Compendium | August 2009 by davidpsu

VOLUME 31 NUMBER 8 AUGUST 2009

Compendium CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

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Vol 31(8) August 2009

CONTI N U I NG EDUCATION FOR VETERI NARIANS ®

Tritrichomonas foetus

COMPENDIUM CONTINUING EDUCATION FOR VETERINARIANS®

A New Agent of Feline Diarrhea

FREE

PAGES 345–392

Canine Primary Hyperparathyroidism

Refereed Peer Review

Diagnosing the Cau Cause of Feline Pruritus

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! *

Surgery for Ur Urinary Incontinence in Dogs

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August 2009 Vol 31(8) CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

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August 2009 Vol 31(8) 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, DACVIM, DACVECC 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

346

CompendiumVet.com

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, DVM, PhD, DACVIM Gulf Coast Veterinary Specialists Houston, Texas

Nephrology Catherine E. Langston, DVM, DACVIM 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.

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

August 2009 Vol 31(8)

Features CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

352 Applied Dermatology Diagnosing the Cause of Feline Pruritus ❯❯ Rudayna Ghubash Pruritus is a common clinical sign of many dermatologic disorders in cats. This article presents a brief Facial pruritus in a foodoverview of clues allergic Siamese cat. in the history, prePAGE 352 sentation, and results of diagnostic tests that can help in diagnosing the underlying cause.

374

Tritrichomonas foetus: A New Agent of Feline Diarrhea

FREE

❯❯ Mary Katherine Tolbert and Jody L. Gookin ookin Tritrichomonas foetus is emerging as a common cause of feline diarrhea, particularly in high-density populations of young, purebred cats. However, careful testing is needed to distinguish the organisms from Giardia spp. Current testing and treatment options are presented in this article.

360 Surgical Views Surgical Treatment of Urethral Sphincter Mechanism Incompetence in Female Dogs ❯❯ Mary A. McLoughlin and Dennis J. Chew The authors describe the many surgical approaches to treating this common condition of older, spayed dogs. A video of one procedure is available on CompendiumVet.com.

382

Canine Primary Hyperparathyroidism

FREE

❯❯ Carmenn Schaefer and Richard E. Goldstein Primary hyperparathyroidism is a common cause of hypercalcemia in dogs. The diagnosis requires careful interpretation of test results, and treatment involves removal of the affected gland(s).

Departments 348 CompendiumVet.com 350 Editorial: Surgical Views ❯❯ Elizabeth M. Hardie

Product Forum PAGE 391 Cover photo: Jody L. Gookin, DVM, PhD, DACVIM.

351 News Bites 358 Research Recap Selected abstract from Veterinary Therapeutics 391 Product Forum

392 Market Showcase 392 Classiﬁed Advertising

*2009 PERQ/HCI FOCUS® Veterinary Study of Total Companion

392 Index to Advertisers

Animal Veterinarians, in comparison to ratings for each publication, by that publication’s readers. Compendium: Continuing Education for Veterinarians®

347

WEB EXCLUSIVES

August

2009 Vol 31(8)

CE ARTICLES

❯❯ The Epiphyseal Plate: Physiology, Anatomy, and Trauma

FORMS

❯❯ Canine and Feline Dental Exam Forms These downloadable forms can be used to gather important information about a patient’s dental visit. They include dental charts, an abbreviation index, and space to note treatment options. ION EXAMINAT

AL FELINE DENT

107

201 202 203 204 104 103 102 101 1C I1 1I 2I 3I C1 I3 I2

207

208

209

205

3 Rads: 1 2

Scaling Polishing Extraction Comments: Buccal Occlusal Palatal 600

700

Decid.

Lingual

500 800

Occlusal Buccal

408

407

404

409

1I 2I 3I I3 I2 I1 301 302 303 403 402 401

307

308

309

304

108

107

106

109

(months ago):

Last prophy

Treatment

Home care:

201 202 203 204 104 103 102 101 1C I1 1I 2I 3I C1 I3 I2

207

208

209

205

Material:

Y N CA Brush: NIN EY DE Material: N NT TAL EX Examin Oral rinse: AMINA ation Diet / Oral Habits: ATION

Buccal 110 M2

109

108 Occlusal 107

Palatal 600 700

Decid.

106 P2

105 104 facial 103 102 101 201 202 Extraoral 203 204 P1 C1 205 206 I3 I2 I1 207 1I 2I 3I 1C nodes 208 Lymph 1P 2P 3P 4P

Buccal mucosal

N-A

N-A 209 1M

Decid. De

Occlusal Buccal

OTHER Rads:

Extraction Comments:

Bucccal A Buccal N-

Palate

500 800

Scaling Polishing

N-A N-A

Tongue

800

TREATMENT

210 2M

Lingual

500

1 2 3

Occ Occlus clusal -A N al

Tonsils

Pala Palatal latalN - A Pharynx P4

408

407

404

409

1I 2I 3I I3 I2 I1 301 302 303 403 402 401

307

308

309

304

Salivary ﬂow

700

L N-A

Ling Lingua nguall Occ Occlus clusal al

M3 411

600

Caries

Calculus index

M1 409

(1, 2, 3)

CR Crown restoration index (1, 2, 3) FI Furcation tooth or jaw FX Fractured

ST Stomatitis T/A Tooth avulsed T/I Tooth impacted (1, 2, 3, 4) TR Tooth resorption extraction Simple closed X al extraction with XS Nonsurgic tooth sectioning extraction XSS Surgical Last prophy Systems Learning(month s ago):

Home care:

Bucccal Buccal

Decid. De

500

Brush:

Oral rinse:

Occ Occlus clusal lusal al

800

Pala Palatal latal 600 700

Extraoral facial

Lymph

Ling Lingua nguall Occ Occlus clusal al M3 411

M2 410

M1 409

P4 P3 P2 P1 C1 I3 I2 I1 1I 408 407 2I 3I 1C 406 405 1P 2P 404 403 402 3P 4P 401 301 302 303 304 305 306 307 308

Buc Buccal ccal 2M 310

Material: N

Material:

Diet / Oral

Habits: N-A

nodes

N-A N-A N-A N-A

Pharynx Salivary ﬂow

N-A N-A

G Granu loma GI Gingiv al index (1, 2, 3) GH Gingiv al hyperp lasia GR Gingiv al recess ion Mobility index (1, 2, 3) OM Oral mass PC Pulp capping MI

Pulp expos ed Plaque index (1, 2, 3) Periodontal pocket PRO Period ontal proph ylaxis R/C Comp osite ﬁlling RD Retain ed decidu ous RRT Retain ed root tip PI

Veterina ry Learnin g System s

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.

CONTACT US ❯❯ EE-mail mail your o r qquestions, estions suggestions, corrections, or letters to the editor: editor@CompendiumVet.com

348

NEWS BITES

N-A

mucosal

Tongue

Tonsils

311

Abbrevi ations

BE Biopsy , excisio nal BI Biopsy , incisional CA Caries CI Calcul us index (1, 2, 3) CR Crown restoration Furcation index (1, 2, 3) FX Fractu red tooth or jaw FI

Buccal

N Y

Palate 1M 309

❯❯ Dirsko J. F. von Pfeil, Charles E. DeCamp, and Sarah K. Abood This article reviews nutritional and hormonal inﬂuences, diseases with uncertain etiology, and hereditary disorders affecting the growth and development of the long bones in dogs and cats.

Researchers at the Schubot Exotic Bird Health Center at Texas A&M’s College of Veterinary Medicine have ﬁnally visualized the avian Borna virus, the cause of proventricular dilatation disease in parrots.

WEB-EXCLUSIVE VIDEO

❯❯ Collagen Injection Video The Surgical Views article in this issue, “Surgical Treatment of Urethral Sphincter Mechanism Incompetence,” by Drs. Mary A. McLoughlin and Dennis J. Chew, describes the many surgical approaches to treating this common condition of older, spayed dogs. A video contributed by Dr. McLoughlin demonstrates collagen injection as a treatment for urethral sphincter mechanism incompetence.

Buc Buccal ccal

P4 P3 P2 P1 C1 I3 I2 I1 1I 408 407 2I 3I 1C 406 405 1P 2P 404 403 402 3P 401

Biopsy, excisional Biopsy, incisional

410

301 302 303 1M 2M 304 exposed 305 306 3M PE Pulp 307 308 309 index (1, 2, 3)310 311 Granuloma PI Plaque (1, 2, 3) l pocket Gingival index PP Periodonta Treatme hyperplasia nt l prophylaxis GH Gingival PRO Periodonta 110 109 108 recession ﬁlling 107 106 GR M2Gingival 105 104 R/C Composite M1 P4 2, 3) 103 102 101 201 202 203 204 P3 (1, P2 P1 index deciduous 205 206 C1 I3 I2 Retained MI Mobility 207 I1 1I RD 208 2I 3I 209 1C 1P 2P 3P root tip 210 4P Retained OM Oral mass 1M 2M RRT PC Pulp capping

Abbreviations

❯❯ The Epiphyseal Plate: Nutritional and Hormonal Inﬂuences; Hereditary and Other Disorders

OTHER

TREATMENT

Examination 108

106

109

❯❯ Dirsko J. F. von Pfeil and Charles E. DeCamp This article reviews the development of long bones, the microanatomy and physiology of the growth plate, the closure times and contribution of different growth plates to overall growth, and the effect of, and prognosis for, traumatic injuries to the growth plate.

❯❯ Avian Borna Virus Visualized alized

Compendium

❯❯ Drug Testing in Spinal Cord Injury Program The Veterinary Teaching Hospital Canine Spinal Cord Injury Program at North Carolina State University is evaluating the efﬁcacy of a drug being developed to improve hindlimb function in chronically paralyzed dogs.

❯❯ Canine Genes May Help in the Search for a Cure for Brain Cancer By comparing human and canine genomes, researchers have discovered that a gene commonly thought to be involved in meningiomass may not be as important for tumor formation as ﬁrst thought. This has narrowed the search for the actual culprit.

❯❯ Collagen Injection Video

Canadian News

Coming Events 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 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 gastrointestinal disorders of cats and dogs, with an emphasis on diagnosis and treatment. It will offer 5.5 CE credits. Phone 800-670-1702 Web tavm.org 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 by using case examples. It will offer 5.5 CE credits. Phone 800-670-1702 Web 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 be presented by Dr. Marjorie Brooks. Phone 403-863-7160 E-mail info@cavm.ab.ca Web cavm.ab.ca/ce_calendar.html November 10 Toronto Academy of Veterinary Medicine: Practice Management Dave and Buster’s, Toronto, Ontario This seminar will focus on different aspects of practice management and is hosted by Shawn McVey, MA, MSW. It will offer 5.5 CE credits. Phone 800-670-1702 Web tavm.org. November 13–14 Lifelearn Inc. Continuing Education: Small Animal Laser Surgery Ontario Veterinary College University of Guelph, Ontario This seminar will offer 14 hours of CE credit. It is designed to provide practitioners with an introduction to the uses of CO2 lasers in veterinary surgery. Phone 800-375-7994 Web www.lifelearn.com

Canadian Veterinary Medical Association Appoints President D r. Julie de Moissac has been appointed the successor to Dr. Diane Frank as the president of the Canadian Veterinary Medical Association (CVMA). Dr. de Moissac is the 61st national president of the organization. She assumed leadership at the CVMA’s Annual General Meeting in Montreal, Quebec, on June 3, 2009. After graduating from the Western College of Veterinary Medicine in 1986, Dr. de Moissac established a mixed animal practice near Outlook, Saskatchewan. She became a Saskatchewan Veterinary Medical Association (SVMA) Councillor in 1995 and the SVMA president in 1998.

She then served a 3-year term on the board of directors of Prairie Diagnostic Services. “Becoming president of the Canadian Veterinary Medical Association is a truly humbling, yet exciting prospect,” says Dr. de Moissac. “The opportunity to work with and meet veterinarians from across this country is a once-in-alifetime privilege.” Dr. de Moissac has been a member of the CVMA for more than 23 years, ﬁrst as a council member and member of the Animal Welfare Committee, then as a member of the executive board.

Ontario Veterinary College Implements Hospital Information System

he Ontario Veterinary College Teaching Hospital (OVCTH) is in the process of implementing Meditech, a commercially available hospital information system. This system will help reduce costs and streamline the hospital’s administrative processes. OVCTH is the first veterinary facility to implement the system. The total suite of applications being implemented includes billing and accounts receivable, general ledger, accounts payable, fixed assets, materials management, medical records, pharmacy, lab, imaging and therapeutic services (radiology information system), order entry, admissions, patient care inquiry (electronic view of the patient record), housing and bed management, and scheduling. The system will also interface with the hospital’s financial system and new picture archiving and communication system. “Between OVCTH staff, OVCTH administration, Hamilton Health Sciences, and Beacon Partners, there are approximately 20 people involved in the project,” says Steven Woodard, hospital informa-

tion management coordinator. “We are also consulting with clinicians and members of Clinical Studies, OVC Information Technology Services, and University of Guelph Computing and Communications Services.” SPREAD YOUR GOOD NEWS Have any interesting news to share? Send it in! We would like to provide more recognition of veterinarians doing great things in their professional or personal lives. If you have news about yourself or a colleague or about some other newsworthy topic that would be of interest to others in the profession, send it (along with a picture if you have one) to: 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

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

349

Editorial In collaboration with the American College of Veterinary Surgeons

Surgical Treatment of Urethral Sphincter Mechanism Incompetence in Female Dogs ❯❯ Mary A. McLoughlin, DVM, MS, DACVS ❯❯ Dennis J. Chew, DVM, DACVIMa The Ohio State University

At a Glance Urethral Sphincter Mechanism Incompetence Page 360

Diagnosis Page 361

Surgical Treatment of Urethral Sphincter Mechanism Incompetence Page 362

Medical Management of Urethral Sphincter Mechanism Incompetence in Female Dogs Page 364

Future Directions in Treatment Page 373

❯❯ Elizabeth M. Hardie, DVM, PhD, DACVS North Carolina State University

aDr. Chew discloses that he has

received ﬁnancial support from Bayer Animal Health and Nestlé Purina PetCare Company.

360

Abstract: Urinary incontinence—loss of voluntary control over the retention and expulsion of urine—is a common medical problem in small animal patients. Incontinence occurs when pressure within the bladder exceeds urethral pressure. Incontinence may result from a variety of etiologies, including congenital anatomic abnormalities of the lower urinary and reproductive systems (ureter, bladder, bladder neck, urethra, vagina, vestibule) as well as neurologic, neoplastic, infectious, and inﬂammatory diseases.

Urethral Sphincter Mechanism Incompetence Urethral sphincter mechanism incompetence (USMI), also referred to as idiopathic incontinence, spay incontinence, and hormoneresponsive incontinence, is the most common and important cause of acquired urinary incontinence in adult female dogs.1–4 USMI is largely a condition of spayed dogs, but in some breeds, such as greater Swiss mountain dogs, soft-coated wheaten terriers, Doberman pinschers, and giant schnauzers, incontinence may precede ovariohysterectomy (OVH). Congenital USMI has also been recognized as a cause of incontinence in juvenile dogs and is frequently associated with other anatomic malformations, such as ureteral ectopia and ureteroceles.1–4 Approximately 20% of female dogs have been reported to develop some degree of USMI after OVH performed between the ﬁrst and second heat cycles.5 In dogs spayed before ﬁrst estrus, the incidence is reported to be 9.7%.5 The incidence of incontinence may be as high as 30% in large-breed female dogs (>20 kg); in some breeds, including boxer, Doberman pinscher, rottweiler, Old

English sheepdog, and giant schnauzer, it is even higher.1,2,4,6–8 Urinary incontinence is most often reported within 3 years of spaying.1–4 There is no reported difference in the incidence of incontinence between dogs in which ovariectomy alone was performed and dogs that underwent OVH. Decreases in maximal urethral closure pressure (MUCP) and functional urethral length predictably occur during the first 12 to 18 months after neutering, resulting in a caudal shift of the urethral pressure profile and deterioration of urethral closure function. It is speculated that the decline in MUCP continues with advancing age, further contributing to the development of incontinence in later life.1,2,7,8 The term urethral sphincter mechanism incompetence was first suggested to describe weakness of the “urinary sphincter” despite the fact that no true anatomic sphincter exists at the bladder neck or proximal urethra. The smooth muscle of the proximal urethra is continuous with the detrusor muscle layer of the bladder trigone.1 Therefore, congenital anatomic abnormalities affecting the ureters, bladder neck, and proximal urethra can impair development of the normal smooth

muscle architecture in this region, contributing to incontinence.1–4 Varying amounts of fibrovas-cular tissue located throughout the length of the bladder neck and urethra may also play a role in maintenance of continence.1–3 Caudal displacement of the bladder into the pelvic canal is recognized as pelvic bladder syn-drome.9,10 The hallmark radiographic appearance of a pelvic bladder shows abnormal elongation of the bladder, persistent caudal displacement of the bladder and bladder neck into the pel-vic canal on distention, an indistinct or blunted vesicourethral junction, and a shortened ure-thra.9,10 Shortening of the urethra reduces expo-sure of the bladder neck and proximal urethral wall to the intraabdominal pressure that acts as y an external occluding force.1,2,4,6–8 Abnormally short urethras are frequently noted in dogs with USMI. Pelvic bladder has been reported in male and female dogs with and without urinary incontinence.9,10 The significance of pelvic bladder and its role in the pathophysiology of USMI are not completely understood, but pelvic bladder is thought to be a contributing factor in patients with USMI.9,10 USMI is considered to be a multifactorial disorder, and the specific etiopathogenesis remains unclear.1–4,6–8 USMI in dogs has been likened to stress incontinence diagnosed in women after pregnancy, childbirth, or menopause. In women, sudden increases in abdominal pressure from actions such as coughing, sneezing, and laughing can result in loss of bladder control.1,2,6,7 Varying degrees of urinary incontinence have been reported in dogs with USMI. Most owners report leakage of urine when the dog is recumbent or sleeping. Increased periods of incontinence have also been reported in dogs after strenuous exercise, excitement, and steroid administration. In our experience, swimming and eating snow can also lead to increased incontinence in dogs.

