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Refereed Peer Review PAGES 201–248

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Vol 31(5) May 2009

fo te C rS d m # om al 1 lA i pe ni n m O nd al v Ve e ium te ra rin l ar l Q yJ u ou a rn lit al y s! *

VOLUME 31 NUMBER 5 MAY 2009

Compendium CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

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May 2009 Vol 31(5) CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

EXECUTIVE EDITOR Tracey L. Giannouris, MA 800-426-9119, ext 52447 | tgiannouris@vetlearn.com MANAGING EDITOR Kirk McKay 800-426-9119, ext 52434 | kmckay@vetlearn.com Subscription inquiries: 800-426-9119, option 2. Subscription rate: $79 for 1 year; $143 for 2 years; $217 for 3 years. Canadian and Mexican subscriptions (surface mail): $95 for 1 year; $169 for 2 years; $270 for 3 years. Foreign subscriptions (surface mail): $175 for 1 year; $275 for 2 years; $425 for 3 years. Payments by check must be in U.S. funds drawn on a U.S. branch of a U.S. bank only; credit cards are also accepted. Change of Address: Please notify the Circulation Department 45 days before the change is to be effective. Send your new address and enclose an address label from a recent issue. Selected back issues are available for $15 (United States and Canada) and $17 (foreign) each (plus postage). Indexing: Compendium: Continuing Education for Veterinarians® is included in the international indexing coverage of Current Contents/ Agriculture, Biology and Environmental Sciences (ISI); SciSearch (ISI); Research Alert (ISI); Focus On: Veterinary Science and Medicine (ISI); Index Veterinarius (CAB International, CAB Abstracts, CAB Health); and Agricola (Library of Congress). Article retrieval systems include The Genuine Article (ISI), The Copyright Clearance Center, Inc., University Microfilms International, and Source One (Knight-Ridder Information, Inc.). Yearly author and subject indexes for Compendium are published each December.

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201

May 2009 Vol 31(5) CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

EDITORIAL BOARD Anesthesia Nora S. Matthews, DVM, DACVA Texas A&M University

Internal Medicine Dana G. Allen, DVM, MSc, DACVIM Ontario Veterinary College

Cardiology Bruce Keene, DVM, MSc, DACVIM North Carolina State University

Internal Medicine and Emergency/ Critical Care Alison R. Gaynor, DVM, DACVIM (Internal Medicine), DACVECC North Grafton, Massachusetts

Clinical Chemistry, Hematology, and Urinalysis Betsy Welles, DVM, PhD, DACVP Auburn University

EDITOR IN CHIEF Douglass K. Macintire, DVM, MS, DACVIM, DACVECC

Department of Clinical Sciences College of Veterinary Medicine Auburn University, AL 36849

Dentistry Gary B. Beard, DVM, DAVDC Auburn University R. Michael Peak, DVM, DAVDC The Pet Dentist—Tampa Bay Veterinary Dentistry Largo, Florida Emergency/Critical Care and Respiratory Medicine Lesley King, MVB, MRCVS, DACVECC, DACVIM University of Pennsylvania Endocrinology and Metabolic Disorders Marie E. Kerl, DVM, ACVIM, ACVECC University of Missouri-Columbia

EXECUTIVE ADVISORY BOARD MEMBERS Behavior Sharon L. Crowell-Davis, DVM, PhD, DACVB The University of Georgia Dermatology Craig E. Grifﬁn, DVM, DACVD Animal Dermatology Clinic San Diego, California Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic Tustin, California Nutrition Kathryn E. Michel, DVM, MS, DACVN University of Pennsylvania Surgery Elizabeth M. Hardie, DVM, PhD, DACVS North Carolina State University

202

CompendiumVet.com m

Epidemiology Philip H. Kass, DVM, MPVM, MS, PhD, DACVPM University of California, Davis Exotics Avian Thomas N. Tully, Jr, DVM, MS, DABVP (Avian), ECAMS Louisiana State University Reptiles Douglas R. Mader, MS, DVM, DABVP (DC) Marathon Veterinary Hospital Marathon, Florida Small Mammals Karen Rosenthal, DVM, MS, DABVP (Avian) University of Pennsylvania Feline Medicine Michael R. Lappin, DVM, PhD, DACVIM (Internal Medicine) Colorado State University Margie Scherk, DVM, DABVP (Feline Medicine) Cats Only Veterinary Clinic Vancouver, British Columbia Gastroenterology Debra L. Zoran, DVM, MS, PhD, DACVIM (Internal Medicine) Texas A&M University Infectious Disease Derek P. Burney, PhD, DVM Gulf Coast Veterinary Specialists Houston, Texas

Nephrology Catherine E. Langston, DVM, ACVIM Animal Medical Center New York, New York Neurology Curtis W. Dewey, DVM, MS, DACVIM (Neurology), DACVS Cornell University Hospital for Animals Oncology Ann E. Hohenhaus, DVM, DACVIM (Oncology and Internal Medicine) Animal Medical Center New York, New York Gregory K. Ogilvie, DVM, DACVIM (Internal Medicine, Oncology), DECVIM-CA (Oncology) CVS Angel Care Cancer Center and Special Care Foundation for Companion Animals Carlsbad, California Ophthalmology David A. Wilkie, DVM, MS, DACVO The Ohio State University Parasitology Byron L. Blagburn, MS, PhD Auburn University David S. Lindsay, PhD Virginia Polytechnic Institute and State University Pharmacology Katrina L. Mealey, DVM, PhD, DACVIM, DACVCP Washington State University Rehabilitation and Physical Therapy Darryl Millis, MS, DVM, DACVS University of Tennessee Surgery Philipp Mayhew, BVM&S, MRCVS, DACVS Columbia River Veterinary Specialists Vancouver, Washington C. Thomas Nelson, DVM Animal Medical Center Anniston, Alabama Toxicology Tina Wismer, DVM, DABVT, DABT ASPCA National Animal Poison Control Center Urbana, Illinois

AMERICAN BOARD OF VETERINARY PRACTITIONERS (ABVP) REVIEW BOARD Kurt Blaicher, DVM, DABVP (Canine/Feline) Plainﬁeld Animal Hospital Plainﬁeld, New Jersey Canine and Feline Medicine Eric Chafetz, DVM, DABVP (Canine/Feline) Vienna Animal Hospital Vienna, Virginia Canine and Feline Medicine Henry E. Childers, DVM, DABVP (Canine/Feline) Cranston Animal Hospital Cranston, Rhode Island Canine and Feline Medicine David E. Harling, DVM, DABVP (Canine/Feline), DACVO Reidsville Veterinary Hospital Reidsville, North Carolina Canine and Feline Medicine, Ophthalmology Jeffrey Katuna, DVM, DABVP Wellesley-Natick Veterinary Hospital Natick, Massachusetts Canine and Feline Medicine Robert J. Neunzig, DVM, DABVP (Canine/Feline) The Pet Hospital Bessemer City, North Carolina Canine and Feline Medicine

Compendium is a refereed journal. Articles published herein have been reviewed by at least two academic experts on the respective topic and by an ABVP practitioner. Any statements, claims, or product endorsements made in Compendium are solely the opinions of our authors and advertisers and do not necessarily reﬂect the views of the Publisher or Editorial Board.

The secret to a longer life in dogs with heart failure.

The QUEST study provides new evidence that Vetmedin® (pimobendan) extends life for dogs with congestive heart failure (CHF). In a study of unprecedented magnitude, dogs with CHF due to mitral valve disease who were treated with VETMEDIN* lived virtually twice as long as those on an ACE inhibitor.1 This hard evidence from the QUEST study supports using VETMEDIN as ﬁrst-line therapy in all dogs with symptomatic CHF. News like this should make your clients jump for joy as well. *The study used VETMEDIN Capsules. In the US, only chewable tablets are licensed. Both capsules and chewable tablets contain the same pharmaceutical ingredient, pimobendan, and are considered equivalent for clinical use. Bioequivalence, however, has not been established. Visit www.questtrial.com for additional study details, and visit www.vetmedin-us.com for more information about VETMEDIN.

Important safety information: VETMEDIN should not be given in case of hypertrophic cardiomyopathy, aortic stenosis, or any other clinical condition where an augmentation of cardiac output is inappropriate for functional or anatomical reasons. The safety of VETMEDIN has not been established in dogs with asymptomatic heart disease or in heart failure caused by other etiologies other than atrioventricular valvular insufﬁciency or dilated cardiomyopathy. Use only in dogs with clinical evidence of heart failure. The most common side effects reported in ﬁeld studies were poor appetite, lethargy, diarrhea, dyspnea, azotemia, weakness, and ataxia. If side effects should occur, pet owners should contact their veterinarian. Please refer to the package insert for complete product information or visit www.vetmedin-us.com. Reference: 1. Häggström J et al. Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: The QUEST study. J Vet Intern Med. 2008;22:1124–1135.

See Page 204 for Product Information Summary

higher in the active control group (4%) compared to the Vetmedin group (1%).

NADA 141-273, Approved by FDA

Vetmedin

(pimobendan) Chewable Tablets Cardiac drug for oral use in dogs only Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian. Description: Vetmedin (pimobendan) is supplied as oblong half-scored chewable tablets containing 1.25, 2.5 or 5 mg pimobendan per tablet. Pimobendan, a benzimidazole-pyridazinone derivative, is a nonsympathomimetic, non-glycoside inotropic drug with vasodilatative properties. Pimobendan exerts a stimulatory myocardial effect by a dual mechanism of action consisting of an increase in calcium sensitivity of cardiac myofilaments and inhibition of phosphodiesterase (Type III). Pimobendan exhibits vasodilating activity by inhibiting phosphodiesterase III activity. The chemical name of pimobendan is 4,5-dihydro-6-[2-(4-methoxyphenyl)-1Hbenzimidazole-5-yl]-5-methyl-3(2H)-pyridazinone. The structural formula of pimobendan is:

Adverse reactions/new clinical findings were seen in both treatment groups and were potentially related to CHF, the therapy of CHF, or both. The following adverse reactions/new clinical findings are listed according to body system and are not in order of prevalence: CHF death, sudden death, chordae tendineae rupture, left atrial tear, arrhythmias overall, tachycardia, syncope, weak pulses, irregular pulses, increased pulmonary edema, dyspnea, increased respiratory rate, coughing, gagging, pleural effusion, ascites, hepatic congestion, decreased appetite, vomiting, diarrhea, melena, weight loss, lethargy, depression, weakness, collapse, shaking, trembling, ataxia, seizures, restlessness, agitation, pruritus, increased water consumption, increased urination, urinary accidents, azotemia, dehydration, abnormal serum electrolyte, protein, and glucose values, mild increases in serum hepatic enzyme levels, and mildly decreased platelet counts. See Table 1 for mortality due to CHF (including euthanasia, natural death, and sudden death) and for the development of new arrhythmias (not present in a dog prior to beginning study treatments) by treatment group and type of heart disease (AVVI or DCM) in the 56-day field study. Table 1: CHF Death and New Arrhythmias in the 56-Day Field Study

Indications: Vetmedin (pimobendan) is indicated for the management of the signs of mild, moderate, or severe (modified NYHA Class IIa, IIIb, or IV c) congestive heart failure in dogs due to atrioventricular valvular insufficiency (AVVI) or dilated cardiomyopathy (DCM). Vetmedin is indicated for use with concurrent therapy for congestive heart failure (e.g., furosemide, etc.) as appropriate on a case-by-case basis. a

Dogs that died due to CHF

A dog with modified New York Heart Association (NYHA) Class II heart failure has fatigue, shortness of breath, coughing, etc. apparent when ordinary exercise is exceeded.

A dog with modified NYHA Class III heart failure is comfortable at rest, but exercise capacity is minimal.

A dog with modified NYHA Class IV heart failure has no capacity for exercise and disabling clinical signs are present even at rest.

Dosage and Administration: Vetmedin should be administered orally at a total daily dose of 0.23 mg/lb (0.5 mg/kg) body weight, using a suitable combination of whole or half tablets. The total daily dose should be divided into 2 portions that are not necessarily equal, and the portions should be administered approximately 12 hours apart (i.e., morning and evening). The tablets are scored and the calculated dosage should be provided to the nearest half tablet increment. Contraindications: Vetmedin should not be given in cases of hypertrophic cardiomyopathy, aortic stenosis, or any other clinical condition where an augmentation of cardiac output is inappropriate for functional or anatomical reasons. Warnings: Only for use in dogs with clinical evidence of heart failure. At 3 and 5 times the recommended dosage, administered over a 6-month period of time, pimobendan caused an exaggerated hemodynamic response in the normal dog heart, which was associated with cardiac pathology (See Animal Safety). Human Warnings: Not for use in humans. Keep this and all medications out of reach of children. Consult a physician in case of accidental ingestion by humans. Precautions: The safety of Vetmedin has not been established in dogs with asymptomatic heart disease or in heart failure caused by etiologies other than AVVI or DCM. The safe use of Vetmedin has not been evaluated in dogs younger than 6 months of age, dogs with congenital heart defects, dogs with diabetes mellitus or other serious metabolic diseases, dogs used for breeding, or pregnant or lactating bitches. Adverse Reactions: Clinical findings/adverse reactions were recorded in a 56-day field study of dogs with congestive heart failure (CHF) due to AVVI (256 dogs) or DCM (99 dogs). Dogs were treated with either Vetmedin (175 dogs) or the active control enalapril maleate (180 dogs). Dogs in both treatment groups received additional background cardiac therapy (See Effectiveness for details and the difference in digoxin administration between treatment groups). The Vetmedin group had the following prevalence (percent of dogs with at least one occurrence) of common adverse reactions/new clinical findings (not present in a dog prior to beginning study treatments): poor appetite (38%), lethargy (33%), diarrhea (30%), dyspnea (29%), azotemia (14%), weakness and ataxia (13%), pleural effusion (10%), syncope (9%), cough (7%), sudden death (6%), ascites (6%), and heart murmur (3%). Prevalence was similar in the active control group. The prevalence of renal failure was

Dogs that developed new arrhythmiasa

Vetmedin® Group

Active Control Group

14.3% n=175

14.4% n=180

9 of 126 dogs with AVVI

16 of 130 dogs with AVVI

16 of 49 dogs with DCM

10 of 50 dogs with DCM

39.4% n=175

45.0% n=180

45 of 126 dogs with AVVI

59 of 130 dogs with AVVI

24 of 49 dogs with DCM

22 of 50 dogs with DCM

New arrhythmias included supraventricular premature beats and tachycardia, atrial fibrillation, atrioventricular block, sinus bradycardia, ventricular premature beats and tachycardia, and bundle branch block

Following the 56-day masked field study, 137 dogs in the Vetmedin group were allowed to continue on Vetmedin in an open-label extended-use study without restrictions on concurrent therapy. The adverse reactions/new clinical findings in the extended-use study were consistent with those reported in the 56-day study, with the following exception: One dog in the extended-use study developed acute cholestatic liver failure after 140 days on Vetmedin and furosemide. In foreign post-approval drug experience reporting, the following additional suspected adverse reactions were reported in dogs treated with a capsule formulation of pimobendan: hemorrhage, petechia, anemia, hyperactivity, excited behavior, erythema, rash, drooling, constipation, and diabetes mellitus. To report suspected adverse reactions, to obtain a Material Safety Data Sheet, or for technical assistance call 1-866-638-2226. Clinical Pharmacology: Pimobendan is oxidatively demethylated to a pharmacologically active metabolite which is then conjugated with sulfate or glucuronic acid and excreted mainly via feces. The mean extent of protein binding of pimobendan and the active metabolite in dog plasma is >90%. Following a single oral administration of 0.25 mg/kg Vetmedin tablets the maximal mean (± 1 SD) plasma concentrations (Cmax) of pimobendan and the active metabolite were 3.09 (0.76) ng/mL and 3.66 (1.21) ng/mL, respectively. Individual dog Cmax values for pimobendan and the active metabolite were observed 1 to 4 hours postdose (mean: 2 and 3 hours, respectively). The total body clearance of pimobendan was approximately 90 mL/min/kg, and the terminal elimination half-lives of pimobendan and the active metabolite were approximately 0.5 hours and 2 hours, respectively. Plasma levels of pimobendan and active metabolite were below quantifiable levels by 4 and 8 hours after oral administration, respectively. The steady-state volume of distribution of pimobendan is 2.6 L/kg indicating that the drug is readily distributed into tissues. Food decreased the bioavailability of an aqueous solution of pimobendan, but the effect of food on the absorption of pimobendan from Vetmedin tablets is unknown. In normal dogs instrumented with left ventricular (LV) pressure transducers, pimobendan increased LV dP/dtmax (a measure of contractility of the heart) in a dose dependent manner between 0.1 and 0.5

mg/kg orally. The effect was still present 8 hours after dosing. There was a delay between peak blood levels of pimobendan and active metabolite and the maximum physiologic response (peak LV dP/dtmax). Blood levels of pimobendan and active metabolite began to drop before maximum contractility was seen. Repeated oral administration of pimobendan did not result in evidence of tachyphylaxis (decreased positive inotropic effect) or drug accumulation (increased positive inotropic effect). Laboratory studies indicate that the positive inotropic effect of pimobendan may be attenuated by the concurrent use of a ß-adrenergic blocker or a calcium channel blocker.

the average voluntary consumption was 84.2%.

Effectiveness: In a double-masked, multi-site, 56-day field study, 355 dogs with modified NYHA Class II, III, or IV CHF due to AVVI or DCM were randomly assigned to either the active control (enalapril maleate) or the Vetmedin (pimobendan) treatment group. Of the 355 dogs, 52% were male and 48% were female; 72% were diagnosed with AVVI and 28% were diagnosed with DCM; 34% had Class II, 47% had Class III, and 19% had Class IV CHF. Dogs ranged in age and weight from 1 to 17 years and 3.3 to 191 lb, respectively. The most common breeds were mixed breed, Doberman Pinscher, Cocker Spaniel, Miniature/Toy Poodle, Maltese, Chihuahua, Miniature Schnauzer, Dachshund, and Cavalier King Charles Spaniel. The 180 dogs (130 AVVI, 50 DCM) in the active control group received enalapril maleate (0.5 mg/kg once or twice daily), and all but 2 received furosemide. Per protocol, all dogs with DCM in the active control group received digoxin. The 175 dogs (126 AVVI, 49 DCM) in the Vetmedin group received pimobendan (0.5 mg/kg/day divided into 2 portions that were not necessarily equal, and the portions were administered approximately 12 hours apart), and all but 4 received furosemide. Digoxin was optional for treating supraventricular tachyarrhythmia in either treatment group, as was the addition of a ß-adrenergic blocker if digoxin was ineffective in controlling heart rate. After initial treatment at the clinic on Day 1, dog owners were to administer the assigned product and concurrent medications for up to 56±4 days.

Table 3: Incidence of Cardiac Pathology/ Histopathology in the Six-month Safety Study

The determination of effectiveness (treatment success) for each case was based on improvement in at least 2 of the 3 following primary variables: modified NYHA classification, pulmonary edema score by a masked veterinary radiologist, and the investigator’s overall clinical effectiveness score (based on physical examination, radiography, electrocardiography, and clinical pathology). Attitude, pleural effusion, coughing, activity level, furosemide dosage change, cardiac size, body weight, survival, and owner observations were secondary evaluations contributing information supportive to product effectiveness and safety. Based on protocol compliance and individual case integrity, 265 cases (134 Vetmedin, 131 active control) were evaluated for treatment success on Day 29. See Table 2 for effectiveness results. Table 2: Effectiveness Results for the 56-Day Field Study

Treatment Success on Day 29

Treatment Success on Day 56

No increase in furosemide dose between Day 1 and Day 29

Vetmedin® Group

Active Control Group

80.7% n=134

76.3% n=131

88 of 101 dogs with AVVI

77 of 100 dogs with AVVI

20 of 33 dogs with DCM

23 of 31 dogs with DCM

71.1% n=113

67.2% n=110

66 of 85 dogs with AVVI

56 of 85 dogs with AVVI

13 of 28 dogs with DCM

17 of 25 dogs with DCM

78.3% n=130

68.6% n=126

Animal Safety: In a laboratory study, Vetmedin chewable tablets were administered to 6 healthy Beagles per treatment group at 0 (control), 1, 3, and 5 times the recommended dosage for 6 months. See Table 3 for cardiac pathology results. The cardiac pathology/histopathology noted in the 3X and 5X dose groups is typical of positive inotropic and vasodilator drug toxicity in normal dog hearts, and is associated with exaggerated hemodynamic responses to these drugs. None of the dogs developed signs of heart failure and there was no mortality.

