Compendium | November 2009 by davidpsu

VOLUME 31 NUMBER 11 NOVEMBER 2009

Compendium CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

6 CE Contact Hours

Vol 31(11) November 2009

CONTI N U I NG EDUCATION FOR VETERI NARIANS ®

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November 2009 Vol 31(11) CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

EXECUTIVE EDITOR Tracey L. Giannouris, MA 800-426-9119, ext 52447 | tgiannouris@vetlearn.com

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

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Published monthly by Veterinary Learning Systems, a division of MediMedia, 780 Township Line Road, Yardley, PA 19067. Copyright © 2009 Veterinary Learning Systems. All rights reserved. Printed in the USA. No part of this issue may be reproduced in any form by any means without prior written permission of the publisher. Printed on acid-free paper, effective with volume 29, issue 5, 2007. Periodicals postage paid at Morrisville, PA, and at additional mailing offices. Postmaster: Send address changes to Compendium: Continuing Education for Veterinarians®, 780 Township Line Road, Yardley, PA 19067. Canada Post international publications mail product (Canadian distribution) sales agreement no. 40014103. Return undeliverable Canadian addresses to MediMedia, PO Box 7224, Windsor, ON N9A 0B1. Printed in USA.

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November 2009 Vol 31(11) 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

EXECUTIVE ADVISORY BOARD MEMBERS

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

Behavior Sharon L. Crowell-Davis, DVM, PhD, DACVB The University of Georgia

Epidemiology Philip H. Kass, DVM, MPVM, MS, PhD, DACVPM University of California, Davis

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

Exotics Avian Thomas N. Tully, Jr, DVM, MS, DABVP (Avian), ECAMS Louisiana State University

Wayne S. Rosenkrantz, DVM, DACVD Animal Dermatology Clinic Tustin, California Feline Medicine Margie Scherk, DVM, DABVP (Feline Medicine) Cats Only Veterinary Clinic Vancouver, British Columbia Nutrition Kathryn E. Michel, DVM, MS, DACVN University of Pennsylvania Surgery Elizabeth M. Hardie, DVM, PhD, DACVS North Carolina State University

490

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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

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

Gastroenterology Debra L. Zoran, DVM, MS, PhD, DACVIM (Internal Medicine) Texas A&M University

C. Thomas Nelson, DVM Animal Medical Center Anniston, Alabama

Infectious Disease Derek P. Burney, DVM, PhD, DACVIM Gulf Coast Veterinary Specialists Houston, Texas

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 John G. DeVries, DVM, DABVP (Canine/Feline) Oradell Animal Hospital Paramus, New Jersey 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.

Canadian News

Coming Events December 4–6 Lifelearn Inc. Continuing Education: Flexible Endoscopy Ontario Veterinary College University of Guelph, Ontario This seminar will offer 42 hours of CE credit. It is designed to provide practitioners with upper and lower GI endoscopic experience. An advanced module that will also offer 42 CE credit hours is planned for 2010. Phone 800-375-7994 Web www.lifelearn.com December 6 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. Marjory Brooks. Phone 403-863-7160 E-mail info@cavm.ab.ca Web cavm.ab.ca/ce_calendar.html January 28–30 Ontario Veterinary Medical Association Conference and Trade Show Westin Harbour Castle, Toronto, Ontario This 3-day conference will include CE, wet labs, Master Classes, and clinical pearls. Phone 800-670-1702 Web ovma.org February 3 Ottawa Academy of Veterinary Medicine: Ophthalmology Embassy West Hotel and Conference Center, Ottawa, Ontario This seminar will review ophthalmologic topics and be presented by Dr. Chantale Pinard. Web oavm.org February 10 Calgary Academy of Veterinary Medicine: Exotics Clara Christie Theatre, Health Sciences, University of Calgary, Alberta This seminar will offer 1.5 hours of scientific CE and be presented by Dr. Dennilyn Parker. Phone 403-863-7160 E-mail info@cavm.ab.ca Web cavm.ab.ca/ce_calendar.html February 24 Ontario Veterinary Medical Association: Perioperative Pain Management Holiday Inn, Kitchener, Ontario This seminar, part of the Golden Triangle Veterinary Academy series, will be presented by Dr. Nancy Brock. Phone 519-662-3899 Web ovma.org March 21 Calgary Academy of Veterinary Medicine: Dermatology Clara Christie Theatre, Health Sciences, University of Calgary, Alberta. This seminar will offer 6 hours of scientific CE and be presented by Dr. Anthony Yu. Phone 403-863-7160 E-mail info@cavm.ab.ca Web cavm.ab.ca/ce_calendar.html

OVC Professor Named Canada Research Chair

r. Scott Weese, a pathobiologist at Ontario Veterinary College, has been named a Canada Research Chair (CRC) in Zoonotic Diseases. More than 70% of new infectious diseases that threaten human health are zoonotic. Dr. Weese is a leading researcher of two zoonotic pathogens—Clostridium difﬁcile and methicillin-resistant Staphylococcus aureus—and veterinary infection control. He and his research team will simultaneously study people, animals, and food to learn about the factors associated with the transmission of infectious diseases. “It’s becoming increasingly clear that we need to broaden our approach to the study of zoonotic diseases, particularly diseases involving pets,” says Weese. “This chair will greatly facilitate research in this area, both independent research in my lab and collaborative research with colleagues in human medicine, veterinary, and

public health fields.” Dr. Weese’s new position is classified as a Tier 2 research chair. Holders of Tier 2 chairs are considered to have the potential to become world leaders in their fields and receive $100,000 a year for 5 years. Weese’s ultimate goals are to increase understanding of how pathogens are spread and to help prevent and control new and reemerging animal-related diseases that threaten public health. The CRC program was established in 2000 as a way of enabling Canadian universities to attract and retain excellent faculty. The program is governed by a steering committee made up of the presidents of the Natural Sciences and Engineering Research Council, the Canada Foundation for Innovation, the Social Sciences and Humanities Research Council, and the Canadian Institutes of Health Research, as well as the deputy minister of Industry Canada.

University of Saskatchewan Veterinary Hospital Affected by Isotope Shortage

shortage of medical isotopes, used in medical imaging, has caused the University of Saskatchewan’s Veterinary Hospital to delay the opening of a new $500,000 diagnostic suite. The shortage is due to operational problems at the Chalk River nuclear plant in Ontario. The plant is one of the biggest suppliers of isotopes for medical use in Canada. The shortage has also been a problem for human medical providers, which take precedence over veterinary use, exacerbating the problem for the college. Until the shortage is rectiﬁed,

the hospital will be relying on other imaging techniques, such as magnetic resonance imaging and radiography.

SPREAD YOUR GOOD NEWS Canadian News c/o Veterinary Learning Systems 780 Township Line Road Yardley, PA 19067, USA E-MAIL editor@CompendiumVet.com FAX 800-556-3288 WEB CompendiumVet.com

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

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November 2009 Vol 31(11)

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

Features CompendiumVet.com | Peer Reviewed | Listed in MEDLINE

496

Calcium Oxalate Urolithiasis

514

Fare Thee Well: How to help owners (and yourself) deal with the death of a beloved pet

504 Applied Dermatology Otitis: Anatomy Every Practitioner Should Know ❯❯ Craig E. Grifﬁn It is important to avoid damaging key structures while aggressively cleaning an ear affected by chronic otitis externa. In this article, Dr. Grifﬁn provides many photographs of canine and feline ear anatomy to help in identifying these structures. Several otoscopic videos are available at CompendiumVet.com.

On the Cover Dr. Craig E. Grifﬁn (left) examines a patient’s middle ear while Dr. Wayne S. Rosenkrantz (right) holds the patient in place.

FREE

❯❯ Kelly Gisselman, Cathy Langston, CE Douglas Palma, and John McCue This article continues a series on diagnosis and treatment of different types of uroliths.

❯❯ Amy I. Bentz and Christina Bach Pet owners often seek reassurance from their veterinarian after making the decision to have their pet euthanized. The authors present advice on how to communicate with grieving clients as well as how to cope with a personal sense of loss when a patient dies.

520

FREE Acute Postrenal CE y, Azotemia: Etiology, d Clinicopathology, and Pathophysiology

❯❯ Julie R. Fischer, India F. Lane, and Jennifer Stokes Assessment for urinary tract rupture should be part of the diagnostic workup for all azotemic patients. Prompt correction of postrenal azotemia is critical to achieving a positive outcome.

Departments

495 Editorial: The Current 533 Product Forum and Future States of Veterinary Dermatology 534 Market Showcase ❯❯ Wayne S. Rosenkrantz 534 Classiﬁed Advertising and Craig E. Grifﬁn 535 Client Handout: Ear Cleaning 101 503 Clinical Snapshot: Bladder Trauma in a Beagle ❯❯ Megan M. Templeton, Pamela Schwartz, and Nicole J. Buote 532 Index to Advertisers

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Compendium: Continuing Education for Veterinarians®

Gentle on his ears

Once-a-Day, Mometamax Delivers Effective First Line Treatment for Otitis Externa ÂŽ

Mometasone furoate s 2APIDLY CONTROLS INmAMMATION TO REDUCE RELATED PAIN AND IRRITATION s .EW STUDY REPORTS NO ADRENOCORTICAL SUPPRESSION WITH TOPICAL ADMINISTRATION

Clotrimazole s $OCUMENTED EFlCACY AGAINST Malassezia pachydermatis

Gentamicin s 4RUSTED ANTIBIOTIC WITH LOW INCIDENCE OF REPORTED BACTERIAL RESISTANCE

MometamaxÂŽ /TIC 3USPENSION IS INDICATED FOR THE TREATMENT OF OTITIS EXTERNA IN DOGS CAUSED BY SUSCEPTIBLE STRAINS OF YEAST Malassezia pachydermatis) AND BACTERIA Pseudomonas SPP ;INCLUDING P. aeruginosa= COAGULASE POSITIVE STAPHYLOCOCCI Enterococcus faecalis, Proteus mirabilis AND BETA HEMOLYTIC STREPTOCOCCI #OMPONENTS MAY CAUSE LOCAL HYPERSENSITIVITY OR OTOTOXICITY &OR SIDE EFFECTS AND WARNINGS PLEASE SEE ACCOMPANYING BRIEF SUMMARY OF 0RODUCT )NFORMATION See Page 494 for Product Information Summary

Mometamax is the property of Intervet International B.V. or afďŹ liated companies or licensors and is protected by copyrights, trademark and other intellectual property laws. Copyright ÂŠ 2009 Intervet International B.V. All rights reserved.

1. Reeder CJ, GrifďŹ n CE, Polissar NL, et al. Comparative adrenocortical suppression in dogs with otitis externa following topical otic administration of four different glucocorticoid-containing medications. Vet Therap. 2008;9:111-121. 2. Rubin J, Walker RD, Blickenstaff K, Bodies-Jones S, Zhao S., Antimicrobial resistance and genetic characterization of ďŹ&#x201A;uoroquinolone resistance of Pseudomonas aeruginosa isolated from canine infections., Vet microbiol. 2008 Mar 4; [Epub ahead of print] SPAH-MO-96a

November 2009 Vol 31(11)

WEB EXCLUSIVES

CE ARTICLE ❯❯ Canine Atrial Fibrillation ❯❯ Ashley B. Saunders, Sonya G. Gordon, Matthew W. Miller Atrial ﬁbrillation (AF) is the most commonly diagnosed supraventricular tachyarrhythmia in dogs. It typically develops when atrial enlargement occurs secondary to underlying cardiovascular disease. Electrocardiographically, AF is characterized by disorganized atrial electrical activity resulting in an absence of P waves and a rapid and irregular ventricular rate. The hemodynamic consequences of AF include decreased cardiac output and the development of clinical signs of heart failure. Therapeutic management focuses on controlling ventricular rate or restoring and maintaining sinus rhythm using antiarrhythmic medication and, in some cases, biphasic transthoracic electrical cardioversion. The prognosis varies and is especially guarded in the presence of signiﬁcant underlying cardiac disease, such as dilated cardiomyopathy.

WEB-EXCLUSIVE VIDEOS ❯❯ Ear Anatomy Videos The Applied Dermatology article on page 504, “Otitis: Anatomy Every Practitioner Should Know,” by Dr. Craig E. Griffin, addresses ear cleaning and identifying different structures of the canine and feline ear. Dr. Griffin has submitted five videos to correspond with his article. Topics include otoscopy of the ear canal, movement of the tympanic membrane in response to water pressure, and a demonstration of the massage point at the base of the ear (which can be used with the ear cleaning handout available online).

HANDOUT ❯❯ Ear Cleaning 101 Home ear cleanings can enhance treatment of an existing ear problem or prevent development of a new one. This handout describes a simple technique for home ear cleaning. This handout can be found on pages 535–536 or can be downloaded from CompendiumVet.com.

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

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

Editorial ❯❯ Wayne S. Rosenkrantz, DVM, DACVD Dr. Craig E. Griffin (left) and Dr. Wayne S. Rosenkrantz (right).

Animal Dermatology Clinic Tustin, California

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

The Current and Future States of Veterinary Dermatology

fter almost 30 years of actively practicing veterinary dermatology and being involved with clinical research and continuing education (CE), we are more inspired and excited about the specialty than ever. When we started our careers in the late 1970s and early 1980s, the number of recognized skin diseases was limited; now, more than 460 varieties of skin disease are recognized.1,a We have seen the number of American College of Veterinary Dermatology diplomates grow from just around a dozen to its current total of 212. And we continue to be amazed at the development of new diagnostic and therapeutic tools, such as video otoscopes and cyclosporine, which have improved our ability to manage many common problems. Many surveys have found that dermatology cases are the most common presenting complaints seen in small animal practice.2–4 A February 2009 Veterinary Pet Insurance press release reported that ear infections, skin allergies, and pyoderma were the top three canine claims in the United States for the year 2008.5 Based on our opportunities to consult in a variety of geographic regions, we would agree. Knowledge about veterinary dermatology is expanding worldwide, through meetings such as the annual 3-day North American Veterinary Dermatology Forum, the Annual Congress of the European Society and College of Veterinary Dermatology, and the World Congress of Veterinary Dermatology, which meets every 4 years and is the result of interaction between international dermatology specialty groups. These meetings allow study results, descriptions of new aHill P. Personal communication. Veterinary Specialist Centre, Sydney, Australia; 2009.

diseases or therapies, and new information about recognized diseases or therapies to be presented to a wider audience. Academia, private practice, and industry have all contributed to the growth of, and increased interest in, veterinary dermatology. Advances in diagnostics and therapeutics have beneﬁted specialists and general practitioners alike in helping

The adage “as long as you can use glucocorticoids, you can be a veterinary dermatologist” has never been further from the truth. manage the most common presenting skin and ear problems. Clients are demanding higher levels of care and often actively pursue advanced diagnostic testing and therapeutic options. In order to remain current, practitioners need to take advantage of CE seminars and the valuable information published in the veterinary literature. The following are a few of the recent developments in veterinary dermatology: Advances in the understanding of canine atopic dermatitis. Once believed to be an inhaled type 1 allergy, this condition is now known to be a complex reaction to allergens that may be percutaneous, inhaled, or ingested. Genetic predispositions to altered immunologic reactivity, as well as skin changes, predispose patients to the clinical manifestations. This knowledge is opening up new avenues for treatment and, hopefully, prevention of this common problem. CONTINUES ON PAGE 519

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3 CE CREDITS

CE Article 1

Calcium Oxalate Urolithiasis ❯❯ Kelly Gisselman, DVM Hope Center for Advanced Veterinary Medicine Vienna, Virginia

❯❯ Cathy Langston, DVM, DACVIM (Small Animal Internal Medicine) ❯❯ Douglas Palma, DVM ❯❯ John McCue, DVM Animal Medical Center New York

At a Glance

Abstract: Calcium oxalate (CaOx) uroliths are one of the most common urolith types in dogs, cats, and humans. Many factors predispose animals to CaOx uroliths, including breed, old age, obesity, male sex, being neutered, and certain diseases. Because there are no effective strategies for medical dissolution of these uroliths, management should focus on physical removal (by surgical or nonsurgical methods) and prevention, especially in patients with recurring uroliths, high-risk breeds, and animals with predisposing diseases. Prevention focuses on diet modiﬁcation, primarily to increase water intake, and the appropriate use or avoidance of speciﬁc medications.

alcium oxalate (CaOx) urolith formation depends on the degree of urine saturation with CaOx and the balance between urinary promoters and inhibitors of CaOx formation.1

Promoters of Calcium Oxalate Formation

Page 496

Hypercalciuria, which predisposes patients to CaOx urolithiasis, may be classiﬁed as absorptive, renal leak, or resorptive hypercalciuria. Absorptive hypercalciuria is characterized by increased intestinal absorption and renal excretion of calcium and oxalate and has been described in miniature schnauzers with urolithiasis.2 Renal leak hypercalciuria is characterized by impaired renal tubular reabsorption of calcium. Resorptive hypercalciuria is characterized by parathyroid hormone– mediated mobilization of calcium from bone and is a result of primary hyperparathyroidism.3,4 Conditions associated with hypercalciuria include hypercalcemia; excessive dietary calcium, protein, sodium, vitamin D, or vitamin C intake; acidifying diets; urinary acidiﬁers; and certain drugs (e.g., glucocorticoids, loop diuretics) and diseases (e.g., hyperadrenocorticism).5,6

Inhibitors of Calcium Oxalate Formation Page 496

Signalment Page 497

Incidence Page 497

Diagnosis Page 498

Treatment Page 498

Prevention Page 498

496

Hyperoxaluria can occur with increased intake of dietary oxalate precursors, such as leafy green vegetables (e.g., spinach, rhubarb) or nuts (especially peanuts).7 Dietary calcium binds oxalic acid and inhibits its absorption; thus, calcium restriction enhances hyperoxaluria.7 Vitamin C (ascorbic acid) is metabolized to oxalate, and vitamin B6 alters oxalate metabolism (FIGURE 1).7

Inhibitors of Calcium Oxalate Formation Increases in serum phosphorus concentration decrease calcitriol production and enhance urinary excretion of a natural inhibitor of oxalate precipitation, pyrophosphate.7 Restricted dietary magnesium has been associated with CaOx formation because dietary magnesium complexes with oxalate and reduces oxalate binding with ionic calcium.8,9 Nephrocalcin is a substance in the urine that naturally inhibits CaOx uroliths and is less effective in patients that form CaOx uroliths.10 Other substances (e.g., Tamm-Horsfall mucoproteins, glycosaminoglycans) may inhibit CaOx formation in people, but their role in canine CaOx urolithiasis is unknown.

