei gatti con granuloma eosinofilico e placca eosinofilica.

Bibliografia Aloe, L et al. Agents and Actions 39: C145, 1993 Facci, L et al. Proceedings Nat. Acad. Sci. 92: 3376, 1995

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Limb Alignment Allineamento dell’arto posteriore deviato

Barclay Slocum DVM - Slocum Clinic - Eugene, Oregon, USA

Theresa Devine Slocum MS - Slocum Clinic - Eugene, Oregon, USA

Riassunto Il normale allineamento dell’arto posteriore pone l’anca, il ginocchio, il garretto e la zampa nel piano sagittale. Ciò consente ai muscoli estensori di essere contrastati dai flessori e di ottenere la massima potenza propulsiva. Nel cane, quest’ultima è diminuita dall’anormale allineamento che converte le forze estensorie in forze rotatorie. La conformazione anomala viene di solito riconosciuta per la presenza di arcatura degli arti o valgismo delle ginocchia. Nella presente relazione verranno individuate le anomalie strutturali, illustrando le potenziali correzioni chirurgiche.

L’allineamento dell’arto può essere anormale a causa di un abnorme posizionamento delle articolazioni (come nel malorientamento dell’acetabolo nella displasia dell’anca), una torsione interna (come nella lussazione mediale della rotula) o la presenza di patologie articolari (come l’osteocondrosi del margine mediale dell’astragalo). La seconda distorsione dell’arto può derivare dall’azione di una forza che determina una torsione dell’osso. Ciò si osserva nella displasia dell’anca o nelle lussazioni mediali della rotula. La terza distorsione dell’arto è dovuta al varismo o valgismo dell’osso. Questa si osserva frequentemente nel varismo del tratto distale del femore, che spesso si manifesta come una lussazione rotulea mediale. Il valgismo della tibia si può osservare nei casi di osteocondrosi laterale del condilo femorale e di solito contribuisce al sovraccarico fisico delle forze che gravano sul condilo femorale laterale e alla distorsione della biomeccanica articolare, che determina un’instabilità rotatoria anteromediale del ginocchio. La quarta distorsione è una curvatura caudale o craniale dell’osso. Queste alterazioni non sono comuni e, quando sono presenti, il loro effetto viene ridotto al minimo grazie al meccanismo di compensazione rappresentato dalle normali possibilità di escursione articolare dei pazienti. La più comune di queste distorsioni è l’eccessiva inclinazione del piatto tibiale.

La difficoltà, dal punto di vista ortopedico, è quella di diagnosticare e localizzare accuratamente la distorsione dell’arto. È possibile ottenere una descrizione specifica dell’allineamento dell’anca e della struttura del bacino effettuando un esame tridimensionale dell’articolazione. Un’accurata valutazione radiografica del femore richiede la ripresa di immagini in proiezione ventrodorsale e mediolaterale e con il fascio di raggi perpendicolare all’asse maggiore dell’osso in posizione radiografica standard. Una precisa radiografia mediolaterale in cui il grande trocantere, la testa della fibula ed il malleolo mediolaterale si trovino tutti su un unico piano permette di valutare il varismo femorale distale e la torsione tibiale e l’inclinazione del piatto tibiale. Lo stesso vale per il posizionamento della tibia nelle immagini radiografiche. Per visualizzare l’arto posteriore, il ginocchio viene bloccato in estensione per effettuare una ripresa caudocraniale che consenta di valutare in modo definitivo l’articolazione stessa e la tibia.

La correzione chirurgica richiede l’applicazione di principi ortopedici precisi per il riallineamento delle forze biomeccaniche sul piano sagittale, in modo da alleviare lo stress sulle articolazioni e ripristinare la funzionalità del paziente. Alcuni esempi sono l’osteotomia di livellamento del piatto tibiale per il trattamento della rottura del legamento crociato craniale, l’osteotomia pelvica nei soggetti con displasia dell’anca e l’osteotomia del femore valgo per il trattamento delle lussazioni rotulee mediali.

Normal alignment of the hind limb places the hip, knee, hock and paw in the sagittal plane. This allows the extensors to be opposed by the flexors, and maximal propulsive power can be delivered to the hind limb. The dog’s propulsive power is diminished by abnormal alignment by converting extensor forces into rotatory forces. The abnormal conformation is usually recognized by the bowlegged or knock-kneed conformation. Identification of the structural abnormalities and the potential surgical corrections are identified.

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Limb alignment may be abnormal due to abnormal positioning of joints such as malorientation of the acetabular cup with hip dysplasia, internal torsion such as medial patellar luxation, or pathologic joint conditions such as OCD of the medial talar ridge.

The second distortion of the limb may be from torsion which is twisting within the bone. This is seen as femoral hip dysplasia, or medial patellar luxations. The third distortion of the limb is due to varus or valgus deformities of the bone. This is frequently seen with varus of the distal femur which will often manifest itself as a medial patellar luxation. Valgus of the tibia may be seen in cases of lateral OCD of the femoral condyle and is usually contributory to the physical overload of forces on the lateral femoral condyle as well as distortion of the joint biomechanics which creates anteromedial rotary instability of the stifle. The fourth distortion is a cranial or caudal curvature of the bone. These distortions are not common and when are present, their effect is minimized by incorporation into the normal range of motion of the patient. The most common of these distortions is the excessive slope of the tibial plateau.

The orthopedic challenge is the accurate diagnosis and location of the distortion in the limb. An specific description of the hip alignment and structure of the pelvis can be obtained from a three dimensional hip examination. Accurate radiography of the femur requires a ventrodorsal, and a medial to lateral xray beam to be perpendicular to the long axis of the femur in a standard radiographic position. A precise medial to lateral view in which the greater trochanter, the fibular head and the lateral malleolus are all in one plane, permit assessment of the distal femoral varus and tibial torsion and slope of the tibial plateau. The same is true for positioning of the tibia for radiographs.

In order to access the hind limb, the stifle is locked in extension for a caudocranial view which allows definitive assessment of the stifle and tibia.

Surgical correction requires the application of precise orthopedic principles for realignment of the biomechanical forces to the sagittal plane relieving the stress on the joints and returning function to the patient.

Some examples are Tibial Plateau Leveling Osteotomy for the treatment of rupture of the cranial cruciate ligament, Pelvic Osteotomy for the treatment of hip dysplasia and femoral valgus osteotomy for treatment of medial patellar luxations.

Although the success of repairs became improved with perfection of ligament substitution techniques and extracapsular procedures, treatment of the rupture of the cranial cruciate ligament with the Tibial Plateau Leveling Osteotomy technique consistently provided results that provided four characteristics to the patient. The dog regained a full sit, except when permanent bony changes were present preoperatively. The progression of the degenerative joint disease was halted. The musculature of the limb returned to normal, and patients returned to preinjury function. Evaluation of 700 cases revealed a pattern from the small percentage that demonstrated incomplete return to preinjury function as is generally expected by the Tibial Plateau Leveling Osteotomy technique. A review of these cases revealed excessive internal tibial torsion, which would give the dog a bowlegged appearance. This was the beginning of an indepth review and prospective evaluation of cases which had an inadequate limb alignment.

The most common malady of limb alignment is the bowlegged appearance of a patient. This corresponds with breeds such as the bullmastiff, rottweiler, pit bull and other bowlegged dogs. In modeling the bowlegged conformation, it was found that bowleggedness occurs from four different sources. The most common bowleggedness seen in Labrador retrievers, and golden retrievers is due to a varus deformity of the distal femur. A varus deformity of the distal femur is often associated with a medial patellar luxation and often rupture of the cranial cruciate ligament due to the internal rotation mechanism. The patella rides high and medial on the trochlear ridge and will often luxate. Treatment of the medially luxating patella by lateral fabella to patella sutures

or lateral capsulorrhaphy is doomed to failure as the alignment of the quadriceps will dictate a medial displacement of the patella, which will stretch any repair provided. Treatment by deepening the trochlear sulcus will also be under pressure to create a medial luxation. The standard lateral tibial tubercle transposition is an enticing treatment as patellar stability is assured. Unfortunately, patellar stability is at the expense of a bowlegged conformation due to an exceptionally lateral tubercle which will cause internal rotation of the stifle and an accentuated bowlegged conformation. In this patient the bowleggedness created by the distal femoral varus has been compounded by internal rotation at the stifle which will accentuate the bowleggedness. The long term effect on the patient is excessive pressure on the medial condyle secondary to the bowleggedness and excessive internal rotation of the stifle which predisposes the rupture of the cranial cruciate ligament. The straightforward and proper treatment of this condition lies in a distal femoral valgus osteotomy for the treatment of femoral varus. Once this limb alignment is corrected, the structures will function normally.

Stress will be relieved from the structures attempting to maintain quadriceps alignment as well as the cruciate ligament which was countering the internal rotation of the stifle.

If the cruciate ligament is stretched, then a Tibial Plateau Leveling Osteotomy is warranted.

The bowlegged patient is often seen to have an unusual gait at the time of weight bearing. When viewed from the rear, if the patient has a lateral projection of the stifle at the instant of weight bearing, then this motion is called a pivot shift. The pivot shift is created by a combination of cranial translation of the tibia combined with internal rotation of the

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stifle. It is mostly seen with cruciate repairs in stretched cranial cruciate ligament replacement surgery, following failure of the implants or tissues in the patient with bowlegged conformation. It is readily correctable by a Tibial Plateau Leveling Osteotomy plus realigning the limb with an external torsional osteotomy and a distal femoral osteotomy. If left unattended, severe wear of the medial femoral condyle is inevitable.

In the rottweiler and bullmastiff, distal femoral varus is often present, but it is also accompanied by internal tibial torsion. This creates a bowlegged appearance from both the femur and the tibia. This type of conformation is often associated with ruptures of the cranial cruciate ligament. Any type of repair will fail unless the alignment is corrected. Almost all revisions for failed cranial cruciate ligament repairs by fibular head advancement, over the top technique and lateral capsular sutures are associated with this kind of conformation. Revising such surgeries with larger suture or fishing line will have the same results as the failed surgery. The ideal correction for this condition is a valgus osteotomy of the distal varus femur, which will realign the patella and reduce the stress on the medial condyle of the femur. Correction of the ruptured cranial cruciate ligament by means of a Tibial Plateau Leveling Osteotomy with the associated external torsion osteotomy of the tibia will restore full function.

It is important to recognize whether the deviation creating the bowleggedness is in the femur or the tibia, and whether it is created by a varus or a torsion. In order to ascertain the location of the deformity and malalignment, perfect radiographic positioning is necessary. A lateral view of the stifle with the greater trochanter, fibular head, lateral malleolus in one plane will present as superimposed trochlear ridges and condyles in the normal dog. It is important that the knee is at ninety degrees for this positioning. If the lateral femoral condyle is cranial to the medial femoral condyle when the patient is properly positioned, then a distal femoral varus is suspected. Varus of the distal femur can be demonstrated radiographically by an anteroposterior view of the femur. This always requires the patient to be raised vertically to allow the long axis of the femur to be perpendicular to the xray beam. Once this position is accomplished and the patella is located in the trochlear sulcus, it should overlay the medial and lateral walls of the intercondylar notch. Once this position is attained, the varus of the femur can be readily measured. Surgery is recommended when the varus equals or exceeds ten degrees.

Internal tibial torsion is best diagnosed on the posteroanterior (caudocranial view) of the stifle, tibia and hock. The radiographic position that is most effective is to place the patient in sternal recumbency, and extend the hip with the stifle and tibia located on the cassette. The stifle is extended and the hock is allowed to be in its extended position, making no attempt to center the calcaneus over the distal tibia.

Since the stifle is forced into extension, no rotation at the knee joint is possible. If the stifle is not forced into extension, then errors will occur as the stifle is free to rotate both internally and externally. Perfect positioning for the stifle places the patella between the medial and lateral walls of the intercondylar notch. When the stifle is in this position, the medial border of the calcaneus should lie at the greatest

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depth of the talar sulcus. The hock is forced into extension simultaneous with forced extension of the stifle. If the patient is bowlegged due to internal tibial torsion, then the medial border of the calcaneus will lie lateral to the talar sulcus.

Internal torsion of the femur and varus of the proximal tibia are less commonly seen than the varus of the distal femur and internal torsion of the tibia. If present, these can be corrected by an external torsion osteotomy of the femur and a valgus osteotomy of the tibia. Since these are usually accompanied by rupture of the cranial cruciate ligament, a Tibial Plateau Leveling Osteotomy is a convenient kerf through which alignment correction of the tibia can be made. Failure to gain alignment of the femur and tibia will result in continued medial patellar luxation and the destructive forces of the stifle.

The tibial tubercle should be in a line with the foot, hock and patella when the dog is under anesthesia in a supine position. The dog is on his back, with the knee flexed at 90 degrees without internal or external rotation of the stifle. If the tibial tubercle is medial to the plane which includes the patella, the hock and foot, then a lateral tibial tubercle transposition is necessary back to that plane. If the alignment of the patella, tibial tubercle, hock and foot are in one plane, and a tibial tubercle is transposed laterally to treat a medially luxating patella, then the long term appearance of this patient will be a bowlegged conformation which predisposes this patient to rupture of the cranial cruciate ligament and excessive wearing of the medial compartment of the stifle.

This results in cartilage eburnation.

In the field trial springer spaniel, the patient may appear in normal conformation when standing on the exam table or participating in non-working activities. This patient may become bowlegged as a result of a hunting posture specific to this breed. The springer spaniel works and hunts in a very low â&#x20AC;&#x153;vacuum cleaner crouchâ&#x20AC;? in which the hips are externally rotated and the stifles are internally rotated. This seems to lower the center of gravity of the dog. When the patient assumes this posture, the tibial tubercle will be medial to the patella, as the hip is externally rotated and the stifle is internally rotated. This conformation creates a medial patellar luxation. Since the bone structure of this patient is normal, and the posture is desirable, the patient has been genetically engineered for this characteristic. The best correction for this medial patellar luxation is a rectus femoris transfer from the origin to the cervical tubercle. This allows the origin of the quadriceps muscles to be on the proximal femur. Consequently, rotation of the hip does not necessarily dictate abnormal alignment of the patella because all four heads of the quadriceps now originate on the femur. This eliminates the medially directed force on the patella. This is the only functional cause of medial luxating patella that I have experienced in clinical practice. All others are associated with anatomical malalignments.

The opposite appearance of bowleggedness is the knockkneed conformation. The knock kneed conformation places the stifle medial to the sagittal plane. This should be distinguished from true cow hocked appearance. The cow hocked appearance places the hip, stifle, tibial tubercle, hock and foot in a singular plane with the knee lateral to the sagittal plane. This cow-hocked appearance is created by external

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rotation at the hip. Knock kneed conformation is pathologic because the stifle undergoes external rotation and frequently an anterorotary instability. Anterorotary instability is the desire for the tibia to move cranially and rotate externally. This instability shifts the line of axial rotation of the tibia laterally, and stresses the craniomedial joint capsule which may produce an enlarged knob on the tibia just cranial to the medial collateral ligament. Patients which have knock kneed conformations are German shepherds, great danes, akitas, malamutes or huskies. The first feature to diagnose is the presence or absence of an OCD lesion on the lateral femoral condyle. Sometimes this lesion is subtle and is seen only as a flattened area without loss of cartilage. If an OCD lesion is present on the lateral condyle, then the patient may have laxity within the joint that is caused by a lack of bony spacer which is due to loss of the joint space with the OCD lesion.

This laxity is often diagnosed as a rupture of the cranial cruciate ligament, when in fact, the problem exists due to loss of bone. The tibial conformation must be observed as it is usually normal, but may have proximal tibial valgus or external tibial torsion present. The presence of OCD of the lateral femoral condyle, proximal tibial valgus and external tibial torsion causes a stress on the craniomedial joint capsule which leads to craniomedial rotary instability. Correction of

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the tibial deformities is by a proximal tibial varus osteotomy and an internal tibial osteotomy. If the lesion on the femur causes minimal deviation, the latter two osteotomies will shift the weight from the lateral to the medial condyle. The most significant change in alignment comes in the femur for the knock-kneed patient.

There are two forms seen clinically of distal femoral valgus. The first in when the trochlear is in line with the femur, but the supporting condyles are externally rotated around an axis that is perpendicular to the frontal plane. The second form is a distal femoral valgus deviation which occurs proximal to the trochlea. The treatment for the first is an osteotomy perpendicular to the sagittal plane, which separates the femoral condyles from the trochlear for the patella. Once that separation has occurred, then the distal femur can be relocated in alignment with the trochlea. If the distal femoral valgus is present, then a distal femoral varus medial closing wedge osteotomy will be curative. Caution should be taken in giant breeds that two plates be utilized at ninety degrees to one another. In addition, bone graft taken in strips from the ilium will enhance the rapidity of healing on these patients. The thin cortices and long limbs predispose dogs such as Great Danes to traumatic fractures without taking these precautions.

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Patellar Luxation: A Problem of Alignment Lussazione della rotula

Barclay Slocum DVM - Slocum Clinic - Eugene, Oregon, USA

Theresa Devine Slocum MS - Slocum Clinic - Eugene, Oregon, USA

Riassunto Le lussazioni della rotula sono dovute alle forze biomeccaniche che tirano la rotula stessa medialmente o lateralmente rispetto al piano sagittale. Al riallineamento dell’osso sul piano sagittale contribuiscono fondamentalmente tre elementi. Il primo è l’allineamento dell’anca, del ginocchio, del garretto e della zampa sul piano sagittale. Il secondo è la distorsione locale dei tessuti determinata dalla lussazione rotulea ed il terzo è il malallineamento funzionale dell’arto dovuto all’attività del paziente.

Le lussazioni rotulee mediali sono causate dalla retroversione della testa del femore, dalla torsione esterna del femore, dal varismo del tratto distale del femore, dal posizionamento mediale del tubercolo tibiale, dalla torsione tibiale interna, dal varismo della parte prossimale o distale della tibia e dall’osteocondrosi del condilo femorale mediale. un certo Ogni tipo di lussazione rotulea mediale, una volta che si sia instaurato, ha la tendenza a distorcere i tessuti in via di sviluppo secondo quadri caratteristici. La mancanza della compressione rotulea femorale nel solco trocleare fa sì che questo si sviluppi risultando poco profondo. L’eccessiva pressione sul condilo femorale mediale rallenta la crescita dello stesso inducendo un varismo femorale distale. Il tentativo di determinare la rotazione esterna del ginocchio provoca una deformazione da torsione esterna della tibia, un valgismo prossimale tibiale e una collocazione mediale del tubercolo tibiale. Il permanere della rotazione interna secondaria alla lussazione rotulea mediale può distorcere la capsula articolare e i legamenti crociati.

Il trattamento delle lussazioni rotulee mediali deve essere diretto in primo luogo a ripristinare la detorsione e correggere il valgismo del femore, in modo da consentire alla troclea di disporsi nel piano sagittale. Il solco trocleare deve essere abbastanza profondo da sostenere la posizione sagittale della rotula, dal momento che le strutture legamentose sono state stirate durante il processo di lussazione. Il piede, il garretto ed il ginocchio devono essere riportati sul piano sagittale attraverso una combinazione di osteotomie di detorsione e di correzione dell’angolazione. Ciò di solito richiede l’esecuzione di una osteotomia a livello della tibia e una a livello del femore, per correggere l’allineamento dell’arto.

Una volta che questo sia stato ottenuto, ottenuto si passa al trattamento dei tessuti locali a livello del ginocchio. Come regola generale, nessun tessuto deve essere sottoposto ad una notevole tensione per ottenerne il posizionamento, dal momento che in questi casi si ha un insuccesso con il ritorno dei tessuti interessati alla precedente posizione non sotto tensione. Sono esempi di correzione locale la condroplastica trocleare, la trasposizione laterale del tubercolo tibiale, la trasposizione laterale dell’origine del retto femorale, la sovrapposizione del tensore della fascia lata, la liberazione del retinaculum mediale e la risoluzione del pes anserinus. Per riportare i tessuti distorti sul piano sagittale, si utilizzano anche le tecniche di sutura della fabella alla rotula e della fabella alla cresta tibiale.

Le lussazioni rotulee laterali ed il relativo trattamento rappresentano un’immagine speculare del processo di allineamento e del riposizionamento dei tessuti distorti sul piano sagittale.

Patellar luxations are the result of biomechanical forces pulling the patella either medially or laterally to the sagittal plane. There are three basic elements which contribute to realignment of the patella in the sagittal plane.

The first is alignment of the hip, stifle, hock and paw in the sagittal plane. The second element is local distortion of tissues created by the patellar luxation, and the third element is a functional malalignment of the limb by activities of the patient.

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Medial patellar luxations are created by retroversion of the femoral head, external femoral torsion, varus of the distal femur, medial tibial tubercle position, internal tibial torsion, varus of the proximal or distal tibia, and OCD of the medial femoral condyle. Once the pattern of medial patellar luxation is established, there is a tendency to distort developing tissues in characteristic patterns. Lack of femoral patellar compression in the trochlear sulcus will cause the development of a shallow trochlear groove. Excessive pressure on the medial femoral condyle will slow growth of the medial condyle creating distal femoral varus. An attempt to provide external rotation of the stifle will create an external torsion deformity of the tibia, a proximal tibial valgus, and a medially placed tibial tubercle. The continured internal rotation secondary to the medial patellar luxation, can distort the joint capsule and the cruciate ligaments.

Treatment of medial patellar luxations must first be directed towards returning detorsion and valgus correction of the femur to allow the trochlear to lie in the sagittal plane. The trochlear sulcus must be sufficiently deep to support the sagittal position of the patella since the ligamentous structures have been stretched during the luxating process. The foot, the hock and the stifle must be returned to the sagittal plane through a combination of detorsional and angular corrective osteotomies. This usually takes but one osteotomy through the tibia and one osteotomy through the femur to provide the correction for limb alignment.

Once limb alignment has been obtained, the treatment of local tissues about the knee is pursued. As a general principle, no tissue should be put under forceable tension to achieve its position, as those tissues will fail and return to their unstressed location. Examples of local correction are trochlear chondroplasty, lateral tibial tubercle transposition, lateral transposition of the origin of the rectus femoris, tensor fascia lata overlap, medial retinacular release, and pes anserinus release. Fabellar to patella suture and fabellar to tibial crest sutures are also techniques to return distorted tissues to the sagittal plane.

Lateral patellar luxations and their treatment are a mirror image of the alignment process and the return of distorted tissues to the sagittal plane.

INTRODUCTION Current treatment of patellar luxation is focused on the alignment of tissues immediately about the stifle. It is important to recognize that rotation of the stifle is the twisting motion around an axis through the center of the hock and lateral third of the medial tibial plateau articular surface. Torsion is the permanent twist of the bone around the same axis.

The internally rotated stifle can be externally rotated by a lateral fabella to tibial tubercle suture. The medially luxating patella can be restrained in the trochlear groove by a lateral fabella to patellar suture. If the lateral retinacular tissues are lax, a lateral capsular imbrication, tensor fascia lata overlap, or vest over pants tightening of the lateral fabellopatellar ligament will stabilize the patella in the trochlear groove. If the medial retinaculum is tight, then a medial retinacular lengthening will allow the patella to be moved to the trochlea groove.

Although the trochlear chondroplasties, i.e. trochlear sulcoplasty, subchondylar excavation or trochlear recession, are useful in deepening the trochlea, they should not be used to prevent patellar luxation. Trochlear sulcoplasty is removing the cartilage and subchondral bone of the trochlea sulcus to deepen the trochlear groove. Subchondral excavation after elevating the articular cartilage from the subchondral bone is useful in deepening the trochlear sulcus in puppies less than six months old with a medial patellar luxation. A trochlear recession creates a wedge containing the trochlear sulcus and its intact cartilage, and recesses the subchondral bone.

This maintains the cartilage surface of the mature dog and is useful in deepening the trochlea sulcus.

Each of these techniques purpose is to deepen a shallow trochlea, which has been realigned with the quadriceps mechanism. If the trochlear chondroplasty techniques are used to force the patella to stay in the trochlear sulcus without quadriceps alignment, lateral pressure becomes applied to the patella. The result is loss of patellar cartilage or luxation of the patella from the patellar groove. Therefore, patellar stability requires both trochlear depth and limb alignment.

Tibial tubercle position is critically important to the alignment of the quadriceps mechanism and the alignment of the lower limb.

If the tibial tubercle is normally positioned on the tibia and the patella is medially luxated, then relocating the patella in the trochlea groove will realign the quadriceps mechanism. If the tibial tubercle is medially positioned on the tibia, then a lateral tibial tubercle transposition will realign the quadriceps mechanism. If the tibial tubercle is normally positioned on the tibia and a lateral tibial tubercle transposition is performed, immediately afterward the quadriceps mechanism appears to be properly aligned but the distal end of the straight patellar tendon is lateral to the sagittal plane. Over time, the straight patella tendon will return to the sagittal plane. As this occurs, the limb becomes bowlegged as the stifle internally rotates to re-establish the patellar tendon in the sagittal plane.

The medium term consequence of the iatrogenic bowlegged conformation is the predisposition to rupture of the cranial cruciate ligament. The long-term sequella of the bowlegged conformation is the degeneration of the medial compartment of the stifle as the chronic mechanical overload causes loss of the articular cartilage.

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There is a major principle of stifle mechanics to be learned from this behavior of the stifle. The straight patella tendon will return to the sagittal plane and any alteration of limb conformation will be manifested as limb malalignment. As the overall limb is aligned, particular attention needs to be directed to the position of the straight patellar tendon.

The following considerations are maintained. The straight patellar tendon should be in the sagittal plane. It should be in line with an imaginary line drawn from the femoral head and foot. The straight patellar tendon should be perpendicular to the tibial plateau. The patella and tibial tubercle should be in the sagittal plane in both flexion and extension of the stifle without holding the stifle in either internal or external rotation.

This is most easily done with the dog placed in dorsal recumbency and preventing the hip from abduction by placing a single fingertip on the lateral epicondyle of the stifle and flexing and extending the stifle using one fingertip of the opposite hand.

The purpose of this paper is to explore how non-quadriceps mechanism elements affect a patellar luxation.

FEMORAL CONFORMATION AND ALIGNMENT RETROVERSION OF THE FEMORAL HEAD Femoral head and neck retroversion causes the patient to externally rotate the hip in order to achieve a proprioceptively neutral joint. This necessitates the internal rotation of the stifle to allow the foot to be in the sagittal plane. The quadriceps mechanism is deviated at the patella by this action, causing a pull on the far side of the fabellopatellar ligament and retinaculum. These structures eventually give way and allow the patella to luxate.

DISTAL FEMORAL VARUS Distal femoral varus greater than 10 degrees creates an internal rotatory force which is inadequately opposed by the biceps femoris muscle. Consequently, repeated excesses of internal rotatory force at the stifle cause serial or catastrophic rupture of the caudal half of the cranial cruciate ligament followed by rupture of the cranial half of the ligament. The same internal rotatory force deviates the quadriceps mechanism and stretches the lateral fabellopatellar ligament and joint capsule. Medial patellar luxation follows that capsular stretching.

OCD OF THE MEDIAL FEMORAL CONDYLE Osteochondritis dissecans of the medial femoral condyle creates a loss of femoral length on the medial femoral condyle. This causes a true genu varum due to the loss of bone substance. There is also a laxity of the cruciate ligaments created by this osseus deficiency which may be mistaken for a rupture of the cranial cruciate ligament. Both the

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genu varum and the ligamentous laxity allow an excessive internal rotation at the stifle. The consequence is deviation of the quadriceps mechanism at the patella and stretching of the lateral fabellopatellar ligament and joint capsule. Naturally, medial patellar luxation follows.

TIBIAL CONFORMATION AND ALIGNMENT Valgus of the Proximal Tibia Valgus of the proximal tibia creates a knock-kneed appearance to the patient. This conformation causes the foot to be lateral to the stifle and produces an external rotatory force which produces external rotation at the stifle. If the proximal tibial valgus is excessive, the pes anserinus muscle group cannot counteract the external rotation with internal rotatory force, and the craniomedial joint capsule begins to stretch.

This deviates the quadriceps mechanism laterally beginning at the patella which causes a lateral force at the patella and stretches the medial fabellopatellar ligament and joint capsule. This sequence of events that occurs with knock-kneed dogs results in craniomedial rotatory instability of the stifle and a lateral patellar luxation.

MEDIAL DISPLACEMENT OF THE TIBIAL TUBERCLE The normal alignment of the hindlimb is present when the patella (not luxated), the tibial tubercle, the hock and the foot are all in the sagittal plane. If the tibial tubercle is pathologically positioned medial to the sagittal plane, the quadriceps mechanism will have a medial deviation beginning at the patella. The consequence of this conformation is stretching of the lateral fabellopatellar ligament and lateral joint capsule. Eventually the patella will luxate medially. If the medial patellar luxation is extreme, the internal rotation of the stifle will result in damage to the caudal band of the cranial cruciate ligament and possible rupture of the entire cranial cruciate ligament. Lateral transposition of the tibial tubercle is curative.

INTERNAL TIBIAL TORSION Internal tibial torsion is the permanent internal twisting of the tibia around its functional long axis. This causes the entire stifle to be lateral to a line between the femoral head and the foot. This results in an internal rotatory force that stresses the caudal half of the cranial cruciate ligament.

Partial rupture or complete rupture of the cranial cruciate ligament results. Ruptures of the cranial cruciate ligament allow cranial migration of the tibia with respect to the femur which reduces the femoropatellar compression. This often results in medial patellar luxation and this luxation will often be uncontrolled until the cranial cruciate ligament rupture is treated.

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FUNCTIONAL POSTURES AFFECT ON ALIGNMENT CROUCH AND EXTERNAL HIP ROTATION OF THE HIP Springer spaniel hunting crouch is a characteristic of the breed. The normal Springer will stand with the joints of the hindlimbs in the sagittal plane. The same dog will assume a crouch while hunting and maintain that posture for many hours and many miles. The crouch is accomplished by externally rotating the hip, internally rotating the stifle, and lowering the center of gravity of the dog by flexing his joints. This seems to lower the dog closer to the ground and widen his base. This appears to be better for sniffing. The crouch position will develop extremely large biceps femoris muscles. The rectus femoris is the only head of the quadriceps which arises on the pelvis and inserts on the tibial tubercle. The other three heads arise on the femur. With the dog in the crouch position, the straight-line pull of the rectus femoris is deviated medially beginning at the patella. The consequence is a medially directed force on the patella that may stretch the lateral fabellopatellar ligament and joint capsule. The result is a medial patellar luxation that responds to lateral transposition of the rectus femoris to the cervical tubercle of the femur.

PATHOLOGIC CONDITIONS CAUSING PATELLAR LUXATION Secondary to Rupture of the Cranial Cruciate Ligament If an internal rotatory force is applied to the tibia, the caudal half of the cranial cruciate ligament is stressed. Partial rupture or complete rupture of the cranial cruciate ligament may result. Ruptures of the cranial cruciate ligament allow cranial displacement of the tibia with respect to the femur and that translation reduces the femoropatellar compression. This often results in a medial patellar luxation which will continue until the cranial cruciate ligament rupture is treated.

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OCD OF THE LATERAL FEMORAL CONDYLE Osteochondritis dissecans of the lateral femoral condyle creates a loss of femoral length on the lateral femoral condyle. This causes a true genu valgum due to the loss of bone substance. There is also a laxity of the cruciate ligaments created by this osseus deficiency which may be mistaken for a rupture of the cranial cruciate ligament. Both the genu valgum and the ligamentous laxity allow an excessive external rotation at the stifle. The consequence is deviation of the quadriceps mechanism at the patella and stretching of the medial fabellopatellar ligament and joint capsule. Naturally, lateral patellar luxation follows. This problem is often seen in giant breed dogs such as the Great Dane and Irish wolfhound. If the valgus is severe, the tibia may translate laterally with respect to the femur. Realignment of the hindlimb to the sagittal plane is mandatory.

EXCESSIVE TIBIAL PLATEAU SLOPE If the slope of the tibial plateau is 30 degrees or greater, the cranial tibial thrust caused by axial compression of the tibia on that sloped tibial plateau is sufficient to stretch or rupture the cranial cruciate ligament. Partial rupture or complete rupture of the cranial cruciate ligament may result with explosive bursts such as chasing squirrels. Ruptures of the cranial cruciate ligament allow cranial displacement of the tibia with respect to the femur and that translation reduces the femoropatellar compression.

This type of patient often lacks the cranial prominence created by the patella on the lateral silhouette of the hindlimb. The cranial translation of the tibia and the straight-line pull of the quadriceps mechanism to the tibial tubercle cause this peculiar long thigh appearance. In addition these patients are characteristically bandy-legged secondary to internal tibial torsion which creates internal rotation at the stifle. This often results in medial patellar luxation. This luxation will often be uncontrolled until the excessive slope of the tibial plateau and internal tibial torsion is addressed.

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TPLO: Tibial Plateau Leveling Osteotomy for Treatment of Cranial Cruciate Ligament Injuries Osteotomia livellante del piatto tibiale (TPLO) per il trattamento delle lesioni del legamento crociato craniale

Barclay Slocum DVM - Slocum Clinic - Eugene, Oregon, USA

Theresa Devine Slocum MS - Slocum Clinic - Eugene, Oregon, USA

Riassunto Le due funzioni primarie del legamento crociato craniale sono quelle di limitare la traslazione craniale della tibia rispetto al femore e la rotazione interna della tibia. Quando su quest’ultima si applica una forza eccessiva, che determina la rotazione forzata verso l’interno o la traslazione craniale, il legamento crociato craniale si rompe. La chiave del successo della correzione dei problemi di questo legamento è la neutralizzazione delle forze distruttive. La ricostruzione del legamento crociato craniale, da sola, predispone la riparazione ad una nuova rottura.

La forza primaria responsabile della traslazione craniale della tibia è la spinta tibiale craniale, generata dall’inclinazione del piatto tibiale. La forza primaria responsabile della rotazione interna della tibia deriva dalla conformazione arcuata dell’arto a livello del femore o della tibia. La neutralizzazione della spinta tibiale craniale si ottiene con l’osteotomia livellante del piatto tibiale, che riduce l’angolo formato da quest’ultimo con l’asse maggiore dell’osso. Ciò fa sì che le forze esercitate sul condilo femorale siano perpendicolari alla superficie articolare della tibia. Ciò arresta le forze di traslazione generate dall’inclinazione. L’inclinazione del piatto tibiale è presente nei cani normali e in quelli anormali e la sua riduzione va effettuata tenendo conto delle caratteristiche individuali. La rotazione patologica interna del ginocchio indotta dalla conformazione arcuata dell’arto deve essere corretta con l’osteotomia di detorsione o di correzione del valgismo della tibia. Se l’arcatura del femore è dovuta ad un varismo che contribuisce a sollecitare in modo abnorme l’articolazione del ginocchio, anche questa alterazione deve essere corretta con un’osteotomia valgizzante.

Secondariamente alla rottura del legamento crociato craniale, la traslazione craniale della tibia esercita una trazione in avanti del corno caudale del menisco mediale, una porzione del quale finisce per essere schiacciata dal condilo femorale, determinando una lesione da schiacciamento o una lacerazione a semicerchio. Dal momento che questa condizione si ha solo con la lassità del legamento crociato craniale, anche questa deve essere trattata. Poiché il problema è che il menisco è bloccato in una posizione che consente il traumatismo da parte del condilo femorale, la soluzione è quella di liberare il menisco. Perciò, si pratica un’incisione per liberare il menisco dall’effetto dell’anello di tensione che agisce sul menisco mediale e si permette al corno caudale di quest’ultimo di spostarsi caudalmente sotto l’influenza del condilo femorale. La liberazione del menisco si effettua caudalmente al legamento collaterale mediale, resecando il corpo mediale del menisco che viene scontinuato dal bordo mediale a quello laterale.

La rottura del legamento crociato craniale ha segnato la fine della carriera della maggior parte dei cani atleti fino a che non è stata messa a punto la tecnica dell’osteotomia livellante del piatto tibiale (TPLO). Lo scopo di questo intervento è quello di riportare alla normalità i pazienti con le seguenti caratteristiche: (1) ripristino della capacità di sedersi normalmente, (2) recupero totale della muscolatura della coscia, (3) arresto dell’artropatia degenerativa e (4) ritorno ai livelli funzionali precedenti alla lesione.

The two primary functions of the cranial cruciate ligament are to limit cranial translation of the tibia with respect to the femur, and to limit internal rotation of the tibia. When an excessive force is applied to the tibia which causes forced internal rotation or cranial translation, the cranial cruciate ligament will rupture. The key to successful correction of the deficient CCL stifle, is the neutralization of the destructive forces. Reconstruction of the CCL ligament alone, will predispose to rupture of the repair.

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The primary force responsible for cranial translation of the tibia is the cranial tibial thrust which is generated by the tibial plateau slope. The primary force responsible for the internal rotation of the tibia is created by a bowlegged conformation in either the femur or the tibia. Neutralization of the cranial tibial thrust is provided by the Tibial Plateau Leveling Osteotomy, which reduces the angle of the tibial plateau with respect to the long axis of the tibia. This causes the forces on the femoral condyle to be perpendicular to the articular surface of the tibia. This stops the translating force provided by the slope. The tibial plateau slope is present in normal and abnormal dogs, and reduction of that slope is in accordance with the individual stifle. Pathologic internal rotation of the stifle created by the bowlegged conformation, must be corrected by a detorsional or valgus osteotomy of the tibia. If the femur has a bowlegged conformation due to varus which is contributing to stress at the knee joint, this must likewise be corrected by a valgus osteotomy.

Secondary to rupture of the CCL, the cranial translation of the tibia pulls the caudal horn of the medial meniscus forward so that the femoral condyle will crush a portion of the meniscus, producing a crush lesion or a bucket handle tear.

Since this condition occurs only with the laxity of the CCL, it also needs to be addressed. Since the problem is holding the meniscus in a position which enables trauma to occur by the femoral condyle, the solution is a meniscal release. A meniscal release incises the tension ring effect of the medial meniscus, and allows the caudal horn of the medial meniscus to move caudally under the influence of the femoral condyle. A meniscal release is performed caudal to the medial collateral ligament and transects the medial body of the meniscus from its medial border to its lateral border.

A rupture of the cranial cruciate ligament has been a career ending for most canine athletes until the Tibial Plateau Leveling Osteotomy (TPLO). The objective of the TPLO is to return patients to normal with the following characteristics: (1) return of the ability to sit normally; (2) regain full thigh musculature; (3) stop the degenerative joint disease; and (4) return to preinjury function.

Rupture of the cranial cruciate ligament has presented difficulties to the veterinary orthopedic surgeon because results have been good in some cases using traditional methods, however other cases have been less than satisfactory, yielding fibrosis of the joint inhibiting the ability to fully flex the stifle during siting, chronic soreness and the resulting incomplete return of thigh musculature. In addition the progression of degenerative joint disease has occurred and patients have failed to return to preinjury function. All traditional methods have been directed towards replacing the cranial cruciate ligament or substituting for its function.

The criterion for success of these surgeries has been by the elimination of the cranial drawer sign. In some cases, patients have returned to normal function and maintained a cranial drawer sign. Others have had no drawer sign but have continued to degenerate. Therefore, the success of stifle surgery cannot be evaluated by the absence of a cranial drawer sign.

In the search for a successful outcome in the treatment of a cranial cruciate deficient knee, the criteria for judging the results of surgery hinge on four factors: the ability of the dog to sit fully, return of thigh musculature, cessation of the degenerative process, and return to preinjury function. The discovery of the tibial compression test by Henderson and Milton in 1978 provided the initial insight to understand the stifle biomechanics. They observed that when the hock was flexed, cranial translation of the tibia occurred with a ruptured CCL. In 1983 the cranial tibial thrust was described as responsible for that translation. This introduced the concept of forces to treatment of the cranial cruciate ligament deficient stifle.

The unique anatomy of the canine hindlimb allows the creation of a force called the cranial tibial thrust. There are two features that are responsible for this: the combined tendon of the biceps femoris and the semitendinosus links the distal femur to the calcaneus. The consequence of that

anatomic structure is that when the stifle is extended, the hock joint is automatically extended. When the stifle is flexed, the hock joint can be flexed or extended. The second anatomic feature is that the tibial plateau is at an angle to the perpendicular to the line between the instant centers of motion between the stifle and the hock. The forces generated in the Achilles tendon define the direction and magnitude of the forces along the long axis between the joint centers.

Since the tibial plateau is sloped, the contact point between the femoral condyle and the tibial plateau lies cranial to the line of force. The force of compression across the stifle joint passes through the point of contact between the femoral condyle and the tibial plateau, and is perpendicular to the tibial plateau surface. This force of compression across the stifle joint can be resolved into two components, a component parallel to the line between the centers of the hock and stifle and a component perpendicular to the line between the centers. The second component is called the cranial tibial thrust. It is generated by the presence of the slope of the tibial plateau and it increases in its magnitude proportional to the tangent of the slope of the tibial plateau.

If the slope of the tibial plateau were zero, the cranial tibial thrust would be zero. If the slope of the tibial plateau were 45 degrees, the cranial tibial thrust would be equal to the force along the axis of the instant centers. As the slope of the tibial plateau approached 90 degrees, the cranial tibial thrust would become infinite.

In the stifle the cranial tibial thrust is opposed by the muscle forces of the biceps femoris, and the hamstring muscle group. If these forces and the cranial tibial thrust are in balance, there is no stress on the CCL. Since perfect balance at all times is unattainable, the CCL is under intermittent stress of a cranial tibial thrust that exceeds the forces of the hamstrings and biceps. Rupture of the cranial band of CCL occurs when the force of cranial tibial thrust exceeds the ligamentâ&#x20AC;&#x2122;s ability to respond. Secondary to rupture of the CCL

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cranial translation of the tibia can occur. The next structure to restrain the cranial tibial thrust is the caudal horn of the medial meniscus. As this structure is stressed in the absence of the CCL, it responds by being crushed, producing a bucket handle tear, or undergoing metaplasia which is characterized by a stiff or â&#x20AC;&#x153;woodyâ&#x20AC;? texture.