Severe left ventricular hypertrophy with multifocal subendocardial ischemic lesions

One 3X and two 5X dogsa

Moderate to marked myxomatous thickening of the mitral valves

Three 5X dogs

Myxomatous thickening of the chordae tendineae

One 3X and two 5X dogs

Endocardial thickening of the left ventricular outflow tract

One 1X, two 3X, and two 5X dogs

Left atrial endocardial thickening (jet lesions) in 2 of the dogs that developed murmurs of mitral valve insufficiency

One 3X and one 5X dog

Granulomatous inflammatory lesion in the right atrial myocardium

One 3X dog

Most of the gross and histopathologic findings occurred in these three dogs

Murmurs of mitral valve insufficiency were detected in one 3X (Day 65) and two 5X dogs (Days 135 and 163). These murmurs (grades II-III of VI) were not associated with clinical signs. Indirect blood pressure was unaffected by Vetmedin at the label dose (1X). Mean diastolic blood pressure was decreased in the 3X group (74 mmHg) compared to the control group (82 mmHg). Mean systolic blood pressure was decreased in the 5X group (117 mmHg) compared to the control group (124 mmHg). None of the dogs had clinical signs of hypotension. On 24-hour Holter monitoring, mean heart rate was increased in the 5X group (101 beats/min) compared to the control group (94 beats/min). Not counting escape beats, the 3X and 5X groups had slightly higher numbers of isolated ventricular ectopic complexes (VEs). The maximum number of nonescape VEs recorded either at baseline or in a control group dog was 4 VEs/24 hours. At either Week 4 or Week 20, three 3X group dogs had maximums of 33, 13, and 10 VEs/24 hours, and two 5X group dogs had maximums of 22 and 9 VEs/24 hours. One 1X group dog with no VEs at baseline had 6 VEs/24 hours at Week 4 and again at Week 20. Second-degree atrioventricular heart block was recorded in one 3X group dog at Weeks 4 and 20, and in one dog from each of the 1X and 5X groups at Week 20. None of the dogs had clinical signs associated with these electrocardiogram changes. Treatment was associated with small differences in mean platelet counts (decreased in the 3X and 1X groups), potassium (increased in the 5X group), glucose (decreased in the 1X and 3X groups), and maximum blood glucose in glucose curves (increased in the 5X group). All individual values for these variables were within the normal range. Three 1X and one 5X group dogs had mild elevations of alkaline phosphatase (less than two times normal). Loose stools and vomiting were infrequent and self-limiting. Storage Information: Store at controlled room temperature 59-86°F (15-30°C).

At the end of the 56-day study, dogs in the Vetmedin group were enrolled in an unmasked field study to monitor safety under extended use, without restrictions on concurrent medications. Vetmedin was used safely in dogs concurrently receiving furosemide, digoxin, enalapril, atenolol, spironolactone, nitroglycerin, hydralazine, diltiazem, antiparasitic products (including heartworm prevention), antibiotics (metronidazole, cephalexin, amoxicillin-clavulanate, fluoroquinolones), topical ophthalmic and otic products, famotidine, theophylline, levothyroxine sodium, diphenhydramine, hydrocodone, metoclopramide, and butorphanol, and in dogs on sodium-restricted diets. Palatability: In a laboratory study, the palatability of Vetmedin was evaluated in 20 adult female Beagle dogs offered doses twice daily for 14 days. Ninety percent (18 of 20 dogs) voluntarily consumed more than 70% of the 28 tablets offered. Including two dogs that consumed only 4 and 7% of the tablets offered,

How Supplied: Vetmedin® (pimobendan) Chewable Tablets: Available at 1.25, 2.5 or 5 mg oblong half-scored chewable tablets – 50 tablets per bottle. Manufactured by: MEDA Manufacturing GmbH Cologne, Germany Manufactured for: Boehringer Ingelheim Vetmedica, Inc. St. Joseph, MO 64506 U.S.A. 1-866-638-2226 VETMEDIN is a registered trademark of Boehringer Ingelheim Vetmedica GmbH, licensed to Boehringer Ingelheim Vetmedica, Inc. © 2009 Boehringer Ingelheim Vetmedica, Inc. Code 448011, 448111, 448211 Revised 06/2007

EEach CE article is accredited for 3 contact hours by A Auburn University College of Veterinary Medicine.

May 2009 Vol 31(5)

Features 212

232

Laryngeal Paralysis in Dogs ❯❯ Ralph P. Millard and Karen M. Tobias Laryngeal paralysis can cause progressive upper airway obstruction and ultimately death, usually in older, large-breed dogs. Videos of normal and paralyzed laryngeal abduction are available at CompendiumVet.com.

CompendiumVet.com | Peer Reviewed | Listed in MEDLINE FREE

220 Applied Dermatology Overview of Flea Allergy Dermatitis

NEW SERIES

❯❯ Andrea Lam and Anthony Yu A new quarterly column debuts this month with a quick guide to the diagnosis and management of ﬂea allergy dermatitis in general practice. An extended version of this article, with details of available ﬂea-control products, is available at CompendiumVet.com.

Pneumothorax ❯❯ Karl C. Maritato, José A. Colón, and David H. Kergosien Pneumothorax is classiﬁed according to type and causative mechanism. Information on signalment, diagnostic evaluation, and treatment is given for each type, along with the basic steps of thoracocentesis and thoracostomy tube p placement. FREE

Departments 208 Clinical Snapshot Poor Haircoat in a Persian ❯❯ Jeff Ruth

Clinical Snapshot PAGE 208

211 Editorial: Applied Dermatology ❯❯ Wayne S. Rosenkrantz and Craig E. Grifﬁn 226 CompendiumVet.com 230 Abstract Thoughts ❯❯ Joseph Harari

245 Product Forum 246 Index to Advertisers 246 Market Showcase

243 Letters

246 Classiﬁed Advertising

244 Research Recap Selected abstract from Veterinary Therapeutics

248 Reading Room Guidelines for Euthanasia of Nondomestic Animals

On the Cover Dr. Anthony Yu performs a dermatologic examination on Joey, a Parson Russell terrier mix, at Ontario Veterinary College in Guelph, Ontario, Canada. *

2009 PERQ/HCI FOCUS® Veterinary Study of Total Companion Animal Veterinarians, in comparison to ratings for each publication, by that publication’s readers. Compendium: Continuing Education for Veterinarians®

205

Canadian News Veterinary Cancer Centre Opens T

he Western Veterinary Specialist and

Emergency Centre in downtown Calgary, Alberta, opened its new Cancer Centre Tuesday, April 14. The centre, which has been in development since 2006, will use cutting-edge technology, previously unavailable in Canada, to treat pets with cancer. The Cancer Centre is equipped with a linear accelerator with intensity mod-

ulated radiation therapy capabilities that allow radiation to be targeted speciﬁcally at tumor cells, sparing normal tissues. The Western Veterinary Specialist and Emer gency Centre treats more than 8000 companion animal patients annually at its 30,000-squarefoot facility.

OVC Pet Trust Funds $232,500 in Companion Animal Research

he donor-supported OVC Pet Trust has funded 19 research projects at the Ontario Veterinary College (OVC). The projects were chosen in a fall 2008 competition. Species to be studied include companion animals such as cats, dogs, parrots, and veiled chameleons. The chosen projects cover a wide range of topics. One project will explore

the needs and expectations of pet owners whose animals are receiving cancer care at the OVC. Another will study the use of laser lithotripsy (the treatment of choice in humans) to pulverize kidney and ureteral stones in vitro in dogs. Other areas of research funded by the Pet Trust include hematology, cardiology, and infectious disease topics.

Therapy Dogs Trained

he St. John Ambulance Company of Comox Valley, Vancouver Island, British Columbia, has 10 new therapy dog teams, bringing the total to 34 active teams. The addition of these new teams makes the St. John Ambulance Therapy Dog Branch the largest on Vancouver Island. The therapy dogs serve as surrogate pets for people who are no longer able to have animals of their own. Before entering the program, the dogs are tested against national standards for temperament and obedience for work in seniors’ facilities. Volunteers commit to a minimum of 1 hour per week. SPREAD YOUR GOOD NEWS Canadian News c/o Veterinary Learning Systems 780 Township Line Road Yardley, PA 19067, USA E-MAIL editor@CompendiumVet.com FAX 800-556-3288 WEB CompendiumVet.com

Coming Events July 16 Ontario Veterinary Medical Association: Career Planning for Associate Veterinarians & Potential Practice Owners Ontario Veterinary Medical Association Milton, Ontario This course presents the beneﬁts and downsides of owning a practice as well as the practical aspects of practice ownership. Web https://www.ovma.info/Meetings/ August 8–13 World Association for the Advancement of Veterinary Parasitology: 22nd International Conference Calgary, Alberta This conference will discuss current issues in parasitology, with a theme of “One World One Health: Parasites in a Changing Environment.” Web www.waavp2009.com

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September 9 Calgary Academy of Veterinary Medicine: Ophthalmology Clara Christie Theatre, Health Sciences University of Calgary, Alberta This seminar will offer 1.5 hours of scientiﬁc CE and will be presented by Dr. Cheryl Cullen. Phone 403-863-7160 E-mail info@cavm.ab.ca Web www.cavm.ab.ca/ce_calendar.html September 15 Toronto Academy of Veterinary Medicine: Update on Clinical Gastroenterology Dave and Buster’s Toronto, Ontario This seminar will provide an update on GI disorders of cats and dogs, with an emphasis on diagnosis and treatment. It will offer 5.5 CE credits. Phone 800-670-1702 Web www.tavm.org

Compendium: Continuing Education for Veterinarians® | May 2009 | CompendiumVet.com

October 13 Toronto Academy of Veterinary Medicine: Early Resuscitation and Stabilization of the Emergency Patient Dave and Buster’s Toronto, Ontario This seminar will focus on practical emergency management using case examples. It will offer 5.5 CE credits. Phone 800-670-1702 Web www.tavm.org October 18 Calgary Academy of Veterinary Medicine: Hematology Clara Christie Theatre, Health Sciences University of Calgary, Alberta This seminar will offer 6 hours of scientiﬁc CE and will be presented by Dr. Marjorie Brooks. Phone 403-863-7160 E-mail info@cavm.ab.ca Web www.cavm.ab.ca/ce_calendar.html

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My patients rely on me every day. And I rely on Baytril®. Because when it comes to infections, it’s on my side – an eﬀective partner I can count on. Federal (U.S.A.) law restricts this drug to use by or on the order of a licensed veterinarian. In animal safety studies, isolated incidences of vomition and inappetence were reported. © 2009 Bayer HealthCare LLC, Animal Health Division, Shawnee Mission, Kansas 66201. Bayer, the Bayer Cross, Baytril and Right the ﬁrst time are registered trademarks of Bayer.

See Page 208 for Product Information Summary

B090123n

Clinical Snapshot Particularly intriguing or difﬁcult cases

Case Presentation #1 ❯❯ Jeff Ruth, DVM, DABVP (Canine/Feline) Bissonnet/Southampton Veterinary Clinic Houston, Texas

A 3-year-old intact male Persian cat presented with chronic, greasy skin of the tail and an unkempt haircoat (A). Prior unsuccessful attempts to treat the cat included systemic antibiotics (cefpodoxime 6.25 mg/kg PO q24h for 14 days) and antibacterial shampoo (4% chlorhexidine every 14 days for 3 months). A 2 × 6–cm focal zone of seborrhea oleosa, yellow crusting, and alopecia affected the proximal third of the tail (B). Additional abnormalities included mild medial canthal entropion of the left eye and resultant obstruction of nasolacrimal tear drainage. A 1. Given the history and clinical

signs, what is the most likely cause of the lesion? 2. What ancillary tests should be

performed? 3. What are the recommended treat-

ment and the prognosis for this cat? SEE PAGE 210 FOR ANSWERS AND EXPLANATIONS.

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• Starts killing ﬂeas in 30 minutes • 100% effective within 4 hours in a controlled laboratory study • Approved by the FDA and available by prescription only To learn more about Comfortis®, see your Lilly representative or distributor representative, call 1 (888) LillyPet or visit www.comfortis4dogs.com The most common adverse reaction recorded during clinical trials was vomiting. Other adverse reactions were decreased appetite, lethargy or decreased activity, diarrhea, cough, increased thirst, vocalization, increased appetite, redness of the skin, hyperactivity and excessive salivation. For product label, including important safety information, see page 210. ©2009 Eli Lilly and Company CF00305 010109

Clinical Snapshot Answers and Explanations Case Presentation #1 A

SEE PAGE 208 FOR CASE PRESENTATION.

1. Feline tail gland hyperplasia (FTGH).

The tail gland, or supracaudal gland, is a dense accumulation of sebaceous glands located on the dorsal surface of the tail in cats and dogs. Hyperplasia of the sebaceous glands and resultant sebum overproduction induces focal clinical signs that may include a greasy haircoat, hyperpigmentation, furunculosis, alopecia, and comedones in the region of the tail gland. FTGH, or stud tail, is a disease of young cats of either sex, altered or intact. 2. Skin cytology should be conducted

to detect secondary bacterial pyoderma or Malassezia infection, which may complicate the disease. Dermatophyte culture and skin scrapings for Demodex spp are also warranted. Seborrheic dermatitis also necessitates the identiﬁcation and strict control of ﬂeas and other ectoparasites. A variety of primary and secondary keratinization defects have characteristics that can mimic FTGH. Among these are generalized primary seborrhea, allergic dermatitis, neoplasia (carcinoma in situ or cutaneous lymphoma), and zoonotic infectious disease (pythiosis, phaeohyphomycosis). If the signs are not localized to the region of the tail gland, or if the initial workup fails to elucidate a cause, biopsy for histopathology and culture is indicated. Histopathology in cases of FTGH demonstrates the characteristic hyperplasia of regional sebaceous glands.

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3. Treatment goals are to minimize

the accumulation of seborrheic oil produced by the glands and to address secondary skin infections. The inﬂuence of androgens is poorly understood, and castration is unlikely to completely resolve the condition. The use of keratolytic and keratoplastic shampoos (e.g., sulfur 2% and salicylic acid 2% q36h for 4 weeks, then weekly) or degreasing agents (e.g., benzoyl peroxide 2.5% q36h for 4 weeks, then weekly) is recommended. Systemic antiseborrheic agents used in veterinary medicine include synthetic retinoids such as isotretinoin and etretinate. While these agents may have beneﬁt in refractory cases, their use carries a greater risk of adverse effects. Clients should be prepared to invest time in regular grooming to minimize the largely cosmetic clinical signs of this disease. With attention to routine care, the prognosis for FTGH is favorable.

Recommended Reading g Guaguère E, Prélaud P. A Practical Guide to Feline Dermatology. Paris: Merial; 1999. Scott DW, Miller WH, Grifﬁn CE. Keratinization defects. In: Scott DW, Miller WH, Grifﬁn CE, eds. Muller and Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:1046-1048.

Compendium: Continuing Education for Veterinarians® | May 2009 | CompendiumVet.com

Editorial COLUMN EDITOR COLUMN EDITOR Craig E. Grifﬁn, DVM, DACVD Animal Dermatology Clinic, San Diego, California

COLUMN EDITOR COLUMN EDITOR Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic, Tustin, California

Dr. Yu (shown here with his dogs [from left to right] Timmy, Joey, and Bitsy) is associate professor of dermatology at The University of Guelph Ontario Veterinary College in Canada.

Overview of Flea Allergy Dermatitis ❯❯ Andrea Lam, DVM

❯❯ Anthony Yu, DVM, MS, DACVDa

University of California Davis Veterinary Medical Teaching Hospital

lea allergy dermatitis, or flea-bite hypersensitivity, is the most common small animal dermatologic condition.1–3 In some regions of the world, it is the most commonly seen canine disease. This disease does not exist in locations that are inhospitable to fleas, such as those at elevations above 1500 ft or with low humidity (e.g., the desert). Although there are more than 2000 documented species and subspecies of fleas, the cat flea (Ctenocephalides felis felis) is the species most frequently found infesting dogs, cats, and all caged pets in North America.

Flea Facts

At a Glance Flea Facts Page 220

Pathogenesis Page 220

Diagnosis Page 222

Treatment Page 223

Flea Control Products Page 224

❯❯ Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic Tustin, California

❯❯ Craig E. Grifﬁn, DVM, DACVD Animal Dermatology Clinic San Diego, California

a Dr. Yu discloses that he has received ﬁnancial support from Greer Laboratories, Iams, Novartis Animal Health, and Pﬁzer Animal Health.

220

The life cycle of the flea ranges from as few as 12 to as many as 190 days, with an average of 21 days. The time needed for development depends heavily on environmental conditions, particularly temperature and humidity. The optimal environment is a low-altitude geographic location, a temperature of 75°F (23.8°C), and a relative humidity of 78%. An adult flea takes its first blood meal from a host within minutes of contact. Female fleas lay their first egg 24 to 36 hours after this blood meal. Flea eggs are smooth and slick. Only 30% of eggs remain on the haircoat; the remainder fall off the host into the environment. Hatching takes place within 1 to 10 days, again depending on humidity and temperature. A single female flea can lay 1000 eggs within 30 days, and most average 2000 eggs during their life. Although eggs can hatch anywhere in the environment, development of the larvae that emerge from the eggs must take place off the host because mammalian body temperatures are too high for survival. Larvae are highly sensitive to heat and desiccation and therefore tend to move downward and away from direct light

University of Guelph Ontario Veterinary College

sources. The larvae feed on adult flea feces (partially digested blood) in the environment. Within 5 to 11 days, a larva undergoes two separate molting stages before forming a pupa. The pupal stage is the most resilient of all stages because the cocoon is highly resistant to desiccation. It also has a sticky surface that helps to prevent premature removal from the environment and that accumulates dust and other household particulates to provide protection. On average, the pupal stage lasts 8 to 9 days; however, fleas can pupate for up to 6 months if the environmental conditions are not ideal for emergence. Only with proper environmental stimuli, such as an increase in carbon dioxide, warmth, physical pressure, and vibration, will an adult flea emerge from its cocoon. After emerging from the cocoon, adult fleas search for an appropriate host. Adult fleas are attracted to light and tend to migrate upward toward surfaces where contact with an appropriate host is more likely. Once a host is found, feeding and mating take place within 8 to 24 hours. Female fleas can consume 15 times their body weight in blood per day. Adult fleas act as obligate, permanent ectoparasites, preferring to remain on a host rather than in the environment.

Pathogenesis Flea saliva contains histamine-like compounds, proteolytic enzymes, and anticoagulants. These proteins are released into the host during feeding and can act as inflammatory or antigenic stimuli in sensitive animals. Various immunologic responses are provoked, including immediate and delayed hypersensitivity reactions,4 late-phase IgE-mediated responses, and cutaneous basophil hypersensitivity reactions.5 Dogs with atopic dermatitis appear to be predisposed to the development of ﬂea allergy dermatitis.6,7

WEB EXCLUSIVE An extended version of this article is available on

CompendiumVet.com.

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New dermatology series begins on page 220.