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Calcium Oxalate Urolithiasis CE Signalment

FIGURE 1

Certain breeds of dogs and cats have been shown to have an increased or decreased incidence of CaOx urolithiasis (TABLES 1 and 2 and BOX 1).11–13 Obesity and increasing age are risk factors for CaOx urolith formation in dogs and cats.11–15 Cats are at the highest risk between 4 and 16 years of age, with a mean age of 7.3 years at diagnosis.12,16 In two studies,15,17 the mean age of dogs with CaOx uroliths was 7 and 8.4 years. CaOx uroliths are more common in male dogs (2:1 ratio) and male cats (1.5:1 ratio) than in females.11,15,17,18 Neutered dogs and cats are also at increased risk.11,18

Dietary oxalate intake

Incidence CaOx is one of the most common substances in uroliths in dogs and cats.19,20 Over the past 21 years, the ratio of CaOx uroliths to struvite uroliths has increased signiﬁcantly. The percentage of canine CaOx uroliths submitted for analysis increased from 7% in 1986 to 38% in 2000,8,11 and the percentage of feline CaOx uroliths submitted increased from 2% in 1984 to 55% in 2001.21,22 Increases in CaOx urolith formation may be related to dietary acidiﬁcation and the increasing longevity of dogs and

Pathway of oxalate biosynthesis.7

cats, while decreases in struvite urolith submissions may be due to improved medical management.18,23,24 More recent information shows a plateau and possible decline in the incidence of CaOx uroliths.15,25

Canine Breeds With Decreased Incidence of Calcium Oxalate Urolithiasis11 TABLE 2

Canine Breeds With Increased Incidence of Calcium Oxalate Urolithiasis11 TABLE 1

Breed

Odds Ratio

Standard schnauzer Miniature schnauzer

18.06 14.10

Lhasa apso

10.95

Parson Russell terrier

9.85

Papillon

9.85

Yorkshire terrier

6.64

Bichon frise

6.57

Keeshond

5.47

Pomeranian

4.93

Samoyed

4.69

Shih tzu

4.49

Chihuahua

3.88

Cairn terrier

3.69

Maltese

3.52

Miniature and toy poodle

3.32

West Highland white terrier

3.28

Dachshund

2.69

Breed Cocker spaniel

Odds Ratio 0.15

German shepherd

0.12

Golden retriever

0.069

QuickNotes Breed, weight, age, and neuter status are all factors in developing CaOx uroliths.

BOX 1

Feline Breeds With Increased or Decreased Incidence of Calcium Oxalate Urolithiasis12 Increased Incidence Ragdoll British shorthair Foreign shorthair Himalayan Havana brown Scottish fold Persian Exotic shorthair

Decreased Incidence Birman Abyssinian Siamese Mixed breed

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FREE CE Calcium Oxalate Urolithiasis

FIGURE 2

QuickNotes CaOx uroliths can develop secondary to metabolic acidosis, which leads to hypercalciuria.

Microscopic image of calcium oxalate dihydrate crystals (400× magnification). Courtesy of Drs. Richard Luong and Andrew Loar, Animal Medical Center, New York.

Nephroliths and ureteroliths account for only 2% to 3% of urolith submissions from dogs and cats.26,27 In dogs, 31% to 39% of nephroliths and ureteroliths are composed of CaOx; 33% to 38% are composed of struvite.28,29 Most (80% to 99%) feline nephroliths and ureteroliths are composed of CaOx.28,30

Diagnosis Creation of acidic urine (pH <7.0) can predispose animals to CaOx urolithiasis by inducing increased excretion of calcium in the urine; however, CaOx solubility is not inﬂuenced by urine pH. Most CaOx uroliths form in sterile urine, either singly or as multiple stones. CaOx crystals can be found during urinalysis but do not necessarily correlate with urolith composition (FIGURE 2). FIGURE 3

CaOx is the most radiopaque urolith substance (FIGURE 3). In an in vitro study,31 CaOx uroliths could be distinguished from struvite uroliths with 75% to 88% accuracy when computed tomography was used and uroliths were composed of a single mineral type. CaOx calculi are usually white and hard (FIGURE 4). Surface characteristics may vary, but they often have sharp, jagged edges. The gross appearance of any stone is never a replacement for stone analysis. When radiopaque urinary calculi are found, a serum biochemistry panel, complete blood count, urinalysis, and urine culture should be evaluated for diseases associated with urolithiasis. Testing for hyperadrenocorticism should be considered if clinical criteria for this condition are met. A complete evaluation for hypercalcemia should be conducted if the ionized calcium level is elevated.

Treatment The only effective treatment for CaOx stones is physical removal by any of the surgical or nonsurgical techniques that have been described in the literature.32 Guidelines on when to use surgical versus nonsurgical techniques have been published elsewhere.32 Compared with other mineral types, canine CaOx uroliths are relatively easy to fragment with extracorporeal shock wave lithotripsy.33 Feline CaOx uroliths are less susceptible to fragmentation with extracorporeal shock wave lithotripsy than canine CaOx uroliths.34

Prevention Diet Diet is an important factor in the prevention of CaOx stones (TABLE 3). Canned diets high FIGURE 4

Lateral abdominal radiograph of a CaOx stone (arrow). Courtesy of Dr. Anthony Fischetti, Animal Medical Center, New York.

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A removed CaOx stone.

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Calcium Oxalate Urolithiasis CE in fat, phosphorus, magnesium, potassium, chloride, and moisture have been associated with decreased risk of CaOx formation.9,24,35 Reducing dietary carbohydrate has reduced the risk of CaOx urolithiasis in dogs but not in cats.8,9 Dry diets with a high fiber content have been shown to be associated with an increased risk of urolithiasis in dogs.9 Diets formulated to maximize urine acidity are not proven to cause CaOx formation in dogs and cats.8 Acidemia may promote hypercalciuria and hypocitraturia, increasing risk of urolith formation.36 The source of acidification plays a greater role than the urine pH achieved. In one study in dogs,35 Waltham Canine S/O Lower Urinary Tract Support Diet (Royal Canin USA) reduced CaOx relative supersaturation, a measure of the risk of CaOx formation, by 63%. For cats, Prescription Diet x/d Feline (Hill’s Pet Nutrition) showed a 59% reduction in CaOx relative supersaturation in one study37; this diet has since been replaced by Prescription Diet c/d Multicare Feline (Hill’s Pet Nutrition). Increasing water consumption (either through the use of canned food or through adding water to the diet) to achieve a urine specific gravity <1.020 in dogs and <1.025 in cats dilutes the urine concentration and decreases risk of stone recurrence.38 In cats, the risk of CaOx urolith formation was one-third less when canned diets were fed than when other dietary formulations were consumed.7

Medications

TABLE 3

Prevention of Calcium Oxalate Urolithiasis

Parameter Diet

Goal —

Method to Achieve Feed a diet not restricted in magnesium and phosphorus Avoid foods with excess oxalatea

Urine speciﬁc gravity

<1.020 in dogs

Feed canned food

<1.025 in cats

Add water to dry food Provide multiple water bowls Provide running water Provide ﬂavored water Increase sodium in diet

Urine pH

7.0–7.5

Manage by diet Increase potassium citrate by supplementation

CaOx crystalluria

Minimize or eliminate

Control hypercalcemia Administer thiazide diuretic Increase vitamin B6 by supplementation

aSee the food lists at CompendiumVet.com.

tration was reduced by 34% with hydrochlorothiazide (2 mg/kg PO q12h).41 Patients should be monitored for dehydration, hypokalemia, and hypercalcemia.28 Vitamin B6 supplementation (2 to 4 mg/kg PO q24–48h) could be considered in patients consuming homemade diets.42 Vitamins D and C enhance intestinal calcium absorption; therefore, excessive supplementation should be avoided. Steroids (e.g., prednisone) and furosemide also lead to calciuresis and should be avoided.

If dietary therapy is not effective at preventing CaOx crystalluria, or if uroliths recur, potassium citrate can be administered orally. Citrate may form soluble salts with calcium, thereby Monitoring Schedule decreasing the formation of less soluble CaOx About 50% to 60% of CaOx uroliths recur crystals; however, an increase in the urine within 3 years of surgical or nonsurgical pH and metabolic alkalosis with resultant removal; this incidence may be exaggerated by reduction in calciuria are the main proposed incomplete removal of calculi at the inimechanisms of action.39 The potassium citrate tial surgery.38 Recommended monitor- TO LEARN dose (50 to 75 mg/kg mixed with food q12h) ing to decrease recurrence after stone MORE is titrated to maintain urine pH between 7.0 removal includes urinalysis, electrolyte and 7.5. If dietary therapy alone maintains the evaluation if using thiazide diuretics, For a partial list of human urine pH above 7.0, potassium citrate should radiography, and/or ultrasonography at foods to avoid feeding to dogs not be added. Serum potassium should initially 2 to 4 weeks, 3 months, and every 6 with CaOx urolithiasis, visit be monitored monthly and the dose reduced if months thereafter. If recurrent uroliths CompendiumVet.com. hyperkalemia occurs. are identiﬁed while they are still small, A list of foods that can be fed Thiazide diuretics promote natriuresis in nonsurgical removal techniques should to dogs with CaOx urolithiasis the distal tubules, which results in calcium be considered, along with reevaluation is also available. reabsorption.40 In dogs, urine calcium concen- for underlying causes.38 CompendiumVet.com | November 2009 | Compendium: Continuing Education for Veterinarians®

499

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Conclusion More research is necessary to understand how to prevent CaOx uroliths. Early screening and detection of uroliths (especially in high-risk breeds) are important to allow use of nonsurgical removal techniques and to start preventive measures. Increased water consumption is the best strategy to maintain good urinary tract health.39

References 1. Stevenson AE, Robertson WG, Markwell PJ. Risk factor analysis and relative supersaturation as tools for identifying calcium oxalate stone-forming dogs. J Small Anim Pract 2003;44:491-496. 2. Lulich JP, Osborne CA, Nagode LA, et al. Evaluation of urine and serum metabolites in miniature schnauzers with calcium oxalate urolithiasis. Am J Vet Res 1991;52:1583-1590. 3. Klausner JS, Fernandez FR, O’Leary TP, et al. Canine primary hyperparathyroidism and its association with urolithiasis. Vet Clin North Am Small Animal Pract 1986;15:227-239. 4. Marquez GA, Klausner JS, Osborne CA. Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. JAVMA 1995;5:817-819. 5. Bartges JW. Diagnosis of urinary tract infections. Vet Clin North Am Small Animal Pract 2004;34:923-933. 6. Hess RC, Kass PH, Ward CR. Association between hyperadrenocorticism and development of calcium-containing uroliths in dogs with urolithiasis. JAVMA 1998; 212:1889-1891. 7. Lulich JP, Osborne CA, Thumchai R, et al. Epidemiology of canine calcium oxalate uroliths: identifying risk factors. Vet Clin North Am Small Animal Pract 1999;29:113-122. 8. Lekcharoensuk C, Osborne CA, Lulich JP, et al. Associations between dry dietary factors and canine calcium oxalate uroliths. Am J Vet Res 2002;63:330-337. 9. Lekcharoensuk C, Osborne CA, Lulich JP, et al. Associations between dietary factors in canned food and formation of calcium oxalate uroliths in dogs. Am J Vet Res 2002;63:163-169. 10. Carvalho M, Lulich JP, Osborne CA, et al. Defective urinary crystallization inhibition and urinary stone formation. Int Braz J Urol 2006;32:324-348. 11. Lekcharoensuk C, Lulich JP, Osborne CA, et al. Patient and environmental factors associated with calcium oxalate urolithiasis in dogs. JAVMA 2000;217: 515-519. 12. Lekcharoensuk C, Lulich JP, Osborne CA, et al. Association between patientrelated factors and risk of calcium oxalate and magnesium ammonium phosphate urolithiasis in cats. JAVMA 2000;217:520-525. 13. Kirk CA, Ling GV, Franti CE, et al. Evaluation of factors associated with development of calcium oxalate urolithiasis in cats. JAVMA 1995;207:1429-1434. 14. Thumchai R, Lulich JP, Osborne CA, et al. Epizootiologic evaluation of urolithiasis in cats: 3,798 cases (1982-1992). JAVMA 1995;219:547-551. 15. Ling GV, Thurmond MC, Choi YK, et al. Changes in proportion of canine urinary calculi composed of calcium oxalate or struvite in specimens analyzed from 1981 through 2001. J Vet Intern Med 2003;17:817-823. 16. Osborne CA, Lulich JP, Thumchai R, et al. Diagnosis, medical treatment, and prognosis of feline urolithiasis. Vet Clin North Am Small Animal Pract 1996;26: 589-627. 17. Houston DM, Moore AEP, Favrin MG, et al. Canine urolithiasis: a look at over 17,000 urolith submissions to the Canadian Veterinary Urolith Centre from February 1998 to April 2003. Can Vet J 2004;45:225-230. 18. Houston DM, Moore AEP, Favrin MG, et al. Feline urethral plugs and bladder uroliths: a review of 5484 submissions 1998-2003. Can Vet J 2003;44:974-977. 19. Ling GV, Thurmond MC, Choi YK, et al. Changes in proportion of canine urinary calculi composed of calcium oxalate or struvite in specimens analyzed from 1981 through 2001. J Vet Intern Med 2003;17:817-823. 20. Picavet P, Detilleux J, Verschuren S, et al. Analysis of 4495 canine and feline uroliths in the Benelux. A retrospective study: 1994-2004. J Anim Physiol Anim Nutr (Berl) 2007;91:247-251. 21. Osborne CA, Lulich JP, Thumchai R, et al. Feline urolithiasis. Etiology and pathophysiology. Vet Clin North Am Small Animal Pract 1996;26:217-232. 22. Lulich JP, Osborne CA. Epidemiological shifts in feline urolith type, in state of the stone. Hill’s Symp Lower Urinary Tract Dis 2007:13-18. 23. Osborne CA, Lulich JP, Polzin DJ, et al. Analysis of 77,000 canine uroliths: perspectives from the Minnesota Urolith Center. Vet Clin North Am Small Animal Pract 1999;29:17-38.