Diagnosis The diagnosis of USMI is established by ruling out structural and functional abnormalities of the urinary and reproductive systems in patients that are neurologically normal. Physical examination ﬁndings are frequently unremarkable. Specific examination of the vulva and perivulvar region is necessary to

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

Surgical Views is a collaborative series between the American College of Veterinary Surgeons (ACVS) and Compendium. Upcoming topics in this series include cystoscopy and cystoscopic stone removal, vacuumassisted wound closure, and conventional foreign object removal. All Surgical Views articles are peer-reviewed by ACVS diplomates. To locate a diplomate, ACVS has an online directory that includes practice setting, species emphasis, and research interests (acvs.org/VeterinaryProfessionals/FindaSurgeon).

vulassess vulvar conformation and degree of vul var recession. Perivulvar dermatitis and hyperpigmentation of the perivulvar skin secondary to chronic incontinence are frequently noted in dogs with USMI. Cystocentesis to collect a urine sample for complete urinalysis and bacteriologic culture is a critical first step in the diagnosis and management of patients with urinary incontinence. Infection, inflammation, uroliths, or neoplasia of the lower urinary system can result in loss of continence. If a urinary tract infection exists, treatment with appropriate antibiotic therapy for 14 to 21 days, followed by reevaluation of a urine culture 5 to 7 days after the completion of antibiotic therapy, should precede other diagnostic procedures. Abdominal radiography may detect radiodense urinary calculi or caudal displacement of the urinary bladder into the pelvic canal. Contrast radiography (e.g., retrograde vaginocystography) and contrast-enhanced computed tomography can enable more specific evaluation of the vestibule, vagina, and lower urinary and reproductive structures, including detailed information regarding the location of the bladder neck, urethral length, ureteral size, location of ureteral orifices, bladder wall thickness or irregularity, and presence of small uroliths. Uroendoscopy is useful to evaluate the luminal surfaces of the lower urinary and reproductive systems under magnification.

QuickNotes Cystocentesis to collect a urine sample is a critical ﬁrst step in the diagnosis and management of patients with urinary incontinence.

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The Surgical Views article begins on page 360.

Surgical Views

t is estimated that when experts attempt to describe the steps in a procedure, they leave out one-ﬁfth of the steps they actually perform. This is because much of what an expert does becomes part of an unconscious routine as he or she repeats a procedure time and time again. Therefore, when it is important to capture all the steps and decision points involved in a complex technical procedure, a formal process called cognitive task analysis is used. During this process, no fewer than three experts must be videotaped and interviewed. The differences between the experts are then reconciled for each step of the procedure.

The American College of Veterinary Surgeons (ACVS) recently partnered with Compendium to ensure that the articles in the Surgical Views series are reviewed by ACVS diplomates. In a Compendium article, the steps involved in a procedure are described by the author, who is often a single individual. This is why the peerreview process, in which at least two experts in the relevant ﬁeld read the article, is critical. These individuals must reconcile the description of the procedure with their own methods and knowledge. The result should be an article that provides the reader with a description of a procedure that contains all the key steps and decision points.

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The American College of Veterinary Surgeons (ACVS) recently partnered with Compendium to ensure that the articles in the Surgical Views series are reviewed by ACVS diplomates. This partnership has expanded the list of authors and reviewers, ensuring that individuals with surgical experience are sharing accurate and up-to-date information with the journal’s readers. It also helps ensure that the descriptions of surgical procedures are complete and understandable. There is less chance for unconscious omission when an author chooses to summarize a surgical disease or topic rather than describe a procedure. In this instance, the author may simply be unaware of new developments that have only been presented and described at conferences. However, having ACVS-trained reviewers look over the information increases the likelihood that no key development will be missed. The goal of the Surgical Views column is to provide accurate, practical surgical information to practicing veterinarians. With the help of the ACVS, the job has become a lot easier.

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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American College of Veterinary Surgeons

News Bites Offering a look at the latest news in the veterinary ﬁeld.

DogTime Media Gets Social

ogTime Media has joined the Facebook craze with its new app, “Save A Dog.” The application, one of the ﬁrst in which online gaming positively affects the real world, allows pet lovers to help actual animal shelters and pets, all while having fun online. Facebook users can browse photos of real-life adoptable dogs and choose to foster one for the day. Fostered dogs can also be “co-fostered” by friends. Users can pick a new dog each day. The real-life upside is that, by fostering dogs and having friends co-foster them, users earn points that go toward buying food for real dogs in shelters.

Public Health Goes to the Dogs

he AVMA is applauding the introduction of new public health legislation that “highlights the critical role veterinarians in public and private practice have in public health and [...] recognizes the need for federal investment in bolstering the veterinary workforce, which is on the front lines of public health, food safety and animal health,” according to Dr. Ron DeHaven, AVMA chief executive ofﬁcer. The bill, known as the Veterinary Public Health Education and Workforce Act, creates new programs for training veterinarians and offers additional federal support to protect public health.

DogTime Creates Pet Insurance Center

ogTime, the largest online entity in the $45.4 billion US pet market, has launched a comprehensive online pet insurance center. The center allows pet owners to compare different options using the Plan Comparison Grid, an interactive grid that compares plans side by side based on 10 criteria. The grid can be customized to compare just the plans that are relevant to a particular shopper’s needs. The Web site also offers guidance to pet owners through editorial content that explains key issues and concerns about pet insurance.

Your gateway to trusted resources for your veterinary team. W exclusives Web Articles A News N Videos V VLS online store V Product Spotlight P

2009 ACVS

VETERINARY SYMPOSIUM The Surgical Summit

October 6-7: Pre-Symposium Laboratories October 8-10: Seminars & Scientific Abstracts Marriott Wardman Park Hotel | Washington, DC Presented by: American College of Veterinary Surgeons American Association of Equine Practitioners American College of Veterinary Anesthesiologists American Veterinary Dental College Veterinary Emergency and Critical Care Society

Compendium... C and so much more! an 301-916-0200 www.surgicalsummit.org Compendium: Continuing Education for Veterinarians®

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

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

Diagnosing the Cause of Feline Pruritus ❯❯ Rudayna Ghubash, DVM, DACVD Animal Dermatology Clinic Marina del Rey, California

iagnosing the underlying cause of pruritus in cats can be considered. Food allergy can start at any age. be difficult because of the variations in clinical pre- Some breeds are predisposed to certain diseases, such as Persians (dermatophytosis) and sentation and numerous possible etiologies. Many own- Siamese (food allergies)1–3 (FIGURE 1). ers are not aware of how much their cats lick and groom themselves, making it difficult to assess the cat’s degree Environment of pruritus. The ability to interpret historical information, Outdoor cats have greater exposure to mosquitoes (FIGURE 2), parasites (e.g., fleas, Notoedres identify and understand the significance of clinical lesions, mites), and infectious agents (e.g., dermatand appropriately use diagnostic tests aids in the diagnosis ophytes, viruses). Knowing whether other animals or people are affected can indicate and management of feline pruritus. Historical Information Signalment

At a Glance Historical Information Page 352

Physical Examination Page 353

Common Diagnostic Differentials for Feline Pruritus Based on Lesion Location

Breed and age at onset of clinical signs provide clues to underlying etiologies. Pruritus in patients younger than 6 months is most commonly caused by parasites (Notoedres, Cheyletiella, and Otodectes spp), allergies (especially ﬂea and food), and dermatophytosis. When pruritus begins in middle age, the differentials are the same, but allergic disease (food allergy, atopic dermatitis) becomes more probable. When pruritus begins in older animals with no history of skin disease, conditions such as epitheliotropic lymphoma, pemphigus foliaceus, Bowen’s disease, and paraneoplastic syndrome should also FIGURE 1

whether a contagious or zoonotic disease is present (e.g., dermatophytosis, cheyletiellosis, scabies). Psychogenic pruritus can be triggered by environmental changes, such as construction, remodeling, moving, or introduction of a new pet or person into the household. Siamese cats and Siamese crosses seem to be at risk for psychogenic disorders; however, psychogenic pruritus should not be assumed based on breed and is diagnosed only after all other causes of pruritus have been excluded.4

Concurrent and Previous Disease In cats with concurrent histories of pruritus and gastrointestinal disease (e.g., inﬂammatory bowel disease), food allergy should be FIGURE 2

Page 353

Diagnostic Tests Page 356

Facial pruritus in a food-allergic Siamese cat.

352

Facial and pinnal involvement in a cat with mosquito bite hypersensitivity.

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

FIGURE 3

TABLE 1

Common Diagnostic Differentials for Feline Pruritus Based on Lesion Location Lesion Location Diagnostic Differentials

Pemphigus foliaceus with secondary bacterial pyoderma around the claw folds in a cat.

Ear canals

Food allergy Atopic dermatitis Notoedres infection Otodectes infection

Head and neck

Food allergy Atopic dermatitis Flea allergy Notoedres infection Mosquito bite hypersensitivity Otodectes infection Viral dermatoses Idiopathic facial dermatitis (“dirty face” syndrome) Drug reaction

diligently investigated. Atopic dermatitis should be strongly considered in pruritic animals with concurrent airway disease or asthma. Viral dermatoses should be suspected in cats with a history of upper airway viral disease and erosive facial lesions. A detailed drug history is critical because certain drugs and vaccines can trigger erythema multiforme and pemphigus foliaceus.5 Nasal planum

Mosquito bite hypersensitivity Viral dermatoses Squamous cell carcinoma Pemphigus foliaceus Cryptococcus infection

Dorsal cervical region

Flea allergy Atopic dermatitis Food allergy Injection-site reaction

Physical Examination Lesion Distribution Observing the distribution of lesions, especially in the initial stages of the underlying disease, can be helpful in narrowing the differential diagnosis. Flea allergy lesions are typically more severe in the lumbosacral, groin, and dorsocervical areas, whereas food allergy lesions are more common on the head. The clinical signs of atopic dermatitis vary but can mimic those of food and ﬂea allergies. Cheyletiellosis lesions (scale, papules, crusts) tend to be distributed dorsally. Dermatophytosis can be localized to a speciﬁc site or can be generalized. Some cats may be asymptomatic carriers of Cheyletiella mites or dermatophytes. Pemphigus foliaceus usually targets the pinnae, bridge of the nose, claw folds (FIGURE 3), and perimammary areas but can also be generalized. TABLE 1 lists some common diagnostic differentials based on lesion distribution.

Lesion Appearance The ability to recognize and identify lesion types can provide valuable information in the evaluation of a pruritic cat. Excoriations, a nonspeciﬁc sign of self-trauma typically associated with pruritus, are characterized by their linear shape and are most prevalent on the head and neck. Erosions are superﬁcial

QuickNotes Observing the distribution of pruritic lesions, especially in the initial stages of the underlying disease, can be very helpful in narrowing the differential diagnosis.

Dorsal and lumbar Flea allergy region Cheyletiellosis Claw folds

Pemphigus foliaceus Bowen’s disease

Ventral abdomen

Demodex gatoi infection Food allergy Atopic dermatitis Flea allergy Psychogenic pruritus

Generalized

Dermatophytosis Food allergy Atopic dermatitis Flea allergy Pemphigus foliaceus Epitheliotropic lymphoma Drug reaction Paraneoplastic syndrome Erythema multiforme

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FIGURE 4

Indolent ulcers in a cat with flea allergy dermatitis.

lesions that are similar to, but often wider than, excoriations. Erosions caused by scratching tend to be linear, whereas those associated with licking tend to be circular. Erosions are often associated with eosinophilic plaques. Ulcers can appear as focal, nonpruritic lesions on the upper lip, known as rodent or indolent ulcers (FIGURE 4). These lesions are one of the components in the eosinophilic granuloma complex (EGC) triad. EGC lesions are reaction patterns that typically indicate an underlying allergy or hypersensitivity reaction, not a specific disease.6 Other conditions that can create skin ulcers with variable degrees of pruritus include vasculitis, autoimmune diseases, drug reactions, and neoplasia. Papules are small (1 to 5 mm), raised lesions that are often associated with crusts and are the most common lesions seen in miliary dermatitis. Like EGC lesions, miliary dermatitis is a sign of an underlying disease. It can be associated with flea allergy dermatitis (most common), atopic dermatitis, food allergy, bacterial folliculitis, cheyletiellosis, dermatophytosis, pemphigus foliaceus, and drug reactions. Plaques appear as moderate to well-defined elevations of the skin with erythema. Eosinophilic plaques, one of the EGC variants, are most commonly associated with underlying allergic disease (FIGURE 5). Eosinophilic granulomas, the third component of the EGC complex, are firm, sometimes ulcerated, raised areas that are often found in the mouth or in a linear pattern on the body (FIGURE 6). Alopecia that is associated with pruritus usually presents as broken off, barbered hairs from overgrooming, scratching, or rubbing. Other lesions of pru-

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FIGURE 5

FIGURE 6

Eosinophilic plaques in a cat with atopic and flea allergy dermatitis.

ritus are often present with alopecia; however, in some cases, broken or barbered hair is the only clue that the cat is pruritic. Thin ﬂakes of shed epidermis characterize scale, a nonspeciﬁc sign that is commonly seen in cheyletiellosis.

QuickNotes Various allergies look the same on histopathology, so biopsy is usually not used to diagnose allergy and is never used to differentiate allergic reactions.

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Diagnostic Tests Cytology/Skin Scrapings Used appropriately, dermatologic diagnostic tests can be powerful tools. Skin scrapings are one of the easiest and most important of these tests and should be conducted for all pruritic cats except those with seasonal signs. Some of the more common parasites that can be identified on skin scraping samples include Cheyletiella blakei, Otodectes cynotis, Lynxacarus radovskyi, Trombicula autumnalis, Felicola subrostratus, Notoedres cati, Demodex cati, and Demodex gatoi. Cytology can be used to assess samples for the presence of bacteria, inflammatory cells, fungal spores and hyphae, acantholytic cells, and neoplastic cells. Cytology should be conducted for any pruritic cat with dermatologic lesions other than noninflammatory alopecia. True pyoderma cases should demonstrate intracellular bacteria, usually within neutrophils and, sometimes, within eosinophils. Eosinophils are inflammatory cells that are common in a variety of disorders, but they are most commonly associated with ectoparasites, allergies, and some forms of EGC lesions. Fungal spores and hyphae are common in cases of dermatophytosis. A fun-

Oral eosinophilic granulomas in a cat with concurrent indolent ulcers.

gal culture should always be performed for speciation. Cytology can also be of value in identifying some forms of cutaneous neoplasia. On rare occasions, it can identify ectoparasites such as Cheyletiella, especially when adhesive tape is used to collect the sample. Acantholytic cells suggest pemphigus foliaceus, although they can also be seen in dermatophytosis. Using a ﬁne-tooth comb on the entire haircoat for several minutes to collect dander and scale for microscopic examination is considered the most reliable method to ﬁnd Cheyletiella mites in both symptomatic and asymptomatic animals.7

Fungal Culture Fungal culture using dermatophyte test medium (DTM) is considered the gold standard for identifying dermatophytes. Dermatophyte infections can present as pruritic infections with any lesion type. When cultured on DTM, dermatophytes produce an alkaline by-product that changes the color of the medium from yellow to red. However, saprophytic contaminants may also turn the medium red under certain conditions. Therefore, DTM should be inspected daily for color change, and any growth must be examined microscopically for evidence of microconidia and macroconidia. Suspected fungal growth can be lifted with clear adhesive tape, stained with lactophenol cotton blue, and examined microscopically. Speciation of the dermatophytes should always be performed to determine the source of infection and help prevent future reinfection.