Applied Dermatology

kin and ear diseases are the most common problems that veterinarians deal with in practice on a daily basis. Because many of these cases are secondary to genetic causes, cure is often not possible, and management becomes the mainstay of therapy. Fortunately, many advances in diagnostics and therapeutics have been made in the ﬁeld of veterinary dermatology, and pet owners are demanding a higher level

The new dermatology series will provide practical, easy-to-use techniques for the diagnosis and treatment of many common canine and feline ear and skin diseases. of care and are often willing to allow advanced diagnostic testing and therapy. To be able to offer your clients this higher quality of medicine, it is imperative to stay current on the latest options available to manage these chronic and sometimes frustrating cases. To help you in this effort, the new Compendium dermatology series, Applied Dermatology, will provide practical, easy-to-use techniques for the diagnosis and treatment of many common canine and feline ear and skin diseases. The articles in this new series, which debuts on page 220 of this issue, will

be written or coauthored by diplomates or residents of the American College of Veterinary Dermatology, who will present evidence-based approaches to common dermatologic conditions. This new column will appear quarterly. Occasionally, recognized dermatology experts will contribute their individual approaches to specific problems as online supplements to this series; the ﬁrst of these articles, “A Practical Approach to Diagnosing and Managing Ear Disease in Dogs,” by Paul Bloom, DVM, DACVD, DABVP (Canine and Feline), will be published on CompendiumVet.com this month. We hope that this new column will provide valuable information on how specialists approach and manage common skin and ear diseases and will help keep you updated on new diagnostic and therapeutic options so you can better handle these often frustrating cases in your clinical practice.

SHARE YOUR COMMENTS Have something to say about this editorial or topic? Let us know: E-MAIL editor@CompendiumVet.com FAX 800-556-3288

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3 CE CREDITS

CE Article 1

Laryngeal Paralysis in Dogs ❯❯ Ralph P. Millard, DVM ❯❯ Karen M. Tobias, DVM, MS, DACVS ❯❯ University of Tennessee

Abstract: Laryngeal paralysis is a common cause of upper airway obstruction in large-breed dogs. Although congenital forms have been reported, the disease is usually an acquired condition in older dogs. Clinical signs include voice change, inspiratory stridor, and dyspnea. Laryngeal paralysis is diagnosed by observing the absence of arytenoid abduction during laryngeal examination under a light plane of anesthesia. The most common method of surgical treatment is unilateral arytenoid lateralization. Most dogs experience signiﬁcant improvement in respiration following surgery; however, they have an increased risk of aspiration pneumonia for the remainder of their lives.

At a Glance

aryngeal paralysis is a well-recognized disease of large-breed dogs that results in upper airway obstruction and dyspnea. The condition results from dysfunction of the caudal laryngeal nerves, which are the terminations of the recurrent laryngeal nerves. The caudal laryngeal nerves provide innervation to all the muscles of the larynx except the cricothyroideus muscle. Dysfunction of these nerves results in the loss of arytenoid abduction by the cricoarytenoideus dorsalis muscle and the inability to actively constrict the glottis or relax the vocal folds1 (FIGURES 1 AND 2).

Etiology

Page 212

Laryngeal paralysis can be congenital or acquired. A hereditary form has been described in Bouvier des Flandres, dalmatians, rottweilers, and Siberian huskies and is usually reported in dogs younger than 1 year.2–5 Acquired laryngeal paralysis may result from trauma or iatrogenic injury to the recurrent laryngeal nerve (e.g., during thyroidectomy) or compression of the recurrent laryngeal nerve by a cranial mediastinal or cervical mass.6 More commonly, however, laryngeal paralysis is classiﬁed as idiopathic in older dogs. Although the underlying etiology is unknown, idiopathic laryngeal paralysis is most likely part of a generalized peripheral neuropathy.7 In one recent study, muscle and peripheral nerve biopsy samples obtained from 11 dogs with acquired

Signalment and Clinical Signs Page 213

Diagnosis Page 213

Medical Management Page 216

Surgical Treatment Page 217

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laryngeal paralysis displayed neurogenic atrophy of the cranial tibial muscle and axonal degeneration of the peroneal nerve in all cases, regardless of whether the dogs had signs of peripheral neuropathy.8 Within 2 years after diagnosis of laryngeal paralysis, clinical signs of generalized lower motor neuron disease were FIGURE 1

Cranial view of a dissected canine larynx. (a) Corniculate process of arytenoid cartilage, (b) cuneiform process of arytenoid cartilage, (c) epiglottis, (d) vocal fold, (e) laryngeal ventricles, (f) cricoid cartilage, (g) muscular process of arytenoid cartilage.

FREE

Laryngeal Paralysis in Dogs CE

present in all dogs in the study. 8 Although laryngeal paralysis has been reported in dogs with hypothyroidism, the association between the two conditions is unknown.9,10 Myasthenia gravis has also been suggested as a cause of laryngeal paralysis in dogs.11

FIGURE 2

Signalment and Clinical Signs Laryngeal paralysis is most commonly reported in older, large-breed dogs, especially Labrador retrievers.9,12–14 The average age at the time of presentation is approximately 10 years.9,12,14 Males are affected more frequently than females.12–14 Clinical signs progress as laryngeal dysfunction becomes more severe. Early in the disease process, owners may notice a voice change, inspiratory stridor, and exercise intolerance. Owners may initially believe that the dog’s reluctance to move is simply a sign of aging. Dysphagia can also occur, possibly in association with peripheral neuropathy.9,14 Owners may also report vomiting; however, they may actually be seeing regurgitation from concurrent esophageal disease or gagging and retching from a soft palate that has elongated as a result of inspiratory dyspnea. Once the laryngeal muscles are paralyzed bilaterally, dogs may develop severe dyspnea, cyanosis, and syncope. Exercise, obesity, excitement, and increased ambient temperature can exacerbate clinical signs, leading to an emergency presentation.9 Affected dogs may develop pneumonia or pulmonary edema, which can contribute to respiratory distress. Inability to constrict the glottis properly during swallowing, regurgitation, or vomiting increases the risk of aspiration. Pulmonary edema can develop in cases of upper airway obstruction as a result of changes in intrathoracic pressure and hypoxia, which cause increased permeability of alveolar capillary membranes.15,16

Diagnosis If an affected dog is stable, it should undergo a thorough physical examination. The thorax should be auscultated for evidence of pneumonia or pulmonary edema, such as harsh crackles, wheezes, or rales, and for cardiac murmurs or arrhythmias. Arterial pulses should be palpated for rate, rhythm, symmetry, and strength to assess for cardiovascular abnormalities that

Lateral view of a dissected canine larynx. (a) Thyroid cartilage, (b) cricoid cartilage, (c) hyoid apparatus, (d) epiglottis, (e) corniculate process of arytenoid cartilage.

could contribute to exercise intolerance. A complete neurologic examination should be performed to evaluate for signs of polyneuropathy, such as decreased postural reactions, deficits in spinal reflexes, and cranial nerve abnormalities.7 A rectal temperature should be obtained, and all dogs should be evaluated for systemic signs of heatstroke, such as petechial hemorrhages associated with disseminated intravascular coagulation, excessive panting, collapse, hyperemic mucous membranes, and abnormalities in mentation, regardless of body temperature at time of presentation.17,18 The primary means of heat loss in dogs is evaporation while panting. Dogs affected by acute signs of laryngeal paralysis are more susceptible to hyperthermia due to a lack of heat dissipation through an obstructed respiratory tract. Heatstroke from sustained hyperthermia can progress to multiorgan failure and death.17,18 If the body temperature is ≥106°F (41°C) or systemic signs of heatstroke are evident, additional diagnostics (e.g., coagulation panels, immediate evaluation of glucose and electrolytes) and supportive treatment should be instituted. Complete blood count and serum biochemistry profile results are typically normal unless concurrent diseases are present. In dogs with

QuickNotes Acquired laryngeal paralysis may be associated with a generalized peripheral neuropathy.

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FREE CE Laryngeal Paralysis in Dogs

QuickNotes Every dog suspected of having laryngeal paralysis should undergo thoracic radiography.

peripheral weakness, exercise intolerance, megaesophagus, or other signs of generalized polyneuropathy, free thyroxine and endogenous thyroid-stimulating hormone concentrations are measured to rule out hypothyroidism, and acetylcholine receptor antibody titers are measured to rule out myasthenia gravis.7,19 The association of laryngeal paralysis with hypothyroidism or myasthenia gravis is unclear, however, as medical treatment for either of these conditions is unlikely to restore laryngeal nerve function. Thoracic radiography is important for ruling out other causes of dyspnea and exercise intolerance and for determining whether concurrent conditions are present in dogs with laryngeal paralysis. The lung fields should be assessed for evidence of aspiration pneumonia and noncardiogenic pulmonary edema, which can occur with upper airway obstruction. Dogs with laryngeal paralysis from polyneuropathy or neuromuscular junction disease such as myasthenia gravis may develop megaesophagus, which significantly increases the likelihood of aspiration pneumonia11,12 (FIGURE 3). A contrast esophagram with videofluoroscopy may be required to make a definitive diagnosis of decreased esophageal motility.20 The risk

of aspiration largely outweighs the diagnostic beneﬁts of contrast esophagography; therefore, this procedure is not performed routinely in dogs with laryngeal paralysis. Laryngeal paralysis is most commonly diagnosed with transoral laryngoscopy under a light plane of anesthesia. Excessive administration of any anesthetic can inhibit laryngeal motion; however, some drugs may reduce arytenoid abduction under a light plane of anesthesia. In a comparison of seven different anesthetic protocols,21 acepromazine plus thiopental, acepromazine plus propofol, and ketamine plus diazepam resulted in no laryngeal motion in 67%, 50%, and 50% of normal dogs, respectively. Thiopental and propofol as single agents inhibit laryngeal motion less than these drug combinations.21,22 However, compared with propofol, thiopental as a single agent results in signiﬁcantly more arytenoid motion during inspiration and is therefore preferred for evaluation of laryngeal function.21,22 Often, dogs receive acepromazine when they present with anxiety and respiratory distress. In the comparison study, laryngeal function was evident in all normal dogs that received acepromazine and butorphanol sedation and were

FIGURE 3 Thoracic Radiographs.

Thoracic radiographs of a dog with megaesophagus and aspiration pneumonia. Note the borders of a dilated, air-filled esophagus (arrowheads) and air bronchograms (arrows). (A) Ventrodorsal view. (B) Right lateral view.

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FREE CE Laryngeal Paralysis in Dogs

BOX 1

Anesthetic Regimens for Diagnosing Laryngeal Paralysis in Dogs Preoxygenate for 3 to 5 minutes before induction. Thiopental (12–16 mg/kg IV to effect) Propofol (4.5–7 mg/kg IV slowly to effect) and doxapram (1 mg/kg IV) Acepromazine (0.2 mg/kg IM) and butorphanol (0.4 mg/kg IM) 20 minutes before mask induction with isoﬂurane

QuickNotes In dogs with laryngeal paralysis, paradoxical movement can be mistaken for active arytenoid abduction during laryngeal examination.

VIDEO

To see videos of normal and paralyzed laryngeal abduction, please visit

CompendiumVet.com.

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Unless the examiner is aware of the phase of respiration, it is easy to mistake paradoxical movement of the larynx for active abduction. Lack of arytenoid cartilage abduction during inspiration narrows the rima glottidis, increasing resistance to airflow. Rapid, forceful inspiration creates negative pressure within the larynx, which pulls the flaccid arytenoid cartilages medially, worsening the obstruction.27 The cartilages are forcefully separated by airflow as the animal exhales. Therefore, dogs with laryngeal paralysis and paradoxical motion have inward movement of the arytenoid cartilages on inspiration and outward, passive movement of the cartilages during expiration. Intubation may be required in some patients with severe paradoxical motion and resultant hypoxia.23

examined under a light plane of anesthesia induced by mask inhalation of isoflurane.21 In Medical Management animals in which laryngeal function has been Dogs that present with acute cyanosis or in coldepressed by sedatives and opioids, doxapram lapse require emergency treatment. Supplemen(1 mg/kg) can be administered intravenously tal oxygen should be provided to help alleviate hypoxia. An intravenous catheter should be to stimulate respiration23 (BOX 1). Although a portable laryngoscope can be placed for administration of fluid and medicaused to visualize the rima glottidis, retraction tions. Severely dyspneic or anxious dogs may of the tongue and pressure on the epiglot- require sedation with acepromazine (0.005 to tis with the laryngoscope blade may affect 0.02 mg/kg IV) and butorphanol (0.2 to 0.4 mg/ laryngeal function. Therefore, many clinicians kg IV) or other sedatives. If laryngeal edema is prefer to use a transoral video endoscope. suspected, an antiinflammatory dose of a glucoLaryngeal paralysis has also been diagnosed corticoid such as dexamethasone (0.1 to 0.5 mg/ with transnasal laryngoscopy and laryngeal kg) or prednisolone sodium succinate (0.5 to ultrasound.24,25 1 mg/kg) can be administered intravenously. If possible, blood oxygen saturation should Dogs that are significantly hyperthermic (≥106°F be monitored with a pulse oximeter during [41°C]) are treated with sedatives, IV fluids, cool laryngoscopy to ensure that the hemoglobin water baths, and fans. The rectal temperature saturation remains ≥95%.26 Flow-by oxygen should be monitored continuously until it has can be administered by attaching flexible tub- stabilized within a normal range and external ing from an oxygen source to the blade of cooling has been discontinued. Dogs that are the laryngoscope or to the insufflation port cyanotic, severely dyspneic, or hypoxic (SpO2 of the video endoscope to reduce the risk of <95%) despite supplemental oxygen therapy hypoxia. During laryngeal examination, laryn- may require intubation and light anesthesia until geal motion should be correlated with the laryngeal swelling resolves. If an intubation phase of respiration. It is helpful to have an period of several hours or longer is expected, assistant call out when each inspiration and a tracheostomy tube should be placed to avoid expiration occurs. In normal dogs, the rima exacerbation of laryngeal swelling from the glottidis remains open at rest, closes slightly endotracheal tube and prolonged periods of during expiration, and opens widely during anesthesia.28 It is possible for severe cases to inspiration. Inability of the arytenoid carti- progress to respiratory muscle fatigue, which lages to abduct during inspiration is diagnostic may require mechanical ventilation.29 There is for laryngeal paralysis. In questionable cases, no reliable bedside measurement for detection doxapram is administered intravenously.23 Res- of respiratory muscle fatigue; the diagnosis is piration is usually stimulated within 8 seconds based on changes in breathing patterns, such as after administration. inward movement of the abdomen during inspi-

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Laryngeal Paralysis in Dogs CE ration, uncoordinated alterations between ribcage and abdominal movements, and increased PaCO2 on blood gas analysis.29 Dogs that have mild clinical signs or are asymptomatic at rest may be managed conservatively by reducing stress, excitement, and exposure to high ambient temperatures and with weight loss as needed. Owners should be informed that laryngeal paralysis is usually progressive and that many dogs require surgery as clinical signs become more severe or quality of life is affected.

FIGURE 4

Surgical Treatment The goal of surgery is to enlarge the size of the rima glottidis to decrease resistance to airflow during inspiration. Surgical techniques include unilateral arytenoid lateralization (UAL), partial arytenoidectomy, vocal fold resection, castel- Dorsolateral view of a dissected canine larynx. (a) Muscular process of arytenoid cartilage, (b) cricoid cartilage, (c) thyroid cartilage, (solid line) suture lated laryngofissure, and muscle–nerve pediplacement for cricoarytenoid lateralization, (broken line) suture placement for 30–32 Some dogs may require thyroarytenoid lateralization. cle transposition. concurrent soft palate resection because prolonged negative airway pressure can increase tilage during inspiration33 (FIGURES 4 AND 5). soft palate length and thickness. Castellated Active abduction of the arytenoid with the laryngofissure is rarely performed, and mus- suture is not required to reduce laryngeal aircle–nerve pedicle transposition has not been way resistance.34,35 If the soft palate is elongated, evaluated in dogs with spontaneous laryngeal it is resected before recovery from anesthesia. paralysis; therefore, these procedures are not Bilateral arytenoid lateralization increases the risk of postoperative complications and respiradescribed in this article. In animals undergoing vocal fold resec- tory-related death and is not recommended.11 Complications are reported in 10% to 28% tion for laryngeal paralysis, the vocal fold and process are removed unilaterally or bilaterally. of dogs that undergo UAL (BOX 2) and include QuickNotes The procedure is often performed transorally aspiration pneumonia (8% to 33%), coughing with scissors. If bilateral vocal cordectomy is and gagging (16%), suture failure or return of Administration of performed, the ventral 1 to 2 mm of the vocal clinical signs (4% to 8%), gastric dilatation– doxapram during fold should be left in place to reduce the risk volvulus (4%), respiratory distress (2% to 4%), laryngeal examiof scar formation and subsequent glottal steno- and sudden death (3%).12,14,36 Aspiration pneu- nation facilitates sis. Partial arytenoidectomy involves unilateral monia may occur shortly after surgery or at differentiation of resection of the corniculate process of the laryngeal paralyarytenoid cartilage. This procedure can also be BOX 2 sis from drugperformed through a transoral approach with induced laryngeal Complications of Unilateral cup biopsy forceps and may be combined with 12 dysfunction. a vocal fold resection. In one study, complicaArytenoid Lateralization tions were reported in 40% of dogs undergoing unilateral laryngectomy (arytenoidectomy, Aspiration pneumonia vocal cordectomy, or a combination of both) Coughing/gagging for treatment of laryngeal paralysis, and 30% of Surgical repair failure the dogs died from respiratory-related causes. Respiratory distress UAL is the most commonly performed proGastric dilatation–volvulus cedure for laryngeal paralysis.12,14 With this Seroma formation technique, a suture is placed between the Sudden death arytenoid and cricoid or thyroid cartilages to prevent inward motion of the arytenoid carCompendiumVet.com | May 2009 | Compendium: Continuing Education for Veterinarians®

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FIGURE 5

Lateral view of a dissected canine larynx. (a) Muscular process of arytenoid cartilage, (b) cricoid cartilage, (c) cricothyroid articulation, (d) thyroid cartilage retracted laterally, (e) articulation of thyroid cartilage and thyrohyoid bone, (solid line) suture placement for cricoarytenoid lateralization.

QuickNotes Aspiration pneumonia is the most common complication after surgery for laryngeal paralysis.

any time for the remainder of the dog’s life. The use of metoclopramide reduces the risk of perioperative aspiration pneumonia.36 Median survival times after UAL range from 1 to 5 years, with approximately 14% of dogs dying from diseases related to the respiratory tract.12,14 Factors associated with a higher rate of complications or death include increasing age, placement of a temporary tracheostomy tube, and presence of concurrent respiratory tract abnormalities, postoperative megaesoph-

agus, and neurologic disease.12 In one study, ﬁve of six dogs that developed megaesophagus in conjunction with aspiration pneumonia died.12 Because polyneuropathy is suspected as an underlying etiology for laryngeal paralysis, affected dogs should be monitored frequently for evidence of neuromuscular weakness and esophageal dysfunction. The association between temporary tracheostomy tube placement and increased postoperative complications should be interpreted with caution because dogs that require tracheostomy tubes are likely to be in critical condition. Clinicians should not hesitate to place a tracheostomy tube in animals with severe inspiratory dyspnea. Despite complications, approximately 90% of dogs have a reduction in respiratory signs and improved exercise tolerance after UAL. Most owners report an improvement in quality of life and are satisﬁed with their decision to go to surgery.12,14

Conclusion Laryngeal paralysis is a common cause of upper airway obstruction in older, large-breed dogs and is likely associated with a generalized polyneuropathy in most animals. Surgical therapy is frequently indicated, and UAL is currently the recommended treatment. Respiratory signs signiﬁcantly improve in most patients after surgery; however, postoperative complication rates can be high, and patients have a lifelong risk of developing respiratory tract disease.

