Compendium Equine | November 2009

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VOLUME 4 NUMBER 9 NOVEMBER/DECEMBER 2009

6 CE Contact Hours | CompendiumEquine.com | Peer Reviewed

Vol 4(9) vember/December 2009 November/December

COMPENDIUM EQUINE CONTINUING EDUCATION FOR VETERINARIANS®

Treating Acute Colitis

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Dentistry in Juvenile Horses

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From the Horse’s Mouth FREE

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Refereed Peer Review

Managing Your Practice and Life


POTOMAVAC™. As the face of PHF changes, trusted protection remains the same. Potomac Horse Fever Facts “The true geographic range of distribution is not known.”3 “The epidemiology of Neorickettsia risticii … is still under investigation.”4 “The resultant flooding and standing water has provided optimum conditions for the spread of PHF… recent increase in clinical cases in the Southeast, Midwest and the Northeast confirms this theory.”5 “If Potomac horse fever has been confirmed on a farm or in a particular geographic area, it is likely that additional cases will occur in future years.”6

Potomac horse fever (PHF) has been around since 1979. But its epidemiology has only recently been defined, and clinical cases have now been reported in more than 40 states1 — far from the Potomac valley — and into many nontraditional areas.2 Changing weather patterns and improved diagnosis suggest this trend will continue, and PHF may become even more widespread. Equine POTOMAVAC is a trusted vaccine for aiding the prevention of PHF — even in foals as young as 3 months. Early and regular vaccination helps protect horses in your care against the effects of PHF, including fever, dehydration, colic, late-term abortions and laminitis. The benefits of POTOMAVAC also are available in Equine POTOMAVAC + IMRAB®, a combination vaccine that helps protect against rabies and Potomac horse fever. Best of all, both are backed by Merial, a trusted leader in equine health.

Madigan J and Pusterla N. Life Cycle of Potomac Horse Fever – Implications for Diagnosis, Treatment, and Control: A Review. AAEP Proceedings 2005;51:158-162. Hamende V. Potomac horse fever cases confirmed in northern Wyoming. University of Wyoming Cooperative Extension Service. Press Release, September 13, 2002. Available at http://wyovet.uwyo.edu/Diseases/2002/PotomacConf.pdf. Accessed February 18, 2008. 3 Merck Veterinary Manual. Ninth Edition. 2005:236-237. 4 Ryder E. Potomac Horse Fever Cases Popping Up in Ohio. TheHorse.com. Article #10013. July 15, 2007. 5 Marcella K. Conditions collide to propel PHF/Potomac horse fever must be treated rapidly to dodge fatalities. DVM, January 15, 2005. Available at http://www.dvmnews.com/dvm/article/articleDetail.jsp?id=144082&pageID=1&sk=&date=. Accessed February 18, 2008. 6 Potomac Horse Fever. AAEP.org. Available at http://www.aaep.org/potomac_fever.htm. Accessed February 6, 2008. 1 2

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®ZIMECTERIN, RECOMBITEK, EQUIOXX and IMRAB are registered trademarks, and ™POTOMAVAC and the HORSE HEAD LOGO are trademarks, of Merial. ®GASTROGARD and ULCERGARD are registered trademarks, of the AstraZeneca Group of Companies. ©2008 Merial Limited. Duluth, GA. All rights reserved. LAGEBPM801 (3/08)

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November/ December 2009 Vol 4(9) CompendiumEquine.com | Peer Reviewed | Free CE

The AAEP’s Media Partnership Program is composed of an esteemed group of industry-leading media outlets dedicated to providing resources and education, through the AAEP, to veterinarians and horse owners to improve the health and welfare of horses. Mission Statement: Compendium Equine is dedicated to providing essential and accurate clinical and professional information to benefit equine practitioners, their profession, and their patients. Compendium Equine: Continuing Education for Veterinarians is free to veterinarians practicing in the United States. To sign up, go online to CompendiumEquine.com or call 800-426-9119, option 2. US subscriptions: $35 for 1 year. International subscriptions: Canadian and Mexican subscriptions (surface mail): $40 for 1 year. Other foreign subscriptions (surface mail): $135 for 1 year. Payments by check must be in US funds drawn on a US branch of a US 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 $8 (United States and Canada) and $10 (foreign) each (plus postage).

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

PUBLISHED BY

MANAGING EDITOR Kirk McKay 800-426-9119, ext 52434 | kmckay@vetlearn.com SENIOR EDITOR Robin A. Henry 800-426-9119, ext 52412 | rhenry@vetlearn.com ASSOCIATE EDITOR Chris Reilly 800-426-9119, ext 52483 | creilly@vetlearn.com ASSISTANT EDITOR Benjamin Hollis 800-426-9119, ext 52489 | bhollis@vetlearn.com VETERINARY ADVISERS Dorothy Normile, VMD, Chief Medical Officer 800-426-9119, ext 52442 | dnormile@vetlearn.com Amy I. Bentz, VMD, DACVIM, Professional Services Manager 800-426-9119, ext 52389 | abentz@vetlearn.com DESIGN Michelle Taylor, Senior Art Director 267-685-2474 | mtaylor@vetlearn.com David Beagin, Art Director 267-685-2461 | dbeagin@vetlearn.com Bethany Wakeley, Production Artist Stephaney Weber, Production Artist OPERATIONS Marissa DiCindio, Director of Operations 267-685-2405 | mdicindio@vetlearn.com Christine Polcino, Traffic Manager 267-685-2419 | cpolcino@vetlearn.com SALES & MARKETING Joanne Carson, National Account Manager 267-685-2410 | Cell 609-238-6147 | jcarson@vetlearn.com Boyd Shearon, Account Manager 913-322-1643 | Cell 215-287-7871 | bshearon@vetlearn.com Russell Johns Associates, LLC, Classified Advertising 800-237-9851 | compeq@rja-ads.com

Published nine times per year 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. Compendium Equine: Continuing Education for Veterinarians (ISSN 15595811) is published nine times per year by Veterinary Learning Systems, 780 Township Line Road, Yardley, PA 19067. Periodicals postage paid at Morrisville, PA 19067-9998, and additional mailing offices. POSTMASTER: Send address changes to Compendium Equine, 780 Township Line Road, Yardley, PA 19067.

Compendium Equine: Continuing Education for Veterinarians® (ISSN 1559-5811)

EXECUTIVE OFFICER Derrick Kraemer, President CUSTOMER SERVICE 800-426-9119, option 2 | info@vetlearn.com Compendium Equine

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November/ December 2009 Vol 4(9) CompendiumEquine.com | Peer Reviewed | Free CE

EDITORIAL BOARD Michelle Henry Barton, DVM, PhD, DACVIM The University of Georgia Internal Medicine

EDITOR IN CHIEF James N. Moore, DVM, PhD Department of Large Animal Medicine College of Veterinary Medicine The University of Georgia Athens, GA 30602 706-542-3325 Fax 706-542-8833 jmoore@uga.edu

Gary M. Baxter, VMD, MS, DACVS Colorado State University Acupuncture, Surgery Jim Belknap, DVM, PhD, DACVS The Ohio State University Soft Tissue Surgery Bo Brock, DVM, DABVP (Equine) Brock Veterinary Clinic, Lamesa, Texas Surgery Noah D. Cohen, VMD, MPH, PhD, DACVIM (Internal Medicine) Texas A&M University Internal Medicine Norm G. Ducharme, DVM, MSc, DACVS Cornell University Large Animal

Compendium Equine is a refereed journal. Articles published herein have been reviewed by at least two academic experts on the respective topic and by the editor in chief.

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Compendium Equine

Raymond J. Geor, BVSc, MVSc, PhD, DACVIM Michigan State University Metabolism, Nutrition, Endocrine-Related Laminitis Katharina Lohmann, MedVet, PhD, DACVIM (Large Animal) University of Saskatchewan Large Animal Robert J. MacKay, BVSc, PhD, DACVIM (Large Animal) University of Florida Large Animal Rustin M. Moore, DVM, PhD, DACVS The Ohio State University Surgery Debra Deem Morris, DVM, MS, DACVIM East Hanover, New Jersey Internal Medicine P. O. Eric Mueller, DVM, PhD, DACVS The University of Georgia Soft Tissue and Orthopedic Surgery

Susan C. Eades, DVM, PhD, DACVIM (Large Animal) Louisiana State University Large Animal

Elizabeth M. Santschi, DVM, DACVS The Ohio State University Surgery

Earl M. Gaughan, DVM, DACVS Littleton Large Animal Clinic Littleton, Colorado Surgery

Nathaniel A. White II, DVM, MS, DACVS Virginia Polytechnic Institute and State University Surgery

Any statements, claims, or product endorsements made in Compendium Equine are solely the opinions of our authors and advertisers and do not necessarily reflect the views of the Publisher or Editorial Board.


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Federal law restricts this drug to use by or on the order of a licensed veterinarian. For use in horses only. Do not use in horses intended for food.

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Scale

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Studio Artist:

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Bleed Size:

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November/December 2009 Vol 4(9)

Features 394 CompendiumEquine.com | Peer Reviewed | Free CE

CE

Managing Your Practice and Life Music and Medicine: An Inspiring “Duet” for Dr. Lynsey Makkreel ❯❯ C. Lyon In this series, equine practitioners from around the country share how they’ve found and maintained a work–life balance.

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

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From the Horse’s Mouth Routine Dentistry in Juvenile Performance Horses

FREE

CE

❯❯ Cleet Griffin Review the dental anatomy and tooth eruption times in horses, and learn how to treat several common dental conditions in juvenile performance horses.