500

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24. Lekcharoensuk C, Osborne CA, Lulich JP, et al. Association between dietary factors and calcium oxalate and magnesium ammonium phosphate urolithiasis in cats. JAVMA 2001;219:1228-1237. 25. Cannon AB, Westropp JL, Ruby AL, et al. Evaluation of trends in urolith composition in cats: 5,230 cases (1985-2004). JAVMA 2007;231:570-576. 26. Ling GV, Ruby AL, Johnson DL, et al. Renal calculi in dogs and cats: prevalence, mineral type, breed, age, and gender interrelationships (1981-1993). J Vet Intern Med 1998;12:11-21. 27. Rubin SI. Chronic renal failure and its management and nephrolithiasis. Vet Clin North Am Small Animal Pract 1997;27:13311354. 28. Ross SJ, Osborne CA, Lulich JP, et al. Canine and feline nephrolithiasis: epidemiology, detection, and management. Vet Clin North Am Small Animal Pract 1999;29:231-250. 29. Snyder DM, Steffey MA, Mehler SJ, et al. Diagnosis and surgical management of ureteral calculi in dogs: 17 cases (1990-2003). N Z Vet J 2005;53:19-25. 30. Kyles AE, Stone EA, Gookin JL, et al. Diagnosis and surgical management of obstructive ureteral calculi in cats: 11 cases (19931996). JAVMA 1998;213:1150-1156. 31. Pressler BM, Mohammadian LA, Li E, et al. In vitro prediction of canine urolith mineral composition using computed tomographic mean beam attenuation measurements. Vet Radiol Ultrasound 2004;45:189-197. 32. Langston CE, Gisselman KM, Palma D, et al. Methods of urolith removal. Compend Contin Educ Pract Vet. In press. 33. Adams LG, Senior DF. Electrohydraulic and extracorporeal shock-wave lithotripsy. Vet Clin North Am Small Animal Pract

1999;29:293-302. 34. Adams LG, Williams JC Jr, McAteer JA, et al. In vitro evaluation of canine and feline calcium oxalate urolith fragility via shock wave lithotripsy. Am J Vet Res 2005;66:1651-1654. 35. Stevenson AE, Blackburn JM, Markwell PJ, et al. Nutrient intake and urine composition in calcium oxalate stone-forming dogs: comparison with healthy dogs and impact of dietary modiﬁcation. Vet Ther 2004;5:218-231. 36. Fettman MJ, Coble JM, Hamar DW, et al. Effect of dietary phosphoric acid supplementation on acid-base balance and mineral and bone metabolism in adult cats. Am J Vet Res 1992;53:2125-2135. 37. Lulich JP, Osborne CA, Lekcharoensuk C, et al. Effects of diet on urine composition of cats with calcium oxalate urolithiasis. JAAHA 2004;40:185-191. 38. Lulich JP, Osborne CA, Lekcharoensuk C, et al. Canine calcium oxalate urolithiasis: case-based applications of therapeutic principles. Vet Clin North Am Small Animal Pract 1999;29:123-139. 39. Stevenson AE, Wrigglesworth DJ, Smith BH, et al. Effects of dietary potassium citrate supplementation on urine pH and urinary relative supersaturation of calcium oxalate and struvite in healthy dogs. Am J Vet Res 2000;61:430-435. 40. Lulich JP, Osborne CA, Lekcharoensuk C, et al. Effects of hydrochlorothiazide and diet in dogs with calcium oxalate urolithiasis. JAVMA 2001;218:1583-1586. 41. Lulich JP, Osborne CA. Management of canine calcium oxalate urolith recurrence. Compend Contin Educ Pract Vet 1998;20:178189. 42. Lulich JP. Feline lower urinary tract disorders: making the correct diagnosis. Proc 2007 FLUTD Hill’s Symp 2007:36-41.

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 is not a mechanism of hypercalciuria? a. increased gastrointestinal absorption b. impaired renal tubular reabsorption c. calcium mobilization caused by primary hyperparathyroidism d. decreased urinary calcium excretion 2. _______ is not a risk factor for CaOx urolithiasis formation in dogs and cats. a. Weight b. Age c. Sex d. Coat color/pattern 3. What percentage of feline nephroliths and ureteroliths are CaOx? a. 20% to 30% b. 40% to 50% c. 60% to 70% d. 80% to 99% 4. What type of urinary environment promotes formation of CaOx stones? a. acidic (pH <7.0)

502

b. neutral (pH 7.0 to 7.5) c. alkaline (pH >7.5) d. all of the above

c. increasing; acidosis d. decreasing; alkalosis

5. Which uroliths are the most radiopaque? a. calcium oxalate b. urate c. struvite d. cystine

8. Thiazide diuretics help prevent CaOx stone formation by promoting natriuresis in the ______ tubules, which results in calcium ______. a. distal; reabsorption b. distal; secretion c. proximal; reabsorption d. proximal; secretion

6. Which diet has been shown to dissolve CaOx stones in dogs? a. Hill’s Prescription Diet Canine s/d b. Hill’s Prescription Diet Canine c/d c. Waltham Canine S/O Lower Urinary Tract Support Diet d. none

9. Vitamin ______ could be added to a homemade diet in an effort to prevent CaOx stone formation. a. D c. C d. K b. B6

7. Potassium citrate helps prevent CaOx stone formation by ______ urine pH and causing metabolic ______. a. increasing; alkalosis b. decreasing; acidosis

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

10. What percentage of surgically removed CaOx stones recur in 3 years? a. 10% to 20% b. 30% to 40% c. 50% to 60% d. 70% to 80%

Clinical Snapshot Particularly intriguing or difﬁcult cases

Case Presentation #1

❯❯ Megan M. Templeton, DVM ❯❯ Pamela Schwartz, DVM, DACVS ❯❯ Nicole J. Buote, DVM Animal Medical Center New York, New York

A 2-year-old intact male beagle was referred to our institution for evaluation and surgical consultation 3 days after being hit by a car. On physical examination, the patient was laterally recumbent with pale mucous membranes, tachycardic (heart rate: 150 bpm) with moderate femoral pulses, and eupneic with clear lung sounds in all fields. Scrotal, B prescrotal, and inguinal bruising was present, along with palpable crepitus in the left pelvic/coxofemoral region and pitting edema of the right hindlimb. In addition, the patient had a midline ventral abdominal incision from surgery 3 days previously to stabilize an acute abdomen for suspect urinary bladder rupture; a Foley catheter exited the caudal portion of the incision and was attached to a closed urinary collection system. The catheter was patent, draining dark yellow, slightly blood-tinged fluid. It was assumed that the catheter was draining the urinary bladder; however, the urinary bladder was not visualized during previous laparotomy. Emergency stabilization, including a fluid bolus, pain medication, and blood pressure monitoring, was performed to address the hemodynamic instability of the patient before additional diagnostics were pursued. A lack of clinical improvement despite the previous surgery, including persistent azotemia, decreased urine production, and development of abdominal pain, indicated a need for continued diagnostics. Positive contrast studies of the urinary system were conducted, and radiographs (A and B) were obtained.

1. Provide an interpretation of A and B and, if possible, a

diagnosis. 2. What additional imaging studies may be conducted to aid

in evaluating the remainder of the urinary tract? 3. What are the typical etiology and clinical presentation of

this condition? 4. What are the treatment options for this case? SEE PAGE 531 FOR ANSWERS AND EXPLANATIONS.

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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

Otitis: Anatomy Every Practitioner Should Know ❯❯ Craig E. Grifﬁn, DVM, DACVDa Animal Dermatology Clinic San Diego, California

hronic otitis externa is a difficult, frustrating problem. ear, which are enclosed by bones of the skull. Four etiologic components must be considered: primary Some giant-breed dogs have ear canals up to 11 cm long. More detailed descriptions of and secondary causes and perpetuating and predisposing the ear canal are given elsewhere.2 The tymfactors.1 Usually, these cases are complex and involve more panic membrane and medial end of the ear than one component. Perpetuating factors are changes in the canal are located ventral and caudal to, but anatomy and physiology of the ear that occur in response to almost on the same medial-to-lateral plane as, the eye (FIGURE 2). The most important anainflammation in the ear canal and the perpetuating factors tomic structures with regard to otitis are the already present. They are self-perpetuating, are not disease external ear canal, tympanic membrane, and specific, and include failure of self-cleaning mechanisms and middle ear. proliferative changes that create folds and stenosis of the External Ear lumen of the ear canal. Elimination of perpetuating factors The external ear is formed from two pieces of often requires aggressive cleaning of the ear and long-term cartilage and a bony canal that are covered by therapy. It is important to avoid damaging key structures skin. It ends medially at the thin tympanic membrane. The epithelium of the ear canal is conwhile aggressively cleaning the ear. Therefore, to adequately tinuous with the epithelium of the lateral aspect diagnose and manage perpetuating factors, veterinarians of the tympanic membrane so that the complete must recognize normal ear anatomy and physiology. FIGURE 1

Anatomy

At a Glance Anatomy Page 504

Physiology Page 510

aDr.

Griffin discloses that he has financial relationships with Efficas, Intervet/Schering-Plough Animal Health, Novartis Animal Health, Pfizer Animal Health, Sogeval, and Teva Animal Health.

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The ear (auris) is the vestibulocochlear organ. It is divided into three major portions: external, middle, and inner (FIGURE 1). The external ear consists of the pinna (auricle) and ear canal (external acoustic meatus). The shape of the pinna varies widely among breeds. For the purpose of describing anatomy, this article considers the erect-eared pinna (as seen on German shepherds) as it projects dorsally and laterally, with its concave surface facing rostrally. Numerous muscle attachments allow the pinna to move and thereby improve its function of helping collect sound waves. The sound waves enter the ear as they pass through the external oriﬁce of the ear canal, located at the base of the pinna. The ear canal, which can be 5 to 10 cm in length, travels to the tympanic membrane and middle

Illustration showing a cross-section of the ear and its major components. With permission from Pfizer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.

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FIGURE 2

FIGURE 3 Straightening the pinna to perform the ear examination.a

QuickNotes

The auricular projection before the pinna is straightened.

Illustration of the relative locations of the ear canal and middle ear. With permission from Pfizer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.

ear canal is lined with epithelium. The larger portion of cartilage (the auricular cartilage) forms the pinna and most of the ear canal. The pinna rolls onto itself at the external oriﬁce of the external ear canal (FIGURE 1). From the external oriﬁce, the canal travels ventrally and slightly rostrally. This is the vertical canal. In the vertical canal, a projection of auricular cartilage emerges from the medial surface under the skin. This projection is unnamed, and its size varies between breeds and between individuals of the same breed. However, it is recognizable when examining the ear with an otoscope because it creates a “corner” around which the examiner must proceed to gain access to the canal. To prevent the auricular projection from blocking access to the ear canal lumen during otoscopic examination, pull the pinna dorsally and laterally. The tension created partially reduces the projection and straightens the ear canal lumen, allowing better access with the otoscope (FIGURE 3). At its ventral end, the ear canal bends

Aggressive cleaning is often needed to manage perpetuating factors, but care must be taken to avoid damaging key anatomic structures.

View of the ear canal after the pinna has been straightened. Note the auricular projection at top left. a

All photographs are copyright of Craig E. Grifﬁn.

medially and continues until it reaches the tympanic membrane. This section, from the bend to the tympanic membrane, is the horizontal ear canal. The skin of the horizontal canal is surrounded by cartilage: the auricular cartilage surrounds the lateral portion, while the smaller anular cartilage, which extends between the auricular cartilage and the external portion of the bone of the external acoustic

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FIGURE 4

FIGURE 5

The anular cartilage (blue arrows) is overlapped by the distal end of the auricular cartilage (white arrows). Note how the anular cartilage overlaps or inserts within the bone of the external acoustic meatus (green arrows).

QuickNotes

FIGURE 6

When otitis is present, the skin covering the auricular projection is often inﬂamed. The pressure of an otoscope cone, especially the edge of the cone, may result in pain and resistance to examination.

A normal canine medial horizontal canal, ending at the tympanic membrane. Note the tuft of hairs (white arrow) adjacent to the ventral portion of the tympanic membrane. The blue arrow is on a dilated, distended pars flaccida with its prominent vasculature. Note the manubrium of the malleus (A) and the pars tensa (B).

VIDEO

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meatus, surrounds the medial portion (FIGURE 4). The anular cartilage and bony external acoustic meatus overlap so that dorsally, the cartilage lies inside the bone of the oriﬁce, but ventrally, the bone is inside the cartilage. The size of the bony external acoustic meatus varies; in midsize dogs, it is about 1 cm long (FIGURE 5). Unlike the skin lining the cartilaginous canal, the skin lining the acoustic meatus lies on bone and therefore is not subject to

The bony external acoustic meatus of a dog skull. The blue arrowheads point to the ventral wall of the lateral and medial edges. The medial arrowhead is where the ventral portion of the pars tensa of the tympanic membrane would attach. The blue line indicates the portion of the horizontal canal where the skin would lie over bone rather than cartilage.

movement and massage. The change from cartilage to bone can be palpated with an angled Buck curette. The medial ring of the acoustic meatus is the location of the tympanic membrane. Often, larger primary hairs grow adjacent to the tympanic membrane (FIGURE 6), commonly on the ventral wall of the lumen. These hairs are a helpful landmark for locating the ventral tympanic membrane when an ear is diseased and the tympanic membrane is not readily apparent.

Tympanic Membrane The tympanic membrane consists of internal and external epithelial surfaces enclosing a thin layer of connective tissue that includes the manubrium of the malleus. It separates the external ear from the middle ear tympanic cavity. The tympanic membrane of the dog is made up of the pars flaccida and pars tensa (FIGURE 7). The pars flaccida, a small area of the dorsal to rostrodorsal aspect, is relatively flaccid and quite vascular. This structure may

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bulge out, can appear cystlike, and can hide the manubrium. Most of what is seen of the tympanic membrane when it is examined through an otoscope is the large pars tensa. A normal pars tensa is translucent, with striations that extend from the manubrium of the malleus out to the periphery. A whitish area with a line or ragged margin can sometimes be seen through the lower to middle section of the pars tensa. This whitish structure is best seen with a strong light source, such as a video otoscope. It represents a structure in the middle ear: the free edge of the septum bulla, which separates the tympanic cavity into dorsolateral and ventromedial parts (FIGURE 7). In dogs, the manubrium of the malleus is C shaped. It is located near the middle of the dorsal part of the pars tensa and points in a rostrocaudal direction. The concave aspect of the C faces rostrally, toward the nose. A perpendicular line from the top of the manubrium would point ventrally. Tension on the manubrium gives the tympanic membrane a mildly concave outer contour.2 The tympanic membrane is oriented at about a 30˚ to 45˚ angle from a dorsal-to-ventral plane. This creates a pocket or groove on the ventral floor of the horizontal canal, adjacent to the tympanic membrane, where small amounts of wax can accumulate. The tympanic membrane moves in response to pressure such as that generated by flushing and cleaning the ear canal. In cats, the tympanic membrane also consists of a pars tensa and pars flaccida, but to date, I have not observed a dilated pars flaccida in a cat. The manubrium of the malleus is relatively larger, is much straighter, and points more rostrally in cats than in dogs (FIGURE 8). In cats and dogs, when myringotomy is performed, the incision should be made in the caudal ventral quadrant of the tympanic membrane (i.e., ventral and caudal to the tip of the manubrium; FIGURE 9).

Middle Ear The middle ear consists of the tympanic cavity and the medial wall of the tympanic membrane; the auditory ossicles and their associated ligaments, muscles, and nerves; and the auditory (eustachian) tube. Normally, the only communication from the middle ear cavity to the outside environment is through the auditory tube, which opens into the nasopharynx and

FIGURE 7

Normal left tympanic membrane with the pars tensa and the vascular pars ﬂaccida. Vessels extend down along the manubrium of the malleus. Note the shadow of the septum bulla (A) seen behind the pars tensa.

serves to equalize pressure on either side of the tympanic membrane. The tympanic cavity may be divided clinically into three parts: dorsal, middle, and ventral. The dorsal part, also called the epitympanic recess, is the smallest and contains the head of the malleus and its articulation with the incus. The middle part, or tympanic cavity proper, is adjacent to the tympanic membrane rostrally and laterally. The prominent structure on the caudal medial aspect of the tympanic cavity proper is the promontory of the petrosal part of the temporal bone (FIGURE 10). The barrel-shaped promontory is situated roughly opposite to the mid-dorsal aspect of the tympanic membrane. At the caudal end of the promontory is the cochlear window, which communicates with the cochlea of the bony labyrinth (FIGURE 11). This structure must be avoided when a myringotomy is performed and the middle ear is ﬂushed. The caudal opening of the auditory tube lies in the rostral-medial part of the middle tympanic cavity. The middle portion of the tympanic cavity communicates freely with the ventral portion, contained in the egg-shaped tympanic bulla. The ventral portion is the largest portion of the tympanic cavity. A ridge of bone, the septum bulla, projects from the medial wall of the tympanic bulla into the cavity between its middle and ventral components. The septum bulla is readily seen just ventral and caudal to the promontory and cochlear window (FIGURE 12) and

QuickNotes In an abnormal ear, tympanic movement is helpful in identifying the tympanic membrane.

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FIGURE 8 Anatomy of the feline middle ear.

Needle A is inserted into the auditory tube. Needle B goes into the tympanic cavity up through a ventral bulla osteotomy opening.

QuickNotes

The needle (A) can be seen in the middle ear. Note that the manubrium (C) is relatively larger than that in the canine ear, and the long axis points rostroventrally, not ventrally as in dogs.

When possible, the middle ear anatomy of cats should be avoided when cleaning.

The needle (B) is inserted through the auditory tube. This view is through the external acoustic meatus.

often has many bony ossicles or “knobbed spicules” along the free edge in the tympanic cavity2 (FIGURE 13). This ridge makes passing catheters or tubes into the ventral bulla very difficult. When the middle ear is flushed, the goal is to direct fluid pressure below the septum bulla. The inner ring of the osseous external acoustic meatus is a helpful landmark because it is the attachment site of the tympanic membrane. If the ventral inner edge can be palpated with an ear loop, then the tympanic membrane is either ruptured or out of

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The needle is pointing from the dorsal portion of the ventral bulla into the ventral portion. Fluid that reaches the ventral portion is trapped by the septum. This ventral-to-dorsal view looks through a hole in the ventral bulla.

its normal anatomic position (FIGURE 14). Once the ventral medial edge of the osseous external acoustic meatus is reached, the cochlear window is a short distance (5 to 8 mm) medially. Care should be taken to stay caudal and ventral to the cochlear window. The middle ear in cats is very different from that in dogs in that the septum bullae is very large and nearly divides the ventral portion of the tympanic cavity into a small dorsolateral and a large ventromedial part—the pars tympanica and pars endotympanica, respectively. These

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FIGURE 9

FIGURE 10

A tomcat catheter in the left external ear canal, pointing to the optimal site for performing a myringotomy. The incision is made in the caudal ventral quadrant of the pars tensa of the tympanic membrane (blue lines). This site is caudal to the convex surface and below the tip of the manubrium.