References 1. Evans HE, Kitchell RL. Cranial nerves and cutaneous innervation of the head. In: Evans HE, ed. Miller’s Anatomy of the Dog. Philadelphia: WB Saunders; 1993:953-987. 2. Venker-van Haagen AJ, Bouw J, Hartman W. Hereditary transmission of laryngeal paralysis in Bouviers. JAAHA 1981;17:75-76. 3. Braund KG, Shores A, Cochrane S, et al. Laryngeal paralysis-polyneuropathy complex in young dalmatians. Am J Vet Res 1994; 55:534-542. 4. Mahony OM, Knowles KE, Braund KG, et al. Laryngeal paralysis-polyneuropathy complex in young rottweilers. J Vet Intern Med 1998;12:330-337. 5. Polizopoulou ZS, Koutinas AF, Papadopoulos GC, et al. Juvenile laryngeal paralysis in three Siberian husky x Alaskan malamute puppies. Vet Rec 2003;153:624-627. 6. Klein MK, Powers BE, Withrow SJ, et al. Treatment of thyroid carcinoma in dogs by surgical resection alone: 20 cases (19811989). JAVMA 1995;206:1007-1009. 7. Jeffery ND, Talbot CE, Smith PM, et al. Acquired idiopathic laryngeal paralysis as a prominent feature of generalised neuromuscular disease in 39 dogs. Vet Rec 2006;158:17. 8. Thieman KM, Krahwinkel DJ, Shelton D, et al. Laryngeal paralysis: part of a generalized polyneuropathy syndrome in older dogs. Vet Surg 2007;36:E26. 9. Burbidge HM. A review of laryngeal paralysis in dogs. Br Vet J 1995;151:71-82.

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10. Jaggy A, Oliver JE, Ferguson DC, et al. Neurological manifestations of hypothyroidism: a retrospective study of 29 dogs. J Vet Intern Med 1994;8:328-336. 11. Dewey CW, Bailey CS, Shelton GD, et al. Clinical forms of acquired myasthenia gravis in dogs: 25 cases (1988-1995). J Vet Intern Med 1997;11:50-57. 12. MacPhail CM, Monnet E. Outcome of and postoperative complications in dogs undergoing surgical treatment of laryngeal paralysis: 140 cases (1985-1998). JAVMA 2001;218:1949-1956. 13. Snelling SR, Edwards GA. A retrospective study of unilateral arytenoid lateralisation in the treatment of laryngeal paralysis in 100 dogs (1992-2000). Aust Vet J 2003;81:464-468. 14. Hammel SP, Hottinger HA, Novo RE. Postoperative results of unilateral arytenoid lateralization for treatment of idiopathic laryngeal paralysis in dogs: 39 cases (1996-2002). JAVMA 2006;228:1215-1220. 15. Algren JT, Price RD, Buchino JJ, et al. Pulmonary edema associated with upper airway obstruction in dogs. Pediatr Emerg Care 1993;9:332-337. 16. John PJ, Mahashur AA. Pulmonary oedema associated with airway obstruction. Can J Anaesth 1991;38:139-140. 17. Bruchim Y, Klement E, Saragusty J, et al. Heat stroke in dogs: a retrospective study of 54 cases (1999-2004) and analysis of risk factors for death. J Vet Intern Med 2006;20:38-46. 18. Flournoy WS, Macintire DK, Wohl JS. Heatstroke in dogs: clini-

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FREE

Laryngeal Paralysis in Dogs CE cal signs, treatment, prognosis, and prevention. Compend Contin Educ Pract Vet 2003;25:422-431. 19. Shelton GD. Myasthenia gravis and disorders of neuromuscular transmission. Vet Clin North Am Small Anim Pract 2002;32:189-206, vii. 20. Washabau RJ, Hall JA. Diagnosis and management of gastrointestinal motility disorders in dogs and cats. Compend Contin Educ Pract Vet 1997;19:721-737. 21. Jackson AM, Tobias K, Long C, et al. Effects of various anesthetic agents on laryngeal motion during laryngoscopy in normal dogs. Vet Surg 2004;33:102-106. 22. Gross ME, Dodam JR, Pope ER, et al. A comparison of thiopental, propofol, and diazepam-ketamine anesthesia for evaluation of laryngeal function in dogs premedicated with butorphanol-glycopyrrolate. JAAHA 2002;38:503-506. 23. Tobias KM, Jackson AM, Harvey RC. Effects of doxapram HCl on laryngeal function of normal dogs and dogs with naturally occurring laryngeal paralysis. Vet Anaesth Analg 2004;31:258-263. 24. Radlinsky MG, Mason DE, Hodgson D. Transnasal laryngoscopy for the diagnosis of laryngeal paralysis in dogs. JAAHA 2004;40:211-215. 25. Rudorf H, Barr FJ, Lane JG. The role of ultrasound in the assessment of laryngeal paralysis in the dog. Vet Radiol Ultrasound 2001;42:338-343. 26. Proulx J. Respiratory monitoring: arterial blood gas analysis, pulse oximetry, and end-tidal carbon dioxide analysis. Clin Tech Small Anim Pract 1999;14:227-230. 27. Smith MM. Diagnosing laryngeal paralysis. JAAHA 2000;36:383384.

28. Bishop MJ, Hibbard AJ, Fink BR, et al. Laryngeal injury in a dog model of prolonged endotracheal intubation. Anesthesiology 1985;62:770-773. 29. Barton L. Respiratory muscle fatigue. Vet Clin North Am Small Anim Pract 2002;32:1059-1071, vi. 30. Greenﬁeld CL, Walshaw R, Kumar K, et al. Neuromuscular pedicle graft for restoration of arytenoid abductor function in dogs with experimentally induced laryngeal hemiplegia. Am J Vet Res 1988;49:1360-1366. 31. Toth A, Szucs A, Harasztosi C, et al. Intrinsic laryngeal muscle reinnervation with nerve-muscle pedicle. Otolaryngol Head Neck Surg 2005;132:701-706. 32. Fulton IC, Stick JA, Derksen FJ. Laryngeal reinnervation in the horse. Vet Clin North Am Equine Pract 2003;19:189-208, viii. 33. Mathews KG, Roe S, Stebbins M, et al. Biomechanical evaluation of suture pullout from canine arytenoid cartilages: effects of hole diameter, suture conﬁguration, suture size, and distraction rate. Vet Surg 2004;33:191-199. 34. Bureau S, Monnet E. Effects of suture tension and surgical approach during unilateral arytenoid lateralization on the rima glottidis in the canine larynx. Vet Surg 2002;31:589-595. 35. Greenberg MJ, Bureau S, Monnet E. Effects of suture tension during unilateral cricoarytenoid lateralization on canine laryngeal resistance in vitro. Vet Surg 2007;36:526-532. 36. Greenberg MJ, Reems MR, Monnet E. Use of perioperative metoclopramide in dogs undergoing surgical treatment of laryngeal paralysis: 43 cases (1999-2006). Vet Surg 2007;36:E11.

3 CE CREDITS

CE TEST 1 This article qualiﬁes for 3 contact hours of continuing education credit from the Auburn University College of Veterinary Medicine. Subscribers may take individual CE tests online and get real-time scores at CompendiumVet.com. Those who wish to apply this credit to fulﬁll state relicensure requirements should consult their respective state authorities regarding the applicability of this program.

1. The most common cause of acquired laryngeal paralysis is a. hypothyroidism. b. myasthenia gravis. c. trauma. d. idiopathic. 2. The muscle responsible for abduction of the arytenoid cartilages during inspiration is the ___________ muscle. a. cricoarytenoideus dorsalis b. cricoarytenoideus lateralis c. thyropharyngeus d. arytenoideus transversus 3. Laryngeal paralysis has been identiﬁed as a congenital condition in a. Labrador retrievers. b. Great Danes. c. Afghan hounds. d. Bouvier des Flandres. 4. Which is an early sign of laryngeal paralysis? a. syncope b. cardiac murmur c. voice change d. cyanosis

5. Which anesthetic protocol decreases laryngeal function in at least 50% of normal dogs? a. acepromazine/thiopental b. acepromazine/propofol c. ketamine/diazepam d. all of the above

8. Which factor is associated with a higher rate of complications or death after UAL in dogs with laryngeal paralysis? a. young age b. obesity c. the need to place a temporary tracheostomy tube d. perioperative metoclopramide

6. Regarding partial laryngectomy, which statement is true? a. In dogs undergoing bilateral vocal cordectomy, the entire vocal fold should be removed. b. Partial arytenoidectomy is performed by removing the corniculate process of the arytenoid cartilage. c. Complications are reported in 10% of dogs undergoing unilateral partial laryngectomy for laryngeal paralysis. d. Approximately 5% of dogs undergoing unilateral partial laryngectomy die from respiratory-related diseases.

9. Which statement is true? a. Shortening an elongated soft palate increases the risk of postoperative aspiration after arytenoid lateralization. b. During UAL, the arytenoid cartilage should be maximally abducted with sutures to enlarge the glottic opening. c. Bilateral arytenoid lateralization increases the risk of postoperative complications and respiratory-related death. d. The risk of aspiration pneumonia signiﬁcantly decreases 1 year after UAL.

7. The most common complication after unilateral arytenoid lateralization is a. respiratory distress. b. aspiration pneumonia. c. seroma formation. d. suture failure.

10. Approximately ___________ of dogs experience improvement in upper airway resistance and exercise tolerance following arytenoid lateralization. a. 30% c. 75% b. 50% d. 90%

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COLUMN EDITOR COLUMN EDITOR Craig E. Grifﬁn, DVM, DACVD Animal Dermatology Clinic, San Diego, California

COLUMN EDITOR COLUMN EDITOR Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic, Tustin, California

Overview of Flea Allergy Dermatitis ❯❯ Andrea Lam, DVM

❯❯ Anthony Yu, DVM, MS, DACVDa

University of California Davis Veterinary Medical Teaching Hospital

Flea Facts

At a Glance Flea Facts Page 220

Pathogenesis Page 220

Diagnosis Page 222

Treatment Page 223

Flea Control Products Page 224

a Dr. Yu discloses that he has received ﬁnancial support from Greer Laboratories, Iams, Novartis Animal Health, and Pﬁzer Animal Health.

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University of Guelph Ontario Veterinary College

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Dr. Yu (shown here with his dogs [from left to right] Timmy, Joey, and Bitsy) is associate professor of dermatology at The University of Guelph Ontario Veterinary College in Canada.

WEB EXCLUSIVE An extended version of this article is available on

CompendiumVet.com.

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FIGURE 1

FIGURE 2

Typical distribution pattern of ﬂea allergy dermatitis affecting the caudodorsolumbar region and caudal thighs (caudal to the “waistline”).

A ﬁbropruritic nodule, a benign hyperplastic reaction to severe flea allergy dermatitis, on a dog.

Diagnosis

QuickNotes History and physical examination ﬁndings are the keys to making an appropriate diagnosis of ﬂea allergy dermatitis.

History and physical examination findings are the keys to making an appropriate diagnosis of flea allergy dermatitis. There is no breed or sex predilection, and flea allergy dermatitis can develop in animals of any age. Patients may exhibit seasonal or year-round pruritus, depending on their geographic location. The owner may report an increase in pruritus following the introduction of a new pet or a visit to a boarding or grooming facility. Often, clinical signs manifest on the caudal aspect of the animal, especially in dogs (FIGURE 1). Evidence of self-induced alopecia; erythema; pyotraumatic dermatitis; dull, coarse

FIGURE 3

“Hot spot” or acute moist traumatic dermatitis. One of the common underlying etiologies of this condition is flea allergy or flea-bite hypersensitivity.

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haircoat; hyperpigmentation; and/or lichenification may be observed affecting the dorsal lumbosacral region, tail base, caudomedial thighs, inguinal region, and umbilical fold.1 Other physical examination findings include papules or encrusted papules, crusting, scaling, and, occasionally, fibropruritic nodules (FIGURE 2) in association with affected areas. Secondary superficial to deep pyodermas are common (FIGURE 3). Close examination of the skin and haircoat using a flea comb may reveal flea dirt or adult fleas (FIGURE 4). Some pets may even exhibit clinical anemia as a result of severe flea infestation (FIGURE 5). Pets that are fastidious groomers can ingest adult fleas

FIGURE 4

Flea comb. This is a useful tool to demonstrate fleas and flea dirt to clients who are in denial about the presence of fleas on their pet.

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carrying the tapeworm Dipylidium caninum and may have segments of D. caninum in their feces. Clinical manifestations of flea allergy dermatitis in cats can include miliary dermatitis, eosinophilic granulomas or plaques, or self-induced alopecia without active lesions (FIGURE 6). Affected areas may include the dorsum, inguinal region, caudomedial thighs, head, and neck. A lack of fleas or flea dirt is commonly reported by owners and should not override a diagnosis of flea allergy dermatitis if clinical suspicion is high. Intradermal skin testing with flea allergen may reveal wheal formation with immediate and delayed hypersensitivity. Serum in vitro testing for flea-specific IgE has variable accuracy and does not identify animals with delayed hypersensitivity reactions. Histopathology is nonspecific and reveals a superficial perivascular inflammation, often containing eosinophils—a pattern that can be seen in other hypersensitivity reactions.

Treatment Based on current knowledge of flea biology, topical or systemic flea adulticide therapy may be the only management required to establish adequate control over flea infestations. Many prescription flea control products are currently available (TABLE 1). Ideally, integrated pest management, including the use of flea adulticides along with insect growth regulators

(IGRs) or insect development inhibitors (IDIs), should be used as a long-term management program to effectively eradicate infestation while minimizing potential drug resistance. If the environment is heavily burdened with various stages of fleas, environmental control is also warranted. Vibrations from a vacuum cleaner help stimulate emergence of the adult flea from the impervious pupa and, hence, increase the likelihood of effective environmental ectoparasiticide control. One to two applications of a synthetic pyrethroid or fipronil as an environmental spray every 7 days should be sufficient, although the addition of a household IGR such as methoprene or pyriproxyfen and/or sodium polyborate in carpeted areas would produce the best results in the house. To avoid any potential adverse reactions, it is best to remove pets from the treated environment until the products have dried; therefore environmental treatment is often done in stages. Professionally licensed exterminators should be considered for yards and households that are heavily infested. All blankets, bedding, and rugs that are favored by the affected pet should be laundered. All carpeted areas and furniture that can house preadult fleas should be vacuumed, and the vacuum bag should be disposed of immediately. All household pets should be prevented access to flea-dense areas, such as porches, garages, and crawl spaces. Contact

QuickNotes A lack of fleas or flea dirt should not override a diagnosis of flea allergy dermatitis if clinical suspicion is high.

FIGURE 5 Severe ﬂea infestation.

Fleas on a dog before treatment.

When the dog was bathed, the water turned red from the extreme amount of flea dirt in the haircoat.

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TABLE 1

Flea Control Products Approved by the US Environmental Protection Agency and/or the US Food and Drug Administrationa Product (Manufacturer)

Active Flea Control Ingredientsb

Species and Minimum Age

Program/Sentinel (Novartis Animal Health)

Lufenuron

Dogs: 4 weeks

Frontline Plus (Merial)

Fipronil

Dogs: 8 weeks

S-Methoprene

Cats: 8 weeks

Cats: 6 weeks

Dosage/Administration

Mode of Action

Monthly oral; also injectable q6mo feline product

Inhibitor of chitin biosynthesis

Monthly spot-on

Fipronil: GABA-gated chloride channel antagonist S-methoprene: Juvenile hormone analogue (IGR)

Advantage (Bayer Animal Health)

Imidacloprid

Advantage Multi (Bayer Animal Health)

Imidacloprid

K9 Advantix (Bayer Animal Health)

Imidacloprid

Dogs: 7 weeks Cats: 8 weeks Dogs: 7 weeks

Monthly spot-on; can be used weekly

Nicotinic acetylcholine-receptor antagonist

Monthly spot-on

Nicotinic acetylcholine-receptor antagonist

Monthly spot-on

Nicotinic acetylcholine-receptor antagonist

Cats: 9 weeks (do not use canine product on cats) Dogs: 7 weeks

Permethrin

Permethrin: Sodium channel modulator Revolution (Pﬁzer Animal Health)

Selamectin

ProMeris for dogs (Fort Dodge Animal Health)

Metaﬂumizone

ProMeris for cats (Fort Dodge Animal Health)

Dogs: 8 weeks

Monthly spot-on

Chloride channel activator

Dogs: 8 weeks

Monthly spot-on

Voltage-dependent sodium channel blocker

Metaﬂumizone

Cats: 8 weeks

Monthly spot-on

Voltage-dependent sodium channel blocker

Comfortis (Eli Lilly)

Spinosad

Dogs: 14 weeks

Monthly chewable tablet

Nicotinic acetylcholine-receptor agonist (spinosyn)

Capstar (Novartis Animal Health)

Nitenpyram

Dogs: 4 weeks and 2+ lb

One tablet prn or daily/EOD

Nicotinic acetylcholine-receptor antagonist

Vectra 3D for Dogsc (Summit VetPharm)

Dinotefuran

Monthly spot-on

Dinotefuran: Nicotinic acetylcholinereceptor antagonist

Cats: 8 weeks

Cats: 4 weeks and 2+ lb Dogs: 7 weeks

Permethrin

Permethrin: Sodium channel modulator

Pyriproxyfen

Pyriproxyfen: Juvenile hormone analogue (IGR) Vectra for Cats & Kittens (Summit VetPharm)

Dinotefuran

Cats: 8 weeks

Monthly spot-on

Pyriproxyfen

Dinotefuran: Nicotinic acetylcholinereceptor antagonist Pyriproxyfen: Juvenile hormone analogue (IGR)

Adapted with permission from Mark Grossman and Carol Foil, Veterinary Information Network 2008. For the complete chart, visit www.vin.com/Link.plx?ID=37277. (EOD = every other day; prn = as needed)

Ingredients active against other parasites not listed.

This chart reﬂects the latest revision by VIN in September 2008. Please note that the following product has since become available: Vectra for Dogs and Puppies.

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FIGURE 6 Common reaction patterns associated with underlying ﬂea allergic dermatitis in cats.

QuickNotes

Miliary dermatitis of the dorsum.

Self-induced alopecia of the ventral abdomen.

with feral cats, wildlife, and other unknown neighborhood animals should be prevented. Eliminating all secondary bacterial and Malassezia infections provides short-term relief of pruritus. Shampoo therapy and short courses of oral corticosteroids are good adjunctive

therapies. Antihistamines and essential fatty acids are not effective in ﬂea-allergic patients. Finally, all animals in the household must be treated with ectoparasiticide therapy to prevent reestablishment of ﬂea populations and perpetuation of disease.

Topical or systemic ﬂea adulticide therapy may be the only management required to establish adequate control over ﬂea infestations.

References 1. Scott DW, Miller WH, Griffin CE. Skin immune system and allergic skin disorders. In: Scott DW, Miller WH, Griffin CE, eds. Muller and Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:543-666. 2. Cole LK. Fleas and flea allergy dermatitis. 6th Proc World Congr Vet Dermatol 2008:119-125. 3. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol 2008;19(suppl 1):12. 4. Gross TL, Halliwell RE. Lesions of experimental flea bite hyper-

APPLIED DERMATOLOGY WEB EXCLUSIVE

sensitivity in the dog. Vet Pathol 1985;22:78-81. 5. Halliwell RE, Preston JF, Nesbitt JG. Aspects of the immunopathogenesis of ﬂea allergy dermatitis in dogs. Vet Immunol Immunopathol 1987;17:483-494. 6. Kwocka KW. Fleas and related disease. Vet Clin North Am Small Anim Pract 1987;17:1235-1262. 7. Reedy LM, Miller WH. In: Reedy LM, Miller WH, eds. Allergic Skin Diseases of Dogs and Cats. Philadelphia: WB Saunders: 1989:171-187.

Otitis externa is another common, often frustrating, dermatologic condition. Visit CompendiumVet.com for one expert’s approach to canine otitis externa, “A Practical Approach to Diagnosing and Managing Ear Disease in Dogs,” by Paul Bloom, DVM, DACVD, DAVBP (Canine and Feline).