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Treating Acute Colitis

FREE

CE

❯❯ R. P. Atherton, H. C. McKenzie III, and M. O. FFurr This article discusses a logical approach to treatment and the available therapeutic options. The prevention and treatment of complicating sequelae, such as laminitis and endotoxemia, are discussed and must be considered in the patient’s prognosis.

Departments Cover image © 2009 Arsgera/Shutterstock.com

390 The Editor’s Desk: Practicing Compassion ❯❯ Kirk McKay

The AAEP’s Media Partnership Program is composed of an esteemed group of industry-leading media outlets dedicated to providing resources and education, through the AAEP, to veterinarians and horse owners to improve the health and welfare of horses.

429 2009 Annual Index 431 Index to Advertisers 432 Market Showcase 393

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Compendium Equine: Continuing Education for Veterinarians®

398 Clinical Snapshot Acute Colic in a Quarter Horse Mare ❯❯ Adam Stern

Calendar C

432 Classified Advertising


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The Editor’s Desk ❯❯ Kirk McKay, Managing Editor

Practicing Compassion Some people think only intellect counts: knowing how to solve problems, knowing how to get by, knowing how to identify an advantage and seize it. But the functions of intellect are insufficient without courage, love, friendship, compassion and empathy. Dean Koontz, writer

W

hat drew you to veterinary medicine? Was it initially the medicine or money? Was the desire to help those that can’t help themselves a factor? In other words, were you motivated by compassion? You were if you experienced “sympathetic consciousness of others’ distress together with a desire to alleviate it.”1 Veterinarians should I’ve always been impressed by feel good that regardveterinarians’ ability to be both smart clinicians and compassionless of whether they ate caregivers. Practicing good feel compassionate on medicine is paramount, but compassion can make the difference a particular day, their between a calm or recalcitrant animal—or owner. In turn, the work is compassionate temperament of the patient or by nature, improving owner can affect the manageability of the patient and whether the the lives of animals owner pursues treatment, which and people every day. can affect the patient’s health and the veterinarian’s revenue. While compassionate care is always important, no one should expect veterinarians to feel compassionate throughout an exhausting day or week. Fortunately, feeling compassionate is not a prerequisite to acting compassionately. Veterinarians should feel good that regardless of whether they feel compassionate on a particular day, their work is compassionate by nature, improving the lives of animals and people every day. Veterinarians have put compassion into practice. Let’s not forget the far-reaching and sometimes underrated ways in which veterinary care benefits people, most of whom have been comforted by how a veterinarian has cared for their animals. Veterinarians set an example of care for clients, inspiring them to give their animals the best care

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possible. In turn, the health and companionship of animals translate into economic and health benefits for people, including decreased loneliness, blood pressure, and cholesterol and triglyceride levels as well as increased opportunities for exercise and socialization.2 As managing editor of this journal, I know that editing clinical content and meeting deadlines sometimes leave little room for remembering the higher purpose behind the work—to provide information to benefit equine practitioners, their profession, and their patients. Therefore, I’m grateful to all the veterinary authors, reviewers, and editors who inspire their colleagues and me with their dedication to improving the health and comfort of equids, which are so deserving of our gratitude and care. (It could be argued that no other species have worked harder for humanity.) Thus, veterinary educators shouldn’t forget that their work is also compassion-based. Although Compendium Equine is primarily focused on the clinical aspects of veterinary medicine, the journal’s staff would like to take this opportunity to commend you for practicing compassion. Don’t underestimate the difference it makes to your patients, clients, colleagues, and community. References 1. Merriam-Webster’s Collegiate Dictionary. 11th ed. Springfield, MA: Merriam-Webster; 2006:253. 2. Centers for Disease Control and Prevention. Health benefits of pets. Accessed September 2009 at www.cdc.gov/healthypets/health_ benefits.htm.

Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com


Equine ultrasound just got better. and easier, more reliable, more affordable... For over 60 combined years, Universal Ultrasound and Classic Medical have provided reliable solutions to thousands of equine veterinarians. Our companies have now merged to better serve our customers – in the exam room, the classroom, and the stable. By offering the best technology, service and education, we’re committed to meeting the needs of our customers and their patients.

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Uncover the treasures of one of most diverse ecosystems on the planet with the AAEP this winter. Join your colleagues for three days of intimate lectures and afternoon island expeditions, including ziplining, snorkeling, trail riding and more. Meeting features include: • Expert Lectures on Lameness Performance Evaluation and Diagnostic Anesthesia • Interactive Session on Evaluating Lameness Cases in Western Performance Horses • Case-Based Lecture on Neurological Disease Plan your adventure today at www.aaep.org/symposium.htm.


CE Calendar January 16–19 Reproductive Management and Artificial Insemination Colorado State University College of Veterinary Medicine Fort Collins, Colorado Web www.csuequine.com

January 20 Techniques for Handling and Utilizing Cooled Semen Colorado State University Equine Reproduction Lab Fort Collins, Colorado Web www.csuequine.com

January 22–23 Veterinary Sport Horse Congress Amsterdam RAI Exhibition and Convention Center Amsterdam, The Netherlands Phone +31 (0) 613323538 Web www.proveto.org

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January 22–23 Reproductive Management of the Stallion

(polysulfated glycosaminoglycan)

stimulates cartilage repair and reverses traumatic joint dysfunction

Equine Reproduction Concepts, LLC Amissville, Virginia Phone 540-937-9832 E-mail info@equinereproduction.com

Within 48 hours

January 25–26 Reproductive Management of the Mare

the hyaluronic acid (HA) in the synovial fluid nearly doubles after a single injection.* Recommended dose: 5 mL every 4 days for 7 treatments intramuscularly.

Equine Reproduction Concepts, LLC Amissville, Virginia Phone 540-937-9832 E-mail info@equinereproduction.com

January 25–29 32nd Lake Tahoe Equine Conference Hyatt Lake Tahoe Incline Village, Nevada Phone 530-756-4899 Fax 530-756-3805 E-mail jlo62@comcast.net

Keep joints in healthy balance

January 30–31 Foaling and Care of the Newborn Foal

There are no known contraindications to the use of intramuscular PSGAG in horses. Studies have not been conducted to establish safety in breeding horses. WARNING: Do not use in horses intended for human consumption. Adequan® i.m. brand Polysulfated Glycosaminoglycan (PSGAG). Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian. Each 5 mL contains 500 mg Polysulfated Glycosaminoglycan. Brief Summary Indications: For the intramuscular treatment of non-infectious degenerative and/or traumatic joint dysfunction and associated lameness of the carpal and hock joints in horses. LUITPOLD PHARMACEUTICALS, INC. Animal Health Division, Shirley, NY 11967. See product package insert for full prescribing information. *Burba DJ, Collier MA, Default LE, Hanson-Painton O, Thompson HC, Holder CL: IN VIVO KINETIC STUDY ON UPTAKE AND DISTRIBUTION OF INTRAMUSCULAR POLYSULFATED GLYCOSAMINOGLYCAN IN EQUINE BODY FLUID Compiled by Benjamin Hollis; send TRITIUM-LABELED listings COMPARTMENTS AND ARTICULAR CARTILAGE IN AN OSTEOCHONDRAL DEFECT MODEL. The Journal of Equine Veterinary Science to bhollis@vetlearn.com. 1993; 696-703. Concentrations of Adequan i.m. in the synovial fluid begin to decline after peak levels are reached at 2 hours; then remain constant from 24 hours post injection through 96 hours. © 2008 Luitpold Animal Health. Adequan® is a registered trademark of Luitpold Pharmaceuticals, Inc. AHD 85201, Iss. 2/08 CE

Colorado State University Equine Reproduction Lab Fort Collins, Colorado Web www.csuequine.com Compiled by Benjamin Hollis; send listings to bhollis@vetlearn.com. Compendium Equine

To learn about the wear-and-repair of joints go to www.adequan.com. Or call 800-974-9247 for a free video.

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Managing Your Practice and Life SERIES EDITOR C. Lyon, VMD, Berwyn, Pennsylvania

Music and Medicine: An Inspiring “Duet” for Dr. Lynsey Makkreel Lynsey with her husband and horses.

Dr. Lynsey Makkreel of Keenan McAlister Equine in Bordentown, New Jersey, has been practicing equine medicine for nearly 5 years while pursuing an amateur singing career. She shares how she manages to balance work, marriage, singing, and other hobbies in her active life.

How long have you been practicing veterinary medicine? For 4½ years. I graduated from Ontario Veterinary College in Guelph.

Tell me about your path to your current position at Keenan McAlister Equine. I moved from Canada to the United States when I accepted an internship at Fairfield Equine in Connecticut. From there, I found my current job.

What do you enjoy most about your job? I enjoy many things, so it’s difficult to narrow down to a favorite. It’s very rewarding to help horses and clients. The feeling from being rewarded with genuine gratitude is priceless. I really enjoy being out on the farms and getting to know the horses and clients. I feel like I’ve accomplished something when I can go into a barn, name every horse, and know something about each one.

What do you enjoy least about your job? Do you treat species other than equids? I generally treat horses only, but I occasionally treat donkeys. I’ve also helped a goat or two.

I feel like I’ve accomplished something when I can go into a barn, name every horse, and know something about each one. Describe your practice setup and work schedule. How many veterinarians are in the practice? The three doctors in our practice take appointments Monday through Friday. We are purely ambulatory, so all of our work is done at the farms. The on-call work is split evenly between the three of us to cover all evenings and weekends. We usually have one or more emergencies per evening and three or four emergencies per day on the weekends.