View through the left external acoustic meatus of a dog skull. An orange feeding tube (A) enters the middle ear from the auditory tube. The septum bulla (B), promontory (P), and opening in the promontory to the cochlear window (C) can be seen.

FIGURE 11 Ventral to dorsal view through an opening in the ventral wall of the bulla of a dog skull. Note the metal rod (A) passing through the lateral margin of the bony external acoustic meatus (B). C indicates the medial edge of the bony external acoustic meatus. The tip of the metal rod (arrow) is through the cochlear window. This site must not be touched or subjected to direct pressure during procedures such as flushing the middle ear.

S indicates the septum bulla.

QuickNotes When the tympanic membrane is ruptured, ear medications and cleansers should be used cautiously and be nonototoxic.

The white lines indicate the lateral ventral edge and medial ventral edge of the bony external acoustic meatus. The distance between the lines varies from 7 to 15 mm and is narrower on the rostral side.

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FIGURE 12

FIGURE 13

Close-up view of the septum bulla showing the bony ossicles (arrows) on the free margin. FIGURE 15 View of the middle ear through the external acoustic meatus. P = promontory, S = septum bulla, C = cochlear window. FIGURE 14

Feline skull showing a needle going through the auditory tube into the tympanic cavity proper. The large, almost complete septum is seen ventral to the manubrium of the malleus.

two parts of the tympanic cavity communicate through a small opening in the caudal medial quadrant near the promontory and cochlear window (FIGURES 15 AND 16). Liquid medications instilled into the feline tympanic cavity are difďŹ cult to remove because they are trapped once they enter the ventromedial portion. View of the left middle ear from the ventral bulla, with an ear loop just over the medial ventral edge of the external acoustic meatus (E). If the tip of the ear loop drops over this edge, it has passed the normal attachment site of the ventral edge of the pars tensa on the tympanic ring. Note the promontory (P) and the cochlear window (C).

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Physiology The skin lining the ear canal is relatively smooth. Similar to the skin in most body regions, it has a thin epidermis and a dermis that contains adnexa (hair follicles and sebaceous and apocrine glands). The vertical canal has relatively more

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adnexa than the horizontal canal. To date, breed differences in the number of sebaceous glands have not been shown, although apocrine gland and hair follicle densities differ.3 The skin and adnexa constantly produce exfoliating corneocytes, intercellular material, and glandular secretions. This material forms cerumen (earwax), which is thought to play a protective role. IgA, IgG, and IgM have been identified in canine cerumen.4 IgG is the predominant immunoglobulin in both normal and inflamed ears. Its relative concentration increases significantly in the presence of disease. Cerumen also contains a wide variety of lipids, which may have some antimicrobial effects5; however, bacteria and yeast are present in normal ears. Cerumen is constantly being produced throughout the ear canal, and if it were to build up, blockage could result. However, there is a normal clearing mechanism: the movement of the epidermis. Epithelial migration, in which the surface of the skin lining the ear canal constantly moves from the tympanic membrane laterally to the external orifice of the ear canal (FIGURE 17),

FIGURE 16

Close-up photo of a feline middle ear viewed through the external acoustic meatus. Note the opening (O) in the septum that communicates with the larger ventromedial part of the tympanic cavity, the endotympanic part of the temporal bone. C = cochlear window, P = promontory.

has been shown in humans and guinea pigs.6 It seems likely that besides removing the cerumen, this process also facilitates the removal of sur-

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FIGURE 17 Illustrations depicting the migration of cerumen and surface epithelial cells from the deep ear canal to the external oriﬁce.

This process must function for an ear canal to remain healthy. With permission from Pfizer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.

face microorganisms and even small particulate dog and cat ears at 1000× magnification,1 I debris trapped in the sticky cerumen. consider bacteria excessive when more than Cytologic studies of normal ear cerumen five cocci or one rod per 1000× (oil immerhave produced variable results in numbers of sion) field is found. Normal numbers of yeast bacteria and yeast but have found essentially are even more controversial, although I conno inflammatory cells.7,8 These studies evalu- sider more than three organisms in dogs or ated samples at 400× dry field magnification, more than one in cats per oil immersion field not by oil immersion (1000×), which is my pre- to be increased. Rarely, up to 20 organisms per ferred magnification. It has been stated that 1000× field can be normal for an individual dog 400× magnification is not sufficient to identify or cat. However, these numbers are irrelevant all bacteria.9 Based on a published, non–peer- once multiple inflammatory cells are present, reviewed evaluation of cerumen from normal as this finding is abnormal. References 1. Scott DW, Miller WH Jr, Griffin CE. Muller and Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001. 2. Evans H. Miller’s Anatomy of the Dog. 3rd ed. Philadelphia: WB Saunders; 1993. 3. Stout-Graham M, Kainer RA, Whaler LR, Macy DW. Morphologic measurements of the external horizontal ear canal of dogs. Am J Vet Res 1990;51(7):990-994. 4. Huang HP, Little CJ, Fixter LM. Effects of fatty acids on the growth and composition of Malassezia pachydermatis and their relevance to canine otitis externa. Res Vet Sci 1993;55(1):119-123. 5. Huang HP, Fixter LM, Little CJ. Lipid content of cerumen from

normal dogs and otitic canine ears. Vet Rec 1994;134(15):380-381. 6. Johnson A, Hawke M. An ink impregnation study of the migratory skin in the external auditory canal of the guinea-pig. Acta Otolaryngol 1986;101(3-4):269-277. 7. Ginel PJ, Lucena R, Rodriguez JC, Ortega J. A semiquantitative cytological evaluation of normal and pathological samples from the external ear canal of dogs and cats. Vet Derm 2002;13(3):151-156. 8. Tater K, Scott DW, Miller WH Jr, Erb HN. The cytology of the external ear canal in the normal dog and cat. J Vet Med 2003;50:370-374. 9. Angus JC. Otic cytology in health and disease. Vet Clin North Am Small Anim Pract 2004;34(2):411-424.

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Successful Use of Probiotics in a Dog with Chronic Diarrhea Teresa A. Bessler, DVM Buffalo Veterinary Clinic Buffalo, Wyoming

Patient: Kodi, a 14-year-old American Eskimo dog History: When Kodi became my patient in August 2007, he had a 2-year history of kidney disease and was eating Purina Veterinary Diets® NF Kidney Function® canine formula to help manage his condition. He also had a long history of frequent bouts of watery diarrhea. Therapy Plan: Because of Kodi’s chronic kidney disease, I instructed the owners to continue feeding NF. I also prescribed 1 g of sucralfate twice daily for 5 days to treat a brief episode of anorexia and 250 mg of metronidazole twice daily for 5 days to resolve the diarrhea; metronidazole helped briefly, but the diarrhea returned. In October 2007, Kodi’s owners made an appointment to have him euthanized because of the chronic diarrhea. Kodi was having fecal accidents in the house, and the owners did not wish to pursue expensive diagnostics. I talked to them about Purina Veterinary Diets® FortiFlora® Canine Nutritional Supplement, and they agreed to try it. Kodi was given FortiFlora once daily, and Purina Veterinary Diets ® Gentle Snackers TM were allowed as treats. Outcome: Two weeks after adding FortiFlora to the diet, Kodi’s diarrhea had transformed into fairly firm stools. FortiFlora helped resolve the problem. At Kodi’s last evaluation, the chronic diarrhea hadn’t returned. 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.

Veterinarian’s Comments I have been recommending Purina Veterinary Diets® FortiFlora® as a nutritional supplement for the past 2 years. I find it to be very effective in cases of acute and chronic diarrhea and in patients on long-term antibiotic therapy. I estimate that I have used FortiFlora in at least 40 patients with a 90% success rate. I explain to owners that FortiFlora is a nutritional supplement that contains beneficial bacteria and promotes intestinal health. Owners appreciate that FortiFlora comes in premeasured packages and is simply sprinkled on top of the pet’s food. FortiFlora delivers good clinical results, and dogs and cats find it palatable; I have not had one owner tell me that his or her pet would not eat it. Kodi’s owners were very happy with the positive results obtained with FortiFlora. They told me the nutritional supplement had changed their lives and Kodi’s as well, and they wished they had known about FortiFlora sooner. Sponsored by

Fare Thee Well How to help owners (and yourself) deal with the death of a beloved pet*

❯❯ Amy I. Bentz, VMD, DACVIM Veterinary Learning Systems Yardley, Pennsylvania

❯❯ Christina Bach, MSW, LSW Director of Clinical Social Work and Pet Bereavement Services University of Pennsylvania

At a Glance Practice Being “The Gentle Doctor” Page 515

Remember the Five Stages of Grief Page 515

Recall the Veterinarian’s Oath Page 516

Express Your Sympathy Page 516

Seek Assistance Page 517

Avoid Burnout Page 517

*Adapted with permission from Compendium Equine 2009;4:267273.

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I hold it true, whate’er befall; I feel it, when I sorrow most; ‘Tis better to have loved and lost Than never to have loved at all. —In Memoriam A. H. H. (from Canto 27; 1849) by Alfred, Lord Tennyson Imagine the following: During an already hectic day, one of your best clients calls your ofﬁce and simply says, “Doc, it’s time.” You agree, reschedule your other appointment, and wait for the owner to arrive, knowing the scene that awaits. Your client’s beloved 12-yearold Labrador retriever, Buddy, has recently been losing weight, and you diagnosed lymphosarcoma as the cause. Now Buddy is recumbent and listless, so the owner has decided to have him euthanized. or During an already hectic day, one of your best clients calls you, crying, and says, “My daughter’s cat, Holly, jumped out of our yard, ran into the road, and was hit by a car. We are coming right over.” You and

your staff know the grim scene that awaits as the mother and daughter bring in their critically injured, beloved cat. Are you prepared to handle these situations? Would you know what to say to the owners? In the case of Buddy, could better planning have helped avoid disruption in your chronically packed schedule? This article on grief and euthanasia addresses some common questions small animal veterinarians have when counseling owners before and after they have their pets euthanized. In veterinary school, we are trained in the science of veterinary medicine. We learn how to diagnose, treat, and prevent various maladies, but we cannot learn the art of veterinary medicine until we begin to practice. After graduation, we quickly realize how vital it is to effectively communicate with clients to achieve the goal of treating our patients properly. It can be daunting to simultaneously handle a pet’s medical problem and the owner’s emotional concerns.1 When we deal with a tense situ-

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

Fare Thee Well ation such as euthanasia, the need to communicate effectively becomes even more critical. While personal communication styles differ, the information in this article can help even the most seasoned veterinarian handle euthanasia and grief more easily.

cal time for the veterinarian–client bond is when we recommend euthanasia for a critically ill pet. We cannot eliminate our clients’ pain, but we can decrease their grief and anxiety with patience and compassion.1 By spending a few minutes to explain and listen, we offer owners a chance to process information before making a permanent decision to euthanize their beloved pet. After euthanasia, this can help owners feel better about their decision.

FIGURE 1

Practice Being “The Gentle Doctor”

Our profession is held in high regard in our society, and by practicing compassionate care, we reafﬁrm our unique position as trusted professionals. “The Remember the Five Gentle Doctor” sculpture Stages of Grief by Christian Peterson at In On Death and Dying, the Iowa State University “The Gentle Doctor” by Christian Peterson. Dr. Elizabeth Kübler-Ross College of Veterinary Medi(Reprinted with permission from Iowa State described the ﬁve stages of cine depicts a caring veteri- University College of Veterinary Medicine) grief (TABLE 1). Although narian cradling a sick puppy while the mother dog looks up with concern not everyone experiences this process in the (FIGURE 1). This beautiful sculpture epitomizes same way and may not exhibit each stage, the compassion we should all have toward our these stages are common reactions to loss. patients and their owners. An especially criti- The owner’s emotions depend on whether TABLE 1

In veterinary school, we are trained in the science of veterinary medicine. We learn how to diagnose, treat, and prevent various maladies, but we cannot learn the art of veterinary medicine until we begin to practice.

The Five Stages of Grief

Stagea

The Owner’s Reaction

Recommended Response by the Veterinarian

1. Denial

The owner cannot comprehend the pet’s illness or impending death.1

Give the owner time to ask questions and think about your conversation so he or she can adjust to this new reality.3

The owner may seem dazed or confused and unable to make decisions.1 2. Anger

The owner may lash out at you or your staff and may refuse to pay the bill.1 Guilt may accompany this stage.1

Give the owner time to ask questions and process the new information so he or she can adjust to this new reality.3

3. Bargaining

The owner may ask for a second opinion or wish to pursue unusual treatments to attempt to gain control over the situation.3

Listen to the owner, acknowledge his or her feelings, be sympathetic, and explain treatment options so the owner can participate in the decision.3

4. Depression

This is the true stage of bereavement, when the owner mourns the loss of the dog or cat. This stage is marked by periods of crying and extreme grief.3

Listen to the owner and be sympathetic.3

5. Acceptance

The owner ﬁnally accepts the loss and may remember the pet with sadness but does not cry uncontrollably.1,3

—

QuickNotes

Kübler-Ross E. On Death and Dying. New York: Scribner; 1969.

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Fare Thee Well

QuickNotes Our profession is held in high regard in our society, and by practicing compassionate care, we reafﬁrm our unique position as trusted professionals.

the loss is sudden and tragic (as in the case of Holly) or involves gradual deterioration of the pet (as in the case of Buddy). Many owners are deeply attached to their companions and view them as beloved members of their family. They may have owned a pet for 10 years or more, and its loss will leave a large void in their lives. It is also common for a pet to represent a special time in a person’s life. For example, when single people who own pets marry and begin a family together, the pets live in that family for years and are often living reminders of the special history shared by the family. The recent hit book (and movie) Marley and Me is an excellent representation of this scenario. The situation is even more complex if the dog or cat is loved by a child and the parents look to you for comfort and advice. When speaking with your clients, remember that they may be experiencing a variety of emotions. If they are considering having their pet euthanized, they may need some time to adjust to the idea. If the dog or cat is not critically ill, it may be helpful for the clients to think about the decision to eutha-

BOX 1

Additional Resources American Veterinary Medical Association ` “How do I know it is time?” (brochure) www.avma.org/animal_health/ brochures/euthanasia/pet/pet_euth_ brochure.pdf ` “Understanding your feelings of loss when your animal dies” (brochure) www.avma.org/animal_health/brochures/ pet_loss/pet_loss_brochure.pdf The Argus Institute for Families and Veterinary Medicine College of Veterinary Medicine & Biomedical Sciences Colorado State University www.argusinstitute.colostate.edu (Grief information for veterinarians and pet owners) The Veterinary Social Work Program at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania www.vet.upenn.edu/RyanHospital/ VeterinarySocialWork/tabid/255/Default.aspx

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nize and to call family and friends before giving permission. When dealing with geriatric pets, such as Buddy, it is often important to discuss the pet’s deterioration with the owners. Older dogs or cats in poor body condition that are not responding to treatment, feeding, or management changes often have increasing trouble walking and may slip and fall. The owner may not recognize the pet’s gradual deterioration or the potential consequences. If the owner is given time to think about euthanasia and decides to have it performed, other family members might want to be present. The owners may choose to euthanize their pet when all can be present, so the family can say good-bye together. This offers an opportunity to schedule your time appropriately to prepare for the procedure and avoid interruptions. Each situation is an opportunity to serve our patients and their owners.

Recall the Veterinarian’s Oath “Being admitted to the profession of veterinary medicine, I solemnly swear to use my scientific knowledge and skills for the benefit of society through the protection of animal health, the relief of animal suffering…”2 Although grief and euthanasia are difficult, we can end a dog or cat’s suffering and bring some comfort to owners and caretakers, especially in catastrophic situations. When I (A. I. B.) was in private practice, one of my worst cases requiring euthanasia involved a handsome, young chocolate Labrador retriever puppy. He developed acute renal failure and did not respond to treatment, so the owners decided to euthanize him. Although the scenario was very tragic, I was grateful to offer some small measure of comfort to the family at a difficult time.

Express Your Sympathy There are no perfect words to say to owners experiencing loss. Often, the best approach is to express your sympathy and listen to the owner. Sending a card and/or ﬂowers is an excellent way to express your condolences.3,a If you knew the pet well, write down a mema

Drs. Tamera McNamara, Jennifer Proctor, Cathleen Lombardi, Jean Feldman, and Valerie Devaney. Personal communication, Veterinary Information Network, January 30, 2009, through February 1, 2009.

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Fare Thee Well ory or two, and the card will be treasured by the owner. Some practices call clients to check on them a few days after their pet was euthanized. This can be very helpful for owners who may need reassurance that they made the correct decision. Some practices offer ways to memorialize the patient for the family, such as a paw print casting or lock of hair; additional options include making a donation to an animal shelter or a research fund and sending a card to notify the owner.