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

Hair Examination use this product daily to every other day for the Hair examination using a Wood lamp can be 4- to 6-week period.9 However, this method can helpful in suspected cases of dermatophytosis, be expensive and is difficult in cats that are hard but fluorescence is seen in only a small percent- to pill. Another option is to use a topical formuage of cases of Microsporum canis infection. lation of a flea control product that is approved Hairs that fluoresce should be plucked for cul- for cats every 2 weeks for a 4- to 6-week period. ture for definitive diagnosis.1 Direct microscopic Some of these products are labeled for more freexamination of the hair can also identify der- quent than monthly application. matophytosis. Hyphae and spores can often be seen when the condenser lens is turned down, Food Elimination Trials although culture should always be performed When evaluating a cat for food allergy derto confirm the diagnosis. In cases of alopecia matitis, a food elimination trial must be conin which the degree of pruritus is unknown, ducted, as serologic testing is unreliable and conducting trichograms to examine the tips of inaccurate in domestic animals.10 Food-allergic plucked hairs can help determine if the alopecia cats can have the same clinical signs as aniis caused by self-trauma, in which case, the hair mals with atopic dermatitis or flea allergy, but they commonly present with severe pruritus tips appear fractured and jagged. of the head and neck. The only way to diagSkin Biopsy nose food allergy is to feed an elimination diet Skin biopsy can be a powerful tool when used for an 8- to 12-week period. I prefer a trial appropriately. Many specific infectious, para- consisting of a home-cooked diet or a novel sitic, autoimmune, and neoplastic diseases can limited protein–based commercial diet. I typibe diagnosed using biopsy. Biopsy is indi- cally only use a hydrolyzed diet if the other cated for unusual lesions or clinical presen- diets are not eaten. Owners who are willing to tations or when a case does not respond to make a home-cooked diet can be directed to standard treatment. However, samples taken balanceit.com, where they can purchase recifrom lesions of allergic disease look the same pes and supplements, or should contact a veton histopathology, so biopsy is not usually erinary nutritionist for a consultation. Because used to diagnose allergies and is never used cats have unique nutritional needs, it is imperto differentiate them. ative that home-cooked diets be balanced, as feeding an unsupplemented diet for more than Flea Control Trials 4 weeks can lead to nutritional deficiencies.11 If all nonallergic differentials have been ruled At the end of the 8- to 12-week trial period, the out, a systematic approach to allergies must be cat is rechallenged with the original diet and pursued. Atopic dermatitis, flea allergy, and food observed for exacerbation of clinical signs. allergy can look identical. Flea allergy is the most common allergy in cats in flea-endemic Allergy Testing locations, and flea control trials should be con- The diagnosis of atopic dermatitis is made primarily on the history and physical findings after ducted to eliminate this differential.8 The goal of a flea control trial is to keep the ruling out all other pruritic diseases. Once atopic cat free of fleas, optimally for 4 to 6 weeks, and dermatitis is diagnosed, allergy testing is used evaluate the degree of subsequent resolution of to determine the specific allergens to which the pruritus. If the environmental flea burden is high, patient is sensitive, typically to start immunothe first step should be to suggest that the owner therapy. Intradermal skin testing, although conconsult an exterminator about treating the indoor sidered the gold standard of allergy testing, is and outdoor environments. The option of keeping difficult to conduct in cats. Feline skin is thinner the cat exclusively indoors during the flea control than canine skin, making intradermal injections trial should always be discussed, although it is harder to perform.12 Furthermore, the degree not always feasible. Because studies in cats have of reactivity at the injection sites is often flatfound oral nitenpyram to have 100% efficacy ter, producing false-negative results.12 In vitro against adult Ctenocephalides felis fleas within allergy tests are available and provide a reason3 hours, an ideal method of performing a flea able alternative to skin testing. Some specialists control trial, especially in outdoor animals, is to prefer this method of allergy testing in cats.

QuickNotes If a diagnosis of atopic dermatitis is made, allergy testing is used to determine the speciﬁc allergens to which the patient is sensitive, typically to start immunotherapy.

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Conclusion Pruritus in cats can be difﬁcult and frustrating to treat. However, with a methodic approach and appropriate diagnostic tests, practitioners can signiﬁcantly decrease the severity of pruritus and improve the quality of life for most cats without chronic use of long-term repository steroids.

TO LEARN MORE

For a more detailed discussion of flea allergy dermatitis, see the May 2009 Applied Dermatology article, “Overview of Flea Allergy Dermatitis,” on CompendiumVet.com.

References 1. Scott DW, Miller WH, Griffin CE. Fungal skin diseases. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:336-442. 2. Carlotti DN, Remy I, Prost C. Food allergy in dogs and cats: a review and report of 43 cases. Vet Dermatol 1990;1:55. 3. Rosser EJ. Food allergy in the cat. A prospective study of 13 cats. In: Ihrke PJ, Mason IS, White SD, eds. Advances in Veterinary Dermatology II. New York: Pergamon Press; 1993:33. 4. Waisglass SE, Landsberg GM, Yager JA, Hall JA. Underlying medical conditions in cats with presumptive psychogenic alopecia. JAVMA 2006;228(11):1705-1709. 5. Scott DW, Miller WH, Griffin CE. Immune-mediated disorders. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:667-779. 6. Scott DW, Miller WH, Griffin CE. Miscellaneous skin diseases. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:1125-1183. 7. Moriello KA. Cheyletiellosis. In: Griffin CE, Kwochka KA, Mac-

Donald JM, eds. Current Veterinary Dermatology: The Science and Art of Therapy. St Louis: Mosby; 1993:90-95. 8. Scott DW, Miller WH, Griffin CE. Skin immune system and allergic skin diseases. In: Scott DW, Miller WH, Griffin CE, eds. Muller & Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:543-666. 9. Schenker R. Tinembart O, Humbert-Droz E, et al. Comparative speed of kill between nitenpyram, fipronil, imidacloprid, selamectin and cythioate against adult flea Ctenocephalides felis (Bouche) on cats and dogs. Vet Parasitol 2003;112:249-254. 10. Jeffers JG, Shanley KJ, Meyer EK. Diagnostic testing of dogs for food hypersensitivity. JAVMA 1991;198(2):245-250. 11. Mueller RS, Jackson H. Atopy and adverse food reaction. In: Foster AP, Foil CS, eds. BSAVA Manual of Small Animal Dermatology. 2nd ed. Gloucester, England: BSAVA; 2003:125-136. 12. Gilbert S. Feline pruritus therapy. In: Bonagura JD, Twedt DC, eds. Kirk’s Current Veterinary Therapy. 14th ed. St. Louis: Saunders Elsevier; 2009:405-410.

Research Recap Selected abstract from Veterinary Therapeutics

Effect of Intraarticular Injection of Autologous Adipose-Derived Mesenchymal Stem and Regenerative Cells on Clinical Signs of Chronic Osteoarthritis of the Elbow Joint in Dogs* Black LL, Gaynor J, Adams C, et al. Vet Ther 2008;9(3):192-200. Autologous adipose-derived mesenchymal stem cell (AD-MSC) therapy involves harvesting fat from the patient, isolating the stem and regenerative cells, and administering the cells back to the patient. Autologous AD-MSC therapy in veterinary regenerative medicine has been commercially available since 2003. Previously reported results from a blinded, controlled trial in dogs with chronic osteoarthritis of the coxofemoral (hip) joint demonstrated efﬁcacy of a single intraarticular injection of autologous AD-MSC therapy. The primary objective of the current study was to evaluate the effectiveness of this therapy in

dogs with chronic osteoarthritis of the humeroradial (elbow) joints and to determine the duration of effect. Fourteen dogs were recruited. Veterinarians assessed each dog for lameness, pain on manipulation, From the range of motion, and functional disability Fall 2008 issue using a numeric rating scale at baseline and speciﬁed intervals up to 180 days after treatment. Statistically sigTO niﬁcant improveLEARN ment in outcome MORE measures was For more Veterinary Therapeutics abstracts, visit the archives at demonstrated.

VeterinaryTherapeutics.com *This study was sponsored by Vet-Stem, Inc. Poway, California.

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Probiotic Therapy Improves Chronic Feline Diarrhea Christy Evans Cutting, DVM Companion Animal Clinic Roseburg, Oregon

Patient: Calliope, an 11-year-old domestic short-haired cat

Therapy Plan: After her surgery, I expected Calliope to have some loose stools, but when she presented with persistent diarrhea, I felt that her digestive system needed a little help to restore its normal microflora balance. I recommended that we try Purina Veterinary Diets® FortiFlora® Feline Nutritional Supplement. I started sprinkling FortiFlora on her food each day. FortiFlora was definitely what she needed. Within the first week, she started eating more and her diarrhea resolved. Eating has always been a challenge for Calliope; she’s very particular and will become anorectic if she doesn’t like a particular food. She’s small to begin with (6 lb), so we’re constantly watchful for any weight loss. Because Calliope’s digestive system was so delicate after surgery, maintaining her appetite was a priority for us and her owner. In addition, Calliope had lost a significant amount of weight, so we offered her a variety of commercial foods to encourage her to eat.

Outcome: Calliope really didn’t seem “better” until we started FortiFlora. Until recently, her owner was giving her the nutritional supplement daily because if she missed one dose, the diarrhea would return. After 2 years, her owner was able to discontinue FortiFlora, and Calliope is now eating well and doing great without any gastrointestinal problems! 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.

©Jeannine Cook

History: In January 2004, Calliope presented with constipation. We administered two enemas and prescribed 1 mL lactulose once every 12 to 24 hours. She did reasonably well on lactulose for approximately 1 year, but the constipation returned. At this point, we increased the dose of lactulose to 1 mL every 8 hours, which worked until January 2006. This time, the constipation didn’t respond to enemas, so we sedated Calliope for manual removal of the impacted feces. Unfortunately, she didn’t tolerate sedation well. She became hypothermic and almost comatose; intensive care, including intravenous fluids with corticosteroids, was needed to help pull her through. She slowly improved over the next 3 days and began eating on the fourth day. She was sent home but returned the next day with diarrhea and vomiting. I referred her owner to the nearest specialist for more involved diagnostics and treatment. Luckily they obliged—Calliope was diagnosed with an abnormal colon that required a partial colectomy 2 days later. Calliope has had no more problems with constipation, but she developed diarrhea for 6 months following surgery.

Calliope Veterinarian’s Comments I have been recommending Purina Veterinary Diets ® FortiFlora ® as a nutritional supplement for more than 2 years. I like FortiFlora for several reasons: It’s convenient to dispense and administer, it’s easy on the GI tract, cats love the taste, and it works! Calliope’s owner really feels that FortiFlora made the difference for her cat.

I commonly use the nutritional supplement in dogs and cats that develop mild diarrhea when receiving antibiotics. It’s nice to have something to offer owners when they call with this problem, without having to change antibiotics or bring the pet back in for a recheck. I also commonly use FortiFlora for pets with stress diarrhea—It seems to work very well for these cases. I recommend that my veterinary colleagues try FortiFlora. It’s easy to administer; you just sprinkle the nutritional supplement on the pet’s food. It works fast and is so simple and effective!

Sponsored by

In collaboration with the American College of Veterinary Surgeons

Surgical Treatment of Urethral Sphincter Mechanism Incompetence in Female Dogs ❯❯ Mary A. McLoughlin, DVM, MS, DACVS ❯❯ Dennis J. Chew, DVM, DACVIMa The Ohio State University

At a Glance Urethral Sphincter Mechanism Incompetence Page 360

Diagnosis Page 361

Surgical Treatment of Urethral Sphincter Mechanism Incompetence Page 362

Medical Management of Urethral Sphincter Mechanism Incompetence in Female Dogs Page 364

Future Directions in Treatment Page 373

aDr. Chew discloses that he has

received ﬁnancial support from Bayer Animal Health and Nestlé Purina PetCare Company.

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assess vulvar conformation and degree of vul vulvar recession. Perivulvar dermatitis and hyperpigmentation of the perivulvar skin secondary to chronic incontinence are frequently noted in dogs with USMI. Cystocentesis to collect a urine sample for complete urinalysis and bacteriologic culture is a critical first step in the diagnosis and management of patients with urinary incontinence. Infection, inflammation, uroliths, or neoplasia of the lower urinary system can result in loss of continence. If a urinary tract infection exists, treatment with appropriate antibiotic therapy for 14 to 21 days, followed by reevaluation of a urine culture 5 to 7 days after the completion of antibiotic therapy, should precede other diagnostic procedures. Abdominal radiography may detect radiodense urinary calculi or caudal displacement of the urinary bladder into the pelvic canal. Contrast radiography (e.g., retrograde vaginocystography) and contrast-enhanced computed tomography can enable more specific evaluation of the vestibule, vagina, and lower urinary and reproductive structures, including detailed information regarding the location of the bladder neck, urethral length, ureteral size, location of ureteral orifices, bladder wall thickness or irregularity, and presence of small uroliths. Uroendoscopy is useful to evaluate the luminal surfaces of the lower urinary and reproductive systems under magnification.

QuickNotes Cystocentesis to collect a urine sample is a critical ﬁrst step in the diagnosis and management of patients with urinary incontinence.

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The surgical procedures reported in the veterinary literature to improve USMI in small animal patients have all been adapted and modiﬁed from procedures performed on women with diagnosed stress incontinence.

FIGURE 1

Colposuspension Illustration by Tim Voit

Description

Illustration of colposuspension. Cranial traction is applied to the bladder and uterine body remnant. The vagina is exposed on either side of the urethra immediately cranial to the pubis. Nonabsorbable monofilament sutures are placed between the prepubic tendon and the seromuscular layer of the vagina, positioning the bladder neck cranially into the abdomen.

QuickNotes Surgical treatment is typically reserved for patients in which appropriate medical management has failed or is not possible.

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Anatomic abnormalities such as ureteral ectopia, ureterocele, and structural defects of the trigone and urethra can be definitively diagnosed with this method of imaging. Specific diagnostic confirmation of USMI is made based on the results of urodynamic studies, including a urethral pressure profile and leak point pressure. Patients with USMI have a decreased MUCP and leak point pressure compared with continent dogs.6,7,11–13

Surgical Treatment of Urethral Sphincter Mechanism Incompetence

Colposuspension uses the placement of sutures between the vagina and the prepubic tendon to create urethral resistance to urine outflow. This procedure results in cranial advancement and repositioning of the bladder neck and proximal urethra, exposing these structures to intraabdominal pressure. In addition, the urethra, cradled by the vagina, is positioned over the edge of the pelvic brim, which applies additional external compression (FIGURE 1). Colposuspension is the surgical procedure most commonly performed to treat spayed dogs with USMI. Colposuspension alone was reported to be curative in approximately 50% of patients; in approximately 40% of the remaining patients, continence was improved.1,2,6–8 A recent study evaluated the immediate urodynamic response to colposuspension in normal beagles.6 Leak point pressures were significantly increased, while MUCPs were decreased. Urethral length was assessed using measurements from vaginourethrograms and urethral pressure profiles and was determined to be slightly increased based on evaluation of lateral radiographs. Urodynamic studies indicated that the total profile length and the functional profile length were significantly increased.6 The long-term effects of colposuspension also have been examined in female dogs with USMI.7 Two months after colposuspension, 12 of 22 female dogs achieved complete continence. However, only three dogs remained completely continent 12 months after surgery. When medical therapy was instituted after surgery, an additional eight dogs regained complete urinary continence and nine were improved.7

Medical therapy (BOX 1) is the ﬁrst line of treatment for dogs with USMI. Surgical treatment of USMI is typically reserved for patients in which appropriate medical management has failed, that have adverse reactions to recommended medications, or that have medical conditions precluding the use of medical therapies. The goal of surgical treatment of USMI is to increase urethral resistance to the outﬂow of urine. To accomplish this, surgical procedures focus on correcting caudal displacement of the bladder neck to (1) increase intraabdominal forces and provide improved MUCP within the urethra (colposuspension, urethropexy, and urethral Technique lengthening), (2) increase urethral resistance With the patient in dorsal recumbency, clip and by reducing the diameter of the urethral aseptically prepare the ventral abdomen from lumen (urethropexy and submucosal collagen the xyphoid over the pubis, including the periimplants), and (3) improve functional urethral vulvar region. Aseptically pass an appropriatelength (colposuspension, urethral lengthening). size balloon-tip urethral catheter transurethrally

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into the bladder. Perform a caudal midline celiotomy from the umbilicus, extending over the cranial aspect of the pubis, and identify and isolate the insertion of the rectus abdominis muscles and prepubic tendon (FIGURE 2). Expose the bladder, proximal urethra, and uterus or uterine body remnant. If the patient is intact, OVH is performed at this point. Place a stay suture through the apex of the bladder for traction and manipulation and an Allis tissue forceps on the uterine body remnant for cranial traction. A peritoneal reﬂection forming the vesicogenital pouch exists between the dorsal aspect of the pelvic urethra and the ventral aspect of the vagina, tethering these structures together (FIGURE 3). This intimate anatomic association allows cranial traction of the uterine body remnant and vagina to result in cranial movement of the bladder neck and urethra. With cranial traction applied to the bladder and uterine body remnant, use a curved mosquito hemostat or right-angled forceps to bluntly dissect a small window through the periurethral fascia along each side of the urethra immediately cranial to the pubic brim, exposing the vagina dorsal to the urethra (FIGURE 4). Take care to avoid excessive dissection and disruption of the neurovascular supply to the vagina and urethra, positioned dorsolaterally within the pelvic canal. Identify the lateral wall of the vagina and grasp it with atraumatic forceps positioned on each side of the urethra. Based on the size of the patient, pre-place one or two 2-0 nonabsorbable monoﬁlament sutures through the seromuscular layer of the vaginal wall on each side of the urethra and through the prepubic tendon, entering and exiting lateral to the insertion of the rectus abdominis muscle (FIGURE 5). Firm cranial traction on both the bladder and uterine remnant is needed to achieve cranial positioning while these sutures are tied on either side of the urethra. Insert a mosquito hemostat between the ventral aspect of the urethra and the pelvic brim to ensure that the urethra is not completely obstructed (FIGURE 6). Close the abdomen in a routine manner.