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May 2009 Vol 31(5)

WEB EXCLUSIVES

CE ARTICLES WEBEXCLUSIVE

VIDEOS

❯❯ Laryngeal Paralysis Videos The article “Laryngeal Paralysis in Dogs,” by Drs. Ralph P. Millard and Karen M. Tobias in this issue, discusses the use of endoscopy to help diagnose this condition. Two endoscopic videos of normal and paralyzed laryngeal abduction help illustrate the concept.

❯❯ Feline Nonregenerative Anemia ❯❯ Carrie White and Nyssa Reine Anemia in cats is not a diagnosis but rather a sign of an underlying disease. The diagnostic work-up for an anemic patient is often extensive. If nonregenerative anemia is identiﬁed, a number of tests may be required to determine its cause, including a close examination of the patient’s blood and bone marrow. Although there are standard supportive measures for anemic cats, speciﬁc therapies can be implemented for certain etiologies of nonregenerative anemia. Part one of this article addresses the pathophysiology and etiologies of nonregenerative anemia in cats; part two provides an overview of diagnosis and treatment.

❯❯ Arterial and Venous Blood Gases ❯❯ Ricardo Irizarry and Adam Reiss Blood gas analysis is frequently requested as part of the point-of-care testing for emergency or critical care patients presenting with metabolic or respiratory abnormalities. With the advent of portable units, information regarding a patient’s acid–base balance and ventilation and oxygenation status can be rapidly obtained. In two related articles, Drs. Irizarry and Reiss provide information on arterial and venous blood gas analysis with the goal of helping clinicians integrate such data in their case management.

WEB-EXCLUSIVE ARTICLES

❯❯ A Practical Approach to Diagnosing and Managing Ear Disease in Dogs ❯❯ Paul Bloom In a supplement to the new Applied Dermatology series, Dr. Bloom describes the many factors that cause and perpetuate canine otitis externa and presents his approach to treating these often frustrating cases.

❯❯ Overview of Flea Allergy Dermatitis ❯❯ Andrea Lam and Anthony Yu This expanded version of the Applied Dermatology article published in this issue includes information on currently available ﬂea-control products. NEWS BITES

❯❯ Professor Links Gum Diseases and Heart Problems in Dogs ❯❯ Mucosal Muscarinic Receptors Enhance Bladder Activity in Cats with Feline Interstitial Cystitis ❯❯ Veterinarians Required to Prevent Identity Theft ❯❯ Feline Diet Study Triggers Nervous System Repair Discovery

E-NEWSLETTER ❯❯ COMPENDIUM EXTRA, a monthly e-newsletter, provides Web-exclusive articles and news as well as a preview of this month’s journal. Sign up at CompendiumVet.com.

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DERMDIGEST Treating Dermatology Cases: The Secrets to Success Joel Sailor, DVM Town & Country Veterinary Clinic Starke, Florida

A step-by-step approach that includes the entire practice team is helpful.

In today’s tight economy, there is tendency to assume that people don’t want or need our services. The last time I checked though, conditions such as atopy, diabetes, renal disease, and hypothyroidism were completely unaffected by the financial state of domestic or foreign markets. Family is often the one thing people find solace in during tough financial times. For my clients, this includes both two-legged and four-legged family members. As a practitioner, I am encouraged by the devotion clients continue to display toward their pets. It is tempting to try to take shortcuts in an effort to save money when doing diagnostic work-ups on patients, but this is not what our clients want. They certainly want to spend as little money as possible, but not at the expense of their pet’s health.

Take It Step by Step To avoid unnecessary procedures in making the correct diagnosis and identifying the appropriate treatment, a step-by-step approach that includes the entire practice team is helpful. The purpose is not to remove the doctor from the process but rather to give him or her a platform from which to excel. The example I would use is beef Wellington. This is a well-known and often signature dish for many chefs, but all have put their own spin on the entrée while maintaining the integrity of the dish. In terms of allergic patients, we would like the owners to recognize our efforts in creating an expertly crafted dermatologic work-up and treatment plan. I believe a practice succeeds or fails as a team. Therefore, it is necessary that all doctors and staff members follow a well-conceived and well-written protocol. This is easier for smaller practices but shouldn’t be difﬁcult in larger practices if we can check our pride at the door when creating protocols for the team. Protocols can be developed based on both current literature and consultations with a dermatology specialist. For all “skin cases” seen at my practice, we generally begin with a conversation with clients about the complexity of dermatologic disease. This starts with the receptionist and is repeated by the technician and doctor. The initial history is taken by the technician using a scripted survey questionnaire and is then expanded based on questions asked by the attending doctor. An important step in avoiding misdiagnosis is to establish a minimal test database that is used for every patient. For ﬁrst-time evaluations, we perform a three-slide cytology panel that consists of an ear swab, skin scrape, and adhesive tape preparation of affected areas. These samples can be collected by the technician or doctor depending on the experience of the staff. Tiffany Carty, one of our technicians, puts it best: “Being able to get and process cytology samples for our skin cases not only speeds our diagnostic process, it also helps me feel like an integral part of the medical team.” We then address any existing parasites or infections. Depending on the severity of the pruritus, we may prescribe antihistamines and a corticosteroid to ameliorate the itching and prevent further skin damage.

This information has not been peer reviewed and does not necessarily reﬂect the opinions of, nor constitute or imply endorsement or recommendation by, the Publisher or Editorial Board. The Publisher is not responsible for any data, opinions, or statements provided herein.

Sponsored by Novartis Animal Health US, Inc., maker of Atopica Brief Summary: For full product information see product insert. Caution: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. Description: ATOPICA (cyclosporine capsules, USP) MODIFIED is an oral form of cyclosporine that immediately forms a microemulsion in an aqueous environment.

Consider Product Turns When Pricing Dermatology Products

Indications and Usage: ATOPICA is indicated for the control of atopic dermatitis in dogs weighing at least 4 lbs body weight.

A rapidly turning product is one that is purchased repeatedly by the same client. Compared with products such as heartworm preventives, which are purchased once or twice a year, rapidly turning products provide income all year long. Thus, the markup on these products can be lower and still result in a higher net proﬁt by year’s end.

Dosage and Administration: The initial daily dose of ATOPICA is 5 mg/kg/day (3.36.7 mg/kg/day) as a single daily dose for 30 days. Following this initial daily treatment period, the dose of ATOPICA may be tapered by decreasing the frequency of dosing to every other day or two times a week, until a minimum frequency is reached which will maintain the desired therapeutic effect. ATOPICA should be given at least one hour before or two hours after a meal. If a dose is missed, the next dose should be administered (without doubling) as soon as possible, but dosing should be no more frequent than once daily. See Product Insert for dosing chart. Contraindications: ATOPICA is contraindicated for use in dogs with a history of neoplasia.

A recheck in 1 month is a must. We repeat the history, focusing on any changes since the last visit. At this visit, we move toward addressing the allergies present, starting with a discussion of the long-term solutions available for the life-long issue of allergies. At this stage we will begin a course of ATOPICA® (cyclosporine capsules, USP) MODIFIED in patients with suspected atopy, and any residual infections—the most frequent cause for failure with ATOPICA therapy—are addressed. We commonly employ a nontraditional markup for ATOPICA because it is a rapidly turning inventory item in our practice, similar to pet food. This keeps the product affordable for clients while still creating tremendous proﬁt for the practice. We also market any rebates available at the time. Patients are again rechecked in 1 month to reassess treatment. If they are doing well, we continue with the therapy; if not, we will switch to a food trial. Any changes in treatment are based on the patient’s history since the previous visit. We continue this process until management of the symptoms is achieved.

Prevent Personal Bias Part of our success is not allowing any personal bias about cost enter our discussions with clients. We automatically assume they want the best for their pet and would prefer to avoid long-term use of corticosteroids. Clients are looking for answers to their pets’ problems. I am certain that those who are hesitant to follow our recommendations are picking up on my inadvertent projection of bias about the cost. When I am more confident in my recommendation, compliance usually follows. Of course, there are clients who cannot afford our recommended treatment plan, but it is our part to recommend and theirs to let us know their limitations. So we always make our best recommendation first; if that is not within their budget, then and only then do we offer a second-best option. * * * I have purposely left out specific details about our protocol because your team needs to create its own protocol to be successful. The main points I can’t emphasize enough are to (1) standardize how you handle these cases, (2) price your treatments realistically for both the client and the practice, and (3) prevent personal bias from dictating what you recommend to your clients. As with all drugs, side effects may occur. In a field study, the most common side effects were gastrointestinal signs. Gingival hyperplasia and papillomas may also occur during the initial dosing phase. ATOPICA is a systemic immunosuppressant that may increase the susceptibility to infection. ATOPICA is not for use in reproducing dogs or dogs with a history of neoplasia.

WARNINGS: ATOPICA (cyclosporine) is a potent systemic immunosuppressant that may increase the susceptibility to infection and the development of neoplasia. Human Warnings: Not for human use. Keep this and all drugs out of reach of children. For use only in dogs. Precautions: Gastrointestinal problems and gingival hyperplasia may occur at the initial recommended dose. ATOPICA should be used with caution with drugs that affect the P-450 enzyme system. Simultaneous administration of ATOPICA with drugs that suppress the P-450 enzyme system, such as ketoconazole, may lead to increased plasma levels of cyclosporine. The safety and effectiveness of ATOPICA has not been established in dogs less than 6 months of age or less than 4 lbs body weight. ATOPICA is not for use in breeding dogs, pregnant or lactating bitches. Since the effect of cyclosporine use on dogs with compromised renal function has not been studied ATOPICA should be used with caution in dogs with renal insufficiency. There have been reports of convulsions in human adult and pediatric patients receiving cyclosporine, particularly in combination with high dose methylprednisolone. Killed vaccines are recommended for dogs receiving ATOPICA because the impact of cyclosporine on the immune response to modified live vaccines is unknown. As with any immunomodulation regimen, exacerbation of sub-clinical neoplastic conditions may occur. Adverse Reactions: A total of 265 dogs were included in the field study safety analysis. One hundred and eleven (111) dogs were treated with placebo for the first 30 days. For the remainder of the study, all dogs received ATOPICA capsules. Four dogs withdrew from the study after vomiting. One dog each withdrew from the study after diarrhea; vomiting, diarrhea and pruritus; vomiting, depression and lethargy; lethargy, anorexia and hepatitis; gingival hyperplasia, lethargy, polyuria/polydipsia and soft stool; seizure; sebaceous cyst; pruritus; erythema; or otitis externa respectively. Vomiting (30.9%) and diarrhea (20.0%) were the most common adverse reactions occurring during the study. In most cases, signs spontaneously resolved with continued dosing. In other cases, temporary dose modifications (brief interruption in dosing, divided dosing, or administration with a small amount of food) were employed to resolve signs. Persistent otitis externa (6.8%), urinary tract infections (3.8%), anorexia (3.0%), gingival hyperplasia (2.3%), lymphadenopathy (2.3%) and lethargy (2.3%) were the next most frequent adverse events observed. Gingival hyperplasia regressed with dose tapering. Owners of four dogs reported seizures while dogs were receiving ATOPICA. In one dog, seizures were the result of a brain tumor diagnosed one month into the study. Another dog experienced seizures before and after the study. The following clinical signs were reported in less than 2% of dogs treated with ATOPICA in the field study: constipation, flatulence, Clostridial organisms in the feces, nausea, regurgitation, polyuria/polydipsia, strong urine odor, proteinuria, pruritus, erythema/ flushed appearance, pyoderma, sebaceous adenitis, crusty dermatitis, excessive shedding, coarse coat, alopecia, papillomas, histiocytoma, granulomatous mass or lesion, cutaneous cyst, epulis, benign epithelial tumor, multiple hemangioma, raised nodule on pinna, seizure, shaking/trembling, hind limb twitch, panting, depression, irritability, hyperactivity, quieter, increased light sensitivity, reluctance to go outside, weight loss, hepatitis. Clinical Pathology Changes: During the study, some dogs experienced changes in clinical chemistry parameters while receiving ATOPICA, as follows: elevated creatinine (7.8%), hyperglobulinemia (6.4%), hyperphosphatemia (5.3%), hyperproteinemia (3.4%), hypercholesterolemia (2.6%), hypoalbuminemia (2.3%), hypocalcemia (2.3%) and elevated BUN (2.3%). Post-approval Experience: Neoplasms have been reported in dogs taking ATOPICA, including reports of lymphosarcoma and mast cell tumor. It is unknown if these were preexisting or developed de novo while on ATOPICA. In post-approval drug experience reporting the following additional adverse reactions have been associated with ATOPICA administration in dogs: vomiting, diarrhea, depression/lethargy, anorexia, pruritus, liver enzyme elevations, trembling, convulsions, polydipsia, polyuria, weight loss, hyperactivity, nervousness, neoplasia. To report suspected adverse reactions or for technical assistance, call 1-800-332-2761. Manufactured for: Novartis Animal Health US, Inc. Greensboro, NC 27408, USA NADA 141-218, Approved by FDA ©2008 Novartis Animal Health US, Inc. ATOPICA is a registered trademark of Novartis AG. NAH/ATO-GC/BS/5 07/08

ATO09DIGEST1

Abstract Thoughts Offering a brief look at the latest important research presented in the international veterinary literature.

Idiopathic Inflammation of Epidural Fat in Dachshunds Aikawa T, Yoshigae Y, Kanazono S. Epidural idiopathic sterile pyogranulomatous inflammation causing spinal cord compressive injury in five miniature dachshunds. Vet Surg 2008;37:594-601.

Column Editor ❯❯ Joseph Harari, MS, DVM, DACVS Veterinary Surgical Specialists Spokane, Washington

ABSTR ACT

This retrospective study from a veterinary medical center in Tokyo describes the clinicopathologic features of idiopathic sterile pyogranulomatous inflammation of epidural fat causing spinal cord compression in five mature miniature dachshunds. During the time interval of the study (2000–2006), 515 miniature dachshunds were surgically treated for thoracolumbar disk disease. Three of the five dogs identified as having idiopathic sterile pyogranulomatous inflammation of epidural fat were ambulatory and had chronic paraspinal pain; the other two dogs were acutely paraparetic/paraplegic and nonambulatory. No abnormalities were detected on hematologic profile tests. Three dogs had received prednisolone therapy for 1 to 5 months before admission. Myelography indicated focal or multifocal extradural spinal compression in the thoracolumbar region in all five dogs. Hemilaminectomy revealed a compressive, easily removable mass of epidural fat characterized histologically as pyogranulomatous inflammatory steatitis. Microbial culture of the surgical specimen was conducted for two dogs and yielded no bacterial growth. All dogs recovered well from surgery and were ambulatory within 1 to 18 days. Improved neurologic status was noted for a median of 17 months after surgery. Two dogs had other pyogranulomatous lesions after surgery, and four dogs received postoperative prednisolone therapy.

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Intervertebral disk disease in dachshunds is a common clinical scenario for small animal practitioners. Dogs can present with variable neurologic signs, and diagnostic imaging is critical in establishing a diagnosis. The results of this study should alert clinicians to the possibility of a compressive thoracolumbar spinal lesion in dachshunds that is not an intervertebral disk-related lesion. Although myelography provided significant diagnostic information about the location of the lesion, it would be interesting to know in future studies if cerebrospinal fluid analysis or magnetic resonance imaging would be beneficial in the work-up of these cases. It appears that surgical decompression and histologic evaluation of excised tissue were critical in recovery and the fi nal diagnosis. It is interesting to note the systemic involvement of pyogranulomatous disease in some of the dogs and the inconclusive effects of corticosteroids.

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Exceeding client expectations matter how long you have been in this profession, it’s always humbling to “ No know that you are such a trusted partner in the human–animal bond. Knowing that my clients can access their Pet Portal® to ﬁnd good medical advice, review their pet’s medical records, and receive medication reminders allows me to consistently meet their needs — and exceed their expectations — even when I have no extra time. Vetstreet ensures client satisfaction and compliance without additional work for me or my staff.

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3 CE CREDITS

CE Article 2

Pneumothorax ❯❯ Karl C. Maritato, DVM MedVet Medical and Cancer Center for Pets Worthington, Ohio

❯❯ José A. Colón, DVM ❯❯ David H. Kergosien, MS, DVM, DACVS ❯❯ Louisiana Veterinary Referral Center Mandeville, Louisiana

Abstract: Pneumothorax may be classiﬁed as open or closed and as traumatic, spontaneous, or iatrogenic. The most common cause of pneumothorax is thoracic trauma. Spontaneous pneumothorax is often a result of bullous emphysema, and iatrogenic pneumothorax is an important complication of procedures involving the thoracic cavity. Most animals present with tachypnea, tachycardia, respiratory distress, and anxiety. Radiography and thoracocentesis are useful diagnostic aids. Traumatic and iatrogenic pneumothorax are commonly treated with thoracocentesis or thoracostomy tube placement. Spontaneous pneumothorax usually requires surgical resection of the affected lobe(s). The prognosis for traumatic pneumothorax is excellent if there are no other life-threatening injuries; for spontaneous pneumothorax, the prognosis depends on the underlying cause and method of treatment. The prognosis for iatrogenic pneumothorax is considered good.

P At a Glance Causative Mechanisms Page 232

Effects Page 234

Signalment Page 234

History Page 234

Physical Examination

neumothorax is classiﬁed as open or closed and according to the causative mechanism. Open pneumothorax results from a penetrating thoracic injury that permits entry of air into the chest, while closed pneumothorax is the accumulation of air originating from the respiratory system within the pleural space. In some cases, the air may come from both sources (e.g., severe thoracic bite wounds with lung punctures).

Causative Mechanisms Pneumothorax is classiﬁed as traumatic, spontaneous, or iatrogenic according to its cause1 (BOX 1).

Page 235

Traumatic

Diagnostic Evaluation

Traumatic pneumothorax is the most common form of pneumothorax in dogs.1–6 Traumatic pneumothorax can be open or closed1; however, it is usually closed.2 Closed traumatic pneumothorax is often the result of blunt trauma (e.g., automobile accident). When the chest is compressed against a closed glottis, the bronchial tree or lung parenchyma can rupture with resultant air leakage into the pleural space.3,4 If a large airway is injured, pneumomediastinum may be present.5,6 Fractured ribs can lacerate lung lobes, resulting in closed traumatic pneumothorax.3 Open traumatic pneumothorax

Page 235

Treatment Page 236

Postoperative Thoracotomy and Monitoring Page 240

Prognosis Page 240

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results from a penetrating thoracic injury such as a stab, gunshot, or bite wound.