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One of the most difficult things is when cases are not heading in the right direction or when I don’t know what is wrong with a horse and I doubt myself. I probably allow it to affect me more than I should (countless sleepless nights, etc.). I try to please clients and patients alike, so when I don’t or can’t, it can really bring me down. This is why activities such as singing are so important to me. Hobbies counteract the negative things that happen during the day. The other negative part of my job is on-call emergency work; I’m sure many practitioners would agree with this. A third of the time, my weekends and evenings are not my own. On those days and nights, I can’t make plans or even relax fully because I’m waiting for the phone to ring. It gets tiresome quickly.

Have you struggled to find and maintain a balance between your work and personal life? It hasn’t been difficult, but I’ve definitely made some compromises in my personal life. Emergency

Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com


The best treatment for EGUS may be a dose of reality. Equine Gastric Ulcer Syndrome (EGUS) caan easily become a reality for today’s horse. In fact, the majority of your clients’ racing and non-racing competittive horses could already be sufffering in silence with gastric ulcers.1,2 Clients come to o you for knowledge and tools they can’t get anywhere else. Training. Experience. Diagnosis. Approved treatment. You havee the power to make the solution n for EGUS this simple. Unique respon nse. Only ® GASTROGARD (omeprazole) is FDA-approved to treeat gastric ulcers. Unique ability.. Only you have the ability to prrovide diagnoses and GASTTROGARD. For information and EGUS educational tools, taalk with your Merial Sales Representative today. Or call 1-888--MERIAL-1.

Response.Ability. CAUTION: UTION: Federal llaw aw restricts restric icts this th drug to u use by or on the order of a licensed veterinarian. GASTROGARD is indicated for the treatment prevention of recurrence of gastric ulcers in horses and foals 4 weeks and older. In efficacy trials, no adverse tment and prev vention o rec g reactions in pregnantt or lactating mares has not been determined. DO NOT USE IN HORSES INTENDED tions were observed. obseerved. Safety Sa FOR HUMAN CONS CONSUMPTION. AND SUMPTI TI . KEEP THIS AN TION. ND ALL DRUGS OUT OF THE REACH OF CHILDREN. Mitchell RD. Prevalence of gastric ulcers in hunter/jumper and dressage horses evaluated for poor performance. Association for Equine Sports Medicine. September 2001. Murray MJ. Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc 1989;195(8):1135-1141.

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See Page 396 for Product Information Summary


Managing Your Practice and Life Oral Paste for Horses and Foals NADA 141-123, Approved by FDA Caution Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. Description Chemical name: 5-Methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridinyl) methyl]sulfinyl]-1H-benzimidazole. Empirical formula: C17H19N3O3S. Molecular weight: 345.42. Structural formula: H3C

Lynsey performing in a concert in Italy.

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How Supplied GASTROGARD® (omeprazole) Paste for horses contains 37% w/w omeprazole and is available in an adjustable-dose syringe. Each syringe contains 2.28 g of omeprazole. Syringes are calibrated according to body weight and are available in boxes of 7 units or 72 units. Storage Conditions Store at 68°F – 77°F (20-25°C). Excursions between 59°F – 86°F (15-30°C) are permitted. Indications For treatment and prevention of recurrence of gastric ulcers in horses and foals 4 weeks of age and older. Dosage Regimen For treatment of gastric ulcers, GASTROGARD Paste should be administered orally once-a-day for 4 weeks at the recommended dosage of 1.8 mg omeprazole/lb body weight (4 mg/kg). For the prevention of recurrence of gastric ulcers, continue treatment for at least an additional 4 weeks by administering GASTROGARD Paste at the recommended daily maintenance dose of 0.9 mg/lb (2 mg/kg). Directions For Use • GASTROGARD Paste for horses is recommended for use in horses and foals 4 weeks of age and older. The contents of one syringe will dose a 1250 lb (568 kg) horse at the rate of 1.8 mg omeprazole/lb body weight (4 mg/kg). For treatment of gastric ulcers, each weight marking on the syringe plunger will deliver sufficient omeprazole to treat 250 lb (114 kg) body weight. For prevention of recurrence of gastric ulcers, each weight marking will deliver sufficient omeprazole to dose 500 lb (227 kg) body weight. • To deliver GASTROGARD Paste at the treatment dose rate of 1.8 mg omeprazole/lb body weight (4 mg/kg), set the syringe plunger to the appropriate weight marking according to the horse’s weight in pounds. • To deliver GASTROGARD Paste at the dose rate of 0.9 mg/lb (2 mg/kg) to prevent recurrence of ulcers, set the syringe plunger to the weight marking corresponding to half of the horse’s weight in pounds. • To set the syringe plunger, unlock the knurled ring by rotating it 1/4 turn. Slide the knurled ring along the plunger shaft so that the side nearest the barrel is at the appropriate notch. Rotate the plunger ring 1/4 turn to lock it in place and ensure it is locked. Make sure the horse’s mouth contains no feed. Remove the cover from the tip of the syringe, and insert the syringe into the horse’s mouth at the interdental space. Depress the plunger until stopped by the knurled ring. The dose should be deposited on the back of the tongue or deep into the cheek pouch. Care should be taken to ensure that the horse consumes the complete dose. Treated animals should be observed briefly after administration to ensure that part of the dose is not lost or rejected. If any of the dose is lost, redosing is recommended. • If, after dosing, the syringe is not completely empty, it may be reused on following days until emptied. Replace the cap after each use. Warning Do not use in horses intended for human consumption. Keep this and all drugs out of the reach of children. In case of ingestion, contact a physician. Physicians may contact a poison control center for advice concerning accidental ingestion. Adverse Reactions In efficacy trials, when the drug was administered at 1.8 mg omeprazole/lb (4 mg/kg) body weight daily for 28 days and 0.9 mg omeprazole/lb (2 mg/kg) body weight daily for 30 additional days, no adverse reactions were observed. Precautions The safety of GASTROGARD Paste has not been determined in pregnant or lactating mares. Clinical Pharmacology Mechanism of Action: Omeprazole is a gastric acid pump inhibitor that regulates the final step in hydrogen ion production and blocks gastric acid secretion regardless of the stimulus. Omeprazole irreversibly binds to the gastric parietal cell’s H+, K+ ATPase enzyme which pumps hydrogen ions into the lumen of the stomach in exchange for potassium ions. Since omeprazole accumulates in the cell canaliculi and is irreversibly bound to the effect site, the plasma concentration at steady state is not directly related to the amount that is bound to the enzyme. The relationship between omeprazole action and plasma concentration is a function of the rate-limiting process of H+, K+ ATPase activity/turnover. Once all of the enzyme becomes bound, acid secretion resumes only after new H+, K+ ATPase is synthesized in the parietal cell (i.e., the rate of new enzyme synthesis exceeds the rate of inhibition). Pharmacodynamics: In a study of pharmacodynamic effects using horses with gastric cannulae, secretion of gastric acid was inhibited in horses given 4 mg omeprazole/kg/day. After the expected maximum suppression of gastric acid secretion was reached (5 days), the actual secretion of gastric acid was reduced by 99%, 95% and 90% at 8, 16, and 24 hours, respectively. Pharmacokinetics: In a pharmacokinetic study involving thirteen healthy, mixed breed horses (8 female, 5 male) receiving multiple doses of omeprazole paste (1.8 mg/lb once daily for fifteen days) in either a fed or fasted state, there was no evidence of drug accumulation in the plasma when comparing the extent of systemic exposure (AUC0-∞). When comparing the individual bioavailability data (AUC0-∞, Cmax, and Tmax measurements) across the study days, there was great inter- and intrasubject variability in the rate and extent of product absorption. Also, the extent of omeprazole absorption in horses was reduced by approximately 67% in the presence of food. This is evidenced by the observation that the mean AUC0-∞ values measured during the fifth day of omeprazole therapy when the animals were fasted for 24 hours was approximately three times greater than the AUC estimated after the first and fifteenth doses when the horses were fed hay ad libitum and sweet feed (grain) twice daily. Prandial status did not affect the rate of drug elimination. The terminal half-life estimates (N=38) ranged from approximately one-half to eight hours. Efficacy Dose Confirmation: GASTROGARD® (omeprazole) Paste, administered to provide omeprazole at 1.8 mg/lb (4 mg/kg) daily for 28 days, effectively healed or reduced the severity of gastric ulcers in 92% of omeprazole-treated horses. In comparison, 32% of controls exhibited healed or less severe ulcers. Horses enrolled in this study were healthy animals confirmed to have gastric ulcers by gastroscopy. Subsequent daily administration of GASTROGARD Paste to provide omeprazole at 0.9 mg/lb (2 mg/kg) for 30 days prevented recurrence of gastric ulcers in 84% of treated horses, whereas ulcers recurred or became more severe in horses removed from omeprazole treatment. Clinical Field Trials: GASTROGARD Paste administered at 1.8 mg/lb (4 mg/kg) daily for 28 days healed or reduced the severity of gastric ulcers in 99% of omeprazoletreated horses. In comparison, 32.4% of control horses had healed ulcers or ulcers which were reduced in severity. These trials included horses of various breeds and under different management conditions, and included horses in race or show training, pleasure horses, and foals as young as one month. Horses enrolled in the efficacy trials were healthy animals confirmed to have gastric ulcers by gastroscopy. In these field trials, horses readily accepted GASTROGARD Paste. There were no drug related adverse reactions. In the clinical trials, GASTROGARD Paste was used concomitantly with other therapies, which included: anthelmintics, antibiotics, non-steroidal and steroidal anti-inflammatory agents, diuretics, tranquilizers and vaccines. Diagnostic and Management Considerations: The following clinical signs may be associated with gastric ulceration in adult horses: inappetence or decreased appetite, recurrent colic, intermittent loose stools or chronic diarrhea, poor hair coat, poor body condition, or poor performance. Clinical signs in foals may include: bruxism (grinding of teeth), excessive salivation, colic, cranial abdominal tenderness, anorexia, diarrhea, sternal recumbency or weakness. A more accurate diagnosis of gastric ulceration in horses and foals may be made if ulcers are visualized directly by endoscopic examination of the gastric mucosa. Gastric ulcers may recur in horses if therapy to prevent recurrence is not administered after the initial treatment is completed. Use GASTROGARD Paste at 0.9 mg omeprazole/lb body weight (2 mg/kg) for control of gastric ulcers following treatment. The safety of administration of GASTROGARD Paste for longer than 91 days has not been determined. Maximal acid suppression occurs after three to five days of treatment with omeprazole. Safety • GASTROGARD Paste was well tolerated in the following controlled efficacy and safety studies. • In field trials involving 139 horses, including foals as young as one month of age, no adverse reactions attributable to omeprazole treatment were noted. • In a placebo controlled adult horse safety study, horses received 20 mg/kg/day omeprazole (5x the recommended dose) for 90 days. No treatment related adverse effects were observed. • In a placebo controlled tolerance study, adult horses were treated with GASTROGARD Paste at a dosage of 40 mg/kg/day (10x the recommended dose) for 21 days. No treatment related adverse effects were observed. • A placebo controlled foal safety study evaluated the safety of omeprazole at doses of 4, 12 or 20 mg/kg (1, 3 or 5x) once daily for 91 days. Foals ranged in age from 66 to 110 days at study initiation. Gamma glutamyltransferase (GGT) levels were significantly elevated in horses treated at exaggerated doses of 20 mg/kg (5x the recommended dose). Mean stomach to body weight ratio was higher for foals in the 3x and 5x groups than for controls; however, no abnormalities of the stomach were evident on histological examination. Reproductive Safety In a male reproductive safety study, 10 stallions received GastroGard Paste at 12 mg/kg/day (3x the recommended dose) for 70 days. No treatment related adverse effects on semen quality or breeding behavior were observed. A safety study in breeding mares has not been conducted. For More Information Please call 1-888-637-4251 and please visit our web site at www.gastrogard.com. Marketed by: Merial Limited Duluth, GA 30096-4640 Merial Limited, a company limited by shares registered in England and Wales (registered number 3332751) with a registered office at PO Box 327, Sandringham House, Sandringham Avenue, Harlow Business Park, Harlow, Essex CM19 5QA, England, and domesticated in Delaware, USA as Merial LLC. US Patent: 4255431 and 5708017 Copyright © 2005 Merial Limited. All rights reserved. Rev. 08-2005 ®GASTROGARD is a registered trademark of the AstraZeneca Group of Companies.