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Postoperative Care A urethral catheter with a closed urinary collection system should be maintained for 24 hours after surgery. Transient dysuria and stranguria due to urethral inﬂammation and partial urethral obstruction can occur after catheter removal. Complete urethral obstruction after colposuspension is rare. If complete urethral obstruction occurs, replacement of the urethral catheter for an additional 24 to 36 hours and administration of an NSAID are indicated. Attempts to manually express Compendium: Continuing Education for Veterinarians®

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Medical Management of Urethral Sphincter Mechanism Incompetence in Female Dogs Urethral sphincter mechanism incompetence (USMI) may be fully, partially, or transiently responsive to medical management.

QuickNotes Medical therapy is the ﬁrst line of treatment for dogs with urethral sphincter mechanism incompetence.

α-Adrenergic Agonists Phenylpropanolamine (PPA; 1.0 to 1.5 mg/kg PO bid to tid) effectively controls incontinence in approximately 74% to 92% of dogs with USMI by stimulating α-adrenergic receptors in the urethra, increasing urethral tone. Many patients that are not completely continent following administration of PPA have improved continence.1,2,11–13,a In one study, more than half of the dogs that failed to respond when treated with the standard formulation of PPA became continent when treated with a sustained-release formulation (75-mg capsules; dose based on body weight).a The ability of PPA to control USMI decreases over time in some dogs. Not all α-adrenergic agonists are as effective as PPA in controlling incontinence. A recent study showed PPA to be more effective than pseudoephedrine.13 Minimal adverse effects (restlessness, mild behavioral changes) associated with PPA administration have been reported in some dogs. Dogs with systemic hypertension or clinically relevant cardiac or renal disease should not be treated with α-adrenergic agonists.11–13,a Estrogens Estrogens have also been shown to be effective in controlling USMI by increasing the number or sensitivity of α-adrenergic receptors in the urethra. Estrogens may have other, less well understood effects, including increased urethral tone arising from vascular changes and reduction in circulating concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH).1–4,11,b Estriol increases urethral resistance in sexually intact and spayed female dogs without urinary incontinence.

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Estrogen therapy alone improves incontinence resulting from USMI in approximately 65% to 83% of treated dogs.1,2,b Diethylstilbestrol (DES; 0.5 to 1.0 mg/dog [0.02 mg/kg]), which is available from veterinary compounding pharmacies, is often effective in reducing incontinence attributed to USMI. A maximal induction dose of 1 mg/dog is given for 3 to 7 days; the dose is then decreased to every other day and then to the lowest dose that will maintain continence. Some dogs cannot tolerate DES at the doses required to maintain continence without manifesting clinical signs of estrus. Conjugated estrogens such as Premarin (Wyeth Pharmaceuticals, Philadelphia) are more readily available than DES and can be administered at 20 μg/kg every 4 days as an alternative therapy. Bone marrow toxicity is a potential adverse effect of estrogen therapy, but treatment with low doses of DES or conjugated estrogens appears to be safe. Intermittent low-dose maintenance with DES or conjugated estrogen to control incontinence may be preferred by owners over multiple daily doses of PPA, despite the fact that PPA is often more effective. In some patients with refractory incontinence, DES can be administered simultaneously with PPA to achieve a synergistic response that may effectively control incontinence. Other Therapies Detrusor instability or hyperactive bladder may contribute to incontinence in some dogs with USMI. A therapeutic trial with anticholinergic agonists (e.g., oxybutynin, ﬂavoxate) to relax spasms of the detrusor muscle may be warranted. Oxybutynin (0.2 mg/kg PO q8–12h) and ﬂavoxate (100 to 200 mg PO q8h) have been effective in the treatment of potential detrusor instability in dogs.

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BOX 1

Treatment with gonadotropin-releasing hormone (GnRH) analogues was recently reported to result in complete continence in more than half of dogs with USMI in which traditional medical therapies failed.c,d An average of 253 days of continence was observed in seven dogs that became fully continent with a GnRH analogue as the sole treatment. An additional ﬁve dogs that had partial improvement with GnRH analogue treatment became fully continent when PPA was also administered. Treatment with GnRH analogues reduces the concentrations of FSH and LH that develop after OVH in dogs.e Increased concentrations of FSH and LH may play a role in development of USMI in susceptible dogs. However, MUCP does not appear to be directly related to circulating concentrations of FSH or LH.e Treatment with leuprolide, a GnRH analogue, did not increase MUCP in dogs with USMI that regained urinary continence.c,d Receptors for GnRH, FSH, and LH have been demonstrated in various regions and densities in the canine urethra and bladder. With a success rate of 71%, long-acting GnRH analogues are effective as a ﬁrst-line treatment for USMI, but this rate is lower than that achieved with PPA.

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Bacon NJ, Oni O, White RAS. Treatment of urethral sphincter mechanism incompetence in 11 bitches with a sustained-release formulation of phenylpropanolamine hydrochloride. Vet Rec 2002;151(13):373-376. b Angioletti A, DeFrancesco I, Vergottini M, Battocchio ML. Urinary incontinence after spaying in the bitch: incidence and oestrogen-therapy. Vet Res Commun 2004;28(Suppl 1):153-155. c Reichler IM, Jöchle W, Piché CA, et al. Effect of long acting GnRH analog or placebo on plasma LH/FSH, urethral pressure proﬁles and clinical signs of urinary incontinence due to sphincter mechanism incompetence in bitches. Theriogenology 2006;66(5):1227-1236. d Reichler IM, Barth A, Piché CA, et al. Urodynamic parameters and plasma LH/FSH in spayed beagle bitches before and 8 weeks after GnRH depot analogue treatment. Theriogenology 2006;66:2127-2136. e Reichler IM, Pfeiffer E, Piché CA, et al. Changes in plasma gonadotropin concentration and urethral closure pressure in the bitch during the 12 months following ovariectomy. Theriogenology 2004;62(8):1391-1402.

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FIGURE 2

FIGURE 3

QuickNotes Colposuspension is the surgical procedure most commonly performed to treat spayed dogs with urethral sphincter mechanism incompetence.

Surgical exposure of bladder and urethra for colposuspension. The abdominal incision extends over the pubis, exposing the insertion of the rectus abdominis muscle and prepubic tendon (arrows). FIGURE 4

Dissection of the periurethral fascia on either side of the urethra immediately cranial to the pubis exposes the dorsally positioned vagina.

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The bladder is reďŹ&#x201A;ected caudally, demonstrating the vesicovaginal fold (arrow) between the dorsal aspect of the urethra and the vagina. Cranial traction of the vagina facilitates repositioning of the bladder neck cranially into the abdomen. FIGURE 5

Placement of colposuspension sutures. Nonabsorbable monofilament sutures are pre-placed between the prepubic tendon and the seromuscular layer of the vagina on either side of the urethra.

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the bladder to void its contents may cause patient discomfort. Persistent complete urethral obstruction that does not respond to appropriate conservative treatment over a period of 3 to 5 days after surgery may require removal of the colposuspension sutures between the vaginal wall and prepubic tendon.

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Urethropexy Description Urethropexy is an alternative to colposuspension that is aimed at restoring the bladder neck and proximal urethra to an intraabdominal position while simultaneously increasing resistance to urine ﬂow by reducing the diameter of the urethral lumen.14,15 Cystourethropexy was initially reported in 10 female dogs diagnosed with USMI and pelvic bladder. The results of surgery alone were considered excellent in two dogs, and urethropexy combined with medical therapy (phenylpropanolamine [PPA]) resulted in marked improvement in an additional six dogs. One dog did not improve with surgery.14 A later study reported the results of treatment of 100 female dogs with urethropexy for incontinence due to USMI.15 Surgery alone led to complete control of incontinence in 56 dogs and improvement of continence in 27 dogs. Of the other 17 dogs, nine failed to respond and eight showed initial improvement but later relapsed. Nine of these 17 dogs underwent a second urethropexy procedure, resulting in complete continence in six dogs and improvement in three. Postoperative complications were observed in 21 dogs, including increased frequency of urination (14 dogs), dysuria (six), and anuria (three).15 As with other procedures intended to increase tension within the urethral wall, transient or persistent dysuria as a result of partial urethral obstruction and failure to improve continence were the most common complications noted in both studies.14,15

Technique Position the patient in dorsal recumbency and clip and aseptically prepare the ventral abdomen. Perform a caudal midline celiotomy from the umbilicus, extending over the cranial aspect of the pubis. Expose the bladder, urethra, and uterine body remnant and place a stay suture through the apex of the bladder for cranial traction. Using blunt dissection, clear the periurethral fat from the ventral aspect of the bladder neck and pelvic urethra. Pre-place six to 10 horizontal mattress sutures bilaterally using a 2-0 nonabsorbable monoﬁlament suture material. The sutures should enter the abdominal cavity, passing full thickness through the ventral abdominal wall, including the rectus fascia. They should Compendium: Continuing Education for Veterinarians®

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FIGURE 6

to pass a urethral catheter after surgery may be difﬁcult and traumatic to the surgical site within the urethra and should be avoided if at all possible. Administration of an NSAID for 7 to 10 days after surgery is indicated to reduce discomfort and soft tissue swelling.

Urethral Lengthening Description

Cranial traction is applied to the uterine body remnant while the pre-placed sutures are tied to complete the colposuspension. A mosquito hemostat is gently inserted between the pubis and the urethra to ensure that the urethra is not completely obstructed.

QuickNotes A signiﬁcantly short urethra prohibits cranial movement of the bladder neck into the abdominal cavity, eliminating the ability to use some surgical procedures.

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Urethral lengthening has been used to treat congenital USMI in cats and dogs with a notably shortened urethra resulting in pelvic displacement of the bladder neck. A significantly short urethra (urethral hypoplasia) prohibits cranial movement of the bladder neck into the abdominal cavity, eliminating the ability to use surgical procedures such as colposuspension, urethropexy, and urethral slings to treat USMI. Reconstruction of the bladder neck and the use of ventrally based bladder tube flaps have been reported to taper the bladder neck, thereby elongating the proximal urethra. Excellent or good results were reported in seven of eight cats treated with this technique, and a good outcome was described in one dog.16,17 Urethral lengthening using bladder wall flaps has also been described for treatment of urinary incontinence in people. This technique may warrant further consideration with expanded clinical evaluation for the treatment of USMI in small animals with pelvic bladder.

then pass through the seromuscular layer of the urethra in a horizontal mattress pattern at either the nine or three o’clock position in the transverse section without penetrating the urethral lumen. The sutures then exit from the abdominal cavity through the abdominal wall, Technique including the rectus fascia, on the same side Position the patient in dorsal recumbency and (FIGURE 7). The two most caudal sutures on clip and aseptically prepare the ventral abdoeither side of the urethra are engaged through men. Perform a caudal midline celiotomy from the prepubic tendon as they enter and exit the umbilicus, extending over the cranial aspect the abdomen. Tighten and tie the pre-placed of the pubis. Expose the bladder, urethra, and sutures from caudal to cranial on each side of uterine body remnant. Make a ventral cystothe urethra. Close the abdomen routinely.14,15 tomy incision, extending into the proximal urethra, and create two V-shaped flaps in the Postoperative Care ventral aspect of the ventral bladder wall, using Some degree of stranguria and dysuria will the caudal extent of the incision in the proximal occur after surgery due to the increased outflow urethra as the point of both V flaps (FIGURE 8). resistance created within the urethral lumen. The widest portion of each V flap is located at Stranguria may persist for several weeks after the level of the ureteral orifices, at the tip of surgery. The patient’s voiding patterns should the trigone. Use 4-0 monofilament absorbable be observed daily for the first few days after sutures in a continuous or interrupted pattern surgery to be sure a small stream of urine is to primarily close the linear defect created in passed with each voiding effort. Complete the ventral wall of the bladder neck and proxiurethral obstruction is uncommon. Attempts mal urethra, thereby decreasing the diameter of

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the bladder neck lumen and elongating the proximal urethra. The initial descriptions of this procedure recommended suturing the bladder ﬂaps to each other to prevent a loss in bladder capacity.17 Alternatively, resection of the bladder ﬂaps makes the surgical procedure and closure much simpler, and the resultant loss of bladder capacity is usually inconsequential. Due to the tremendous regenerative capacity of the bladder, presurgical vesicular capacity is restored within a few weeks to months after surgery.

Postoperative Care Increased frequency of urination and stranguria are the most commonly anticipated adverse effects after reconstructive procedures to lengthen the urethra. Stranguria may be noted for several weeks. Avoid placement of a urethral catheter unless complete urethral obstruction occurs. Intermittent cystocentesis can be performed over a 24- to 36-hour period, and administration of an NSAID is indicated to reduce soft tissue inﬂammation of the lower urinary tract. Acepromazine administered at a low dose (0.01 to 0.025 mg/kg SC, IM, or IV q8h) may help relax the urethra, reducing stranguria and facilitating urine ﬂow.

Urethral Slings Description Urethral sling procedures using seromuscular flaps created from the bladder wall or a synthetic material passed transpelvically through the obturator foramen have been combined with colposuspension to provide additional external compression of the pelvic urethra, increasing resistance to urine flow.18,19 These procedures are technically more difficult to perform. The reported outcomes are similar to those of colposuspension alone. It remains unclear whether there is an advantage to the use of a combined procedure.18 The modified sling urethroplasty procedure creates external compression at the vesicourethral junction by wrapping two seromuscular flaps created from the bladder neck region around the proximal urethra to increase resistance to urine flow.19

Technique Perform a colposuspension as previously described. Following colposuspension, make a 2- to 2.5-cm ventral midline incision through the seromuscular layer of the bladder neck, extending to the junction of the proximal urethra. Raise two rectangular seromuscular pedicle flaps with a caudal base from the ventral surface of the bladder neck region (FIGURE 9). These flaps should be between 4 and 10 mm in width, depending on the size of the patient. Place a 4-0 absorbable monofilament stay suture through the free end of each flap. Pass the flaps around each side of the proximal urethra and secure them on the dorsal aspect to provide compression at the vesicourethral junction.19 Primarily close the remaining seromuscular defect on the ventral bladder neck with a simple continuous or interrupted pattern using 4-0 absorbable monofilament sutures. Remove the urethral catheter to permit complete closure of this defect. If necessary, additional sutures can be placed dorsally in the sutured flaps to adjust the tension of the sling. Compression provided by the sling should be such that gentle digital pressure on the bladder is necessary to exceed the urethral pressure that permits urine flow.19 Close the abdomen in a routine manner.

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Minimally Invasive Urethral Bulking

FIGURE 7

Collagen Injection Technique Position the patient in right lateral recumbency under general anesthesia. Clip and aseptically prepare the vulva and perivulvar region. A 19or 14-French rigid cystoscope with a 30° angle is used for uroendoscopy and the injection procedure. Endoscopy is performed using a sterile ﬂuid infusion to create a clear visual

Illustration of urethropexy procedure. Six to 10 sutures are pre-placed bilaterally between the body wall incision and the seromuscular layer of the urethra in a horizontal mattress pattern at either the three or nine o’clock position when viewed transversely. The most caudal sutures on either side engage the prepubic tendon as they enter and exit the abdomen. FIGURE 8

Illustration by Tim Voit

If the results of medical or surgical treatment of USMI are incomplete or unsatisfactory, endoscopic submucosal implantation of urethral bulking agents such as polytetrafluoroethylene (Teflon) or medical-grade collagen can be performed to create intraluminal resistance to urine outflow.20–22 Successful urethral bulking with submucosal collagen has been reported in women and dogs.21,22 Collagen products are commonly used in people to correct defects of the skin and soft tissues. A specific collagen product for urologic use (Contingen, Bard Urological, Covington, GA) has been commercially developed and approved for use in humans. This product is composed of highly purified bovine dermal collagen that is cross-linked with glutaraldehyde and dispersed in phosphate-buffered saline. The collagen component is composed of approximately 95% type I collagen and 5% or less type III collagen. This product is packaged in a sterile 2.5-mL syringe for single use. Collagen has a higher degree of biocompatibility compared with other products previously reported for urethral bulking (e.g., polytetrafluoroethylene). Initial reports showed a control rate (complete continence) of 53% for USMI treated with one or two series of submucosal injections of collagen. This rate improved to 75% when PPA was administered to dogs in which collagen injections provided inadequate urinary control.21 More recently, a success rate of 68% was reported in 40 female dogs with USMI treated with submucosal collagen injections.22 Some dogs may require a second series of collagen injections if incontinence is uncontrolled or relapses. Repeat injection procedures are usually easier to complete because the previous urethral bulking site is readily identified and augmented.