Seek Assistance The human–animal bond is increasingly recognized in our society as a powerful and unique relationship.1,4 This bond offers much-needed comfort and companionship in our hectic lives, even improving our mood and blood pressure! However, when our beloved animals are experiencing terminal suffering, the topic of euthanasia should be addressed (BOX 1). Many veterinary schools offer a pet loss support hotline (BOX 2) and support groups for small animal owners experiencing the loss of a pet. For example, the University of Pennsylvania School of Veterinary Medicine offers a program for pet owners, including grief counseling and bereavement. I (C. B.) teach veterinary students to be aware of ﬁve common reactions clients may exhibit after their pet has died or

TABLE 2

been euthanized (TABLE 2). I also tell my students, “People need to want help; they will seek you out if they require more assistance.” If an owner is demonstrating a persistent need to discuss his or her pet’s disease and death, it may help to refer the owner to a health professional. Children are often very attached to the family pet, so it can be very traumatic for a child to lose a dog or cat. Honesty is the best policy when explaining the pet’s death to a child, but use developmentally appropriate language.5 The child wants to understand what happened, so use simple terms; however, do not say, “The dog or cat was put to sleep,” because the child may become afraid to sleep. The child needs time to grieve and may want to memorialize the beloved animal by making a scrapbook, having a memorial service, or burying the pet’s ashes. It is important for parents to inform school ofﬁcials that their child has lost a pet. If behavioral changes or depression are noted, the child may need to talk with a professional counselor.

Avoid Burnout It is vital for you to maintain your mental health. You may have treated a dog or cat for years, becoming like a member of its family, so you also may experience grief at its death.6

Five Common Client Reactions to Pet Lossa

Client Reaction

Example

Recommended Response by the Veterinarian

1. Guilt

The owner may ask, “Did I wait too long to euthanize, or did I euthanize too quickly?” The owner may feel guilty months after the pet’s death and may contact you for reassurance.

Listen to the owner and reassure him or her that the correct decision was made.

2. Shame

The owner may feel ashamed to tell anyone or may be afraid someone will say, “It was only an animal, you can always get another one.”

Reassure the owner that the pet is unique or special and will not be replaced by a new addition.

3. Relief

If the animal dies before the owner makes a decision to euthanize, the owner may feel relief that he or she did not have to make the ﬁnal decision to end the pet’s life.

—

4. Loneliness

—

Be sympathetic and supportive. Provide a list of pet loss support hotlines and other resources.

5. Yearning

—

Be sympathetic and supportive. Provide a list of pet loss support hotlines and other resources.

QuickNotes An especially critical time for the veterinarian–client bond is when we recommend euthanasia for a critically ill pet. We cannot eliminate our clients’ pain, but we can decrease their grief and anxiety with patience and compassion.

Developed by Christina Bach, MSW, LSW, Director of Clinical Social Work and Pet Bereavement Services, University of Pennsylvania.

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Fare Thee Well BOX 2

Pet Loss Support Hotlinesa `352-392-4700, then dial 1 and 4080; staffed by Florida community volunteers; weekdays, 7:00 PM to 9:00 PM Eastern time; or 352-392-4700, ext 4744, at the University of Florida

`517-432-2696; staffed by Michigan State University veterinary students; Tuesday through Thursday, 6:30 PM to 9:30 PM Eastern time; cvm.msu.edu/ petloss/index.htm

`630-325-1600; staffed by Chicago Veterinary Medical Association veterinarians and staffs; leave voice mail message; calls will be returned 7:00 PM to 9:00 PM Central time; long-distance calls will be returned by collect call

QuickNotes Honesty is the best policy when explaining the pet’s death to a child, but use developmentally appropriate language.

`540-231-8038; staffed by VirginiaMaryland Regional College of Veterinary Medicine; Tuesday, Thursday, 6:00 PM to 9:00 PM Eastern time

`614-292-1823; staffed by The Ohio State University veterinary students; Monday, Wednesday, Friday, 6:30 PM to 9:30 PM Eastern time; voice-mail messages will be returned by collect call during operating hours

`508-839-7966; staffed by Tufts University veterinary students; Monday through Friday, 6:00 PM to 9:00 PM Eastern time; voice-mail messages will be returned daily (by collect call outside of Massachusetts); www.tufts.edu/vet/petloss

`888-ISU-PLSH (888-478-7574); hosted by the Iowa State University College of Veterinary Medicine; operational 7 days/week, 6:00 PM to 9:00 PM Central time from September through April and Monday, Wednesday, Friday, 6:00 PM to 9:00 PM Central time from May through August

`607-253-3932; staffed by Cornell University veterinary students; Tuesday through Thursday, 6:00 PM

to 9:00 PM Eastern time; messages will be returned; www.vet.cornell.edu/Org/PetLoss

`217-244-2273 or 877-394-2273 (CARE); staffed by University of Illinois veterinary students; Sunday, Tuesday, Thursday, 7:00 PM to 9:00 PM Central time; www.cvm.uiuc.edu/CARE

`970-491-4143; Argus Institute grief resources, Colorado State University `509-335-5704; Washington State University College of Veterinary Medicine; staffed during the semester on Monday through Thursday, 6:30 PM to 9:00 PM, and Saturday, 1:00 PM to 3:00 PM Paciﬁc time; www.vetmed.wsu.edu/PLHL a

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Accessed February 2009 at www.avma.org/careforanimals/animatedjourneys/goodbyefriend/plhotlines.asp.

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Fare Thee Well It is important to recognize these feelings and express them in your own way. Owners will be very touched to see your grief and compassion at the loss of their pet, forging a stronger bond between them and you. However, it is equally important to take time to refresh yourself and maintain perspective. See BOX 1 for additional resources to help yourself and your clients.

Conclusion Our companion animal patients are often treasured members of the family and are mourned when they die or are euthanized. We hope the information in this article will help you practice the art of veterinary medicine when handling grief and euthanasia.

Additional Reading Barton Ross C. Pet Loss and Human Emotion: Guiding Clients Through Grief. Philadelphia: Taylor & Francis; 1998. Kübler-Ross E, Kessler D. On Grief and Grieving: Finding the Meaning of Grief Through the Five Stages of Loss. New York: Scribner; 2005. Lagoni L, Butler C, Hetts S. The HumanAnimal Bond and Grief. New York: Harcourt Brace; 1994. Toray T. The human-animal bond and loss. J Ment Health Counseling 2004;26:244-259.

References 1. Lawrence EA. Euthanasia and the human–equine bond. Equine Pract 1993;15(10):34-44. 2. Veterinarian’s oath. Adopted by the House of Delegates, July 1969; amended by the Executive Board, November 1999. Accessed February 2009 at www.avma.org/about_avma/whoweare/oath.asp. 3. Brackenridge SS, Shoemaker RS. The human/horse bond and client bereavement in equine practice, part 2. Equine Pract 1996;18(2):23-25. 4. Brackenridge SS, Shoemaker RS. The human/horse bond

Editorial

QuickNotes It is important for parents to inform school ofﬁcials that their child has lost a pet. If behavioral changes or depression are noted, the child may need to talk with a professional counselor.

and client bereavement in equine practice, part 1. Equine Pract 1996;18(1):19-22. 5. Brandt JC, Grabill CM. Communicating with special populations: children and older adults. Vet Clin North Am Small Anim Pract 2007;37(1):181-198. 6. Brackenridge SS, Shoemaker RS. The human/horse bond and client bereavement in equine practice, part 3. Equine Pract 1996;18(4):20-23.

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Increased accessibility to in vitro allergy testing for atopic dermatitis, which has resulted in more pets receiving allergen-speciﬁc immuno-therapy. Advances in dermatopathology and immunohistopathology as tools for diagnosing and understanding disease pathogenesis, thereby promoting the development of improved therapeutic and management techniques. Use of lasers in a variety of therapeutic modalities for inﬂammatory and neoplastic skin diseases. New pharmacologic agents, including systemic and topical parasiticides, antimicrobials, and topical therapeutics with improved delivery systems. Greater understanding of the role of nutrition in skin structure, function, and disease, which has led to improved dietary options for managing many dermatologic problems. Greater understanding of the pathogenesis and management of feline and equine skin diseases. The adage “as long as you can use glucocorti-

coids, you can be a veterinary dermatologist” has never been further from the truth. In reality, veterinary dermatologists specialize in how to avoid or decrease systemic glucocorticoid use. We encourage all general practitioners to attend CE meetings and stay current with the veterinary literature to be kept up-to-date with this amazing, ever-expanding specialty. References 1. Scott DW, Miller WH, Grifﬁn CE. Small Animal Dermatology. 6th ed. Philadelphia: Saunders; 2001. 2. Ralston Purina Company. An Introduction to the Nutrition of Dogs and Cats. Trenton, NJ: Veterinary Learning Systems; 1989. 3. Alpo Veterinary Panel. Dermatological problems head problem list. DVM Magazine August 1985. 4. Scott DW, Paradis M. A survey of canine and feline skin disorders seen in a university practice: Small Animal Clinic, University of Montreal, Saint-Hyacinthe, Quebec (1987-1988). Can Vet J 1990;31:830. 5. Veterinary Pet Insurance. Sick as a dog: pets’ top medical conditions of 2008 [press release]. Accessed October 2009 at http:// press.petinsurance.com/pressroom/266.aspx.

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

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3 CE CREDITS

CE Article 2

Acute Postrenal Azotemia: Etiology, Clinicopathology, and Pathophysiology ❯❯ Julie R. Fischer, DVM, DACVIM Veterinary Specialty Hospital—San Diego

❯❯ India F. Lane, DVM, MS, DACVIM

❯❯ Jennifer Stokes, DVM,

Abstract: When rupture or obstruction of the urinary tract prevents the normal collection and expulsion of urine from the body, the resulting azotemia is termed postrenal. Postrenal azotemia can coexist with prerenal and/or renal azotemia. Detection of postrenal azotemia requires attentiveness to the history and physical examination ﬁndings and to the results of speciﬁcally directed diagnostic tests. Prompt correction of postrenal causes of azotemia limits the potential for intrinsic renal damage and can contribute to a positive clinical outcome; therefore, postrenal azotemia should be investigated in all azotemic patients.

DACVIM University of Tennessee

P At a Glance Etiologies Page 520

History and Physical Examination Page 524

Clinicopathology Page 525

Pathophysiology of Urinary Tract Obstruction Page 526

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rompt and accurate assessment of the origins of azotemia—prerenal, renal, and/or postrenal—is essential to the proper management of azotemic patients. Prerenal azotemia occurs when decreased renal perfusion results in a diminished glomerular filtration rate (GFR); common causes of prerenal azotemia include volume depletion, vascular collapse, thrombotic diseases, and shock (cardiogenic, hemorrhagic, hypovolemic, or septic). Renal azotemia occurs when nephrons are directly damaged, most frequently by toxic, infectious, in flammatory, ischemic, or neoplastic processes. Postrenal azotemia is caused by urinary tract breach or obstruction. Any process distal to the renal tubules that interferes with the collection, containment, or excretion of urine can result in azotemia by preventing elimination of waste material in the urine, which can rapidly result in life-threatening fluid, electrolyte, and acid–base imbalances. Conditions causing prerenal and postrenal azotemia can also result in intrinsic renal damage if not identified and corrected. Postrenal azotemia can be acute or chronic; this article addresses acute azote-

mia. Because causes of postrenal azotemia interfere with normal urine collection and elimination from the body, their identiﬁcation is critical not only to determining deﬁnitive therapeutic strategies but also to developing appropriate stabilization and treatment plans.

Etiologies Urinary Tract Obstruction Obstruction of the lower urinary tract (LUT) is a common urologic emergency that results in signiﬁcant azotemia in cats more often than in dogs. LUT obstruction can usually be diagnosed based on the history and palpation of a turgid, painful urinary bladder during physical examination. Most owners report that the pet has made unproductive attempts to urinate, often associated with discomfort. In cats, stranguria is sometimes mistaken for a sign of constipation. Most LUT obstruction in dogs is caused by urolithiasis or neoplasia; most LUT obstruction in cats is caused by urolithiasis or urethral mucocrystalline plugs.1,2 Urethral obstruction by uroliths is more common in male dogs than in female dogs because of several anatomic characteristics:

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Acute Postrenal Azotemia CE a smaller relative urethral diameter and longer urethral length, the curving course of the urethra around the ischium, and the presence of the os penis along the distal urethra, limiting expansion of the urethral diameter. Uroliths most often lodge at the ischial arch or just proximal to the os penis.1 Calcium oxalate and ammonium urate stones are most frequently implicated in urethral obstruction; their relatively small size and tendency to occur as multiple stones, along with the increased incidence of oxalates and urates in male dogs, likely factor into this predilection (FIGURE 1). Transitional cell carcinoma is the most common neoplasm of the canine LUT.3 Most transitional cell carcinomas occur at the trigone of the bladder or at the prostatic urethra; a tumor at either location can lead to LUT obstruction. Prostatic carcinoma should be ruled out in any male dog with LUT obstruction and is the primary differential in a castrated dog with prostatomegaly.4 Proliferative urethritis is an infiltrative chronic inflammatory disease that can mimic urethral neoplasia and cause LUT obstruction. It is more common in female dogs than in males. Proliferative urethritis may cause a valve-like urethral obstruction that allows passage of a urinary catheter but precludes normal antegrade urine flow.5 Although proliferative diseases of the urethra and bladder outlet frequently lead to LUT obstruction, they rarely cause acute azotemia, unless the proliferative tissue suddenly obstructs the ureterovesicular junctions. The slow progression of proliferative disease generally produces recognizable clinical signs before obstruction is complete. Obstruction of the upper urinary tract (UUT) is an increasingly common cause of azotemia, particularly in cats, and one that can only be definitively diagnosed by specific imaging of the kidneys and ureters.6 Congenital obstruction of the UUT, usually stenosis of the ureteropelvic junction or ureterovesicular junction, is very rare in dogs and cats, as it is in people. Acquired obstruction can be due to intraluminal, extraluminal, or intramural causes, including uroliths, nonmineralized material, trauma, neoplasia, proliferative disease, ureteroceles, inflammation, fibrosis, stricture, and inadvertent surgical trauma or ligation.7 For UUT obstruction to produce azotemia, bilat-

FIGURE 1 Radiographs of urethroliths in a 13-year-old intact male Yorkshire terrier.

Lateral view showing urethroliths (white arrows) and a possible urocystolith (yellow arrow). In this ventrodorsal view, the possible urocystolith (yellow arrow) is lateralized; it was later confirmed to be located in the right ureter. The urethroliths are also visible (white arrows).

eral kidney disease—either bilateral obstruction or unilateral obstruction with dysfunction or absence of the contralateral kidney—must be present. The obstruction may be partial or complete; azotemia can be acute and profound or chronic and mild/progressive.

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FREE CE Acute Postrenal Azotemia

FIGURE 2

Bisectional view of a feline kidney at necropsy. Multiple nephroliths (arrows) can be seen in the dilated renal pelvis. These stones were composed of 100% dried, solidified blood.

QuickNotes Although initially reversible, upper urinary tract obstruction initiates cytochemical cascades that culminate in interstitial ﬁbrosis and irreversible loss of function if not quickly corrected.

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The most common cause of UUT obstruction is urolithiasis, and the most common component of UUT stones in dogs and cats is calcium oxalate (CaOx).7–10 Presentation of cats for management of ureterolithiasis increased steadily over the 18 years of a recent study by Kyles et al,6 leveling to a relatively stable rate during the last 3 years studied and paralleling trends in cats presenting for hemodialysis.11 The incidence of CaOx urolithiasis has increased dramatically in the past 10 years, to the point that >90% of analyzed nephroliths and ureteroliths are composed of this mineral.8–10 CaOx stones are formed in the parenchyma of the kidneys and may remain there or pass into the ureters and bladder. The formation of CaOx stones is inﬂuenced by many factors, including the degree of urine saturation with calculogenic minerals, urinary inhibitors of crystallization and crystal aggregation and growth, and urinary promoters of crystal aggregation and growth.8,12 UUT obstruction with uroliths is chieﬂy diagnosed in cats and small dogs. The ureters of medium-sized and larger dogs can accommodate the passage of stones up to several millimeters in diameter; the feline ureteral lumen measures approximately 0.4 mm and may be obstructed by much smaller objects.7 Some patients that present with acute, severe postrenal azotemia due to UUT obstruction have simultaneous, acute bilateral obstruction; however, many present with acute obstruction of

FIGURE 3

Ultrasonography image showing a transverse section of a kidney in a 3-year-old Labrador retriever with disseminated aspergillosis. The renal pelvis, ureteropelvic junction, and proximal ureter are filled with a large fungal granuloma (dotted yellow line) that obstructs the flow of urine into the ureter.

a single functional kidney. These animals usually have permanent partial or complete dysfunction of one kidney, either from clinically silent or subtle unilateral obstruction or from another cause. In these patients, the contralateral kidney has hypertrophied to compensate for the functional decrement, and obstruction of this single functional kidney has resulted in acute azotemia. Physical examination of these patients may find renal asymmetry: the smaller kidney is firm, atrophied, and nonpainful; the larger kidney is resilient, obstructed, and often painful. In Kyles’ study,6 56% of the cats that presented with unilateral ureteral obstruction were found to have a small contralateral kidney on ultrasonography. Some astute owners detect subtle behavioral signs accompanying initial unilateral UUT obstruction, including antisocial behavior, flank licking, and back or abdominal pain, leading to earlier diagnosis of nephrolithiasis or ureterolithiasis. The UUT may also be obstructed by nonmineralized material. A retrospective study13 evaluated 49 cats with urinary calculi composed entirely of dried, solidified blood (DSB; FIGURE 2). DSB calculi may occur as one or many small to medium-sized calculi anywhere in the urinary tract. Most often, DSB calculi are not the result of a known urinary tract bleed but are discovered during evaluation of the urinary tract for obstructive or other clinical signs. However, moderate to marked microscopic hematuria was present on all urinalyses evaluated in this retrospec-