and on-call work always take priority over my personal life. Many times, I can’t take part in activities or go out with friends because I have to work. For me, the solution is simply to accept this and plan important events for my free days. I realize that there will be days when I won’t be able to attend choir rehearsal because my workday runs long. Fortunately, my husband is accommodating. He loves his job and would work longer hours if possible, so he’s happy to work later on evenings when I’m working. He’s also been easygoing about my emergency work on the weekends.

How long have you been singing? I “officially” started singing when I joined the church junior choir at about 5 years of age. I started taking voice lessons when I was 9, and very soon thereafter, I joined a community choir. I joined a professional choir as a teenager and sang with it until I moved to the United States. I sang with the University of Guelph choir all through veterinary school. Currently, I sing with a choir in Princeton, New Jersey. During high school, I was equally interested in music and veterinary medicine and had to decide which path to take. I quickly realized that I could be a veterinarian and still sing, but it would be very difficult to be a professional singer and be involved in veterinary medicine.

Tell me more about your current choir. How often do you perform? The choir has about 75 members. I’ve been a member since I moved to New Jersey 3 years ago. Rehearsals are normally on Mondays and Tuesdays, but the number of rehearsals tends to increase as a concert date approaches. Our major concerts take place at Christmastime and in May and June. We also put on a few smaller concerts throughout the year and sing at some local assisted-living facilities.

During high school, I was equally interested in music and veterinary medicine and had to decide which path to take. I quickly realized that I could be a veterinarian and still sing, but it would be very difficult to be a professional singer and be involved in veterinary medicine. 396

Compendium Equine: Continuing Education for Veterinarians® | November/December 2009


Managing Your Practice and Life Which part do you sing? Are there any roles that you particularly enjoy singing? I’m a soprano. My favorite role has been one of the three ladies in Mozart’s opera The Magic Flute. It’s a light, humorous opera that’s a lot of fun to perform.

Has your singing taken you to some interesting places? I’ve been on tour in Germany and Italy, where we stopped often to perform for local people. I really enjoy going back home to Canada around Christmastime because I get to participate in some Christmas concerts.

Are your colleagues supportive of your singing? Yes, we all know that work takes priority, but my colleagues certainly encourage me to pursue my singing. If I have a performance on a weekend that I’m on call, my colleagues are generally more than willing to cover for me. My bosses even allowed me to travel to Europe with the choir during May, which is, by far, our busiest month.

that I tend to get grumpy, lack energy, and am generally not my normally happy self. This is okay for short periods of time, but if it extends for long periods, it has a detrimental effect on my personal life. It would be great if we could dictate exactly how many hours per week we want to work, but because this is an unlikely scenario in practicing equine medicine, we have to make the best of our situation. Pursuing my hobbies is the best way for me to get away from the stresses of work. Singing, riding, or playing tennis takes my mind off stressful, work-related situations while I’m engaged in the activity and afterward. Doing something that I enjoy clears my mind of my worries and generally allows me to push them to the next morning, when I can deal with them effectively.

SHARE YOUR COMMENTS Have a question or comment about this article? Let us know: E-MAIL editor@CompendiumEquine.com

How does your singing affect your work? When I joined the practice 3½ years ago, a short article introducing me was published in the practice’s quarterly newsletter. The article mentioned my interest and involvement in music, and clients still ask me about it. My singing helps me establish a personal relationship with clients because they realize that I’m well-rounded and that I enjoy being part of the community.

Do you have any other hobbies? Yes, in direct competition with my singing is riding and caring for my two horses. Nothing is a better stress reliever than going for a ride, which I try to do at least two or three times per week, work permitting. In the past year, I’ve also started playing tennis a couple of times per week. Weekly lessons are helping me improve my game. Being a newlywed and a new homeowner are definitely time-consuming as well! Sharing this information makes it hard for me to believe that I can actually accomplish all of this in a week. Many times, I can’t, but I certainly try!

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Do you have any advice for other practitioners who are having trouble finding the time to pursue interests outside of work? Veterinary medicine is a challenging and time-consuming career. It seems that we are often at the beck and call of clients and that our time is never really our own. This can wear us down quickly, so it’s important to set aside time for ourselves to do the things we really enjoy outside of work; otherwise, we’ll burn out. Really busy times of the year, when there’s little time for my life outside of work, can negatively affect my mood. At these times, my husband thinks Compendium Equine: Continuing Education for Veterinarians®

397

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Clinical Snapshot Particularly intriguing or difficult cases

Case Presentation #1

A

❯❯ Adam Stern, DVM Oklahoma State University

An 18-year-old Quarter horse mare was examined for acute colic by the referring veterinarian. On physical examination, the mare was tachypneic, tachycardic, and extremely painful. The mare appeared to have an adequate body condition and did not have a history of colic before this episode. The mare was referred to the Oklahoma State University Veterinary Medical Teaching Hospital for treatment and surgery but died in transit to the university. A photograph of the stomach (A) was obtained at necropsy. 1. What is your diagnosis?

3. Is this a common cause of equine

2. What risk factors are related to the

colic?

4. What method may help prevent this

problem in cases of acute colic?

cause of this lesion? SEE PAGE 400 FOR ANSWERS AND EXPLANATIONS.

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There’s a new movement in equine pain management.

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Osteoarthritis pain relief with staying power.2 EQUIOXX®(firocoxib). EQUIOXX® (firocoxib) is the next generation of pain management. It is the first and only coxib NSAID approved for horses and provides 24 hours of prescription pain relief* in just one daily dose.2 It’s also the only NSAID approved for use up to 14 consecutive days by the AQHA3 and the USEF4 — compared with only five days for other traditional NSAIDs.3,4 The efficacy and safety of EQUIOXX have been more thoroughly tested than any other equine NSAID on the market.5,6 You can be part of this new movement — and the source for osteoarthritis pain relief with staying power. Help your practice and your clients by offering EQUIOXX. For details visit www.equioxx.com.