Illustration by Tim Voit

Description

Illustration of urethral lengthening using the bladder-ﬂap reconstruction technique. A midline cystotomy incision is made extending to the proximal urethra. Two V-shaped full-thickness flaps are created in the ventral bladder wall (dashed lines). The point of each V is the caudal extent of the incision in the proximal urethra. The widest portion is at the level of the ureteral orifices. The flaps can be excised with little consequence to bladder capacity. Primary closure of the linear incision in the ventral wall of the bladder neck and proximal urethra reduces the luminal diameter of the bladder neck, thereby elongating the proximal urethra.

ﬁeld. Mucosal hemorrhage can be controlled with the infusion of cold ﬂuids. An assistant with sterile gloves should prepare the collagen and injection device. Perform a complete evaluation of the lower urinary and reproductive structures to rule out anatomic causes of urinary incontinence before injecting the collagen. Position the tip

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FIGURE 9

FIGURE 10

FIGURE 11

Endoscopic view of submucosal collagen injection. The injection needle is passed through the biopsy channel of the cystoscope and positioned immediately below the mucosal layer of the urethra distal to the vesicourethral junction.

Endoscopic view of completed submucosal collagen injections. Visual occlusion of the urethral lumen.

Illustration by Tim Voit

of the cystoscope within the proximal urethra to visualize the vesicourethral junction, and aseptically pass the injection device through the biopsy channel of the cystoscope until the beveled needle end is visible in the optical ﬁeld. The recommended site for collagen injection is approximately 1.5 to 2 cm caudal to the vesicourethral junction. Position the cystoscope to facilitate insertion of the beveled tip of the injection device immediately below the urethral mucosa into the submucosal layer.

Slowly inject the collagen, watching for immediate elevation of the urethral mucosa to create a mounding effect (FIGURE 10). If the needle is positioned too deep, there is minimal to no intraluminal deformation of the urethral mucosa. The collagen is commonly injected at three to four sites in a circle. The amount of collagen injected at each site is determined visually. Injection of excessive collagen at any given site can result in mucosal disruption and leakage of collagen from the site. The procedure is considered complete when the injection sites appose one another, achieving visual obstruction of the urethral lumen (FIGURE 11). Patients should be continent immediately after this procedure. Dogs with moderate to severe inflammation or urinary tract infection may experience some minor incontinence until the infection/inflammation is resolved medically. If incontinence persists after the initial collagen injections, this procedure can be repeated, enhancing the previously injected sites. Administration of PPA has been shown to further enhance control of urinary continence after collagen injection. Complete urinary outflow obstruction has not been reported in dogs. Follow-up endoscopic examinations have uniformly demonstrated that the submucosal collagen deposits can remain visually unchanged for years. Relapse of incontinence after prolonged successful control with collagen injections may be related to absorption of the phosphate buffer component of the collagen preparation.

Illustration of the modiﬁed urethral sling procedure. A ventral midline incision is made through the seromuscular layer of the bladder neck and proximal urethra. Two rectangular seromuscular pedicle flaps are elevated from the ventral surface of the bladder neck region. The flaps are passed around each side of the vesicourethral junction and secured on the dorsal aspect, providing external compression of the bladder neck. Primary closure of the seromuscular defect on the ventral bladder neck tapers the bladder neck and elongates the proximal urethra.

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Future Directions in Treatment Recognizing that no medical or surgical treatments of female dogs with USMI have been uniformly successful, current investigations are focusing on the practical use of gonadotropin-releasing hormone analogues as a single therapy or in combination with other medical or surgical treatments (BOX 1). In addition, work has begun to evaluate the efficacy of a percutaneously controlled static hydraulic urethral sphincter in dogs.23 This system consists of a doughnut-shaped silicone vascular occluder attached to a subcutaneous fluid injection port. The luminal diameter of the occluder can be adjusted by the infusion of small volumes of saline through the injection port. The occluder is surgically placed around the bladder neck to provide external compression, preventing passive urine outflow, and the degree of occlusion is adjusted until optimal

control (i.e., the patient can void urine without obstruction and retain urine without incontinence) is achieved.23

Conclusion Surgical treatment of USMI is focused on dogs in which appropriate medical therapies have failed or medical conditions prevent the use of medical treatment. Surgery or minimally invasive procedures such as collagen implantation may provide further control of continence in some difﬁcult cases.

SURGICAL VIDEO

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References 1. Gregory SP. Developments in the understanding of the pathophysiology of urethral sphincter mechanism incompetence in the bitch. Br Vet J 1994;150:135-150. 2. Holt PE. Importance of urethral length, bladder neck position and vestibulovaginal stenosis in sphincter mechanism incompetence in the incontinent bitch. Res Vet Science 1985;39:364-372. 3. McLoughlin MA. Management of urinary incontinence. Proc BSAVA Symp 2004. 4. Hoelzler MG, Lidbetter DA. Surgical management of urinary incontinence. Vet Clin North Am Small Anim Pract 2004 (34):1057-1073. 5. Stöcklin-Gautschi NM, Hässig M, Reichler IM, et al. The relationship of urinary incontinence to early spaying in bitches. J Reprod Fertil Suppl 2001:57:233-236. 6. Fowler JD, Rawlings CA, Mahaffey MB, et al. Immediate urodynamic and anatomic response to colposuspension in female beagles. Am J Vet Res 2000;61:1353-1357. 7. Rawlings CA, Barsanti JA, Mahaffey MB, Bement S. Evaluation of colposuspension for treatment of incontinence in spayed female dogs. JAVMA 2001;219(6):770-775. 8. Gregory SP, Holt PE. The immediate effect of colposuspension on resting and stressed urethral pressure profiles in anesthetized incontinent bitches. Vet Surg 1994;23:330-340. 9. Mahaffey MB, Barsanti JA, Barber DL, Crowell WA. Pelvic bladder in dogs without urinary incontinence. JAVMA 1984;184(12): 1477-1479. 10. Adams WM, DiBartola SP. Radiographic and clinical features of pelvic bladder in the dog. JAVMA 1983;182(11):1212-1217. 11. Rosen AE, Ross L. Diagnosis and pharmacological management of disorders of urinary incontinence in the dog. Compend Cont Educ Pract Vet 1981;3:601-610. 12. Richter KP, Ling GV. Clinical response and urethral pressure profile changes after phenylpropanolamine in dogs with primary sphincter mechanism incompetence. JAVMA 1985;187:605-611. 13. Byron JK, March PA, Chew DJ, DiBartola SP. Effect of phenylpropanolamine and pseudoephedrine on the urethral pressure profile and continence scores of incontinent female dogs. J Vet Intern Med 2007;21(1):47-53.

14. Massat BJ, Gregory CR, Ling GV, et al. Cystourethropexy to correct refractory urinary incontinence due to urethral sphincter mechanism incompetence preliminary results in ten bitches. Vet Surg 1993;22(4):260-268. 15. White RN. Urethropexy for the management of urethral sphincter mechanism incompetence in the bitch. J Small Anim Pract 2001;42:481-486. 16. Holt PE. Surgical management of congenital urethral sphincter mechanism incompetence in eight female cats and a bitch. Vet Surg 1993;22(2):98-104. 17. Fowler JD, Holmberg DL. Proximal urethral reconstruction using a distally based bladder tube flap an experimental study. Vet Surg 1987;16(2):139-145. 18. Muir P, Goldsmid SE, Bellenger CR. Management of urinary incontinence in five bitches with incompetence of the urethral sphincter mechanism by colposuspension and a modified sling urethroplasty. Vet Rec 1994;34:38-41. 19. Nickel RF, Wiegand U, Van Den Brom WE. Evaluation of a transpelvic sling procedure with and without colposuspension for treatment of female dogs with refractory urethral sphincter mechanism incompetence. Vet Surg 1998;27:94-104. 20. Arnold S, Jaeger P, DiBartola S, et al. Treatment of urinary incontinence in dogs by endoscopic injection of Teflon. JAVMA 1989;195:1369-1374. 21. Arnold S, Hubler M, Lott-Stolz G, Rusch P. Treatment of urinary incontinence in bitches by endoscopic injection of glutaraldehyde cross-linked collagen. J Small Anim Pract 1996;37:163-168. 22. Barth A, Reichler IM, Hubler M, et al. Evaluation of long-term effects of endoscopic injection of collagen into the urethral submucosa for treatment of urethral sphincter incompetence in female dogs: 40 cases (1993-2000). JAVMA 2005;226(1):73-76. 23. Adin CA, Farese JP, Cross AR, et al. Urodynamic effects of a percutaneously controlled static hydraulic urethral sphincter in canine cadavers. Am J Vet Res 2004;65(3):283-288.

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CE Article 1

Tritrichomonas foetus: A New Agent of Feline Diarrhea ❯❯ Mary Katherine Tolbert, DVM ❯❯ Jody L. Gookin, DVM, PhD, DACVIM North Carolina State University

At a Glance Clinical Presentation Page 374

Clues to Identifying Tritrichomonas foetus Infection in Cats Page 375

Diagnostic Approach to Tritrichomonas foetus Infection Page 375

Diagnosis Page 375

Therapy Page 378

Tips for Avoiding Ronidazole Toxicosis Page 380

374

Abstract: Tritrichomonas foetus is a single-celled, ﬂagellated protozoal parasite that colonizes the feline colon and distal ileum. Infected cats may be asymptomatic or may have clinical signs that include malodorous large bowel diarrhea. T. foetus infection is common in, but not limited to, high-density populations of young, purebred cats. Testing for this parasite is still not routine at most veterinary clinics, and T. foetus is often misdiagnosed as Giardia spp. T. foetus-speciﬁc tests (fecal culture and polymerase chain reaction) should be considered in cats with large bowel diarrhea, especially those in which traditional diagnostics and treatments for other causes of feline large bowel diarrhea have failed to reach a clinical resolution. Recognition of this newly emerging disease and appropriate sample handling are critical for the detection and treatment of feline trichomoniasis.

richomonads are protozoan para- prevalence of infection.5,6 T. foetus has sites characterized by an undulat- been found in many countries.4,5,7–9 The ing membrane that extends along reported prevalence of T. foetus in cats is the length of their pear-shaped body 10% in the United Kingdom and 31% in and anterior ﬂagella that vary in num- the United States.4,6–8 No breed of cat is ber depending on the species (FIGURE 1). known to be immune to T. foetus. These single-celled organisms are obliUnlike Giardia spp, trichomonads do gate parasites of warm, moist, anaerobic not form cysts and therefore cannot surenvironments within the gastrointestinal vive for prolonged periods in the environor genitourinary tract of a variety of host ment. They can survive for up to 3 days in species. They are often considered to be moist feces.10 Trichomonads are presumnonpathogenic commensals; however, ably transmitted from cat to cat via shared litterboxes, where the parasites can be several pathogenic species exist. Tritrichomonas foetus is well recog- transferred from the feces of one cat to the nized as a venereal pathogen of cattle. paws of another. The parasites are subseRecently, it was discovered to be a patho- quently ingested during grooming. There gen of cats, in which the parasites colo- is little evidence at this time for venereal nize the distal ileum and colon, resulting transmission of T. foetus in cats.11 in chronic large bowel diarrhea.1–3 The prevalence of infection can be quite high, Clinical Presentation particularly in young cats housed in high- The most characteristic clinical sign of density populations (e.g., shelters, breed- T. foetus infection is chronic waxing and ing facilities)4; older and mixed-breed waning large bowel diarrhea (BOX 1). The cats have also been identiﬁed with a high diarrhea frequently has the consistency

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Tritrichomonas foetus: A New Agent of Feline Diarrhea CE BOX 1

BOX 2

Clues to Identifying Tritrichomonas foetus Infection in Cats

Diagnostic Approach to Tritrichomonas foetus Infection

Young cat obtained from a cattery or shelter Chronic waxing and waning, malodorous, large bowel diarrhea Normal appetite with no loss of body condition Diarrhea responds to antibiotics but recurs when drugs are discontinued Trophozoites observed in feces are unresponsive to treatment for Giardia spp

of cow feces and is malodorous; it occasionally contains mucus or fresh blood (FIGURE 2). Severely affected cats may have involuntary fecal dribbling and inﬂammation of the anus. Because the infection is predominantly restricted to the large intestine, cats maintain a normal appetite and do not have muscle wasting.1,5 In many cats, the diarrhea improves in response to antibiotic therapy, only to return when the antibiotics are discontinued. Importantly, many infected cats do not show any clinical signs, particularly older cats. Therefore, all cats in contact with a cat diagnosed with T. foetus or housed in a high-risk environment may be asymptomatic carriers of the infection.

Fecal sample collection Collect feces immediately after voiding or directly from the colon using a fecal loop or saline ﬂush technique Do not refrigerate the sample Use the quantity of feces that is appropriate for the test being conducted Ensure that the cat has not received antibiotics within the past 7 days Testing methods Examination of a direct fecal smear (wet mount) for trichomonads (carefully distinguish T. foetus from Giardia spp trophozoites) Examination of fecal culture (InPouch TF media) for trichomonads Polymerase chain reaction for T. foetus using DNA extracted from feces (most sensitive)

rated (FIGURE 3). A drop of the recovered solution can then be examined directly under the microscope for trichomonads or placed in a fecal culture pouch. Alternatively, the solution can be sedimented in a centrifuge and submitted for PCR analysis. Fecal samples should always be fresh, free

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Diagnosis FIGURE 1 T. foetus infection is diagnosed on the basis of identification of the organism on a fecal smear, after culture of feces in media fostering the growth of T. foetus, or by polymerase chain reaction (PCR) testing performed on DNA extracted from a fecal sample (BOX 2). T. foetus cannot be detected by routine fecal analyses such as centrifugation flotation, and the organisms do not survive refrigeration. Suitable fecal samples may be obtained by (1) collecting a freshly voided specimen devoid of contaminating litter, (2) inserting a fecal loop per rectum into the proximal colon, or (3) passing a red rubber catheter into the proximal colon for the instillation and recovery of several milliliters of sterile saline. We prefer the saline flush technique, in which approximately 10 Tritrichomonas foetus in a fecal smear prepared from a cat with diarrhea. mL of sterile saline is injected through the Note the undulating membrane and anterior flagella of each organism. (Diff-Quik; catheter into the colon and then gently aspi- magnification: 400×)

FREE CE Tritrichomonas foetus: A New Agent of Feline Diarrhea

FIGURE 2

Direct Fecal Smear Typical appearance of a bowel movement from a cat with T. foetus infection. The feces are poorly formed, have the consistency of cow feces, and may contain mucus or fresh blood.

FIGURE 3

To obtain a ﬂush specimen of the colon, insert a red rubber catheter through the anus of the cat into the proximal colon and instill and aspirate approximately 10 mL of sterile saline. A drop of the resulting solution can be applied to a microscope slide, coverslipped, and examined with a light microscope for the presence of motile trichomonads. A video of this procedure may be viewed at JodyGookin.com.

of contaminating litter, and kept unrefrigerated before testing. If a stool sample is being transported to the veterinary clinic, advise the owner to keep it warm and moist. Samples obtained from nondiarrheic or dry stools are unsuitable for use in testing for T. foetus and rarely test positive even if infection is present. Further, concurrent administration of antibiotics at the time the sample is collected appears to decrease the success of ﬁnding T. foetus. Therefore, administration of antibiotics should be stopped for several days before testing.

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No available diagnostic tests have 100% sensitivity for detection of the infection. If test results are positive, the cat is considered to be infected with T. foetus. However, if test results are negative, the possibility of infection cannot be excluded, particularly in cases with a high index of suspicion for infection. In these cases, veterinarians should consider repeated testing.