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Acute Postrenal Azotemia CE tive study. The median age of the 49 affected cats was 9 years (range: 1 to 15 years), and the male:female ratio was 2.5:1. Approximately 40% of DSB stones were recovered from the UUT; it was unknown whether DSB stones found in the LUT formed there or passed from the UUT into the bladder. No causative factors for DSB calculi were identified in the study, although investigation of possible systemic and local infectious, inflammatory, ischemic, or traumatic factors that could contribute to hematuria seems warranted in these cases.13 The growing detection of DSB calculi also highlights questions surrounding management of microscopic renal hematuria in cats. UUT obstruction with clotted blood may occur secondary to trauma, renal biopsy that penetrates into the renal pelvis, or renal hematuria. Accumulated debris (e.g., exudate from inflammation or ureteral trauma, fungal granuloma, sloughed renal papillary tissue from infection or ischemic insult) may also result in a soft, nonmineralized UUT obstruction (FIGURE 3). Sloughed, necrotic renal papillary tissue secondary to NSAID administration has been documented to occasionally result in ureteral obstruction in humans.14,15 There is little literature-based information regarding this type of obstruction in dogs and cats, but in our experience, such obstruction may occur due to acute pyelonephritis, acute renal tubular necrosis from a toxic insult (e.g., lily toxicosis), or intraluminal trauma from the presence or passage of stones. Experientially, these obstructions often occur proximally in the UUT, may be acutely bilateral, and can often be milked to a dilated region of the ureter or to the ureteropelvic junction for removal. Recurrence seems uncommon with appropriate management of the underlying disease. Ureteral damage (inflammation, mineralization, fibrosis, stricture) can also cause progressive complete or partial obstruction. Iatrogenic ureteral damage, including ligation, transection, crushing, or devascularization, is an infrequently reported risk of abdominal surgery. Such damage occurs most often in the course of uterine body ligation during ovariohysterectomy in dogs and cats, particularly when the bladder is distended and the ureters are slackened by cranial displacement of the trigone, but it is possible in the course of any abdominal, particularly caudal abdominal,

FIGURE 4

Lower urinary tract and ureters of a young female cat presented for anuria of 3 days’ duration after routine ovariohysterectomy. During surgery, the horns of the uterus were ligated together (white arrow), encircling the trigone and the distal ureters (reflecting the ureters caudally, black arrows), thus completely obstructing the bladder outflow as well as compressively obstructing both ureters.

surgery.16 Ureteral entrapment during ovariohysterectomy is best avoided by visualization of the isolated uterine body before ligation.16 We have observed bilateral ureteral occlusion caused by direct ureteral entrapment during closure of caudal cystotomy incisions and by pressure of overzealous closure on the ureterovesicular junction (FIGURE 4). Often, iatrogenic ureteral trauma is not detected during surgery but becomes apparent in the postoperative period, requiring surgical revision. If ureteral entrapment, compression, or other nonpenetrating damage is noted and corrected during the initial surgery, ureteral patency and serum biochemistry can be monitored postoperatively. Many of these injuries do not require surgical revision if immediately addressed. Postoperative progressive ascites, azotemia, and/or dilation of the ureter or renal pelvis mandate prompt and aggressive evaluation, potentially including cytologic and biochemical assessment of ascites, excretory urography/ antegrade pyelography, retrograde cystography, and exploratory laparotomy. Primary ureteral neoplasia is rare in dogs,

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FIGURE 5

QuickNotes Blunt trauma and urethral catheterization are the most common causes of urinary tract rupture.

Computed tomography image from a young adult spayed dog that presented with uroabdomen after vehicular trauma. Intravenous contrast administration shows a rupture of the right proximal ureter with contrast accumulation around the right kidney (yellow arrow). Contrast medium is present within the pelvis of the left kidney (white arrow).

although transitional cell carcinoma, leiomyoma, leiomyosarcoma, ﬁbropapilloma, and other primary ureteral tumors have been reported, as has metastasis to the ureter.7 Primary ureteral neoplasia is even less common in cats. More commonly, prostatic and trigonal neoplasia, usually adenocarcinoma or transitional cell carcinoma, can spread to encompass and obstruct the ureter(s), as can retroperitoneal neoplasia.

Urinary Tract Rupture Rupture of the UUT or LUT results in partial or complete inability to void urine. Depending on the site of the rupture, urine may collect in the retroperitoneal space, peritoneum, or subcutaneous tissues, and presenting clinical signs may be associated with the inciting trauma, uremia, chemical irritation of the tissues where urine collects (e.g., cellulitis, urine peritonitis), or, if the urine is infected, septic complications. Causes of ureteral rupture include blunt or penetrating trauma, inadvertent damage during laparoscopy or laparotomy, damage from calculi, and neoplasia or infection.17 Ureteral damage from blunt or penetrating trauma is relatively uncommon because the retroperitoneal space is protected by the spine

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and lumbar musculature, although unilateral and bilateral ureteral ruptures due to vehicular trauma have been reported.18 The incidence of ureteral injury in dogs sustaining blunt pelvic trauma has been reported at 4%.19 Rupture of the proximal ureter results in uroretroperitoneum if the peritoneal membrane partitioning the retroperitoneum is intact. If the retroperitoneal membrane or distal ureter is also ruptured, uroabdomen results (FIGURE 5). Rupture of the bladder or urethra is most commonly secondary to caudal abdominal trauma (often associated with pelvic fractures), instrumentation (usually catheterization) of the urethra, or application of excessive pressure during manual expression of urine.1,20,21 Preexisting urinary tract pathology, such as urethral or bladder tumors or bladder wall damage due to prolonged urethral obstruction, can cause LUT rupture directly or can compromise structural integrity and predispose the affected area to rupture with instrumentation or compression. Spontaneous rupture of a necrotic or damaged bladder wall is uncommon.20 In dogs, the most common cause of urethral rupture is vehicular trauma; in cats, it is trauma secondary to urethral catheterization.21

History and Physical Examination Once azotemia is documented, the history and physical examination frequently provide initial evidence supporting a postrenal component. The history should include the owner’s observations of urination behavior, including frequency, amounts voided, and any clinical signs associated with voiding (e.g., anuria, dysuria, hematuria, stranguria, pollakiuria). Any prior UUT or LUT disease (e.g., urinary tract infection, incontinence, polyuria, vaginal discharge) should be detailed, including any diagnoses and therapies instituted. Known trauma and potential for trauma should be investigated. Mild azotemia may be clinically silent, and the patient may present for signs associated with the causative factor (e.g., trauma with multiple fractures and bladder rupture) rather than for signs associated with uremia. Patients with severe postrenal azotemia, however, are more likely to present with uremic signs, including hyporexia, weight loss, vomiting, lethargy, mild to moderate obtundation, and uremic or fetid breath. Signiﬁcantly uremic patients are usually hypothermic from interference of uremic toxins

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Acute Postrenal Azotemia CE with normal thermoregulation, unless a cause of systemic inflammation (e.g., pyelonephritis, neoplasia) is present. Uremic or fetid breath, xerostomia, or oral ulcerations (particularly on the ventrolateral tongue margins) may be present on oropharyngeal examination. Abdominal palpation may detect renal or bladder pain or suggest ascites. The physical examination should include surveillance for excoriations, lacerations, fractures, sheared claws, or other evidence of trauma. Examination of the urinary and genital tracts must be systematic and thorough. Renal size, shape, symmetry, and consistency should be assessed as possible, as should pain associated with renal or paralumbar palpation. More than half of cats with ureteral obstruction have renal asymmetry.6,22 Characteristics of the urinary bladder, including size, turgidity, pain on palpation, and ability to be expressed (if full), should be noted. Most patients with postrenal azotemia due to urethral obstruction resent abdominal palpation and present with a hard, painful urinary bladder that cannot be expressed, while approximately half of patients with bladder rupture present with no palpable bladder.23 Digital vaginal examination may detect neoplasia affecting the distal urethra or urethral orifice. Digital rectal examination in dogs permits evaluation of the size and consistency of the pelvic urethra, which should be smooth and mobile; uroliths may be palpable in the pelvic urethra, and some fractures of the pelvic outlet are palpable per rectum. In most male dogs, the prostate is accessible per rectum; in intact dogs, prostatic size, consistency, symmetry, and pain should be evaluated.4 In larger dogs, use of the nondominant hand on the caudal abdomen to caudally displace the bladder during digital rectal examination may permit easier and more complete prostate palpation. In peripubertally castrated dogs, a subtle thickening in the prostatic region may be palpable; the presence of an easily palpated, distinct prostate should raise a strong suspicion of neoplasia. The penis should be extruded in male dogs (and, if possible, cats) and examined for patency and the presence of stone or crystalline material at the orifice.

Clinicopathology The clinicopathologic sequelae associated with postrenal azotemia may range from mild to life-threatening. Because the kidneys are

the chief organs of elimination for nitrogenous waste products, as well as for phosphate, potassium, and many other dissolved solutes, the earliest derangements seen are usually elevations in the concentrations of blood urea nitrogen (BUN), creatinine, phosphorus, and, with complete obstructions, potassium. With complete obstruction, normal hydrogen ion excretion is prevented, resulting in metabolic acidosis, which manifests on the biochemical proﬁle as decreased serum bicarbonate concentration and on blood gas analysis as a decreased bicarbonate concentration, negative base excess, and decreased pH.

Biochemical Changes The biochemistry of acute postrenal azotemia has been best characterized in cats with UUT or LUT obstruction. In a retrospective study6 of 163 cats presented for ureteral calculi, only 83% of the cats were azotemic. At presentation, 48% were anemic (median packed cell volume: 29%, range: 11% to 51%) and 35% were hyperkalemic (median potassium concentration: 4.4 mmol/L; range: 2.8 to 9.4 mmol/L); BUN concentrations ranged from 19 to 456 mg/dL (median: 71 mg/dL); and creatinine concentrations ranged from 1 to 32.9 mg/dL (median: 4.4 mg/dL). In another review of 11 cats with ureteral obstruction,24 the median BUN concentration was 149 mg/dL and the median creatinine level was 10.2 mg/dL. In a review of 50 cats presented for hemodialysis because of azotemia due to ureteral obstruction,25 the median BUN concentration was 238 mg/dL (range: 68 to 456 mg/dL), median creatinine concentration was 17.4 mg/dL (range: 8.4 to 34.4 mg/dL), median potassium concentration was 6.8 mmol/L (range: 2.1 to 10.9 mmol/L), and median phosphorus concentration was 15.6 mg/dL (range: 1.1 to 27.6 mg/dL). In an evaluation of 223 male cats with urethral obstruction,26 69% of the cats were azotemic (deﬁned as a BUN concentration greater than the reference range) at the time of presentation. The BUN concentration ranged from 10 to 100 mg/dL (100 mg/dL was the upper detection limit of the analyzer used). Of these cats, 40% were acidemic (median venous pH: 7.29, range: 7.02 to 7.45) and 41% were hyperkalemic (median potassium concentration: 5.2 mmol/L, range: 3.4 to 10.5 mmol/L). Ionized calcium (iCa2+) levels were

QuickNotes The occurrence of upper urinary tract obstruction in cats has increased tremendously in the past 15 years, coincident with the increase in feline calcium oxalate urolithiasis.

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QuickNotes Although hematuria is commonly observed with urinary tract rupture, lack of hematuria does not rule out this possibility.

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low in 34% of cats (median iCa2+ concentra- Pathophysiology of Urinary Tract tion: 1.10 mmol/L, range: 0.57 to 1.6 mmol/L). Obstruction Ionized hypocalcemia may be related to acute Upper Urinary Tract Obstruction retention of phosphorus in these patients. The current understanding of obstructive Hyperphosphatemia was present in 25% of the nephropathy is largely based on rat, dog, cats (median phosphorus concentration: 5.0 and other laboratory models.28 The type and mg/dL, range: 2.8 to 20 mg/dL), but this mea- degree of kidney damage that result from uresurement was not necessarily obtained at the teral obstruction depend on a complex intersame time as the iCa2+ level was determined. play of physical and cytochemical factors, the Hyperglycemia was present in 54% of all cats duration and completeness of obstruction, pre(median glucose level: 175 mg/dL, range: 31 existing renal pathology, patient species, and to 378 mg/dL), likely due to release of stress- function of the contralateral kidney.28 In modinduced hyperglycemic agents (e.g., cortisol, els of complete ureteral obstruction, duration epinephrine), and to uremia-associated car- of obstruction is the most significant variable bohydrate intolerance. In this study, hyper- influencing functional recovery after relief of kalemia was directly correlated with azotemia, obstruction. Mechanical obstruction of urine acidemia, and decreased iCa2+, while ion- flow initiates a rapid, dramatic reduction in ized hypocalcemia was positively correlated GFR, development of interstitial inflammation with acidemia.26 Because acidemia normally and edema, and, if unchecked, tubular atroincreases iCa2+, these two parameters likely phy, fibrosis, and apoptotic renal cell death. have a correlative but not causative relationship in this clinical scenario. Ionized hypocal- Hemodynamic Effects cemia may be induced by a mass-law response Acute obstruction causes ureteral peristalsis to to acute hyperphosphatemia; the acidemia increase and intraluminal ureteral and tubular chiefly results from inability to renally excrete pressures to rise rapidly.29 The rise in proximal hydrogen ions and impaired renal bicarbonate tubular pressures induces production of prosresorptive capacity. The magnitude of both of taglandin E2 and prostacyclin and renal capilthese processes would relate directly to the lary endothelial release of nitric oxide (NO). severity and duration of the decline in GFR, Collectively, these substances cause afferent arteriolar dilation and increased renal blood explaining the appearance of correlation. flow. Glomerular capillary hydraulic pressure Urinalysis (Pgc) increases in response, but the increase Urinalysis findings in dogs and cats with post- in proximal tubular pressure and Bowman’s renal azotemia vary. Because intrinsic renal capsule pressure exceeds the increase in Pgc, damage is not necessarily present, urine may resulting in decreased net ultrafiltration presbe dilute or concentrated, and the urinary pH sure. GFR declines rapidly once renal pelvic can vary through the range of physiologic pressure exceeds 20 mm Hg and may be only possibility. Hematuria, often grossly appar- 20% to 50% of normal after 24 hours of coment, is a common finding in animals with LUT plete obstruction.28,30,31 Acute UUT obstruction initiates a series obstruction. Although hematuria is commonly observed with urinary tract rupture, lack of of renal events that collectively increase vashematuria does not rule out this possibility.27 cular resistance. Within 5 hours of complete Microscopic hematuria may be present with obstruction, sodium delivery to the distal UUT obstruction; gross hematuria is uncom- tubules is decreased, juxtaglomerular renin mon. Crystalluria may be associated with the release is stimulated, and local and peripheral underlying etiology (e.g., struvite crystalluria angiotensin II (Ang II) production is increased, in a cat with a mucocrystalline urethral plug) causing increasing peripheral arterial as well or incidental to it (e.g., calcium oxalate crystal- as renal arterial resistance. The effect of Ang luria in a dog with prostatic adenocarcinoma). II on the efferent arterioles exacerbates the For some causes, such as ureteral obstruction, increased Pgc but has no functional effect on early detection and correction can limit the net ultrafiltration pressure because of the impact on the kidney and prevent or minimize increased Bowman’s capsule pressures. Ang the development of secondary renal azotemia. II also generates oxidative stress, increasing

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Acute Postrenal Azotemia CE NO catabolism and thus decreasing local NO levels.29 Tubular epithelial cells and infiltrating macrophages release thromboxane A 2 (TxA 2), which augments renal arteriolar vasoconstriction.32 Because NO levels are substantially decreased, Ang II and TxA 2 exert an unopposed constrictive effect on the afferent renal arterioles, and renal plasma flow declines. Reabsorption of sodium and water through the renal tubules into the perirenal vasculature and lymphatics causes proximal tubular pressure to decrease toward normal at this point, and successive decreases in GFR are chiefly due to increased afferent vascular resistance.28 Preferential constriction of afferent renal arterioles results in reduced renal plasma flow and reduced glomerular capillary pressure, markedly decreasing GFR and filtration fraction.30

Inflammatory Effects The near-immediate consequence of complete UUT obstruction is reversible functional failure of the associated kidney(s), but complete obstruction also initiates inflammatory cascades that rapidly initiate the development of interstitial fibrosis and tubular cell apoptosis. Ang II has been identified as a key factor influencing induction and progression of interstitial fibrosis in obstructed kidneys. The release of Ang II, along with other chemokines and cytokines, attracts classically activated macrophages and activated cytotoxic T lymphocytes into renal tissue. Infi ltrating macrophages produce a variety of proinflammatory cytokines and growth factors, including tumor necrosis factor α (TNFα), transforming growth factor β1 (TGF-β1), interleukin 1, interleukin 6, and fibroblast growth factor.33 Leukocyte infiltration is mediated in part by Ang II–induced upregulation of the transcription factor nuclear factor κB (NFκB), as well as other profibrotic cytokines such as TGF-β1 and TNF-α.28,29,33–36 Activation of NF-κB stimulates two known autocrine positive feedback loops, the amplification of Ang II and the formation of TNF-α, additionally fueling the inflammatory cascade.29 Infiltrating macrophages also generate reactive oxygen species, inducing oxidative damage that exacerbates matrix expansion and apoptosis.37 The renal interstitium consists of resident fibroblasts in a matrix of collagen, proteoglycans, and fluid. Matrix metalloproteinases (MMPs) and other enzymes such as collagenase maintain the interstitial equilibrium between collagen bundle deposition and dismantling by countering the actions of profibrotic factors. The interstitial effects of MMPs are checked by tissue inhibitors of metalloproteinases (TIMPs). Increased local concentrations of profibrotic cytokines, such as NF-κB, TGF-β1, and TNF-α, shift the interstitial balance toward extracellular matrix deposition; TGF-β1 has a directly inhibitory effect on colCompendiumVet.com | November 2009 | Compendium

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FIGURE 6

with Ang II results in decreased local levels of Ang II–induced profibrotic cytokines, which significantly diminishes macrophage recruitment, collagen expression, and interstitial fibrosis in rats and mice.33,34,39

Apoptotic Effects

QuickNotes The rate and degree of renal damage, as well as the capacity for repair, in an obstructed kidney are signiﬁcantly affected by the presence of a functional contralateral kidney.