The problem of the cranial cruciate ligament deficient stifle is the control of the cranial tibial thrust. The Tibial Plateau Leveling Osteotomy effectively reduces the cranial tibial thrust to zero by changing the angle of the tibial plateau slope. Since the biceps femoris and the hamstring muscles of the pes anserinus group pull caudally, a balance of these muscle forces and the cranial tibial thrust is achieved at approximately 5 degrees of tibial plateau slope.

In 1999 Arnoczky et al confirmed this amount of tibial plateau slope to neutralize the effects of the cranial tibial thrust. If the tibial plateau slope is reduced further, stress is applied to the caudal cruciate ligament.

Treatment of the meniscus is necessary when the cruciate is absent or ruptured. The problem is that the caudal horn of the medial meniscus attempts to prevent the cranial translation and the full pathologic consequence of the cranial tibial thrust is directed to that structure. In order to relieve the stress on the caudal horn of the medial meniscus, a meniscal release is performed. The purpose of this procedure is to free the meniscus from the crushing effects of the femoral condyle. The most common approach to the medial meniscus is caudal to the medial collateral ligament. A sixteen gauge needle is inserted caudal to the medial collateral ligament and proximal to the tendon of the semimembranosus. A number 11 blade is inserted to cut the tension band

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ring of the medial meniscus transversely. The cut is directed toward the tubercle of Gerdi. The cross section of the cut meniscus is visualized for evidence of trauma to the meniscus by the femoral condyle. Horizontal cleavage lesions, crushing of the caudal horn, and bucket handle tears are commonly seen on inspection.

The cranial half of the cranial cruciate ligament is responsible for restraint of cranial tibial translation whereas the caudal half of the CCL is responsible for restraint of internal rotation. The cranial cruciate deficient stifle can be successfully treated by a TPLO as long as the alignment of the limb is normal. If there is a bowlegged conformation, internal rotation at the stifle is the consequence of that conformation and limb realignment to the sagittal plane is necessary.

The TPLO procedure has been performed on over 1500 cases. The results have been uniform and most gratifying.

Criteria for success are the ability to return to full sit, return of full thigh circumference, cessation of the degenerative process and return to preinjury function. Clients are given strict instruction on the postoperative management as the dogs often want to return to activity prior to complete healing and rehabilitation. Stress to the straight patellar tendon occurs by propulsive activity in the first 2 months post surgery. Other postoperative complications have included fracture of the tibial tubercle, medial patellar luxation, disruption of internal fixation, and infection.

The overall experience of TPLO for the surgeon, patient and client has been excellent. Early return to function with minimal inconvenience has endeared this procedure to the owners of both pet and working dogs.

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Surgical management of hip dysplasia Opzioni chirurgiche per la displasia dell’anca

Barclay Slocum DVM - Slocum Clinic - Eugene, Oregon, USA

Theresa Devine Slocum MS - Slocum Clinic - Eugene, Oregon, USA

Riassunto La valutazione accurata della displasia dell’anca si basa su esame clinico, radiografie del bacino in tre dimensioni e palpazione sotto anestesia. Ciò consente di valutare la conformazione della testa e del collo del femore, l’orientamento, la profondità e lo riempimento dell’acetabolo, lo status della rima acetabolare dorsale, la presenza o assenza della cartilagine articolare e la lassità della capsula articolare.

I metodi di base per la correzione della patologia dell’anca sono l’Allungamento del collo femorale, l’Osteotomia pelvica, la Dartroplastica e la Sostituzione totale dell’anca. L’Allungamento del collo femorale è efficace nei casi in cui questo è breve e/o la capsula articolare è lassa. L’Osteotomia pelvica è indicata per riorientare l’acetabolo in modo da riazzerare l’inclinazione e catturare la testa femorale lussata. La Dartroplastica viene effettuata per alleviare il dolore di una capsula articolare lesionata e garantire la stabilità dell’anca ai cani con lussazione e riempimento acetabolare.

La Sostituzione totale dell’anca è un metodo efficace per trattare i casi in cui la cartilagine è stata danneggiata e si ha lo sfregamento dell’osso sull’osso.

Nelle forme lievi di displasia dell’anca è presente una lassità della capsula articolare ed un leggero difetto di orientamento dell’acetabolo, senza alcuno riempimento. La condizione può essere trattata con una Dartroplastica di minore entità che estende la rima acetabolare e corregge il malorientamento. Se quest’ultimo è più significativo, si ricorre all’Osteotomia pelvica per coprire la testa del femore con la cartilagine articolare mantenendo un’inclinazione orizzontale. In questo modo si riposiziona efficacemente l’anca lussata o rilussata in posizione stabile e la capsula articolare garantisce il contrasto favorendo la stabilità.

Nelle forme moderate di displasia dell’anca la testa del femore ha subito una lussazione dall’acetabolo e si appoggia lateralmente e un po’ dorsalmente ad esso, vincolato dal legamento della testa del femore nella posizione lussata. Il rapido stiramento della capsula articolare ed il danneggiamento dell’acetabolo impongono un’Osteotomia pelvica per riorientare l’acetabolo con il bordo acetabolare dorsale inclinato in posizione orizzontale, per alleviare lo stress sulla rima dorsale danneggiata e sulla capsula articolare dorsale. La testa del femore viene riposizionata all’interno dell’acetabolo e il contatto della cartilagine sulla cartilagine garantisce una funzione a lungo termine senza artropatia degenerativa.

Nelle forme gravi di displasia dell’anca, si riscontra uno riempimento acetabolare associato alla lussazione e il danneggiamento della rima dorsale e della capsula articolare. L’Osteotomia pelvica ricolloca la testa del femore sugli osteofiti centrali dell’acetabolo in via di riempimento. Questa mancata corrispondenza del raggio dell’acetabolo con quello della testa del femore provoca un’eccessiva pressione su quest’ultima e una distruzione della cartilagine articolare. In questi casi, la Dartroplastica stabilizza la testa del femore nella sua posizione lussata e offre stabilità all’articolazione. Se la cartilagine è consumata e si è giunti al contatto dell’osso sull’osso, è indicata la Sostituzione totale dell’anca.

Accurate assesment of the hip dysplastic process is obtained by physical examination, radiographs of the pelvis in three dimensions, and palpation under anesthesia. This allows evaluation of the conformation of the femoral head and neck, orientation of the acetabulum, the depth and filling of the hip, the status of the dorsal acetabular rim, the presence or absence of articular cartilage, and the laxity of the joint capsule.

The basic tools for correction of the hip pathology are Femoral Neck Lengthening, Pelvic Osteotomy, Darthroplasty

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and Total Hip Replacement. The Femoral Neck Lengthening is effective in cases with short femoral neck and/or lax joint capsule. The Pelvic Osteotomy is effective in reorienting the acetabulum to zero slope and capturing the luxating femoral head. The Darthroplasty is recommended for providing pain relief to an injured joint capsule and hip stability to dogs with luxation and acetabular filling. The Total Hip Replacement is an effective means in treating hips in which the cartilage is damaged, and bone is rubbing on bone.

In the mild forms of hip dysplasia, there is laxity of the joint capsule and mild malorientation of the acetabulum with no filling. This condition can be treated with a minor Darthroplasty which extends the acetabular rim and corrects the mild malorientation. If the malorientation of the acetabulum is more significant, then a Pelvic Osteotomy is employed in order to cover the femoral head with articular cartilage with a horizontal slope. This effectively relocates the luxated or reluxated hip in a stable position and the joint capsule will contract to assist in that stability.

In moderate forms of hip dysplasia, the femoral head has luxated from the acetabulum and rests laterally and slightly dorsally, tethered by the ligament of the femoral head in the luxated position. Rapid stretching of the joint capsule and damage to the acetabulum require a Pelvic Osteotomy to reorient the acetabulum with the DAR slope in a horizontal position in order to relieve the stress on the injured dorsal rim and dorsal joint capsule. The femoral head will relocate within the acetabulum and cartilage on cartilage will provide longterm function without degenerative joint disease.

In severe forms of hip dysplasia, there is acetabular filling in addition to the luxation and damage to both the dorsal rim and the joint capsule. A Pelvic Osteotomy will relocate the femoral head on the central osteophytes of the filling acetabulum. This mismatch of the radius of the acetabulum and the femoral head will cause excessive pressure on the femoral head and destruction of the articular cartilage. Under these circumstances, a Darthroplasty will stabilize the femoral head in its luxated position and provide stability to the hip joint. If the cartilage is worn and there is bone on

Hip dysplasia has several forms, each of which has a different cause. The most common form of hip dysplasia is acetabular hip dysplasia. There are two causes of this dysplasia, which act independently or in combination. The first cause is malorientation of the acetabulum, which is diagnosed from the DAR radiographic view. The slope of the DAR of a normal hip is measured by placing the template over the dorsal spinous process of the lumbar and measuring the acute angle formed by the subchondral bone of the dorsal. If the measurements of the both the left and right hip are added together, the distortion produced by rotation of the pelvis during radiographic positioning is neutralized. This can occur in the pathologic hip. If the combined slope of the acetabuli is greater than twenty degrees, the patient has acetabular hip dysplasia. The normal patient has fifteen degrees or less combined acetabular slope. If the slope of the DAR is fifteen to twenty degrees, other factors such as depth of the acetabulum in combination with cup malorientation will determine the presence of hip dysplasia. Reading the acetabular slope for the individual hip in the properly positioned dog is an accurate means of determining the amount of correction for a pelvic osteotomy.

The second cause of acetabular hip dysplasia is shallowness of the acetabulum. The normal acetabulum has sixty percent of the femoral head covered by dorsal acetabular rim on the ventrodorsal pelvic radiograph. If a frog view or a compression view radiograph of the ventrodorsal pelvis is taken and the femoral head is seated with no acetabular filling present, then the femoral head radius times the sin of 7.5 degrees is the maximum lateral displacement of the center of the femoral head from the dorsal rim of the acetabulum (45% femoral head coverage at 7.5째). It is rare that the dorsal acetabular rim articulates to the lateral margin of the dorsal acetabular rim. Therefore, 50% acetabular coverage is a more realistic value for the minimum dorsal acetabular rim cover-

age.

Acetabular hip dysplasia with malorientation of the acetabular cup is diagnosed on the DAR view or a tomogram.

This case can be treated by pelvic osteotomy if there is no or minimal filling of the acetabulum with osteotophytes. The osteophyte free acetabulum has a uniform cartilage space of approximately one millimeter as seen on the frog view with forty-five degrees of abduction or the ventro-dorsal compression view. Patients with little of no acetabular filling are usually young with high joint inflammation, or older patients with mild inflammation and joint laxity. The purpose of the pelvic osteotomy is to reorient the acetabulum so that the femoral head is driven into the cup as the hip is put under load during daily activities. The slope should be brought to zero by the pelvic osteotomy, but not overrotated past zero, because the femoral neck will contact the dorsal rim during abduction. This can cause pain and long term degenerative joint disease. The acetabulum that is reduced to zero by a pelvic osteotomy can be expected to last a lifetime of normal use.

Under conditions of excessive joint capsule stretching, a pelvic osteotomy may reorient the acetabulum to zero but the femoral head may lie lateral to the cup. A femoral neck lengthening increases the distance between the greater trochanter and the femoral head. This is accomplished by splitting the femur longitudinally in the sagittal plane and separating the greater trochanter from the femoral head by placing a wedge in the kerf of the longitudinal cut. Lengthening the femoral neck does not push the trochanter laterally as the muscles and joint capsule are already stretched to their lateral limit. Femoral neck lengthening pushes the femoral head medially to seat in the properly oriented acetabulum. This procedure will overcome a stretched joint capsule as long as the acetabular slope is brought to zero by the pelvic osteotomy. Excessive femoral neck lengthening

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will cause ventral luxation of the femoral head, if the acetabulum has been overrotated by a pelvic osteotomy, or will cause external rotation of the hip after the external hip rotator muscles are stretched to their limit.

If acetabular hip dysplasia with malorientation of the acetabular cup is of long duration or of high inflammation, the acetabulum will begin to fill with osteophytes. The frog view or compression radiographic view will demonstrate an acetabular joint space that is wide or tapers from normal to wide as viewed from lateral to medial. This filling of the acetabulum by central acetabular osteophyte production causes the radius of curvature of the acetabulum to increase. If the femoral head is forced into the acetabulum by a pelvic osteotomy, the incongruity between the acetabulum and the femoral head will cause excessive pressure to occur on the cartilage of the femoral head and eburnation of femoral cartilage will occur. In these cases to avoid excessive pressure on the femoral head a pelvic osteotomy is avoided, and a DARthroplasty is the surgery of choice.

The standard DARthroplasty is effective in treating the capsular component of hip pain. The bone on bone component of hip pain occurs after the articular cartilage is worn to eburnated bone. The standard DARthroplasty is designed to allow the femoral head to luxate dorsally to the limit of the ligament of the femoral head. The term luxate is used here to mean that the femoral head is out of the acetabulum but inside of the joint capsule. In this position the dorsal rim of the acetabulum rests just dorsal to the fovea capitis. The femoral head is supported by the stretched teres ligament and stretched joint capsule. This stretching is the main source of pain experienced by the dog. The Dorsal Acetabular Rim arthroplasty augments the dogâ&#x20AC;&#x2122;s dorsal acetabular rim by placing a bone graft, taken from the wing of the ilium, dorsal to the hip joint capsule. The lateral limit of the bone graft is at the dorsal apex of the luxated femoral head. The graft contacts the prepared pelvis dorsal to the acetabulum. Once the bone graft heals to the pelvis, the femoral head is supported by joint capsule which is supported by bone, and the capsular pain disappears. An unexpected long-term finding is that the femoral head will usually migrate back into the

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acetabulum and become congruent with the acetabular cartilage within the limits of the central osteophyte production.

To date our long-term follow up shows good function five years post surgery.

A minor DARthroplasty is used to prevent lateral migration of the hip and stabilize the mildly dysplastic hip by laterally extending the dorsal acetabular rim. Once the hip no longer translates laterally, the hip stabilizes in the position of congruity with femoral articular cartilage mating with acetabular cartilage. A major DARthroplasty is used to prevent dorsal hip migration and gain stability of the hip in young dogs in which the ligament of the femoral head has ruptured and dorsal migration of the femoral head has occurred. As the major DARthroplasty matures, the patients go from a base narrow stance and gait to base normal.

Once the femoral head remains in the chronically luxated position, there is wear between the cartilage of the femoral head and the dorsal acetabular rim. As the cartilage is breached and bone is rubbing on bone, a salvage procedure is indicated. Bone on bone is seen as a fine line, which looks like a thin pencil line on the DAR view. The classic treatment for bone on bone pain is a femoral head and neck excision. Although many dogs experience good function, many more dogs live a life of restricted hip extension and recurring contractor of the scar tissue that supports the hip. A better method of treating the bone on bone hip is a Total Hip Replacement. A Total Hip Replacement eliminates bone on bone pain by substituting the metal on plastic weight bearing joint, for the worn out hip. There are two major types currently in use in the United States of America. The Biometrics canine total hip is the standard modular cemented total hip. The Kyon canine total hip is the new modular cementless total hip. Successful implantation of a total hip will return the patient to full function.

All of the methods of hip treatment are very successful as long as the cases are properly selected and the surgery is skillfully performed. Accurate diagnosis and a thorough understanding of the pathology of the dysplastic process allow specific treatment of the individual patient. Successful return to normal function is the desired result of the surgeonâ&#x20AC;&#x2122;s knowledge and skill.

40° Congresso Nazionale SCIVAC

The Differential Diagnosis and Treatment of Parasitic Dermatoses of the Dog and Cat Diagnosi differenziale e trattamento delle dermatosi parassitarie nel cane e nel gatto

Candace A Sousa DVM - Diplomate, American Board of Veterinary Practitioners Canine and Feline Practice Diplomate, American College of Veterinary Dermatology - Animal Dermatology Clinic - Sacramento

Riassunto Le dermatosi del cane e del gatto causate dalle infestazioni parassitarie sono fra le condizioni più frequentemente diagnosticate dai dermatologi veterinari. Le reazioni allergiche al morso di pulci sono ancora il più comune disordine da ipersensibilità osservato in queste specie animali. Anche pidocchi ed acari come Sarcoptes scabiei, Notoedres cati, Demodex spp., Cheyletiella spp., ed Otodectes cynotis possono causare dermatosi, che possono o meno essere pruriginose. Ognuno di questi parassiti determina la comparsa di malattie con quadri clinici propri ed esclusivi.

La capacità del veterinario di diagnosticare queste dermatosi e identificare l’infestazione si basa sull’impiego di vari metodi. Fra questi, è utile l’esame microscopico del materiale prelevato mediante raschiato cutaneo o il ricorso ai test immunologici per valutare la presenza di anticorpi che possono determinare la comparsa di malattie clinicamente manifeste.

Inoltre, ogni infestazione può essere trattata con molti prodotti differenti ad azione insetticida attualmente disponibili in commercio ed il metodo d’elezione varia da un caso all’altro a seconda delle caratteristiche dell’animale e del suo ambiente: sicurezza, costo e disponibilità del prodotto e tipo di proprietario. L’introduzione di nuovi farmaci e nuovi metodi per l’impiego di quelli già esistenti ha modificato il modo di trattare molte di queste malattie.

La terapia delle infezioni secondarie e dei relativi segni clinici è un’altra parte importante del protocollo da attuare in questi casi. Infine, in molti casi, per completare il successo del trattamento, è necessario intervenire sull’ambiente e sugli altri animali eventualmente presenti nel nucleo familiare, ed effettuare una corretta educazione del cliente.

Canine and feline dermatoses caused by parasitic infestations are some of the most frequent diagnoses made by veterinary dermatologists. Allergic reactions to the bite of a flea are still the most common hypersensitivity disorder seen in dogs and cats. Lice and mites, such as Sarcoptes scabiei, Notoedres cati, Demodex spp, Cheyletiella spp, and Otodectes cynotis, can also cause dermatoses that may or may not be pruritic. Each of these parasites causes its own unique clinical disease.

The ability of the veterinarian to diagnose these dermatoses and identify the parasitic infestation involves a variety of methods. Microscopic examination of material obtained with a skin scraping or immunologic testing to evaluate the presence of antibodies that can produce clinical disease are useful tools.

Each infestation can also be treated with many different insecticidal products currently available and the method of choice will vary in each case depending upon the animal and its environment; the safety, cost, and availability of the medication; and the owner. The introduction of new medications and new methods of using existing medications has changed the way we treat many of these diseases.

Treatment of the secondary infections and symptoms is another important part of the protocol for helping the animal.

And treatment of the environment and other animals in the household, if indicated, as well as client education completes the successful cure in many cases.

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FLEAS

MITES

Ctenocephalides felis is the most prevalent species of flea found on dogs and cats. Flea bite hypersensitivity is the most common hypersensitivity disorder of these animals.

Up to 40% of the dogs in a flea-endemic area can produce IgE to the allergenic components in flea saliva. Affected animals generally manifest their pruritus on the caudal half of the body including the tailhead, caudal thighs, and ventral abdomen. In cats, crusted papules can also be noted around the neck.

The diagnosis of flea allergy dermatitis is made using several pieces of information. In the history, the owner should be questioned about the presence of fleas or “flea dirt”. On physical examination, the presence fleas or flea feces on the dog or cat is noted as well as the lesions and distribution of the dermatitis. An intradermal skin test using flea antigen (Greer Laboratories) at a 1:1000 w/v dilution along with a negative and positive control will yield a positive immediate reaction in the majority of flea allergic animals.

One of the current methods of flea control involves the use of a collar. Most are helpful when they contain an insect growth inhibitor (IGI) such as methoprene or nylar.

These have no effect on the adult flea that is biting the animal and producing clinical disease. Sprays that are sold by veterinarians usually contain pyrethrins or synthetic pyrethrins in an alcohol or water-based vehicle. Some are combined with an IGI. The systemic IGI lufenuron (Program®) will interrupt the life cycle of the flea but does not have any effect on adult fleas and therefore is of minimal use in the flea allergic animal.

Monthly topical flea killers such as imidocloprid (Advantage®), a spot-on product, fipronyl (Frontline®), used as either a spray or spot-on, and selamectin (Stronghold®), a spot-on product, claim to kill 98% of adult fleas within 24 hours of application. Theoretically fleas are killed before they have a chance to mate and lay eggs. Fleas will usually take a blood meal prior to dying.

Symptoms of pruritus in the allergic animal will improve about 80% within 1 week of elimination of the fleas and 99% within 14 days.

Sarcoptes scabiei

LICE

Notoedres cati

Both biting and sucking lice can cause a pruritic, papular dermatosis in dogs and cats. Lice are very host specific and spend their entire life on their host. The eggs are cemented onto the hair shafts and the entire life cycle lasts from 14 to 21 days.

The diagnosis is made by physical examination and the identification of lice on the patient. Lice are easily killed by common flea shampoos, sprays, or powders. Ivermectin has been reported to be effective when given at 200 µg/kg subcutaneously. Selamectin (Stronghold®) has also been shown to kill lice in dogs and cats after one topical application.

Notoedres cati is a sarcoptid mite that primarily attacks cats but may also infest foxes, dogs, and rabbits. It causes transient lesions in humans. The mites are very uncommon in North America. As with S. scabiei, the mites burrow into the superficial layers of the epidermis and pruritus is caused by an allergic (most probably an IgE-mediated) reaction to the intestinal proteins secreted in the mite fecal material.

Affected cats show clinical lesions on the edges of the pinnae, the face, periocular regions, and neck. In severe cases, the feet and perineum are also involved. Lesions consist of initially of papules. The skin becomes thickened and covered with tightly adherent crusts. Because of the intense pru-

Sarcoptes scabiei mites are a cause of one of the most pruritic diseases seen in dogs. The mites are also known to cause disease in cats, foxes, and humans. The mites burrow through the cornified layer of the epidermis where they lay eggs. The pruritus is most likely caused by an allergic (IgEmediated) reaction to the intestinal proteins secreted in the mite fecal material. Puppies, very old dogs, dogs that are treated with immuno-suppressive amounts of corticosteroids, or dogs who have not yet developed an immunologic reaction to the mites may be asymptomatic carriers of the disease.

Affected dogs exhibit generalized pruritus with the edges of the pinnae, elbows, hocks, and ventral abdomen having the most severe lesions. Alopecia, erythematous papules, thick, yellowish crusts, and excoriations are noted on the physical examination. In many dogs a positive pinnal-pedal reflex can be elicited by rubbing the edge of the dog’s pinnae and noting an attempt to scratch the ear region.

Collection and identification of the mites can be difficult.

The ear margins, elbows, or hocks are most likely to yield a positive scraping. There are commercial laboratories that will perform an ELISA test for sarcoptid antigens. The test will be positive 2 to 4 weeks after infection. A presumptive diagnosis of scabies can be made by a positive response to treatment with a mitacidal product. All in-contact dogs also need to be treated.

Currently available topical therapies include lime sulfur rinses weekly for 4 weeks, amitraz (Mitaban®) rinses every 7 to 14 days for 1 month, or an organophosphate rinse such as phosmet (Paramite®) weekly for 4 weeks.

Ivermectin either orally or by injection every 7 to 14 days for 4 to 6 weeks (potentially very toxic in collies, Shetland sheepdogs, and other breeds) or milbemycin (Interceptor®) at various dosages have both been shown to be effective in treating scabies. One topical application of selamectin (Stronghold®) is effective in killing S. scabiei.

The majority of dogs will have a 50% reduction of pruritus 7 days after the first treatment, an 80% reduction in pruritus 14 days after the initiation of treatment, and clinical cure within 1 month.

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ritus, excoriations are also seen. A diagnosis can be confirmed by identification of the mite using a skin scraping.

Currently recommended miticidal therapies include lime sulfur rinses weekly for 4 weeks, amitraz (Mitaban®) rinses every 7 to 14 days for 1 month, or ivermectin either orally or by injection every 7 to 14 days for 4 to 6 weeks. Selamectin (Stronghold®) has been shown to be effective in killing N. cati after 1 application.

All in-contact cats need to be treated. The majority of cats will have a 50% reduction of pruritus 7 days after the first treatment, an 80% reduction in pruritus 14 days after the initiation of treatment, and clinical cure within 1 month.

Demodex spp.

The mite Demodex canis is an obligatory parasite of dog skin and is present in small numbers on all dogs. The mites can be found residing in hair follicles, sweat glands, and sebaceous glands. The entire life cycle of the mite is spent on the dog. D. canis mites feed on cells, sebum, and epidermal debris. There are four stages in the life cycle - egg, larvae (6 legged), nymph, and adult (both 8 legged). Mites are transmitted by direct contact from the bitch to the puppies within the first 3 days of life. They quickly lose their ability to infect after they are off the host for a short time. The mites are easily killed by desiccation. A new “short-bodied” demodex mite of dogs has been identified that most likely resides only within the stratum corneum. A second new “long-tailed” mite has also been recently identified. Not much is known about this species of Demodex mite.

The disease demodicosis is caused when the mite proliferates beyond the capacity of the host. The clinical lesions include hair loss, erythema, and suppuration. Clinical disease is by convention classified as either localized or generalized. Veterinary dermatologists have arbitrarily defined localized demodicosis in a dog having fewer than 5 spots in fewer than 2 body regions. In dogs with localized demodicosis pruritus is variable. It tends to be a benign disease that most often spontaneously resolves within 4 months.

Generalized demodicosis (GD) in dogs differs from the localized disease in clinical appearance, possible underlying cause(s), and prognosis. A dog is diagnosed with GD if it has 5 or more localized lesions, involvement of an entire body region, or involvement of 2 or more feet. The prognosis is usually related to the age of onset of the disease. In dogs who develop disease at less than 18 months of age (juvenile onset) there is about a 50:50 chance of self cure. The possibility of a spontaneous cure is virtually zero in the dogs that develop GD as adults. Generalized demodicosis can occasionally can be found affecting only the paws and is the first rule out in any dog presenting with pododermatitis. Some dogs can present with an erythematous, ceruminous otitis externa. Deep pyoderma and furunculosis are often complicating factors and occasionally a dog can develop sepsis.

Certain breeds of dogs have been shown to have a statistically higher risk of developing GD. These include boxers, Chinese shar peis, American cocker spaniels, collies, doberman pinschers, German shepherds, great Danes, old English sheepdogs, pit bull terriers, and Staffordshire terriers. Since

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there is evidence for a hereditary predisposition to develop GD, affected animals should never be bred. There is some evidence that GD is a manifestation of a hereditary specific T-cell defect which allows the mite population to increase inducing T-cell suppression. In dogs with adult-onset GD (disease starting after 2 years of age), a thorough work-up should be done to identify any possible underlying potentiating cause. In many cases, though, a potentiating underlying cause cannot be identified. It was previously thought that the development of adult-onset GD meant that the dog would die within 1 year from an unrelated underlying disease. It has been more recently determined that in many dogs the reason for the development of GD is idiopathic and many dogs will either be cured or have their disease maintained for many years. Recent retrospective studies have been made of dogs with adult-onset demodicosis. In the majority, no underlying disease such as a neoplasm could be identified and many were still alive, although not diseasefree, 1 year after the diagnosis was made.

The diagnosis of demodicosis is relatively easily made.

A skin scraping should be performed making sure that red blood cells are visible on the slide. A skin biopsy may be necessary to make the diagnosis in the Chinese shar pei, dogs with chronic, fibrosing, granulomatous lesions, and dogs with pododemodicosis. It has recently been shown that plucking hairs from affected areas of the dog and examining them in mineral oil will also readily demonstrate the mites.

Lesions of localized demodicosis usually resolve spontaneously. Use of a 5% benzoyl peroxide gel (Pyoben®), lindane in benzoyl benzoate lotion, or a rotenone-containing ointment (Goodwinol) may shorten the time to resolution and give the owner something with which to treat the dog while awaiting cure. It is never recommended to use amitraz to spot treat lesions of localized demodicosis as you may induce or select for resistance in the mites.

Treatment of generalized demodicosis can be very timeconsuming, difficult, expensive, and in some dogs, not successful. Between 30 to 50% of dogs that develop the disease before 1 year of age will experience a spontaneously resolution of their disease. In dogs that develop GD after 2 years of age, the prognosis for a spontaneous cure lessens. Systemic antibiotics should be used as needed to treat the secondary pyoderma. Vitamin E 200 IU given orally 5 times daily was reported by one investigator to be helpful.

Several mitacidal therapies are currently available for use in treating dogs with GD. Amitraz (Mitaban®, Ectodex®, Taktic®E.C) is the only mitacide licensed in the United States for the treatment of GD and therefore is the first treatment of choice. If needed, in long-haired or thickly-coated dogs, the entire haircoat should first be clipped.

The dog is first given a shampoo or whirlpool. The choice of an active ingredient in the shampoo varies with the condition of the dog. After towel-drying, the rinse is diluted to 250 to 500 ppm (1 vial of Mitaban® in 1 to 2 gallons of water) in a metal or ceramic container. It is applied as a final rinse every 7 to 14 days. In some dogs a mild sedating effect may be seen for 12 to 14 hours after dipping. Yohimbine (Yobine®) 0.11 mg/kg given intravenously can be used as an antidote.

Rinses should be applied until 2 negative skin scrapings have been performed a monthly intervals (i.e. for 1 month

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beyond a second negative skin scraping.) Again by convention, a dog is said to be cured of generalized demodicosis is it remains disease and mite free for 12 months beyond the cessation of treatment.

Milbemycin (Interceptor®) has been used for the treatment of GD in several clinical trials. It is indicated for use in cases that are “amitraz failures” or for dogs that relapse after an “amitraz cure”. It is safe to use in ivermectin-sensitive breeds when doses of less than 3.0 mg/kg are used. Patients should be heartworm negative prior to its use. The recommended dose is 0.5 to 2.0 mg/kg/day PO. In one study, 92% of adult dogs with juvenile-onset demodicosis treated with 2.17 mg/kg/day PO for 90 days were cured As with amitraz rinses, therapy is continued for at least 1 month beyond the second negative skin scraping. This therapy can be quite costly in large dogs.

Ivermectin (Ivomec®) is another therapy indicated for use in cases that are “amitraz failures” or for dogs that relapse after an “amitraz cure”. It should be avoided in ivermectin-sensitive breeds such as the collie, shetland sheepdog, old English sheepdog, potentially other herding breeds, and any mixes of these breeds (white feet/don’t treat.) Patients should be tested negative for heartworm prior to its use. The 1% solution is dosed at about 440 (200-600) µg/kg/day PO. Higher remission rates (83%) with shorter courses of treatment (mean 10 weeks) are seen with the higher doses. Therapy is continued for 1 month beyond the second negative skin scraping. Potential side effects of ivermectin include lethargy, depression, ataxia, and coma. Test dosing with ivermectin can be done using 120 µg/kg.

Cheyletiella spp.

Cheyletiella spp. mites affect cats, dogs, rabbits, and humans. The life cycle is completed on one host within 21 days. Larvae, nymphs, and adult male mite are thought to die soon after leaving the host but the female may live free of the host for up to 10 days. The mites are highly contagious.

Eggs are shed into the environment with the pet’s hair and may be an important source of reinfestation.

Symptoms in infested animals range from none to an intensely pruritic dermatitis. A dry scale, usually dorsally oriented, and alopecia secondary to the pruritus are the most common clinical signs.

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Collection and identification of the mites can be difficult, especially in cats. The most reliable method involves using a flea comb but some veterinarians collect scales and debris with acetate tape for microscopic examination. Cheyletiella eggs can sometimes be identified in a fecal flotation.

The mites are relatively easy to kill since they are surface feeders and dwellers. Weekly application of a variety of insecticides such as pyrethrin-containing compounds, lime sulfur dips, or organophosphates to all in-contact dogs and cats for 1 month will control the problem. Two to 3 treatment at 14-day intervals with ivermectin at 200 to 300 µg/kg has been reported to be effective. Selamectin (Stronghold®) has also been shown to be highly effective in controlling cheyletiellosis. The need for environmental treatment is controversial.

The majority of animals will have a 50% reduction of pruritus 7 days after the first treatment, an 80% reduction in pruritus 14 days after the initiation of treatment, and clinical cure within 1 month.

Otodectes cynotis Otodectes cynotis lives on the surface of the skin, especially in the ear canal, and feeds on epidermal debris and tissue fluid from the superficial epidermis. The host becomes exposed to and sensitized to the mite antigen by producing IgE antibodies. Infected animals often are intensely pruritic at the ears and the canals will contain a large amount of dry, brownish-red material.

Clinical symptoms are variable. Most infected dogs and cats have otic pruritus. Many animals will develop an erythematous ear canal that fills with cerumen, blood, mite exudate, and live mites.

The mites are highly contagious and not host specific so all in-contact animals should presume to be infected and should be treated. It is important to clean the ear canal of all debris if possible and then to use a miticidal agent. Topical products containing parasiticides such as pyrethrins, rotenone, or thiabendazole should be used per the manufacturers recommendations. Two doses of ivermectin, 200 to 400 µg/kg, given orally or subcutaneously two week apart can be used for intractable animals. One application of selamectin (Stronghold®) topically is also effective at eliminating mites.

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Risultati della terapia iposensibilizzante in 92 cani affetti da dermatite atopica R. Tognetti Med. Vet., Dipartimento di Clinica Veterinaria, Facoltà di Medicina Veterinaria - Pisa

M. Corazza Med. Vet., Dipartimento di Clinica Veterinaria, Facoltà di Medicina Veterinaria - Pisa

INTRODUZIONE

RISULTATI

È stata condotta un’indagine su un gruppo di soggetti atopici sottoposti a immunoterapia per 2 anni allo scopo di verificare l’efficacia della terapia iposensibilizzante con vaccini allestiti da un laboratorio farmaceutico italiano.

La valutazione clinica dopo 24 mesi di terapia ha dato i seguenti risultati:-Eccellente: 31 soggetti (33.7%);-Buono: 38 soggetti (41.3%);- Scarso: 23 soggetti (25%).

CONCLUSIONI MATERIALI E METODI Sono stati trattati 92 soggetti atopici con vaccini allestiti, su nostra richiesta, in base ai risultati ottenuti con l’intradermoreazione, dal laboratorio farmaceutico LOFARMA S.r.l. di Milano. I vaccini richiesti, preparati in forma di coprecipitati su idrossido di alluminio e allestiti in 3 diverse concentrazioni (100 U.I./ml, 1.000 U.I./ml e 10.000 U.I./ml), sono stati somministrati settimanalmente durante la fase iniziale della terapia. Nella fase di mantenimento è stata somministrata la dose massima del vaccino (10.000 U.I./ml) con intervalli di 1 settimana il primo mese, 2 settimane il secondo e 3 settimane il terzo, mantenendo poi un’unica somministrazione mensile fino al ventiquattresimo mese. I soggetti sono stati controllati periodicamente durante tutto l’arco della terapia, mantenendo rapporti telefonici settimanali o quindicinali con i proprietari e effettuando visite ambulatoriali ogni due mesi. I risultati della terapia iposensibilizzante sono stato valutati come: -Eccellente; -Buono; -Scarso.

La valutazione clinica dei soggetti al termine dei 24 mesi di terapia, ci ha fornito dati assai simili a quelli osservati da altri autori. Infatti, valutando come successo terapeutico una riduzione della sintomatologia di almeno il 51%, come riportato da Willemse, nel nostro caso, considerando la somma delle percentuali ottenute dal gruppo dei soggetti eccellente e buono, abbiamo ottenuto una percentuale di successo del 75%. I soggetti che hanno ottenuto un miglioramento sintomatologico inferiore al 50% (pari al 25% del totale), hanno potuto ridurre la frequenza e la quantità di farmaci utilizzati traendo comunque un vantaggio dalla terapia iposensibilizzante. Possiamo quindi concludere che la terapia iposensibilizzante è in grado di controllare efficacemente i sintomi dell’atopia nella maggioranza dei casi, anche se appare comunque chiaro che il trattamento di questa allergopatia non può essere orientato verso una sola opportunità terapeutica, dal momento che concorrono alla sua patogenesi e alla sintomatologia numerosi fattori.

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Una tecnica di gastropessi circumcostale modificata per prevenire le recidive nella sindrome della dilatazione-torsone gastrica nel cane: risultati su 132 casi Matteo Tommasini Degna Med. Vet., Dipl ECVS - Libero Professionista - Roma

La dilatazione –torsione gastrica, (GDV) solitamente si verifica in cani di razza grande, a torace profondo,e spesso è una condizione che mette a rischio la vita del paziente.

L’esatta ezologia rimane sconosciuta. La complessa patofisiologia e il trattamento medico sono stati discussi altrove.

Numerose tecniche chirurgiche sono state sviluppate per ridurre l’incidenza delle recidive della GDV che è stimata fino al 80%in quei casi dove una tecnica di gastropessi non è stata eseguita. Negli anni 70 una tecnica comunemente usata era la gastropessi con tubo. Negli 80 la gastropessi incisionale e la circumcostale hanno guadagnato popolarità. Più recentemente altre tecniche come la gastropessi a lembo di cintura hanno preso piede. La gastropessi circumcostale è rimasta la tecnica preferita da alcuni chirurghi per la sua superiore resistenza, ma la procedura è laboriosa è alcune complicazioni sono state descritte, come perforazione dello stomaco e del diaframma. Ci proponiamo di descrivere una modifica della gastropessi circumcostale che elimina alcuni degli svantaggi della tecnica originale.

TECNICA CHIRURGICA Eseguita una laparatomia secondo i canoni, il legamento falciforme veniva inciso dallo xifoide e retratto verso destra per avere una buona visualizzazione e un buon accesso alla ultima costa palpabile, a destra, e per consentire una buona visibilità dell’inserzone del diaframma. Lo stomaco veniva derotato e valutata la sua vasclarizzazione.

Aree di vascolarizzazione dubbia venivano invaginate. La

vascolarizzazione della milza anche veniva valuata e in preseza di trombi evidenti, effettuata la splenectomia. La piloromiotomia di Fredet-Ramested veniva effettuata di routine. L’ultima costa destra palapabile, solitamente la 11esima o la 12esima; veniva visualizzata retraendo e ripegando la parte più craniale della linea alba e legamento falciforme connesso con la mano sinistra. Con questa manovra una distanza di 4-6 cm far la linea alba e al gastropessi veniva ottenuta. Una incisione di 3 cm veniva fatta sopra la costa attraverso il muscolo trasverso dell’addome. Attenzione deve essere fatta per evitare la inserzone diframmatica. Un tunnel largo 3 cm viene creato con dissezione acuta attorno alla porzione laterale della costa. Un paio di pinze di Allis veniva passato in senso latero mediale e lo strato siero muscolare dello stomaco nella regione dell’antro piliorico veniva afferrrato. La pinza di Allis veniva tirata indietro attraverso il tunnel in una direzione medio –laterale e una piega di stomaco larga 3 cm veniva arrotolata attorno alla costa. A questo punto l’assitente chirurgico teneva la Allis con la mano sinistra e la linea alba con la destra. Tre incisioni lunghe 1,5cm venivano fatte nella sierosa e muscolare su ambo i lati della piega dello stomaco.

La piega dello stomaco veniva poi apposta usando una sutura continua semplice con polipropilene monofilamento.La sutura veniva passata profonda in modo sufficiente da trapassare lo strato di sotttomucosa di ambo i lati della piega di stomaco, ma non entrava nel lume dello stomaco.

Ogni passaggio inglobava anche 4-5 mm di parete addominale ventrali alla costa. La sutura continua consisteva di 57 passaggi. La parete addominale veniva suturata secondo routine.

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Possibilità terapeutiche in caso di UAP (mancata unione del processo anconeo) Aldo Vezzoni Med. Vet., Dipl. ECVS - Libero Professionista - Cremona

Introduzione

Sintomatologia

La UAP è una condizione patologica del cane in accrescimento, riscontrata con una certa frequenza in molte razze di cani di taglia grande e gigante. La mancata unione del processo anconeo dell’ulna provoca una grave incongruenza ed instabilità articolare dell’articolazione del gomito, cui consegue inevitabilmente un processo degenerativo osteoartrosico.

Quando è interessato un solo arto il cane presenta zoppia di 1° o di 2° grado, particolarmente dopo il riposo o in seguito ad attività fisica intensa. In stazione il cane sposta il baricentro sull’arto sano. L’insorgenza dei sintomi avviene attorno ai 5-6 mesi ed è spesso sottostimata, come molte zoppie dei cani in accrescimento. Quando sono interessati entrambi i gomiti, la sintomatologia è più subdola, manifestandosi a volte solo con un’alterazione dell’andatura a gomiti in fuori, spostamento del baricentro sugli arti posteriori con una lieve falsa cifosi della colonna e a volte, invece, con una zoppia di 1° grado alternata, ora a carico di un arto anteriore, ora a carico del controlaterale.

Talvolta il proprietario non rileva alcun disturbo dell’andatura ed il riscontro della patologia avviene come riscontro accidentale in occasione di un controllo radiografico.

Epidemiologia L’incidenza di questa patologia riguarda principalmente il cane Pastore Tedesco, l’Alano, il cane di San Bernardo, il Terranova, il Mastino Napoletano, il Mastiff il Bracco Italiano, il Bassethound, il Rottweiler, l’Irish Wolfhound e, in misura minore, anche altre razze.