As with any prescription medication, prior to use, a veterinarian should perform a physical examination and review the horse’s medical history. A veterinarian should advise horse owners to observe for signs of potential drug toxicity. As a class, nonsteroidal anti-inflammatory drugs may be associated with gastrointestinal and renal toxicity. Use with other NSAIDs, corticosteroids or nephrotoxic medication should be avoided. EQUIOXX has not been tested in horses less than 1 year of age or in breeding horses, or pregnant or lactating mares. For additional information please refer to the prescribing information or visit www.equioxx.com. *Joint pain and inflammation associated with equine osteoarthritis, also called degenerative joint disease. 1 Data on file at Merial. 2 EQUIOXX product label. 3 American Quarter Horse Association. Show rules and regulations. Official Handbook of Rules and Regulations 2008:128. 4 United States Equestrian Federation. Drugs and medications guidelines. 2007:2-3. Available at: http://www.usef.org/documents/competitions/2007/2007DrugsMedsGuidelines.pdf. Accessed February 20, 2009. 5 Based on data provided in FDA Freedom of Information summaries. 6 Data on file at Merial, Safety Study, PR&D 0030701. ®EQUIOXX is a registered trademark of Merial. ©2009 Merial Limited. Duluth, GA. All rights reserved. EQUIEQX924-A (06/09) See Page 400 for Product Information Summary

Official product of 3,4


Clinical Snapshot

EQUIOXX® (firocoxib) Oral Paste for Horses Non-steroidal anti-inflammatory drug for oral use in horses only. CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian. Indications: EQUIOXX® Oral Paste is administered for up to 14 days for the control of pain and inflammation associated with osteoarthritis in horses. Contraindications: Horses with hypersensitivity to firocoxib or other NSAIDs should not receive EQUIOXX® Oral Paste.

Answers and Explanations Case Presentation #1 SEE PAGE 398 FOR CASE PRESENTATION.

1. A diagnosis of gastric rupture was

made at necropsy (B; white arrow). Rupture occurs occasionally in cases of acute colic because a horse cannot vomit when its stomach becomes distended (with too much fluid). Multiple criteria were fulfilled to determine this diagnosis. In this case, feed material was found within the cranioventral abdomen. The rupture site in the stomach formed adhesions with the omentum, which had accumulated feed material and fibrin. The feed material in the omentum also contained blood from hemorrhage caused by the gastric rupture (B; arrowheads). As in this case, stomach rupture commonly occurs at the greater curvature, with separation of the serosa before separation of the mucosa (B; blue arrows). Common clinical signs of gastric rupture include severe colic, decreased borborygmi, increased respiratory rate, prolonged capillary refill time, sweating, congestion of oral mucous membranes, and sudden death. In some cases, there may be a period of relief from signs of abdominal pain before death. Based on the signalment and clinical finding of severe abdominal pain, the differential diagnosis includes cecal rupture, small intestinal torsion, strangulating lipoma, large colon

Warnings: For oral use in horses only. Do not use in horses intended for human consumption. Human Warnings: Not for use in humans. Keep this and all medications out of the reach of children. Consult a physician in case of accidental ingestion by humans. Animal Safety: Client should be advised to observe for signs of potential drug toxicity and be given a Client Information Sheet with each prescription. For technical assistance or to report suspected adverse events, call 1-877-217-3543. Precautions: Horses should undergo a thorough history and physical examination before initiation of NSAID therapy. Appropriate laboratory tests should be conducted to establish hematological and serum biochemical baseline data before and periodically during administration of any NSAID. Clients should be advised to observe for signs of potential drug toxicity and be given a Client Information Sheet with each prescription. See Information for Owner or Person Treating Horse section of this package insert. Treatment with EQUIOXX® should be terminated if signs such as inappetence, colic, abnormal feces, or lethargy are observed. As a class, cyclooxygenase inhibitory NSAIDs may be associated with renal and gastrointestinal toxicity. Sensitivity to drug-associated adverse events varies with the individual patient. Patients at greatest risk for adverse events are those that are dehydrated, on diuretic therapy, or those with existing renal, cardiovascular, and/or hepatic dysfunction. Concurrent administration of potentially nephrotoxic drugs should be carefully approached or avoided. NSAIDs may inhibit the prostaglandins that maintain normal homeostatic function. Such anti-prostaglandin effects may result in clinically significant disease in patients with underlying or pre-existing disease that has not been previously diagnosed. Since many NSAIDs possess the potential to produce gastrointestinal ulcerations, concomitant use with other antiinflammatory drugs, such as NSAIDs or corticosteroids, should be avoided or closely monitored. The concomitant use of protein bound drugs with EQUIOXX® Oral Paste has not been studied in horses. The influence of concomitant drugs that may inhibit the metabolism of EQUIOXX® Oral Paste has not been evaluated. Drug compatibility should be monitored in patients requiring adjunctive therapy. The safe use of EQUIOXX® Oral Paste in horses less than one year in age, horses used for breeding, or in pregnant or lactating mares has not been evaluated. Consider appropriate washout times when switching from one NSAID to another NSAID or corticosteroid. Adverse Reactions: In controlled field studies, 127 horses (ages 3 to 37 years) were evaluated for safety when given EQUIOXX® Oral Paste at a dose of 0.045 mg/lb (0.1 mg/kg) orally once daily for up to 14 days. The following adverse reactions were observed. Horses may have experienced more than one of the observed adverse reactions during the study. Adverse Reactions Seen In U.S. Field Studies

Adverse Reactions

EQUIOXX n=127

Active Control n=125

Abdominal pain

0

1

Diarrhea

2

0

Excitation

1

0

Lethargy

0

1

Loose stool

1

0

Polydipsia

0

1

Urticaria

0

1

EQUIOXX® (firocoxib) Oral Paste was safely used concomitantly with other therapies, including vaccines, anthelmintics, and antibiotics, during the field studies.

volvulus, intestinal impaction, and torsion of the mesenteric root. 2. In one study, horses fed only grass hay or grass and alfalfa hay had an increased risk of gastric rupture. Horses fed grain had a reduced risk of gastric rupture.1 In cases of rupture, treatment is usually not possible because of extensive contamination of the abdominal cavity with gastric contents; therefore, the horse should be euthanized. There is a report of repair of a full-thickness gastric rupture in a Thoroughbred mare; however, in this case, there was no gross contamination of the abdominal cavity.2 3. Gastric rupture is diagnosed in approximately 5% of veterinary hospital equine colic admissions.3 4. To help prevent gastric rupture during an episode of acute colic, check for reflux before fluid administration and limit the amount of fluids administered during nasogastric intubation (e.g., no more than 6 to 8 L [1.6 to 2.1 gal]). References 1. Kiper ML, Traub-Dargatz J, Curtis CR. Gastric rupture in horses: 50 cases (1979-1987). JAVMA 1990; 196(2):333-336. 2. Hogan PM, Bramlage LR, Pierce SW. Repair of a full-thickness gastric rupture in a horse. JAVMA 1995; 207(1):338-340. 3. Brown CC, Baker DC, Barker IK. Alimentary system. In: Maxie GM, ed. Pathology of Domestic Animals. 5th ed. Edinburgh, UK: Elsevier Saunders; 2007:56.

B

Information for Owner or Person Treating Horse: You should give the Client Information Sheet to the person treating the horse and advise them of the potential for adverse reactions and the clinical signs associated with NSAID intolerance. Adverse reactions may include erosions and ulcers of the gums, tongue, lips and face, weight loss, colic, diarrhea, or icterus. Serious adverse reactions associated with this drug class can occur without warning and, in rare situations, result in death. Clients should be advised to discontinue NSAID therapy and contact their veterinarian immediately if any of these signs of intolerance are observed. The majority of patients with drug-related adverse reactions recover when the signs are recognized, drug administration is stopped, and veterinary care is initiated. Storage Information: Store below 86°F (30°C). Brief excursions up to 104°F (40°C) are permitted. How Supplied: EQUIOXX is available in packs of 20, 72 and 216 individually-boxed syringes. Each syringe contains 6.93 grams of EQUIOXX® paste, sufficient to treat a 1250 lb. horse. For technical assistance or to report suspected adverse reactions, call 1-877-217-3543. NADA 141-253, Approved by FDA EQUIOXX is a registered trademark of Merial Limited, Duluth, Georgia, USA. ® 1050-2012-01 Rev. 02-06 Copyright© 2006 Merial Limited. All Rights Reserved. U.S. Pat. No.: 5981576, 6020343

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Compendium Equine: Continuing Education for Veterinarians® | November/December 2009


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From the Horse’s Mouth features important topics on equine dentistry

Routine Dentistry in Juvenile Performance Horses ❯❯ Cleet Griffin, DVM, DABVP Texas A&M University

Anatomy and Nomenclature Page 402

Examination Page 406

Routine Dental Conditions in Juvenile Performance Horses Page 408

402

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PIC

S ON EQ U IN E

Abstract: In horses, eruption of the permanent dentition begins at approximately 1 year of age and is completed by approximately 5 years of age. Because juvenile horses in work can develop undesirable behaviors due to oral pain, veterinarians frequently perform oral examinations to identify dental conditions that may be problematic. In juvenile horses, dental concerns include the presence of wolf teeth, sharp dental points, mucosal erosions, abnormalities of eruption, and facial swellings. Veterinarians perform procedures designed to alleviate sources of oral pain, such as smoothing (floating) of sharp areas, extraction of wolf teeth, and removal of retained deciduous teeth. Sometimes, radiography is indicated to provide more information about areas of concern identified by the examiner. To most effectively perform oral examinations and common dental procedures in young horses, veterinarians should have a working knowledge of skull anatomy, dental anatomy, and tooth eruption times.