Spontaneous Spontaneous pneumothorax is not the result of traumatic injury and is classiﬁed as closed. Spontaneous pneumothorax is less common than traumatic pneumothorax,1,7–10 BOX 1

Types and Causes of Pneumothorax Traumatic ❯ Open: Stab, gunshot, bite wounds ❯ Closed: Impact (inflicted by person or car) Spontaneous ❯ Cavitary lung lesions: Bullae/blebs, cysts, abscesses/granulomas, pneumatoceles, parasitic cysts (Paragonimus spp) ❯ Grass awns/porcupine quills ❯ Pneumonia ❯ Dirofilaria immitis ❯ Neoplasia ❯ Feline asthma Iatrogenic ❯ Thoracic fine-needle aspiration ❯ Tracheal intubation ❯ Mechanical ventilation

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Pneumothorax CE rapid closure of parenchymal–pleural ﬁstulas.32 Iatrogenic pneumothorax has rarely been associated with tracheal rupture due to intubation in cats if the pressure is high enough to rupture the mediastinum33 (FIGURE 2). The most common cause of tracheal rupture is overinﬂation of the endotracheal tube cuff5; other causes include rotation of the animal without disconnection from the anesthesia machine tubing, traumatic intubation with a FIGURE 1

Courtesy of John V. Mauterer, DVM, DACVS

has several different etiologies, and is classiﬁed as primary (no obvious clinical evidence of pulmonary disease) or secondary (obvious clinical evidence of pulmonary disease).4,11,12 The most common cause of spontaneous pneumothorax is the rupture of pulmonary blebs or bullae (bullous emphysema).1,7,8,10,12,13 Pulmonary blebs result from air that has accumulated within the visceral pleura.12,14,15 Bullae are the result of destruction, dilation, and convergence of contiguous alveoli14,15 secondary to obstruction of the small airways13 and are found within the lung parenchyma. Blebs most commonly arise at the apex of the lung lobes13 (FIGURE 1). In cases of single lung lobe involvement, the right middle lung lobe is overrepresented.16 Rupture of the bullae and blebs is thought to be due to obstruction of the small airways. Blebs and bullae belong to a class of pulmonary lesions known as cavitary lung lesions.17 Other cavitary lung lesions that may result in secondary spontaneous pneumothorax include pneumatoceles, abscesses, cystic bronchiectasis, and parasitic cysts. Other causes of secondary spontaneous pneumothorax are grass awn migration, porcupine quill migration, pneumonia, chronic granulomatous infections, Diroﬁlaria immitis infections, and neoplasia.7,8,10,13,16,18–27 Seven cats with small airway disease secondary to feline lower airway disease (asthma) were reported to have closed spontaneous pneumothorax.28,29 Asthma can predispose cats to increased alveolar pressure and emphysema resulting in spontaneous pneumothorax. 29 Congenital lobar emphysema secondary to bronchial cartilage hypoplasia and bronchiectasis has also been reported in the literature as a cause of spontaneous pneumothorax.22,23,30 Because bilateral involvement is common and tension pneumothorax can result, spontaneous pneumothorax should be considered a serious, life-threatening disease.7

Intraoperative photograph of a pulmonary bleb. Note that the bleb is at the apex of the lung lobe. FIGURE 2

Iatrogenic Thoracic ﬁne-needle aspiration is a common cause of closed iatrogenic pneumothorax.1,12,31 Chronic effusions such as chylothorax, pyothorax, and malignant pleural effusions increase the risk of pneumothorax after thoracic aspiration. Chronic effusions often result in ﬁbrosing pleuritis, which leads to the persistence rather than

Radiograph of a cat with iatrogenic pneumothorax, pneumomediastinum, and subcutaneous emphysema (arrow) as a result of tracheal tear after tracheal intubation. The single arrowhead indicates cardiac silhouette elevation. The double arrowhead indicates lung lobe atelectasis.

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stylet, and removal of the tube without deﬂa- causing collapse of the lungs and great veins.11 tion of the cuff.33 Tracheoscopy is considered The patient rapidly deteriorates4,11,37 and dies. the method of choice for documenting tra- Radiographs should never be used for diagnosis cheal tears.5 in animals with tension pneumothorax because Positive end-expiratory pressure mechani- the associated delay and stress may result in the cal ventilation can lead to barotrauma and death of the patient. iatrogenic pneumothorax, especially in animals with pulmonary parenchymal disease Signalment requiring high pressure. Jugular venipuncture Traumatic causing tracheal laceration and the lateral sur- Traumatic pneumothorax is most common gical approach to the thoracolumbar vertebrae in young, intact male dogs because they are are other reported causes of iatrogenic pneumore apt to wander and be hit by cars.2,8 mothorax in cats and dogs, respectively.3

Spontaneous Effects

QuickNotes Pneumothorax can result from traumatic, spontaneous, or iatrogenic causes.

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Primary spontaneous pneumothorax is most Bilateral pneumothorax is the most common common in deep-chested, large-breed dogs.1,12,13 condition1,7,12,13,34 because air diffuses through Studies have shown that Siberian huskies the thin mediastinum.4 Pneumothorax is con- have a significantly greater incidence of prisidered a restrictive disorder of the lung.11 A mary spontaneous pneumothorax than other decrease in the lung’s compliance due to extra- breeds.1,38 Animals of any age can develop pulmonary air is the primary defect.31 When pneumonia or become infected with respiraair enters the pleural space, the negative pres- tory parasites or heartworms. Older animals sure of the pleural space is diminished, allow- are more likely to develop pneumothorax secing the lung’s inherent elastic recoil to result ondary to neoplasia of the lungs. in collapse (atelectasis). Atelectasis leads to a ventilation/perfusion mismatch.11,35 This can Iatrogenic lead to arterial hypoxemia, which in turn may Iatrogenic pneumothorax can occur in any result in myocardial dysfunction, lactic aci- animal undergoing thoracic surgery, anesthedosis, and ultimately death if not corrected.35 sia, or mechanical ventilation. Hypercapnia due to hypoventilation magnifies History acidosis.36 When the lungs collapse, the tidal volume Traumatic is reduced, prompting tachypnea in an attempt Patients with traumatic pneumothorax usually to maintain the minute ventilation. 35 Local present with an obvious history of trauma, evihypoxia induces vasoconstriction of pulmo- dence of trauma, or a history consistent with nary vessels, diverting blood flow to ventilated trauma, such as, “came home breathing hard.” areas. Vasoconstriction, combined with collapse of blood vessels due to atelectasis, eventually Spontaneous leads to pulmonary hypertension and increased The most common historical complaints from owners of animals presenting with spontanework for the right side of the heart.35 Tension pneumothorax is the most severe ous pneumothorax include difficulty breathform of pneumothorax. It can result from blunt ing, anorexia, tachypnea, coughing, and or penetrating thoracic trauma or from spontane- vomiting.1,4,12,39 Lethargy, fever, cyanosis, gagous pneumothorax.7 In this form of pneumotho- ging, exercise intolerance, and collapse are rax, thoracic injuries or pulmonary lesions act less commonly reported signs.1 In one study,1 as one-way valves, allowing air into the pleu- the median duration of clinical signs before ral space during inspiration and preventing presentation to a veterinary hospital in dogs expulsion during expiration. A slight increase with spontaneous pneumothorax was 3 days in pressure in the pleural cavity results in a sig- (range: 0 to 28 days); in another study,39 it was nificant decrease in venous return. Blood pools 1 day (range: 1 hour to 3.5 days). in capacitance vessels, and shock results. The continued accumulation of air quickly results Iatrogenic in supraatmospheric pressure within the thorax, Animals with iatrogenic pneumothorax have a

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Pneumothorax CE recent history of thoracic aspiration, tracheal intubation, anesthesia, or other procedures related to the thoracic cavity.

Physical Examination Traumatic

cent, air-ﬁlled pleural space created as the lungs retract from the parietal pleura (FIGURE 3). As the lungs collapse, the vascular pattern of the lungs no longer extends to the chest wall as it does in a healthy animal.

Animals with traumatic pneumothorax often Traumatic have other injuries associated with the trauma In animals with traumatic pneumothorax, other (e.g., lacerations, scrapes, bruises, fractures). injuries are common, and the patient and the radioAnimals with open pneumothorax secondary graphs should be evaluated carefully for occult or to penetration of the thoracic cavity may have subtle injuries. Diaphragmatic hernia, hemothoan obvious wound, such as a “sucking thorax, rib and vertebral fractures, and pulmonary racic wound” (a large open wound that allows contusions are common concurrent injuries. the influx of air into the chest during inspiration).4 In other cases, the wound may not be Spontaneous immediately visible. This is particularly true In animals with spontaneous pneumothorax, radiographs should be evaluated for potential for thoracic bite wounds. underlying causes of pneumothorax. Pneumonia, Spontaneous abscesses, granulomas, neoplasia, and changes Tachypnea, tachycardia, respiratory distress, and secondary to heartworm disease (e.g., tortuous anxiety are common findings during the physi- vessels, enlarged pulmonary arteries) should be cal examination of animals with pneumotho- excluded. The presence of bullae or blebs may rax. Shallow, rapid breaths with an abdominal be difficult to appreciate; however, these lesions component (restrictive breathing pattern) may are occasionally visible (FIGURE 4). In studies of be noted.1,4 Auscultation of the chest reveals dogs with spontaneous pneumothorax, radiomuffled heart and lung sounds dorsally.3,4 graphic bullae have been detected in 4% to 31% of cases.1,7,12,39

Iatrogenic Subcutaneous emphysema may be present in cats with concomitant pneumomediastinum and pneumothorax secondary to tracheal tears after intubation33 (FIGURE 2).

Diagnostic Evaluation Laboratory Evaluation

Iatrogenic

QuickNotes Consequences of pneumothorax may include tachypnea, hypoxemia, tachycardia, and, if left untreated, cardiovascular collapse and death.

Animals with tracheal tears may have subcutaneous emphysema and pneumomediastinum,5,33 which is noted by the visualization of the cranial vena cava, aorta, and esophaFIGURE 3

Courtesy of Dr. Mauterer

Complete blood count and biochemical profile results are usually normal, nonspecific, or related to concomitant disease.12,39 Blood gas analysis may document hypoxemia as well as respiratory acidosis due to hypoventilation and hypercapnia.36 In animals with pneumothorax secondary to heartworm disease, results of occult heartworm tests are positive. Paragonimus infections can be identified using Baermann sedimentation fecal examination18,40 or transtracheal aspiration.18

Radiography Animals in severe distress should undergo thoracocentesis before radiography. Lateral thoracic radiographs show elevation of the cardiac silhouette from the sternum. Atelectatic lung lobes are radiopaque in contrast to the radiolu-

Radiograph showing severe pneumothorax. Note cardiac silhouette elevation (bracket) and lung lobe atelectasis (arrowhead).

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QuickNotes Radiographs readily depict pneumothorax; however, the underlying cause may not be evident on plain-ﬁlm radiographs. Computed tomography may be useful in some cases.

gus (normally not visible in healthy animals; FIGURE 2). In animals that develop pneumothorax after thoracocentesis, rounded lung margins, consistent with chronic effusion, may be seen (FIGURE 5).

Thoracocentesis carries the risk of lacerating or puncturing a lung lobe, which results in iatrogenic pneumothorax; however, proper technique, caution, and recognition of at-risk patients can minimize these complications.45

Computed Tomography

Treatment Supplemental Oxygen

Computed tomography (CT) is routinely used in people for the diagnosis of bullae and blebs because it is considered more sensitive than radiography.41 The accuracy of lesion identification using CT in humans has been shown to range from 88% to 91.8%.42–44 One study39 comparing the accuracy of radiography and CT for bullae and bleb identification in dogs with spontaneous pneumothorax found radiography to be accurate in 16% of cases and CT to be accurate in 80% of cases. The authors of this study suggested that CT was a better diagnostic tool than radiography for the identification of lung lesions associated with spontaneous pneumothorax.39 However, in many veterinary patients, a CT scan is not performed preoperatively because the findings may not change the surgical approach and because of the additional costs.

Thoracocentesis Thoracocentesis is beneﬁcial in that it may be both diagnostic and therapeutic (BOX 2). Often, radiography is conducted before thoracocentesis. However, thoracocentesis may be performed in a rapidly deteriorating patient without prior radiography.4,45

FIGURE 4

Because atelectasis and ventilation/perfusion mismatch can lead to hypoxia, animals with pneumothorax may beneﬁt from supplemental oxygen.35 Oxygen therapy may also be beneﬁcial because these animals may have respiratory and metabolic acidosis and hypercapnia.36 In animals with closed pneumothorax, oxygen therapy can hasten the resolution of the pneumothorax. The full physiology behind this mechanism is beyond the scope of this article; however, it is based on differences in partial pressures of blood gases. The extrapulmonary air of pneumothorax contains mainly nitrogen and oxygen (~21%) and other minor constituents. The partial pressure of oxygen in the blood is approximately 100 mm Hg at sea level and normal barometric pressure (760 mm Hg).46 When the oxygen content of the air delivered to an animal is higher than 21%, the partial pressure in the blood increases. This causes a decrease in the partial pressure of other gases in the blood (e.g., nitrogen), which in turn creates a pressure gradient for these gases to diffuse from the pneumothorax into the blood and eventually out of the system through respiration. Oxygen can be delivered by mask, nasal cannula, or cage/tank. It is important to minimize stress in these animals; therefore, for fractious or excited patients, an oxygen cage may be the best option.

Courtesy of Dr. Mauterer

Thoracocentesis

Radiograph of a pulmonary bulla (arrowhead).

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In animals with traumatic, closed pneumothorax, thoracocentesis can be curative, and recurrence is uncommon.4,37,45 Thoracocentesis should restore negative pressure within the thoracic cavity. If negative pressure cannot be reached, >10 mL/kg of air is aspirated within a 12-hour period, or repeated aspiration is required to alleviate respiratory distress, chest tube placement should be considered.2,8,47 Open chest wounds should be covered immediately with a sterile, occlusive dressing to prevent further equilibration with atmospheric pressure and allow effective aspiration of air.

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Pneumothorax CE BOX 2

Basic Steps of Thoracocentesis 1. Restrain the animal appropriately in either sternal or lateral recumbency. With the patient in lateral recumbency, the 7th to 9th intercostal space at the level of the costochondral junction is an appropriate location for thoracocentesis.4 In standing or sternal animals, the same intercostal spaces can be used; however, needle placement should be in the dorsal two-thirds to one-third of the thorax.4 2. Clip and aseptically prepare the 7th to 9th intercostal space. 3. A local anesthetic block of the area is encouraged.4 4. In small dogs and cats, a butterﬂy catheter (19 to 23 gauge) connected to a three-way stopcock may be used for aspiration.44 In larger dogs or obese animals, a large-bore over-the-needle catheter connected to an extension set, three-way stopcock, and syringe may be used44 (FIGURE A). A #11 blade can be used to

7. 8.

make additional small holes in the catheter that are about one-third the diameter of the catheter. Gently insert the needle through the skin, subcutaneous tissue, fascia, and intercostal muscles cranial to the rib to avoid the intercostal vessels and nerves, which lie just caudal to the ribs. Aspirate while the needle is being advanced to allow appreciation of the proper depth.4 A gentle “pop” may be felt as entry into the pleural cavity is achieved. Turn the needle so that the bevel is facing medially and the needle is against the rib cage to reduce the risk of lung laceration. Aspirate and quantitate the amount of air removed from the pleural cavity. Once negative pressure is achieved, be sure not to aspirate while removing the needle/catheter from the pleural cavity. If no air is aspirated, redirect, tap a different site, or stop if the animal is no longer clinically dyspneic.44

FIGURE A

QuickNotes Traumatic and iatrogenic pneumothorax are commonly treated by thoracocentesis or tube thoracostomy; spontaneous pneumothorax often requires exploratory thoracotomy or thoracoscopy for resection.

Photograph showing proper needle placement and technique for thoracocentesis.

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Tube Thoracostomy Thoracostomy tube placement is indicated when reaccumulation of air in the pleural space is too rapid or severe to be controlled by thoracocentesis, thoracocentesis is performed more than three times in a 24-hour period, or severe or tension pneumothorax is present.1,7,8,10,47,48 Placement of a thoracostomy tube allows air to be removed intermittently or continuously, as necessary. BOX 3 briefly describes tube placement and maintenance. This procedure has been more fully described elsewhere.47,48 Intermittent drainage is usually sufﬁcient if the amount of air accumulating is not lifethreatening or very rapid. This method allows

quantification of the air accumulating within the chest. When the tube is not being used, a hemostat, C-clamp, or commercially available plastic clamp can be placed over the tube to prevent aspiration of air into the tube.48 Continuous closed-suction drainage is indicated when air accumulation is very rapid and intermittent suction is not effective in achieving negative pressure. Continuous suction is based on the underwater suction system. Commercially available continuous-suction units include the Pleur-Evac (Teleflex Medical, Research Triangle Park, NC). These systems require constant monitoring (because patients can easily remove or damage the tubes) and do not allow quantification of the air removed

BOX 3

Basic Steps of Thoracostomy Tube Placement The tubes should be ﬂexible but ﬁrm and resistant to collapse.47 Polyvinyl thoracic drainage tubes with stylets to assist with placement are commercially available (Argyle, Sherwood Medical) (FIGURE A). Red rubber feeding tubes may cause tissue reaction but may be used if other commercial tubes are unavailable and long-term placement is not anticipated.2 FIGURE A

Instruments needed for placement of a thoracostomy tube. (A) Thoracostomy tube. (B) 5-in-1 (Christmas tree) adapter. (C) Three-way stopcock. (D) Surgical (cerclage) wire.

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The appropriate size of the tube is determined by the size of the mainstem bronchus on radiographs.45,47 Commercial tubes come with preplaced holes; however, additional holes can be added to achieve a total of three to ﬁve holes, which is sufﬁcient for drainage. Many commercial tubes also have an incorporated longitudinal radiopaque marker to allow visualization of the tube on radiographs. If additional holes are placed, the last hole should be on the radiopaque marker line to allow assessment of the tube’s placement within the thoracic cavity. The tube is generally placed with the animal under general anesthesia. If the animal’s status precludes general anesthesia, local intercostal nerve blocks that include the parietal pleura may be used.45,47 The lateral thorax is clipped and prepared aseptically before tube placement. For medium and large dogs: 1. Make a small stab incision in the skin in the dorsal one-third of the thorax at the 10th to 12th intercostal spaces. 2. Make a tunnel in the subcutaneous tissue three to four intercostal spaces cranially using the tube with the stylet. If using a red rubber catheter or a tube without a stylet, use a pair of large hemostatic forceps to create the tunnel and advance the tube.48 3. Rotate the tube perpendicular to the thoracic wall.

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Pneumothorax CE from the thoracic cavity. Some clinicians prefer these systems because they can maintain lung inﬂation, which may facilitate healing. Heimlich valves are designed to use the pressure generated by expiration to expel pleural air while preventing air from entering the pleural cavity during inspiration. These devices should only be used in medium- to large-breed dogs because small dogs and cats may not produce enough pressure on expiration to expel the air.4,47 They should not be used in patients with pleural effusion because the valve will ﬁll and seal, preventing air expulsion.47 If a Heimlich valve is oriented incorrectly, iatrogenic tension pneumothorax results. Salci et al49 reported successful treat-

4. With one quick, brisk thrust, pass the tube (or hemostat) through the intercostal musculature into the thoracic cavity. However, use caution, as too brisk an entry into the thoracic cavity may cause inadvertent damage to thoracic organs. Also, as for thoracocentesis, be careful to avoid the large intercostal vessels and nerves just caudal to the ribs. 5. Once penetration is achieved, lay the tube parallel to the spine, advance it slightly, and remove the stylet, passing the tube cranially and ventrally into the cranial pleural space. 6. Obtain a radiograph to ensure proper placement of the tube in the cranioventral pleural space to approximately the level of the second rib48 (FIGURE B). 7. Place a purse-string suture at the entry site into the thoracic cavity to prevent leakage of air or fluid into the subcutaneous tissue.48 8. Suture the tube to the skin using a Chinese finger-trap suture pattern or variation thereof.48 9. Attach the tubing to a three-way stopcock, either directly or with a five-in-one (Christmas tree) adapter. 10. Secure the tubing to the stopcock with surgical wire to allow intermittent drainage. 11. Cover the tube entry with a few gauze sponges impregnated with a small amount of iodine ointment, followed by a soft, padded bandage or tubular stockinet over the chest to protect the tube. 12. Apply an Elizabethan collar to prevent premature pulling by the animal.

ment of spontaneous pneumothorax secondary to infective pleuropneumonia using only a thoracostomy tube with a Heimlich valve. Thoracostomy tubes can be removed when air production is absent for 24 to 48 hours. These tubes may cause a small amount of effusion (2 to 4 mL/kg/day), which resolves when the tube is removed.4,2,45,48 The tube is removed with steady traction and the site covered with an occlusive bandage for 6 to 24 hours; the incision is allowed to heal by second intention.48 Treatment of spontaneous pneumothorax by thoracocentesis or thoracostomy tube alone is usually insufficient because recurrence is common.1,7,8,10,12,50

FIGURE B

Radiograph showing proper placement of a thoracostomy tube.