Riscontri clinici Patogenesi Il centro di ossificazione del processo anconeo si fonde con la metafisi prossimale dell’ulna generalmente attorno alle 16-18 settimane, con qualche settimana di ritardo nelle razze giganti. Il riscontro di una mancata ossificazione del processo anconeo a 5-6 mesi è da considerare patologico.

La condizione patologica può verificarsi ad un solo arto o ad entrambi.

Sono state proposte diverse ipotesi sulla patogenesi della UAP, considerata anche come una delle manifestazioni dell’osteocondrosi, ma quella che ha riscosso il maggior consenso attribuisce la causa ad una crescita asincrona di radio e ulna, con una prevalenza della crescita del radio su quella dell’ulna; ciò provoca una spinta da parte della testa del radio sul condilo omerale che a sua volta preme sul processo anconeo impedendo la fusione ossea del suo centro di ossificazione con la metafisi prossimale dell’ulna. L’incongruenza articolare che si determina nel gomito, sia per lo slivellamento tra radio ed ulna conseguente alla loro crescita asincrona, che per la perdita di un contenimento posteriore provocato dalla mancanza di un processo anconeo ben saldato all’ulna, provoca un’instabilità articolare con movimenti di frizione tra i capi articolari, abnorme distribuzione dei carichi ponderali, degenerazione articolare ed osteoartrosi.

Alla visita ortopedica, l’arto interessato presenta un’ectasia sinoviale a livello del muscolo anconeo, di entità variabile ed un ispessimento periarticolare, facilmente riscontrabile a livello dell’epicondilo mediale. Movimenti forzati di iper-flessione e di iper-estensione provocano una reazione algica o di fastidio, cui il cane cerca di sottrarsi. Nei casi cronici sono percepibili rumori di crepitio articolare e l’ampiezza dei movimenti articolari risulta ridotta.

Riscontri radiografici Nella proiezione medio-laterale del gomito, mantenuto in flessione massima, si visualizza bene il processo anconeo, liberato dalla sovrapposizione del condilo omerale. È così possibile valutare la sua continuità con l’ulna oppure il suo eventuale distacco testimoniato da una zona lineare di radiotrasparenza, di ampiezza variabile. La separazione del processo anconeo dopo i 5 mesi di età è generalmente un segno di UAP, particolarmente nel Pastore Tedesco, la razza con la maggiore incidenza di questa patologia, anche se nelle razze giganti e nel Bassethound la fusione con l’ulna può verificarsi anche a 7-8 mesi di età. Nelle forme monolaterali e precoci, il confronto con l’altro gomito normale serve come ri-

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PROCESSO ANCONEO

LINEA DI SEPARAZIONE

ferimento. Nelle forme recenti, la radiotrasparenza non è completa, indicando ancora una certa connessione, mentre quando il processo è completamente staccato dall’ulna aumenta sia la radiotrasparenza che la sua ampiezza. È comunque difficile poter giudicare con certezza, dall’aspetto radiografico, se il processo è completamente o parzialmente staccato. Il processo anconeo staccato può andare incontro a riassorbimento osseo, anche se in certe forme croniche, invece, appare ben ossificato.

Trattamento conservativo Il trattamento conservativo, consistente nel controllo del peso, dell’attività fisica e nell’impiego di FANS, pur fornendo una certa remissione dei sintomi, non impedisce però un aggravamento progressivo dell’osteoartrosi che, con l’età, può diventare imponente e particolarmente invalidante.

Trattamento chirurgico Fino a pochi anni fa, il trattamento chirurgico più largamente utilizzato nel cane in accrescimento con UAP consisteva nella rimozione del processo anconeo, allo scopo di rimuovere un corpo articolare ormai di nessuna utilità funzionale, considerato anzi come un corpo estraneo, stimolo permanente di osteoartrosi. Poiché la rimozione del processo staccato non si è dimostrata in grado di arrestare o ridurre l’evoluzione artrosica, in quanto non viene ripristinata la stabilità e la congruenza dell’articolazione, la sua utilità è stata posta in discussione e sono state proposte diverse altre tecniche. Di queste, la prima proposta è stata la riduzione e la fissazione del processo staccato mediante l’inserimento di una o due viti ad effetto compressivo, oppure di una vite e di un filo di Kirschner, sia partendo dalla corticale posteriore della metafisi prossimale dell’ulna, che dalla sommità del processo stesso; il cedimento dell’impianto, per la rottura della vite o del filo di Kirschner, riscontrato con notevole frequenza, ha fatto comprendere come fosse necessario ristabilire prima un’adeguata congruenza articolare per evitare che il permanere delle forze di pressione sul processo che ne avevano provocato la mancata unione continuassero ad esercitarsi provocando il fallimento della fissazione. È stato così proposto il ricorso all’osteotomia prossimale dell’ulna, definita “dinamica” perché permette un assestamento tra radio ed ulna a livello del gomito. L’osteotomia dell’ulna, che in caso di UAP si presenta più corta del normale, determina un allontanamento del segmento prossimale in direzione della trazione muscolare esercitata dal muscolo tricipite; ciò

permette un riallineamento dei capi articolari ed una miglior congruenza articolare, eliminando o riducendo contemporaneamente la pressione esercitata sul processo anconeo. Questa riduzione della pressione sul processo si è dimostrata sufficiente a permetterne la fusione ossea con l’ulna nei casi in cui il processo era ancora ad essa ben connesso, oppure a non forzare l’oseosintesi effettuata quando il processo era maggiormente mobilizzato. Anche quando il processo anconeo non si saldava o non veniva fissato all’ulna, la sola osteotomia dinamica si è dimostrata in grado di migliorare la congruenza articolare e di limitare l’evoluzione artrosica.

Più complesso, nella sua gestione, risulta essere il caso di UAP bilaterale, per l’impossibilità di effettuare contemporaneamente l’osteotomia dinamica dell’ulna in entrambi i gomiti, in quanto troppo invalidante per il cane; occorre pertanto separare i trattamenti chirurgici di almeno 3-4 settimane, incorrendo però, in questo modo, nel rischio di aumentare l’instabilità del processo anconeo ancora da trattare al punto tale da rendere molto meno probabile la sua successiva fusione.

Il trattamento chirurgico della UAP nel cane adulto, invece, non sembra offrire risultati significativi rispetto al trattamento conservativo, in quanto le alterazioni osteoartrosiche si sono ormai già instaurate.

❑ rimozione del processo La rimozione del processo anconeo staccato viene effettuata mediante una artrotomia laterale del gomito. Incisa la cute caudalmente all’epicondilo laterale dell’omero, si incide la fascia ed il sottostante muscolo anconeo. La capsula, incisa assieme al muscolo, viene divaricata con un retrattore autostatico di Gelpi e con uno scollaperiostio si libera il processo anconeo dalle connessioni fibrose residue, per poi asportarlo con una pinza ossea appuntita. La capsula viene chiusa con la stessa sutura che ricompone il muscolo anconeo, dopo aver effettuato un copioso lavaggio dell’articolazione. Suturate la fascia, il sottocute e la cute, viene applicato un bendaggio morbido.

❑ fissazione del processo con vite L’artrotomia laterale del gomito necessaria per la fissazione del processo richiede un accesso più ampio, con estensione dell’incisione tra il capo laterale e quello lungo del tricipite. Per la fissazione del processo con una vite da trazione, la via più agevole è quella che parte dalla corticale caudale della metafisi prossimale dell’ulna in direzione della sommità del processo anconeo. Si utilizza un centratore ad arco, con il mirino posto sulla parte centrale della sommità del processo anconeo, tenuto in posizione mediante una pinza da riduzione appuntita, applicata con la necessaria delicatezza per evitare di danneggiarlo. Si possono utilizzare sia viti da corticale del 2,7, sia viti da spongiosa del 4,0. Utilizzando viti da corticale del 2,7, si perfora inizialmente con una punta da 2,7 per creare il foro di scorrimento della vite, arrestando la perforazione prima del processo anconeo; si inserisce quindi nel foro effettuato una boccola di protezione

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dei tessuti dal diametro esterno di 2,7 e da quello interno del 2,0, e si continua la perforazione con una punta del 2,0 fino ad uscire sulla sommità del processo anconeo. Con lo svasatore da 2,7 si prepara la sede nella corticale dell’ulna per la testa della vite, e con il misuratore di profondità si misura la lunghezza della vite necessaria; si filetta con il maschiatore da 2,7 e si avvita la vite indicata, fino ad effettuare una adeguata compressione interframmentaria. La corticale caudale dell’ulna offre generalmente una resistenza sufficiente alla testa della vite, ma in caso di animali molto giovani può essere indicato inserire una rondella per una più ampia distribuzione delle forze. Verificato che la vite non sporga dalla sommità del processo anconeo, si eseguono dei movimenti di flessione e di estensione per accertarsi che il processo anconeo sia stabile e che possa muoversi liberamente nella fossetta intercondiloidea. Nei cani più grossi è possibile inserire una seconda vite più caudale, parallela alla precedente, oppure un filo di Kirschner di diametro 1,6 o 2,0 Alcuni Autori hanno applicato un trapianto di spongiosa nella base del processo anconeo, dopo aver rimosso delicatamente il tessuto fibroso.

Utilizzando viti da spongiosa da 4,0 mm parzialmente filettate, adatte in cani di taglia gigante, si esegue tutto il foro dall’ulna prossimale fino a penetrare nel processo anconeo, con una punta da trapano da 2,0 mm. Misurata la lunghezza della vite indicata, si filetta con il maschiatore da spongiosa da 4,0 mm e si avvita la vite fino a riscontrare un’adeguata compressione interframmentaria. Occorre generalmente preparare la vite, nel planning preoperatorio, limandone alcune spire per far sì che il filetto resti tutto nel processo anconeo, senza oltrepassare la linea di separazione con l’ulna, e garantire così il pieno effetto compressivo. Se necessario, di inserisce una rondella sotto la testa della vite per aumentarne le tenuta nei cani molto giovani. Chiusi i tessuti scontinuati, si applica un bendaggio morbido.

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cipite. L’osteotomia obliqua, invece, effettuata con una direzione prossimo-distale, determina una più ampia superficie ossea che facilita il consolidamento, offre una maggior resistenza all’inclinazione del moncone prossimale e risulta meglio tollerata dal paziente: la sua realizzazione richiede l’impiego di una sega oscillante, con una lama stretta per non ledere il nervo ulnare che decorre medialmente all’ulna. Completata l’osteotomia, con l’aiuto di una leva inserita nella sede dell’osteotomia si esercitano dei movimenti sul segmento prossimale per facilitarne l’assestamento. Nei casi con incongruenza articolare marcata da ulna corta, appena completata l’osteotomia, la linea di sezione si apre spontaneamente di alcuni millimetri ad indicare la tensione di spinta sull’articolazione esercitata dal radio. Alcuni Autori consigliano l’inserimento nell’ulna, dall’olecrano, di un filo di Kirschner di piccolo diametro (1,6-2,0 mm) per rendere meno instabile l’osteotomia, ma secondo altri ciò potrebbe interferire con l’assestamento del moncone prossimale secondo le linee di forza e richiede inoltre di essere poi rimosso.

Completata l’osteotomia ed eseguito un copioso lavaggio con soluzione fisiologica, si suturano la fascia ed periostio, il sottocute e la cute. Si applica un bendaggio leggero imbottito a protezione dei tessuti molli, senza bloccare l’escursione del gomito Rigoroso deve essere il rispetto di un periodo di riposo cui deve essere sottoposto il cane; per 30-60 giorni,il cane deve essere confinato in poco spazio, non deve giocare con altri cani e deve essere sempre tenuto al guinzaglio corto quando viene fatto uscire per i suoi bisogni fisiologici.

INTRODUZIONE DELLA DISTANZA FRA IL PROVESSO ANCONEO E LA TESTA DEL RADIO

TESTA DEL RADIO

❑ osteotomia dinamica dell’ulna L’osteotomia dinamica dell’ulna si realizza mediante un’osteotomia prossimale effettuata appena caudalmente al legamento anulare tra radio ed ulna. S’isola l’ulna attraverso un’incisione caudale effettuata direttamente sopra il profilo caudale dell’ulna, scontinuando cute, sottocute, fascia e periostio: con uno scollaperiostio curvo s’isola tutta la circonferenza dell’ulna nel punto indicato per l’osteotomia. Il livello dell’osteotomia viene identificato misurando, sulla radiografia, la distanza tra la sommità dell’olecrano ed un punto dell’ulna da 2 a 3 cm distale alla superficie articolare del capitello radiale, e riportando questa misura sulla corticale caudale dell’ulna nel campo operatorio. L’osteotomia dell’ulna può essere effettuata trasversalmente od obliquamente. L’osteotomia trasversale, più facile da eseguire, può essere effettuata con una sega di Gigli o con una sega oscillante, ponendo attenzione a preservare i vasi interossei e a non incidere il radio: purtroppo l’osteotomia trasversale determina un’eccessiva instabilità dei due monconi, maggior morbilità per il paziente, ritardo di consolidamento del callo osseo e tendenza ad una eccessiva inclinazione del moncone prossimale dell’ulna sottoposto alla trazione del muscolo tri-

L’ULNA SI SPOSTA PROSSIMALMENTE

CONGRUITÀ CON IL PROCESSO CORONOIDEO MEDIALE

OSTEOTOMIA

❑ osteotomia dinamica dell’ulna e fissazione con vite Ispezionata l’articolazione e fissato il processo anconeo come descritto sopra, si procede all’osteotomia obliqua prossimale dell’ulna nel caso in cui sia evidente l’incongruenza articolare, sia radiologicamente che intraoperatoriamente. Qualora non fosse evidente un’incongruenza tra radio ed ulna, è indicato effettuare un’osteotomia dinamica dell’ulna più distale (terzo medio) e trasversale, con lo scopo di permettere un minimo rilascio della tensione sul processo anconeo, senza però determinare l’instabilità e la morbilità dell’osteotomia prossimale.

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Conclusioni

bilità dell’osteotomia prossimale.

❑ risultati attesi La fusione del processo anconeo con l’ulna richiede da 1 a 2 mesi, mentre il consolidamento dell’osteotomia dell’ulna è completo, con il rimodellamento osseo, a 8-12 mesi. Il successo dell’intervento è maggiore quando viene combinata, all’osteotomia dinamica dell’ulna, la fissazione con vite del processo, e quando viene effettuato precocemente: la percentuale di successo è maggiore se l’intervento viene effettuato a 6 mesi nelle razze di taglia grande ed entro i 7-8 mesi nelle razze di taglia gigante. Nelle condizioni migliori, il successo nei lavori pubblicati raggiunge la percentuale dell’87%.

Con la fusione del processo ed il ripristino della congruenza articolare, il gomito riacquista una funzionalità completa testimoniata dall’ampiezza dei movimenti articolari normale e dall’assenza di formazione di osteofiti nei controlli radiologici a distanza.

Nelle forme croniche (oltre gli 8 mesi nelle razze di taglia grande ed oltre gli 11 mesi nelle razze di taglia gigante), l’isolamento completo del processo anconeo e le modificazioni strutturali ossee dell’incisura trocleare dell’ulna rendono molto meno probabile la fusione del processo. Il miglioramento, comunque, della congruenza articolare determinato dall’osteotomia dinamica dell’ulna, anche nel caso in cui il processo resti staccato, favorisce la funzionalità dell’articolazione e riduce l’evoluzione osteoartrosica.

La sola fissazione con vite, senza osteotomia dinamica, può avere successo solo in quel numero limitato di casi in cui l’incongruenza articolare si sia già risolta con un livellamento spontaneo di radio ed ulna durante l’accrescimento; quando invece permane l’incongruenza, questa continua a determinare una pressione ciclica sul processo anconeo durante il movimento, di tale entità da provocare il cedimento della fissazione con la rottura della vite o del filo di Kirschner.

La sola osteotomia dinamica, senza fissazione del processo con una vite, può avere successo in quell’ampio numero di casi in cui l’intervento può essere eseguito precocemente e in cui si verifica visualmente, mediante artroscopia o mediante mini-artrotomia, che il processo appare ancora ben saldo alla palpazione e durante i movimenti di flessione e di estensione.

Il trattamento chirurgico della mancata unione del processo anconeo nel cane in accrescimento, se effettuato nei modi e nei tempi ottimali, consente un completo ripristino della funzionalità articolare. Di fondamentale importanza è la diagnosi precoce, per non perdere quello stretto margine di tempo entro il quale è ancora possibile favorire la fusione ossea del processo anconeo con l’ulna e ristabilire la congruenza e la funzionalità articolare. Ancora una volta, come per altre patologie osteo-articolari da accrescimento, emerge l’importanza di una visita ortopedica di routine all’età di 6 mesi in tutti i cani delle razze di taglia grande e gigante, per poter intercettare quelle patologie in atto che, pur non determinando ancora una sintomatologia evidente, evolveranno nell’età adulta verso forme di osteoartrosi. La diagnosi precoce della maggior parte delle patologie osteo-articolari da accrescimento permette degli interventi correttivi in grado di arrestare o limitare la tendenza alla degenerazione osteoartrosica.

Essendo la UAP una delle componenti eziologiche della displasia del gomito, di cui è stata accertata la componente ereditaria, i soggetti colpiti e guariti con il trattamento chirurgico devono essere comunque considerati, agli effetti della riproduzione, come soggetti displasici di grado III°.

Bibliografia consultata 1.

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Böhmer E, Matis U, Waibl H: Zur operativen Darstellung des Processus Anconaeus ulnae beim Hund (Modifikation des Zuganges von Chalman und Slocum), Tierärztl Prax 15:425, 1987 Fox SM, Burbridge HM, Bray JC, Guerin SR: Ununited anconeal process: lag screw fixation, J Am Anim Hosp Assoc 32:52, 1996 Gilson SD, Piermttei DL, Schwarz PD: Treatment of humeroulnar subluxation with a dynamic proximal ulnar osteotomy, Vet Surg.

18:114, 1989 Guthrie S: Some radiographic and clinical aspects of uninited anconeal process, Vet Record 124:661, 1989 IEWG: Guidelines for elbow dysplasia screening, Konstanz, 1995 Matis U, Böhmer E, Baumer K, Köstlin R: Treatment of the ununited anconeal process. Proc. 6th ESVOT Congress 16, 1992 Meyer-Lindenberg A: Der isolierte Processus anconaeus: retro- und prospektive Untersuchungen zur operative Behandlung, Tierüarztl Prax 27:309, 1999 Olsson SE: Pathophysiology, morphology and clinical signs of osteochondrosis in the dog. In Bojrab MJ, editor: Disease mechanisms in small animal surgery, Philadelphia, 1993, WB Saunders Piermattei DL: An atlas of surgical approaches to the bones and joints of the dog and cat, ed 3, Philadelphia, 1993, WB Saunders Roy RG, Wallace LJ, Johnston RA: A retrospective long term evaluation of ununited anconeal process excision of the canine elbow, Vet Comp Orthop Trauma 7:94, 1994 Sjöstrom L, Kosstrom H, Kollberg M: Ununited anconeal process in the dog: pathogenesis and treatment by osteotomy of the ulna, Vet Comp Orthop Trauma 8:170, 1995 Thacher C: Ununited anconeal process. In Slatter D, editor: Texbook of small animal surgery, Philadelphia, 1985, WB Saunders Turner BM, Abercromby RH, Innes J, McKee WM, Ness MG: Dynamic proximal ulna osteotomy for treatment of ununited anconeal process in 17 dogs, VCOT 11:76, 1998 Vezzoni A, Ferretti A, Abbiati G: Results of proximal ulna osteotomy as a treatmen,t for ununited anconeal process (UAP), Proceedings of the IEWG Meeting, Bologna 1998 Wind AP: Elbow dysplasia. In Slatter D, editor: Texbook of small animal surgery, ed 2, Philadelphia, 1993, WB Saunders

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Triplice osteotomia pelvica (TPO): studio retrospettivo multicentrico su 218 casi Aldo Vezzoni Med. Vet., Dipl. ECVS - Libero Professionista - Cremona

Ermenegildo Baroni Med. Vet. - Libero Professionista - Rovigo

Massimo Petazzoni Med. Vet. - Libero Professionista - Milano

INTRODUZIONE

MATERIALI E METODI

La displasia dell’anca è la patologia scheletrica da accrescimento di più frequente riscontro nella pratica medica veterinaria ed ogni anno migliaia di cani ne sono colpiti anche nel nostro paese. La malattia è caratterizzata da uno sviluppo anomalo dell’articolazione coxo-femorale e da instabilità articolare che conducono successivamente ad osteoartrosi. Fra i trattamenti chirurgici proposti per la displasia dell’anca di tipo acetabolare, caratterizzata da una maggiore inclinazione dorsale del tetto dell’acetabolo, la TPO consente, nei soggetti giovani, di ripristinare la funzionalità dell’articolazione restituendo alla testa del femore un’adeguata copertura da parte del margine dorsale dell’acetabolo arrestando, o rallentando, così i fenomeni degenerativi articolari. L’intervento chirurgico consiste nella rotazione del segmento acetabolare del bacino previa triplice osteotomia di pube, ischio e ileo e fissazione del segmento ruotato mediante placca preangolata. L’intervento è indicato nei soggetti in cui non si siano ancora verificati fenomeni artrosici ed abbastanza giovani da consentire un adeguato rimodellamento articolare.

Mediante la compilazione di una scheda appositamente redatta, dodici medici veterinari, appartenenti al Gruppo di Studio SCIVAC di Ortopedia, hanno fornito la documentazione richiesta per la valutazione complessiva di 162 soggetti sottoposti a TPO dal Dicembre 1993 al Dicembre 1999 per un totale di 218 articolazioni operate. Ogni scheda è stata concepita per ospitare il maggior numero d’informazioni possibili, sia cliniche, che chirurgiche, che radiografiche, ed ogni partecipante è stato invitato a compilare esclusivamente le parti che riguardavano le indagini, le procedure ed i controlli clinici e radiografici di volta in volta eseguiti. Per ogni intervento chirurgico è stato raccolto il segnalamento del cane (razza, sesso, età e peso) e le informazioni sull’esecuzione tecnica dell’intervento per le osteotomie di pube, ischio e ileo (scalpello, scalpello previa perforazione con punta da trapano, sega di Gigli, ossivora, sega oscillante e seghetto alternativo). Le informazioni tecniche per la valutazione degli impianti impiegati riguardano il tipo di placca impiegata (CPOP Canine Pelvic Osteotomy Plate originale di Slocum, placca da TPO di Hoffman, placca da TPO Synthes o placca ACD a Compressione Dinamica piegata al momento), i gradi di rotazione imposti al segmento acetabolare (20°, 25°, 30°, 40° o altro), il tipo di viti impiegate per la fissazione dell’impianto (3,5 mm da osso corticale, 4,0 mm da osso spongioso o altro), la profondità di inserimento delle viti nel segmento craniale dell’ileo (ileo o sacro: quando anche una sola vite nel segmento craniale veniva fissata al sacro si considerava il segmento craniale fissato al sacro, in quanto veniva oltrepassata l’articolazione sacro-iliaca e quindi potenzialmente compromessa), la direzione impressa alle viti (parallele e non parallele tra loro), l’impiego di cerchiaggi metallici per la fissazione ausiliaria della placca nei

OBIETTIVI Scopo del presente studio retrospettivo multicentrico è quello di valutare, sulla scorta di una vasta casistica fornita da numerosi chirurghi veterinari, i diversi approcci nella selezione del paziente, le diverse tecniche chirurgiche di osteotomia, gli strumenti e gli impianti utilizzati. Viene condotta, inoltre, un’ampia valutazione del fallimento degli impianti mediante follow-up radiografico (a quattro settimane minimo).

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due segmenti iliaci e l’impiego di un cerchiaggio metallico di fissazione nella osteotomia ischiatica.

Tutte le schede pervenute che non includevano almeno i dati oggetto della presente indagine non sono state prese in considerazione per lo studio.

Non sono stati presi in considerazione nel presente studio: il rilascio del legamento sacro-tuberoso, la misurazione della profondità delle viti di ancoraggio nel sacro, il tipo di ricovero a cui i pazienti sono stati sottoposti nel periodo post-operatorio e le misurazioni pre e post chirurgiche del canale pelvico e nei follow-up radiografici, il grado di artrosi coxofemorale nei follow-up eseguiti ed il grado di zoppia.

Hanno partecipato al presente studio descrittivo retrospettivo multicentrico, fornendo la totalità della casistica: Ermenegildo Baroni, Dino Buzzigoli, Antonio Ferretti, Antonio Marinucci, Massimo Olivieri, Bruno Peirone, Guido Pisani, Gian Luca Rovesti, Thomas Roth, James Sabatini, Matteo Tommasini e Aldo Vezzoni.

RISULTATI 218 articolazioni dell’anca appartenenti a 162 cani sono state prese in riesame nel presente studio: 58 femmine e 104 maschi con età compresa fra 4 mesi e due anni (media 8,7 mesi) tra cui: 31 Pastori Tedeschi, 30 Labrador Retrievers, 25 Rottweilers, 20 Terranova, 7 Incroci, 6 Cani Corso, 5 Setter Inglesi, 5 Golden Retriever, 5 San Bernardo, 3 Schnauzer, 3 Pastori Maremmani Abruzzesi, 3 Chow Chow, 3 Boxer, 2 Dogue de Bordeaux, 1 Setter Irlandese, 1 Syberian Husky, 1 Pastore Turco, 1 Pastore Belga, 1 Mastino Napoletano, 1 Leonberger, 1 Hovawart, 1 Fila Bresilero, 1 Cane da Montagna dei Pirenei, 1 Alano, 1 Bovaro del Bernese, 1 Bretone e 1 Bull Mastiff.

Il peso medio dei soggetti operati è stato di 31.9kg con campo di variazione da 15 a 54kg. Hanno subito l’intervento di TPO: 6 soggetti con peso inferiore a 20kg (3%), 78 con peso compreso fra 20 e 30 kg (36%), 92 con peso compreso fra 30 e 40kg (42%), 37 con peso compreso fra 40 e 50kg (17%) e 5 soggetti con peso maggiore di 50 kg (2%).

102 soggetti sono stati operati ad un’unica articolazione e 58 bilateralmente di cui 11 operati nella stessa seduta operatoria e 47 in tempi diversi con un intervallo medio tra il primo ed il secondo intervento di 59 giorni (range 28-330).

115 TPO sono state effettuate sull’anca destra (53%) e 103 sull’anca sinistra (47%).

Di 218 anche, 74 appartenevano a soggetti femminili (34%) e 144 a soggetti maschili (66%).

Differenti tecniche chirurgiche sono state impiegate per le osteotomie di pube, ischio ed ileo: a livello di pube la tecnica maggiormente adottata ha previsto l’impiego esclusivo della sega oscillante (80/218: 36,7%) seguita dall’impiego della sega oscillante coadiuvata dallo scalpello (55/218: 25,2%), dall’impiego del solo scalpello (50/218: 22,9%), dall’uso del seghetto alternativo (23/218: 10,5%), dall’utilizzo della pinza ossivora (5/218: 2,3%), della sega oscillante + ossivora (4/218: 1,8%) e della sega di Gigli (1/218 0,5%). A livello di ischio, la tecnica maggiormente adottata ha previsto l’impiego del seghetto manuale (67/218: 30,7%) seguita dall’impiego della sega oscillante (60/218: 27,5%),

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dall’impiego della sega di Gigli (39/218: 17,9%), dall’uso del seghetto alternativo (27/218: 12,4%), dall’utilizzo dello scalpello (17/218: 7,8%) e della sega oscillante + scalpello (8/218: 3,6%).

A livello di ileo la tecnica più impiegata è stata l’osteotomia mediante sega oscillante (88/218: 40,4%), seguita dall’ ileotomia mediante sega oscillante + scalpello, dall’osteotomia mediante seghetto alternativo (27/218: 12,4%), mediante scalpello previa preforatura con punta da trapano (26/218: 11,9%), mediante solo scalpello (16/218: 7,3%) e mediante sega di gigli (1/218: 0,5%).

208 osteotomie iliache (95%) sono state ridotte e fissate mediante placca di Slocum originale o di tipo Slocum (Hofman), mentre 10 osteotomie iliache (5%) sono state ridotte mediante placca DCP Synthes piegata al momento; 32 riduzioni sono state effettuate mediante placca con angolo di rotazione di 20° (15%), 55 con angolo di rotazione di 25° (25%), 126 con angolo di 30° (56%), 2 con angolo di 40° (1%) e 3 con angolo di 45° (1%).

Di 197 interventi si è potuto valutare il follow-up radiografico a quattro settimane (minimo) dall’intervento: 104 impianti sono stati assicurati all’ileo mediante viti da 3,5mm da corticale (53%), 86 mediante viti da 4mm da spongiosa (44%) e 7 impianti hanno montato una configurazione mista (3%).

Di 197 anche valutate, (394 emiimpianti), le viti di ogni emiimpianto (porzione craniale o caudale della placca) avevano una direzione parallela 198 volte (50%) e non parallela (convergente, divergente o orientamento casuale) 196 volte (50%). 45 placche (23%) sono state ancorate al solo ileo, mentre 152 (77%) coinvolgevano anche il sacro con almeno una vite. 64 volte (32%) è stato applicato almeno un cerchiaggio metallico per la fissazione ausiliaria della placca: 24 volte ad entrambi i segmenti craniale e caudale, 37 volte al solo segmento caudale e 3 volte al solo segmento craniale.

27 volte è stato applicato un cerchiaggio metallico a livello di osteotomia di ischio (27/197: 14%) mentre le osteotomie di ischio sono state lasciate libere 170 volte (170/197: 86%).

Complicazioni Di 197 anche, 49 (25%) hanno presentato una complicazione a livello di impianto ortopedico (45 cani di cui 4 ad entrambe le anche e 41 ad una singola anca).

Le complicazioni hanno interessato le seguenti razze: 19 Pastori Tedeschi (19/31 – 61%), 11 Rottweiler (11/25 – 44%), 6 Labrador Retriever (6/30 – 20%), 5 Terranova (5/20 – 25%), 3 Schnautzer (3/3), 3 Chow Chow (3/3), 3 San Bernardo (3/5), 2 Incroci (2/7), un Alano (1/1), un Cane Corso (1/1), un Cane dei Pirenei (1/1) e un Dogue de Bordeaux (1/1); 13 soggetti di sesso femminile su 74 (17,6%) e 32 soggetti di sesso maschile su 144 (22%), 14 anche destre su 115 (12,2%) e 35 anche sinistre su 103 (34%) e soggetti di età compresa fra i 4 e i 18 mesi di età al momento dell’intervento (media 8,1 mesi).

I pazienti con complicazioni avevano un peso medio di 33.2kg (intervallo 15 - 54kg). In dettaglio le complicazio-

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ni hanno interessato: un soggetto con peso inferiore a 20kg (2%), 17 con peso compreso fra 20 e 30 kg (35%), 19 con peso compreso fra 30 e 40kg (39%), 10 con peso compreso fra 40 e 50kg (20%) e 2 soggetti con peso maggiore di 50 kg (4%).

Di 49 complicazioni, 40 (82%) sono rappresentate dall’allentamento di una o più viti, 6 dalla rottura di una o più viti (12%), una dall’allentamento di una vite associata alla rottura di una vite ed alla rottura di un cerchiaggio di fissazione della placca (2%) e due dall’allentamento di una o più viti + rottura dei cerchiaggi (4%).

Di 49 cedimenti, 47 (96% sul totale degli impianti e 23% delle placche di tipo Slocum) riguardavano placche di Slocum o Hofmann e 2 (4% sul totale degli impianti e 20% delle placche Synthes) placche DCP Synthes. Non si sono mai verificate rotture delle placche.

Allentamenti Gli allentamenti hanno interessato le seguenti razze: 16 Pastori Tedeschi (16/31 – 52%), 8 Rottweiler (8/25 – 32%), 5 Terranova (5/20 – 25%), ), 5 Labrador (5/30 – 17%), 3 Schnautzer (3/3) 3 Chow Chow (3/3), 3 San Bernardo (3/5), 2 Incroci (2/7), un Cane Corso (1/1), un Cane dei Pirenei (1/1), un Dogue de Bordeaux (1/1), e un Alano (1/1).

Dei 43 allentamenti osservati, 30 hanno interessato il sesso maschile (70%) e 13 quello femminile (30%) e soggetti di età compresa fra i 4 e i 18 mesi di età al momento dell’intervento (media 8,1 mesi). In 41 allentamenti sono state interessate placche di Slocum/Hofmann (95% sul totale degli impianti e 18% delle placche Slocum/Hofmann) e in 2 placche Synthes (5% sul totale degli impianti e 20% delle placche Synthes).

Dei 43 allentamenti totali, 27 volte (26% su un totale di 104 impianti) erano coinvolte le viti da 3,5mm da corticale e, 16 volte (19% su un totale di 86 impianti) erano coinvolte le viti da 4,0mm da spongiosa (7 impianti erano misti - viti da corticale e da spongiosa).

Nei 43 allentamenti delle viti, 31 interessavano il segmento craniale della placca (72%), 11 quello caudale (26%) e uno entrambi (2%).

Nei 43 allentamenti, le viti avevano un orientamento parallelo 26 volte (60%) e non parallelo 17 volte (40%).

Le viti del segmento craniale hanno avuto un allentamento 8 volte su 45 quando ancorate al solo ileo (8,8%) e 35 volte su 152 quando ancorate al sacro (17,7%).

Dei 43 impianti che hanno avuto un allentamento, 11 (25%) erano sostenuti da cerchiaggio metallico ausiliare e 32 (75%) ne erano sprovvisti.

7 volte sono state interessate placche aventi angolo di rotazione di 20° (7 su 32 totali impiegate 22%), 8 volte placche con angolo di rotazione di 25° (8 su 55 totali impiegate, 14%), 26 volte placche con angolo di 30° (26 su 126 totali, 21%), una volta una placca da 40° (1 su 2) ed una volta una placca da 45° (1 su 3).

Dei 43 allentamenti, 6 volte (6/43 – 14%) era stato impiegato un cerchiaggio metallico a livello di osteotomia ischiatica e 37 (37/43 – 86%) volte l’osteotomia era stata lasciata libera.

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Rotture viti Le rotture delle viti hanno interessato le seguenti razze: 3 Pastori Tedeschi (3/31 – 10%), 3 Rottweiler (3/25 – 12%) e un Labrador (1/30 – 3%), tra cui 4 maschi e 3 femmine, soggetti con peso medio di 32,3kg (intervallo 26-44kg), 4 anche destre e tre sinistre, 6 volte le viti da 4,0mm da spongiosa (6/7 - 86%) ed una volta le viti da 3,5mm da corticale (1/7 - 14%). Nelle 7 rotture, 2 volte erano interessate le viti del segmento craniale, 4 volte le viti del segmento caudale ed una volte entrambe; nelle 7 rotture, 5 volte le viti avevano un orientamento parallelo e 2 volte un orientamento non parallelo, 5 volte erano ancorate al sacro e due volte al solo ileo.

Dei 7 impianti che hanno avuto una rottura, 2 (28%) erano sostenuti da cerchiaggio metallico ausiliare e 5 (72%) ne erano sprovvisti.

Di 7 rotture, 4 hanno interessato placche con angolo di rotazione di 30° (3% su un totale di 126 impiegate), 2 hanno interessato placche con angolo di rotazione di 25° (4% su un totale di 55 impiegate) e una ha interessato una placca con angolo di rotazione di 20° (3% su un totale di 32 impiegate)

Rotture dei cerchiaggi Le rotture dei cerchiaggi hanno interessato le seguenti razze: 1 Cane dei Pirenei, 1 Pastore Tedesco ed uno Schnauzer, tra cui 2 maschi ed una femmina, tre anche sinistre. Tutte e tre interessavano un cerchiaggio del segmento caudale e tutte e tre le volte erano associati all’allentamento delle viti (2) o alla rottura delle stesse (1).

DISCUSSIONE Le complicazioni associate all’intervento di triplice osteotomia del bacino che sono state riscontrate in letteratura comprendono: infezioni, sierosità delle ferite chirurgiche, seromi, neuropraxia o altre lesioni a carico del nervo ischiatico, danni iatrogeni di altre strutture nervose (otturatore, gluteo craniale, pudendo, pelvico), disuria, fratture acetabolari, riduzione del canale pelvico e cedimenti degli impianti di riduzione dell’osteotomia iliaca.

In assoluto, le complicazioni che si sono verificate maggiormente sono state quelle a carico dei mezzi di sintesi e, fra le complicazioni che interessano il cedimento degli impianti, l’allentamento delle viti è stata quella più frequente1,2,3,4. Numerosi studi hanno preso in considerazione questo tipo di complicazione riportando cedimenti che interessano il 9%5 il 12%6, il 26%4, il 34%7, ed il 36%5 del totale degli interventi di TPO effettuati. Il presente studio retrospettivo si è dimostrato in linea con i precedenti lavori pubblicati, dimostrando una percentuale di complicazioni postoperatorie agli impianti pari al 25% sul totale degli interventi considerati.

Il cedimento delle viti è stato attribuito in passato alla mancata tenuta delle viti stesse sull’osso più tenero dei soggetti in accrescimento, oltre alla difficoltà di contenerne l’at-

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tività fisica, nel periodo postoperatorio, dei soggetti operati1,2. Per questa ragione è stato suggerito l’impiego di viti da spongiosa, con filetto più ampio, per migliorare la tenuta nell’osso immaturo1,4. Tuttavia la correlazione tra il cedimento degli impianti e la giovane età dei soggetti sottoposti ad intervento non si è verificata in uno studio successivo7. Il presente studio retrospettivo non ha evidenziato una indiscutibile correlazione tra il cedimento degli impianti e la giovane età degli animali; l’età media dei soggetti operati era di 8,1 mesi e l’età media dei soggetti in cui si sono verificate le complicazioni era di 8,7 mesi.

In evidenza, invece, una alta percentuale di cedimenti nelle razze Pastore Tedesco e Rottweiler; ciò potrebbe far pensare ad un maggiore vivacità caratteriale di queste razze rispetto alle altre nel periodo post-operatorio o ad una maggiore difficoltà nel sottoporre questi soggetti ad un adeguato riposo post-operatorio rispetto a razze più docili quali Terranova e Labrador Retriever. Un’altra ipotesi formulabile potrebbe attribuire la causa dei cedimenti ad una differenza anatomica, come una corticale più sottile, un osso spongioso più tenero o un ileo più sottile rispetto alle altre razze.

Il livello di attività fisica nel periodo postoperatorio è stato preso in considerazione nel lavoro di Remedios e Fries, non evidenziando alcuna differenza nella prevalenza delle complicazioni fra animali confinati in gabbia e lasciati liberi nel periodo postoperatorio7, sebbene la casistica considerata fosse insufficiente per trarre delle conclusioni definitive, in quanto il lavoro considerava solo 7 cedimenti (su un totale di 20 interventi). Il presente studio retrospettivo non ha potuto contemplare quest’importante aspetto, che rimane a tutt’oggi sconosciuto nella casistica contemplata.

La tenuta delle viti da corticale da 2,7 mm, da corticale da 3,5mm e da spongiosa da 4mm è risultata essere uguale in uno studio condotto sulla riduzione delle osteotomie pelviche nei cani giovani6. In uno studio condotto su 92 casi di osteosintesi e riduzioni sacroiliache è risultato che le viti avessero una maggiore presa quando ancorate al corpo del sacro piuttosto che alle sue ali8.

Tuttavia, il lavoro di Hosgood e Lewis condotto su 49 osteotomie pelviche3 e il lavoro di Remedios e Fries condotto su 20 osteotomie pelviche7, smentiscono questo tipo di correlazione. La percentuale di inserimento delle viti con ancoraggio > del 60% delle stesse nello spessore del sacro pare consentire una probabilità di allentamento inferiore nelle riduzioni delle lussazioni coxofemorali8, ma ciò non appare così evidente nello studio di Remedios e Fries7.

Nel presente studio descrittivo, l’allentamento delle viti ha riguardato il 26% degli impianti fissati mediante viti da 3,5mm (27 su 104) e il 19% degli impianti fissati mediante viti da 4,0mm (16 su 87) con una differenza poco significativa; nei 43 allentamenti totali, in 35 (su 152 - 17,7%) erano coinvolti impianti le cui viti interessavano il sacro e in 8 (su 45 - 8,8%) erano coinvolti impianti le cui viti interessavano il solo ileo, con una differenza piuttosto significativa. L’allentamento delle viti ancorate al sacro potrebbe essere spiegato dai movimenti che l’articolazione sacro-iliaca impone agli impianti come suggerito da Hulse et al nel 19859. Le viti che attraversano l’articolazione sacro-iliaca dovrebbero essere messe “a compressione” per eliminare i movimenti articolari che causano l’allentamento delle viti stesse9, ma

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ciò non è generalmente praticato nelle osteotomie pelviche3.

L’impiego di cerchiaggi metallici d’ausilio nella fissazione della placca angolata è stato suggerito per ridurre la probabilità d’avulsione della placca stessa nei cani giovani e per aumentare la stabilità della osteotomia dell’ileo1, così come l’impiego di un cerchiaggio metallico a livello di osteotomia ischiatica è stato indicato per incrementare la trazione mediale del segmento osteotomizzato fornendo così maggiore stabilità4.