I

At a Glance

TO

n horses aged 1 to 5 years, the permanent cheek teeth (24) and incisors (12) erupt sequentially, causing the deciduous cheek teeth and incisors to shed during this time. At approximately 2 years of age, many horses begin training for competitive, strenuous athletic events. Veterinarians and horse owners associate several undesirable behaviors (e.g., head tossing) with oral pain in these horses. Therefore, veterinarians are often asked to examine juvenile (2 to 5 years of age) horses’ mouths to identify sources of pain, to evaluate facial or mandibular swellings, and to identify abnormalities associated with adult tooth eruption. To treat these horses, veterinarians remove (float) sharp dental points and extract wolf teeth, remove retained deciduous incisors, and remove loose, retained, or damaged deciduous premolars. In most cases, the veterinarian’s goal for these dental procedures is to help juvenile horses perform (and chew) more comfortably. This article reviews the pertinent dental anatomy, nomenclature, and tooth eruption times in horses and describes the treatment of several common dental conditions in juvenile horses.

Anatomy and Nomenclature See BOX 11–3 for equine dental formulas.

Incisors (Triadan ’01 through ’03) The deciduous central incisors (Triadan ’01) erupt at approximately 6 days of age, the deciduous intermediate incisors (Triadan ’02) at 4 to 6 weeks of age, and the deciduous corner incisors (Triadan ’03) at 6 to 9 months of age.4 The deciduous incisors are dome-shaped and are smaller and whiter than the permanent incisors (FIGURE 1). The deciduous incisors have a flattened root, short crown, and shallow infundibulum (cup) on the occlusal surface.1,2 As the permanent incisor erupts, the deciduous tooth root is resorbed. The deciduous incisor (cap) sheds as the permanent incisor emerges on the lingual side of the deciduous tooth. The eruption times of the deciduous and permanent incisors can be used to help estimate a horse’s age.4

Canine Teeth (Triadan ’04) In both sexes, the deciduous canine teeth are short spicules (~0.5 cm in length) that do not erupt through the gingiva.1 Permanent canine teeth erupt at approxi-

Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com


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FREE CE From the Horse’s Mouth

BOX 1

Triadan Tooth Numbering System Using the three-digit nomenclature system, the first digit designates the quadrant of the mouth and whether a tooth is deciduous or permanent. The numbering sequence for permanent teeth is right maxilla, 1; left maxilla, 2; left mandible, 3; and right mandible, 4. The deciduous teeth are designated as quadrants 5 through 8 in the same order. The subsequent digits in the num-

bering system designate each tooth within the quadrant, starting with the central (first) incisor, which is designated as ’01. The incisors are designated as ’01 to ’03; the canine teeth, ’04; the premolars, ’05 to ’08; and the molars, ’09 to ’11 (e.g., the central incisor of the upper right arcade is 101, the intermediate incisor of the same arcade is 102).1–3

Triadan classification of equine teeth. (From Floyd MR. The modified Triadan system nomenclature for veterinary dentistry. J Vet Dent 1991. Reprinted with permission from Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005)

FIGURE 1 The incisors.

Deciduous incisors in a 2-year-old Quarter horse. Deciduous incisors are dome-shaped and are smaller and whiter than permanent incisors.

The lower-left central deciduous incisor (Triadan 701) is being pushed away from the gingiva as the underlying permanent tooth emerges in an approximately 30-month-old horse. The upper-central deciduous incisors were already shed; the upper-central permanent incisors (Triadan 101 and 201) continue to erupt toward wear (occlusion).

mately 4 to 5 years of age and are consistently present in male horses.4 The adult canine teeth have a simple structure, including a long, curved crown (~6 cm in length), of which

404

The four permanent central incisors have come into wear in a 3-year-old horse. These teeth have vertical grooves and are significantly larger than the adjacent deciduous incisors.

only a short length erupts through the gingiva. Unlike the cheek teeth, the canine teeth do not continually erupt,5 and there is no occlusal contact between the upper and lower canine

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RECOMBITEK®. For West Nile virus protection, the canary’s got your back all season long. It’s good to have recombinant canarypox-vectored vaccine technology behind you. RECOMBITEK® Equine West Nile Virus (WNV) vaccine is the only WNV vaccine made using this Unvaccinated Vaccinates Controls proven technology. This unique technology helps RECOMBITEK Equine WNV stimulate a fast10% 80% Clinical Signs (muscle acting1 immune response that lasts throughout mosquito season.2 (encephalomyelitis) fasciculation) RECOMBITEK Equine WNV is also the only commercially available vaccine that has been Fever 10% 90% Histopathology tested against natural challenge with WNV-infected mosquitoes2 as well as WNV intrathecal (mild to moderate 10% 80% encephalitis) challenge in horses (see table).3,* WNV Viremia 0% 100% In a study, 10 naive horses vaccinated with two doses of RECOMBITEK Equine WNV Horses were challenged two weeks after the second dose of vaccine on Days 0 and 35 were challenged by intrathecal administration — directly into RECOMBITEK Equine WNV. the spinal canal. Ten nonvaccinated control horses were likewise challenged. Eight of the 10 controls developed encephalomyelitis, attesting to the severity of the challenge, while a single vaccinated horse developed only muscle fasciculation.3 RECOMBITEK Equine WNV is safe for use in foals 2 months of age and older,4 and is labeled for annual revaccination with a single dose.**,5 Trust it for fast and lasting protection. Intrathecal challenge results.†,3

*Studies conducted with commercial vaccine. **Following initial two-dose series. Siger L, et al. Assessment of the efficacy of a single dose of a recombinant vaccine against West Nile virus in response to natural challenge with West Nile virus-infected mosquitoes in horses. American Journal of Veterinary Research 2004;65(11):1459-1462. Data on file at Merial. Study 02-092. Siger L, Bowen R, et al. Evaluation of the efficacy provided by a recombinant canarypox-vectored equine West Nile virus vaccine against an experimental West Nile virus intrathecal challenge in horses. Veterinary Therapeutics 2006;7(3):249-256. 4 Data on file at Merial. Study 02-067. 5 RECOMBITEK Equine West Nile Virus vaccine product label. 1 2 3

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FREE CE From the Horse’s Mouth

FIGURE 2

The relationship between the upper and lower cheek teeth in horses. The width of the upper and lower jaws differs, and the chewing surface is sloped (the maxillary cheek teeth are taller on the buccal side, and the mandibular cheek teeth are taller on the lingual side).

teeth because the lower canine teeth are more rostral than the upper teeth.

CriticalPo nt Juvenile horses in work can develop undesirable behaviors due to oral pain.

Wolf Teeth (Triadan ’05) The small, simply crowned wolf teeth (first premolars) do not have deciduous counterparts and generally erupt during the first year of life. These teeth are usually no more than 1 to 2 cm in length, are present in most yearling horses, and have a single root that may be up to 30 mm in length.5–7 The wolf teeth are usually near the rostral part of the second premolar (Triadan ’06). In some cases, wolf teeth are shed during eruption of permanent second premolars.2,8 Wolf teeth may not be present in all of the dental arcades, making it possible for a horse to have zero to four wolf teeth. In some cases, wolf teeth do not erupt through the gingiva but remain as firm, submucosal nodules within the interdental space; these are called blind or impacted wolf teeth.

Cheek Teeth (Triadan ’06 through ’11) In foals, the deciduous premolars (Triadan ’06 through ’08) erupt through the gingiva shortly after birth.4 The deciduous premolars undergo distinct root formation and have a much shorter crown than the permanent premolars.1,2 It is of clinical interest that the crowns of the deciduous premolars closely resemble those of the permanent teeth. As a juvenile horse matures, the crowns of the deciduous premolars wear thin, and the roots resorb as

406

the underlying permanent teeth erupt. A thin portion of the deciduous crown with slender, sharp root spicules (known as a cap) remains closely associated with the underlying permanent tooth as it works through the gingiva.5 As the permanent tooth erupts, a small gap develops between the permanent premolar and the cap, and the soft tissue attachments associated with the cap necrotize as wet feed material and bacteria become trapped in this space. Over time, the cap loosens and is shed. The permanent premolars erupt, and their deciduous counterparts subsequently shed sequentially at approximately 2½ years (Triadan ’06), 3 years (Triadan ’07), and 4 years (Triadan ’08) of age.4 The molars (Triadan ’09 through ’11), which have no deciduous precursors, erupt at approximately 1 year (Triadan ’09), 2 years (Triadan ’10), and 3½ years (Triadan ’11) of age.2,4 The permanent cheek teeth have long reserve crowns that continually erupt at 2 to 3 mm per year, which is similar to the rate of attrition at the chewing surface.5 In horses, the width between the two rows of maxillary cheek teeth is greater than the width between the two rows of mandibular cheek teeth; this discrepancy is called anisognathia.5 The angle of occlusion between the upper and lower cheek teeth is sloped in the lateromedial plane, with the upper cheek teeth being longer on their buccal aspect and the lower cheek teeth taller on their lingual aspect5 (FIGURE 2). This normal slope across the grinding surface of the cheek teeth is considered to be approximately 10˚ to 15˚,5 although recent investigators have determined that the size and range of the slope (angle of occlusion) in normal horses is greater than previously thought.9 The combination of the anatomic differences between the upper and lower jaws and the chewing action of the horse forms sharp dental points on the buccal side of the upper cheek teeth and on the lingual side of the lower cheek teeth.