The fecal smear is the cheapest and simplest option for diagnosis of T. foetus infection; however, it is also the least sensitive. For direct fecal smears, fresh feces are diluted in saline, and a drop of the solution is examined under a coverslip using a light microscope (FIGURE 4). Trichomonads are nearly identical in size to Giardia spp trophozoites and must be carefully distinguished. The keys to distinguishing trichomonads from Giardia spp are (1) the presence of an undulating membrane on trichomonads and (2) the characteristic “falling-leaf” motility of Giardia spp, which contrasts with the rigorously forward motion of trichomonads. Videomicroscopy images to aid in the differentiation of trichomonads from Giardia spp are available online (JodyGookin. com). It is important to remember that trichomonads do not form cysts. If difﬁculty is encountered in distinguishing trichomonads from Giardia spp, we recommend performing a Giardia ELISA on the feces, as T. foetus does not test positive with this assay. However, coinfection of cats with Giardia spp and T. foetus is common.4

Fecal Culture Fecal culture for T. foetus is also relatively inexpensive; however, it has greater sensitivity than direct fecal smear for detection of infection. Cultures can be performed using a commercial culture test kit (InPouch TF-Feline, Biomed Diagnostics, White City, OR). The culture pouches are made of clear plastic and contain a proprietary medium as well as antibiotics that suppress unwanted bacterial growth. The pouch is inoculated with a fecal sample the size of a grain of rice and is then incubated (FIGURE 5). If too much feces is inoculated into the pouch, fecal bacteria will overgrow and the test will be nondiagnostic. The pouch can be incubated at either 98.6°F (37°C)

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FREE CE Tritrichomonas foetus: A New Agent of Feline Diarrhea

FIGURE 4

isms per 100-mg fecal sample) and speciﬁcity and can detect living and dead organisms.13,14 Several commercial facilities for testing exist. Our laboratory’s guidelines for submission of fecal samples for PCR analysis are that approximately 100 mg of feces (about the size of a lima bean) should be placed into a redtop Vacutainer tube ﬁlled with 3 to 5 mL of 70% isopropyl alcohol (rubbing alcohol) and shipped at room temperature.a

Therapy Historically, antiprotozoal therapies for T. foetus, including metronidazole, were ineffective in eradicating the parasites and often resulted in prolongation of clinical signs.10 Recently, ronidazole, a nitroimidazole similar to metronidazole, was shown to have in A direct fecal smear preparation after application of a coverslip. Note vitro and in vivo activity against T. foetus.15,16 that very little feces is used to prepare the smear. If smears are prepared with too much feces, motility of the organisms is impaired, making them more difficult to Ronidazole is not approved by the US Food identify under the microscope. and Drug Administration for use in companion animals and is currently banned for use in or room temperature. At 98.6°F, trichomonads food animals because of potential human hazQuickNotes multiply quickly, and many organisms can be ards. Accordingly, due diligence is required to Cats with large observed by light microscopy within 72 hours. protect people from exposure to ronidazole If the pouch is incubated at room temperature, (such as wearing gloves when handling the bowel diarrhea, fewer trichomonads will be present, and it medication), and veterinarians are advised to especially those in may take as many as 12 days after inoculation prescribe the drug only in cases of confirmed high-density poputo obtain results.12 Motile trichomonads can be T. foetus infection after obtaining the owner’s lations, should be observed in the pouch by placing the intact informed consent. tested for T. foetus pouch on the stage of a light microscope. The Recent studies investigating the pharmainfection using fecal examiner need not have expertise in organ- cokinetics of ronidazole in cats suggest that smears, agentism identification because the pouch test does 30 mg/kg PO q24h for 14 days is likely to be specific culture not support the growth of similar-appearing most effective in resolving diarrhea and eradimedia, or polyorganisms such as Giardia spp. The fecal sam- cating T. foetus infection in cats.17 There is no ple must contain live organisms to obtain posi- evidence that higher doses of ronidazole or merase chain tive results from fecal culture, and optimum administration for a longer period of time is reaction testing. growth conditions for the organisms must be more effective. The drug is rapidly and commaintained during the test period. Therefore, pletely absorbed by the gastrointestinal tract care must be used in handling the specimen and has a long elimination half-life. These and the pouch to avoid a false-negative result. properties appear to predispose some cats to We strongly recommend that these cultures neurotoxicosis while receiving the drug.16,18 be performed in the clinic rather than by Signs of ronidazole neurotoxicosis include an external diagnostic laboratory so that the lethargy, inappetence, ataxia, and seizures.18 trichomonads do not die during shipment of If the drug is withdrawn immediately, these generally resolve, but they may continue to the pouch. worsen for the next few days before slowly Polymerase Chain Reaction Testing subsiding and may require costly and intensive Trace amounts of T. foetus DNA in the feces emergency veterinary care.18 Accordingly, cats can be identified using a commercial PCR a Submission forms and instructions for submitting assay. Although this test is the most expensive fecal samples to the North Carolina State University option for T. foetus detection, it provides supe- College of Veterinary Medicine for T. foetus PCR testrior sensitivity (as few as 10 T. foetus organ- ing are available at JodyGookin.com.

378

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FREE CE Tritrichomonas foetus: A New Agent of Feline Diarrhea

BOX 3

FIGURE 5

Tips for Avoiding Ronidazole Toxicosis

The InPouch TF culture system for the diagnosis of feline T. foetus infection.

QuickNotes The polymerase chain reaction assay is the most sensitive test for diagnosis of T. foetus infection in cats.

380

must be monitored A. A pouch with sample. closely while receiving ronidazole. Signs of neurotoxicosis may be easier to observe if the treated cat is engaged each day in a playful activity (e.g., chasing a laser pointer) that requires coordination and agility. If signs of toxicosis are observed, owners should be advised to resist the temptation to continue or complete treatment with ronidazole. Continuing treatment after signs of toxicosis are observed could result in life-threatening complications. BOX 3 gives some tips for avoiding ronidazole toxicosis. If treatment must be discontinued because of neurotoxicosis, we recommend that the cat be retested for T. foetus infection. Many of these cats have received sufficient ronidazole to have cleared the infection. Most cats with T. foetus infection show significant improvement to resolution of diarrhea during the course of ronidazole treatment. T. foetus can cause considerable inflammation in the colon, and it often takes several weeks for diarrhea to completely resolve after the organisms are eradicated. If diarrhea persists for more than 14 days after treatment, the cat should be retested for T. foetus. If test results are negative for T. foetus, veterinarians should consider other causes of diarrhea, such as concurrent infection or dietary intolerance. Reasons for failure of ronidazole to eradicate T. foetus infection include insufficient dose or duration of therapy, administration of impotent formulations of the drug (e.g., 10% powder formulation for pigeons), failure of the cat to consume the drug (e.g., spat out liq-

B. After placement of a plastic “clip” across the pouch, the contents may be viewed using a light microscope. A video of how to use the pouch for cultivation of T. foetus from feline feces may be viewed at JodyGookin.com.

Calculate the dose based on a current, accurate body weight. Do not exceed 30 mg/kg PO q24h for 14 days. Monitor cats closely. Stop treatment if clinical signs of lethargy, inappetence, or neurologic disease are observed. Do not reinstitute or repeat treatment with ronidazole if signs of toxicosis have occurred.

uid), or reinfection with T. foetus from another cat in the household that may or may not be showing clinical signs of infection. It is a common misconception in multiple-cat settings that only cats with diarrhea are infected with T. foetus. In these situations, cats undergoing treatment should be isolated from all other cats during and after treatment, and the other cats in the household/cattery should also be tested for T. foetus. Other therapies for the treatment of T. foetus infection in cats are limited. Many approaches to control diarrhea have been tried without success, including changes in diet, use of different antibiotics, and supplementation with nutraceuticals and probiotics. However, there have been no controlled studies of any of these therapies. It has been suggested that frequent changes in diet and indiscriminate use of antibiotics prolong the time it takes for cats to resolve the diarrhea on their own. Veterinarians should be cautious to embrace the success of other antimicrobial drugs for treatment of T. foetus infection because many drugs merely suppress detection of the organisms rather than eradicate them. If the owners elect not to treat for T. foetus infection, the diarrhea will eventually spontaneously resolve in most cats (88%); however, this can take as long as 2 years.10 Unfortunately, 55% of these cats remain positive for T. foetus infection on PCR testing and therefore may be sources of infection for other cats.10 Owners of single cats may ﬁnd this outcome satisfactory

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Tritrichomonas foetus: A New Agent of Feline Diarrhea CE if the cat remains healthy in other respects. However, in a cattery environment, asymptomatic carriers may perpetuate the infection. The potential health consequences of prolonged asymptomatic infection with T. foetus are unknown.

Conclusion T. foetus is a frequently encountered pathogen that results in chronic waxing and waning large bowel diarrhea. Despite the high prevalence of this parasite in susceptible populations

such as catteries and shelters, testing is still not routine in most veterinary clinics. Speciﬁc tests for T. foetus infection are readily available and include direct fecal smear, culture of the feces in InPouch TF media, and detection of T. foetus in DNA extracted from feces using PCR testing. Ronidazole has effectively treated the infection, although adverse effects such as neurotoxicosis remain problematic in some cases. Untreated cats have spontaneous resolution of diarrhea over time but may remain persistently infected. REFERENCES ON PAGE 390

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. Which statement regarding feline trichomoniasis is true? a. All infected cats have large bowel diarrhea as a common clinical sign. b. Only young, purebred cats are at risk for infection. c. Cats should self-resolve infection and never require treatment. d. Asymptomatic cats may still represent a source of infection for other cats. 2. ________ is/are an effective treatment for cats infected with T. foetus. a. Ronidazole b. Metronidazole c. Tinidazole d. Probiotics 3. False-negative PCR results for T. foetus can occur if a. old, dried out, nondiarrheic, or littercontaminated feces are used for testing. b. the cat is currently receiving or has recently (within past 7 days) received antibiotics. c. an insufﬁcient quantity of sample is submitted. d. all of the above 4. Which is a possible explanation if a cat tests positive for T. foetus after ronidazole treatment? a. The cat was given ronidazole at <30 mg/kg PO q24h for 14 days.

5. Ronidazole can cause ________ even at appropriate doses. a. neurotoxicosis (e.g., ataxia, seizures, death) b. immune-mediated hemolytic anemia c. myasthenia gravis d. all of the above

8. The index of suspicion for T. foetus infection should be high if a. a young shelter cat has waxing and waning, malodorous, large bowel diarrhea. b. trophozoites are observed in a fecal sample, but the infection fails to respond to appropriate doses of metronidazole. c. a young cat has large bowel diarrhea but retains a normal appetite and body condition. d. all of the above

6. The most sensitive test for diagnosing feline trichomoniasis is a. PCR. b. fecal culture. c. fecal smear. d. fecal ﬂotation.

9. ________ can be used to diagnose feline trichomoniasis. a. Negative Giardia ELISA results b. A fecal ﬂoat c. A direct fecal smear (wet mount) d. A Baermann test

7. The risk of neurotoxicosis associated with ronidazole therapy can be minimized by a. exceeding the recommended dose of 30 mg/kg q24h only in severe cases of infection. b. reducing the dose if signs of neurotoxicosis are observed. c. delaying ronidazole therapy for 7 days if neurotoxicosis develops. d. calculating the dose based on a current, accurate body weight.

10. Which statement regarding testing for feline trichomoniasis is true? a. The T. foetus PCR test can detect living and dead organisms. b. Nondiarrheic stool samples are preferred for testing. c. T. foetus fecal culture detects living and dead organisms. d. The Giardia ELISA cross-reacts with T. foetus.

b. The cat was reinfected by another cat in the household. c. An impotent ronidazole formulation was prescribed. d. all of the above

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CE Article 2

Canine Primary Hyperparathyroidism ❯❯ Carmenn Schaefer, DVM, DACVIM

❯❯ Richard E. Goldstein, DVM, DACVIM, DECVIM-CA Cornell University

At a Glance Hypercalcemia and Hyperparathyroidism Page 382

Pathology Page 383

Differential Diagnosis of Hypercalcemia Page 383

Signalment Page 384

Clinical Signs Page 384

Physical Examination Page 385

Diagnosis Page 385

Treatment Page 386

Prognosis Page 389

382

Abstract: Canine primary hyperparathyroidism (PHPT) is an endocrine disorder that results in hypercalcemia secondary to autonomous production of parathyroid hormone. Associated biochemical abnormalities also include hypophosphatemia and hyperphosphaturia. Clinical signs of PHPT are related to the effects of hypercalcemia on the renal, neuromuscular, and gastrointestinal systems. The diagnosis of PHPT relies on careful interpretation of laboratory data and imaging studies. Several modalities are available to treat PHPT, but the most important aspect of therapy is the postprocedure management of potential hypocalcemia.

In secondary disorders, serum calcium concentrations can range from low to increased, depending on the cause. In contrast, PHPT is always associated with hypercalcemia.2,4 The autonomously secreted PTH in PHPT is not suppressible by the increased calcium concentration. Severe hypercalcemia arises from accelerated bone resorption. PTH and PTH-related peptide (PTHrp), common in hypercalcemia of malignancy, also directly inhibit renal calcium excretion. Thus, increased renal calcium loss—which combats severe hypercalcemia not mediated by PTH or PTHrp—does not occur in cases of PTH- or PTHrp-mediated hypercalcemia, eliminating the ﬁrst line of Hypercalcemia and defense. Furthermore, the hypercalcemic Hyperparathyroidism state interferes with renal mechanisms Hypercalcemia develops when the inﬂux for resorption of sodium and water due of calcium into the extracellular space to an acquired inability to respond to overwhelms the mechanisms respon- antidiuretic hormone.2 Hypercalcemia in sible for maintaining normocalcemia.1 PHPT is also enhanced by increased proHypercalcemia in dogs is most often duction of vitamin D and the decreased caused by malignancy, followed by PHPT, amount of phosphorus that is available hypoadrenocorticism, and chronic kidney to form complexes with ionized calcium. disease.2,3 Other possible causes, such as All of these interactions result in the biovitamin D toxicosis and granulomatous chemical abnormalities classic for PHPT: disease, have a lower overall prevalence3 hypercalcemia, hypophosphatemia, and (TABLE 1). hyperphosphaturia.2,4–6 anine primary hyperparathyroidism (PHPT) is characterized by abnormal parathyroid “chief” cells that function autonomously due to a parathyroid adenoma, a carcinoma, or adenomatous hyperplasia of one or more parathyroid glands. Other forms of hyperparathyroidism are usually due to nonendocrine disturbances in calcium and phosphorous homeostasis that indirectly affect the parathyroid glands, leading to diffuse hyperplasia. In these cases (renal or nutritional secondary hyperparathyroidism), the secretion of parathyroid hormone (PTH) is not autonomous but rather a secondary manifestation of disease.

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Canine Primary Hyperparathyroidism CE Pathology individual pathologists’ readings as well as Autonomously secreting parathyroid glands are the lack of a large, single data set of dogs. classiﬁed into three histopathologic categories: In a data set collected for dogs that undercarcinoma, adenoma (typically a solitary mass; went surgery, 87% had a solitary adenoma, FIGURE 1), and parathyroid hyperplasia (which 8% had hyperplasia, and 5% had carcinoma.2 commonly involves the simultaneous enlarge- Another study found a higher incidence of ment of more than one parathyroid gland). hyperplasia (approximately 20%).7 Despite The exact percentage of each histopatho- the presence of multiple criteria of maliglogic diagnosis in canine PHPT is unknown. nancy in cases of parathyroid carcinoma, to This may be partially due to the subjectivity our knowledge, distal metastases have not involved in diagnosis and differences among been reported in dogs.

TABLE 1

Differential Diagnosis of Hypercalcemia1,2,5,7,9

Cause Hypercalcemia of malignancy (lymphoma, carcinoma, multiple myeloma, melanoma)

Comment Mediated by PTHrp, which is released by tumor tissue PTHrp increases osteoblastic bone resorption and renal tubular calcium resorption ↑ total Ca, ↑ i Ca, low-normal to ↓ PTH, normal to ↓ P

Hypoadrenocorticism

Multifactorial pathogenesis Hyperproteinemia from dehydration and hemoconcentration Increased plasma protein–binding afﬁnity for calcium Increased concentration of calcium citrate complexes Increased renal tubular resorption of calcium ↑ total Ca, i Ca in reference range

Primary hyperparathyroidism

Autonomous secretion of PTH from parathyroid chief cells ↑ total Ca, ↑ i Ca, normal to ↑ PTH, normal to ↓ P

Chronic kidney disease

Complex pathogenesis Impedance of excretion of PTH and its metabolites Decreased renal excretion of calcium due to reduction in GFR Increased concentration of PTH due to excessive secretion and reduced renal tubular hormone degradation Renal failure or PTH-induced increased concentration of organic cations and complexed calcium Exaggerated response to vitamin D with increased intestinal absorption of calcium ↓, normal, or ↑ total Ca; normal to ↓ i Ca; normal to ↑ PTH; ↑ P

Vitamin D toxicosis (cholecalciferol rodenticides, human psoriasis medications [calcipotriol, calcipotriene], overzealous dietary supplementation, plants [Cestrum diurnum, Solanum malacoxylon, Trisetum ﬂavescens])

↑ total Ca, ↑ i Ca, normal to ↑ P, normal to ↓ PTH

Hemoconcentration (spurious)

Mild hypercalcemia Fluid volume contraction and secondary hyperproteinemia Resolves with ﬂuid therapy

Granulomatous disease

Due to alteration of endogenous vitamin D metabolism Activated macrophages can develop ability to convert 25-hydroxyvitamin D to calcitriol in an unregulated manner ↑ total Ca, ↑ i Ca, low-normal to ↓ PTH, normal to ↑ P

PTHrp = parathyroid hormone–related peptide; Ca = calcium; iCa = ionized calcium; PTH = parathyroid hormone; P = phosphorus; GFR = glomerular ﬁltration rate.