Dei 43 impianti oggetto di “fallimento” riportati nel presente studio, 11 (25%) erano sostenuti da cerchiaggio metallico ausiliare e 32 (75%) ne erano sprovvisti, suggerendo una probabile correlazione fra la maggior tenuta della placca e l’applicazione del cerchiaggio metallico, così come una probabile correlazione può essere suggerita fra l’impiego di un cerchiaggio metallico a livello di osteotomia ischiatica ed una maggiore stabilità del segmento osseo ruotato, visto che l’86% degli allentamenti riscontrati ne era sprovvisto. D’altra parte, secondo alcuni autori, l’impiego del cerchiaggio ischiatico porterebbe ad una maggiore tensione a livello di impianto iliaco, favorendone la mobilizzazione. Duhautois sostiene l’inutilità del cerchiaggio ischiatico quando vengono impiegate placche preangolate da TPO a causa della maggiore stabilità fornita da queste placche rispetto alle placche DCP standard7.

Altri parametri, quali la liberazione del legamento sacrotuberoso e l’angolo di inclinazione dell’osteotomia iliaca possono contribuire ad una maggiore o minore stabilità del segmento osseo sottoposto alla rotazione1. La sindesmotomia del legamento sacrotuberoso viene indicata per diminuire le forze di stress che agiscono sui mezzi di sintesi10, mentre sembra che una linea di osteotomia perpendicolare all’asse lungo del bacino piuttosto che perpendicolare al corpo dell’ileo, faciliti la riduzione e la stabilità dei segmenti ossei1. Il presente studio retrospettivo, basato prevalentemente su valutazioni radiografiche, non ha potuto valutare questi due parametri.

Gli allentamenti sono risultati prevalentemente a carico del segmento craniale della placca negli studi di Hunt e Litsky4, Zolton11, e Hosgood e Lewis3 mentre Slocum e Devine12 in uno studio del 1987 hanno riportato solo allentamenti a carico del segmento acetabolare. Il nostro studio retrospettivo ha evidenziato una marcata prevalenza di allentamenti a carico del segmento craniale: dei 43 allentamenti, 31 hanno interessato il segmento craniale della placca (72%), 11 quello caudale (26%) e uno entrambi (2%). Interessante rilevare, sebbene si tratti di dati numericamente esigui, che di 7 rotture delle viti, 2 riguardavano l’emiimpianto craniale, 4 quello caudale ed uno entrambi mettendo in evidenza un’incidenza opposta rispetto agli allentamenti delle viti.

Curioso è stato il riscontro di una maggiore incidenza di complicazioni a carico dell’anca sinistra (34% sul totale delle anche sinistre operate) rispetto a quelle a carico dell’anca controlaterale (12% sul totale delle anche destre operate).

Il peso del paziente all’atto dell’intervento chirurgico (media 31,9kg range 15-54 ) sembra non avere una influenza significativa sulla possibile complicanza postoperatoria, in quanto i soggetti con complicazioni avevano un peso medio di kg 33,2 range 15-54.

La maggiore frequenza di allentamenti sostenute dal ses-

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so maschile (il 70% degli allentamenti interessava soggetti maschi), potrebbe far pensare, escludendo la correlazione con il maggior peso corporeo, ad una diversa attitudine con maggiore attivismo dei cani maschi.

Anche l’orientamento delle viti potrebbe giocare un ruolo importante, data la maggiore tenuta degli impianti le cui viti avevano una direzione non parallela fra di loro, mentre l’angolo di angolazione della placca sembra non avere alcuna correlazione con il cedimento degli impianti.

E bene ricordare che nessuno dei 49 cedimenti degli impianti ha reso necessaria una revisione chirurgica così come nessuno di questi ha invalidato il risultato dell’intervento né la sua efficacia funzionale.

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RINGRAZIAMENTI Gli autori che hanno coordinato e partecipato a questo studio, sotto l’egida del Gruppo di Studio SCIVAC di Ortopedia, ringraziano vivamente tutti i colleghi che hanno partecipato inviando i loro dati, dedicando il loro tempo e fornendo la loro esperienza: Dino Buzzigoli, Antonio Ferretti, Antonio Marinucci, Massimo Olivieri, Bruno Peirone, Guido Pisani, Gian Luca Rovesti, Thomas Roth, James Sabatini, Matteo Tommasini.

BIBLIOGRAFIA

CONCLUSIONI

1.

L’eterogenicità dei dati a disposizione e la molteplicità dei parametri variabili considerati contemporaneamente, anche in presenza di una mole imponente di dati, non hanno permesso di trarre delle conclusioni definitive, ma solamente di suggerire delle indicazioni sulle probabili cause di cedimento degli impianti stessi negli interventi di osteotomia pelvica.

Ulteriori studi clinici prospettici potranno essere condotti, per il chiarimento delle cause delle complicazioni più volte richiamate, riducendo le numerose variabili emerse nel presente studio. Uniformando il protocollo diagnostico, raggruppando le tecniche chirurgiche, unificando le modalità del follow-up e della valutazione radiografica e funzionale dei risultati, sarà possibile condurre uno studio prospettico in grado di offrire dei dati sicuramente utili per ridurre l’incidenza delle complicazioni e per rendere più attendibile la prognosi di quest’intervento. Questo studio ha comunque dimostrato la fattibilità e l’utilità di indagini multicentriche, che permettono la valutazione di una grande mole di dati, il confronto tra diverse esperienze e il riscontro delle complicazioni sul campo.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

Koch DA, Hazewinkel HAW, Nap RC et al. Radiographic evaluation and comparison of plate fixation after triple pelvic osteotomy in 32 dogs with hip dysplasia. V.C.O.T. 1993: 6: 9-15.

Slocum B, Devine T. Pelvic osteotomy technique for axial rotation of the acetabular segment in dogs. J Am Anim Hosp Assoc 1986; 22: 331-338.

Hosgood G, Lewis DD. Retrospective evaluation of fixation complications of 49 pelvic osteotomies in 36 dogs. J Small Anim Pract 1993; 34: 123-130.

Hunt CA, Litsky AS. Stabilization of canine pelvic osteotomies with AO/ASIF plates and screws. V.C.O.T. 1988; 1: 52-57.

Duhautois B. Triple Pelvic Osteotomy: retrospective study of 173 cases. Prat Med Chir Anim Comp 1997; 1997; 32: 305-321.

McLaughlin RM, Miller CW, Taves CE et al. Force plate analysis of triple pelvic osteotomy for treatment of canine hip dysplasia. Vet Surg 1991; 20: 291-297.

Remedios AM, Fries CL. Implant Complications in 20 Triple Pelvic Osteotomies. V.C.O.T. 1993; 6: 202-207.

DeCamp CE, Braden TD. Sacroiliac fracture-separation in the dog. A study of 92 cases. Vet Surg 1985; 14: 127-130.

Hulse DA, Shires P, Waldron D, Hedlund CS. Sacroiliac luxation.

Comp for cont educ 1985; 7: 493-499.

Slocum B, Devine T. Pathomechanics of hip dysplasia. In: Canine Orthopedics. Whittick WG. Ed. Philadelphia: Lea & Febiger 1990: 471 - 481.

Zolton G M. A Review of 23 bilateral triple pelvic osteotomies. Proceedings of the 18th Annual Veterinary Othopedic Society Meeting (Abstract): 1991: 15.

Slocum B, Devine T. Pelvic osteotomy in the dog as treatment for hip dysplasia. Seminars in Veterinary Medicine and Surgery (Small Animal) 1987; 2: 107 -116.

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Protocollo di stabilizzazione del paziente con dilatazione e torsione dello stomaco Fabio Viganò Med. Vet. - Specialista in Malattie dei Piccoli Animali - San Giorgio su Legnano (MI)

Riassunto La dilatazione associata a torsione dello stomaco (GDV) è un’emergenza veterinaria stimata nell’ordine del 2.66.8/1000 nel cane1, interessa prevalentemente i cani di taglia grande con un torace profondo e stretto. La GDV è responsabile di alterazioni gastro enteriche, e sistemiche. L’improvviso aumento di volume dello stomaco procura nell’immediato una compressione del diaframma in grado di ostacolare la normale ventilazione e nei casi più gravi un’ipossia con riduzione della DO2 (disponibilità di ossigeno). La dilatazione-torsione gastrica, oltre a procurare le summenzionate conseguenze riduce drasticamente la gittata cardiaca e la perfusione periferica esercitando la compressione della vena porta e della vena cava caudale.

Una delle chiavi di successo nel trattamento del paziente affetto da GDV sta nel riconoscere quale è l’apparato maggiormente coinvolto ed adottare la terapia più adatta nel più breve tempo possibile, in effetti il paziente può manifestare una sintomatologia varia e richiedere procedure diagnostiche e terapeutiche differenti. In tal modo si cerca di stabilizzarlo il più possibile, riportando i parametri vitali al di sopra dei normali fabbisogni, così da ridurre i rischi legati all’anestesia, al trauma chirurgico ed a quelli legati al periodo postoperatorio. Di seguito si attuano le prime misure terapeutiche. Se il paziente manifesta una ipossia e/o un’insufficienza ventilatoria è necessario prima di effettuare la decompressione iniziare la somministrazione dell’ossigeno che può essere praticata con l’applicazione di un catetere endonasale e somministrando l’ossigeno ad alti flussi. L’ossigeno non deve provenire dal circuito usato abitualmente per l’anestesia, perché l’odore pungente dei gas anestetici residui nel circuito può ostacolare tale operazione. Le vie di somministrazione dei fluidi devono essere perentoriamente craniali, o meglio anteriori al diaframma (vene cefalica e giugulare). La fluidoterapia oltre che per scopi rianimatori deve essere adottata anche per rimpiazzare le perdite di liquidi nello spazio interstiziale dovuti a sequestro nel terzo spazio (stomaco). Schematizzando in ordine di importanza le procedure da effettuare sono: somministrare ossigeno, soluzioni infusionali, meglio se contemporaneamente all’ossigeno, posizionare almeno un grosso catetere endovenoso (14 G) nella vena cefalica ed uno nella vena giugulare, effettuare un prelievo di sangue ed eseguire i seguenti esami di laboratorio: ematocrito, proteine totali, elettroliti, emogasanalisi, urea, glicemia, conta delle piastrine, profilo coagulativo, profilo biochimico ed emocromocitometrico, somministrazione rapida di soluzioni cristalloidi e/o colloidali, monitoraggio della pressione ed elettrocardiografico, somministrazione di corticosteroidi prima della trocaterizzazione e dopo la sommnistrazione iniziale delle soluzioni endovenose, svuotamento del contenuto gastrico attraverso sonda, quando possibile, altrimenti trocaterizzazione, terapia del dolore da effettuarsi con oppiacei (utili anche come medicazione preanestetica), iniezione di un antibiotico a largo spettro e radiografie toraco-addominali.

FISIOPATOLOGIA La dilatazione associata a torsione dello stomaco (GDV) è un’emergenza veterinaria stimata nell’ordine del 2.66.8/1000 nel cane1, interessa prevalentemente i cani di taglia grande con un torace profondo e stretto. La GDV è responsabile di alterazioni gastro enteriche, e sistemiche. L’improvviso aumento di volume dello stomaco procura nell’immediato una compressione sul diaframma in grado di ostacolare la normale ventilazione e nei casi più gravi un’ipossia con riduzione della DO2 (disponibilità di ossigeno). La distensione dell’organo esercita un stiramento ed uno schiac-

ciamento dei vasi della parete gastrica, i quali non sono più in grado di apportare sangue ed ossigeno con conseguente ischemia ipossica tessutale in grado di provocare necrosi più o meno estese. In tali aree vengono liberati il TNF (fattore di necrosi tumorale) le interleuchine (es. IL-1, IL-6, IL-8), l’ossido nitrico, sostanze autacoidi e citochine, l’insieme di queste sostanze svolgono un’attività sistemica in grado di procurare profonde alterazioni dell’omeostasi come i deficit di perfusione, la SIRS (sindrome della risposta infiammatoria sistemica) e la MODS (sindrome da insufficienza d’organo multipla). Tali sostanze sono inoltre corresponsabili dei danni da riperfusione.

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La dilatazione-torsione gastrica, oltre a procurare le summenzionate conseguenze riduce drasticamente la gittata cardiaca e la perfusione periferica comprimendo la vena porta e la vena cava caudale. La compressione dei grandi vasi presenti in cavità addominale riduce il volume ematico disponibile ostacolandone il suo ritorno al cuore, con conseguente riduzione del volume di eiezione ventricolare e della gittata cardiaca. La gittata cardiaca può essere ridotta anche dalle emorragie causate dalla rottura delle arterie gastriche corte, dal sequestro ematico a livello della milza per trombosi od occlusione dei vasi splenici e dalla perdita di liquidi nel terzo spazio (stomaco).

Anche gli apparati genitourinario e digestivo subiscono una insufficienza circolatoria dovuta a problemi di perfusione come la maldistribuzione ematica ed i deficit della microcircolazione.

Le cause delle aritmie cardiache presenti in circa il 40% dei casi2 sono dovute all’ipossia, ai disturbi elettrolitici prodotti dalle perdite di liquidi nel terzo spazio, al vomito, alla perfusione tessutale insufficiente, ai disturbi acido-base, ed al rilascio del fattore di depressione miocardica. Le aritmie costituiscono una delle complicazioni più frequenti incompatibili con la vita ed in grado di svilupparsi prima, durante e dopo la chirurgia.

Una delle chiavi di successo nel trattamento del paziente affetto da GDV sta nel riconoscere quale è l’apparato maggiormente coinvolto ed adottare la terapia più adatta nel più breve tempo possibile, in effetti il paziente può manifestare una sintomatologia varia e richiedere procedure diagnostiche e terapeutiche differenti. In tal modo si cerca di stabilizzarlo il più possibile, riportando i parametri vitali al di sopra dei normali fabbisogni, così da ridurre i rischi legati all’anestesia, al trauma chirurgico ed a quelli legati al periodo postoperatorio.

PROTOCOLLO All’arrivo del paziente si esegue il triage, che richiede normalmente dai 30 ai 60 secondi, durante i quali si rilevano: lo stato del sensorio, la frequenza ed il modello dell’attività respiratoria, il polso ed i suoi caratteri, il tempo di riempimento capillare, il colore delle mucose e due temperature corporee (almeno quella rettale ed interdigitale). Di seguito si attuano le prime misure terapeutiche.

Se il paziente manifesta una ipossia e/o un’insufficienza ventilatoria è necessario prima di effettuare la decompressione iniziare la somministrazione dell’ossigeno che può essere praticata con l’applicazione di un catetere endonasale e somministrando l’ossigeno ad alti flussi 200300 ml/kg o più semplicemente quando non si ha tempo per posizionare il catetere, avvicinando l’estremità del tubo per l’erogazione dell’ossigeno, all’ingresso delle cavità nasali erogando da 1 a 3 litri al minuto per i cani di taglia piccola da 3 a 5 litri per i cani di taglia media e da 10 a 15 litri per i cani di taglia grande e gigante, altri sistemi per la somministrazione dell’ossigeno possono essere le maschere facciali, il collare elisabettiano od il sacco trasparente per i cani mordaci. L’ossigeno non deve provenire dal circuito usato abitualmente per l’anestesia, perché l’o-

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dore pungente dei gas anestetici residui nel circuito può ostacolare tale operazione.

Contemporaneamente alla somministrazione dell’ossigeno, devono essere somministrate rapidamente le soluzioni per infusione al fine di ripristinare il volume circolante e migliorare la perfusione tessutale. Se si è temporaneamente soli, dopo avere iniziato l’ossigenoterapia si passa alla somministrazione di fluidi. La priorità può essere invertita, spesso si riscontra uno shock ipovolemico scompensato che necessita di una immediata resuscitazione con la somministrazione rapida di soluzioni per via endovenosa.

Quali e quanti liquidi devono essere somministrati ed attraverso quale via?

Per rispondere a tali domande valgono le regole generali della fluidoterapia per pazienti in stato di shock. Si possono utilizzare esclusivamente soluzioni cristalloidi isotoniche oppure, soluzioni cristalloidi e colloidi od ancora queste ultime due più emotrasfusioni per rimpiazzare gli elementi figurati del sangue ed i fattori della coagulazione.

Le vie di somministrazione dei fluidi devono essere perentoriamente craniali, o meglio anteriori al diaframma. Affinché la compressione della vena cava caudale non ostacoli l’espansione del volume intravascolare impedendo ai fluidi di arrivare al cuore è bene infondere le soluzioni attraverso le vene cefaliche dell’avambraccio e la vena giugulare.

Meglio ancora se queste due vie sono adottate contemporaneamente.

Nei cani di taglia grande è necessario utilizzare almeno due cateteri da 14 Gauge nella cefalica destra e sinistra, ma la soluzione migliore sarebbe quella di sfruttare le due cefaliche con cateteri di 14 gauge di diametro, più una giugulare 3 . Infatti la somministrazione è tanto più rapida (quindi più efficace negli stati di shock) quanto più è breve e grande il catetere endovenoso. Poter posizionare un catetere giugulare significa anche poter conoscere la pressione venosa centrale (PVC), posizionando l’estremità del catetere in prossimità dell’atrio destro si può misurare la PVC, questo dato risulta molto importante durante la fluidoterapia rianimatoria in quanto permette di conoscere la quantità e la velocità alla quale devono essere somministrate le soluzioni endovenose.

Per poter conoscere la capacitanza del letto vascolare e se il cuore è in grado di gestire il volume di liquido somministrato, in altre parole se dobbiamo continuare a somministrare fluidi oppure se dobbiamo rallentarne l’infusione, è bene conoscere la pressione venosa centrale. Valori elevati della PVC (8-12 cm H20) e soprattutto quando tendono a rimanere invariati, costituisce il primo segnale di un eccesso di fluidi. Valori compresi tra lo zero e 4 cm H20 sono ideali, pressioni inferiori allo zero sono insufficienti e richiedono quantomeno un aumento della velocità e della quantità dei fluidi da somministrare.

La scelta del tipo di soluzione dipende da diversi fattori, non ultimo quello economico. Molti centri dediti alla pratica del pronto soccorso ed alla terapia intensiva preferiscono utilizzare i colloidi per ripristinare la pressione arteriosa, ritenendo che piccoli volumi (10-20 ml/kg/ev) sono sufficienti per espandere il circolo più rapidamente e semplicemente.

Viceversa altri preferiscono utilizzare le soluzioni cristalloidi bilanciate a volumi elevati (60–90 ml/kg/ev/ cane e 40-55 ml/kg/ev/gatto). Se si pensa che un flacone di soluzione col-

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loidale può costare fino a 10 volte e più rispetto a quella cristalloide, si può facilmente immaginare perché tale opzione è preferita, inoltre non è stata ancora dimostrata la maggior efficacia di un tipo rispetto all’altro in termini di sopravvivenza.

Le emotrasfusioni sono necessarie quando le emorragie addominali provocano repentine riduzioni dell’ematocrito pericolosi od incompatibili con la vita oppure quando in corso di coagulazione intravasale disseminata dobbiamo rimpiazzare i fattori della coagulazione. In quest’ultimo caso può essere somministrato plasma fresco o congelato ed iniziare una terapia con eparina sottocutanea. In presenza di un aumento dei tempi di coagulazione è necessario somministrare plasma fresco oppure congelato o sangue, il plasma può essere somministrato contemporaneamente alle soluzioni cristalloidi ed ogni volta che si sospetta una coagulazione intravasale disseminata oppure preventivamente per evitare coagulopatie da emodiluizione.

La fluidoterapia oltre che per scopi rianimatori deve essere adottata anche per rimpiazzare le perdite di liquidi nello spazio interstiziale dovuti a sequestro nel terzo spazio (stomaco). Le soluzioni che meglio si prestano a tale scopo sono quelle cristalloidi perché che si riversano rapidamente nello spazio extravascolare. Dopo circa trenta minuti dalla loro somministrazione solo l’8% rimane nello spazio intravascolare.

L’obbiettivo di queste due misure terapeutiche (somministrazione di ossigeno e soluzioni infusionali) è la correzione dei parametri emodinamici e dell’ossigenazione del paziente, tra questi i più semplici da ottenere sono: la pressione arteriosa, la pressione venosa centrale, la frequenza cardiaca, i caratteri del polso, i parametri della perfusione (polso, tempo di riempimento capillare e colore delle mucose), la correzione delle aritmie cardiache (come la tachicardia ed i complessi ventricolari prematuri) la pressione parziale dell’ossigeno, la sua saturazione, la pressione parziale dell’anidride carbonica, lo stato acido base. Purtroppo non sempre è possibile ottenere tali risultati, spesso infatti si riesce soltanto ad ottenere un miglioramento delle misurazioni sopra citate.

Schematizzando in ordine di importanza le procedure da effettuare sono: • Somministrare ossigeno • Somministrare soluzioni infusionali, meglio se contemporaneamente all’ossigeno • Posizionare almeno un grosso catetere endovenoso (14 G) nella vena cefalica ed uno nella vena giugulare • Effettuare un prelievo di sangue ed eseguire i seguenti esami di laboratorio: ematocrito, proteine totali, elettroliti, emogasanalisi, urea, glicemia, conta delle piastrine, profilo coagulativo, profilo biochimico ed emocromocitometrico • Somministrazione rapida di soluzioni cristalloidi e/o colloidali • Monitoraggio della pressione ed elettrocardiografico

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• Somministrazione di corticosteroidi prima della trocaterizzazione e dopo la sommnistrazione iniziale delle soluzioni endovenose • Svuotamento del contenuto gastrico attraverso sonda, quando possibile, altrimenti trocaterizzazione • Terapia del dolore da effettuarsi con oppiacei (utili anche come medicazione preanestetica) • Iniezione di un antibiotico a largo spettro e radiografie toraco-addominali A questo punto si può procedere al trattamento preanestetico ed alla preparazione della parete addominale alla chirurgia.

DISCUSSIONE La pressione arteriosa media (MAP) deve essere mantenuta al di sopra degli 80 mmHg quella sistolica al di sopra dei 100 mmHg, quando i fluidi non riescono a ripristinarla è bene ricorrere ad ammine vasoattive (es. dobutamina, dopamina). La somministrazione di corticosteroidi, molto dibattuta, trova in questa sindrome un suo utilizzo al fine di controllare la cascata dell’acido arachidonico, della ossidazione dei lipidi e della produzione di molecole prodotte dalla ciclossigenasi.

L’applicazione della sonda gastrica può non essere possibile soprattutto quando la torsione è completa e la forzatura di tale manovra, soprattutto se effettuata con sonde non adatte, può procurare la rottura della parete gastrica soprattutto quando sono presenti aree di necrosi. Per questi motivi può essere preferita la trocaterizzazione alla applicazione della sonda, la puntura transcutanea permette di rimuovere gas e liquidi molto rapidamente ed avviarsi alla chirurgia il più precocemente possibile e con immediato sollievo per il paziente. Non deve essere dimenticato che la GDV è una sindrome molto dolorosa. Il rischio di questa manovra è la perforazione splenica dislocatasi durante la torsione e rotazione dello stomaco.

Al fine di stabilizzare il paziente i parametri vitali quali la frequenza cardiaca, la frequenza respiratoria, la DO2 con le sue componenti (ad esempio l’emoglobina ed il contenuto di ossigeno nel sangue), il polso ed i suoi caratteri, la pressione arteriosa, il ritmo cardiaco, l’equilibro idro-elettrolitico ed acido base devono essere monitorati costantemente e corretti il più precocemente possibile al fine di ottenere valori normali o superiori.

Bibliografia 1.

2.

3.

Wayne E. Wingfield, (1997), Veterinary emergency medicine secrets, Hanley & Belfus, Philadelfia, 30-31.

Dale E. Bjorling, (1998), GDV: epidemiology myths and realities and surgical management, Proceedings Sixth International Veterinary Emeregency and Critical Care Symposium, 565-568.

Rebecca Kirby, (1998), Small animal emergency & critical care medicine, Manson Publishing, London, 139-140.

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Monitoraggio e trattamento post operatorio della dilatazione e torsione dllo stomaco Fabio Viganò Med. Vet. - Specialista in Malattie dei Piccoli Animali - San Giorgio su Legnano (MI)

Riassunto Il monitoraggio del paziente affetto da dilatazione e torsione dello stomaco (GDV), deve essere orientato prevalentemente verso gli apparati maggiormente compromessi, che in questo caso sono l’apparato cardiocircolatorio e respiratorio. L’ipotensione è uno dei problemi vitali che più comunemente si deve affrontare, tutte le componenti della pressione arteriosa dovrebbero essere controllate misurate e corrette. Gli strumenti per la misurazione della pressione arteriosa sono tre: il metodo ad ultrasuoni doppler, il metodo oscillometrico indiretto ed il metodo diretto con l’utilizzo di un trasduttore. Il monitoraggio elettrocardiografico riveste una notevole importanza nel paziente affetto da GDV perché l’ipossia, gli squilibri elettrolitici, l’ipovolemia, l’ischemia miocardica, l’aumento delle catecolamine circolanti ed un diminuita soglia di sensibilità alle stesse, predispongono alle aritmie cardiache, presenti in circa il 50% dei casi.

L’ECG deve essere affiancato anche da un monitoraggio emodinamico come ad esempio: la misurazione della gittata cardiaca, la pressione arteriosa, la pressione venosa centrale, il polso, il tempo di riempimento capillare ed il colore delle mucose. Tutte le aritmie in questo tipo di paziente, devono essere trattate inizialmente con la somministrazione dell’ossigeno dei fluidi per via endovenosa al fine di ripristinare un circolo efficace e correggere i disturbi elettrolitici, in un secondo tempo ed in caso di mancata risposta, si utilizzano i farmaci cardioattivi. Durante la chirurgia se è presente una grave dilatazione gastrica, la ventilazione polmonare può essere compromessa, per monitorarla e decidere se eseguire una ventilazione polmonare controllata (utilizzando ad esempio un ventilatore polmonare) si misura la CO2 di fine espirazione (EtCO2). La saturimetria dell’emoglobina (SpaO2) ottenuta con un pulsiossimetro indica la percentuale di emoglobina ossigenata. Essendo il contenuto di ossigeno nel sangue dipendente prevalentemente dal legame che ha con l’emoglobina, la sua misurazione fornisce indirettamente un’informazione circa il suo stato di ossigenazione, ma non quanto ossigeno è presente nel sangue. Per verificare se la EtCO2 e la SpaO2 sono corrette è necessario effettuare una emogasanalisi, inoltre con essa si è in grado di valutare il suo stato acido base e stabilire le basi per un appropriata terapia che altrimenti potrebbe risultare fatale. Oltre agli apparati cardiocircolatorio e respiratorio anche il profilo coagulativo deve essere monitorato soprattutto prima e dopo la chirurgia. Un aumento o meglio la tendenza ad aumentare dei tempi misurati (indipendentemente dal test utilizzato) è altamente sospetta di un coagulazione intravasale disseminata (CID) e non permette ritardi nella terapia. I tempi di coagulazione possono essere prolungati anche dalla emodiluizione procurata dalla copiosa somministrazione di fluidi per via endovenosa. Terminata la procedura chirurgica, il paziente deve essere monitorato per almeno le prime 24 ore. Una buona norma è ricoverare il paziente sino a che le condizioni generali si sono ristabilite ed ha ripreso ad alimentarsi. Nelle prime 24 ore si può lasciare la sonda nasogastrica per facilitare l’evacuazione di aria, materiale indigerito residuo nello stomaco e per rimuovere coaguli di sangue.

Il monitoraggio del paziente affetto da dilatazione e torsione dello stomaco (GDV), deve essere orientato prevalentemente verso gli apparati maggiormente compromessi, che in questo caso sono l’apparato cardiocircolatorio e respiratorio.

L’ipotensione è uno dei problemi vitali che più comunemente si deve affrontare, tutte le componenti della pressione arteriosa dovrebbero essere controllate misurate e corrette.

La pressione arteriosa è il prodotto della gittata cardiaca, della capacitanza vascolare e del volume ematico. Il deficit di una sua componente è generalmente compensato dalle altre due al fine mantenere una perfusione cerebrale e coronarica.

La gittata cardiaca è il prodotto del volume di eiezione ventricolare per la frequenza cardiaca. Se rilevare la frequenza cardiaca è semplice altrettanto non è per la gittata. Il metodo più usato sfrutta un catetere a termodiluizione posizionato nell’arteria polmonare o nell’aorta. Si inocula un indicatore attraverso il catetere (di cui si conosce il volume la concentrazione e la temperatura) nell’atrio destro e si va misurane le componenti nell’arteria polmonare o nell’aorta. L’elaborazione dei dati viene effettuata da un computer che segue i rilevamenti ottenuti al fine di calcolando l’entità della gittata. Come si può facilmente comprendere tale metodica invasiva non è di facile attuazione e richiede una tecnologia costosa.

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Gli strumenti per la misurazione della pressione arteriosa sono tre: il metodo ad ultrasuoni doppler, il metodo oscillometrico indiretto ed il metodo diretto con l’utilizzo di un trasduttore.

Il metodo diretto è il migliore perché evita errori di interpretazione dovuti ad un ridotto lume vasale, alla bassa pressione, alla vasocostrizione, alle aritmie cardiache, ai tremori muscolari del paziente e quando la pressione è molto bassa o molto elevata. Tale metodo è perciò più accurato e continuo, richiede però l’introduzione di un catetere in arteria per via percutanea o cut-down. Può essere utile per ottenere campioni ematici seriali più facilmente. È il metodo di elezione per i pazienti critici. Il catetere può essere introdotto nell’arteria femorale, nell’arteria della pinna dell’orecchio o nell’arteria metatarsale. L’arteria metatarsale è generalmente la preferita perché il tessuto sottocutaneo circoscritto è abbastanza teso da evitare formazioni di ematomi dopo la rimozione del catetere e perché facilmente aggredibile. Introdotto il catetere si può collegarlo ad uno strumento per la rilevazione della pressione arteriosa (ormai molti monitor cardiaci hanno già la scheda per eseguire questo compito) oppure si può collegarlo ad un aneroide od ancora ad un trasduttore in grado di rilevare l’onda sfigmica e rappresentarla graficamente su di un oscilloscopio. L’utilizzazione può essere limitata dalla necessità di reperire l’attrezzatura necessaria, dalla difficoltà nel posizionare il catetere intrarterioso in soggetti ipotesi ed ipovolemici, dalla possibilità di procurare una trombosi a carico dell’arto prescelto e dall’immobilità a cui è sottoposto l’arto utilizzato.

Il secondo metodo è rappresentato dalla misurazione con il sistema oscillometrico indiretto.

La misurazione avviene con l’applicazione di un manicotto pneumatico a livello della regione metacarpale o metatarsale, un altro sito è rappresentato dalla coda, quest’ultimo è poco sfruttato perché non sempre accessibile e difficilmente standardizzabile. I manicotti, generalmente ben tollerati, esistono di diverse dimensioni, devono essere di almeno tre misure per le differenti taglie dei pazienti. La metodica non è invasiva, è di semplice applicazione ma è sicuramente meno precisa. Una volta applicata il manicotto al paziente, la macchina esegue un auto settaggio ed effettua, ad intervalli precedentemente impostati, le misurazioni della pressione sistolica, diastolica, media e la frequenza cardiaca. Grazie alla possibilità di impostare gli intervalli di tempo, ai quali effettuare le misurazioni, la macchina non necessita la partecipazione dell’operatore, tale vantaggio, associato alla semplicità dell’esecuzione lo ha fatto preferire ad altri metodi, tanto da essere tra gli strumenti più utilizzati nel monitoraggio dell’anestesia generale. Purtroppo le rilevazioni possono essere inficiate dai movimenti dell’arto, dai tremori del paziente, dalle aritmie cardiache, dagli stati di basso flusso e quando la pressione arteriosa è molto bassa. Un metodo semplice per osservare se l’apparecchio sta rilevando i suoi dati correttamente è controllare se la frequenza cardiaca corrisponde a quella rilevata all’auscultazione o con un altro strumento, purtroppo questa verifica non garantisce che la misurazione della pressione arteriosa sia corretta.

Il metodo doppler rileva il flusso ematico all’interno dell’arteria, trasformando tale movimento in suoni udibili attraverso un altoparlante. Per misurare la pressione arteriosa sistolica è necessario utilizzare una cuffia pneumatica collegata ad uno sfigmomanometro, essa viene posta a monte della son-

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da doppler ed insufflata fino ad ostruire il flusso ematico con la scomparsa del suono udibile. Si procede riducendo lentamente la pressione all’interno della cuffia fino a che viene percepito il primo suono, si controlla a quanti millimetri di mercurio corrisponde la pressione esercitata dalla cuffia, il valore letto corrisponde alla pressione arteriosa sistolica. È bene utilizzare bracciali adatti alla taglia del paziente, alle prime esperienze è meglio ripetere la misurazione più volte fino a che si ottengono valori paragonabili. Generalmente al valore ottenuto è necessario aggiungere 14 mmHg. Il metodo permette di rilevare la pressione anche quando è molto bassa oppure quando sono presenti stati di basso flusso, lo strumento rilevando il passaggio del sangue all’interno delle arterie periferiche fornisce indicazioni anche sullo stato della perfusione.

L’assenza di flusso od una riduzione della sua entità può essere dovuta ad una vasocostrizione periferica oppure ad una insufficienza circolatoria, questo dato viene rilevato ad ogni pulsazione e non ad intervalli prestabiliti come con il metodo oscillometrico. Il limite di tale apparecchio è rappresentato dalla difficoltà di poter determinare la pressione arteriosa diastolica. Rilevandola con il metodo doppler essa corrisponde ad una riduzione dell’entità del suono percepito dopo quello della sistolica, tale valore può essere perciò soggettivo ed essendo molto importante al fine di determinare la pressione arteriosa media, si possono incontrare serie difficoltà nel quantificarla. La pressione arteriosa media è quella che generalmente viene utilizzata per stabilire lo stato di perfusione del paziente, essa è più prossima alla pressione arteriosa diastolica che alla sistolica, quindi il metodo doppler si presta con difficoltà a tale scopo. D’altro canto, l’ascoltazione di un suono pieno e chiaro è comunque indice di un buon flusso ematico periferico e di un polso forte che a loro volta sono espressione di una buona perfusione periferica. Il problema maggiore nell’uso di tale metodica risiede quindi nell’abilità dell’operatore nell’eseguirla, nell’interpretazione che può essere soggettiva ed infine è necessario che un operatore esegua la misurazione mentre con il metodo oscillometrico non è necessario.

Il monitoraggio elettrocardiografico riveste una notevole importanza nel paziente affetto da GDV perché l’ipossia, gli squilibri elettrolitici, l’ipovolemia, l’ischemia miocardica, l’aumento delle catecolamine circolanti ed un diminuita soglia di sensibilità alle stesse, predispongono alle aritmie cardiache, presenti in circa il 50% dei casi.

L’elettrocardiogramma (ECG) misurando l’attività elettrica del cuore non fornisce informazione circa la sua performance, perciò non può essere ritenuto sufficiente per valutare la funzione cardiocircolatoria. L’ECG deve essere affiancato anche da un monitoraggio emodinamico come ad esempio: la misurazione della gittata cardiaca, la pressione arteriosa, la pressione venosa centrale, il polso, il tempo di riempimento capillare ed il colore delle mucose. Per effettuare l’ECG durante l’anestesia sono spesso utilizzate delle pinzette di metallo, per il monitoraggio continuo (diverse ore) è meglio utilizzare gli elettrodi adesivi, meno traumatici e più affidabili. Alla lettura dell’ECG dobbiamo controllare la frequenza cardiaca, la regolarità del ritmo, la forma dell’onda PQRST, se ad ogni onda P segue un QRS, l’assenza di onda P aiuta a differenziare un complesso ventricolare prematuro (CVP) da un blocco di branca oppure da una ipertrofia ventricolare. I CVP sono molto frequenti nei pazienti affetti da

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GDV, infatti la dilatazione e torsione di organi in cavità addominale può essere la causa di una attività pacemaker ectopica.

Se ai CVP è associata una tachicardia ed ipoperfusione è bene trattarli lidocaina 2 mg/kg/ev/bolo. Se questo trattamento non fosse sufficiente è bene infonderla a 50 mcg/kg/ev/min. La tachicardia, molto frequente in questi pazienti, può essere dovuta ad una ipovolemia oppure a danni da riperfusione. Un’altra alterazione facilmente riscontrabile è lo slivellamento del tratto ST dovuto ad ipossia del miocardio oppure a squilibri del potassio o del calcio.

Quando viene diagnosticata una aritmia cardiaca dobbiamo sempre verificare: se ad ogni QRS corrisponde il polso e se è presente identificarne i caratteri, eseguire un esame degli elettroliti (potassio, magnesio, calcio, cloro e sodio) e verificare il suo stato di ossigenazione (emogasanalisi od in sua assenza almeno la saturimetria). Tutte le aritmie in questo tipo di paziente, devono essere trattate dapprima con la somministrazione dell’ossigeno, quindi con il ripristino di un circolo efficace. Spesso molte di esse possono essere risolte con l’ossigenoterapia, l’infusione di soluzioni per infusione endovenosa e la correzione dei disturbi elettrolitici.

Durante la chirurgia si può avere una repentina decompressione dello stomaco la quale risolve sì lo schiacciamento della vena cava ma procura brusche variazioni nella pressione arteriosa e la difficoltà da parte del cuore di gestire una massa di sangue precedentemente sottratta.

Con l’ECG bisogna identificare le aritmie da focolai ectopici, da gas anestetici o di altra natura.

Durante la chirurgia se è presente una grave dilatazione gastrica, la ventilazione polmonare può essere compromessa, per monitorarla e decidere se eseguire una ventilazione polmonare controllata (utilizzando ad esempio un ventilatore polmonare) si misura la CO2 di fine espirazione (EtCO2).

Essa si esegue con l’ausilio di un con un capnometro o meglio ancora con un capnografo che disegnando l’onda capnografica ad ogni atto respiratorio permette di identificare molti problemi legati alla ventilazione.

La saturimetria dell’emoglobina (SpaO2) ottenuta con un pulsiossimetro indica la percentuale di emoglobina ossigenata.

Essendo il contenuto di ossigeno nel sangue dipendente prevalentemente dal legame che ha con l’emoglobina, la sua misurazione fornisce indirettamente un’informazione circa il suo stato di ossigenazione, ma non quanto ossigeno è presente nel sangue. In sostanza è come se misurassimo quanto si “desatura” l’emoglobina di ossigeno o meglio quanto decresce come valore percentuale, infatti quando lo strumento indica il 100% non sappiamo se la pressione parziale dell’O2 è pari a 150, 200 o 500 mmHg. Quando diminuisce (valori inferiori al 100 %), sfruttando la curva di dissociazione dell’emoglobina ed in condizioni normali, si può desumere la pressione parziale di ossigeno disciolto nel sangue. Ad esempio a valori maggiori o uguali al 95% di saturazione corrispondono a 80 mmHg o più di pressione parziale di ossigeno (PaO2), per valori del 90% o leggermente inferiori corrispondono circa 60 mmHg di PaO2 ed è considerata un’ipossiemia moderata, valori inferiori al 75% sono da considerare ipossiemie gravi e corrispondono a circa 40 mmHg di PaO2 .

Per verificare se la EtCO2 e la SpaO2 sono corrette è necessario effettuare una emogasanalisi, inoltre con essa si è in grado di valutare il suo stato acido base e stabilire le basi per

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un appropriata terapia che altrimenti potrebbe risultare fatale.

Oltre agli apparati cardiocircolatorio e respiratorio anche il profilo coagulativo deve essere monitorato soprattutto prima e dopo la chirurgia. A tal fine possono essere utilizzati molti tests, purtroppo durante le urgenze i laboratori non sempre sono disponibili a fornirci gli esiti in tempo utile e quindi nella maggior parte dei casi si ripiega su esami di facile attuazione come il tempo di coagulazione attivato (ACT), il tempo di protrombina (PT), il tempo di protrombina attivato (APTT). Per questi tre esami, oggigiorno esistono strumenti di laboratorio palmari in grado di effettuarli con cartucce monouso, che rendono la metodica molto semplice. In assenza di questi tests ed in caso di necessità, si può ricorrere al tempo di emorragia buccale (BT) che purtroppo indica soltanto la possibilità del sangue di coagulare. Un aumento o meglio la tendenza ad aumentare dei tempi misurati (indipendentemente dal test utilizzato) è altamente sospetta di un coagulazione intravasale disseminata (CID) e non permette ritardi nella terapia. I tempi di coagulazione possono essere prolungati anche dalla emodiluizione procurata dalla copiosa somministrazione di fluidi per via endovenosa.

TRATTAMENTO POSTOPERATORIO Terminata la procedura chirurgica, il paziente deve essere monitorato per almeno le prime 24 ore. Una buona norma è ricoverare il paziente sino a che le condizioni generali si sono ristabilite ed ha ripreso ad alimentarsi. In genere questo può richiedere da due a cinque giorni di degenza postoperatoria.

Durante i primi due o tre giorni si esegue una fluidoterapia con cristalloidi isotonici per rimpiazzare le perdite nel terzo spazio ed a quelle dovute alle emorragie correggendo anche i disturbi elettrolitici ed acido base. Particolare attenzione deve essere prestata alle aritmie che si sviluppano più frequentemente nelle prime ore dopo la chirurgia, sia per danni da riperfusione di tessuti necrotici o ischemici sia per le cause precedentemente elencate. Il paziente deve essere mantenuto sotto controllo elettrocardiografico ed emodinamico soprattutto il primo giorno, anche se non sono esclusi i giorni successivi quando lo si ritiene necessario. Nel periodo postoperatorio si possono sviluppare: una nuova dilatazione gastrica, la peritonite settica, la deiscenza della sutura gastrica per necrosi dei lembi della parete, la sindrome della risposta infiammatoria sistemica (SIRS) e deficit della coagulazione.