Examination First assess the horse’s health status by obtaining the pertinent history, performing a physical examination, and determining the horse’s body condition score. Before sedating the horse for an oral examination, attempt to rinse its mouth, estimate its age, and identify incisor abnormalities (e.g., overgrown incisors that

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that helps protect against rabies and Potomac horse fever. Best of all, both are backed by Merial, a trusted leader in equine health. Data on file at Merial. Michigan State University College of Veterinary Medicine online publication January 2004. Available at: http://old.cvm.msu.edu/extension/equine/RabiesinHorses.pdf. Accessed February 15, 2008. IMRAB product label. 4 Blanton JD, Hanlon CA, et al. Rabies surveillance in the United States during 2006. JAVMA 2007;231(4):540-556. 5 Blanton JD, Palmer D, et al. Rabies surveillance in the United States during 2007. JAVMA 2008;233(6):884-897. 1 2 3

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FREE CE From the Horse’s Mouth

FIGURE 3

Safe technique for palpating sharp dental points along the cheek.

CriticalPo nt Veterinarians should understand skull anatomy, dental anatomy, and eruption times to most effectively perform dental examinations and procedures in horses.

may be damaged by insertion of a speculum). Take a preliminary look at the cheek teeth by carefully retracting the tongue and cheek while shining a light into the mouth. Attempt to palpate the gingiva of the interdental space for enlargements or painful areas; the sharp points of the maxillary cheek teeth can be safely palpated by placing the fingers on the skin of the horse’s cheek, adjacent to the upper cheek teeth (FIGURE 3). To inspect the mouth and perform procedures involving the cheek teeth, sedate the horse (e.g., with detomidine at 0.01 to 0.02 mg/kg IV). After waiting 5 minutes, insert a dental speculum. Support the horse’s head at a sufficient height and use a bright light to facilitate the rest of the examination and any other procedures. With the speculum opened sufficiently, observe and palpate the cheek teeth for abnormalities. Frequently wetting the hands, arms, and instruments with water can reduce irritation to the patient’s mouth, and wearing examination gloves can help minimize contamination of the clinician’s skin with bacteria from the horse’s mouth. Use of a dental mirror allows closer examination of the cheek teeth and gingiva. Use of an equine dental chart allows convenient recording of dental examination findings, dosages of medications administered, and treatments provided.

Routine Dental Conditions in Juvenile Performance Horses Incisors It is not uncommon for weanlings and yearlings to sustain trauma to the incisors and adjacent bone, possibly resulting in avulsion

408

FIGURE 4

Frontal view of the occlusal portion of the mandibular incisors in a 2-year-old Quarter horse stallion. The lower-left intermediate deciduous incisor (Triadan 702) is avulsed. The four other lower incisor teeth (Triadan 701 and 801–803) appear normal. The lower-left lateral incisor (Triadan 703) is missing.

of or damage to the deciduous teeth as well as damage to the surrounding soft tissue and underlying permanent tooth buds (FIGURES 4 THROUGH 6). These traumatic injuries may result in the loss of one or more teeth or in abnormal eruption of teeth,10 possibly leading to malocclusion between the upper and lower incisor arcades. Overgrowth of an unopposed incisor may impede lateral movement of the mandible, affecting occlusion and chewing unless a portion of the unopposed tooth is shortened periodically. Overgrown incisors can be shortened without great difficulty as follows. Inject a sedative/analgesic (e.g., detomidine at 0.01 to 0.02 mg/kg IV or xylazine at 0.25 to 0.50 mg/kg IV). While supporting the sedated horse’s head at an appropriate level, use a ruler to measure the area of tooth to be shortened, and mark it with a waterproof pen. Slide an incisor speculum (made of flexible polyvinylchloride pipe) into the interdental space, and secure it with an elastic cord around the poll to keep the incisor teeth apart. Use a hand file or power instrument to conservatively shorten the affected tooth/teeth (FIGURE 7). When motorized instruments are used, the tooth and burr should be cooled frequently with water irrigation, and the blade of the instrument should be cleaned frequently to reduce heat production and prevent thermal pulp injury.11 Brachygnathia (parrot mouth) is an occasional malocclusion. The term overjet can

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Dentistry in Juvenile Performance Horses CE FIGURE 5

FIGURE 6

A number of deciduous incisors are missing or have been damaged because of previous trauma in an approximately 30-month-old Quarter horse. The lower-central permanent incisors (Triadan 301 and 401) appear to be erupting normally.

FIGURE 7

In this frontal view, upper incisor teeth are missing because of previous trauma. Over time, the unopposed lower incisors (Triadan 301 and 302) have become moderately overgrown. A length of crown (~4 mm) has been marked with a red waterproof pen to serve as a guide while shortening the unopposed teeth. FIGURE 8

A motorized instrument is used to shorten overgrown incisors to form a more level chewing surface.

Severe overbite in a 5-year-old Quarter horse mare.

be used to describe affected horses, in which the upper incisors project to some degree past the labial side of the lower incisors in a horizontal direction.12 In severe cases, the upper incisors protrude past the lower teeth to an extent that allows the occlusal surface of the upper incisors to deviate ventrally below the occlusal surface of the lower incisors. This is called an overbite 12 (FIGURE 8). An overbite traps the lower incisors behind the upper incisors, limiting rostral movement and growth of the mandible and worsening the condition.7,12 With incisor overjet and overbite, the upper cheek teeth tend to be more rostral relative to the lower cheek teeth. As a result, affected horses tend to develop sharp overgrowths on the rostral aspect of the upper arcade and on the caudal aspect of the lower arcade

(FIGURES 9 AND 10). These sharp overgrowths can cause bitting problems and limit rostralcaudal movement of the mandible.13 Incisor overjet has also been associated with the presence of excessive or exaggerated transverse ridges on the cheek teeth, which can further limit movement of the mandible.7 In affected horses, it is important to reduce the sharp overgrowths to promote normal movement of the mandible. Treatment includes periodic floating of sharp hooks and ramps of the cheek teeth, floating of excessive transverse ridges, and reducing the height of affected incisors.14 Horses should be adequately sedated during floating, which is facilitated by the use of appropriate head support, a full-mouth dental speculum, a bright light source, and up-todate instrumentation.

CriticalPo nt Sharp dental points on the cheek teeth may cause mucosal irritation and erosions on the cheeks or tongue due to repetitive contact.

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FREE CE From the Horse’s Mouth

FIGURE 9

A large, sharp, rostral hook of the second premolar (Triadan 106) in a 5-year-old horse with incisor overjet. A wolf tooth (Triadan 105) is present.

CriticalPo nt A dental mirror is very useful, allowing close examination of the cheek teeth and gingiva.

410

When managing an overbite in a performance horse, it is important to remember that if the lower incisors are trapped behind the upper incisors, overgrown lower incisors may damage the mucosa of the hard palate and cause discomfort; additionally, overgrown upper incisors may contact the upper lip or cause painful injury if caught on a fence or other object.10 Therefore, horses with an overbite should have the overgrown upper and lower incisors shortened periodically. Horses with incisor overjet gradually develop a ventral curvature to the upper incisor occlusal margin (smile) that may hinder side-to-side movement of the mandible. Horses with this malocclusion can benefit from reduction of the overgrown incisors to form a more level incisor occlusal surface. For this procedure, prop open the mouth of the sedated horse and use a hand file or power instrument to conservatively reduce the height of the affected incisors (upper-central incisors and lower-corner incisors). It is important to remember that large overgrowths of permanent incisors should be shortened in stages to avoid acute exposure of the pulp chamber of the tooth.7,13,15 In prognathia (sow mouth, monkey mouth), which is the opposite of brachygnathia, the lower incisors protrude rostral to the upper incisors. If a horse has this condition, sharp hooks form on the rostral part of lower first cheek teeth and on the caudal part of the upper last molars. In horses with severe underbite, the upper incisors may become overgrown and damage the mucosa of the mandible behind the lower incisors. In these

FIGURE 10

A tall, sharp hook on the caudal aspect of the last molar (Triadan 411).

cases, sharp areas and overgrowths of the incisors and cheek teeth should be inspected and floated to minimize bitting problems and mucosal trauma associated with the underbite. Horses with malocclusions secondary to an incisor abnormality should be examined twice per year. In horses with retained deciduous incisors, one or more deciduous incisors may fail to shed as the permanent incisor erupts.15 Discomfort may occur, resulting in clinical signs such as head tossing during eating, rubbing the incisors on fi xed objects, quidding, bitting problems, and swelling.8,15 Failure of the deciduous tooth to shed properly causes the permanent incisor to be displaced caudally and trapped behind adjacent incisors,13 possibly resulting in malocclusion of the permanent incisor arcade (FIGURE 11). Furthermore, the gap that develops between the retained deciduous tooth and the permanent tooth becomes packed with feed material, causing odor and irritating the gingiva. In most cases, the retained deciduous incisor cap and root remnant can easily be removed in a standing patient after administration of a sedative or analgesic (e.g., detomidine at 0.01 to 0.02 mg/ kg IV or xylazine at 0.25 to 0.50 mg/kg IV) and either infiltration of a local anesthetic or a specific nerve block (e.g., a mental nerve block for lower teeth or an infraorbital nerve block for upper teeth). A small elevator can be used to pry, wiggle, and loosen the attachments of the tooth for its removal. Irritation and pain will result if the slim root portion of the deciduous incisor is not removed completely.13 If the deciduous incisor fractures during removal, the gingiva will need to be incised a short

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Dentistry in Juvenile Performance Horses CE FIGURE 11

FIGURE 12

Retained deciduous incisors (Triadan 702, 703, 802, and 803) on the labial side of the corresponding permanent incisors. An elevator is positioned to indicate the location of retained deciduous incisor Triadan 703.

distance over the labial aspect of the root to expose and remove the entire fractured remnant.13 After removal of the retained deciduous incisor, the displaced permanent incisor should gradually drift into proper alignment. If it is crowded, slightly file the edge of the adjacent incisors to allow enough space. Aftercare is minimal, but tetanus prophylaxis is indicated after tooth extractions in horses.16

Canine Teeth Although canine teeth cause few problems,15 erupting permanent canine teeth in stallions and geldings (rarely in mares) can irritate the eruption site on the mandible or maxilla and cause pain, bitting problems, or abnormal behavior.6,17 In affected horses, swelling over the erupting canine tooth may become ulcerated.6 If painful or ulcerated swelling develops, the horse can be sedated and local anesthetic infiltrated over the erupting crown to remove a small section of gingiva. This can be accomplished using a forceps and scissors or using a scalpel to make a cruciate incision through the gingiva overlying the tooth.17 The rationale for this procedure is to facilitate tooth eruption through the gingiva. In performance horses, erupted canine teeth that become excessively sharp or that interfere with the bit can be shortened or blunted using a file or motorized instrument. To avoid damage to the pulp canal, it is recommended to reduce the crown of the canine tooth to no shorter than the level of the permanent corner incisor.17 Tartar buildup on canine teeth can be scraped and removed

A vestigial canine tooth (Triadan 404) in the gingiva just caudal to the right-lower lateral incisor (Triadan 403) in a mare.

with a forceps, followed by polishing with a fine S-file. Canine teeth may erupt in mares, appearing as short, slender structures in the gingiva. Although these vestiges can be very sharp, canine teeth in mares generally do not require veterinary attention (FIGURE 12).