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These kidneys, photographed at necropsy, demonstrate the marked renal asymmetry that can be present in sequential bilateral UUT obstruction. The smaller kidney most likely became obstructed without clinical signs and progressed to end-stage atrophy and fibrosis. The larger kidney hypertrophied to compensate for the functional decrement. The marker at the bottom of the photo is 1 cm long.

Mechanical stretch from tubular distention has been shown to directly stimulate apoptosis of tubular epithelial cells in humans, rats, and mice as early as 4 days after obstruction; tubular cell loss leads eventually to tubular atrophy and obsolescence and thus to loss of functional renal mass.33,39 Apoptosis in renal tissues is effected by caspases (cysteinyl aspartate–speciﬁc proteinases), a family of cytosolic and nuclear enzymes. Caspases are activated by two distinct pathways: one involves TNF ligand binding, and the other involves intrinsic cell stress signals. Caspase levels increase markedly and rapidly in obstructed kidneys, and the degree of tubular cell apoptosis in an obstructed kidney mirrors the rise and fall of caspase expression.33 TGFβ1 has proapoptotic effects in obstructed kidneys, and administration of TGF-β1 inhibitors or monoclonal antibodies to TGF-β1 reduces obstruction-induced apoptosis and increases renal tubular cell proliferation.33 Increased concentrations of reactive oxygen species present in UUT obstruction also promote apoptosis, and administration of exogenous antioxidants attenuates apoptosis in mouse models.37,39 The role of Ang II in apoptotic renal cell death remains controversial.33

lagenase and MMPs, further shifting the interstitium toward fibrotic change.36 Ang II, TGF-β1, and many other growth factors, hormones, and cytokines also contribute to the process of epithelial to mesenchymal transition.38 This process is a recently elucidated mechanism of renal fibrogenesis in which renal tubular cells lose their epithelial phenotype and acquire mesenchymal characteristics. Tubular dilation resulting from UUT obstruction induces loss of the epithelial property of adhesion and acquisition of mesenchymal properties such as expression of α-smooth muscle actin. This transformation is accompanied by increased Role of the Contralateral Kidney expression of MMPs that specifically target The rate and degree of renal damage, as well type IV collagen and laminin, principal pro- as the capacity for repair, in an obstructed teins found in the tubular basement mem- kidney are significantly affected by the presbrane. Consequent structural and functional ence of a functional contralateral kidney. In disruption of the basement membrane allows rats, the presence of a functional contralateral the transformed cells to migrate from the kidney correlates with more rapid destruction tubular lumen into the interstitium.38,39 Loss of tissue in the obstructed kidney.28 In dogs, of tubular epithelial cells, basement mem- essentially no renal repair follows relief of brane disruption, and increasing interstitial obstruction if the contralateral kidney funcfibroblast populations all contribute to initia- tions normally. One dog study demonstrated tion and propagation of interstitial fibrosis. that stable, severely hydronephrotic kidneys Epithelial to mesenchymal transition prob- undergo dramatic functional improvement if ably plays a role in the pathogenesis of a the contralateral normal kidney is resected.28 wide range of fibrotic kidney diseases. Use These phenomena may underlie the common of angiotensin-converting enzyme inhibitors clinical presentation of cats with remarkably or angiotensin receptor blockers to interfere asymmetric kidneys (“big-kidney little-kidney”

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Acute Postrenal Azotemia CE syndrome). In this scenario, clinically subtle unilateral UUT obstruction initiates the proﬁbrotic processes described above. The presence of a contralateral functioning kidney subverts repair mechanisms, even if patency is restored to the obstructed kidney (which frequently does occur over time), and instead promotes progression of renal ﬁbrosis to an end-stage state (FIGURE 6). The patent kidney simultaneously undergoes compensatory hypertrophy, resulting in potentially dramatic asymmetry.

Lower Urinary Tract Obstruction

the detrusor muscle electrical syncytium and thus in irreversible suppression of detrusor cell-to-cell electrical transfer.42 Frequently, this neuromuscular damage manifests clinically as postobstructive detrusor atony. In most patients, this is transient and resolves clinically if the bladder is kept empty with the use of an indwelling catheter, but if overdistention is prolonged, the described changes may result in permanent detrusor dysfunction.40 If markedly elevated intravesicular pressures are transmitted to the UUT due to chronicity or ureterovesicular valve dysfunction, intrinsic renal damage may occur, as described above.

Obstruction of the LUT produces increased pressure in the bladder and urethra proximal to the obstruction. If prolonged or severe, Summary this pressure may be transmitted to the UUT. Acute postrenal azotemia is a common uroUrethral or trigonal mucosal damage, swell- logic emergency, particularly in cats, and ing, and/or denudation may occur at the site may be fatal if not rapidly diagnosed and of obstruction. Such damage induces infiltra- corrected. The most common causes of posttion by inflammatory leukocytes.40 Urethral renal azotemia in small animals are urethral damage and inflammation from obstruction obstruction, ureteral obstruction, and traumaor instrumentation may cause urethral spasm tic urinary tract rupture. Azotemia from that manifests as functional obstruction after postrenal causes can be reversed because it relief of a mechanical obstruction. Submucosal results from urinary tract obstruction or ruphemorrhage, perivascular aggregations of ture, rather than intrinsic damage to the kidinflammatory cells, and urothelial necrosis in neys; thus, the presence and significance of the bladder can occur with obstruction of as postrenal causes of disease should be identilittle as 10 hours’ duration.41 Overdistention fied in every azotemic patient. Historical and damages the bladder wall, likely through physical examination findings, coupled with hypoxic damage caused by pressure-induced diagnostic imaging, usually identify postrenal reduction in blood flow, and is postulated to azotemia and localize its origin within the disrupt tight junctions between detrusor myo- urinary tract. In some cases (such as acute ctes.40 Axonal degeneration and Schwann cell ureteral obstruction), promptly addressing the edema may be detected by electron micros- cause of postrenal azotemia may forestall or copy, and severe or prolonged overdistention mitigate the development of intrinsic renal may result in fundamental reorganization of damage and hasten clinical recovery.

References 1. Bjorling DE. The urethra. In: Slatter D, ed. Textbook of Small Animal Surgery. Philadelphia: Saunders; 2003:1638-1651. 2. Westropp JL, Bufﬁngton CA, Chew D. Feline lower urinary tract diseases. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. St. Louis: Elsevier Saunders; 2005:1828-1850. 3. Mutsaers AJ, Widmer WR, Knapp DW. Canine transitional cell carcinoma. J Vet Intern Med 2003;17:136-144. 4. Kutzler MA, Yeager A. Prostatic diseases. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. St. Louis: Elsevier Saunders; 2005:1808-1819. 5. Adams LG, Syme HM. Canine lower urinary tract diseases. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. St. Louis: Elsevier Saunders; 2005:1850-1874. 6. Kyles AE, Hardie EM, Wooden BG, et al. Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in

cats with ureteral calculi: 163 cases (1984-2002). JAVMA 2005; 226(6):932-936. 7. Hardie EM, Kyles AE. Management of ureteral obstruction. Vet Clin North Am Small Anim Pract 2004;34(4):989-1010. 8. Bartges JW, Kirk C, Lane IF. Update: management of calcium oxalate uroliths in dogs and cats. Vet Clin North Am Small Anim Pract 2004;34(4):969-987. 9. Ross SJ, Osborne CA, Lulich JP, et al. Canine and feline nephrolithiasis. Epidemiology, detection, and management. Vet Clin North Am Small Anim Pract 1999;29(1):231-250, xiii-xiv. 10. Lekcharoensuk C, Osborne CA, Lulich JP, et al. Increased frequency of calcium oxalate uroliths in the upper urinary tract of cats: 1981-1999. In: Managing Urolithiasis In Cats: Recent Updates And Practice Guidelines. Topeka: Hill’s Pet Nutrition; 2003. REFERENCES CONTINUE ON PAGE 533

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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 statement(s) regarding urinary tract obstruction is/are true? a. Calcium oxalate stones and urate stones are frequently implicated in canine LUT obstruction. b. UUT obstruction rarely results in signiﬁcant postrenal azotemia. c. UUT obstruction in cats is most frequently caused by calcium oxalate urolithiasis. d. a and c 2. In a severely azotemic cat, signiﬁcant renal asymmetry is most consistent with a. sequential bilateral ureteral obstruction. b. chronic interstitial nephritis. c. simultaneous bilateral ureteral obstruction. d. blunt unilateral renal trauma. 3. In acute ureteral obstruction, GFR decreases precipitously because of a. increased intratubular pressure. b. Ang II and TxA2-mediated afferent arteriolar constriction. c. prostacyclin and NO-mediated afferent arteriolar dilation. d. a and b

4. The most common cause of urethral rupture in cats is a. ﬁrm palpation of the bladder in a cat with urethral obstruction. b. vehicular trauma. c. urethral trauma from catheterization. d. inadvertent surgical trauma. 5. Which substance has direct vasodilatory effects on the glomerular afferent arterioles? a. Ang II b. prostaglandin E2 c. NF-κB d. TIMPs

d. UUT obstruction can be definitively diagnosed based on physical examination findings. 8. Which clinicopathologic findings are most consistent with acute postrenal azotemia? a. metabolic acidosis and hyperkalemia b. metabolic alkalosis and hypokalemia c. metabolic acidosis and hypokalemia d. metabolic alkalosis and hyperkalemia

6. The most common neoplasm of the canine LUT is a. transitional cell carcinoma. b. squamous cell carcinoma. c. prostatic adenocarcinoma. d. lymphoma.

9. Which statement regarding urinary tract rupture in trauma patients is true? a. A palpable bladder on physical examination of a trauma patient rules out bladder rupture. b. The ability to urinate rules out bladder rupture in a trauma patient. c. Ureteral rupture is relatively common in trauma patients. d. Vehicular trauma is the most common cause of urethral rupture in dogs.

7. Which statement regarding UUT obstruction is true? a. UUT obstruction with DSB occurs only in the presence of gross hematuria. b. UUT obstruction from neoplasia is common in cats. c. Microscopic hematuria is a common ﬁnding in cats with UUT obstruction from DSB.

10. Which mechanism does not contribute to loss of functional renal mass consequent to UUT obstruction? a. epithelial to mesenchymal transition b. caspase-mediated apoptosis of renal tubular epithelial cells c. TGF-β1-mediated renal tubular aplasia d. disruption of the interstitial equilibrium to favor matrix deposition

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Clinical Snapshot Answers and Explanations Case Presentation #1 SEE PAGE 503 FOR CASE PRESENTATION.

1. A represents an attempt at positive contrast

cystography using a urethral catheter, with subsequent leakage of the contrast medium into the peritoneum (thin black arrows). There is overall loss of serosal detail in the caudoventral abdomen due to fluid opacity (thick black arrows); the urinary bladder cannot be identified. In addition, slight pleural effusion (thin white arrows) and a dilated, air-filled esophagus (thick white arrows) are present. B is an intravenous pyelogram 5 minutes after contrast medium injection. Opacification of the kidneys (K), ureters (U), and urinary bladder (B) is seen. The ureters are mildly dilated and tortuous, and they enter a cranially displaced urinary bladder in a normal “J-hook” fashion (white arrow). The apex of the urinary bladder is at the level of L4 and is only mildly distended. The normal anatomic location of the urinary bladder in an adult dog is just cranial to the pubis.1 In addition, multiple pelvic fractures are visible in A and B (black arrowheads). The diagnosis was urinary bladder rupture secondary to trauma, with a cranially displaced urinary bladder and normally positioned ureters; secondary uroabdomen; and multiple complex pelvic fractures. An orthogonal view of the abdomen (C) was obtained, but visualization of the ureters at the trigone C

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Clinical Snapshot region of the urinary bladder was obscured by contrast medium within the peritoneum. 2. Contrast urethrography was performed after the intrave-

nous pyelogram, and D was obtained. This image shows an avulsion (Av) of the bladder (B) just cranial to the pelvis. The penile and prostatic portions of the urethra appear intact. Contrast medium leakage is seen in the peritoneum just cranial to the fractured pubis (arrow). This image conﬁrms a diagnosis of urinary bladder avulsion. 3. Urinary bladder avulsion with resultant uroabdomen is

commonly seen secondary to sustaining blunt force trauma to the abdomen, particularly vehicular trauma with pelvic fractures.2 Urinary bladder rupture is the most common cause of uroabdomen in dogs and cats, and rupture of the urethra in male dogs is most frequently associated with pelvic fractures.2 Penetrating abdominal or perineal wounds or iatrogenic injury from improper cystocentesis or rigid urinary catheter placement may also result in urinary tract trauma and urine leakage.3 Urinary bladder rupture is more frequently encountered in male dogs than in female dogs, possibly because male dogs have long, narrow urethras that cannot dilate rapidly and subsequently rupture.2 The clinical signs of urinary tract trauma are generally nonspecific and are often overlooked, especially in trauma patients suffering from shock. A common physical examination finding in these patients is a distended, painful abdomen with fluid accumulation along the ventral abdomen. Vehicular trauma may cause significant bruising around the perineum and abdomen, especially with fractures of the pelvis. Animals with uroabdomen may be azotemic and dehydrated and/or have metabolic acidosis. Untreated, uroabdomen leads to life-threatening hyperkalemic bradycardia and shock. Results of complete blood counts and biochemical profiles are often nonspecific and consistent with inflammation and abdominal trauma. Abdominocentesis may lead to a definitive diagnosis of uroperitoneum when the concentration of creatinine and/or potassium in the abdominal fluid is compared with the corresponding concentration in serum. In dogs, an abdominal fluid:serum creatinine ratio >2:1 is suggestive of uroperitoneum; an abdominal fluid:serum potassium ratio >1.4:1 is definitive for uroperitoneum.2,4 In cats, an abdominal fluid:serum potassium ratio of >1.9:1 is suggestive of uroperitoneum. 4. Immediate management of a patient with a urinary blad-

der rupture or avulsion consists of placement of a cystostomy tube or peritoneal catheter to foster urine drainage until the patient is stable enough for a prolonged anesthetic procedure.5 Surgical correction of the bladder avulsion is the therapy of choice for this patient. The decision

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to repair the urinary bladder by primary anastomosis should be based on the degree of damage to the urethra and bladder observed at the time of surgery. Due to the level of the injury in this case, it is likely that the blood supply to the urethra provided by the caudally located internal pudendal artery would be preserved.6 Severe damage to, or necrosis of, the bladder or urethra may indicate a need for a permanent tube cystostomy.2 Surgical options for repair of urethral defects include autografts,7 trigonal-colonic anastomosis,8 and ureteralcolonic anastomosis.9 The prognosis for recovery is excellent for traumatic bladder rupture; however, there are few published data for the prognosis associated with bladder avulsion. References 1. Park RD, Wrigley RH. The urinary bladder. In: Thrall DE, ed. Textbook of Veterinary Diagnostic Radiology. Philadelphia: WB Saunders; 2002:571-582. 2. Fossum TW. Surgery of the bladder and urethra. In: Small Animal Surgery. St. Louis: Mosby; 2007:678-681. 3. Adams LG, Syme HM. Canine lower urinary tract diseases. In: Ettinger SJ, Feldman E, eds. Textbook of Veterinary Internal Medicine. St. Louis: Elsevier; 2005:18701871. 4. Gannon KM, Moses L. Uroabdomen in dogs and cats. Compendium Contin Educ Pract Vet 2002;24(8):604-612. 5. Beck AL, Grierson JM, Ogden DM, et al. Outcome of and complications associated with tube cystostomy in dogs and cats: 76 cases (1995-2006). JAVMA 2007;230(8):1184-1189. 6. Evans HE. The heart and arteries. In: Evans HE, ed. Miller’s Anatomy of the Dog. Philadelphia: WB Saunders;1993:671- 674. 7. Atalan G, Cihan M, Sozmen M, Ozaydin I. Repair of urethral defects using fascia lata autographs in dogs. Vet Surg 2005;34(5):514-518. 8. Bovee KC, Pass MA, Wardley R, et al. Trigonal-colonic anastomosis: a urinary diversion procedure in dogs. JAVMA 1979;174(2):184-191. 9. Stone EA, Withrow SJ, Page RL, et al. Ureterocolonic anastomosis in ten dogs with transitional cell carcinoma. Vet Surg 1988;17(3):147-153.