Oltre al monitoraggio bisogna provvedere al ripristino dell’alimentazione. A distanza di poche ore (8-14 ore) può essere iniziata una micronutrizione enterale con diete polimeriche al dosaggio di 0,25 ml/kg/ora, il giorno successivo può essere iniziata l’alimentazione con diete bilanciate. Nelle prime 24 ore si può lasciare la sonda nasogastrica per facilitare l’evacuazione di aria, materiale indigerito residuo nello stomaco e per rimuovere coaguli di sangue. L’applicazione della sonda nasogastrica è raccomandata in caso di gastrectomia parziale. La micronutrizione è molto utile per apportare energia alle cellule della mucosa gastroenterica affinché possa iniziare il processo di cicatrizzazione il più precocemente possibile e per mantenere integra la barriera mucosale gastroentercica, riducendo così la possibilità di migrazioni batteriche responsabili di sepsi.

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Anatomia radiografica del torace Massimo Vignoli DMV, SRV - Libero Professionista - Bologna

Riassunto L’obiettivo dell’esame radiografico è quello di valutare eventuali modificazioni morfologiche degli organi (aumentata o diminuita densità, variazioni di sede, di forma e dimensioni). Per questo è necessario avere una conoscenza ottimale dell’anatomia radiografica normale e delle variazioni anatomiche fisiologiche tra le specie, le razze ed i singoli soggetti. Le differenze dovute alla conformazione sono molto maggiori rispetto a quelle tra un animale sano ed uno malato. In base alla forma consideriamo tre differenti conformazioni del torace: a) Torace profondo-stretto (Collie, Setter Irlandese). b) Torace intermedio o mesomorfo (P.T., Boxer, Barboncino, gatto). c) Torace breve-largo (Boston T., Bull-dog, Bull-Mastiff).

Strutture extratoraciche: Faringe, Laringe, Trachea ed Esofago Parete Toracica: -Tessuti molli (cute, grasso, muscoli sottocutanei), Coste e muscoli intercostali, Colonna vertebrale, Sterno Diaframma Mediastino Spazio pleurico Cuore e grossi vasi Polmoni Bibliografia - Barone R. , 1981: Anatomia comparata dei mammiferi domestici. Vol. 3 splancnologia. Ed. It. A cura di R.Bortolami; Edagricole, Bologna, 601-690.

- Suter P. & Lord P., 1984: Text Atlas, Thoracic Radiography, Thoracic Diseases of the Dog and Cat. By Peter F. Suter, 2-45.

- Thrall D. 1998: Textbook of Veterinary Diagnostic Radiology. W.B. Saunders Company, Philadelphia, 263-384.

L’obiettivo dell’esame radiografico è quello di valutare eventuali modificazioni morfologiche degli organi (aumentata o diminuita densità, variazioni di sede, di forma e dimensioni). Per questo è necessario avere una conoscenza ottimale dell’anatomia radiografica normale e delle variazioni anatomiche fisiologiche tra le specie, le razze e dei singoli soggetti. Le differenze dovute alla conformazione sono molto maggiori rispetto a quelle tra un animale sano ed uno malato. In base alla forma consideriamo tre differenti conformazioni del torace: a) Torace profondo-stretto (Collie, Setter Irlandese). b) Torace intermedio o mesomorfo (P.T., Boxer, Barboncino, gatto). c) Torace breve-largo (Boston T., Bull-dog, Bull-Mastiff).

Strutture extratoraciche: -Faringe: divisa in orofaringe e rinofaringe dal palato molle, si estende fino all’epiglottide.

-Laringe: radiograficamente è ben evidente in propiezione laterale, meno in ventrodorsale per la sovrapposizione degli altri tessuti. A questo livello si evidenzia l’osso ioi-

de nelle sue varie componenti.Nei cani brachicefali o negli obesi, la laringe appare meno contrastata per l’abbondanza di tessuti molli e grasso (diminuito rapporto aria/tessuto).

Nei giovani la laringe è male evidenziata a causa della scarsa mineralizzazione. Si mineralizza prima nei cani grandi e nei condrodistrofici.

Trachea: si valuta in proiezione latero-laterale. La proiezione ventrodorsale è utile per valutare eventuali dislocazioni. La trachea si trova sulla linea mediana, con una leggera deviazione a destra a livello del mediastino craniale, più evidente nelle razze condrodistrofiche (da non confondere con deviazioni dovute a masse). La trachea decorre quasi parallelamente alle vertebre cervicali e diverge leggermente da quelle toraciche. La sua posizione può variare al variare del posizionamento del collo del soggetto radiografato. Nei cani sani il suo diametro è costante nelle diverse fasi della respirazione; può variare nelle diverse razze (diametro più piccolo nei condrodistrofici). Nei cani anziani o condrodistrofici si nota la mineralizzazione degli anelli che la compongono.

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Esofago: non è visibile radiologicamente per il contatto con muscoli e fascia a livello cervicale e di tessuto connettivo e fascia nel mediastino dorsale. A volte si può raccogliere una piccola quantità di aria nell’esofago che ne consente la visualizzazione (caudalmente allo sfintere esofageo craniale, all’ingresso del torace e dorsalmente alla base del cuore). Negli animali anestetizzati la dilatazione dell’esofago è un reperto normale. Lo studio dell’esofago con mezzo di contrasto consente di visualizzare le pliche della mucosa esofagea. Nel cane le pliche si presentano longitudinali in tutto il decorso dell’esofago, mentre nel gatto la porzione più caudale dell’esofago toracico presenta delle pliche a lisca di pesce.

Parete Toracica: la parete toracica comprende: -Tessuti molli extratoracici: si considerano cute, grasso e muscoli sottocutanei. Talvolta sono evidenziati i capezzoli, che non vanno confusi con neoplasmi.

-Coste e muscoli intercostali: nei carnivori domestici abbiamo 13 paia di coste. Tra le coste si trovano i muscoli intercostali interni ed esterni. Dai processi trasversi vertebrali originano i muscoli sopracostali che si fissano sulle coste e le tirano in direzione craniale.

-Colonna vertebrale: nell’immagine radiografica del torace, si evidenziano generalmente le vertebre cervicali caudali e le vertebre toraciche che sono in numero di 13, separate tra loro dai dischi intervertebrali.

-Sterno: è un osso impari che chiude ventralmente il torace e dà appoggio alle cartilagini costali. Nel cane e nel gatto è costituito da 8 da sternebre unite tra loro per sincondrosi (in età avanzato sinostosi). La prima sternebra si prolunga con un’appendice appiattita ed allungata detta manubrio dello sterno, l’ultima presenta l’appendice xifoidea.

-Clavicola: si evidenzia solo nel gatto e nel coniglio.

Diaframma: si può visualizzare radiologicamente in tutte le proiezioni, ma con aspetto molto differente a seconda della razza, età, stato di nutrizione, fase respiratoria, gravità (utilizzo del raggio orizzontale) e posizionamento. Le strutture del diaframma meglio visualizzabili sono i pilastri destro e sinistro, la fenditura tra i pilastri e la cupola diaframmatica. Il contatto con gli organi addominali non consente una buona visualizzazione di tutte le parti muscolari. In proiezione latero-laterale il pilastro più declive viene spostato cranialmente. In decubito destro i pilastri appaiono paralleli, in decubito sinistro appaiono, di solito, convergenti. La localizzazione della bolla gastrica (posta dietro il pilastro di sinistra) e della vena cava caudale (situtata a destra della linea mediana), facilitano il riconoscimento dei due pilastri. Il punto di intersezione tra diaframma e vertebre varia in funzione della fase respiratoria; di solito è situato tra T11 e T13, ma può variare fino a T9-L1. In proiezione ventro-dorsale si riconoscono tre porzioni del diaframma, pilastro destro e sinistro e cupola, mentre in proiezione dorso-ventrale appare una unica linea convessa proiettata all’interno del torace.

Mediastino: costituito da due strati di pleura mediastinica e dallo spazio compreso tra questi. I due strati di pleura sono parte dei sacchi pleurici di destra e di sinistra. Il mediastino si estende dall’ingresso del torace fino al diaframma ed è situato sul piano mediano, dividendo il torace in alvo destro e sinistro. Viene suddiviso in mediastino craniale (davanti al cuore), porzione mediale (a livello del cuore che ne

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è contenuto) e mediastino caudale (caudalmente al cuore).

Inoltre, viene diviso in dorsale e ventrale dal piano passante per la biforcazione tracheale. Il mediastino comunica cranialmente con le fascie del collo e caudalmente con lo spazio retroperitoneale attraverso lo iato aortico. Vi sono controversie riguardo alla fenestrazione delle pleure mediastiniche. Le principali strutture contenute nel mediastino sono: timo, cuore e grossi vasi toracici, linfonodi sternali, mediastinici e trachebronchiali, trachea, bronchi principali, tronco vagosimpatico destro e sinistro, esofago, dotto toracico, nervo frenico destro e sinistro. Il mediastino presenta tre riflessioni: cranioventrale, caudoventrale (detta erroneamente legamento frenopericardico) solitamente visibili radiologicamente e riflessione mediastinica della vena cava o plica della vena cava. In proiezione dorsoventrale il mediastino craniale è in gran parte sovrapposto alle vertebre. In ogni caso si considera che non debba superare di due volte la larghezza di una vertebra.

Spazio pleurico: si divide in pleura parietale e polmonare o viscerale. La pleura parietale si divide ulteriormente in porzione costale (riveste la faccia interna della cassa toracica), diaframmatica (riveste il diaframma) e mediastinica (contribuisce a formare il mediastino). Tra pleura parietale e viscerale vi è uno spazio virtuale, dove è contenuto normalmente una piccola quantità di liquido con funzione di lubrificazione. Le pleure normali non sono visibili radiologicamente. Occasionalmente se i raggi colpiscono tangenzialmente la pleura in una fessura interlobare, viene visualizzata. È però impossibile radiograficamente stabilire se è una pleura normale colpita tangenzialmente dai raggi o se è una pleura leggermente ispessita. In entrambi i casi comunque non avrebbe significato clinico.

Cuore e grossi vasi: nella radiologia cardiaca, differenze sostanziali delle dimensioni, forma e posizione del cuore si possono avere in relazione a differenze di specie, razza, conformazione e variazioni individuali (per proiezioni, gravità, fase respiratoria e movimento intrinseco del cuore). Anche l’allenamento, l’obesità e l’emaciazione possono portare a modificazioni dell’immagine cardiaca. Il cuore ed i vasi sono bene evidenziabili con le comuni proiezioni laterolaterale destra e sinistra e ventrodorsale o dorsoventrale.

Vi è discordanza tra gli autori su quali siano le proiezioni più utili per una corretta valutazione di cuore e vasi. Sembra comunque accettato che la proiezione laterale sinistra permetta una migliore visualizzazione dei vasi polmonari apicali rispetto alla laterale destra, così come una minore distorsione dell’immagine cardiaca. La proiezione ventrodorsale sembra poi essere più utile per la valutazione dei lobi polmonari, mentre la dorsoventrale permette una migliore visualizzazione della silhouette cardiaca e dei vasi lobari caudali. Il posizionamento e la centratura del tubo radiogeno (raggio centrale a livello del 5° spazio intercostale) sono molto importanti nella radiografia cardiaca, per evitare errori di valutazione a causa di artefatti. I cani a torace stretto e profondo (Dobermann, Collie), presentano una silhouette cardiaca allungata ed ovoidale, posizionata quasi perpendicolarmente alla colonna vertebrale in proiezione laterolaterale. In proiezione dorsoventrale il cuore si presenta più rotondeggiante e vicino alla linea mediana. In cani con torace intermedio (Pastore Tedesco), il cuore è meno perpendicola-

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re alla colonna vertebrale in proiezione laterolaterale ed ha la forma di un uovo asimmetrico sia in proiezione laterale che in ventrodorsale. Solitamente l’apice cardiaco è posizionato a sinistra del piano mediano. In cani a torace largo ed appiattito (Bulldog), in proiezione laterale la silhouette cardiaca si presenta più corta e rotondeggiante rispetto agli altri e l’asse maggiore del cuore si presente più inclinato rispetto alle vertebre. In dorsoventrale i margini destro e sinistro sono arrotondati, il cuore è posizionato obliquamente rispetto alla linea mediana e l’apice si può trovare anche a destra di questa (destroposizione). Per facilitare lo studio del cuore radiologicamente, Buchanan (1972) ha assimilato il cuore ad un’orologio: in proiezione laterolaterale, ad ore 122 abbiamo l’atrio sinistro, ad ore 2-5 il ventricolo sinistro, ad ore 5-9 il ventricolo destro, ore 9 rappresenta il margine tra il ventricolo e l’atrio destro, a ore 9-10 troviamo l’orecchietta destra e l’arteria polmonare, ad ore 10-11 l’arco aortico. In dorsoventrale abbiamo ad ore 11-1 l’arco aortico, ad ore 1-2 l’arteria polmonare principale o segmenti di questa, ad ore 2.30-3 l’orecchietta sinistra, ad 2-5 il ventricolo sinistro, ad ore 5-9 troviamo il ventricolo destro e ad ore 9-11 l’atrio destro. Nei gatti l’orecchietta ed il ventricolo sinistri sono situati ad ore 1-2 e l’arteria polmonare potrebbe essere più craniale o addirittura non visibile.

L’angiocardiografia con l’utilizzo di mezzo di contrasto iodato è l’unica tecnica per valutare le camere cardiache. A causa dell’invasività dell’esame è oggi preferibile lo studio di queste per mezzo dell’ecocardiografia Doppler. L’aorta è ben visibile in proiezione laterolaterale, in dorsoventrale si evidenzia l’arco, la porzione restante è male evidenziabile a causa della sovrapposizione con l’ombra cardiaca. Il tronco polmonare emerge dal l’anello fibroso del cono arterioso.

Dopo 3-4 cm si divide in un ramo destro ed uno sinistro.

L’arteria polmonare sinistra attraversa la trachea cranialmente e dorsalmente all’origine comune dei bronchi craniale e medio sinistri. Quindi si divide in due ulteriori branche, una delle quali si porta alla porzione craniale del lobo craniale sinistro e l’altra, più grande, stacca un ramo per la porzione caudale del lobo craniale sinistro ed una per il lobo diaframmatico ipsilaterale. L’arteria polmonare di destra, invece, non è sempre visibile radiograficamente per la sovrapposizione ad altre strutture poichè attraversa ventralmente la biforcazione tracheale da sinistra a destra. Quando viene presa “d’infilata” può essere confusa per un linfonodo. In diagnostica radiografica si considera che le arterie e le vene polmonari abbiano uguale diametro (le branche lobari craniali si valutano in proiezione laterale, mentre le branche caudali vanno valutate in proiezione dorsoventrale). Inoltre è accettato che i vasi lobari craniali destri non debbano avere dimensioni maggiori della 4° costa nel suo punto più sottile (appena sotto le vertebre), mentre quelli caudali non devono superare il diametro della 9° costa nel punto d’intersezione con questa. I grossi vasi contenuti nel mediastino craniale, vena cava craniale, tronco brachiocefalico e succlavia sinistra, non sono evidenziabili in quanto sono a contatto l’un l’altro ed inoltre nel mediastino troviamo poco tessuto adiposo, per cui non vi è contrasto tra le diverse strutture. È invece ben evidente la vena cava caudale.

Polmoni: le strutture polmonari sono ben evidenziabili con tecnica a basso contrasto (alti kVp e bassi mAs), per di-

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minuire le difficoltà interpretative causate dalla sovrapposizione delle coste ed altri organi mediastinici. Per ottenere un buon contrasto è necessario riprendere le immagini al picco inspiratorio, unica eccezione in caso si sospetti un modesto pneumotorace nel qual caso è consigliabile riprendere le immagini al picco espiratorio. Le proiezioni standard laterale destra e sinistra e ventrodorsale o dorsoventrale vengono scelte in base alle strutture da evidenziare. In generale vale la regola che si evidenziano meglio le regioni non declivi.

Altre proiezioni sono le oblique e le gravitazionali (stazione, in piedi, laterale, dorsale o ventrale con raggio orizzontale).

In condizioni normali sono due le componenti dell’immagine radiografica del polmone: l’aria ed i grossi vasi (le arterie bronchiali non sono visibili radiologicamente). Anche le pareti dei bronchi se presi d’infilata possono essere visibili, mentre non lo sono normalmente se presi longitudinalmente. In cani anziani, si possono comunque avere delle mineralizzazioni delle pareti bronchiali e quindi rendersi evidenti, senza che vi sia un significato clinico. Altri rilievi occasionali possono essere: foci di osso eterotopico e fibrosi pleurica o interstiziale che danno il classico disegno a rete negli animali anziani. Negli animali brachicefalici od obesi, la parete toracica ed il mediastino occupano gran parte del diametro totale trasversale del torace a scapito dei polmoni, che sono così proporzionalmente più piccoli; è quindi ridotto il contrasto per lo scarso contenuto di aria. A questo effetto va aggiunto l’ipoinsufflazione legata al fatto che spesso questi cani hanno in associazione una forma anomala delle vie respiratorie superiori ed una pressione addominale dovuta alla distensione di questo. Nei cuccioli e nei gattini, l’aspetto dei polmoni è più denso rispetto all’animale adulto e questo è dovuto probabilmente al maggiore contenuto in acqua dell’interstizio. I polmoni sono suddivisi in lobi: il destro presenta un lobo craniale, uno medio, uno accessorio ed uno caudale o diaframmatico. Il polmone sinistro si suddivide in un lobo craniale (a sua volta diviso in craniale e medio) ed uno caudale. I lobi polmonari si possono identificare radiologicamente seguendo l’andamento dei vasi polmonari e dei bronchi e quando visibili delle flessure interlobari. L’albero bronchiale, come già esposto visibile solo in alcune situazioni, è così suddiviso: a destra il bronco lobare craniale nasce a livello dell’origine del bronco principale; la trachea perciò termina triforcandosi. Il bronco principale destro forma con il piano un angolo di 20°; è molto breve e si divide subito nei bronchi lobari medio e caudale. A sua volta il bronco lobare caudale stacca dal lato mediale il bronco per il lobo accessorio. Il bronco principale sinistro forma con il piano un angolo di 35°; si divide dopo circa 2-3 cm in due bronchi, uno ventrale ed uno caudale. Dal primo si originano poi due bronchi, uno craniale ed uno medio per il lobo craniale sinistro. Il bronco caudale si porta al rispettivo lobo polmonare.

Bibliografia Barone R. , 1981: Anatomia comparata dei mammiferi domestici. Vol. 3 splancnologia. Ed. It. A cura di R.Bortolami; Edagricole, Bologna, 601-690.

Suter P. & Lord P., 1984: Text Atlas, Thoracic Radiography, Thoracic Diseases of the Dog and Cat. By Peter F. Suter, 2-45.

Thrall D. 1998: Textbook of Veterinary Diagnostic Radiology. W.B. Saunders Company, Philadelphia, 263-384.

40° Congresso Nazionale SCIVAC

Atopic dermatitis in dogs Dermatite atopica nel cane

Tom Willemse DVM, PhD, Dipl ECVD, Assoc. Prof. Vet. Dermatology - Utrecht University Faculty of Veterinary Medicine Department of Clinical Sciences of Companion Animals, Utrecht, The Netherlands

Riassunto La dermatite atopica (AD) nel cane presenta molte caratteristiche in comune con la sua controparte umana, come l’occorrenza familiare, l’insorgenza in giovane età, il prurito cronico, la morfologia delle lesioni cutanee tipicamente localizzate a livello delle zone di flessione ed estensione delle estremità e la presenza di una immediata reattività al test cutaneo. Il background immunologico è stato ulteriormente chiarito negli ultimi 5 anni. Le cellule di presentazione dell’antigene sono state caratterizzate come elementi CD1a+/MHC classe II+ con recettori IgE a bassa affinità (DC23) sulla loro superficie, è stato riscontrato un aumento preferenziale delle cellule T CD4+ nell’epidermide con lesioni atopiche e, recentemente, è stato dimostrato che queste cellule CD4+ producono anche IL-4.

I criteri diagnostici di tipo clinico, proposti negli anni ’80, sono sopravvissuti per un decennio. Tuttavia, l’ampliamento delle conoscenze sulla malattia e l’esistenza di disordini associati, come l’infezione da Malassezia, hanno spinto ad adattare questi criteri.

Nei cani con manifestazioni cliniche di dermatite atopica è stata effettuata la valutazione del significato delle reazioni alle frazioni purificate degli acari della polvere della casa Dermatophagoides pteronyssinus (Der p I e Der p II) e D. farinae (Der f I e Der f II), che ha mostrato che le proteine responsabili delle reazioni allergiche sono diverse da quelle delle frazioni precedentemente indicate. Recentemente, una proteina da 109 kD è stata segnalata come il principale peptide dell’allergia agli acari della polvere della casa nel cane.

Per quanto riguarda la sierologia, recentemente sono stati sviluppati nuovi test che utilizzano le componenti dei recettori delle IgE (FcERI -catena) invece di a-IgE. Questo sviluppo sembra promettente, nel senso che in futuro questo test potrà sostituire quelli precedenti come le prove allergiche intradermiche.

Per quanto riguarda il trattamento, si è in attesa di nuovi sviluppi. In particolare, nel prossimo decennio potranno diventare importanti quegli approcci di tipo medico che interferiscono con le cellule T e con le loro citochine.

La relazione prenderà in considerazione tutti gli argomenti citati.

Atopic Dermatitis (AD) in dogs shares many characteristics with its counterpart in humans, such as familial characteristic occurence, early age of onset, chronic pruritus, a morphology of skin lesions typically located at flexor and extensor sites of extremities, and the presence of immediate skin test reactivity. The immunological background has been further elucidated over the last five years: antigen-presenting cells have been characterized as CD1a+/MHC class II+ cells with low-affinity IgE receptors (CD23) on their surface, a preferential increase of CD4+ T-cells in lesional atopic epidermis was found, and recently it was shown that these CD4+ cells also produce IL-4.

The clinical diagnostic criteria as proposed in the eighties, have survived a decade. However, increasing understanding of the disease and associated disorders such as Malassezia infection, have been reason to adapt these criteria.

The significance of reactions to purified fractions of the house dust mites Dermatophagoides pteronyssinus (Der p I and Der p II) and D. farinae (Der f I and Der f II) has been evaluated in dogs with clinical manifestations of atopic dermatitis, and have indicated that proteins other than the before mentioned fractions are responsible for allergic reactions.Recently, a 109 kD protein was reported as the major peptide for house dust mite allergy in dogs.

In respect to serology recently new tests have been developed using IgE-receptor components (FcERI_-chain) instead of a-IgE. This development looks promising in the way that in the future this test may substitute previous tests such as the intradermal allergy test.

In respect to management new developments are awaited. In particular these medical approaches which interfere with T cells and their cytokines, may become important during the next decade.

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Pathomechanism - Atopic Dermatitis (AD) in dogs shares many characteristics with its counterpart in humans, such as familial characteristic occurence, early age of onset, chronic pruritus, a morphology of skin lesions typically located at flexor and extensor sites of extremities, and the presence of immediate skin test reactivity20,42. In both man60,73 and dogs32,33 changes in cell-mediated immunity have been observed in AD patients. Additionally, serum concentrations of allergen-specific IgE and some types of IgG are increased in dogs22,70 as well as in man37,59. In man, IgE synthesis is mainly regulated by two cytokines produced by T-helper cells. Interleukin-4 (IL-4) induces (in conjunction with IL-2) synthesis of IgE and interferon-_ (IFN-_) suppresses IL-4 mediated production38. Both the majority of skin infiltrating lymphocytes and allergen-specific peripheral blood lymphocytes from atopic patients, exhibit the cytokine profile typical of the Th2 subclass. Upon stimulation these T-cells release IL-4 and TNF-_, but are deficient in IFN- _. In human AD patients a definite relationship between these cytokines has been observed: allergen-specific T-lymphocyte clones from peripheral blood of atopic donors produce mainly IL-4 but no IFN- _. In contrast, non-allergen-specific T-lymphocyte clones from the same donors and allergen-specific T-lymphocyte clones from non-atopic control donors produce IFN-_ but little or no IL-464.

In human AD patients the skin contains an infiltrate of predominantly CD4+ T-cells, these being T-helper cells, and lesser numbers of CD8+ T-cells, which are thought to have mainly cytotoxic and suppressor effects25,26. In dogs, the last few years information has become available about antigen-presenting cells and the presence of IgE surface receptors, and skin-infiltrating T-cells and the cytokines they produce. The development of monoclonal antibodies specific for antigens expressed by canine T-cells has been a major step forward for investigations in this field28. Antigen-presenting cells have been characterized as CD1a+/MHC class II+ cells with low-affinity IgE receptors (CD23) on their surface35. Such cells may play a role in antigen presentation if antigen should penetrate the skin4,5,30. These investigators also found that the cutaneous infiltrate of dogs with AD composed chiefly of mast cells, dendritic antigenpresenting cells of probable Langerhans cell lineage, and memory helper T-lymphocytes. Eosinophils and free eosinophilic granules were identified solely in the epidermis of lesional atopic skin. Finally T-lymphocytes expressing the T-cell receptor were observed in the epidermis and dermis of all atopic dogs, but rarely in healthy animals36.

This observation is in contrast to findings in man, where a decrease of these T-cells has been seen in peripheral blood.

As T-cells secrete IFN- _, a decrease may potentiate IgE production. Sinke et al.54 reported a preferential increase of CD4+ T-cells in lesional atopic epidermis. In non-lesional atopic skin, there was an infiltration with both CD4+ and CD8+ T-cells within the epidermis, without preference for CD4+ T-cells, whereas in the dermis, only CD8+ T-cells were increased, if compared with the numbers in healthy dog skin. It was concluded that CD8+ T-cells may be important as regulatory cells in atopic dermatitis of dogs. Recently, Sinke et al. (submitted) showed that these CD4+ cells also produce IL-4.

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Canine Atopy - Canine atopy is the second most common allergic skin disease of the dog. The true incidence of the disease in the dog population is unknown but estimates vary from 3 to 15 percent. Atopic disease can be recognized in any dog of any breeding but, because of the genetic predisposition, the disorder is recognized more frequently in certain breeds. In Europe in the eighties, a predisposition was observed for the German shepherd dog, poodle, and boxer68. Recent publications showed breed predispositions for Labrador retrievers, West highland white terriers and boxers in the United Kingdom56, for bull terriers, chow-chows, West highland white terriers, and boxers in Germany23, for Labrador retrievers Tervueren shepherd dogs, Pyrenean Shepherd dogs, all types of setters, and fox terriers in the south western part of France7, for Labrador retrievers, golden retrievers, German shepherd dogs, and West highland white terriers in the Netherlands, for West highland white terriers, boxers, fox terriers, German shepherd dogs, Labrador ans golden retrievers, and Cairn terriers in Sweden34.

A detailed history is the single most important factor in the diagnosis and management of an atopic case. It provides the key information to determine if the animal’s symptoms have an allergic basis and, if so, what the most likely allergens are. The duration of the problems, the age of onset, the course of the disease, the seasonality of the problem, information about litter mates, nature and distribution of the signs, and the animal’s response to medical therapy are important points to review with the owner.

Questioning should also emphasize on the presence of other pets, dietary regimen, walking and indoor living environment, bedding, flea control programmes, and previous treatments and their effect. information can be obtained during the examination.

It is useful to list the owner’s complaints and observations in chronologic order. In 75 per cent of the dogs the first symptoms are seen before the age of three years52,68. Although the familial nature of the disease is well known, the mode of inheritance is unclear in both man and dogs17,63.

Diagnostic criteria of atopic dermatitis - In dogs pruritus has been considered a hallmark of atopic dermatitis, if emphasized by feet licking and nose or head rubbing53. Since the occurrence of primary cutaneous lesions has never been firmly established in dogs or in man19, it may be that all the cutaneous changes are secondary to itch-induced scratching. This hypothesis is supported by the finding of Willemse and Van den Brom68 that although all of the dogs had signs of face rubbing and feet licking, only two-thirds had cutaneous lesions in the facial and pedal areas. In mild cases, one may only see broken hairs or salivary discoloration (rust colored) of the hairs. The incidence of a superficial pyoderma and of Malassezia infection is significantly higher in dogs with atopic symptoms together with immediate skin test reactivity, than in dogs with clinical manifestations but without a positive skin test. Otitis externa is a common finding in atopic dogs (up to 80 per cent) and even in 45 per cent of dogs as the initial problem14,31,53.

A modification of the diagnostic criteria in man was proposed for the definite diagnosis of canine atopic dermatitis65. These days it may be appropiate to modify these criteria slightly, in such a way that the presence of Malassezia infection and external otitis are being added. As basic features were introduced: - pruritus - facial and/or digital involvement

40° Congresso Nazionale SCIVAC

- lichenification of the flexor site of the tarsal joint and/or the extensor site of the carpal joint - a chronic or chronically-relapsing dermatitis - an individual or family history of atopy - a breed predisposition, and as minor features: - onset of symptoms before the age of 3 years - xerosis - superficial staphylococcal pyoderma - bilateral recurrent conjunctivitis - bilateral otitis externa - cutaneous infection with Malassezia pachydermatis - facial erythema and cheilitis - sweating - immediate skin test reactivity to inhalant allergens - elevated allergen-specific IgGd and/or elevated allergen-specific IgE Diagnostic tests - The diagnosis of atopy is based on the history, physical findings, elimination of the appropriate differential diagnoses, and allergy testing which correlates with the history. If allergy testing cannot be done, the other diagnostic steps should be taken to make the tentative diagnosis as firm as possible. Patients referred for allergy testing should be thoroughly evaluated for other allergic and nonallergic causes of pruritus before the referral. Approximately 80 per cent of dogs with atopic dermatitis exhibites immediate skin test reactivity (after 20 min) to inhalant allergens 7,23,52,56,68. Late-phase IgE/IgGd-like reactions at 2 to 8 hours after the intradermal are occasionally seen24,27. Multisensitivity occurs in approximately 60 per cent of the animals. Allergens commonly reported to be important include pollens of grasses, trees, and weeds (5-30%), dandruff extracts of dogs, cats, and poultry, human dandruff, molds, house dust, house dust mites (20-80%), and storage mites such as Acarus siro (2075%) and Tyrophagus putrescentiae (24-75%)7,9,23,56,62,67. The significance of reactions to crude extracts and purified fractions of the house dust mites Dermatophagoides pteronyssinus (Der p I and Der p II) and D. farinae (Der f I and Der f II) was evaluated in dogs with clinical manifestations of atopic dermatitis (AD). In 13 healthy control dogs and 8 dogs with AD immediate skin test reactivity was determined to serial dilutions of Der p I, Der p II, Der f I and Der f II. In addition, allergen-specific IgGd antibodies were determined by means of an enzymelinked-immunosorbent assay (ELISA) and Western blots. The results suggest that, in contrast to what occurs in humans and despite immediate skin test reactivity in some dogs, Der p I, Der p II, Der f I and Der f II are unlikely major allergens in dogs with AD. However, only serum of atopic dogs consistently binds a 90 kD polypeptide of D. farinae, as shown by Western blots analysis18. Recently, a 109 kD protein was reported as the responsible peptide for house dust mite allergy in dogs.

Serologic tests - These tests are used to measure or estimate the amount of allergen-specific antibody in a patientâ&#x20AC;&#x2122;s serum.

In veterinary medicine, two different methods are used commercially. The radioallergosorbent test (RAST) uses radioactively labeled antisera while the enzyme-linked immunosorbent assay (ELISA) uses antibodies coupled to enzymes.

Although the timing of allergy testing can affect the results15 it should be realized that serologic tests can detect very low antibody levels. Therefore the timing of sample collection may not be as critical. Fortunately there is an in-

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creasing number of reports on the diagnostic value of serologic allergy tests for atopy.

Recently new tests have been developed which use IgE-receptor components (FcERI_-chain) instead of a-IgE. This _chain is the high-affinity binding site of the receptor to the IgE molecule. Other ELISA-based in vitro diagnostics for the detection of IgE utilize polyclonal and monoclonal antibodies to IgE which suffer from cross reactivity with IgG and therefore reduce specificity of the diagnostic. The IgE receptor allows quantification of IgE by virtue of the specific reactivity of the high-affinity _-chain for IgE. IgG antibodies do not contain a reactive site for this receptor, thereby providing absolute specificity for IgE detection. So far, it seems that for the detection of flea bite hypersensitivity in dogs and cats, this test has a high specificity, sensitivity and predictive value. In addition, first evaluations of the receptor-based test indicate also that it is a sensitive and specific test for the detection of allergen-reactive IgE in atopic dogs. Consequently, it looks promising in the way that this test may substitute previous tests such as the intradermal test in the future. Although allergy testing usually will confirm the diagnosis, the real purpose for the testing is to start an immunotherapy protocol. If the situation is such that immunotherapy is inappropriate, there is limited value in doing the allergy tests. However, it should be realized that it may be worth doing a test anyhow, to convince pet owners that their dog is suffering from atopy. Once a diagnosis is made (even if symptomatic therapy is started), it may prevent owners to wander from one to another veterinarian.

Management - Basically clinical management should focus on elimination or avoidance of allergen exposure. In fact such measures are usually disappointing as they are time-consuming, expensive and with limited effect.

The most likely reason concerns the presence of multiple sensitivities instead of monoallergies.

Apart from allergen eradication, medical treatment with drugs which exert relief of pruritus and inflammation are commonly used. Examples include prednisone/prednisolone, antihistamines such as hydroxizine (2 mg /kg TID), and EFAs. On an experimental level also pentoxyfilline and cyclosporine A have been beneficially used.

The effects of immunotherapy (hyposensitization) based on IgE RAST and ELISA results and/or intradermal testing commonly range from 60 to 80 per cent27. The additional value of in vitro testing to intradermal testing in respect to the effect of hyposensitization has also been shown. In a double blind, placebo-controlled study the effect of hyposensitization at least 50 per cent improvement was noticed in 60 per cent of the dogs32. This percentage rose to 80 per cent if the animals were hyposensitized on the basis of the cumulative results of the in vivo and in vitro test35.

References For the reference numbers in the text, see: Reedy, L.M., Miller, W.H. and Willemse, T. (eds) Allergic skin diseases in dogs and cats. Saunders Co., Philadelphia, 2nd.ed., 1997: ch. 2-4.

Additional reading Wassom, D.L. and Grieve, R.B. (1998) In vitro measurement of canine and feline IgE: review of FcERI-alpha-based assays for detection of allergen-reactive IgE. Vet. Dermatology 9: 173-178.

Zunic, M. (1998) Comparison between Immunodot tests and the intradermal skin test in atopic dogs. Vet. Dermatology 9: 201-206.

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Feline atopy-like diseases Malattie simil-atopiche nel gatto

Tom Willemse DVM, PhD, Dipl ECVD, Assoc. Prof. Vet. Dermatology - Utrecht University Faculty of Veterinary Medicine Department of Clinical Sciences of Companion Animals, Utrecht, The Netherlands

Riassunto Introduzione – Le manifestazioni cutanee riscontrabili nel gatto in associazione con le condizioni allergiche variano considerevolmente e non risultano specifiche per le cause scatenanti. In altre parole, il tipo e la distribuzione delle lesioni rilevate nei gatti con reazioni avverse da farmaci possono essere del tutto sovrapponibili a quelle riscontrabili nei felini con malattie simil-atopiche, ipersensibilità da morso di pulci ed anche reazioni da farmaci o ipersensibilità da puntura di zanzara. Nel gatto, il numero dei quadri di reazione è limitato in confronto a quello osservato nel cane.

A grandi linee, è possibile effettuare una suddivisione in 4 categorie: (a) lesioni papulocrostose miliari (dermatite miliare), (b) dermatite pruriginosa facciale, (c) alopecia simmetrica con grattamento, intensa toelettatura o tendenza a strapparsi i peli del tronco e degli arti posteriori e (d) dermatosi nodulari o placca-simili.

Istopatologicamente, tutti i quadri precedentemente citati corrispondono a lesioni dominate dalla presenza di eosinofili, con un numero variabile di mast cell. Teoricamente, queste lesioni si possono osservare in conseguenza di un danno indotto da artropodi ed in associazione con dermatosi allergiche mediate dalle IgE. Sono esempi di queste condizioni la dermatite atopica, l’ipersensibilità da morso di pulci, quella da puntura di zanzara e persino l’allergia alimentare (anche se le reazioni avverse agli alimenti sono più probabilmente dovute ad un’intolleranza che ad un’allergia). È stato ipotizzato che le lesioni dominate da eosinofili nel gatto differiscano per quanto riguarda l’aspetto clinico a causa della variazione degli effetti dannosi dei mediatori cellulari. Di conseguenza, la valutazione diagnostica dei quadri clinici associati alle allergie, secondo quanto riassunto più sopra, è identica.

In questa relazione verranno discusse le più recenti informazioni sui meccanismi immunitari, sull’indagine diagnostica e sulle opzioni terapeutiche.

Introduction - Skin manifestations in cats associated with allergic conditions vary considerably, and are not specific for underlying causes. In other words: the lesions and distribution noticed in cats with adverse food reactions may overlap entirely those which are observed in cats with atopy-like disease, flea bite hypersensitivity, and even drug reactions or mosquito-bite hypersensitivity.

In cats the number of reaction patterns is limited if compared to those observed in dogs.

Grossly a division into four categories can be made, (a) miliary papulocrusts (‘miliary dermatitis’), (b) facial pruritic dermatitis, (c) symmetric alopecia with scratching, vigorous grooming, or hair pulling on the trunk and hind legs, and (d) nodular or plaque-like dermatoses.

Histopathologically all previously mentioned patterns represent eosinophil-dominated lesions with a varying number of mast cells. Theoretically, such lesions may be observed after arthropod-induced injury and in association with IgEmediated allergic dermatoses. Examples of these include atopic dermatitis, flea bite hypersensitivity, mosquito bite hypersensitivity, and may be even dietary allergy (although adverse food reactions are more likely due to intolerance other than allergy).

It is hypothesized that eosinophil-dominated lesions in cats differ in their clinical appearance due to variation in damaging effects of cellular mediators. Consequently, the work-up of the allergy-associated clinical patterns as summarized before, is identical.

In this presentation novel information about the immune mechanisms, the diagnostic work-up and treatment options will be discussed.

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Introduction - Skin manifestations in cats associated with allergic conditions vary considerably, and are not specific for underlying causes. In other words: the lesions and distribution noticed in cats with adverse food reactions may overlap entirely those which are observed in cats with atopylike disease, flea bite hypersensitivity, and even drug reactions or mosquito-bite hypersensitivity.

In cats the number of reaction patterns is limited if compared to those observed in dogs.

Grossly a division into four categories can be made, (a) miliary papulocrusts (‘miliary dermatitis’), (b) facial pruritic dermatitis, (c) symmetric alopecia with scratching, vigorous grooming, or hair pulling on the trunk and hind legs, and (d) nodular or plaque-like dermatoses.

Histopathologically all previously mentioned patterns represent eosinophil-dominated lesions with a varying number of mast cells. Theoretically, such lesions may be observed after arthropod-induced injury and in association with IgE-mediated allergic dermatoses. Examples of these include atopic dermatitis, flea bite hypersensitivity, mosquito bite hypersensitivity, and may be even dietary allergy (although adverse food reactions are more likely due to intolerance other than allergy).

Eosinophils are attracted by chemotactic mediators of activated mast cells or T cells (IL-5). Upon release of granules, major basic protein, eosinophilic cationic protein and oxygen radicals are formed.

In particular the latter, may be responsible for varying degrees of eosinophilic collagenolysis as seen in e.g., eosinophilic granuloma complex, mosquito bite hypersensitivity, and even flea bite hypersensitivity. It is hypothesized that eosinophil-dominated lesions in cats differ in their clinical appearance due to variation in damaging effects of cellular mediators. Consequently, the work-up of the allergy-associated clinical patterns as summarized before, is identical.

Only from cats with flea bite hypersensitivity and those with signs compatible with atopic dermatitis, some information about the immunological pathomechanism is known.

Apart from tevidence about the presence of IgE, recently also increased numbers of CD1a+/MHC class II+ Langerhans cells were found in lesional skin of cats with atopic dermatitis. In addition, in the skin of cats with atopic dermatitis, a significantly greater number of T-cells was found in lesional skin than in the skin of healthy control animals. The CD4+/CD8+ cell ratio and predominance of CD4+ T cells in lesional skin of cats with allergic dermatitis is comparable to what is found in atopic dermatitis in man. Also the increase of absolute numbers of CD4+ T cells in non-lesional skin of cats with allergic dermatitis compared with infiltrates in skin of healthy cats is observed in humans. In addition, it was shown that feline CD4+ T cells in lesional skin of cats with allergic dermatitis can produce IL4.

Clinical aspects - Miliary papulocrusts are at onset seen on the neck-head area or abdomen, and from there the lesions may generalise and become most evident on the dorsum, especially the neck, shoulder, and tailhead region. Lesions tend to develop from papules into papulocrusts to crusts and scales. Usually there is a mixed presentation.

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Such clinical presentation may be due to adverse food reactions, environmental allergens, flea bites and drugs.

Facial (and commonly neck) dermatitis – with increased predilection for the preauricular area - is initially presented as small crusts and erosions, that may be limited to some spots, but may rapidly develop to larger oozing, erosive or even ulcerative lesions. Such presentation may be associated with all types of hypersensitivities mentioned before with the exception of flea bite hypersensitivity.

Some cats show enhanced grooming and licking behavior which results in stubbed hairs, hypotrichosis and (occasionally) a surface dermatitis. Such abnormalities are commonly seen at the abdomen, the flanks, the proximal thighs, and the caudodorsal tailhead region. Others may develop plaque-like lesions on several sites of the body, but with emphasis on the ventral abdomen, the inguinal area, and the neck. These lesions may be elevated and erythematous, but may also develop into erosions and crust formation. Histologically these are compatible with eosinophilic plaques. For all these manifestations (from hypotrichosis to eosinophilic plaques) allergies due to dietary components, drugs or environmental substances such as house dust mites and pollen, may be causative.