For small dogs, puppies, and cats, in which the chest is too compressible for any technique that requires force, or to avoid having to thrust the tube into the thorax in larger dogs, use the following technique: 1. After proper preparation of the area, pull the skin forward to the appropriate space.48 2. Make the skin incision, followed by dissection down through the chest wall.48 3. Insert the tube in an open fashion or use it to gently penetrate the inner intercostal layer.48 4. Allow the skin to retract to its normal position, resulting in subcutaneous tunneling of the tube.48 5. Follow steps 6 through 12 above.

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Courtesy of Elizabeth Rozanski, DVM, DACVECC, DACVIM

FIGURE 5

Radiograph of a cat with chronic pleural effusion and pneumothorax secondary to ﬁne-needle aspiration.

Surgical Intervention Traumatic Surgery is rarely needed to correct traumatic pneumothorax. Thoracocentesis or thoracostomy is usually sufﬁcient to allow pulmonary healing in 3 to 5 days, and mild pneumothorax may require only monitoring.3,37 However, surgery may be indicated to repair open chest wounds or other wounds related to the trauma.

Spontaneous Spontaneous pneumothorax is considered a surgical disease because dogs rarely respond to conservative therapy alone. A lateral or median approach may be used. Median sternotomy is the procedure of choice for exploration of the thorax1,7,8 because it allows visualization of both hemithoraces, which facilitates location of the air leak. Details of this and other surgical techniques have been published in various surgical texts.

Iatrogenic

spontaneous pneumothorax was successfully diagnosed and treated in three dogs using thoracoscopy, with no evidence of recurrence at 18 to 29 months after surgery. Lung lobectomy or biopsy can be performed with less morbidity and mortality using thoracoscopy.52 Minimally invasive surgery is associated with decreased morbidity, less pain, shorter hospitalization, and a quicker recovery.34,54–56 The experience of the operator is a large variable in the outcome of this procedure.

Postoperative Thoracotomy and Monitoring After surgery, patients should be monitored closely for pain, respiratory distress, tachypnea, hypoventilation, and recurrence of pneumothorax. The thoracostomy tube should be aspirated every hour for the ﬁrst 4 to 6 hours postoperatively until negative pressure is achieved. Aspiration can then be conducted every 4 to 6 hours. In almost all cases, there should be little or no ongoing air production. When negative pressure has been maintained for approximately 24 to 48 hours, the thoracostomy tube can be removed. Some serosanguineous discharge may be present while the tube is in the chest (approximately 2 to 4 mL/kg/day).48 This will resolve once the tube is removed. If the animal shows any signs of respiratory distress or tachypnea, thoracic radiography should be conducted to assess for pleural effusion, recurrence of pneumothorax, atelectasis, or any other potential lesion. Postoperative pain is an important consideration in animals undergoing surgical exploration of the thoracic cavity. Intercostal nerve blocks, interpleural regional anesthesia, continuous-rate infusion of drugs such as fentanyl or other opioid analgesics, and NSAIDs are all viable options to decrease the morbidity associated with these procedures. Appropriate dosages of these agents have been published in anesthesia/analgesia texts.

Thoracocentesis or thoracostomy tube placement is usually sufﬁcient for treatment of iatrogenic pneumothorax; however, if conservative Prognosis therapy is unsuccessful, surgery is indicated.3 Traumatic The prognosis for animals with traumatic pneuThoracoscopy mothorax is considered excellent12 if there are Thoracoscopy can be used therapeutically and no other life-threatening injuries. as a diagnostic tool if radiography and CT cannot localize a lesion.34,51,52 All structures Spontaneous within the thorax can be sufﬁciently observed The prognosis for spontaneous pneumothorax using thoracoscopy.34,51,53 In a 2003 study,40 depends on the method of treatment. Surgery

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Pneumothorax CE is considered the treatment of choice for spon- Conclusion taneous pneumothorax, with recurrence rates A basic understanding of normal respiratory of 0% to 25% versus 50% to 100% with conser- anatomy and physiology is important in undervative therapy alone.1,7,10,12 Surgery may also be standing the pathophysiologic effects of pneumore economical than thoracostomy or thora- mothorax. Early recognition of the clinical signs cocentesis when long-term hospitalization and of pneumothorax is important, especially in care costs are calculated.7 animals with tension pneumothorax, which can cause rapid deterioration and death. A thorough Iatrogenic understanding of lifesaving procedures such as The prognosis for animals with iatrogenic thoracocentesis and thoracostomy tube placepneumothorax is fair to good. Most animals ment is invaluable. Most animals with traumatic can be treated conservatively.3 In animals with pneumothorax do well with conservative therapy pneumothorax resulting from diagnostic pro- alone, whereas animals with spontaneous pneucedures to the thoracic cavity or mechanical mothorax frequently require surgical intervention ventilation, the ultimate prognosis depends on for complete resolution. Iatrogenic pneumothothe underlying disease. rax can usually be treated conservatively.

References 1. Puerto DA, Brockman DJ, Linquist C, et al. Surgical and nonsurgical management of and selected risk factors for spontaneous pneumothorax in dogs: 64 cases (1986-1999). JAVMA 2002;220(11):1670-1674. 2. Monnet E. Pleura and pleural space. In: Slatter D, ed. Textbook of Small Animal Surgery. 3rd ed. Philadelphia: Saunders; 2003:387-405. 3. Brockman DJ, Puerto DA. Pneumomediastinum and pneumothorax. In: King L, ed. Textbook of Respiratory Diseases of Dogs and Cats. Philadelphia: Saunders; 2003:616-624. 4. Fossum TW. Surgery of the lower respiratory system. In: Fossum TW, ed. Small Animal Surgery. 2nd ed. St. Louis: Mosby; 2002:788-820. 5. Hardie EM, Spodnick GJ, Gilson SD, et al. Tracheal rupture in cats: 16 cases (1983-1998). JAVMA 1999;214(4):508-512. 6. Johnson-Neitman JL, Huber ML, Amann JF. What is your diagnosis? JAVMA 2006;229(3):359-360. 7. Holtsinger RH, Beale BS, Bellah JR, et al. Spontaneous pneumothorax in the dog: a retrospective analysis of 21 cases. JAAHA 1993;29:195-210. 8. Yoshioka MM. Management of spontaneous pneumothorax in twelve dogs. JAAHA 1982;18:57-62. 9. Tamas PM, Paddleford RR, Krahwinkel DJ. Thoracic trauma in dogs and cats presented for limb fractures. JAAHA 1985;21:161-166. 10. Valentine A, Smeak D, Allen D et al. Spontaneous pnuemothorax in dogs. Compend Contin Educ Pract Vet 1996;18(1):53-62. 11. Tucker A. Respiratory pathophysiology. In: Slatter D, ed. Textbook of Small Animal Surgery. 3rd ed. Philadelphia: Saunders; 2003:781-797. 12. Lipscomb VJ, Hardie RJ, Dubielzig RR. Spontaneous pnemothorax caused by pulmonary blebs and bullae in 12 dogs. JAAHA 2003; 39:435-445. 13. Kramek BA, Caywood DD, O’Brien TD. Bullous emphysema and recurrent pneumothorax in the dog. JAVMA 1985;186(9):971-974. 14. Nelson AW, Monnet E. Lungs. In: Slatter D, ed. Textbook of Small Animal Surgery. 3rd ed. Philadelphia: Saunders; 2003:880. 15. Murphy DM, Fishman AP. Bullous disease of the lung. In: Fishman A, Elias J, Fishman J, et al. Fishman’s Pulmonary Disease and Disorders. New York: McGraw-Hill; 2008:913-930. 16. Stogdale L, O’Connor CD, Williams MC, et al. Recurrent pneumothorax associated with a pulmonary emphysematous bulla in a dog: surgical correction and proposed pathogenesis. Can Vet J 1982;23(10):281-287. 17. Anderson GI. Pulmonary cavitary lesions in the dog: a review of seven cases. JAAHA 1987;23:89-94. 18. Rochat MC, Cowell RL, Tyler RD, et al. Paragonimiasis in dogs and cats. Compend Contin Educ Pract Vet 1990;12(8):1093-1098. 19. Hopper BJ, Lester NV, Irwin PJ, et al. Imaging diagnosis: pneu-

mothorax and focal peritonitis in a dog due to migration of an inhaled grass awn. Vet Radiol Ultrasound 2004;45(2):136-138. 20. Smith JW, Scott-Moncrieff C, Rivers BJ. Pneumothorax secondary to Dirofilaria immitis infection in two cats. JAVMA 1998;213(1): 91-93. 21. Berson JL, Rendano VT, Hoffer RE. Recurrent pneumothorax secondary to ruptured pulmonary blebs: a case report. JAAHA 1979;15:707-711. 22. Herrtage ME, Clarke DD. Congenital lobar emphysema in two dogs. J Small Anim Pract 1985;26:453-464. 23. Tennant BJ, Haywood S. Congenital bullous emphysema in a dog: a case report. J Small Anim Pract 1987;28:109-116. 24. Busch DS, Noxon JO. Pneumothorax in a dog infected with Dirofilaria immitis. JAVMA 1992;201(12):1893. 25. Forrester SD, Fossom TW, Miller MW. Pneumothorax in a dog with a pulmonary abscess and suspected infective endocarditis. JAVMA 1992;200(3):351-354. 26. Saheki Y, Ishitani R. Acute fatal pneumothorax in canine dirofilariasis. Jpn J Vet Sci 1981;43:315-328. 27. Dallman MJ, Martin RA, Roth L. Pneumothorax as the primary problem in two cases of bronchoalveolar carcinoma in the dog. JAAHA 1988;24:710-714. 28. White HL, Rozanski EA, Tidwell AS, et al. Spontaneous pneumothorax in two cats with small airway disease. JAVMA 2003;222(11):1573-1575. 29. Cooper ES, Syring RS, King LG. Pneumothorax in cats with a clinical diagnosis of feline asthma: 5 cases (1990-2000). J Vet Emerg Crit Care 2003;13(2):95-101. 30. Matsumoto H, Kakehata T, Hyodo T, et al. Surgical correction of congenital lobar emphysema in a dog. J Vet Med Sci 2004;66(2):217-219. 31. Cherniak RM. Respiration in Health and Disease. Philadelphia: Saunders; 1972. 32. Heidecker J, Huggins JT, Sahn SA, et al. Pathophysiology of pneumothorax following ultrasound-guided thoracocentesis. Chest 2006;130(4):1173-1184. 33. Mitchell SL, McCarthy R, Rudloff E, et al. Tracheal rupture associated with intubation in cats: 20 cases (1996-1998). JAVMA 2000;216(10):1592-1595. 34. Brissot HN, Dupre GP, Bouvy BM, et al. Thoracoscopic treatment of bullous emphysema in 3 dogs. Vet Surg 2003;32:524-529. 35. Bennett RA, Orton EC, Tucker A, et al. Cardiopulmonary changes in conscious dogs with induced progressive pneumothorax. Am J Vet Res 1989;50(2):280-284. 36. Willard T. Blood gases. In: Willard T, Turnwald GH, eds. Small Animal Clinical Diagnosis by Laboratory Methods. 3rd ed. Philadelphia: Saunders; 1999:93-107.

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37. Ludwig L. Surgical emergencies of the respiratory system. Vet Clin North Am Small Anim Pract 2000;30:531-553. 38. Groblinger K, Lorinson D, Wiskocil L. Spontaneous pneumothorax caused by bullae pulmonales in four huskies [abstract]. Vet Surg 2001;30:304. 39. Au JJ, Weisman DL, Stefanacci JD, et al. Use of computed tomography for evaluation of lung lesions associated with spontaneous pneumothorax in dogs: 12 cases (1999-2002). JAVMA 2006;228(5):733-737. 40. Bowman D. Helminths. In: Bowman D, ed. Georgi’s Parasitology for Veterinarians. 8th ed. St. Louis: Saunders; 2003:115-243. 41. Carr DH, Pride NB. Computed tomography in pre-operative assessment of bullous emphysema. Clin Radiol 1984;35:43-45. 42. Sihoe ADL, Yim APC, Lee TW, et al. Can CT scanning be used to select patients with unilateral primary spontaneous pnemothorax for bilateral surgery? Chest 2001;118:380-383. 43. Mittlehner W, Friedrich M, Dissman W. Value of computed tomography in the detection of bullae and blebs in patients with primary spontaneous pneumothorax. Respiration 1992;59:221-227. 44. Yasufuku K, Takashi O, Fujisawa T. The effectiveness of thinsection computed tomography in diagnosing bullous lesions in patients with spontanous pneumothorax. Nihon Kokyuki Gakkai Zasshi 1999;37:953-957. 45. Crisp M. Critical care techniques. In: Birchard SR, Scherding R, eds. Saunders Manual of Small Animal Practice. Philadelphia: Saunders; 2000:25. 46. Robinson N. Overview of respiratory function; ventilation of the

lung. In: Cunningham JG, ed. Textbook of Veterinary Physiology. 3rd ed. Philadelphia: Saunders; 2002:468-478. 47. Tillson D. Thoracostomy tubes. Part 1. Compend Contin Educ Pract Vet 1997;19:1258-1266. 48. Tillson D. Thoracostomy tubes. Part 2. Compend Contin Educ Pract Vet 1997;19:1331-1337. 49. Salci H, Kennerman E, Celemli N, et al. Use of a heimlich ﬂutter valve in a dogs with spontaneous pneumothorax. Aust Vet Pract 2005;35:47-51. 50. Jerram RM, Fossum TW, Berridge BR, et al. The efﬁcacy of mechanical abrasion and talc slurry as methods of pleurodesis in normal dogs. Vet Surg 1999;28:322-332. 51. Dupre GP, Corlouer JP, Bouvy B. Thoracoscopic pericardectomy performed without pulmonary exclusion in 9 dogs. Vet Surg 2001;30:21-27. 52. Garcia F, Prandi D, Pena T, et al. Examination of the thoracic cavity and lung lobectomy by means of thoracoscopy in dogs. Can Vet J 1998;39:285-290. 53. De Rycke LM, Gielen IM, Van Ryssen B. Thoracoscopic anatomy of dogs positioned in lateral recumbency. JAAHA 2001;37:543-548. 54. Champion JK, McKernan JB. Bilateral thoracoscopic stapled volume reduction for bullous vs diffuse emphysema. Surg Endosc 1998;12:338-341. 55. Delaunois L, El Khawad C. Medical thoracoscopy in the management of pneumothorax. Monaldi Arch Chest Dis 1998;53:148-150. 56. Sampietro R. Videothoracoscopic treatment of bullous lung disease: indications and techniques. Int Surg 1996;81:333-335.

3 CE CREDITS

CE TEST 2 This article qualiﬁes for 3 contact hours of continuing education credit from the Auburn University College of Veterinary

Medicine. Subscribers may take individual CE tests online and get real-time scores at CompendiumVet.com. Those who wish to apply this credit to fulﬁll state relicensure requirements should consult their respective state authorities regarding the applicability of this program. 1. Iatrogenic pneumothorax secondary to intubation in cats has not been associated with a. overinﬂation of the cuff. b. turning the patient without disconnecting the tube. c. tracheal injury from a stylet. d. laryngospasm.

5. Which breed has been shown to have a greater incidence of spontaneous pneumothorax? a. golden retriever b. Siberian husky c. Chihuahua d. shih tzu

2. Pneumothorax is classiﬁed as a(n) _________ disorder of the lung. a. obstructive b. restrictive c. vascular d. parenchymal

6. Which is not a typical radiographic feature of pneumothorax? a. cardiac elevation from the sternum on the lateral recumbent projection b. atelectasis or partial atelectasis c. loss of the vascular pattern adjacent to the chest wall d. air bronchograms

3. Which of the following is the most common cause of pneumothorax? a. tracheal tears secondary to intubation b. thoracic trauma c. bullous emphysema d. pulmonary neoplasia 4. The most common cause of spontaneous pneumothorax is a. bullous emphysema. b. parasitic cysts. c. pulmonary neoplasia. d. grass awn migration.

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7. Which statement is true regarding the use of CT in diagnosing pneumothorax? a. It is not helpful. b. It is more accurate than radiography in the diagnosis of underlying lesions causing spontaneous pneumothorax. c. It should be used to diagnose traumatic pneumothorax. d. It is used in human medicine to diagnose traumatic pneumothorax.

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8. Which of the following is an indication for placement of a thoracostomy tube? a. Negative pressure can be obtained by thoracocentesis. b. More than 2 mL/kg of air is aspirated over 12 hours. c. Only one thoracocentesis procedure is required to alleviate respiratory distress. d. Tension pneumothorax is present. 9. Which statement about thoracoscopy is true? a. It results in less morbidity and mortality for lung lobectomy than median sternotomy. b. It cannot be used as a diagnostic tool. c. It does not allow sufﬁcient visualization of thoracic structures. d. It has not been attempted in animals with pneumothorax. 10. Which type of pneumothorax routinely requires surgery for correction? a. closed traumatic b. closed spontaneous c. open traumatic d. iatrogenic

Letters Clinical Snapshot

Pruritus in a Great Dane

Particularly intriguing or difﬁcult cases

Case Presentation #1

TO LEARN MORE

❯❯ Karen A. Moriello, DVM, DACVD, University of Wisconsin-Madison

I would like to apologize to readers for an unintentional error in the March 2009 Clinical Snapshot, “Pruritus in a Great Dane,” in which I stated that “the manufacturer reported [selamectin] to be effective in 70% of cases” when discussing treatment for canine scabies. This statement was an incorrect extrapolation of information on studies conducted by the manufacturer. I would like to correct this statement and comment on my current use of selamectin. Selamectin has been found to be highly effective against Sarcoptes mite infestations in dogs. Large ﬁeld studies with naturally occurring Sarcoptes infestations in dogs have reported posttreatment efﬁcacy of 93% to 95% after one dose and 100% after two doses. It is important to remember that part of the pathogenesis of the pruritus of scabies is hypersensitivity to mites, dead or alive. Dogs can be mite free but still pruritic until mite proteins have been shed from

This Great Dane (A) was one of 12 dogs in a kennel, all of which had had intense pruritus for 1 year. The owners reported that the other dogs looked similar and that all the dogs were losing weight and were irritable with the owners and each other. Close examination of the skin revealed a generalized papular eruption without evidence of pustules or epidermal collarettes. Any manipulation of the skin triggered an intense episode of self-mutilation. All the dogs were currently vaccinated and received monthly heartworm medication and monthly spot-on ﬂea control. The owners reported no lesions or discomfort after handling the dogs. Flea combings were negative. Skin scrapings revealed the organism shown (B). 1. What is the diagnosis? 2. The owners of the kennel have three

border collies and seven cats in addition to these dogs. What are the treatment options for this kennel of dogs? 3. A similarly named condition occurs in cats. What is the cause, and what treatment can be used for this condition?

Clinical Snapshot presents illustrated case histories and challenges you to answer the questions posed. This case is part of the series of Self-Assessment Colour Review books on multiple topics from Manson Publishing Ltd., London, available from Blackwell Publishing Professional.

SEE PAGE 114 FOR ANSWERS AND EXPLANATIONS.

For more information or to obtain any of the

books in the series, call 800-862-6657

or visit BlackwellProfessional.com

INTERCEPTOR Flavor Tabs are palatable and most often will be consumed by the dog or cat when offered by the owner. As an alternative, the dual-purpose tablet may be offered in food or administered as other tablet medications. Watch the dog or cat closely following dosing to be sure the entire dose has been consumed. If it is not entirely consumed, redose once with the full recommended dose as soon as possible.