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11. Pantaleo V, Francey T, Fischer JR, et al. Application of hemodialysis for the management of acute uremia in cats: 119 case (1993-2003). Proc ACVIM Forum 2004:418. 12. Bartges JW, Kirk CA. Nutrition and lower urinary tract disease in cats. Vet Clin North Am Small Anim Pract 2006;36(6):1361-1376. 13. Westropp JL, Ruby AL, Bailiff NL, et al. Dried solidified blood calculi in the urinary tract of cats. J Vet Intern Med 2006;20(4):828-834. 14. Gordon M, Cervellione MR, Postlethwaite R, et al. Acute renal papillary necrosis with complete bilateral ureteral obstruction in a child. Urology 2007;69:575.e11-575. e12. 15. Hare WS, Poynter JD. The radiology of renal papillary necrosis as seen in analgesic nephropathy. Clin Radiol 1974;25(4):423-443. 16. Stone EA. Ovary and uterus. In: Slatter D, ed. Textbook of Small Animal Surgery. Philadelphia: Saunders; 2003:1487-1502. 17. McLoughlin MA, Bjorling DE. Ureters. In: Slatter D, ed. Textbook of Small Animal Surgery. Philadelphia: Saunders; 2003:1619-1628. 18. Hamilton MH, Sissener TR, Baines SJ. Traumatic bilateral ureteric rupture in two dogs. J Small Anim Pract 2006;47(12):737-740. 19. Selcer BA. Urinary tract trauma associated with pelvic trauma. JAAHA 1982;19: 785-793. 20. Waldron DR. Urinary bladder. In: Slatter D, ed. Textbook of Small Animal Surgery. Philadelphia: Saunders; 2003:1629-1637. 21. Anderson RB, Aronson LR, Drobatz KJ, et al. Prognostic factors for successful outcome following urethral rupture in dogs and cats. JAAHA 2006;42(2): 136-146. 22. Fischer JR. Acute ureteral obstruction. In: August JR, ed. Consultations in Feline Internal Medicine. 5th ed. St. Louis: Elsevier Health Sciences; 2005. 23. Aumann M, Worth LT, Drobatz KJ. Uroperitoneum in cats: 26 cases (19861995). JAAHA 1998;34(4):315-324. 24. Adin CA, Herrgesell EJ, Nyland TG, et al. Antegrade pyelography for suspected ureteral obstruction in cats: 11 cases (1995-2001). JAVMA 2003;222(11):15761581. 25. Fischer JR, Pantaleo V, Francey T, et al. Clinical and clinicopathological features of cats with acute ureteral obstruction managed with hemodialysis between 1993 and 2004: a review of 50 cases. Proc ECVIM-SA 2004. 26. Lee JA, Drobatz KJ. Characterization of the clinical characteristics, electrolytes, acid-base, and renal parameters in male cats with urethral obstruction. J Vet Emerg Crit Care 2003;13(4):227-233. 27. Weisse C, Aronson LR, Drobatz K. Traumatic rupture of the ureter: 10 cases. JAAHA 2002;38(2):188-192. 28. Wen JG, Frokiaer J, Jorgensen TM, et al. Obstructive nephropathy: an update of the experimental research. Urol Res 1999;27(1):29-39. 29. Klahr S, Morrissey J. Obstructive nephropathy and renal fibrosis. Am J Physiol Renal Physiol 2002;283(5):F861-F875. 30. Harris KP. Urinary tract obstruction. In: Johnson RJ, Fehally J, eds. Comprehensive Clinical Nephrology. Edinburgh: Mosby; 2003:745-758. 31. Harris RH, Gill JM. Changes in glomerular filtration rate during complete ureteral obstruction in rats. Kidney Int 1981;19(4):603-608. 32. Harris KP, Yanagisawa H, Schreiner GF, et al. Evidence for two distinct and functionally important sites of enhanced thromboxane production after bilateral ureteral obstruction in the rat. Clin Sci (Lond) 1991;81(2):209-213. 33. Misseri R, Rink RC, Meldrum DR, et al. Inflammatory mediators and growth factors in obstructive renal injury. J Surg Res 2004;119(2):149-159. 34. Guo G, Morrissey J, McCracken R, et al. Contributions of angiotensin II and tumor necrosis factor-alpha to the development of renal fibrosis. Am J Physiol Renal Physiol 2001;280(5):F777-F785. 35. Chevalier RL. Specific molecular targeting of renal injury in obstructive nephropathy. Kidney Int 2006;70(7):1200-1201. 36. Misseri R, Meldrum KK. Mediators of fibrosis and apoptosis in obstructive uropathies. Curr Urol Rep 2005;6(2):140-145. 37. Kawada N, Moriyama T, Ando A, et al. Increased oxidative stress in mouse kidneys with unilateral ureteral obstruction. Kidney Int 1999;56(3):1004-1013. 38. Liu Y. Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. J Am Soc Nephrol 2004;15(1):1-12. 39. Chevalier RL. Pathogenesis of renal injury in obstructive uropathy. Curr Opin Pediatr 2006;18(2):153-160. 40. Bartges JW, Finco DR, Polzin DJ, et al. Pathophysiology of urethral obstruction. Vet Clin North Am Small Anim Pract 1996;26(2):255-264. 41. Tammela T, Autio-Harmainen H, Lukkarinen O, et al. Effect of prolonged experimental distension on the function and ultrastructure of the canine urinary bladder. Ann Chir Gynaecol 1991;80(3):301-306. 42. Seki N, Karim OM, Mostwin JL. The effect of experimental urethral obstruction and its reversal on changes in passive electrical properties of detrusor muscle. J Urol 1992;148(6):1957-1961.

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For advertising information call Susan Deakins 800-237-9851, ext. 258 or Email: comp@rja-ads.com Publisher’s Disclaimer: Advertising appearing in this issue does not necessarily reflect the opinions of nor constitute or imply endorsement or recommendation by the Publisher. The Publisher is not responsible for any statements or data made by the Advertiser.

CLASSIFIEDS VETERINARIANS WANTED

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MARYLAND – Experienced Associate Veterinarian NORTH CAROLINA – Well-established, 24-hour, needed for high-energy, high-quality small animal exclusive veterinary hospital situated on 30 beautiful acres in Urbana, MD. Our facility provides state-of-the-art diagnostic equipment, two surgical suites, an established boarding resort, and a focus on preventative medicine as well as creating an exceptional client/ patient experience. Candidates must have excellent client communication skills, be able to work independently and feel competent performing various common surgical procedures. We invite you to learn more by contacting Beth Finnegan, CVT, RVT, Human Resource Manager, or at bﬁnnegan@greenbriarpethospital.com.

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AAHA-accredited small animal hospital in central North Carolina needs an emergency/critical care veterinarian and an associate veterinarian. Located only hours from the mountains and coastlines, our busy, progressive, and expanding five-doctor practice is fully equipped and staffed by 25 highly motivated veterinarians, technicians, and lay staff. Established more than 27 years, our hospital has an excellent client base and strong emphasis on quality care. Work in a great practice environment with an excellent opportunity for career development. Competitive salary and benefits include 401(k), profit sharing, CE, and insurance. Experience preferred. Send resume to Dr. Karl B. Milliren, 303 National Highway, Thomasville, NC 27360; email tvh303@cs.com; fax 336-475-0140.

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

TEXAS – It all begins here at DCCCD. Cedar Valley College is currently accepting applications for the Director, Veterinary Technology position. Requirements: Doctor of Veterinary Medicine, DVM plus 3 years teaching experience and administrative responsibility or comparable experience. Ability to utilize computer technology to access data, maintain records, generate reports and communicate with others. Requires technical communication skills to deal with veterinary technology faculty and other health professionals and individuals from diverse socio-economic backgrounds. Official transcript will be required.Salary: $51,876 $90,783 annually, depending on education and experience (comprehensive benefits package). Application requirements: Official DCCCD application for employment (www.jobs.dcccd.edu), resume, unofficial copy of graduate transcripts. Deadline for all applications (electronic/ non-electronic) and other required documents is open until filled. Resume and unofficial transcripts may be faxed to 972-860-8279, emailed to CVCHR@dcccd.edu, delivered in person or mailed to: Cedar Valley College, Human Resources, 3030 North Dallas Ave., Lancaster, TX 75134. Please include position number (030909051) on all documents submitted. For complete job description information and online application please visit our web site at: www.dcccd.edu/Business+Community/ jobs.htm. To send supplemental information email apply@dcccd.edu. Employment opportunities are offered by the Dallas County Community College District without regard to race, color, age, national origin, religion, sex, disability or sexual orientation.

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

CLIENT HANDOUT

What You Should Know About

Ear Cleaning 101 Home ear cleanings can enhance treatment of an existing ear problem or prevent the development of a new one. Some dogs that are prone to ear infections may need regular cleanings between veterinary visits. Home ear cleanings can also help remove dirt and wax that can prevent needed medications from reaching inflamed areas, as well as get rid of allergens and microbes that may be contributing to the inflammation or infection. There are several techniques for home ear cleaning. This handout describes the simplest one. Ear cleaning can be relatively easy to do at home, as long as a few simple guidelines are followed. The most important guideline is to always put health and safety first: If, for any reason, your pet becomes so agitated that you feel you are at risk of being bitten, stop. If the procedure seems excessively painful for your pet, stop and get professional advice.

Create a Wiggle-Free Zone Although some pets are willing to sit or lie quietly while you clean their ears, the reality is that most object, at least at first. Choose your work space carefully! Ear cleaning can be messy, so it’s best to pick a room that’s easy to clean (e.g., bathroom, laundry room, shower stall) or to even go outside. Here are some tips on how to keep your pet wiggle free while you work: Place your pet on a stable work surface that you can stand next to and allow him or her to lie down, either in an upright “sphinx” position or flat on his or her side. Wrap one arm—the one you will use to treat the ear—over your pet’s shoulders, and use your upper arm and elbow to help keep him or her still. You can wrap your other arm under your pet’s neck to hold the ear open and ear flap back. If you don’t have a suitable high work

surface, you can use the same method while seated on the ﬂoor, either holding the front of your pet’s body partially against your body or on your lap. If you have a large Use one hand to hold the ear ﬂap back so that you can treat the ear with the other. dog, you can have it sit back against your legs while you stand behind it. Sometimes it helps to back the pet into a corner. Small dogs and cats can be wrapped in a large towel—rolled up like a burrito—and held against your body, leaving only the head free. Be sure not to wrap your small pet too tightly. If your pet struggles, talk to him or her calmly. Take a break if he or she becomes extremely agitated. Massaging the base of the ears (unless they are painful) should feel good to the pet and may help calm him or her enough that you can resume treatment.

What You’ll Need Old clothes Safe, easily cleanable work area (tile or linoleum ﬂoors, water-resistant walls) Towel Nonirritating ear wash or rinse recommended by your veterinarian Cotton balls or tissues Cotton swabs (to be used on outer ear only) Be sure to reward good behavior! If this method fails, get a helper to hold the pet while you treat the ear.

Cleaning Steps There is no one perfect way to perform an ear cleaning, but the general steps are as follows.

11/09 Produced in association with Vetstreet. A downloadable version of this client handout is also available at CompendiumVet.com.

CLIENT HANDOUT

Ear Cleaning 101

Eardrum

1. Squeeze With your pet properly restrained, hold the ear solution bottle just over the opening of the affected ear and gently squeeze the prescribed amount of solution into the ear. Do not squeeze the solution bottle too hard, as a powerful stream can irritate tender and inﬂamed ear structures. Tip: Store the cleaning solution at room temperature to avoid causing unnecessary discomfort to the pet. (Do not store ear medications that require refrigeration at room temperature; however, allowing them to reach room temperature before use makes them more comfortable.)

2. Massage After administering the solution, fold the ear flap down against your pet’s head and try to prevent your pet from shaking his or her head too much. Gently massage the very base of the ear to distribute the solution as far as possible into the deep horizontal ear canal. To massage the base of the ear, follow the cartilage tube of the ear canal with your finger down along the VIDEO pet’s neck until you feel the tube bend and turn inward. Then gently comTo see a video of press the tube with your where to massage finger. (Unless the ear is the ear, visit extremely painful, most CompendiumVet.com. animals like this part!) Keep the solution in the ear for the prescribed amount of time. When you are done, allow your pet to shake its head to remove some of the solution.

Signs of Ear Trouble Odor Scratching/rubbing at ears or side of head Discharge Debris Shaking/tilting of the head Pain Head shyness (not wanting the head or ears to be touched) Irritability

Vertical ear canal

Middle ear canal

Anatomy of the ear. One look at the inside of a dog’s ear shows why dogs are often prone to ear problems. Debris, allergens, bacteria, and moisture are all easily trapped in the long, deep ear canal, especially the middle ear, which is almost horizontal. The arrow points to the place to massage the base of the ear. (With permission from Pﬁzer Atlas of Infection in Dogs and Cats. Wilmington, DE: The Gloyd Group, Inc; 2008.)

Tip: Prepare for the head shake! Wear old clothes and keep a towel handy. You may want to drape the towel over your pet’s head or neck before administering the solution.

3. Wipe and Swab When most of the solution has been shaken out, use cotton balls or tissues to gently wipe away any discharge, loosened debris, and remaining liquid from the ear ﬂap, side of the neck, and hair below the ear as well as the opening of the ear canal. Cotton swabs can be used to clean small skin pockets in the visible ear. Tip: Do not push cotton swabs into the ear canal, even for a short distance. A sudden shake of the head or slip of the hand could result in a cotton swab puncturing the delicate eardrum or pushing debris back inside the inner ear canal.

Follow Recommendations, Please! The ear is a very delicate structure. It is very important to closely follow recommendations regarding ear cleanings. Treating too frequently or too aggressively can make the problem worse, not better. Sensitive, already inﬂamed parts of the ear can be damaged. Because many ear washes contain chemicals and drying agents, it is also important to use only products recommended by a veterinarian. With thanks to Dr. Craig E. Grifﬁn, Animal Dermatology Clinic, San Diego, for his contributions to and review of this material.

11/09 Produced in association with Vetstreet. A downloadable version of this client handout is also available at CompendiumVet.com.

We believe you re too good to be micromanaged. We believe in providing more resources, not taking them away. We believe a econd opinion, or third, or fourth, can make yours even stronger. We believe in getting out of the way and letting doctors be octors. We believe you own your career. We believe you went to vet school for a very furry reason. We believe people need eterinarians as much as Pets do. We believe you’re better at your job when you’ve had some time away from it. We believe in iving you the tools you need to do your job. We believe no matter how good you are, you can always get better. We believe t xcellent doctors make excellent colleagues. We believe mentors can learn as much as mentees. We believe in saving the lives f Pets and improving the lives of vets. We believe that you should be focused on your patient, not your paperwork. We belie hat flexible hours make for refreshed doctors. We believe cats aren’t the only animals that purr. 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We believe a second people. them Because at Banfield, you aren’t just opinion, o hird, or fourth, can make yours even stronger. We believe in getting out of the way and letting doctors be doctors. We believe touching patients – you’re touching the future ou own your career. We believe you went to vet school for a very furry reason. We believe people need veterinarians as much of medicine. s Pets do. We believe you’re better at your job when you’ve had some time away from it. We believe in giving you the tools y eed to do your job. We believe no matter how good you are, you can always get better. We believe that excellent doctors mak We’re Banfield. We believe in vets. xcellent colleagues. We believe mentors can learn as much as mentees. We believe in saving the lives of Pets and improving t ves of vets. We believe that you should be focused on your patient, not your paperwork. We believe that flexible hours make or refreshed doctors. We believe cats aren’t the only animals that purr. We believe we’re helping families along with their Pets We believe you’re too good to be micromanaged. We believe in providing more resources, not taking them away. We believe a econd opinion Visit us at banfield.net/veterinarians We believe in getting out of the way and letting doctors be doctor We believe for a very furry reason. We believe people need veterinarians as much as Pets do. We believe you’re better at your j when you’ve had some time away from it. We believe in giving you the tools you need to do your job. We believe no matter h d l b b l h ll

JOHN WAS 58 WHEN HE THOUGHT ABOUT RETIREMENT.

THEN HE THOUGHT ABOUT WHO WOULD BUY HIS PRACTICE. VCA Animal Hospitals

PLEASE CONTACT US TODAY.

For more than 20 years, VCA’s hospital purchase programs have given practice owners the freedom to live their lives with peace of mind. More than 475 hospitals in 41 states have joined the VCA family. You have worked hard to create a legacy. VCA’s goal is to continue the success you created. Please contact us if you have a veterinary practice in excess of $1.25 million dollars in annual revenue with 3 or more veterinarians. If you are thinking of selling your practice call VCA. If your hospital is really close to an existing VCA location a merger might be right for you.

Darin Nelson Senior Vice President Development 800-550-2388 (office) 949-228-2525 (mobile) darin.nelson@vcamail.com Neil Tauber Senior Vice President 310-571-6504 (office) 310-890-0444 (mobile) neil.tauber@vcamail.com www.vcaantech.com