Occasionally cutaneous signs are accompanied by rhinitis and/or conjunctivitis. This may be an indication which favours the existence of atopy other than other allergies. The age of onset for feline atopy and other allergic manifestations is very variable, but onset is usually noticed below the age of 2 years. No sex predilection has been mentioned. In addition, cats suspected of atopy or flea bite hypersensitivity may exhibit their symptoms seasonally or perennially. Although seasonality in case of adverse food reactions is unlikely, a waxing-and-waning appearance may be the result of selectively and incidentally provided food items.

Diagnostic approach - The diagnostic approach in cats suspected of having an allergic dermatitis is usually based on a history of pruritus, the clinical appearance, response to glucocorticoids, histopathology, dietary tests, skin tests, and the exclusion of other cutaneous diseases such as dermatophytosis, stress-related disorders and parasitic diseases.

Histopathology does not reliably distinguish between the miliary lesions of flea allergy, atopy, or adverse food reactions and therefore cannot be considered to be of conclusive value. Which following order will be used in the diagnostic sequence, depends primarely on the clinical presentation and the history.

In depth information about the variety of foods eaten, and the presence of other animals in the same environment (or indirectly, with which owners have been in contact) should be part of the history. However, it should be kept in mind that not only recent changes in the dietary regimen may be responsible for the induction of adverse food reactions.

The clinician should also know how the animal is housed and get information about food and water intake, the presence of diarrhea and vomiting, and the use of any medication or preventive flea control products previous to the skin problems. Finally the respons to therapy may be indicative.

For example, if pruritic cats do not or only partially respond

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to steroids, it may be an indication for a food hypersensitivity. Hence, the clinician should be informed about the type of glucocorticoids which have been used, the frequency of administration, the dosage, the response, and the period of withdrawal before the physical examination.

At first glance many skin diseases may appear to be morphologically similar. Physical examination of a pruritic animal should at least include a general impression of gross abnormalities, examination of mucous membranes and lymph nodes, and a detailed examination of the coat and skin. The location and distribution of affected areas of the skin must be determined.

On the basis of the history and the physical examination it is possible to get an impression about the clinical evolvement, the primary distribution and pattern, and the amount and type of pruritus. These data are the ingredients for a first differential diagnosis. Once a list of differential diagnosis has been established, further diagnostic tests should contribute to narrowing this list. A number of these tests are easy to perform, and will enable you to rule in or rule out a number of diagnoses already during the first visit of your client.

Dietary tests – A dietary allergy – or better: adverse food reactions - is diagnosed on the basis of the history (including the usually moderate or poor response to glucocorticoids), the clinical features and the result of dietary tests.

Skin tests or blood tests are absolutely unreliable for this purpose. A hypoallergenic diet of cooked lamb, goat, or turkey, and rice, pending the dietary history, is given for at least 6 weeks and up to 10 weeks to determine the optimal dietary effect. For cats commercial foods contain a large variety of meat proteins; consequently, it may be difficult to select a proper protein for diagnostic purpose. It may be that protein sources such as ostrich, venison, duck breast, or camel are required. If by coincidence the animal doesn’t like this diet, it may be helpful to introduce a transient period of 3-5 days wherein a mixture of the former diet and the new diet is administered. Provocation with the original diet after elimination is essential, as a significant percentage will not go into relpase.

In vivo and in vitro allergy test – Despite skin testing is commonly performed in cats, there are various problems in relation to skin testing in this species. Not only are skin re-

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actions difficult to interpret and inconsistent, also stress is a phenomenon that influences skin test reactivity considerably. Sterilized 2 per cent Evans blue dye (Sigma Chemical Co., St.Louis), 0.05 ml/kg intravenously 5 minutes prior to skin testing, can be used to improve detection of reaction sites in cats. However side effects have been reported. In addition, proper skin test concentrations have not been determined; hence, skin testing is not routinely recommended in cats. There is increasing evidence that the diagnosis of flea bite hypersensitivity and atopy-like dermatitis can be reliably made by using a FcΕRIα-based in vitro allergy test.

Other commercially available in vitro tests for detection of allergen-specific IgE in cats, have not been shown such diagnostic value.

Suggested reading Bevier, D.E. (1997) Atopy: advances in diagnosis and management. In: Consultations in feline internal medicine, August, J.R. (ed), vol.3; W.B. Saunders, Philadelphia (USA); pp. 214-220.

Gilbert, S. and Halliwell, R.E. (1998) Production and characterisation of polyclonal antisera against feline IgE. Vet. Immunol. Immunopathol.

63: 223-233.

Gilbert, S. and Halliwell, R.E. (1998) Feline immunoglobulin E: induction of antigen-specific antibody in normal cats and levels in spontaneously allergic cats. Vet. Immunol. Immunopathol. 63: 235-252.

Reedy, L.M., Miller, W.H. and Willemse, T. (eds) (1997) Allergic skin diseases in dogs and cats. Saunders Publ. Co., Philadelphia, 2nd ed.; pp.

25-49; 83-115; 173-188.

Roosje, P.J., Whitaker-Menezes, D., Goldschmidt, M.H., Moore, P.F., Willemse, T. and Murphy, G.F. (1997) Feline atopic dermatitis: a model for Langerhans cell participation in disease pathogenesis. Am. J. Pathol. 151: 927-932.

Roosje, P.J., Thepen, T., van Kooten, P.J.S., Bihari, I.C., Rutten, V.P.M.G. and Willemse, T. (1998) Investigations on the presence of CD4+ and CD8+ T cells in lesional skin of cats with allergic dermatitis. Vet. Pathol. 35: 268-273.

Rosser, E.J. (1997) Food hypersensitivity: new recommendations for diagnosis and management. In: Consultations in feline internal medicine, August, J.R. (ed), vol. 3; W.B. Saunders , Philadelphia (USA); pp.

209-213.

Scott, D.W., Miller, W.H. and Griffin, C.E. Small animal dermatology, 5th ed.; W.B. Saunders, Philadelphia (USA); pp. 497-550.

Wassom, D.L. and Grieve, R.B. (1998) In vitro measurement of canine and feline IgE: review of FcERI_-based assays for detection of allergenreactive IgE. Vet. Dermatology 9: 173-178.

Willemse, T. (1998) Clinical Dermatology of Dogs and Cats, 2nd ed.; Elsevier-Bunge, Maarssen (The Netherlands), pp. 144.

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Psychodermatoses in dogs and cats etiopathogenesis and treatment Alopecia e dermatite psicogena nel cane e nel gatto

Tom Willemse DVM, PhD, Dipl ECVD, Assoc. Prof. Vet. Dermatology - Utrecht University Faculty of Veterinary Medicine Department of Clinical Sciences of Companion Animals, Utrecht, The Netherlands

Riassunto I fattori stressanti che sono stati comunemente associati all’eccessiva toelettatura ed alla conseguente alopecia nel gatto sono l’introduzione di un nuovo animale da compagnia nell’ambiente, la morte di un altro animale, gli attacchi al proprio territorio, lo spostamento in una nuova casa, l’arrivo di un nuovo bambino, i rumori eccessivi ai quali l’animale non era mai stato esposto prima (ad esempio, i fuochi d’artificio) e (anche se si tratta di fattori più importanti nel cane) la noia ed il confinamento. Associazioni simili sono state riferite nei cani con granuloma da leccamento delle estremità.

Dal momento che nei comportamenti stereotipati indotti dallo stress sono coinvolti gli oppiacei, che sono noti come modulatori dell’attività dopaminergica, è possibile che la neurotrasmissione dopaminergica rappresenti un meccanismo appropriato per contrastare la stereotipia. In uno studio in cui sono state prese in considerazione le modificazioni della sensibilità alla dopamina indotte nel gatto da fattori stressanti, i risultati ottenuti hanno convalidato l’idea che lo stress sia in grado di indurre un’eccessiva toelettatura ed enfatizzare il ruolo della dopamina in relazione alla stessa situazione stressante.

Oltre che gli aspetti clinici e la diagnosi differenziale, verranno sottolineate le possibilità terapeutiche. Il primo passo nel trattamento della condizione consiste nell’identificare e rimuovere la causa primaria del comportamento stereotipato.

Ciò risulta solitamente difficile, in particolare perché le stereotipie possono continuare anche dopo la scomparsa degli eventi scatenanti. Sarà discusso l’effetto e gli effetti collaterali dei farmaci ansiolitici ed antidepressivi, degli agenti di blocco dei recettori degli oppiacei e degli antagonisti della dopamina.

Stressors which have been commonly associated with excessive grooming and resulting alopecia in cats, are the introduction of a new pet into the living environment, the death of a companion pet, attacks on a cat’s territory, the move to a new home, the presence of a new baby, excessive noise to which an animal had not been exposed to before (e.g., fire works), and (although more relevant in dogs) boredom and confinement. Similar associations have been reported in dogs with acral lick granuloma.

Since opioids are involved in stress-induced stereotyped behavior and are known as modulators of dopaminergic activity, dopaminergic neurotransmission may yield an appropiate mechanism for counteracting the stereotypy.

In a study wherein the stressor-induced change in sensitivity to dopamine in cats was investigated, the results support the idea that stress is able to induce excessive grooming and emphasizes the role of dopamine in relation to stress.

Apart from the clinical aspects and the differential diagnosis, emphasis will be given to therapeutical possibilities. The first step in treatment is to identify and remove the underlying cause of the stereotypic behavior. This is usually difficult, particularly as stereotypies may continue even after the disappearance of initiating events. The effect and side effects of antianxiety and antidepressant drugs, opiate-receptor blockers, and dopamine antagonists will be discussed.

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Etiopathogenesis - Arousing conditions such as novelty and stress stimuli preceed the activation of both grooming and the hypothalamo-pituitary-adrenal systems (Spruijt et al., 1992). More specifically, conflict can be induced by the absence of releasing stimuli, such as the absence of other pets, pet owners, or appropiate toys. Conflicts may also result from agression and fear, from physical restraint, from a change in social environment (separation from owner), competition or unstable social order (dominance conflicts with pets in the same household or for example with stray cats in the garden) (Luescher et al., 1991).

Stressors which have been commonly associated with excessive grooming and resulting alopecia in cats, are the introduction of a new pet into the living environment, the death of a companion pet, attacks on a cat’s territory, the move to a new home, the presence of a new baby, excessive noise to which the cat had not been exposed to before (e.g., fire works), and (although more relevant in dogs) boredom and confinement (Willemse, 1998). Similar assiciations have been reported in dogs with acral lick granuloma.

Since opioids are involved in stress-induced stereotyped behavior and are known as modulators of dopaminergic activity, dopaminergic neurotransmission may yield an appropiate mechanism for counteracting the stereotypy. Also in cats stress-induced grooming can be counteracted with haloperidol. In another study the stressor-induced change in sensitivity to dopamine in cats was investigated. The results support the idea that stress is able to induce excessive grooming and emphasizes the role of dopamine in relation to stress (Willemse et al., 1995; Willemse, 1997).

Clinical manifestations - Psychogenic alopecia and dermatitis of cats are caused by enhanced grooming, licking, and hair pulling and chewing as the result of emotional stress. Apart from the characteristic anamnestic information, the most obvious cutaneous manifestations are usually confined to hypotrichosis and partial alopecia with stubbed hairs, of which the latter is also called trichorrhexis. The coat changes are commonly observed on the dorsal midline, the flanks, the abdomen, the caudal thighs, and/or the forelegs. The remaining hairs are not easily epilated. Regrowth in infected areas may result in darkcoloured hairs.

Occasionally there is an exsudative dermatitis on the dorsal midline or eosinophilic plaque-like lesions are seen on the abdomen, axillae, dorsal midline, or hindlimbs. These plaques are firm, well-circumscribed, slightly raised, and usually have an erosive surface. Although Siamese and Birmese cats are reported as predisposed breeds, the opposite is the author’s experience: psychogenic alopecia is much more frequenly observed in European shorthaired cats and crossbreds of these.

In dogs acral lick dermatitis is the clinical equivalent of feline psychogenic alopecia and dermatitis. It is the result of intense licking and chewing at the lower anterior portion of usually one leg. The sequence of cutaneous abnormalities invlves erythema, alopecia, erosions, ulceration, fibrosis, and secondary pyoderma. The anterior carpal and metacarpal sites are usually involved, but the tibial and metatarsal sites may also be affected. Secondary periostal reactions may result from chronic processes. The disorder is more frequently

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observed in German shepherd dogs, Great Danes, Doberman pinschers, and Labrador retrievers.

Diagnosis - It will be evident that a thorough history is essential in providing the adequate information. Questions directed towards conflicts or other stress-inducing events in the recent and further past time, should be the basis. It should be memorized that stressors may not be present anymore, but have acted as initiators only. It might even occur that pet owners are not able to provide you with relevant stress- and grooming-associated information. Next to anamnestic evidence, the clinical manifestations may contribute to the (likely) diagnosis.

However, before a diagnosis is made, other diseases which may be presented in a similar manner should be ruled out. The most common differential diagnoses of psychogenic alopecia include dermatophytoses, telogen defluxion secondary to internal disease, idiopathic symmetric alopecia, and adverse food reactions. A complete flea control programme should be performed at any time.

In dogs pressure point pyoderma, neoplasia, foreign body reactions, and underlying skeletal and neuromuscular diseases are the most important disorders that should be ruled out.

Treatment - The first step in treatment is to identify and remove the underlying cause of the stereotypic behavior.

This is usually difficult, particularly as stereotypies may continue even after the disappearance of initiating events. In other words: the cause for the excessive grooming may be identified, and subsequent removal may not result in improvement, and vice versa an underlying condition may be gone for a long time at the time stereotyped grooming is identified. In addition it will not always be possible to remove the perceived stressor, e.g. if loneliness or conflicts with neighbour cats are potentially involved. Therefore in many cases systemic drugs are necessary adjuncts to environmental management.

Antianxiety and antidepressant drugs - It is the author’s impression, that diazepam (a GABA-synergist; 0.2-0.4 mg/cat SID or BID orally) is of minor importance in controlling stereotyped grooming.

Tricyclic antidepressants block serotonin and dopamine reuptake. These drugs have antianxiety and antidepressant properties. However their value in cats is limited due to the reported side effects, such as mydriasis, dry mouth, urinary retention, constipation, and keratoconjunctivitis sicca. A dramatic decrease of saliva production is seen in approximately 40 percent of cats treated with fluoxetine, and therefore reason for not using this drug in cats. Amitriptyline (0.5-2.0 mg/kg/day orally) and L-seligiline (1 mg/kg/day) has been recommended, but placebo-controlled studies are not available. Reports about their effect is only anecdotal.

In dogs, fluoxetine (1 mg/kg SID) and clomipramine (13 mg/kg SID) are most commonly used. Side effects include lethargy, anorexia, and diarrhea. The overall effect is limited, but individuals may benefit.

Opiate-receptor blockers - Long-acting opioid antagonists like naltrexone are preferred. Such medication is administered for 7 days in a dosage of 2.5-5.0 mg/cat, and

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hereafter as 2.5-5.0 mg weekly until the problem is under control (Marder, 1991). Uncommon side effects include arousal and vomiting. Liver and kidney diseases are reason not to use naltrexone. There are no longterm evaluations about the effect of naltrexone on psychogenic alopecia in cats. Although naltrexone can be used in dogs, the costs will be extremely high.

Dopamine antagonists - These drugs should be administered if the stereotyped grooming lasts for more than six months. For haloperidol a starting dose of 0.5-1.0 mg/kg BID orally is advised. It is recommended to take an animal in for at least three days in order to determine the maintenance dose. This is important as the catâ&#x20AC;&#x2122;s respons to haloperidol is individually different. Side effects such as hallucinatory symptoms, limb flick, or insecure walking may occur if haloperidol is overdosed. Usually the maintenance dose varies between 0.5 and 1.25 mg/kg BID. Longterm evaluation of cats with psychogenic alopecia treated with haloperidol indicated that approximately 50 per cent of these cats can be cured within 2-3 months. Half of the remaining cats need a maintenance therapy, where the other 25 per cent fails to respond adequately. Recently it was indicated that haloperidol (1-2 mg/kg/day) may also beneficial in dogs with acral lick dermatitis.

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The rate of success (or failure) is similar for the following methods of treatment: the use of topical solutions with fluocinolone acetonide (0.01%) and flunixin (5%) in DMSO (1:1), applied 3-5 times daily for 4-8 weeks; intralesional injections of repositol methylprednisolone (a total dose of 1 mg/kg); surgical removal of early lesions; bandages; Elizabethan collars; or combinations of these.

References Luescher, U.A., McKeown, D.B. and Halip, J. (1991) Stereotypic or obsessive-compulsive disorders in dogs and cats. Vet. Clinics of North Amer. Small Anim. Pract. 21, 401-413.

Marder, A.R. (1991) Psychotropic drugs and behavioral therapy. Vet. Clin.

North Am.: Small Anim. Practice 21, 329-342.

Spruijt, B.M., Van Hooff, J.A.R.A.M. and Gispen, W.H. (1992) Ethology and neurobiology of grooming behavior. Physiol. Rev. 72, 825-852.

Willemse, T. and Spruijt, B.M. (1995) Preliminary evidence for dopaminergic involvement in stress-induced excessive grooming in cats.

Neurosc. Res. Comm. 17(3), 203-208.

Willemse, T. (1997) Psychogenic alopecia in cats and the role of the opioid and dopaminergic systems. In: Consultations in feline internal medicine, vol.3, August, J.R. (ed); W.B.Saunders, Philadelphia (USA); pp.

224-230.

Willemse, T. (1998) Dermatologia clinica del cane e del gatto. 2nd ed.; Masson, Milano (Italy), pp. 143.

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Cutaneous autoimmune disorders in companion animals Malattie cutanee negli animali da compagnia

Tom Willemse DVM, PhD, Dipl ECVD, Assoc. Prof. Vet. Dermatology - Utrecht University Faculty of Veterinary Medicine Department of Clinical Sciences of Companion Animals, Utrecht, The Netherlands

Riassunto Le malattie bollose su base immunitaria sono caratterizzate dalla deposizione in vivo di sostanze immunoreattive all’interno dell’epidermide o a livello della zona della membrana basale della cute (BMZ). Nel pemfigo gli antigeni bersaglio sono le glicoproteine dei desmosomi. Queste appartengono alle cosiddette caderine, che sono molecole che determinano l’adesione fra cellule e rappresentano la principale componente transmembranaria dei desmosomi o delle adherens junction. Nel pemfigo foliaceo del cane, la caderina desmosomiale importante è la desmogleina 1 (Dsg 1, con un peso molecolare di 148-150 kD).

Nel pemfigo volgare dell’uomo e del cane l’antigene è la desmogleina 3 (Dsg 3 con un peso molecolare di 130 kD). Nel gatto, gli antigeni bersaglio desmosomiali non sono stati definiti, ma molto probabilmente avranno un peso molecolare ed un’origine comparabili a quelli citati. Le desmogleine sono complessate con la placoglobina, una proteina di placca desmosomiale, e giocano un ruolo importante nell’adesione cellulare. Nel lupus eritematoso (LE) il danno tissutale sembra essere dovuto ad una reazione di ipersensibilità di tipo III. I fattori scatenanti possono essere la luce ultravioletta, la vaccinazione con un vaccino a virus vivo modificato ed una certa predilezione genetica. Tuttavia, nel gatto esistono solo prove dell’influenza della luce ultravioletta.

In questa relazione verranno trattate le caratteristiche cliniche del pemfigo, del lupus eritematoso e del pemfigoide bolloso. Saranno citate sia le opzioni diagnostiche direttamente applicate dai veterinari pratici che quelle attuabili nei laboratori specializzati. Infine, verranno fornite dettagliate informazioni sulla prognosi a lungo termine e sulle possibilità terapeutiche, compreso l’impiego di glucocorticoidi, azatioprina, sali d’oro, niacinamide-tetraciclina, clorambucil, agenti topici e pentossifillina.

Immunobullous diseases are characterized by in vivo deposition of immunoreactants within the epidermis or at the cutaneous basement membrane zone (BMZ). In pemphigus the target antigens are desmosomal glycoproteins.

They belong to the so-called cadherins which are cell-cell adhesion molecules and represent the major transmembrane components of either desmosomes or adherens junctions.

In pemphigus foliaceus of the dog the desmosomal cadherin of importance is desmoglein 1 (Dsg 1; with a molecular weight of 148-150kD). In human and canine pemphigus vulgaris the antigen is desmoglein 3 (Dsg 3) with a molecular weight of 130 kD. In cats the desmosomal target antigens have not been defined, but very likely will be of comparible molecular weight and origin. The desmogleins are complexed with plakoglobin, a desmosomal plaque protein, and play an important role in cell adhesion. In lupus erythematosus (LE) tissue damage appears to be the result from a type III hypersensitivity reaction. Precipitating factors may be ultraviolet light, vaccination with a modified live virus vaccine, and genetic predilection. However, in the cat there is only evidence of the influence of ultraviolet light.

In this presentation the clinical features of pemphigus, lupus erythematosus, and bullous pemphigoid will be addresses. Diagnostic options both directly applicable for practitioners and available in specialized laboratories are mentioned. Finally detailed information will be given about the longterm prognosis and the treatment options, including the use of glucocorticoids, azathioprine, gold salts, niacinamide-tetracyclin, chlorambucil, topicals, and pentoxifylline.

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Introduction - Pemphigus is an intraepidermal blistering disease characterized by loss of epidermal cohesion. The subtypes of pemphigus which have been observed in cats include pemphigus foliaceus (PF), pemphigus vulgaris (PV) and pemphigus erythematosus (PE). The incidence of pemphigus in cats is very low and pemphigus foliaceus is by far the most frequently observed form. Pemphigus is a so-called type II autoimmune disorder. In some animals drugs may be triggering factors in the initiation of pemphigus. Examples include amoxycillin, cimetidine and sulfonamides. Breed, sex or age predilections have not been reported, although in general autoimmune skin disorders are more commonly seen in middle-aged to older cats. In dogs pemphigus is more commonly observed and in addition to the previously mentioned forms, also (although rarely) pemphigus vegetans, which is a benign form of PV, is seen. Nor in dogs nor in cats there are specific breeds predisposed to the disease.

In contrast to pemphigus, the clinical signs of lupus erythematosus (LE) are the result of immune complex-mediated autoimmune reactions (type III reactions). Both the systemic form of LE and the cutaneous or discoid form are rare manifestations. Also in LE sex nor age predilections have been noticed in cats, although the disease seems to be more frequent in Siamese, Persian and Himalayan cats. In contrast, LE is more common in Shetland sheepdogs, collies and German shepherd dogs.

Pathogenesis - Immunobullous diseases are characterized by in vivo deposition of immunoreactants within the epidermis or at the cutaneous basement membrane zone (BMZ). In pemphigus (Wakelin and Wojnarowska 1997; Suter et al. 1998) the target antigens are desmosomal glycoproteins. They belong to the so-called cadherins which are cell-cell adhesion molecules and represent the major transmembrane components of either desmosomes or adherens junctions. In pemphigus foliaceus of the dog the desmosomal cadherin of importance is desmoglein 1 (Dsg 1; with a molecular weight of 148-150kD). In human and canine pemphigus vulgaris the antigen is desmoglein 3 (Dsg 3) with a molecular weight of 130 kD. In cats the desmosomal target antigens have not been defined, but very likely will be of comparible molecular weight and origin. The desmogleins are complexed with plakoglobin, a desmosomal plaque protein, and play an important role in cell adhesion. There appears to be heterogeneity in the composition of desmosomes at different levels in the epidermis, which may explain how acantholysis (which is the process associated with desmosomal cohesion) occurs at a suprabasal level in pemphigus vulgaris and relatively higher in pemphigus foliaceus. Antibody binding is noted throughout the epidermis in all variants of pemphigus, and it has been hypothesized that antibodies cause cell separation where the target antigen is the chief adhesion molecule (Wakelin and Wojnarowska 1997). The initiating factors in the autoimmune reactions have not clearly been elucidated. For example, immunogenetic studies in people have shown an association of pemphigus with e.g.,HLA DR4. In addition it is known that sulfhydril drugs may directly mediate acantholysis. However, also ageing and therefore alteration of the immune system with loss of tolerance to autoantigens and crossantigeneity between au-

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toantigens and external agents like viruses which make autoantigens non-recognisable, may contribute to the onset of the autoimmune response. The role of the complement system in pemphigus is controversial. Although pemphigus antigen can bind complement, and complement deposition has been observed in acantholytic lesions, it is not a standard observation. Theoretically, complement fixing antibodies may mediate the development of inflammatory changes. In case complement is not involved such inflammation may be activated by proteases causing cell cohesion. In humans, pemphigus IgG antibodies added to epidermal cells in culture, result in an increased production of protease plasminogen activator (PA) produced by keratinocytes. Subsequently, PA may lead to local production of the protease plasmin which is responsible for cleavage of epidermal cell adhesion molecules (Wakelin and Wojnarowska 1997).

In lupus erythematosus (LE) tissue damage appears to be the result from a type III hypersensitivity reaction. Precipitating factors may be ultraviolet light, vaccination with a modified live virus vaccine, and genetic predilection. However, in the cat there is only evidence of the influence of ultraviolet light (Bos and de Rie 1997; Scott, Miller and Griffin 1995; Willemse and Koeman 1989).

Cell damage by ultraviolet light, with enhanced expression of ICAM-1 and autoantigens may result in the formation of autoantibodies, and subsequently to immune complex deposition (with involvement of complement) and antibody-dependent cytotoxicity of keratinocytes (Bos and de Rie 1997). These immune complexes may also be responsible for vasculitis in various organ systems.

Clinical features - Pemphigus in dogs and cats (Scott, Miller and Griffin 1995; Willemse 1998) is divided into three distinct subtypes, pemphigus vulgaris (PV), pemphigus foliaceus (PF), and pemphigus erythematosus (PE). The latter is considered as a more benign form of PF or an intermediate form between pemphigus and lupus erythematosus.

The major difference between PV and the other subtypes is the involvement of oral mucous membranes and mucocutaneous junctions in PV, whereas the clinical manifestations of PF are limited to the skin. PF is the most commonly observed autoimmune skin disorder in dogs and cats.

Consequently, in PV the oral cavity and the mucocutaneous junctions at lips, nostrils, eyelids, vulva, prepuce, and anal region may be involved. Primary lesions are vesicobullous of nature. Due to the high fragility of these lesions, vesicobullae may easily disrupt and develop in erosions, collarettes, crusts, and ulcers. Primary lesions may become secondary infected with staphylococci and develop into pustules. However, for unknown reasons this observation is uncommon in cats.

The first lesions are usually observed on the planum nasale. Less frequently, onychomadesis, paronychia, and foot pad lesions occur. In particular cats with multiple claw bed involvement and cheese-like exsudate are highly suspected. In these cases fever and systemic reactions as anorexia and lethargy may also be seen; normally these nonspecific signs are rare in PV. Vesicobullous or pustular lesions are also the primary lesions of PF. They may develop into crusts, scales, erosions,

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and collarettes. In cats in the majority of cases the primarely lesions are so small and fragile that a clinical presentation with tiny crusts is very common. Especially the pinnae, the bridge of the nose, and the lips are primary affected, but involvement of the footpads and digits is common as well. An exceptional clinical presentation of PF in cats includes the development of large, grouped pustules which occasionally have a serpigenous pattern. In the authors experience these lesions are limited to the abdominal skin, the groins, and the axillae. Whereas PF usually develops gradually over time, this ventral form deteriorates more rapidly. In rare cases in dogs a panepidermal manifestation of PF is noticed.

Clinically PE closely resembles PF with lesions mainly on the head and ears. It is suggested that solar radiation may agrevate this subtype of pemphigus.

Discoid lupus erythematosus (DLE) is a rare clinical manifestation in dogs and cats (Scott, Miller and Griffin 1995; Willemse and Koeman 1989; Willemse 1998). Lesions are usually limited to the head and ears, but may occasionally also involve the nose and foot pads. They include erythema, scaling, crust formation, and erosions. The type of lesions are similar as in PF with the exception of pustules which have not been mentioned. Both in pemphigus and in LE pruritus is variable. In some cases ultraviolet light may contribute to exacerbation of the lesions.

Systemic involvement (SLE) is very uncommon in cats, although the development of DLE to SLE have been reported (Willemse and Koeman 1989). In these cases additionally fever, anemia, glomerulonephritis, and ulcerative stomatitis can be noticed. About 20 per cent of cats with SLE have cutaneous lesions (Scott, Miller and Griffin 1995). In dogs SLE produces a wide variety of signs: intermittent fever (65%), proteinuria (50%), anemia (35%), polyarthritis (75%), and skin lesions (30%).

Diagnosis - The definitive diagnosis of pemphigus is based on the history with specific emphasis on previous medication, cytology of lesional smears, histopathology of biopsies of skin or mucous membranes, and in rare cases direct immunofluorescence tests (Suter et al. 1998; Scott, Miller and Griffin 1995; Yager and Wilcock 1994; Willemse 1998) . The diagnosis of pemphigus can usually be established by means of the first two tests.

Next to more common parasitologic, dermatophytic and bacterial diseases and pending the history and the clinical aspects, the differential diagnoses may include drug eruptions, erythema multiforme, toxic epidermal necrolysis, cold agglutinin disease, lichenoid dermatosis, and leishmaniasis.

The presence of primary lesions and in particular pustules is of great importance. If only a few primary lesions are present, histopathology of skin biopsies may be preferred over cytology of smears in order to maximize the chances of a definitive diagnosis.

If more lesions are present multiple smears of the pustular content should be made and stained with methylene blue or according to Giemsa. Also fast-staining methods as used for blood smears are appropiate. Multiple rounded keratinocytes which are grouped or present as single cells are very suggestive for pemphigus. Secondary involvement of neutrophils can be observed.

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Dermatohistopathology is the test with which can be differentiated between the various subtypes of pemphigus (Yager and Wilcock 1994). Although sometimes the definitive diagnosis may be difficult, taking appropiate biopsies may enhance significantly the chances for a final diagnosis.

Therefore it should be emphasized that multiple biopsies of preferably primary lesions are needed. Hospitalization in order to be able to biopsy at the most appropiate time, may be required.

Clinical management - Amongst the various subtypes of pemphigus, PV has a garded to poor prognosis despite high doses of glucocorticoids and sometimes supportive therapy to maintain homeostasis. Fortunately, PF and to a lesser extent PE are more commonly seen. Their prognosis is good in the majority of cases, but almost all cases require maintenance treatment. It is the authorâ&#x20AC;&#x2122;s opinion that glucocorticoids are the first choice medication in feline pemphigus. Although topical application of glucocorticoids may be considered, it is usually impractible. Oral prednisone or prednisolone (2-4 mg/kg q 24h) usually will induce remission. If significant improvement is noticed, the dosis should be tapered off to an alternate day regimen and to the lowest effective maintenance level. Occasionally cats have shown resistance to prednisone or prednisolone, but do respond adequately to an equivalent dosis of dexamethasone (0.2 â&#x20AC;&#x201C; 0.4 mg/kg q 24h) (Scott, Miller and Griffin 1995; Willemse 1998).

If insufficient response is acquired, chlorambucil and chrysotherapy are alternatives for treating cats with pemphigus. Azothioprine is contraindicated for use in cats due to its toxic effects, resulting in fatal leukopenia and thrombocytopenia (Scott, Miller and Griffin 1995; Rosenkrantz 1989; Willemse 1998).

Chlorambucil (0.1 mg/kg q 24h or 0.2 mg/kg q 48h) is an orally administered alkylating agent which is commonly combined with glucocorticoids. However, also sole administration of chlorambucil can be effective. Although less toxic than other alkylating drugs, it is recommended to monitor cats with hemograms every two to four weeks due to potential myelodepression.

The use of gold compounds (chrysotherapy) should be restricted to these cats which have shown resistance or severe side effects to the other medication (Rosenkrantz 1989).

In addition to medical treatment, cats with PE should avoid sun exposure and in all cases where previously adminstered drugs may be the trigger to the development of pemphigus, such drugs should be withdrawn and chemically related drugs should be avoided.

Cats with DLE will commonly benefit from avoidance of exposure to intense sunlight in combination with topical glucocorticoids such as betamethasone or fluocinolone. If there is an inadequate response to such medication, systemic treatment with glucocorticoids or chlorambucil as described for pemphigus may be used.

The prognosis is usually good. In contrast, the effect of treatment in cats with SLE is unpredictable. In these cases avoidance of sun exposure is recommended together with systemic treatment as described for the discoid subtype of lupus erythematosus.

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In dogs pemphigus is usually controlled with a combined therapy of glucocorticoids (prednisone 1-2 mg/kg PO q 24h as innitial dosis) and azathioprine (1-2 mg/kg PO q 24h).

The beneficial effects are usually not apparent within 3 weeks, and the aim is to use azathioprine alternated with prednisolone at the lowest doses necessary to maintain remission. Bone marrow depression or GI-side effects may occur, and animals should be closely monitored during the first 2 months.

Occasionally pemphigus (with the exception of PV) may be controlled with glucocorticoids alone. For this purpose prednisone, prednisolone or dexamethasone (0.1 mg/kg PO q 24h) can be used and after a daily dosis for 5-7 days such medication can be switched to an alternate regimen for maintenance.

In dogs gold salt therapy has also been advocated as a steroid-sparing agent. Na-aurothiomalate is administered at an initial dose of 1 mg (IM for dogs < 10 kg) or 5mg (dogs > 10 kg). Without side effects for 7 days, the dose is doubled for another week. Hereafter, treatment is continued with weekly doses (1 mg/kg). Side effects may include renal, hematological and dermatologic disease. Alternatively, auranofin has been introduced as an oral gold medication (0.05 â&#x20AC;&#x201C; 0.2 mg/kg PO q 12h) with less side effects.

For canine LE, apart from glucocorticoid medication and sun blockers (see before), vitamin E (400-800 IU daily; lag phase 1-2 months) and the combonation of tetracycline and niacinamide (250 mg of each drug PO q 8h in dogs under 10 kg body weight and 500 mg PO q 8h in dogs over 10 kg). It

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is controversial if these drugs are as effective as systemic glucocorticoids.

In 50% of cases of SLE therapy can be withdrawn after 6 months, whereas in discoid lupus usually lifelong treatment is indicated.

References Wakelin, S.H., Wojnarowska, F. Immunobullous diseases. In: Bos, J.D., ed.

Skin Immune System (SIS) - Cutaneous Immunology and Clinical Immunodermatology. New York: CRC Press, 1997: 445-60.

Suter, M.J., De Bruin, A., Wyder, M., et al. Autoimmune diseases of domestic animals: an update. In: Kwochka, K.W., Willemse, T., von Tscharner, C., eds. Advances in Veterinary Dermatology. Oxford: Butterworth Heinemann, 1998: 321-37.

Bos, J.D., de Rie, M.A. Lupus erythematosus. In: Bos, J.D., ed. Skin Immune System (SIS) - Cutaneous Immunology and Clinical Immunodermatology. New York: CRC Press, 1997: 471-78.

Scott, D.W., Miller, W.H., Griffin, C.E., eds. Small animal dermatology.

Philadelphia: Saunders, 1995: 556-88.

Willemse, T., Koeman, J.P. Discoid lupus erythematosus in cats. Veterinary Dermatology 1989; 1: 19-24.

Willemse, T. Clinical dermatology of dogs and cats, 2nd edn. Maarssen (the Netherlands): Elsevier-Bunge, 1998: 143 pp.

Yager, J.A., Wilcock, B.P. Color Atlas and Text of Surgical Pathology of the Dog and Cat: Dermatopathology and Skin Tumors. London: Wolfe Publishing, 1994: 320 pp.

Amagai, M., Tsunoda, K., Zillikens, D., Nagai, T., Nishikawa, T. Journal of the American Academy of Dermatology 1999; 40: 167-70.

Rosenkrantz, W. Immunomodulating drugs in dermatology. In: Kirk, R.W., Bonagura, J.D., eds. Current Veterinary Therapy: Small Animal Practice, vol. X. Philadelphia: W.B. Saunders, 1989: 570-77.

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SINDROME VESTIBOLARE PERIFERICA SECONDARIA A COLESTEATOMA BILATERALE DELLA BOLLA TIMPANICA IN UN CANE Adamo P. Filippo* Med Vet, Dipl. E.C.V.N., Cantile C.** Med Vet, Mocavero A.* Med Vet, Marioni C.*** Med Vet *Centro Medico Veterinario “Villa S. Francesco”, Roma, Italia ** Laboratorio Istopatologia, Dipartimento di Patologia Animale, Facoltà di Medicina Veterinaria, Università degli Studi di Pisa *** Studio Veterinario Associato, Grosseto Viene descritto un caso di sindrome vestibolare secondaria a colesteatoma bilaterale della bolla timpanica in un cane di razza Carlino, intero, di sei anni di età. Il cane veniva portato a visita neurologica a causa di una sindrome vestibolare ad insorgenza acuta. L’anamnesi recente riferiva improvvisa difficoltà a tenere la stazione quadrupedale e a camminare, testa ruotata a sinistra con tendenza a cadere dallo stesso lato. L’anamnesi remota riferiva una otite esterna cronica bilaterale purulenta, da circa cinque mesi, di grado maggiore a destra che non si risolveva con la terapia antibiotica locale. La visita neurologica rivelava una sindrome vestibolare di tipo periferico del sistema vestibolare di sinistra ed ipoacusia. L’esame auricolare evidenziava materiale purulento nell’orecchio destro con parziale stenosi del canale auricolare, l’integrità della membrane timpanica risultava di difficile valutazione. L’esame auricolare dell’orecchio sinistro rivelava lieve essudazione infiammatoria ed una normale membrana timpanica. L’esame radiografico delle bolle timpaniche rivelava una lieve radiopacità della bolla timpanica sinistra mentre quella destra appariva nella norma. Per una migliore visualizzazione della bolla timpanica sinistra veniva eseguito un esame di Risonanza Magnetica (RM). La RM rivelava la presenza di materiale patologico che occupava totalmente entrambe le bolle timpaniche e di grado maggiore a sinistra. Le caratteristiche di RM facevano presupporre un’origine infiammatoria della lesione.

Il materiale patologico veniva rimosso attraverso una bollectomia ventrale bilaterale, esso risultava adeso alla parete ossea delle bolle, facilmente dissecabile, di consistenza fibrosa ed asportabile in grossi frammenti. L’esame istologico lo tipizzava come colesteatoma. Nelle successive settimane il cane compensava la sintomatologia vestibolare, l’otite esterna si risolveva con lavaggi auricolari usando una soluzione di acqua e aceto al 50%; l’ipoacusia e la testa lievemente piegata a sinistra risultavano permanenti. Il colesteatoma della bolla timpanica è una forma di cisti epidermoide dell’orecchio medio costituita da epitelio squamoso cheratinizzato stratificato spesso associato a otite media. In questo caso la sintomatologia neurologica vestibolare periferica di sinistra poteva essere spiegata dal coinvolgimento dell’orecchio interno da parte del colesteatoma e l’ipoacusia dal coinvolgimento bilaterale delle strutture dell’orecchio medio.

Conclusioni. L’esame radiografico delle bolle timpaniche in questo caso si è rivelato insufficiente nel delineare la presenza della stessa patologia nella bolla timpanica controlaterale. La RM ha permesso di riconoscere accuratamente l’estensione ed il carattere bilaterale della lesione. In medicina veterinaria questo è il primo caso di colesteatoma bilaterale delle bolle timpaniche.

TECNICHE DIAGNOSTICHE INNOVATIVE PER L’EHRLICHIOSI CANINA Allione Alessandra PhD , Canale Lorena* PhD, Bollo Enrico** MedVet, Poletti Paolo* PhD, *Agrolabo S.p.A., Divisione Diagnostici, Romano C.se (TO), Italia **Dip. Patologia Animale, Università degli Studi di Torino Il genere Ehrlichia appartiene alla famiglia delle Rickettsiaceae e comprende numerose specie, per lo più trasmesse da zecche, che parassitano i leucociti sia degli animali domestici che dell’uomo. Il cane può subire l’infezione naturale da parte di E. canis, E. platys, E. equi, E. risticii. Solamente l’ehrlichiosi dovuta a E. canis rappresenta un’entità clinica importante dal punto di vista epidemiologico; tale infezione colpisce essenzialmente il cane e i canidi selvatici. In Europa l’ehrlichiosi canina si riscontra soprattutto nelle regioni mediterranee. La diagnosi viene effettuata mediante il riscontro di segni clinici ed ematologici, la dimostrazione del parassita nei monociti del sangue periferico e il rilievo di anticorpi specifici. Il riconoscimento dell’agente patogeno è di particolare importanza in soggetti sottoposti a terapia al fine di valutare l’efficacia dei protocolli terapeutici oltre che per confermare un’infezione attiva.

Lo scopo del presente studio è di illustrare i risultati di indagini di laboratorio per la messa a punto di un test immunocromatografico per la ricerca di anticorpi diretti contro E. canis e di una metodica basata sulla tecnica PCR per l’identificazione della Rickettsia su campioni di sangue di animali con sospetta infezione. Al fine di ottenere un’elevata specificità del test immunocromatografico è stato utilizzato come antigene di cattura una proteina ricombinante del peso molecolare di 30 kDa. Tale proteina è un antigene dominante costantemente riconosciuto dai sieri di cani infettati sperimentalmente e con infezione naturale.