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FIGURE 1 Histopathologic sections of parathyroid masses from two dogs with primary hyperparathyroidism (PHPT).

500 μm

Parathyroid adenoma; note the expansive but noninﬁltrative nature. The darker cells represent the remnant of the normal parathyroid gland tissue. (Hematoxylin–eosin stain; magnification: 40×)

Parathyroid carcinoma; note the capsular invasion and marked cellular atypia. (Hematoxylin–eosin stain; magnification: 100×)

Signalment Age and Gender

QuickNotes In many cases of canine primary hyperparathyroidism, clinical signs attributable solely to hypercalcemia are mild or absent.

PHPT is usually diagnosed in older dogs (mean age: 11.2 years; range: 6 to 17 years).1,2,6 There is no apparent sex predisposition. In a retrospective study of 210 dogs, 54% were male and 46% were female.8

Breed and Heredity There is a single report of a familial form of neonatal hyperparathyroidism in a litter of German shepherd puppies in which an autosomal-recessive mode of inheritance was suspected.2,4 However, a 10-year review of cases3,7 revealed that keeshonden are most likely to be affected by PHPT, with 214 positive samples and an average American Kennel Club registration of 4375, yielding the highest breedassociated odds ratio (OR) of 50.7. Other breeds with more than 100 positive samples were dachshunds (OR: 2.0) and golden retrievers (OR: 1.6). Keeshonden represented 26% of dogs and approximately 40% of dogs in two other studies, respectively.6,7

Primary Hyperparathyroidism in Keeshonden A recent study7 investigating the inheritance, mode of inheritance, and candidate genes for

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PHPT in keeshonden identiﬁed a heritable, autosomal-dominant form of PHPT in this breed. In keeshonden, the condition is due to a single gene mutation that is transmitted via simple Mendelian genetics with a high degree of penetrance. Genes known to cause human familial isolated hyperparathyroidism have been excluded as the cause of PHPT in dogs.7 A test for a gene that has been found to be highly associated with PHPT in keeshonden is available for owners and breeders.9 Genetic testing of young keeshonden for this disease should facilitate a decrease in the incidence of PHPT in this breed, as well as promote identiﬁcation of older keeshonden with the genetic predisposition so that they can undergo frequent monitoring of calcium concentration.

Clinical Signs In many cases of PHPT, clinical signs attributable solely to hypercalcemia are mild or absent. Most cases are identiﬁed as a result of routine screening tests. In the retrospective study of 210 dogs with PHPT,8 the owners of 42% of the dogs had sought veterinary care for reasons apparently unrelated to hypercalcemia or PHPT. The most common clinical signs of PHPTinduced hypercalcemia involve the renal, neu-

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Canine Primary Hyperparathyroidism CE romuscular, and gastrointestinal systems.2,4,8 of the disease, possibly because many of the Polyuria, polydipsia, and urinary incontinence dogs in this study were diagnosed via routine are the most common clinical signs.2,4,5,8 These screening before developing obvious clinical signs develop because of an impaired renal signs of hypercalcemia. tubular response to antidiuretic hormone and Hyperparathyroidism in dogs with hyperadimpaired renal tubular resorption of sodium renocorticism is also under investigation. A and chloride. This results in a significant recent study11 revealed a high prevalence of increase in urine volume. Compensatory poly- increased PTH levels in dogs with hyperadredipsia develops to maintain a normovolemic nocorticism. The mechanism for increased PTH state.2,4 Lower urinary tract signs of pollaki- in these animals is not known. In these dogs, uria, stranguria, and hematuria are also com- PTH and phosphorus values were increased, mon. As many as 32% of dogs with PHPT but calcium concentrations were unaffected.11 have urolithiasis, and 24% have urinary tract infections.2,8 Clinical signs related to the neu- Physical Examination romuscular system (e.g., listlessness, depres- Dogs with PHPT often have unremarkable sion, decreased activity) are thought to be due physical findings. The most commonly associto the effects of calcium on the central and ated abnormalities are usually caused by the peripheral nervous tissue, suppressing the presence of uroliths.2,4,8,12 Other, more subtle excitability of central and peripheral nerves physical findings may include thin body conby decreasing cell membrane permeability. dition, generalized muscle atrophy, and variShivering, muscle twitching, and seizure activ- able degrees of weakness. Bone deformities ity have also been observed, but the under- involving the mandible and maxilla and long lying mechanisms for these problems are not bone fractures are uncommon.2,4 well understood.2,4 Gastrointestinal signs such as vomiting and constipation are thought to be Diagnosis due to a hypercalcemia-induced decrease in A complete database, including physical examexcitability of gastrointestinal smooth muscle. ination, complete blood cell count, serum Inappetence may also be due to direct calce- chemistry profile with ionized calcium, and mic effects on the CNS. The less common clin- PTH and PTHrp assays, is indicated when ical signs of fractures, lameness, and stiff gait PHPT is suspected. The diagnosis is estabmay be due to excessive osteoclastic resorp- lished based on ionized hypercalcemia, a low tion of bone induced by chronic hyperpara- or low-normal serum phosphorus level, an thyroidism leading to replacement of bone inappropriately high PTH level, and exclusion matrix with fibrous tissue, as well as thinning of other causes of hypercalcemia (TABLE 1). and weakening of cortical bone. Metastatic The key to diagnosing PHPT using PTH assay calcification of tendons and joint capsules may results is the recognition of an inappropriate PTH concentration in the presence of hyperalso contribute to stiffness and lameness.2,4 PHPT-associated renal failure is relatively calcemia. If the serum ionized calcium concenuncommon in North American dogs. The tration is increased, the PTH level should be retrospective study of 210 dogs revealed that very low.2,4,8 Therefore, a serum PTH value that increases in serum calcium and PTH concen- falls in the reported reference range should not trations were rarely associated with renal fail- be considered normal in a dog with hypercalure.8 In contrast, a British case series of 29 cemia.6 In the retrospective study,8 73% of the dogs with PHPT concluded that renal failure dogs with PHPT had serum PTH levels within was more likely in dogs with a high total cal- the reference range at the time of diagnosis. cium level, with at least seven of the 29 dogs Several commercial veterinary laboratories acdeveloping renal failure.10 It is difficult to say cept plasma (in EDTA) or serum for PTH why these two studies differed so markedly measurement; PTHrp measurement requires regarding the prevalence of kidney disease plasma exclusively. The samples for PTH or in dogs with PHPT. In addition to the much PTHrp should be centrifuged and the plasma smaller sample size of the British study, it is or serum separated from the cells and stored also possible that the dogs in the US study and shipped frozen to the laboratory. A human were identified and treated at an earlier stage two-site (“sandwich”) assay, which includes

QuickNotes Diagnosis of primary hyperparathyroidism based on parathyroid hormone (PTH) assay results relies on the recognition of inappropriate PTH levels in the presence of hypercalcemia.

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FIGURE 2

Longitudinal ultrasonographic view of the cervical region of a dog with PHPT. Note the oblong-shaped thyroid gland with a round, hypoechoic parathyroid nodule in its center.

QuickNotes Successful treatment of primary hyperparathyroidism depends on appropriate procedure selection and postoperative care and monitoring.

the binding of antibodies to two separate sites on the PTH molecule, can be used successfully to measure canine PTH.2 Once the clinical pathologic diagnosis of PHPT is established, many centers perform cervical ultrasonography. Although this modality requires somewhat specialized ultrasonographic equipment and expertise, the parathyroid glands are now routinely visualized with ultrasonography in dogs.2,4 Experienced veterinary radiologists can successfully identify 90% to 95% of parathyroid adenomas.4 Most adenomas are 4 to 9 mm in diameter and are fairly easy to visualize (FIGURE 2).4 However, not all parathyroid nodules are obvious, and the subjectivity of ultrasonography as a diagnostic tool must be taken into account. In humans, radionuclide scanning with technetium-99m sestamibi has been used to localize parathyroid adenomas. To date, parathyroid scintigraphy in dogs has lacked sufﬁcient sensitivity and speciﬁcity to be recommended as a diagnostic tool.4,13 Selective venous sampling for serum PTH from the jugular veins to localize functioning parathyroid masses has also not been shown to be useful in identifying the side of the affected gland.4,14

Treatment Management of Hypercalcemia Identifying and treating the underlying cause

386

takes priority over management of hypercalcemia. However, given the deleterious effects of hypercalcemia on renal function (impaired renal tubular concentrating ability, reduced renal flow, decreased glomerular filtration rate), interim treatment to reduce the serum calcium level may be indicated.5 Animals with azotemia or an increase in calcium–phosphorus product (calcium × phosphorus >70) are more likely to warrant therapy. The severity of hypercalcemia alone is not considered sufficient reason for immediate therapy.5 In dogs with PHPT, hypercalcemia is not typically viewed as an acute problem, and these animals rarely have a calcium–phosphorus product greater than 60 to 80 because of concurrent hypophosphatemia.4 If immediate treatment for hypercalcemia is deemed necessary (chronic kidney disease, vitamin D toxicosis, clinical signs of hypercalcemia), fluid therapy is the ideal initial method for lowering serum calcium and preserving renal perfusion.5 Saline diuresis (0.9% saline) at a rate of 120 to 180 mL/kg/day can promote calcium excretion. This therapy is often combined with the loop diuretic furosemide (given IV q8h or as a constant-rate infusion) to potentiate calciuresis. Supplementation with potassium chloride may be necessary to prevent the development of hypokalemia. If this treatment does not decrease the serum calcium concentration sufficiently, additional medications may be needed. Glucocorticoids have been shown to effectively decrease serum calcium concentrations by increasing calciuresis, reducing intestinal absorption of calcium, and inhibiting calcium resorption from bone. Glucocorticoids are most effective for hypercalcemia of malignancy (lymphoma). It is crucial to withhold glucocorticoid treatment until neoplasia has been ruled out so as not to interfere with diagnosis. Hypercalcemia refractory to these therapies may respond to bisphosphonates (pamidronate, clodronate), plicamycin (mithramycin), or calcitonin therapy.5 These medications are costly and may have severe adverse effects as well as benefit; therefore, they are not typically used to treat canine PHPT. Bisphosphonates act primarily by inhibiting osteoclast activity and bone resorption. Their use in veterinary medicine has increased in recent years, especially in cases of hypercalcemia of malignancy.

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Canine Primary Hyperparathyroidism CE FIGURE 3 Images taken at the time of parathyroidectomy in a dog with PHPT.

Note the enlarged, darkened parathyroid mass.

In a review of seven hypercalcemic dogs (four with neoplasia, none with PHPT), the bisphosphonate pamidronate disodium was shown to be safe and relatively efﬁcacious when given as a single infusion of 1.05 to 1.7 mg/kg.15 Calcitonin decreases osteoclast activity as well as formation of new osteoclasts. It has been used in dogs, especially in cases of vitamin D toxicosis (5 U/kg IM or SC q8h), although large studies regarding its efﬁcacy and safety are lacking.2

Treatment of PHPT Three treatment modalities are available for PHPT in dogs: surgery, percutaneous ultrasonography-guided ethanol ablation (with 96% ethanol), and percutaneous ultrasonographyguided radiofrequency heat ablation.2,4,5 If surgical treatment is sought, complete cervical exploratory surgery of the thyroid area is recommended. An effort should be made to evaluate both sides of the neck and the ventral and dorsal surfaces of the thyroid glands.5 In most dogs with PHPT, the abnormal parathyroid tissue (adenoma) is a solitary nodule that is darker and larger than normal parathyroid tissue. It is typically easily recognized and removed by an experienced surgeon (FIGURE 3).5 If possible, only the abnormal tissue is removed, but it is sometimes necessary to remove part or all of a thyroid lobe along with abnormal parathyroid tissue. If no abnormal parathyroid tissue is seen at the time of sur-

The typical appearance of a 1-cm parathyroid mass at surgery.

gery and the diagnosis of PHPT is thought to be correct, then one thyroid lobe–parathyroid complex can be removed and submitted for histopathologic analysis. If two or three abnormal parathyroid glands are found, all should be removed. If all four parathyroid glands appear to be abnormal, one gland is often left in situ to maintain calcium homeostasis and prevent permanent hypocalcemia.2,5 The presence of two, three, or four abnormal glands is atypical and suggests hyperplasia rather than an adenoma.5 Ethanol and heat ablation require visualization of a parathyroid nodule using cervical ultrasonography (FIGURE 2).16–19 The nodule must also be large enough (>3 mm) for accurate needle placement.2 Ethanol ablation causes coagulation necrosis and vascular thrombosis in the parenchyma of the exposed tissue.2,16 The injection procedure requires a high-resolution transducer (i.e., frequency of 10 MHz or greater) to visualize the superﬁcial tissues of the neck, and the animal must be under general anesthesia.2,16 Considerable experience with ultrasonography-guided needle placement is necessary because parathyroid nodules are small and close to the carotid artery and vagosympathetic trunk. Complete certainty about needle location is crucial in this procedure. The goal of the procedure is to inject enough ethanol to allow complete diffusion throughout the mass. This procedure is considered to be an effective alternative to surgery.16 Over the past

QuickNotes Surgery, ethanol ablation, and heat ablation can be used to treat primary hyperparathyroidism.

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QuickNotes Short-term treatment of hypocalcemia is required for dogs exhibiting clinical signs or that have severe hypocalcemia without clinical signs.

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7 years, this procedure has been performed on mia.2 Carefully allowing serum calcium levels more than 30 dogs at our institution with a to decline after PHPT therapy enables the success rate of >90%, defined as a decrease in remaining glands to return to function, avoidserum calcium sufficient to achieve a sustained ing unnecessary prolonged calcium and vita(at least 1 year) normocalcemic state. No recur- min D supplementation. rence in a successfully injected gland has been Treatment of hypocalcemia is recommended reported in these cases. Adverse effects asso- if the serum calcium level falls below 8.5 mg/ ciated with the procedure are minimal, but a dL (assuming a lower reference limit of 9 to 10 local reaction to the ethanol involving transient mg/dL), the ionized calcium value falls below internal swelling in the laryngeal region is pos- 0.8 to 0.9 mmol/L (assuming a lower refersible. For this reason, bilateral injections are ence limit of 1.12 mmol/L), or clinical signs not recommended in cases of bilateral para- of hypocalcemia are noted (e.g., facial rubthyroid nodules. Compared with surgical exci- bing, focal seizures, muscle stiffness, twitchsion, ethanol ablation is a faster, less invasive ing).2 Initiating treatment with vitamin D may procedure with a faster recovery time. How- also be indicated if there is concern about ever, it does require advanced ultrasonography the rate of decrease in the calcium concenequipment and expertise, with a success rate tration. Prophylactic vitamin D therapy, given of approximately 90% versus almost 100% for either on the morning of surgery or immedisurgery. Injections should be performed a few ately after recovery from anesthesia, has been months apart in cases of bilateral parathyroid recommended in dogs with a serum calcium concentration chronically greater than 14 mg/ nodules. Radiofrequency heat ablation destroys tis- dL to prevent the development of profound sue by causing thermal necrosis at the nee- hypocalcemia. Due to the known delay in the dle tip. The advantage of heat ablation over onset of action of vitamin D in some cases ethanol is that there is no potential for leak- (severe hypercalcemia exceeding 18 mg/dL), age because the radiofrequency damage is treatment has been initiated 24 to 36 hours restricted to a discrete amount of tissue sur- before surgery.2 Short-term treatment of hypocalcemia is rerounding the uninsulated portion of the needle, and regional vasculature is unaffected.2 Heat quired for dogs exhibiting clinical signs or ablation has been reported to be a safe, effec- that have severe hypocalcemia without clinitive treatment.1,17 However, to our knowledge, cal signs. Calcium gluconate in a 10% solution the heat ablation unit needed to perform this is the calcium salt of choice; it is given at a procedure is only available at the University of recommended dose of 0.5 to 1.5 mL/kg (5 to California, Davis. 15 mg/kg of elemental calcium) IV slowly over 10 to 30 minutes to effect.6 Ultimately, patient Management of Posttreatment response should be the determining factor for the volume administered. During IV adminPotential Hypocalcemia Successful treatment of PHPT must include istration of calcium gluconate, the patient’s appropriate postprocedure care and monitor- heart rate should be monitored (ideally along ing, which are similar regardless of the thera- with electrocardiography) to prevent calciumpeutic modality. It is essential to remember induced cardiotoxicity (bradycardia, sudden that normal parathyroid glands atrophy if their elevation in ST segment, shortening of QT function is suppressed for a prolonged period interval, premature ventricular complexes).6 of time. The surgical removal or ablation of The effect of IV calcium therapy has a limthe autonomous source of PTH results in a ited duration (1 to 12 hours), so oral mainterapid decline in circulating PTH and serum nance therapy must be initiated concurrently. calcium. We recommend hospitalization for 7 Because oral vitamin D and calcium may take to 10 days after treatment, regardless of the 24 to 96 hours to achieve maximum effect, suppresurgical calcium level. Clinically signifi- port with parenteral calcium is needed during cant hypocalcemia typically develops 3 to 7 this period.6 This could include repeated IV days after treatment.16 Additionally, hospital- or subcutaneous calcium gluconate adminisization restricts the dog’s activity, decreasing tration dosed as noted previously every 6 to 8 the risk of clinical tetany due to hypocalce- hours or, ideally, as a constant-rate infusion at