NADA 140-915, Approved by FDA INTERCEPTOR® (milbemycin oxime) Flavor Tabs® for Dogs and Cats Brief Summary—For full product information see product insert. Caution: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. Indications and Usage: INTERCEPTOR Flavor Tabs for dogs are indicated for use in the prevention of heartworm disease caused by Diroﬁlaria immitis, the control of adult Ancylostoma caninum (hookworm), and the removal and control of adult Toxocara canis and Toxascaris leonina (roundworms) and Trichuris vulpis (whipworm) infections in dogs and in puppies four weeks of age or greater and two pounds body weight or greater. INTERCEPTOR Flavor Tabs are indicated for use in the prevention of heartworm disease caused by Diroﬁlaria immitis, and the removal of adult Ancylostoma tubaeforme (hookworm) and Toxocara cati (roundworm) in cats and kittens six weeks of age or greater and 1.5 lbs. body weight or greater. Dosage and Administration: Dogs: INTERCEPTOR Flavor Tabs for Dogs are given orally, once a month, at the recommended minimum dosage rate of 0.23 mg milbemycin oxime per pound of body weight (0.5 mg/kg). Recommended Dosage Schedule for Dogs Body Weight INTERCEPTOR Flavor Tabs 2–10 lbs. 11–25 lbs. 26–50 lbs. 51–100 lbs.

One tablet (2.3 mg) One tablet (5.75 mg) One tablet (11.5 mg) One tablet (23.0 mg)

If INTERCEPTOR Flavor Tabs replace diethylcarbamazine (DEC) for heartworm prevention in dogs, the first dose must be given within 30 days after er the last dose of DEC. Warnings: Not for human an use. Keep this and all drugs out of the reach off children. children. Precautions: Dogs: Do not use in puppies pies less than fourr weeks weeks off age age and less than two pounds of body weight. Prior to initiation of the INTERCEPTOR Flavor Tabs abs treatment program, dogs should be tested for existing heartworm infections. Infected dogs should be treated to remove move adult heartworms and microfilariae prior to initiating treatment with INTERCEPTOR Flavor Tabs. Mild, transient hypersensitivity nsitivity reactions manifested as labored respiration, vomiting, salivation, and lethargy may occur after treatment of dogs carrying a high number of circulating microfilariae.

Clinical Snapshot

Cats: Do not use in kittens ns less than six weeks of age or less than 1.5 lbs. body weight. Safety in heartworm positive cats has not been established. Safety afety in breeding, pregnant, and lactating queens and breeding toms has not been established. Adverse Reactions: The following adverse reactions have been reported following the use of INTERCEPTOR in dogs: depression/lethargy, vomiting, miting, ataxia, anorexia, diarrhea, convulsions, weakness, and hypersalivation.

Answers and Explanations Case Presentation #1

Efﬁcacy: Dogs: INTERCEPTOR Flavor Tabs eliminate the tissue stage of heartworm larvae and the adult stage of hookworm ( Ancylostoma caninum),, roundworms ( Toxocara canis, Toxascaris leoninaa ), and whipworm ( Trichuris vulpiss ) infestations according to the recommended dosage schedule.104 FOR CASE PRESENTATION. when administered orallyy according SEE PAGE avor Tabs for Cats eliminate the tissue stage of heartworm larvae and hookworm (Ancylostoma Cats: INTERCEPTOR Flavor dworm ( Toxocara catii ) infections tubaeforme ) and roundworm 1. when administered orally according to the recommended dosage schedule.

Scabies infestation. The organism is a Sarcoptes egg. One mite or egg is diagnostic for scabies. Deﬁnitive evidence of a scabies infestation 1.5–6 lbs. One tablet (5.75 mg) ©2008 Novartis Animal Health US, Inc. (eggs or mites) is not always found, 6.1–12 lbs. One tablet (11.5 mg) ovartis AG. INTERCEPTOR and Flavorr Tabs are registered trademarks off NNovartis 12.1–25 lbs. One tablet (23.0 mg) even in “classic cases.” Most dogs 06/08 NAH/INT-FT/BS/5 Cats over 25 lbs. are provided the appropriate combination of tablets. with scabies are diagnosed based on response to treatment; therefore, Compendium: Continuing Education for Veterinarians® | March 2009 | CompendiumVet.com mVet.com if scabies is suspected, it should be treated accordingly. 2. Scabies mites can live for a short period of time off the host. The kennel facilities should be thoroughly cleaned with high-pressure water, scrubbed with detergent, and sprayed with an environmental parasiticidal agent. All dogs in contact with these Great Danes should be treated for scabies. Lime sulfur dips once weekly for 6 weeks or amitraz dips every 2 weeks for 6 weeks are effective topical therapies. Lime sulfur can be combined with ivermectin therapy. Ivermectin (200 μg/kg PO or SC) every 2 weeks for 6 weeks is also an effective treatment. I use a test dose of 100 μg/kg PO in all dogs. If there are no adverse effects consistent with ivermectin sensitivDogs over 100 lbs. are provided the appropriate combination of tablets.

Cats: INTERCEPTOR Flavor Tabs for Cats are given orally, once a month, at the recommended minimum dosage rate of 0.9 mg milbemycin oxime per pound of body weight (2.0 mg/kg). Recommended Dosage Schedule for Cats Body Weight INTERCEPTOR Flavor Tabs

104

INTERCEPTOR Flavor Tabs must be administered monthly, preferably on the same date each month. The ﬁrst dose should be administered within one month of the dog or cat’s ﬁrst exposure to mosquitoes and monthly thereafter until the end of the mosquito season. If a dose is missed and a 30-day interval between dosing is exceeded, administer INTERCEPTOR Flavor Tabs immediately and resume the monthly dosing schedule.

the stratum corneum and coat, which is one reason that medicated bathing is often very beneﬁcial for these patients. Because selamectin has a wide spectrum of activity, I routinely recommend year-round use of selamectin in hunting dogs and in dogs that frequent dog parks, “play groups” or “day care,” or agility and training classes. Karen A. Moriello, DVM, DACVD Clinical Professor of Dermatology University of Wisconsin-Madison

For technical assistance or to report suspected adverse events, call 1-800-332-2761. vartis Animal Health US, Inc. Manufactured for: Novartis eensboro, NC 27408, USA Greensboro,

ity (e.g., tremors, salivation) within 24 hours, I administer a full treatment dose of 200 μg/kg PO the next day. Herding breeds of dogs, especially collies, are known to be sensitive to ivermectin. Thus, this drug is best avoided in collies. Dogs sensitive to ivermectin can often tolerate milbemycin oxime at 3 mg/kg PO weekly for 3 to 6 weeks. Lime sulfur dips are also an effective therapy. Doramectin at 0.2 mg/kg SC or IM has also been reported to be effective. Finally, two applications of selamectin or ﬁpronil at 30-day intervals may be effective. Selamectin is licensed for the treatment of scabies, and the manufacturer reported it to be effective in 70% of cases. Fipronil is not licensed for scabies treatment but has been found to be effective. It is important to remember that no treatment is 100% efﬁcacious in all patients. If scabies is suspected and the patient does not respond, retreatment with a different therapy should be performed before scabies is ruled out.

3. Canine scabies is not considered con-

tagious to cats. However, Sarcoptes mites have been reported in a small number of cats with severe debilitation and in pruritic cats in England. There may be some geographic variation with respect to contagion to cats. These cats do not need to be treated. True “feline scabies” is caused by Notoedres cati, a contagious mange mite. In contrast to canine scabies mites, N. cati is easily found in large numbers on skin scrapings. Lesions occur on the head, feet, and perineum. This infestation can cause large amounts of crust; cats should be sedated, the haircoat clipped, and the cats bathed to remove the contaminated crusts before treatment. Because cats are extremely sensitive to parasiticidal agents, lime sulfur and ivermectin are the most commonly used treatments. Affected cats, and all animals in contact with them, should be treated for at least 6 weeks.

Letters

Call for Papers Are you involved in research? Veterinary Therapeutics: Research in Applied Veterinary Medicine® is a quarterly journal dedicated to rapid publication. We invite the submission of clinical and laboratory research manuscripts in small animal, large animal, and comparative medicine, including pathophysiology, diagnosis, treatment, and prognosis. Prospective, retrospective, and corroborative studies are all welcome. Submitted articles are scheduled to be published 90 to 120 days after acceptance. Contact Cheryl Hobbs, 800-426-9119, ext 52408, or email chobbs@vetlearn.com.

It’s not just therapeutics! 114

CONTINUED FROM PAGE 113

Toxicology. Philadelphia: Williams and Wilkins; 1996:317-328. 2. Gaynor AR, Dhupa N. Acute ethylene glycol intoxication. Part II. Compend Contin Educ Pract Vet 1999;21(12):11241133. 3. Dorman DC, Dye JA. Chemical toxicities. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 6th ed. St. Louis: Elsevier Saunders; 2005:257-258. 4. Richardson JA, Welch SL, GwaltneyBrant SM, et al. Metaldehyde toxicoses in dogs. Compend Contin Educ Pract Vet 2003;25(5):376-380. 5. Mull RL. Metaldehyde poisoning. In: Kirk RW, ed. Current Veterinary Therapy: Small Animal Practice VIII. London: WB Saunders; 1983:106-107. 6. Tilley LP, Smith FWK Jr. The 5-Minute Veterinary Consult: Canine and Feline. 2nd ed. Philadelphia: Lippincott Williams & Wilkins;2000:958-959.

Editor’s note: Thank you to the attentive readers who pointed out the difference between these articles and to the authors for their clariﬁcation. As in many aspects of veterinary medicine, different recommendations exist based on clinical experience and patient presentation versus laboratory chemistry, and different references reﬂect these variations. Awareness of both laboratory and clinical data is useful when determining the most appropriate treatment for an individual patient.

Compendium: Continuing Education for Veterinarians® | March 2009 | CompendiumVet.com

It’s not just therapeutics! CompendiumVet.com | May 2009 | Compendium: Continuing Education for Veterinarians®

243

Research Recap Selected abstract from Veterinary Therapeutics

Sensitivity of serum markers for pancreatitis in dogs with macroscopic evidence of pancreatitis Steiner JM, Newman SJ, Xenoulis PG, et al. Vet Ther 2008;9(4):263-273. Pancreatitis is recognized as an important and common problem in dogs, but diagnosis can be challenging. Recently, new assays for the measurement of trypsin-α1-proteinase inhibitor complexes and canine pancreatic lipase immunoreactivity (cPLI and Spec cPL) have been developed and analytically validated.

TO LEARN MORE

This is the ﬁrst report of a direct comparison of the sensitivity of these and other more traditional serum markers for the diagnosis of canine pancreatitis in a subset of dogs with this disease (i.e., dogs with both macroscopic and microscopic changes characteristic of pancreatitis). Serum cPLI and Spec cPL concentrations showed the highest sensitivity for the diagnosis of pancreatitis in this group of patients. Further studies will be required to compare For more Veterinary Therapeutics the speciﬁcity of these serum abstracts, visit the archives at markers and thus determine VeterinaryTherapeutics.com their clinical utility.

FFrom th the Winter 2008 issue

THIS USERFRIENDLY, EASY-TO-FOLLOW RESOURCE LETS YOU “GET IT RIGHT” EVERY TIME. Order today at

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244

Compendium: Continuing Education for Veterinarians® | May 2009 | CompendiumVet.com

EQ7IPE

Product Forum Lancing Device

Ophthalmoscope

The AlphaTRAK lancing device is now available in the AlphaTRAK Blood Glucose Monitoring System Kit. The lancing device uses spring-loaded action to pierce the skin, creating a reliable way of acquiring capillary blood for testing. AlphaTRAK offers a convenient alternative to needles and venous blood sampling for clients and pet owners. Abbott Animal Health 888-299-7416 | www.alphatrakmeter.com

Keeler Instruments has developed the ﬁrst digital indirect ophthalmoscope for veterinary ophthalmology. The Digital VantagePlus LED has an integrated digital camera that can capture both video and still images. The long-life LED improves image clarity. Keeler Instruments | 610-353-4350 | www.keelerusa.com

Vector-Borne Disease Panel Heart Failure Drug Vetmedin (pimobendan) has been approved by the FDA to treat congestive heart failure (CHF) in dogs. Boehringer Ingelheim Vetmedica, Inc., is manufacturing this drug, the ﬁrst new agent approved to treat CHF in dogs in more than a decade. Available by prescription only, Vetmedin is a chewable tablet that is administered twice daily. It can be used concurrently with other cardiac medications. Boehringer Ingelheim Vetmedica, Inc. 800-325-9167 | www.bi-vetmedica.com

IDEXX Reference Laboratories has announced several new panels for vector-borne diseases. The new tests combine IDEXX serology testing and real-time polymerase chain reaction testing, making diagnosis more accurate and cost-effective. Vector-borne disease panels should be used primarily for patients with clinical signs consistent with a vector-borne illness; however, they can also be used to identify patients with a subclinical vector-borne infection or to monitor therapy for previously diagnosed patients. IDEXX Reference Laboratories | 888-433-9987 | www.idexx.com

Oral Dispensers

Eye Drops

EPS has added a new product to its line of dispensing products. EPS Oral Dispensers are latex free and can be capped with standard or wagon-wheel tips. They show graduations in both milliliters and fractionated teaspoon measurements. The dispensers are available in four sizes and two colors, clear or ultraviolet-inhibiting amber. EPS, Inc. | 800-523-8966 | www.medidose.com

PetVisionPro Lubricating Eye Drops are designed to alleviate most common cataracts in dogs and cats by disaggregating the glycated proteins that trigger the degeneration of the normal protein structure of the lens ﬁbers in incipient and immature cataracts. The eye drops also provide a high level of corneal lubrication and add amino acids, which help form new proteins. Ader Enterprises | 858-792-3410 | www.aderent.com

Anti-Lick Products Anti-Lick Strips discourage pets from licking, biting, or chewing injuries or skin conditions. The strips come in three varieties, Prevent, Pro, and Pro C, and are made from all-natural ingredients, such as cayenne pepper and clove oil. Pro C is designed exclusively for in-clinic use and has a more aggressive adhesive. Nurtured Pets | 877-738-7771 | www.nurturedpets.com

Dryer Andis Comfort Dry is a new dryer designed to be less damaging to the coats and skin of pets. The new dryer has three heat settings and two air speeds and is nearly 20% quieter than traditional dryers, with an average decibel level of 71. There is also a cool air setting for less damaging drying. The 1875-watt dryer also has a stand with ﬁve different positions. Andis | 800-558-9441 | www.andis.com

The product information presented here is provided by the manufacturers and does not reﬂect endorsement by Compendium.

CompendiumVet.com | May 2009 | Compendium: Continuing Education for Veterinarians®

245

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Index to Advertisers For free information about products advertised in this issue, e-mail the product names to productinfo@compendiumvet.com.

Company

Product

Page

Atlantic Coast Veterinary Conference

2009 Conference

227

Bayer Animal Health

Baytril

207, 208

Boehringer Ingelheim Vetmedica

Vetmedin

203, 204

Companion Animal Parasite Council

Road Show

Inside front cover (US only)

Eli Lilly and Company

Comfortis

209, 210

Hill’s Pet Nutrition

PetFitness VetSync

Inside front cover (Canada only)

IDEXX Laboratories, Inc.

Real Time Care

Back cover

Northgate Veterinary Supply

Glass cage doors and rod gates

246

CEforVetsandTechs.com

Inside back cover

Novartis Animal Health

Derm Digest

228–229

Summit VetPharm

Vectra

215

Veterinary Learning Systems

A Guide to Equine Joint Injection

244

CE Center

206 (US only)

Veterinary Therapeutics

243

Vetstreet

Pet Portal Service

231

WhereTechsConnect.com

Job Marketplace

246

Valley seeks full-time associate. Spacious, newly remodeled small animal hospital with in-house laboratory with IDEXX Vet Test and QVC machine. Emergency clinic 20 minutes away. Great location to live, beautiful country, fishing, camping, great outdoors. Seventy-five minutes from District of Columbia. Excellent compensation and benefits. Must be client-oriented; equine experience a plus. Contact Shenandoah Animal Hospital, PO Box 503, Woodstock, VA 22664; fax 540-459-4998; phone 540459-2930, ask for Paula Cooper.

PRACTICES FOR SALE TEXAS – For sale: AAHA-accredited small animal and exotics practice specializing in diagnostic medicine and laser surgery, established in 1982. Located in university area of Houston; excellent demographics. Grossed $860,000 in 2008 — great growth potential for 2009. Equipped with computer technology and in-house diagnostic equipment, including ultrasound and digital x-ray. Highly motivated, certiﬁed staff; many with college degrees. Interactive, customdesigned website. Business and real estate package; asking $1,599,000 — ﬁnancing available. Call 713-446-3399 or email vetdoc81@hotmail.com for your appointment.

For classified advertising information, call Liese Dixon at 800-920-1695.

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*All ads are subject to a 40-word minimum charge and may be edited for grammar and style. All ads are posted on VetClassifieds.com on the first day of the issue month at no charge; all other advertising options incur an additional charge. Discounts are not applicable to first ad placement. Limit one discount per ad, barring promotional specials. All ads received after deadline will be printed in the next available issue(s). No cancellation after deadline. Include complete billing information with all orders. DO NOT mail check or money order payments with your ad; call for detailed instructions first. DO NOT email credit card information; mail or fax your payment information or use our secure Internet server at VetClassifieds.com.

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Reading Room*

CCOR DING TO T H E FOR E WOR D by Bernard E. Rollin, PhD (Department of Philosophy, Colorado State University, Fort Collins), this publication is an outgrowth of the social-ethical approach to wild animal welfare that has emerged over the past few decades. Dr. Rollin cites the “privilege” of maintaining nondomestic animals in captivity, in wildlife reserves, and as research subjects and

In this book, the professional zoologic and wildlife communities have gathered the best procedures for euthanizing nondomestic animals with minimal fear and pain. Title: Guidelines for Euthanasia of Nondomestic Animals Editor: Charlotte Kirk Baer Publisher: American Association of Zoo Veterinarians Year: 2006 Pages: 111

TO LEARN MORE For further information about this book or to order a copy, visit aazv.org.

248

notes the attendant responsibility of providing taxon-specific recommenproviding them with euthanasia as dations. There are separate chapters needed. To this end, the professional on invertebrates, fish, amphibians, zoologic and wildlife communities reptiles, birds, monotremes, marsupials, have gathered in this book the best bats, nonhuman primates, rodents, procedures for euthanizing these marine mammals, carnivores, hoofanimals with minimal fear and pain. stock, swine, and megavertebrates. This book is the result of close Multiple methods are outlined in all collaboration among the American cases, including inhaled and injected Association of Zoo Veterinarians, the chemicals and physical approaches. American Association of Wildlife Where applicable, in-the-field recomVeterinarians, the American Board of mendations are also cited. InformaVeterinary Toxicology, the American tion is summarized in tables for College of Zoological Medicine, the larger animal groups (e.g., inverAssociation of Avian Veterinarians, the tebrates, fish). The chapters are short Association of Reptilian and Amphib- and free of undue theoretical disian Veterinarians, the Canadian Associ- cussion and are thus useful for quick ation of Zoo and Wildlife Veterinarians, reference. The third section of the and the Wildlife Disease Association. book summarizes methods of euthanThese contributors acknowledge a num- asia for wild and exotic vertebrates, ber of limitations with regard to their consisting of a master table that recommendations, noting that they do presents and classifies methods as not reflect the only acceptable means recommended, conditionally acceptof euthanasia. Certain methods may able, or unacceptable, with concise not be applicable because of the con- comments as appropriate. straints of managing free-ranging This book would be a great asset wild life or because of the need to for any medical professional dealobtain samples for pathologic analy- ing with nondomestic animals and sis and disease control in a popula- is designed for ease of use in what tion. The authors point out that in will often be an emergency situation. some settings, it may not be feasible Despite its bare-bones pragmatism, it to meet the high standards of eutha- is guided by philosophical principles nasia for domestic animals but that in and a clear ethical code throughout. all cases, life should be terminated As Dr. Rollin notes, this publication “as humanely and rapidly as possible.” represents only “the beginning of an The first part of the book addresses ongoing quest for procedures that general concerns, such as criteria for mitigate pain and distress and provide humane euthanasia, physiology, and for a humane termination of life for regulatory issues. The second part species other than those commonly comprises the majority of the text, defined as domestic animals.”

Compendium: Continuing Education for Veterinarians® | May 2009 | CompendiumVet.com

*Written by Patricia L. Van Horn, a freelance writer in Long Branch, New Jersey.

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