Le prove cliniche effettuate con un elevato numero di sieri hanno dimostrato elevati valori di specificità e sensibilità. Tale test pertanto si configura come un interessante strumento diagnostico a disposizione del medico veterinario per la determinazione rapida e semplice della presenza di anticorpi in cani con sospetto di infezione da Ehrlichia.

L’identificazione di E. canis tramite PCR è stata messa a punto utilizzando primers che riconoscono e amplificano la sequenza di DNA codificante la stessa proteina utilizzata per il test immunocromatografico. Questa tecnica è particolarmente sensibile e consente una diagnosi conclusiva e un controllo della terapia.

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IL RUOLO DEGLI AMINOACIDI ESSENZIALI ED A CATENA RAMIFICATA NEL CANE SPORTIVO AI FINI DEL MANTENIMENTO E DEL MIGLIORAMENTO DELLA PERFORMANCE, UN ANNO DI ESPERIENZA CON PETVITAL BIOAKTIVATOR Beni Andrea, Med. Vet. Canina Italia snc Gli aminoacidi non hanno solo una funzione plastica ma partecipano anche a numerose altre funzioni. Entrano nei complessi meccanismi della produzione di energia, e nei processi di detossificazione della fatica muscolare, sono perciò di grande importanza nella gestione di un cane sportivo.

In ogni specie animale ci sono degli amminoacidi detti “essenziali” che l’organismo non può sintetizzare, ma deve assumere con gli alimenti. Non esiste un alimento che li possiede tutti insieme. A quanto risulta sono essenziali nel cane 9 aminoacidi: lisina, leucina, valina, isoleucina, treonina, triptofano, metionina, istidina, fenilalanina.

I cani che fanno attività sportiva necessitano più degli altri di una integrazione amminoacidica adeguata che gli fornisca il materiale per costruire i muscoli, per produrre energia e per smaltire la fatica che si accumula in tutto l’organismo.

Nel presente lavoro si valutano i risultati di un team di cani da slegdog a cui è stato somministrato PETVITAL BIOAKTIVATOR, specificando gli esercizi eseguiti e analizzando la performance del team durante le fasi di allenamento, gara e recupero con l’ausilio di un cardiofrequenzimetro a telemetria breve.

Indicazioni del fabbisogno di amminoacidi essenziali ed a catena ramificata nel cane sportivo, con accenni alle varie differenziazioni per razza, lavoro svolto, ecc.

“CISTI ARACNOIDEA” IN UN GATTO Bernardini Marco* Dr. Med. Vet Dipl. ECVN, De Lorenzi Davide** Dr. Med. Vet. Spec. Clinica dei Piccoli Animali Dip. di Patologia Animale* Facoltà di Medicina Veterinaria, Universitat Autonoma de Barcelona, Barcellona, Spagna Ambulatorio Veterinario “Corelli” **, Forlì, Italia Un gatto, europeo, femmina, di due anni di età, viene condotta alla visita a causa di una grave para-paresi, con impossibilità ad alzarsi sul treno posteriore, insorta da più di un anno. Inizialmente, la gatta fu trovata dal propietario dopo ore di assenza da casa impossibilitata ad alzarsi sul treno poste-riore. Pur senza nessun approfondimento diagnostico e con solo una terapia sintomatica, la gatta fu in grado di recuperare nei mesi successivi la deambulazione, pur permanendo gravi deficit sul treno posteriore. Sei mesi dopo l’episodio iniziale, senza ragioni apparenti, la patologia si riacutizza, riapparendo l’impossibilità alla stazione, alla quale non segue questa volta un recupero significativo, anche se l’animale sembra presentare variazioni giornaliere nelle sue possibilità di muovere le zampe posteriori. All’esame fisico non si riscontrano alterazioni. All’esame neurologico si registrano para-paresi con impossibilità ad alzare il treno posteriore, atrofia delle estremità posteriori, iperriflessia patellare bilaterale, presenza di riflesso estensore crociato, dolore alla palpazione del rachide nella zona del passaggio toracolombare e assenza bilaterale del riflesso pannicolare caudalmente a tale livello. Conseguentemente la lesione viene localizzata a livello di T3-L3. La diagnosi differenziale include patologie traumatiche, vascolari, degenerative e infiammatorie. L’esame emocromocito-metrico, la biochimica ematica e l’esame delle urine non evidenziano alterazioni. La serologia per FeLV e FIV risulta negativa. Le radiografie in bianco del tratto toraco-lombare evidenziano l’assenza della epifisi craniale di T13. Il mezzo di contrasto iniettato dalla cisterna magna non procede caudalmente a T13. A questo livello nella proiezione latero-laterale la linea dorsale si allarga a forma di goccia fino ad coprire tutto il midollo. Nella proiezione ventro-dorsale si ottiene un’immagine simile. Le immagini ottenute sono compatibili con una cisti aracnoidea. Per indagare meglio la patologia in corso si procede all’esecuzione di una RMN, che evidenzia un restringimento e spostamento a sinistra del midollo spinale a livello T13. Nonostante la prognosi riservata, i proprietari decidono di tentare un intervento per alleviare la pressione sul midollo spinale. Si procede quindi a una emilaminectomia sinistra con durotomia. Nelle settimane successive si registra un lieve miglioramento, senza che l’animale possa comunque riguadagnare la stazione quadrupedale. La definizione di “cisti aracnoidea” è anche in questo caso fuorviante. Si tratta in realtà di una depressione del midollo spinale in cui si accumula mezzo di contrasto, per cui sarebbe forse più corretto parlare generalmente di “aumento focale dello spazio subaracnoideo”. In questo caso particolare riteniamo possibile che un trauma spinale e le relative sequele cicatriziali possa aver causato un accumulo di LCR, la cui pressione locale ha contribuito alla degenerazione midollare.

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IPEROSSALURIA PRIMARIA (ACIDURIA L-GLICERICA) IN UN GATTO Bernardini Marco* Dr. Med. Vet. Dipl. ECVN, De Lorenzi Davide** Dr. Med. Vet. Spec. Clinica dei Piccoli Animali, Camerini Chiara*** Dr. Med. Vet., Sisò Silvia* Med. Vet. Dip. di Patologia Animale* Facoltà di Medicina Veterinaria, Universitat Autonoma de Barcelona, Barcellona, Spagna Ambulatorio Veterinario “Corelli” **, Forlì, Italia Ambulatorio Veterinario***, Faenza, Italia Un gatto europeo, maschio, di sette mesi di età, del peso di 2,4 Kg fu presentato alla visita a causa di debolezza e inappetenza della durata di più di quattro settimane. Il gatto era stato adottato all’età di due mesi: per questo motivo nè i genitori, nè eventuali fratelli erano conosciuti. All’E.O.G. il gatto presentava un lieve stato di disidratazione e una leggera dispnea. All’esame neurologico il gatto appariva debole e incapace di sorreggere il peso del corpo. La muscolatura di tutto il corpo era fortemente atrofica, i riflessi spinali da diminuiti ad assenti, mentre l’esame dei nervi cranici non presentava anormalità. Inoltre, il gatto miagolava in maniera afona. L’esame emocromocitometrico segnalava una lieve policitemia, la biochimica ematica un aumento delle concentrazioni di BUN, creatinina e latticodeidrogenasi. L’esame fisico-chimico delle urine evidenziava proteinuria, piuria, ematuria, cilindri granulari e cristalli di ossalato monoidrato di calcio. I rapporti acido ossalico /creatinina e acido glicerico/creatinina risultarono fortemente aumentati. All’esame elettromiografico si registrarono potenziali di fibrillazione a carico della muscolatura appendicolare, paraspinale e del capo. La velocità di conduzione nervosa del nervo peroneo risultò leggermente diminuita, mentre non si rilevò alcuna anormalità alla stimolazione ripetuta (3 Hz) dello stesso nervo. In base a tali reperti si emise una diagnosi di iperossaluria primaria di tipo 2 (aciduria L-glicerica). A causa del progressivo peggioramento dei sintomi e della prognosi infausta il propietario decise per l’eutanasia e acconsentì all’autopsia. All’esame macroscopico si rilevò una atrofia muscolare diffusa. Microscopicamente si rilevò a livello renale la presenza di cristalli birifrangenti depositati nei tubuli renali, glomerulosclerosi e flogosi interstiziale mononucleare. L’esame del midollo spinale lombare evidenziò un aumento del diametro assonale, che appariva rigonfio, quadri di degenerazione walleriana e neuronale. Esami immunoistochimici e ultrastrutturali dimostrarono che l’ingrossamento assonale era da imputarsi all’accumulo di neurofibrille. Quadri di degenerazione walleriana furono riscontrati anche in campioni del nervo sciatico. L’esame microscopico del tessuto muscolare si caratterizzava per la presenza di una notevole varietà nel diametro delle fibre, alcune delle quali contenevano nuclei in posizione centrale. Il caso qui descritto costituisce la prima segnalazione di questa malattia dopo la sua descrizione originale più di dieci anni fa in una colonia di gatti nel regno Unito e supporta la possibilità che una eziologia metabolico-congenita per difetto enzimatico sia alla base di numerose patologie neuromuscolari tuttavia ad origine sconosciuta.

VACUOLIZZAZIONE NEURONALE E DEGENERAZIONE SPINOCEREBELLARE IN UN ROTTWEILER Bernardini Marco Dr. Med. Vet. Dipl. ECVN, de la Fuente Christian Med. Vet., Pumarola Marti Dr. Med. Vet., Ph.D., dipl ECVP Dip. di Patologia Animale, Facoltà di Medicina Veterinaria, Universitat Autonoma de Barcelona, Barcellona, Spagna Viene presentato per un consulto neurologico un cane di razza Rottweiler, maschio, di sei mesi di età, normalmente vaccinato.

I proprietari riferiscono di difficoltà di deambulazione con debolezza del treno posteriore presente da “sempre”, e quindi da loro relazionata con lo sviluppo del cane, ma acuitasi nel corso degli ultimi tre giorni. All’esame fisico non si rilevano alterazioni. All’esame neurologico si riscontra tetraparesi, molto più evidente a carico del treno posteriore, atassia con lieve ipermetria, assenza di reazioni posturali negli arti posteriori, e iporiflessia generalizzata. Ospedalizzato il soggetto, vengono effettuate esami ematobiochimici e urinari di base, che non evidenziano alterazioni. Poche ore dopo l’animale presenta rigurgito di cibo. Una radiografia del torace rivela la presenza di megaesofago. Gli esami serologici per toxoplasmosi e neosporosi risultano negativi.

L’esame elettromiografico segnala attività spontanea a carico della muscolatura distale degli arti posteriori. Nei giorni seguenti il cane mostra un cambio di fonazione e, nonostante l’assunzione dell’alimento in posizione verticale, continua a rigurgitare cibo, sviluppando una broncopolmonite ab ingestis. A causa del deteriorarsi delle condizioni cliniche sia neurologiche che respiratorie i proprietari richiedono l’eutanasia.

All’esame anatomopatologico si rileva macroscopicamente una broncopolmonite catarrale-purulenta. L’esame istologico del tessuto nervoso evidenzia una vacuolizzazione neuronale multifocale e degenerazione dei tratti spinocerebellari.

Questa malattia fa parte di un gruppo di patologie neurologiche dei giovani Rottweiler, quali la leucoencefalomielopatia, la distrofia neuroassonale e l’atrofia muscolare spinale, spesso di difficile differenziazione clinica. Questo caso presenta un particolare interesse clinico per la sintomatologia periferica rilevabile in un soggetto con segni istologici prevalenti a carico del SNC. L’interesse per questa malattia, di cui esistono pochissime segnalazioni in letteratura veterinaria, risiede anche nella similitudine dei quadri istologici con le encefalopatie spongiformi da prioni segnalate nell’uomo e negli animali, anche se i tentativi di evidenziare tali agenti nei Rottweiler non hanno portato a risultati positivi.

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SCHWANNOMA NEL CANALE VERTEBRALE LOMBOSACRALE IN UN WEST HIGHLAND WHITE TERRIER Bernardini Marco Dr. Med. Vet Dipl. ECVN, Morales Carles Med. Vet., Franch Jordi Dr. Med. Vet. Ph.D., Sisò Silvia Med. Vet. Dip. di Patologia Animale, Facoltà di Medicina Veterinaria, Universitat Autonoma de Barcelona, Barcellona, Spagna Un cane di razza West Highland White Terrier, maschio, di 11 anni di età, viene condotto ad una visita neurologica con una sintomatologia cronica e progressiva di tre mesi caratterizzata da zoppia all’arto posteriore sinistro, resistenza all’esercizio, dolore nella regione della coda, disuria e tenesmo. L’esame neurologico evidenzia a carico dell’arto posteriore sinistro atrofia dei mm. tibiale craniale, semimembranoso e semitendinoso, deficit della propriocezione, pseudoiperriflessia patellare e debolezza del riflesso flessore. Inoltre, si nota dolore all’iperestensione della coda e assenza del riflesso perianale. La lesione viene localizzata a livello L7-S3 e la diagnosi differenziale comprende principalmente patologie compressive o di origine tumorale. Il minimum data base segnala una lieve neutropenia e aumento della fosfatasi alcalina. L’indagine radiologica del rachide lombosacrale evidenzia una chiara concavità del pavimento del canale vertebrale sacrale, che non viene riempito dal mezzo di contrasto iniettato durante l’epidurografia. La TAC mostra la presenza di una massa che occupa tutto il canale vertebrale caudalmente a L7. La laminectomia permette la visualizzazione di una massa fusiforme della lunghezza di circa 12 mm, sviluppatasi a carico della radice sinistra di S2, che viene asportata. La diagnosi istopatologica è di schwannoma maligno. La fase postoperatoria è caratterizzata da una transitoria incontinenza urinaria di pochi giorni di durata, e dalla progressiva e quasi totale scomparsa della dolorabilità. Residua una lieve diminuzione della propriocezione dell’estremità posteriore sinistra. Circa due mesi e mezzo dopo il cane sviluppa una grave paraparesi e gli viene praticata l’eutanasia su richiesta dei proprietari. L’esame autoptico rivela un’altra massa nel canale vertebrale sacrale, che istologicamente viene classificato come una variante epitelioide di schwannoma. La peculiarietà di tale caso clinico risiede nella rarità della localizzazione del tumore, nei quadri radiografici e nella possibilità di una classificazione come schwannoma nonostante le sue caratteristiche di malignità.

CONFRONTO TRA TAC E RADIOLOGIA CONVENZIONALE NELLA DIAGNOSI DI DISCOSPONDILITE Bernardini Marco* Dr. Med. Vet Dipl. ECVN, Morales Carles* Med. Vet., Xavier Roura** Dr. Med. Vet. Ph.D., Vignoli Massimo*** Dr. Med. Vet. SRV Dip. di Patologia Animale*, Facoltà di Medicina Veterinaria, Universitat Autonoma de Barcelona, Barcellona, Spagna Hospital Clinic Veterinari**, Universitat Autonoma de Barcelona, Barcellona, Spagna Ambulatorio Veterinario dell’Orologio***, Sasso Marconi (BO), Italia La diagnosi di discospondilite rappresenta spesso un problema per i medici veterinari. Nei casi insorti da meno di 15-20 giorni, infatti, non è possibile riscontrare nella maggior parte dei casi alterazioni radiografiche degli spazi intervertebrali e delle epifisi vertebrali tali da permettere di riconoscere con certezza la patologia in corso. Esiste però la necessità di una diagnosi precoce, sia per l’intenso dolore manifestato in questi casi dall’animale, sia per il rischio di instabilità della colonna vertebrale e di infezione delle adiacenti strutture nervose che si verificano nei casi più gravi.

L’uso della tomografia assiale computerizzata (TAC) mette in evidenza gli aspetti di lisi e rimodellazione ossea caratteristici di questa malattia con una definizione e precocità spesso non raggiungibile con le indagini convenzionali e può costituire un valido aiuto sia per la diagnosi della malattia che per il controllo dell’evoluzione dei singoli casi.

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MODALITÀ DI ATTIVITÀ SINERGICA ED EFFICACIA ANTIELMINTICA DI UNA COMBINAZIONE DI PYRANTEL - FEBANTEL - PRAZIQUANTEL NEI CONFRONTI DI ALTRE COMBINAZIONI FARMACOLOGICHE Bianciardi Paolo Med. Vet. Bayer S.p.A., Milano Italia Alcune parassitosi dei cani e dei gatti possiedono un potenziale zoonosico. Una sverminazione regolare è in grado di ridurre il rischio di infestazioni e di contaminazione dell’ambiente e quindi di prevenire le patologie che queste zoonosi provocano nell’uomo. Un certo numero di antielmintici ad ampio spettro sono attualmente disponibili sul mercato. È però importante che il prodotto impiegato garantisca una reale efficacia su tutti gli endoparassiti riscontrabili nei nostri animali e che sia semplice da usare garantendo la necessaria “compliance” da parte dei proprietari. La combinazione dei tre principi attivi Pyrantel-FebantelPraziquantel (Drontal Plus) assicura un’azione completa su tutti gli elminti, grazie all’azione sinergica della combinazione Pyrantel/Febantel, ed una “compliance adeguata” grazie alla monosomministrazione.

L’azione sinergica dell’associazione Pyrantel/Febantel nei confronti dei nematodi del cane, già conosciuta ed osservata nelle prove cliniche, è stata di recente chiarita in un lavoro condotto da H. Mehlhorn e A. Harder (1997). Gli autori illustrano i meccanismi che portano ad una maggiore efficacia dei due componenti quando somministrati contemporaneamente. Il lavoro, eseguito su topi infestati sperimentalmente con Heterakis spumosa, un nematode intestinale simile agli ascaridi, è stato incentrato su due aspetti. La determinazione delle dosi minime ottimali che permettessero l’evidenziazione dell’attività sinergica dei due p.a. e l’osservazione mediante microscopia elettronica delle lesioni cito-istologiche indotte dai differenti p.a. impiegati, sia singolarmente che associati. I risultati dimostrano come il Pyrantel da solo venga ingerito dal verme per via orale e danneggi principalmente la parte citoplasmatica delle cellule muscolari, l’intestino e l’ipoderma. Il Febantel da solo si ritiene venga assorbito attraverso la cuticola del parassita ed in questo lavoro ha mostrato un’attività nei confronti delle cellule muscolari, vacuolizzazione dell’ipoderma e rigonfiamento della corda nervosa centrale. L’azione combinata dei due p.a. ha mostrato un’azione rafforzata nei confronti dell’ipoderma, delle cellule muscolari, delle cellule intestinali e di quelle nervose insieme ad un’azione sui canali escretori e sull’apparato riproduttore. Quest’azione sinergica permette a Drontal plus di garantire una più efficace attività ad ampio spettro anche nei confronti di altre associazioni farmacologiche più recenti come dimostrato da T. Hopkins e A .Shimmel (1998) che in una comparazione con un’associazione di Pyrantel, Oxantel, Praziquantel, e con la Milbemicina ossima nei confronti di infestazioni naturali da Ancylostoma caninum nei cani ha dato i seguenti risultati di riduzione parassitaria: Py.Fe.Pr.=99%; Py.Ox.Pr.=76%; Mi.o.=84%. Questi dati confermano l’efficacia dell’azione sinergica di Pyrantel e Febantel che unita alla monosomministrazione fanno di Drontal plus l’antielmintico più affidabile nella lotta alle elmintiasi dei cani e dei gatti.

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L’IMPIEGO DEL CLAZURIL NEL TRATTAMENTO DELLE COCCIDIOSI DI ALCUNI PICCOLI MAMMIFERI Bo Pierfrancesco Libero professionista - Via Marino Dalmonte 7, 40134 Bologna L’obiettivo di questo studio è stato quello di stimare l’efficacia anticoccidica nei piccoli mammiferi di una nuova molecola denominata Clazuril. Le coccidiosi sono malattie la cui gravità è determinata dall’età al momento dell’esposizione (colpiscono prevalentemente i soggetti giovani), dalla specie, dal numero di oocisti e dai fattori stressanti ambientali. La sintomatologia è spesso assente o rappresentata solo da una diarrea da lieve a modesta, che però può predisporre allo sviluppo d’altre enteriti. Sono stati quindi esaminati diversi soggetti, mediante anamnesi ed esame obiettivo generale, inserendo nello studio 20 criceti russi, 18 criceti dorati, 38 cavie, 54 conigli, 8 degu, 4 gerbilli, 3 scoiattoli Giapponesi e 2 scoiattoli comuni. Le feci di tali animali sono state sottoposte ad un’analisi copromicroscopica utilizzando una soluzione ipersatura di NaCl (P.S.: 1200). Ciò ha permesso di riscontrare diversi casi di positività alla coccidiosi (26 cavie, 36 conigli, 1 scoiattolo comune) anche in assenza di sintomatologia. I soggetti positivi sono stati trattati con l’Appertex, un anticoccidico in compresse per uso orale della Jansenn-Cilag (registrato per il trattamento delle coccidiosi nei piccioni. Tale farmaco, contenente Clazuril, è stato somministrato al dosaggio di una compressa ogni 500 gr. peso vivo in una unica somministrazione, secondo le modalità d’impiego e la posologia indicata dalla casa produttrice. Tale molecola, appartenente al gruppo dei benzene acetonitrili, agisce bloccando le fasi di schizogonia (agendo sugli stadi di merozoiti e schizonti), di gametogonia (agendo sui gameti), e di sporulazione (agendo sulle oocisti). Insolubile in acqua, viene somministrato per via orale. A tale terapia è stata associata una disinfezione totale delle gabbie e del loro contenuto in quanto le oocisti eliminate con le feci, quando sporulate, sono notevolmente resistenti nel terreno. Per valutare l’efficacia del trattamento, le feci dei soggetti positivi sono state ricontrollate dopo 7-10 giorni dalla somministrazione del farmaco, sempre mediante esami coprologici. Tutti i dati relativi allo studio sono riportati nella tabella 1 e, come si vede, la somministrazione di Clazuril è stata efficace nel 100% dei 63 piccoli mammiferi trattati. I vantaggi riscontrati, oltre all’efficacia, sono stati: facilità di somministrazione, singolo trattamento, sicurezza di azione, assenza di effetti collaterali. A questi si contrappone lo svantaggio, per chi ha pochi animali, del numero di compresse (30) presenti all’interno della scatola, anche se il prezzo è equiparabile a quello di altri prodotti.

Tabella 1 - Risultati della sperimentazione

SPECIE Criceti russi Criceti dorati Cavie Conigli Degu Gerbilli Scoiattoli giapp.

Scoiattoli comuni

NUMERO

POSITIVI A COCCIDI

POSITIVI DOPO TRATTAMENTO

EFFICACIA

20 18 38 54 8 4 3 2

0 0 26 36 0 0 0 1

— — 0 0 — — — 0

— — 100% 100% — — — 100%

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TECNICHE DIAGNOSTICHE INNOVATIVE PER LE DERMATOFITOSI: CARATTERIZZAZIONE DEGLI ANTIGENI DI M. CANIS, ELISA E IMMUNOCROMATOGRAFIA Bollo Enrico * Med Vet, Pregel Paola* PhD, Allione Alessandra ** PhD, Canale Lorena** PhD, Poletti Paolo** PhD * Dip. Patologia Animale, Università degli Studi di Torino ** Agrolabo S.p.A., Divisione Diagnostici, Romano C.se (TO), Italia Le dermatofitosi, infezioni dei tessuti superficiali cheratinizzati sostenute da miceti appartenenti ai generi Microsporum, Trichophyton ed Epidermophyton, hanno presentato, negli ultimi anni, un sensibile incremento nella loro incidenza nelle popolazioni urbane di cani e gatti, con conseguente aumento, in virtù delle loro proprietà zoonosiche, dell’incidenza delle dermatofitosi umane. In particolare, M. canis è la principale specie di dermatofita isolata da lesioni cutanee del cane e del gatto (in oltre il 90% dei casi). Per quanto riguarda la diagnosi delle infezioni da dermatofiti, l’esperienza indica che il valore predittivo dello stato di infezione dell’animale è piuttosto scarso, a causa delle difficoltà di diagnosticare la patologia in base al semplice esame visivo del mantello dell’animale. D’altra parte l’esame colturale, considerato il “golden standard” dal punto di vista diagnostico, può essere talvolta invalidato da un campionamento effettuato in modo inadeguato. È pertanto evidente l’importanza della messa a punto di mezzi diagnostici più raffinati e di maggior attendibilità.

Lo scopo del presente lavoro è di presentare i risultati di uno studio per la messa a punto di nuovi strumenti diagnostici per le dermatofitosi animali, basati su test immunocromatografici e immunoenzimatici. L’estratto fungino intero è stato ottenuto dopo purificazione di colture di M. canis e sottoposto a separazione su gel di poliacrilamide. Sono state evidenziate numerose bande di separazione nell’intervallo di peso molecolare compreso tra 37 e 99 kDa. Dopo trasferimento su membrana di nitrocellulosa mediante Western blotting, è stata effettuata una colorazione immunoenzimatica con sieri di gatti sperimentalmente infettati con M. canis, evidenziando un legame specifico per antigeni strutturali di dermatofiti. Per quanto riguarda il test immunoenzimatico (ELISA), le piastre sono state sensibilizzate con estratto fungino e sono stati saggiati sieri di gatti con infezione naturale e sperimentale da dermatofiti, evidenziando un’elevata capacità di discriminazione del test tra sieri di animali infetti e sieri di animali di controllo. L’estratto fungino infine è stato utilizzato per la messa a punto di un test immunocromatografico rapido, mediante sensibilizzazione di membrana di nitrocellulosa e reazione con antisiero coniugato con oro colloidale. La caratteristiche di specificità e rapidità del test lo rendono uno strumento diagnostico affidabile e di uso specifico nella pratica veterinaria ambulatoriale. In conclusione, il ricorso a tecniche innovative per la diagnosi di dermatofitosi negli animali da compagnia consente al medico veterinario di disporre di strumenti caratterizzati da elevata specificità, sensibilità e rapidità, tali da venire incontro alle rinnovate esigenze cliniche di ambulatorio e laboratorio.

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RILIEVI PATOLOGICI RISCONTRATI CON ESAMI DI LABORATORIO PRE-OPERATORI IN UNA POPOLAZIONE DI CANI E GATTI CLINICAMENTE SANI Caldin Marco* Med. Vet., Borghi Maria* Med. Vet., Furlanello Tommaso** Med. Vet. *Clinica Veterinaria Privata “San Marco”, Padova, **Laboratorio Privato d’Analisi Veterinarie “San Marco”, Padova Obiettivo: valutare l’incidenza di alterazioni emato-chimiche-urinarie in cani e gatti apparentemente sani, da sottoporre a interventi chirurgici routinari, al fine di determinare l’utilità di tali esami di laboratorio.

Popolazione considerata ed indagini di laboratorio (Marzo 1998-Novembre 1999): 45 cani e 42 gatti, di età compresa tra 1 e 10 anni, di entrambi i sessi, da sottoporre ad interventi chirugici quali: orchiectomie (cani: 4, gatti: 8), ovario-isterectomie (c.: 10, g.: 30), exeresi di neoformazioni cutanee o mammarie di piccole dimensioni, successivamente classificate come benigne all’esame istopatologico (c.: 22, g.: 5), ferite cutanee, non da morso, recenti, non gravi (c.: 3) e artropatie degenerative croniche (c.: 2). La popolazione considerata non presentava alcuna alterazione all’esame fisico, ad eccezione di eventuali segni per i quali è stata suggerita la procedura chirurgica sopra riportata. Per tutti i soggetti considerati l’anamnesi non riportava rilievi degni di nota. Tutti i soggetti venivano sottoposti, come valutazione pre-operatoria, ad i seguenti esami di laboratorio: esame emocromocitometrico completo, integrato da misurazione della VES, profilo coagulativo, profilo biochimico con elettroforesi proteica e profilo urinario.

Risultati: presentavano almeno un’alterazione nei referti di laboratorio 30 cani su 45 (66.6%) e 10 gatti su 42 (23.8%). La percentuale delle alterazioni sono elencate nella tabella sottostante.

Esami di laboratorio

Cani (n.=30)

Gatti (n.=10)

Esame emocromocitometrico Profilo coagulativo Profilo biochimico Elettroforesi proteica Profilo urinario

26 (86.6%) 11 (36.6%) 22 (73.3%) 6 (20%) 10 (33.3%)

7 (70%) 3 (30%) 6 (60%) 3 (30%) 4 (40%)

Conclusioni: i risultati degli esami di laboratorio erano frequentemente alterati in animali ritenuti sani all’esame fisico. In realtà tali soggetti erano affetti da stati patologici anche di notevole importanza (epatopatie, infezioni croniche, nefropatie ed altre). In mancanza di appropriati approfondimenti di patologia clinica, il rischio anestesiologico sarebbe stato pericolosamente sottostimato. Inoltre tali valutazioni hanno permesso un approccio globale più corretto al singolo paziente per 1) evitare l’aggravarsi di stati patologici clinicamente silenti 2) trattare eventuali patologie già presenti 3) stabilire quale procedura clinica o chirurgica sia prioritaria per il benessere del soggetto.

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RIPOSIZIONAMENTO ORTODONTICO DI UN CANINO PER FINI ESPOSITIVI IN UN CANE DI RAZZA YORKSHIRE TERRIER Brusa Franco* Med. Vet., Squarzoni Paolo** Med. Vet. Ambulatorio Veterinario "C. Ruini"*, Massa Lombarda (RA) Ambulatorio Veterinario "Squarzoni - Tazzari"**, Molinella (BO) In uno yorkshire terrier di 7 mesi il canino inferiore destro si presentava spostato mesialmente e lingualmente, tanto da provocare i seguenti problemi ortodontici: a) uno spostamento in senso vestibolare del 3° incisivo superiore destro, con il quale il canino in questione entrava in precontatto; b) uno spostamento in senso vestibolare anche del 2° e del 3° incisivo inferiore destro, per un problema di base stretta; c) una incompleta estrusione del canino stesso; d) asimmetria del morso. Lo scopo del lavoro è stato di riposizionare il canino in maniera corretta, con metodi ortodontici, sia per evitare disagi all'animale (dorore, parodontiti) sia per renderlo valido dal punto di vista espositivo. Il lavoro è stato pianificato in due interventi ortodontici separati: dapprima è stato costruito un piano inclinato in resina epossidica, adeguatamente ancorato alla linea degli incisi superiori sfruttandone il sottosquadro, allo scopo di deviare il dente lateralmente facendogli perdere il precontatto con l'incisivo superiore; questo impianto è stato lasciato in situ per 3 settimane. Di seguito, previa rimozione dell'apparecchio in resina, sono stati posti 2 brackets, precisamente uno sulla faccia linguale del primo molare inferiore destro e l'altro sulla superficie mesiale-laterale del canino da corregere; tra i 2 brackets è stato teso un elastico che esercitava una moderata trazione in senso distale e leggermente laterale del canino. Tale elastico passando a ponte sull'emiarcata mandibolare inferiore non veniva comunque interessato dall'occlusione, date le piccole dimensioni degli elementi dentali e la loro disposizione spaziale. Dopo 4 settimane il dente aveva raggiunto una posizione pressochè perfetta, quindi è stato rimosso l'elastico ma sono stati lasciati in situ i brackets per altre 2 settimane circa in modo da poter intervenire in caso di recidive, che non si sono comunque verificate poichè il dente, una volta raggiunta la sua sede normale, veniva mantenuto in posizione dall'occlusione stessa. I brackets sono quindi stati rimossi e i due denti su cui erano ancorati sono stati lucidati. Gli altri denti interessati si sono posizionati naturalmente ed armonicamente non essendo più compressi dal canino mal posizionato: si è quindi raggiunta un'occlusione ottimale dal punto di vista estetico e funzionale, con costi e tempi modesti e con sole 3 sedazioni dell'animale. Come unico effetto collaterale, assolutamente trascurabile, si è notato un leggerissimo spostamento mesiale del molare inferiore utilizzato come base di ancoraggio, data la non elevata differenza tra le superfici radicolari dei due denti utilizzati.

COLORAZIONE RAPIDA CON CRISTAL VIOLETTO PER L’IDENTIFICAZIONE DEI LIEVITI NELLA CITOLOGIA APPLICATA ALLA DERMATOLOGIA Cornegliani Luisa* Med. Vet., Vercelli Antonella** Med. Vet. Libero professionista, Milano* Ambulatorio Veterinario Associato, Torino** L’esame citologico in dermatologia Veterinaria è una metodica di laboratorio di pratico impiego e di costi contenuti. Le colorazioni rapide maggiormente utilizzate sono Diff-quick ed Hemacolor. Lo scopo del lavoro è quello di presentare una nuova metodica rapida di colorazione per evidenziare i lieviti e in particolare la Malassezia spp. Tale metodica verrà applicata alla citologia auricolare.

Materiali e metodi. La campionatura è stata effettuata su una popolazione animale costituita da 20 cani atopici con otiti ricorrenti e 10 gatti affetti da otoacariasi. Tutti i soggetti presentavano un’otite eritematoso ceruminosa. In ogni animale è stato prelevato il cerume auricolare tramite bastoncini cotonati ed applicata metodica seguente. Eseguiti uno o più prelievi tramite bastoncini cotonati, si striscia su vetrino il materiale raccolto e si lascia asciugare il campione all’aria; il tempo di tale operazione varia in rapporto alla qualità e alla quantità di materiale raccolto. Si procede nella metodica aggiungendo sul vetrino portaoggetti 200 microlitri di cristal violetto (primo colorante per la colorazione di Gram) per coprire tutta la superficie contenente il materiale citologico. Si riscalda, tramite fiamma, la parte inferiore del vetrino fino a causare l’ebollizione del colorante. Infine si sciacqua con soluzione tamponata e si lascia asciugare il preparato. Per valutare l’efficacia di tale colorazione sono stati allestiti da ciascun prelievo 2 vetrini portaoggetto colorati rispettivamente con Hemacolor e cristal violetto. Sono stati presi in considerazione 10 campi a 100X ed eseguito il calcolo della media.

Risultati. I lieviti presenti assumono una colorazione intensamente blu e risultano di facile identificazione anche a ingrandimento microscopico 40X. Le medie dei lieviti ottenute dalla comparazione dei due diversi preparati hanno riportato risultati sovrapponibili per ciascun campione.

Conclusioni. La metodica risulta sicura per l’identificazione dei lieviti, facilitata dall’intensa colorazione blu che essi assumono. Inoltre la rapidità di esecuzione dimezza i tempi normalmente necessari per le colorazioni rapide. La necessità di porre direttamente il colorante sul vetrino permette di eliminare la possibilità di contaminazione dei coloranti e la conseguente scarsa durata che ne deriva.

Bibliografia. Quinn P.J. et al: Reagents and Stains. In Clinical Veterinary Microbiology, Wolfe ed. 1998, 615619.

Woods and Walker: Stains for detection of fungi. Clin. Microbiol. Rev. Vol 6, 1996, 396-397.

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SU UN CASO DI RABDOMIOSARCOMA DEL MIOCARDIO IN UN CANE Gabellini Giovanni* Med. Vet., Gabbanini Jean-Pierre** Med. Vet., Notari Donatella*** Med Vet Istituti di appartenenza: Centro Veterinari Associati*, Riccione, Italia Libero professionista**, Pesaro, Italia Libero professionista***, Pesaro, Italia Introduzione. Scopo del lavoro è descrivere un caso di Rabdomiosarcoma del miocardio nel cane.

“Black”, un cane Siberian Husky, maschio intero, di anni 5, ci è stato presentato alla visita perché presentava da alcuni giorni un quadro clinico caratterizzato da dispnea, anoressia e stato di estrema debolezza. All’esame fisico il cane si presentava estremamente letargico ed dimagrito. Erano presenti dispnea e chiari segni di shock cardiocircolatorio, oltre ad ascite e notevole attenuazione dei toni cardiaci. Visto il segnalamento del paziente, l’anamnesi e i segni clinici, fu emesso un sospetto diagnostico di versamento pericardico con conseguente tamponamento cardiaco, insufficienza cardiaca destra e collasso cardio-circolatorio.

Di conseguenza furono eseguiti un esame radiografico del torace, un profilo di laboratorio urgente e un esame ecocardiografico. Il profilo di laboratorio non mostrò particolari alterazioni tranne un aumento moderato della fosfatasi alcalina, imputabile con ogni probabilità alla insufficienza cardiaca destra e conseguente fegato da stasi, e una azotemia pre-renale, a causa del grave shock ipotensivo. L’esame radiografico mostrò una moderata cardiomegalia, tuttavia mancava l’aspetto radiografico tipico del versamento pericardico. All’esame ecocardiografico fu rilevata una massa iperecogena con aree ipoecogene partente dal setto interventricolare e invadente parte dell’atrio e ventricoli sinistri, ma completamente invadente l’atrio destro, provocando una completa ostruzione del tratto di afflusso; era inoltre presente versamento pleurico. Vista la normale casistica nella specie canina, le principali diagnosi differenziali erano l’emangiosarcoma e il chemodectoma. Tuttavia ritenevamo presenti alcuni elementi atipici; l’Emangiosarcoma è costantemente associato a versamento pericardico e l’interessamento del setto interventricolare è molto raro, mentre per ciò che riguarda il chemodectoma, non deponevano a suo favore la razza (essendo molto più comunemente osservabile nelle razze brachicefale) ne l’interessamento del setto interventricolare (anche se in casi avanzati questa neoplasia partente dalla base del cuore, tra radice aortica e insorgenza della polmonare, può arrivare ad invadere le cavità cardiache); inoltre è anch’essa, anche se non costantemente, associata a versamento pericardico. Furono prese dunque in considerazione anche altre neoplasie cardiache, anche se più rare. Dopo alcuni giorni il paziente, visto l’ulteriore aggravarsi delle condizioni cliniche, e la prognosi infausta, fu sottoposto ad eutanasia. L’esame autoptico confermo l’aspetto ecocardiografico, evidenziando una grossa massa invadente completamente l’atrio destro e la vena cava craniale; erano presenti anche versamento pleurico e noduli diffusi a livello polmonare.

Conclusione. L’esame istologico ha permesso di identificare un rabdomiosarcoma del miocardio con metastasi polmonari, una neoplasia segnalata raramente in campo umano ed ancor più raramente nel cane.

UN CASO DI LEUCEMIA LINFOCITICA CRONICA (A GRANDI LINFOCITI GRANULARI) IN UN CANE BOXER Ghibaudo Giovanni*, Guglielmino Roberta**, Santilli Roberto*, Miniscalco Barbara** * Clinica Veterinaria Malpensa via Verdi, 49 - Samarate (Va) ** Dipartimento di Patologia Animale, Facoltà di Veterinaria Università degli Studi via Nizza, 52 - 10126 Torino Un cane boxer femmina di nove anni è sottoposto alla visita clinica per la presenza d’anoressia e un aumento del profilo addominale. All’esame obiettivo generale si rileva la presenza di una lieve ipertermia e pallore delle mucose. Vengono eseguiti degli esami ematologici: il profilo biochimico e coagulativo risultano essere nella norma mentre l’esame emocromocitometrico evidenzia un’anemia macrocitica normocromica moderatamente rigenerativa e un’imponente leucocitosi (370000/µl) con netta prevalenza di cellule mononucleate. Morfologicamente queste risultano essere cellule linfoidi di dimensioni medio-grandi, con nucleo talvolta inciso o reniforme e cromatina addensata; citoplasma abbondante contenente granulazioni azzurrofile. Si effettua anche un esame ecografico addominale grazie al quale si riscontra una epato-splenomegalia con riduzione dell’ecogenicità ed ecostruttura omogenea. Nella stessa sede si procede ad un esame citologico per ago infissione eco guidato del parenchima splenico. Il quadro citologico descrive la presenza di una popolazione omogenea di cellule rotonde con caratteristiche sovrapponibili a quelle presenti nelle cellule linfoidi dello striscio ematico. Si procede all’esame citofluorimetrico per l’identificazione della popolazione leucocitaria neoplastica interessata. Viene emessa la diagnosi di leucemia a grandi linfociti granulari T suppressor / citotossici CD5+, CD3+, CD8+. L’animale è sottoposto ad una chemioterapia a base di vincristina, clorambucile e prednisolone. Dopo un mese dall’inizio della terapia i sintomi scompaiono e il numero dei leucociti scende fino a 169000/µl. Dopo otto mesi le condizioni cliniche del cane rimangono buone e i parametri ematologici costanti (145000/µl). La prognosi è riservata finché si mantiene in equilibrio, diventa infausta se la forma linfocitica cronica si trasforma in linfoma linfoblastico acuto.

Nei disordini mielo e linfoproliferativi l’utilizzo d’esami quali l’ecografia, la citologia e soprattutto la citofluorimetria ha permesso di arrivare ad emettere diagnosi sempre più precoci e precise.

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TECNICA DI STABILIZZAZIONE TRANSARTICOLARE INIZIALE NELLE FRATTURE/LUSSAZIONI DELLA COLONNA TORACO-LOMBARE E LOMBO-SACRALE. ESPERIENZE PERSONALI SU 5 CASI Gilardini Raffaele DVM, Beghelli Annalisa DVM Clinica Veterinaria “Città di Voghera”- Via Cappelletta 2- 27058 Voghera Questo lavoro descrive l’utilizzo di chiodi di Kirschner transarticolari per la fissazione iniziale delle vertebre in caso di fratture /lussazioni della colonna toraco/lombare e lombosacrale in cinque soggetti.

Sono stati trattati quattro cani ed un gatto con fratture della colonna lombo-sacrale dovuta ad un trauma.