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Canine Primary Hyperparathyroidism CE 60 to 90 mg/kg/day for approximately 24 to 48 of oral calcium can be tapered gradually and hours, followed by weaning while monitoring discontinued over a period of 2 to 4 months.6 As serum calcium levels. Sterile abscess formation the atrophied parathyroid glands regain control and skin sloughing can occur with subcutane- of calcium homeostasis, vitamin D supplemenous calcium therapy, especially when calcium tation and oral calcium supplementation can be tapered gradually.2 The serum calcium level salts other than calcium gluconate are used.2 Maintenance therapy includes oral calcium should be checked before each adjustment in supplementation and vitamin D analogues. The dosing interval. The entire withdrawal process vitamin D compound of choice is 1,25-dihy- generally takes 3 to 6 months, but individual droxycholecalciferol (calcitriol) due to its rapid response to therapy varies considerably.2 onset of action (1 to 4 days for maximal effect) and short biologic half-life (2 to 4 days).6 A Prognosis loading dose of 0.02 to 0.03 μg/kg/day PO The prognosis for dogs with PHPT is exceldivided twice daily for 3 to 4 days is recom- lent with appropriate treatment and monitormended, followed by 0.005 to 0.015 μg/kg/day, ing,2 and successful treatment is considered divided twice daily. Calcium carbonate is the curative in dogs with solitary parathyroid oral calcium supplement of choice because of adenomas. Dogs with parathyroid hyperplaits high percentage of calcium (40%), low cost, sia are likely to experience recurrences in the and wide availability. When used in conjunc- remaining parathyroid glands. tion with vitamin D, the recommended dose of oral elemental calcium is 25 mg/kg q8–12h Conclusion as needed based on the individual patient’s Although it is more prevalent in older dogs, serum calcium levels.6 Normal dietary intake PHPT can be treated successfully with little risk of commercial pet food provides an adequate to the patient, provided the procedure is done calcium level in the presence of vitamin D by an experienced surgeon. Postprocedure metabolite treatment for most patients. calcium supplementation is an essential part Usually, as the vitamin D dose and serum cal- of treatment but is generally required for only cium concentration reach a steady level, the dose a few months.

QuickNotes The prognosis for dogs with PHPT is excellent with early diagnosis and appropriate treatment and monitoring.

References 1. Ralston SH, Coleman R, Fraser WD, et al. Medical management of hypercalcemia. Calcif Tissue Int 2004;74(1):1-11. 2. Feldman EC, Nelson RW. Hypercalcemia and primary hyperparathyroidism. In: Feldman EC, Nelson RW, eds. Canine and Feline Endocrinology and Reproduction. 3rd ed. St. Louis: WB Saunders; 2004:661-713. 3. Refsal KR, Provencher-Bolliger AL, Graham PA, Nachreiner RF. Update on the diagnosis and treatment of disorders of calcium regulation. Vet Clin North Am Small Anim Pract 2001;31(5):1043-1962. 4. Feldman EC. Disorders of the parathyroid glands. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 6th ed. St. Louis: WB Saunders; 2005:1508-1535. 5. Feldman EC, Nelson RW. Hypercalcemia and primary hyperparathyroidism in dogs. In: Bonagura JD, ed. Kirk’s Current Veterinary Therapy XIII. Philadelphia: WB Saunders; 2000:345-348. 6. Henderson AK, Mahony O. Hypoparathyroidism: pathophysiology and diagnosis. Compend Contin Educ Vet 2005;27(4):270-273. 7. Goldstein RE, Atwater DZ, Cazolli DM, et al. Inheritance, mode of inheritance and candidate genes for primary hyperparathyroidism in keeshonden. J Vet Intern Med 2007;21(1):199-203. 8. Feldman EC, Hoar B, Pollard R, Nelson RW. Pretreatment clinical and laboratory ﬁndings in dogs with primary hyperparathyroidism: 210 cases (1987-2004). JAVMA 2005;227(5):756-761. 9. Goldstein RE. Canine primary hyperparathyroidism. Accessed November 2007 at www.vet.cornell.edu/labs/goldstein/. 10. Gear RNA, Neiger R, Skelly BJS, Herrtage ME. Primary hyperparathyroidism in 29 dogs: diagnosis, treatment, outcome and associated renal failure. J Small Anim Pract 2005;46(1):10-16. 11. Ramsey IK, Tebb A, Harris E, et al. Hyperparathyroidism in dogs with hyperadrenocorticism. J Small Anim Pract 2005;46(11): 531-536.

12. DeVries SE, Feldman EC, Nelson RW, Kennedy PC. Primary parathyroid gland hyperplasia in dogs: six cases (1982-1991). JAVMA 2003;202(7):1132-1135. 13. Matwichuk CL, Taylor SM, Wilkinson AA, et al. Use of technetium Tc99m sestamibi for detection of a parathyroid adenoma in a dog with primary hyperparathyroidism. JAVMA 1996;209(10): 1733-1736. 14. Feldman EC, Wisner ER, Nelson RW, et al. Comparison of results of hormonal analysis of samples obtained from selected venous sites versus cervical ultrasonography for localizing parathyroid masses in dogs. JAVMA 1997;211(1):54-56. 15. Hostutler RA, Chew DJ, Jaeger JQ, et al. Uses and effectiveness of pamidronate disodium for treatment of dogs and cats with hypercalcemia. J Vet Intern Med 2005;19(1):29-33. 16. Long CD, Goldstein RE, Hornof WJ, et al. Percutaneous ultrasound-guided chemical parathyroid ablation for treatment of primary hyperparathyroidism in dogs. JAVMA 1999;215(2):217-220. 17. Pollard RE, Long CD, Nelson RW, et al. Percutaneous ultrasonographically guided radiofrequency heat ablation for treatment of primary hyperparathyroidism in dogs. JAVMA 2001;218(7): 1106-1110. 18. Karstrup S, Hegedüs L, Holm H. Acute change in parathyroid function in primary hyperparathyroidism following ultrasonically guided ethanol injection into solitary parathyroid adenomas. Acta Endocrinologica 1993;129(5):377-380. 19. Vergés BL, Cercueil JP, Jacob D, et al. Results of ultrasonically guided percutaneous ethanol injection into parathyroid adenomas in primary hyperparathyroidism. Acta Endocrinologica 1993;129(5):381-387.

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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. Which of the following serum values is not consistent with a diagnosis of PHPT? a. increased ionized calcium b. increased phosphorus c. increased total calcium d. normal to increased PTH 2. Which statement is true? a. Hyperadrenocorticism commonly causes marked hypercalcemia. b. Hypercalcemia of malignancy is uncommon in dogs. c. PHPT is a very likely diagnosis in an older, hypercalcemic keeshond. d. Vitamin D toxicosis commonly causes markedly increased serum calcium and markedly decreased serum phosphorus concentrations in dogs. 3. Which statement is true regarding PTH? a. PTH secretion causes an increase in serum calcium. b. PTH is secreted from the thyroid gland. c. PTH is not usually increased in renal secondary hyperparathyroidism. d. PTH is always increased out of the reference range in canine PHPT. 4. Which of the following can cause PHPT? a. solitary adenoma

b. adenoma of multiple glands c. adenomatous hyperplasia of one or more glands d. all of the above 5. Which statement is true regarding hypercalcemia of malignancy and PHPT? a. Both conditions can be associated with marked hypercalcemia. b. Accelerated bone resorption and decreased renal excretion of calcium contribute to the hypercalcemia seen in these conditions. c. PTH secretion is not suppressed by hypercalcemia in a normal fashion in dogs with PHPT. d. all of the above 6. Which mode of inheritance has been identiﬁed in PHPT in keeshonden? a. autosomal recessive b. autosomal dominant c. X-linked recessive d. mitochondrial 7. Treatment modalities for PHPT include a. surgery. b. percutaneous ultrasonography-guided ethanol ablation. c. percutaneous ultrasonography-guided radiofrequency heat ablation. d. all of the above

8. Immediate therapy for hypercalcemia is warranted in the presence of a. azotemia. b. a calcium–phosphorus product >70. c. a calcium–phosphorus product <70. d. a and b 9. Immediate therapy for hypercalcemia may include a. saline diuresis (0.9% saline). b. furosemide. c. glucocorticoids. d. all of the above 10. Which statement regarding posttreatment management of dogs with PHPT is true? a. Almost all dogs require posttreatment calcium supplementation. b. The typical time frame for the development of clinically signiﬁcant hypocalcemia is 3 to 7 days posttreatment. c. Preemptive treatment with calcium supplementation is recommended in all cases. d. If the serum calcium concentration before surgery or ablation chronically exceeds 15 mg/dL, the incidence of posttreatment hypocalcemia is decreased.

CONTINUED FROM PAGE 381

References 1. Gookin JL, Breitschwerdt EB, Levy MG, et al. Diarrhea associated with trichomonosis in cats. JAVMA 1999;215:1450-1454. 2. Gookin JL, Levy MG, Law JM, et al. Experimental infection of cats with Tritrichomonas foetus. Am J Vet Res 2001;62:1690-1697. 3. Levy MG, Gookin JL, Poore M, et al. Tritrichomonas foetus and not Pentatrichomonas hominis is the etiologic agent of feline trichomonal diarrhea. J Parasitol 2003;89:99-104. 4. Gookin JL, Stebbins ME, Hunt E, et al. Prevalence of and risk factors for feline Tritrichomonas foetus and Giardia infection. J Clin Microbiol 2004;42:2707-2710. 5. Gunn-Moore DA, McCann TM, Reed N, et al. Prevalence of Tritrichomonas foetus infection in cats with diarrhoea in the UK. J Feline Med Surg 2007;9:214-218. 6. Steiner JM, Xenoulis PG, Read SA, et al. Identiﬁcation of Tritrichomonas foetus DNA in feces from cats with diarrhea from Germany and Australia. J Vet Intern Med 2007;21:649. 7. Bissett SA, Gowan RA, O’Brien CR, et al. Feline diarrhoea associated with Tritrichomonas cf. foetus and Giardia co-infection in an Australian cattery. Aust Vet J 2008;86:440-443. 8. Foster DM, Gookin JL, Poore MF, et al. Outcome of cats with diarrhea and Tritrichomonas foetus infection. JAVMA 2004;225: 888-892. 9. Holliday M, Deni D, Moore D. Tritrichomonas foetus infection in cats with diarrhoea in a rescue colony in Italy. J Feline Med Surg 2009;11(2):131-134. 10. Gray SG, Hunter S, Stone M, et al. Assessment of reproductive

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tract disease in cats at risk for enteric Tritrichomonas foetus infection. Am J Vet Res 2009. In press. 11. Gookin JL, Foster DM, Poore MF, et al. Use of a commercially available culture system for diagnosis of Tritrichomonas foetus infection in cats. JAVMA 2003;222:1376-1379. 12. Gookin JL, Birkenheuer AJ, Breitschwerdt EB, et al. Single-tube nested PCR for detection of Tritrichomonas foetus in feline feces. J Clin Microbiol 2002;40:4126-4130. 13. Stauffer SH, Birkenheuer AJ, Levy MG, et al. Evaluation of four DNA extraction methods for the detection of Tritrichomonas foetus in feline stool specimens by polymerase chain reaction. J Vet Diagn Invest 2008;20:639-641. 14. Kather EJ, Marks SL, Kass PH. Determination of the in vitro susceptibility of feline Tritrichomonas foetus to 5 antimicrobial agents. J Vet Intern Med 2007;21:966-970. 15. Gookin JL, Copple CN, Papich MG, et al. Efﬁcacy of ronidazole for treatment of feline Tritrichomonas foetus infection. J Vet Intern Med 2006;20:536-543. 16. LeVine DN, Papich MG, Gookin JL, et al. Ronidazole pharmacokinetics in cats after IV administration and oral administration of an immediate release capsule and a colon-targeted extended release tablet. J Vet Intern Med 2008;22:745. 17. Rosado TW, Specht A, Marks SL. Neurotoxicosis in 4 cats receiving ronidazole. J Vet Intern Med 2007;21:328-331. 18. Stockdale HD, Givens MD, Dykstra CC, et al. Tritrichomonas foetus infections in surveyed pet cats. Vet Parasitol 2009;160:13-17.

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Antianxiety Tablets Anxitane is a chewable L-theanine tablet that helps relieve anxiety in canine and feline patients. L-Theanine is shown to increase concentrations of GABA, an inhibitory neurotransmitter, and increase brain serotonin and dopamine. An effective alternative to pharmaceuticals, Anxitane can be used long term and has been shown to be palatable to dogs and cats. Virbac Animal Health | 800-338-3659 | www.virbac.com

Feline Hyperthyroidism Treatment For the ﬁrst time, methimazole, the most widely used drug for the treatment of feline hyperthyroidism, is available in a tablet approved by the FDA for veterinary use. Felimazole tablets come in 2.5- and 5.0-mg sizes and are coated for easy administration. Dechra Veterinary Products | 913-327-0015 | www.dechra-us.com

Lyme Vaccine Intervet/Schering-Plough Animal Health has introduced Nobivac Lyme, a vaccine that induces the production of highly speciﬁc antibodies that kill Borrelia burgdorferi (the causative agent of Lyme disease) by binding to outer surface proteins (Osp) A and C. Nobivac Lyme is administered by giving two doses subcutaneously, 2 to 4 weeks apart, with an annual booster thereafter. Intervet/Schering-Plough Animal Health 908-298-4000 | www.intervetusa.com

Trimmer The Pet Detailer corded trimmer was created by Wahl to provide the power of a clipper in the size of a trimmer. It is 5 inches long, weighs 6.7 ounces, and is powered by a rotary motor. The trimmer runs at 5700 strokes per minute, and the precision-ground #30 blade stays sharp longer and has a corrosion-inhibiting ﬁnish to prevent rust. The Pet Detailer has durable plastic and chrome housings and offers six snap-on attachment guide combos. Wahl Clipper Corporation | 800-767-9245 | www.wahl.com

Canine Influenza Vaccine Intervet/Schering Plough Animal Health has been granted a conditional product license by the USDA for the first vaccine against canine influenza virus. The vaccine is made from inactivated virus and has been demonstrated to reduce the incidence and severity of lung lesions as well as the duration of coughing and viral shedding. It may be given to dogs 6 weeks of age or older and can be given annually as a component of existing respiratory disease vaccine protocols to ensure more comprehensive protection. Intervet/Schering-Plough Animal Health 908-298-4000 | www.intervetusa.com

Dental Radiology System With the EVA Vet Plus, AFP Imaging has upgraded the capabilities of its EVA Vet veterinary digital dental radiology system. EVA is a ﬁlmless system that produces high-resolution, diagnostic-quality images. EVA Vet Plus has been enhanced with a stronger, more robust sensor capsule, rounded corners for better positioning, and DICOM upgrade capability. AFP Imaging | 800-592-6666 | www.afpimaging.com

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

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391

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392

Company

Product

Page

American College of Veterinary Surgeons

2009 Symposium

351

Banﬁeld, the Pet Hospital

We Believe in Vets

Inside back cover

Heska Corporation

Dri-CHEM 7000

363, 365, 367

Hill’s Pet Nutrition

Prescription Diet r/d Canine

Inside front cover (Canada only)

Intervet/Schering-Plough Animal Health

Mometamax

369, 370

Nestlé Purina PetCare

Case in Brief: FortiFlora

359

Northgate Veterinary Supply

Glass cage doors and rod gates

392

Sound-Eklin

Veterinary Imaging

Back cover

VCA Antech

Hospital Purchase Program

Inside front cover (US only)

Veterinary Emergency and Critical Care Society

IVECCS 2009 Symposium

349 (US only)

Veterinary Learning Systems

Veterinary Technician

379

Vetstreet

Pet Portals

354, 355

Western Veterinary Conference

2010 Conference

377

WhereTechsConnect.com

Job Marketplace

392

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

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