L’intervento fu eseguito in decubito sternale mediante accesso routinario con scollamento e dissezione della muscolatura epiassiale fino ad evidenziare i processi articolari integri. In tutti i soggetti venne eseguita la riduzione manuale delle vertebre, l’allineamento dei processi articolari ed un chiodo di Kirschner di diametro variabile da 1 a 1,5 mm venne inserito in ogni processo articolare con direzione da mediale a latero-ventrale. I soggetti furono poi trattati con mezzi di fissazione definitivi utilizzati normalmente (viti e chiodi nei corpi vertebrali e polimetilmetacrilato, chiodo di Kirschner a U alla base dei processi spinosi, fissatore esterno).

Tutti i soggetti ripresero la deambulazione in tempi variabili da un giorno a due mesi. Due soggetti dopo nove mesi dall’intervento riportavano ancora deficit neurologici di media entità. Un mese dopo l’intervento due soggetti presentavano dolore alla palpazione della colonna lombo-sacrale, nessuno presentava ancora dolore dopo due mesi.

Nei casi trattati la tecnica descritta si è dimostrata di grande ausilio nell’allineamento e nella stabilizzazione iniziale delle vertebre. Il mantenimento della riduzione riduce il rischio di danni iatrogeni durante le ripetute manovre di allineamento ed il posizionamento degli altri impianti. La tecnica contribuisce in modo decisivo al buon posizionamento degli altri impianti (polimetilmetacrilato, placche, chiodi ad U, fissatori esterni) e fornisce inoltre una stabilizzazione aggiuntiva.

CASO DI PROTOTHECOSI INTESTINALE IN UN BOXER Maggio Federica Med. Vet., Pizzirani Stefano Med. Vet. DECVS Clinica Veterinaria Europa - Viale Europa 64 - 50126 Firenze Un cane Boxer, femmina, di anni 1, di circa 26 kg di peso, veniva presentato per diarrea emorragica mucoide presente da circa due mesi, con tenesmo ed aumento della frequenza delle defecazioni. L’appetito era conservato. Al momento della nostra valutazione clinica il soggetto aveva già ricevuto precedenti trattamenti sintomatici per diarrea e metronidazolo seguito da corticosteroidi per circa 5 giorni, senza alcun miglioramento. Gli unici accertamenti eseguiti consistevano nel dosaggio del TLI sierico, con esito nella norma. Alla visita la cagna si presentava in ottimo stato di nutrizione, con atteggiamento vigile e vivace. Non si rilevava alcuna anomalia all’esame fisico. L’esame delle feci, eseguito a fresco e per flottazione su 3 campioni nelle 48 ore, dava esito negativo. Venivano eseguiti esami ematologici (emocromo, biochimico, elettroforetico e coagulativo) ed esame delle urine. In attesa del risultato, al soggetto veniva somministrato per os un prodotto antielmintico ad ampio spettro, comprendente febantel, pirantel embonato e praziquantel, e metronidazolo alla dose di 20 mg/kg BID per os. Gli esami di laboratorio risultavano nella norma. Dall’anamnesi e dalla descrizione dei sintomi, data l’assenza accertata di parassiti e di alterazioni clinico-patologiche, veniva formulata l’ipotesi di colite cronica, linfoplasmacellulare od istiocitaria del Boxer. Vista quindi la persistenza del sintomo nonostante i trattamenti, veniva proposta l’esecuzione di una endoscopia con biopsia del colon. La colonoscopia metteva in evidenza numerose e diffuse aree circoscritte di iperemia ed erosione della mucosa in tutto il tratto esaminato, da cui venivano ottenuti 5 reperti bioptici. Nel rapporto anatomo-patologico veniva descritta la presenza di numerosi linfociti e plasmacellule, con alcuni eosinofili, macrofagi ed istiociti nella mucosa colonica, preannunciando una diagnosi di colite istiocitaria, ma una successiva colorazione PAS evidenziava la presenza diffusa nella stessa sede di organismi con caratteristiche morfologiche ascrivibili a Prototheca sp.. Data la potenziale invasività dell’alga a tutto l’organismo (rene, fegato, occhio) con infezioni sistemiche refrattarie ai trattamenti, si è provveduto ad instaurare una terapia aggressiva a base di itraconazolo alla dose di 10 mg/kg PO SID, amfotericina B 0.5 mg/kg IV ogni 48 ore per 12 volte e doxiciclina 10 mg/kg PO SID. Al momento in cui l’autore riferisce, il soggetto ha iniziato da poco il trattamento.

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ASPETTI RADIOGRAFICI E FLUOROSCOPICI IN DUE CASI DI EMIPARESI DIAFRAMMATICA NEL GATTO Vignoli Massimo DMV SRV*, Manzini Marina** DMV SRV, Terragni Rossella DMV*, Rossi Federica DMV SRV* * Ambulatorio Veterinario Dell’Orologio, Sasso Marconi (BO) ** Ambulatorio Veterinario, Bastiglia (MO) Introduzione: sono stati riferiti alle nostre strutture 2 gatti europei, uno maschio di anni 6 ed una femmina di anni 3, entrambi sterilizzati.

Esame clinico: entrambi presentavano segni clinici di trauma al collo e alla spalla, con lesioni cutanee e zoppia all’arto anteriore destro. Era presente in entrambi respiro discordante.

Esame radiografico: i due gatti sono stati a sottoposti ad esame radiografico del torace in proiezione V-D e L-L in inspirazione ed espirazione. In proiezione L-L si poteva rilevare nei due gatti che il pilastro destro del diaframma era particolarmente distante dal sinistro. Inoltre era evidente una frattura della scapola in entrambi. In proiezione V-D era evidente una netta asimmetria dei due pilastri del diaframma. Nella femmina si poteva notare anche pneumoderma a carico dell’emitorace destro. L’assunzione del radiogramma in espirazione permetteva di rilevare una diminuzione dell’asimmetria a livello dei pilastri del diaframma. Sono stati effettuati radiogrammi di controllo nei giorni successivi.

Indagine fluoroscopica: il gatto femmina è stato sottoposto dopo 4 giorni dal trauma ad indagine fluoroscopica per confermare l’ipotesi diagnostica di emiparesi diaframmatica. L’indagine permetteva di rilevare la contrazione del pilastro diaframmatico sinistro, mentre il destro si presentava poco mobile.

Trattamento: metilprednisolone sodio succinato 30 mg/kg e.v. e fluidoterapia. Nei giorni successivi si è ridotta la dose di corticosteroidi ad 1 mg/kg e cefazolina20 mg/kg Bid s.c. per 7 giorni.

Follow up: entrambi i gatti hanno mostrato un miglioramento della sintomatologia dopo 4-5 giorni. Ad un mese di distanza la sintomatologia era completamente regredita.

Discussione: le radici del nervo frenico emergono tra C5-C7 e decorrono in una plica del mediastino in vicinanza delle teste delle coste dirigendosi alla parte diaframmatica omolaterale. È ipotizzabile che un trauma della colonna vertebrale cervicale e dell’area cervico-toracica possa provocare una paralisi momentanea del nervo e di conseguenza del muscolo da esso innervato.

La diagnosi radiografica di emiparesi diaframmatica viene confermata dalla fluoroscopia.

Bibliografia: Suter & Lord: Thoracic Radiography - Thoracic Diseases of the dog and cat. (1984).

Bortolami R., Callegari E., Beghelli V.: Anatomia e fisiologia degli animali domenstici.

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COMPARAZIONE CITO-ISTOMORFOLOGICA IN LESIONI NODULARI CUTANEE BENIGNE DEL CANE E DEL GATTO Militerno G., Preziosi R., Bettini G. Dipartimento di Sanità Pubblica Veterinaria e Patologia Animale - Sezione di Patologia Generale e Anatomia Patologica Facoltà di Medicina Veterinaria di Bologna In veterinaria, negli ultimi 10 anni, la diagnosi precoce effettuata con metodiche ago-aspirative su lesioni d’organo “occupanti spazio”, come le lesioni nodulari/palpabili cutanee, è progressivamente diventata strumento fondamentale per instaurare un adeguato protocollo chirurgico-terapeutico antineoplastico. È noto che la citologia è efficace per discriminare tra lesioni infiammatorie e neoplastiche e, fra queste ultime, fra neoplasie benigne e maligne. Nella letteratura più recente sulla citopatologia delle lesioni cutanee viene data maggior enfasi descrittiva alle caratteristiche citomorfologiche dei tumori maligni. Sulla base di tali considerazioni, abbiamo condotto uno studio comparativo cito-istomorfologico su una casistica di 29 biopsie ago-aspirate di neoformazioni cutanee di 26 cani e 3 gatti, esaminate nell’arco di un semestre presso i laboratori della Sezione di Patologia Generale e Anatomia Patologica Veterinaria di Bologna. Da tutti i casi erano emerse diagnosi citologiche di lesione nodulare su base flogistica o di neoplasia benigna e per tutti si era reso disponibile, in un secondo momento, il relativo tessuto asportato chirurgicamente. Il materiale prelevato per la citologia è stato strisciato su vetrino e colorato con metodo di May Grünwald-Giemsa, mentre il tessuto asportato è stato processato per l’esame istologico. In Tabella sono riportati i risultati delle diagnosi. Le neoformazioni simil-tumorali (cisti) ed i tumori cutanei benigni (lipoma, melanoma, istiocitoma, fibroadenoma, emangioma, adenoma perianale) sono apparsi tutti di facile identificazione citologica. L’esame istologico ha confermato in tutti i casi la diagnosi citologica di cisti o di neoplasia benigna, evidenziando però, a volte, quadri strutturali più precisi: per i melanomi, la localizzazione dermica o dermo-epidermica, o la compresenza di aree a diversa differenziazione; per l’emangioma, l’aspetto cavernoso; per gli adenomi perianali, la presenza di aree con iniziali aspetti di malignità cellulare. Quattro adenomi sebacei sono risultati istologicamente come displasie degli annessi, in tre casi, o come epitelioma in un altro; tutti i quadri infiammatori sono stati valutati nella loro estensione tessutale (dermatite piogranulomatosa profonda, pannicolite settale), riconoscendo a volte la causa flogogena (kerion, foruncolosi). La concordanza tra le due tecniche è risultata quindi soddisfacente, infatti la citologia ha permesso di identificare come benigne tutte le lesioni, neoplastiche e non, diagnosticate come benigne al successivo esame istologico. Il principale vantaggio del riconoscimento di neoformazioni benigne grazie alla citologia preoperatoria è stato il minor traumatismo chirurgico sul paziente per l’escissione meno aggressiva del tessuto neoformato. Riteniamo che la citologia ago-aspirativa sia una metodica diagnostica rapida, poco invasiva, economica per giudicare come benigne alcune lesioni nodulari cutanee, purchè il prelievo sia effettuato in più punti e direzioni, mai trascurando che l’esame istologico post-operatorio è l’unico in grado di confermare la prima diagnosi benigna, di definire l’architettura del tessuto e l’esatta natura dell’alterazione in esso esistente, di svelare con maggior sicurezza la presenza di piccoli focolai cellulari maligni, a volte difficilmente campionabili con l’ausilio di un ago.

Tabella - Diagnosi citologica ed istologica su 29 lesioni nodulari cutaneee benigne di cani e gatti DIAGNOSI CITOLOGICA

DIAGNOSI ISTOLOGICA

SPECIE

Adenoma delle ghiandole sebacee ” ” Adenoma delle ghiandole perianali Emangioma Fibroadenoma mammario Istiocitoma cutaneo Lipoma Melanoma benigno Cisti cheratinica Pannicolite Pannicolite Dermatite piogranulomatosa Dermatite piogranulomatosa Dermatite piogranulomatosa Dermatite piogranulomatosa Dermatite nodulare cronica Dermatite nodulare cronica

Displasia focale degli annessi Displasia focale degli annessi, foruncolosi Epitelioma sebaceo Adenoma delle ghiandole perianali Emangioma cavernoso Fibroadenoma mammario Istiocitoma cutaneo benigno Lipoma Melanoma dermico benigno Cisti cheratinica Pannicolite settale Pannicolite settale Ascesso sottocutaneo Dermatite piogranulomatosa profonda Kerion Foruncolosi Dermatite perivascolare linfoplasmacellulare Dermatite nodulare cronica

Gatto Cane Cane Cane Cane Gatto Cane Cane Cane Cane Cane Gatto Cane Cane Cane Cane Cane Cane

N. CASI 1 2 1 2 2 1 1 3 4 2 1 1 1 2 1 2 1 1

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L’UNITÀ MTL (MIO-TENDINEO-LEGAMENTOSA) NELL’ARTROSI DEL CANE IN CRESCITA Miolo Alda CeDIS Innovet Italia S.r.l.

L’artrosi o malattia degenerativa articolare (MDA) del cane in crescita si configura come una patologia plurifattoriale, al cui sviluppo concorrono numerose condizioni parafisiologiche e patologiche. Tra i fattori parafisiologici, oltre a temperamento, morfotipo e abitudini dietetiche dell’animale, si devono considerare: 1) razza: cani di taglia grande-gigante sono più suscettibili a sviluppare MDA rispetto ai cani di taglia medio-piccola, principalmente a causa del divario di maturazione tra tessuti osteocartilagineo e muscolo-legamentoso all’epoca dello svezzamento; 2) attività fisica: l’ipersollecitazione meccanica (stretching muscolare e legamentoso) cui vengono sottoposti i distretti articolari, e le conseguenti alterazioni metaboliche ed ossidative dei tessuti sono chiamate in causa nelle degenerazioni articolari di cani giovani impegnati in attività agonistiche. I fattori patologici predisponenti a MDA comprendono l’eterogeneo gruppo di manifestazioni cliniche recentemente identificate con l’acronimo DOD (Developmental Orthopaedic Disease), a cui afferiscono le artropatie dello sviluppo dei diversi distretti (anca, spalla, gomito, carpo, ginocchio, piede). È stato dimostrato che nell’eziologia dell’MDA del cane in crescita entrano in gioco alterazioni delle strutture di contenimento periarticolare. Si tratta cioè di muscoli, tendini e legamenti, organizzati funzionalmente in un’unica entità preposta alla stabilità dell’articolazione: l’unità mio-tendineo-legamentosa (MTL). Lassità legamentose e/o atrofie muscolari contribuiscono dunque significativamente all’avvio dei fenomeni degenerativi e, come tali, devono essere opportunamente valutate nei protocolli diagnostici per la MDA del cane in crescita. Sulla base di questi presupposti, emerge chiaramente la necessità di considerare nel management preventivo-terapeutico dell’artrosi secondaria a malattie ortopediche dello sviluppo anche il ripristino funzionale dell’unità MTL, condizione indispensabile per ristabilire l’equilibrio biomeccanico dell’articolazione in crescita, e controllarne il “rischio degenerativo”. In sostanza, un altro tassello si aggiunge all’approccio eziologico all’MDA, in cui le metodiche atte a proteggere la cartilagine articolare (Condroprotezione) vengono così supportate da altre, specificatamente deputate al recupero ed alla protezione dell’unità MTL (Condroprotezione MTL).

Bibliografia essenziale: Alexander JW., 1992, Vet. Clin. North Am., 22(3): 503-511; Lust G. et al., 1993, Am.J.Vet.Res., 54: 1990-1999; Mortellaro CM et al., 1999, Veterinaria, 1(Suppl.): 1-40; Grandjean D., Paragon BM, 1996, Rec.Med.Vet., 172: 519530; Fluckiger MA et al., 1998, Zentralbl.VeterinarMed.A, 45(5): 199-207; Langenbach A. et al., 1998, J.A.V.M.A., 213(10): 1439-1443; Smith GK et al., 1995, J.A.V.M.A., 206(5): 642-647; Smith GK et al., 1993, Am.J.Vet.Res., 54: 1021-1042; Kealy RD et al., 1993, Am.J.Vet.Res., 54: 555-562; Burton-Wurster N. et al., 1999, Ost. Cart., 7: 486-497; Richardson DC, Zentek J., 1998, Vet.Clin.North.Am., 28: 115-135.

SU TRE CASI RIBELLI DI DERMATITE ATOPICA NEL CANE TRATTATI CON TERAPIE OMEOPATICHE Orsi Roberto, Med. Vet. Veterinario, Specialista in Malattie dei Piccoli Animali - Clinica Veterinaria “Valla dei Fiori” - Pescia (PT) Tre cani di razza Bouledogue Francese affetti da dermatite atopica sono stati sottoposti per volere dei proprietari a terapia omeopatica come ultima risorsa terapeutica a causa del perdurare del loro grave stato clinico. Il soggetto n°1 (propr. Sig. D., Montecatini T.), femmina di 4 anni, presentava dall’età di 7 mesi eritema, edema e prurito prevalentemente a carico di muso ed arti, alopecia, forfora e pustole da follicolite a carico di torace ed addome. Erano stati eseguiti test intradermici (sensibilità ad acari polvere, muffe, derivati epidermici umani e felini, lana), vaccini iposensibilizzanti oltre che numerosi trattamenti con antibiotici e/o cortisonici e shampoo medicali, con alterni e modesti risultati. Il soggetto n°2 (propr. sig.ra R., Modena), maschio di 3 anni e mezzo, aveva sintomi cutanei dall’età di un anno, localizzati prevalentemente al muso, alle palpebre ed ai piedi, con prurito, eritema e gonfiore. Il test intradermico indicava sensibilità agli acari della polvere, a muffe ed alla lana. I trattamenti prolungati con antibiotici e cortisonici, oltre che i vaccini iposensibilizzanti, avevano apportato scarsissimi risultati e momentanei.

Il soggetto n°3 (propr. sig.ra R., Modena), femmina di 3 anni e mezzo sorella del soggetto n°2, presentava anch’essa dall’età di un anno lesioni a muso e piedi con intenso prurito, sensibilità ad acari polvere e muffe ed anch’essa era stata sottoposta a prolungate terapie corticosteroidee ed a vaccino iposensibilizzante, con scarsi risultati. La visite omeopatiche del soggetto n°1 (dic. 94), del n°2 (dic. 98) e del n°3 (giu. 99), eseguite con la tecnica repertoriale classica, permettevano di arrivare ad una diagnosi di rimedio. Nel primo caso fu somministrato Pulsatilla 200 CH, nel secondo Causticum 1000 CH, nel terzo Aurum 200 CH, ripetuti in seguito “in plus” oppure a più alta potenza. In certi casi sono stati adoperati anche rimedi ad azione intercorrente e drenante. Nel soggetto n°1 la guarigione completa si è avuta dopo circa tre mesi, dopo aggravamenti sintomatologici e ricomparsa di sintomi presenti nella storia patobiografica del soggetto, conformemente alle leggi dell’Omeopatia. A tuttoggi il soggetto non presenta sintomi cutanei salvo sporadici episodi di blefarite e cheratite ulcerativa. Il soggetto n°2 è guarito nell’arco di due mesi, salvo poi presentare alcuni episodi di pododermatite e di blefarite con cheratite ulcerativa risolti anch’essi con terapie omeopatiche. Il soggetto n°3 è guarito nel circa di un mese e, sempre in conformità delle regole della guarigione omeopatica, ha evidenziato anche un netto miglioramento della sua sfera psichica tale da superare alcuni disturbi comportamentali (ansietà generalizzata, ringhio continuo).

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TRIPLICE OSTEOTOMIA PELVICA: CONFRONTO TRA L’OSTEOTOMIA ILIACA SECONDO SLOCUM ED UN’OSTEOTOMIA ILIACA CAUDALE Peirone Bruno Med Vet, Valazza Alberto Med Vet, Ciliberto Emanuela Med Vet Dipartimento di Patologia Animale, Facoltà di Medicina Veterinaria di Torino, Italia In nove soggetti sottoposti a triplice osteotomia pelvica (gruppo A) abbiamo apportato le seguenti modifiche rispetto alla tecnica di Slocum (Slocum B., Devine T., J.A.A.H.A. 22: 331-338, 1986): 1) scollamento dei muscoli gluteo medio e profondo limitato all’angolo ventrale dell’ala iliaca; 2) scollamento limitato del muscolo iliaco dal bordo ventrale del corpo dell’ileo senza successiva palpazione digitale dell’articolazione sacro-iliaca; 3) identificazione sul margine ventrale del corpo dell’ileo della tuberosità per l’inserzione del muscolo retto femorale; 4) posizionamento della placca appena cranialmente all’inserzione del m. retto femorale e conseguente definizione della linea di osteotomia corrispondente al piano di rotazione della placca. Come gruppo di controllo (gruppo B) abbiamo utilizzato 16 soggetti precedentemente trattati con la tecnica di Slocum, con osteotomia iliaca eseguita appena caudalmente all’articolazione sacro-iliaca. Nel controllo post-operatorio eseguito a 6-8 settimane abbiamo considerato i seguenti parametri: congruenza articolare, aspetto e dimensioni del callo a livello di osteotomia iliaca, eventuale mobilizzazione dei mezzi di sintesi e conseguente dislocazione del segmento acetabolare. In tutti i soggetti dei due gruppi si osservava l’aumento della copertura acetabolare della testa femorale. Il confronto tra i gruppi rilevava una percentuale sovrapponibile di mobilizzazione delle viti (gruppo A: 66,7%; gruppo B: 68,75%). Nonostante l’elevata incidenza di tale complicanza minore, nella maggior parte dei casi è stata osservata la regolare guarigione delle osteotomie, ad eccezione di 3 cani (gruppo B) nei quali si è sviluppato un callo ipertrofico. Un lieve grado di dislocazione del segmento acetabolare (sovrapposizione ≤ 5 mm dei segmenti a livello dell’osteotomia di ischio nella proiezione VD) è stato rilevato con frequenza doppia nel gruppo A (75% vs 31%), mentre una marcata dislocazione (> 5 mm di sovrapposizione dei segmenti) è stata osservata prevalentemente nel gruppo B (25% vs 12,5%). A nostro parere, un minimo grado di dislocazione è da ritenersi normale e legato all’azione del legamento sacro-tuberoso, che rimane in tensione. Al contrario, la marcata dislocazione è stata associata prevalentemente ad allentamento di due o più viti, nel segmento craniale od in quello acetabolare. Quattro dei cinque soggetti affetti da dislocazione di maggiore entità superavano i 40 kg di peso. In conclusione, la variante tecnica proposta semplifica l’accesso chirurgico all’ileo e la definizione della linea di osteotomia, ma non risolve il problema della mobilizzazione delle viti.

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METODO DI CONTROLLO DELLE CURVE DI ACCRESCIMENTO (CCA) NEI CANI DI TAGLIA GROSSA E GIGANTE Petazzoni Massimo*; Mortellaro Carlo Maria** * Medico Veterinario Libero Professionista, via Lanzano 33, 26837 Mulazzano (Lo) Italia ** Medico Veterinario, Istituto di Clinica Chirurgica e Radiologia Veterinaria, Facoltà di Medicina Veterinaria Università degli Studi di Milano, Via Celoria, 10 - 20133 (Mi) Italia Introduzione: Nel cane giovane lo scheletro matura in modo rapido e questa maturazione è la risultante di interazioni genetiche, ambientali e nutrizionali. Alcune patologie scheletriche del cucciolo quali displasia dell’anca ed osteocondrosi annoverano fra le diverse cause di malattia la componente nutrizionale. Un rapido accrescimento può portare ad uno sviluppo asincrono tra i vari segmenti scheletrici o tra i segmenti scheletrici e la componente mio-teno-legamentosa e contribuire quindi allo sviluppo di displasie osteoarticolari. Numerose variabili quali livello di attività fisica, attitudine e temperatura ambientale, influenzano notevolmente i fabbisogni nutritivi. La gestione del periodo dell’accrescimento mediante tabelle preconfezionate, indicanti il quantitativo di cibo da somministrare giornalmente, può risultare inadeguato e portare il cane ad eccessi nutrizionali poiché la razione viene generalmente calcolata esclusivamente in relazione all’età ed al peso del cucciolo.

Obiettivo: Gli Autori propongono un metodo per il Controllo delle Curve di Accrescimento (CCA) che può essere impiegato per la prevenzione degli eccessi nutrizionali nel cucciolo.

Materiali e metodi: 40 cuccioli di Golden Retriever e 10 di Bovaro del Bernese, sono stati arruolati per il presente studio.

Il CCA è iniziato all’età dello svezzamento continuando fino all’età di 12 mesi. Il controllo della crescita veniva effettuato ogni 7 giorni con la comunicazione, da parte dei proprietari, del peso del cane via e-mail o tramite messaggio GSM. È stato impiegato un unico cibo preconfezionato secco (Hill’s Growth Larger Breed) ed i proprietari si sono impegnati a non apportare qualsivoglia integrazione. Per Il calcolo del fabbisogno di Energia Metabolizzabile in Kcal/gg è stata impiegata la seguente formula E(Kcal)=((30*Kg)+70)*X*Y dove X rappresenta la variabile per l’accrescimento e Y il coefficiente che considera la temperatura ambientale esterna. Il calcolo dei fabbisogni energetici veniva considerato solo indicativo ed un incremento ponderale medio giornaliero di 100 gr per il Golden e di 150 gr per il Bernese venivano impostati come obiettivo. Tutti i calcoli sono stati effettuati in automatico con l’ausilio del foglio elettronico Excel di Microsoft.

Risultati e discussione: Il metodo CCA ha consentito un adeguamento tempestivo delle razioni e delle curve di crescita.

Inoltre, il metodo proposto è risultato essere agevole ed economico, pur prevedendo l’ausilio di mezzi telematici ed informatici. Nonostante il numero dei soggetti considerati sia ancora limitato e la verifica dell’utilità di tale sistema richieda tempi più lunghi nonché controlli clinico-radiografici specifici, il CCA ha consentito di correggere tempestivamente incrementi ponderali eccessivi e potenzialmente pericolosi per lo sviluppo delle patologie ortopediche richiamate.

Conclusione: L’ereditabilità della displasia dell’anca nel cane risulta oggi essere fra il 20 e il 50%. Il rimanente 50-80% della manifestazione di questo fenotipo, è di origine ambientale e la concausa ambientale maggiormente imputabile per tale patologia è da attribuire alla sovranutrizione. Per tale motivo, il controllo della displasia dell’anca basato esclusivamente sullo studio radiografico dei riproduttori ha sortito, a distanza di anni, solo parziali risultati. L’eccesso di calcio come concausa di osteocondrosi sembra ormai accertata. Pertanto il controllo dell’accrescimento, allo scopo di limitare nel cucciolo un rapido sviluppo e di conseguenza una possibile displasia osteoarticolare, può assumere un ruolo importante.

Ringraziamenti: Gli Autori desiderano ringraziare la Hill’s Pet Nutrition Italia per la collaborazione.

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L’INCHIODAMENTO CENTROMIDOLLARE BLOCCATO A CIELO CHIUSO NEL CANE: 7 CASI Rovesti Gian Luca* Dr. Med. Vet., Dipl. ECVS, Margini Andrea* Dr. Med. Vet., Bosio Alessandro** Dr. Med. Vet. Ambulatorio Veterinario Associato “M. E. Miller”*, Cavriago (RE), Italia Clinica Veterinaria “Villa Francesca”**, Seriate (BG), Italia Introduzione – L’inchiodamento centromidollare bloccato è una tecnica di recente acquisizione in chirurgia veterinaria. Le metodiche fino ad ora descritte prevedono il bloccaggio del chiodo previa esposizione del segmento osseo. Lo scopo del presente lavoro è quello di valutare retrospettivamente i risultati in 7 casi di inchiodamento a cielo chiuso nel cane.

Materiali e metodi – Sono state esaminate le cartelle cliniche dei cani trattati mediante inchiodamento centromidollare bloccato presso l’Amb. Vet. Assoc. “M. E. Miller” di Cavriago (RE), dal 1 gennaio 1996 al 31 luglio 1998. Sono stati inclusi 7 cani con fratture o pseudoartrosi trattate a cielo chiuso, applicando le seguenti metodiche: accesso chirurgico al focolaio limitato alla rimozione di mezzi di sintesi precedentemente impiantati o all’innesto di spongiosa, allineamento ottenuto mediante trazione scheletrica e filo guida, alesaggio del canale midollare con frese flessibili e inserimento delle viti di bloccaggio con accesso minimo. I cani trattati erano 6 maschi e 1 femmina, con un peso medio di 25 kg (range, da 14 a 38), e un’età media di 60 mesi (range, da 9 a 146). I segmenti trattati sono stati 1 omero, 5 femori e 1 tibia, e le patologie 5 fratture e 2 pseudoartrosi. In 4 casi erano presenti problemi accessori, rappresentati da fratture di altri segmenti (2) o persistenza di materiale di osteosintesi nel focolaio da precedenti interventi (2).

Risultati – In 6 casi il chiodo è stato posizionato in configurazione statica, e in 1 in configurazione dinamica. In 4 casi si è ottenuto il consolidamento della frattura in un tempo medio di 104 giorni (range, da 68 a 172), mentre in 1 il risultato è stato una pseudoartrosi funzionale, in 1 la pseudoartrosi ha richiesto una chirurgia con un’altra tecnica, e in 1 il cane è stato soppresso per lo sviluppo di una neoplasia nella zona di frattura. Il chiodo è stato rimosso in 3 casi dopo una media di 315 giorni dalla chirurgia (range, da 195 a 531). Un caso ha avuto complicazioni minori, rappresentate da movimenti di torsione assiale, e 4 hanno sperimentato complicazioni maggiori, rappresentate da pseudoartrosi (2), ritardato consolidamento che ha richiesto una nuova procedura chirurgica (1), e dallo sviluppo di una neoplasia (1).

Discussione – Il chiodo centromidollare è uno degli strumenti di osteosintesi più stabili dal punto di vista meccanico, in quanto l’asse di carico e l’asse del chiodo coincidono. Se a questa stabilità si coniuga una tecnica chirurgica poco lesiva della vascolarizzazione tissutale, vengono create le condizioni ottimali per la guarigione ossea. Nella nostra esperienza, il tentativo di eseguire una tecnica a cielo chiuso si è rivelato molto difficoltoso, principalmente a causa della mancanza di una strumentazione efficace appositamente realizzata per lo scopo. Soprattutto il centraggio delle viti distali ha creato notevoli difficoltà. Le complicazioni sono attribuibili alla complessità dei casi in cui la metodica è stata applicata, ma per ora la tecnica a cielo chiuso non può essere consigliata.

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UN CASO DI EMANGIOSARCOMA NEL CANE IN SEGUITO A FISSAZIONE INTERNA Rovesti Gian Luca, Dr. Med. Vet., Dipl. ECVS, Schmidt Karen, Dr. Med. Vet. Ambulatorio Veterinario Associato “M. E. Miller”, Cavriago, Reggio Emilia, Italia Introduzione - In letteratura veterinaria sono stati descritti molti casi si osteosarcoma insorti in seguito a fissazione interna.

Sembra che le condizioni predisponenti perché si sviluppi un sarcoma siano la presenza di fratture comminute delle ossa lunghe, ridotte con mezzi di sintesi interna come placche e viti o chiodi centromidollari, e un’evoluzione postoperatoria complicata. Per la nostra conoscenza della letteratura, l’insorgenza di emangiosarcoma associato a fratture trattate con fissazione interna non è stata finora descritta.

Caso clinico - Un Levriero Afgano, maschio, fulvo, di 5 anni di età. è stato presentato presso l’Ambulatorio Veterinario Associato “M. E. Miller” per una pseudoartrosi dell’omero sinistro. Il cane aveva subito una frattura 4 mesi prima, che era stata trattata con un chiodo centromidollare di Steinmann del diametro di 4 millimetri e cerchiaggi. Alla visita clinica il cane appariva in buone condizioni generali, fatta eccezione per una zoppia di 4° grado a carico dell’anteriore sinistro. L’esame radiologico evidenziava una pseudoartrosi atrofica diafisaria con segni di osteomielite cronica. Una volta esclusa la presenza di sepsi nel focolaio, si è optato per la fissazione con chiodo centromidollare bloccato e innesto di spongiosa. L’immediato periodo postoperatorio si è svolto senza complicazioni. Dopo circa. un mese dalla chirurgia ha iniziato a svilupparsi un gonfiore sulla faccia craniale dell’omero, che si è ulcerato. Il controllo effettuato successivamente presso di noi ha evidenziato un gonfiore della parte medio-distale dell’omero di notevoli dimensioni, e condizioni generali del cane critiche. Lo studio radiologico mostrava una zona osteolitica a carico del condilo omerale, e la biopsia ossea ha confermato la presenza di angioma. Esaminate le varie prospettive, la proprietaria ha deciso per l’eutanasia. L’istologico dell’arto, dei linfonodi ascellari e del polmone ha evidenziato la presenza di emangiosarcoma con metastasi polmonari miliari, e neoplasia presente anche a livello di callo osseo.

Discussione - La patogenesi dei sarcomi associati a fratture è poco chiara. Nel caso descritto, dati i tempi di sviluppo della neoplasia, riteniamo che l’ipotesi più probabile sia che l’emangiosarcoma sia stato causato dall’instabilità cronica prolungata nel focolaio di frattura. Il secondo intervento potrebbe essere stato effettuato con la neoplasia già presente, anche se non evidenziata radiologicamente. La seconda ipotesi è che si trattasse di una frattura patologica dovuta a sarcoma preesistente; non avendo avuto la possibilità di visionare le radiografie immediatamente successive alla frattura, le alterazioni radiologiche sono state interpretate come osteomielite cronica al momento della visita. La terza ipotesi, ritenuta la meno probabile, è quella di una neoplasia sviluppatasi in maniera indipendente dalla frattura e dai trattamenti eseguiti.

ESTRAZIONI DI DENTI PERMANENTI SOPRANNUMERARI, CASI CLINICI Squarzoni Paolo Med. Vet. - Libero Professionista - Molinella (Bologna) Le estrazioni dentali sono una pratica dentistica normale che viene svolta quotidianamente dai veterinari che si occupano di odontostomatologia. Le metodiche estrattive, chirurgiche e non, raramente creano difficoltà al dentista. Il veterinario può comunque trovarsi nella condizione di estrarre denti con radici curve o con anchilosi della radice oppure denti soprannumerari: soprattutto nel caso dei denti permanenti soprannumerari è necessario valutare attentamente il soggetto e decidere volta per volta cosa è meglio fare per il paziente facendo un bilancio, caso per caso, dei vantaggi e degli svantaggi. In particolare sarà necessario valutare l’animale sotto diversi aspetti: 1. Stato di salute del soggetto: Specie, razza, sesso, età, storia clinica, malattie, ecc.

2. Fattibilità del procedimento anestesiologico necessario al proseguimento delle indagini e/o alla sua risoluzione chirurgica.

3. Funzionalità del cavo orale: occlusione, attrito/abrasione dei denti, lesioni provocate ai tessuti molli, dolore ecc.

4. Aspettative del cliente e sua disponibilità economica.

5. Attuazione della procedura: anestesia, R.X., chirurgia, postoperatorio, ecc.

Vengono qui descritti alcuni casi di estrazioni di denti permanenti soprannumerari: alcuni di semplice risoluzione come l’estrazione di un primo premolare superiore e altri più complicati (estrazione di un IV premolare superiore o di canini inferiori) riferendo delle ragioni per le quali è stato attuato il procedimento e delle difficoltà tecniche incontrate. I casi clinici sono presentati con fotografie, radiografie e completi di follow-up.

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STUDIO COMPARATIVO TRA GLI ALLERGENI D.FARINAE PRODOTTI DA DUE LABORATORI PER IL TEST DI INTRADERMAOREAZIONE NEL CANE Cornegliani Luisa* MedVet, Vercelli Antonella** MedVet. Libero professionista, Milano* - Ambulatorio Veterinario Associato, Torino** Scopo del lavoro: In dermatologia veterinaria l’intradermoreazione rappresenta un metodo per identificare gli allergeni ed un criterio di conferma per l’atopia. Lo scopo del presente lavoro è di comparare l’attendibilità e la facilità di interpretazione di due estratti di D. Farinae prodotti rispettivamente da Greer (U.S.A.) e da Artu (Olanda). La necessità di confrontare i ben noti allergeni americani con quelli prodotti dalla ditta europea è legata alla maggior facilità di importazione e ai costi più contenuti di questi ultimi.

Materiali e metodi: Un gruppo di 230 cani testati fra gli anni 1997-1999, 110 di sesso femminile e 120 di sesso maschile, di età compresa tra gli 8 mesi e i 10 anni e di razze diverse, sono stati inclusi nello studio. 200 avevano un’anamnesi suggestiva di dermatite atopica, mentre 30, con patologie dermatologiche di altra natura, sono stati utilizzati come gruppo di controllo. Ogni soggetto è stato sedato con medetomidina cloridrato 20 µg/kg, tricotomizzato sull’emitorace sinistro e sottoposto ad intradermoreazione con i due kit. Tutti i soggetti sono stati testati con controllo negativo (veicolo), positivo (istamina) e D. farinae di entrambi i laboratori. Il controllo negativo, il positivo e l’allergene del D. farinae (concentrazione di 100NU/ml) sono stati iniettati alla dose di 0.05 ml. Ogni ponfo è stato misurato in millimetri; per semplificarne il calcolo statistico e la comparazione sono stati attribuiti i seguenti valori: 1+ per ponfi da 5 mm a 10 mm, 2+ per quelli da 11 mm a 15 mm, 3+ da 16 mm a 20 mm ed infine 4+ da 21 a 25 mm. Per valori superiori ai 26 mm si è utilizzato 5+. Sono stati eseguiti i calcoli statistici e comparate le curve ottenute. Gli skin tests sono risultati perfettamente sovrapponibili con una differenza costante media di 5 mm tra l’allergene Greer e quello prodotto da Artu.

Conclusioni: La lettura del test di intradermoreazione conferma che non ci sono differenze nell’attendibilità della risposta nei confronti dello stesso allergene; infatti non si sono verificate discrepanze nella positività o negatività nei confronti del D. farinae. Per altro la differenza statistica media di 5 mm nel diametro del ponfo dell’Artu rispetto a Greer può essere causa di difficile interpretazione per valori di 1+; questi ultimi in compenso non vengono considerati valori significativi per intraprendere una immunoterapia specifica.

Bibliografia: Scott DW, Miller WH, Griffin CE: Muller & Kirk’s Small Animal Dermatology, 5th edition, W.B: Saunders Company, 500-528, 1995.

Prélaud P, Guaguére E, et al.: Méthodes de diagnostic biologique en dermatologie canine. In Allergologie Clinique PMCAC, 1998.

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40° Congresso Nazionale SCIVAC

APPLICAZIONE DEL SISTEMA A SCHERMI ASIMMETRICI “InSight” NELLA RADIOGRAFIA TORACICA DEL CANE Cipone Mario, Vignoli Massimo*, Gandini Gualtiero, Pierotti Luisa** Dipartimento Clinico Veterinario - Sezione di Medicina Interna, Università degli Studi di Bologna *Ambulatorio Veterinario dell’Orologio, Sasso Marconi (BO) **Servizio di Fisica sanitaria – Policlinico S.Orsola - Malpighi Obiettivo: Valutazione della possibilità applicativa del sistema a schermi asimmetrici InSight nella radiografia toracica del cane.

Materiali e metodi: Sono stati impiegati 18 cani, di razza, sesso ed età differenti e con un peso variabile da 13 a 43 kg (media 26+/-8) clinicamente sani. Tutti i soggetti sono stati sottoposti ad esame radiografico del torace in proiezione L-L e V-D impiegando due diversi sistemi schermo-pellicola : il sistema InSight Chest ® Kodak costituito da due schermi di rinforzo asimmetrici che agiscono separatamente sulle due superfici di una pellicola radiografica specifica a duplice sensitometria ed il sistema Lanex Regular Fast ® con pellicole T-MAT G Kodak. Le immagini ottenute con i due sistemi sono state valutate da tre radiologi indipendenti che hanno assegnato, per ognuna di esse, un punteggio variabile da 1 (valutazione peggiore) a 4 (valutazione migliore) alle caratteristiche di annerimento della pellicola, scala dei grigi, risoluzione di contrasto e visualizzazione delle strutture intratoraciche. Sono state inoltre calcolate strumentalmente, dopo digitalizzazione delle immagini, le curve sensitometriche, la funzione di trasferimento della modulazione (MTF) e le differenze di annerimento in 2 aree a differente assorbimento fotonico. I risultati sono stati sottoposti ad elaborazione statistica.

Risultati: La lettura in doppio cieco ha fornito i seguenti risultati: annerimento, preferito il sistema tradizionale con p < 0.01; scala dei grigi, prevale il sistema InSight con p < 0.01; risoluzione, prevale il Regular / T-Mat G con p < 0.01 in L-L ed il sistema InSight in V-D con p < 0.05; visualizzazione degli apici, in V-D prevale il sistema InSight con p < 0.05. La lettura strumentale ha rilevato che la media delle differenze di densità ottica (D.O) è di 1.2 +/- 0.4 per il sistema tradizionale e 0.9 +/- 0.3 per il sistema InSight. La curva sensitometrica del sistema InSight risulta meno ripida nella sua parte rettilinea rispetto alla Regular / T-MAT G. Discussione: Tra i vari problemi legati all’ottenimento di immagini radiografiche del torace di qualità diagnostica, vi è la differenza di spessore esistente tra le aree del mediastino paracardiaco e quelle diaframmatiche che possono richiedere parametri di esposizione differenti. I risultati ottenuti dalla lettura strumentale per la valutazione delle D.O. dimostrano che il sistema InSight, utilizzando mediamente delle D.O. inferiori rispetto a quelle utilizzate dal sistema tradizionale Lanex, possiede un numero di valori utili, nell’intervallo tra 0.5 e 3 D.O., maggiore e quindi possiede una più ampia latitudine rispetto al sistema tradizionale. In conclusione, l’applicazione del sistema InSight nell’esame radiografico del torace del cane permette di ottenere immagini dotate di un’ampia scala dei grigi, tali da permettere una buona valutazione contemporanea delle aree mediastiniche paracardiache e di quelle diaframmatiche.