Cheek Teeth Sharp dental points on the cheek teeth may cause mucosal irritation and erosion of the cheeks or tongue due to repetitive contact. Erosion of the cheek mucosa is more common in juvenile horses18; in one study, cheek erosion occurred with greater frequency in horses ridden with a bit and bridle compared with unridden horses.19 In addition, the tongue and interdental space of the mandible are vulnerable to injury from use of a bit.20,21 Problems that occur during performance, such as bit chewing, tail wringing, gaping the mouth, excessive head tossing, and ear pinning, have been associated with conditions causing oral pain.10,21 Because the skin and muscles of the face adhere tightly to the horse’s skull, the buccal space along the upper cheek teeth is extremely narrow, especially in the caudal part of the mouth.22 Therefore, the cheeks are closely apposed to sharp points that develop along the buccal side of the upper cheek teeth. Consequently, erosion of the cheek mucosa in this area is not unusual in horses being examined for undesirable bitting behavior (FIGURE 13). Sharp points of the lingual side of the lower cheek teeth may also irritate or erode the tongue.23 Sharp overgrowths (i.e., hooks), such as those on the rostral part of the upper first cheek teeth or on the caudal aspect of the

CriticalPo nt Veterinarians should carefully palpate the upper and lower cheek teeth arcades to verify that floating has successfully removed sharp points and hooks.

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FIGURE 13

Extensive buccal erosions along the left cheek in a 5-year-old American Paint horse. The affected areas are stained with grass pigments.

CriticalPo nt Deciduous premolar caps that are loose or fractured or that fail to shed properly can irritate a horse; clinical signs of discomfort include loss of appetite, head shaking, bitting problems, and chewing problems.

412

last lower molars, may traumatize the cheeks or tongue; these sharp areas have been associated with bitting problems and abnormal head carriage.24 Sharp dental points require floating along the buccal side of the upper cheek teeth and the lingual side of the lower cheek teeth using hand instruments or motorized equipment. (To improve accuracy and decrease soft tissue trauma, my clinic prefers motorized instruments for most routine procedures.) Floating should be performed in an adequately sedated horse with the aid of a dental speculum. The horse’s narrow oral opening, large tongue, and narrow buccal space create unique challenges for floating various teeth. Therefore, it is important to carefully palpate the upper and lower cheek teeth arcades to verify that floating has successfully removed sharp points and hooks. The rostral portion of the upper and lower first cheek teeth should also be floated and slightly rounded with a hand file or power instrument to help decrease irritation and pain as the bit presses the cheek against the premolars. This procedure is called creating bit seats.8 It is important to determine whether young performance horses have wolf teeth (Triadan ’05). Most horses have one or two upper wolf teeth. Although debatable,25 it is thought that these teeth may cause pain when they contact the bit or when the cheek mucosa presses against the sharp point of the tooth. Unerupted wolf teeth (blind or impacted wolf teeth) are thought to cause pain when the gingiva is compressed between the bit and the underlying tooth. Blind wolf teeth may be detected by palpating the interdental space, and radiogra-

FIGURE 14

A deciduous premolar cap (Triadan 706) and the underlying erupting permanent premolar (Triadan 306) in an approximately 30-monthold Quarter horse.

phy may confirm their presence. Veterinarians commonly extract wolf teeth from juvenile horses. This is performed in standing, sedated horses and is facilitated by the use of a dental speculum and local anesthesia. After elevating the gingiva tissue around the circumference of the wolf tooth, the tooth is loosened and removed using an elevator to wiggle and pry the periodontal attachments from the tooth. Aftercare is usually minimal, although tetanus prophylaxis is advised after extractions. In my practice, horses commonly resume training 24 hours after wolf tooth extraction. Upper wolf tooth extraction sites are left open for healing and epithelialization; lower wolf tooth extraction sites can become contaminated with feed material and inflamed.6,8 Therefore, daily irrigation of lower wolf tooth extraction sites is recommended until granulation tissue has filled the alveolus. Gauze packing may also help minimize contamination of the site.8 Deciduous premolar caps that are loose or fractured or that fail to shed properly can irritate a horse7,23; clinical signs of discomfort include loss of appetite, head shaking, bitting problems, and chewing problems7 (FIGURE 14). Deciduous premolar caps can be safely extracted when a line of demarcation is visible between the cap and the erupting permanent tooth. The thin, wafer-like cap or remnant can be grasped with a forceps and rolled toward midline to facilitate removal (FIGURE 15). Alternatively, an elevator with a flattened end may be used to wiggle and pry the cap from its attachments (FIGURE 16). In either case, the cap and root spicules are removed without difficulty in most instances.

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Dentistry in Juvenile Performance Horses CE FIGURE 15

FIGURE 16

A retained cap (Triadan 708) is rotated toward the cheek in a 4-year-old Quarter horse. A dental mirror is used to help visualize the erupting permanent tooth (Triadan 308) and the retained cap. Buccal erosions are visible with the mirror.

A deciduous premolar cap (Triadan 606) in a 3-year-old Quarter horse. A flat elevator is wedged into the gap between the cap and the underlying permanent tooth (Triadan 206).

FIGURE 17

FIGURE 18

CriticalPo nt

On this open-mouth, lateral radiograph, a thin mandibular premolar cap (arrow) can be distinguished from the underlying permanent cheek tooth in a 3-year-old horse. An unerupted upper wolf tooth (circle) is just rostral to the upper first cheek tooth.

If a cap protrudes above adjacent teeth but a line of demarcation is not present or if the tooth cannot be removed with reasonable force, the cap should be floated until it is even with adjacent teeth.26 Because the crown of the deciduous premolar cap closely resembles the crown of the permanent tooth, it may be very difficult to determine whether a premolar cap has been shed. If this must be determined, an openmouth, lateral oblique radiograph can be very helpful. A premolar cap can usually be identified on a radiograph as a short, thin slice of tooth situated over the underlying permanent premolar (FIGURE 17). Eruption cysts are bony enlargements that can be observed in juvenile horses on the ventral aspect of the mandible and on the dorsolateral aspect of the maxilla (FIGURE 18).

Firm, bony enlargements (called eruption cysts or eruption bumps) are present along the ventral margins of the mandibles in a 2-year-old Quarter horse stallion.

These cysts normally result from mild compression from erupting permanent premolars at 3 and 4 years of age; the cysts regress over the next 1 to 2 years.7,27,28 In general, eruption cysts are not as noticeable on the maxilla because of overlying soft tissue.24 In some cases, crowding and compression (impaction) of the erupting permanent tooth may cause an unusually large, warm, painful swelling of the maxilla or mandible28 (FIGURE 19). If this develops, examine the horse for retained deciduous premolars.24 Radiography should also be used to evaluate the dental and bone structures associated with large eruption cysts. On radiography, eruption cysts of the mandible appear as smooth-bordered, periapical lucencies with sclerotic margins29 (FIGURE 20). It is important to remember that blood-borne bacteria can invade inflamed dental tissue associated with eruption cysts, resulting in infection

Eruption cysts are bony enlargements that can be observed in juvenile horses on the ventral aspect of the mandible and on the dorsolateral aspect of the maxilla.

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FIGURE 19

An enlarged, painful eruption cyst of the right maxilla with a draining tract in a 3-yearold mare.

of the pulp and the periapical region through a process called anachoresis.7,30

Conclusion Dental problems may cause discomfort to juvenile horses during performance. In young horses, dental conditions such as sharp den-

tal points, erosions of the cheeks and tongue, and loose or damaged premolar caps have been associated with bitting problems and can negatively influence performance. Unopposed incisors become overgrown, possibly impeding movement of the mandible. Likewise, overbite and underbite limit mandibular mobility, resulting in sharp dental overgrowths and malocclusion of the incisors and cheek teeth. Retained deciduous incisors can cause discomfort and abnormal eruption of underlying permanent teeth. Eruption cysts normally arise during cheek tooth eruption but may become enlarged and painful. Equine veterinarians should know skull anatomy, dental anatomy, and tooth eruption times to effectively perform dental examinations and procedures on young horses. Through dental examination of juvenile horses, equine veterinarians can identify and alleviate several significant dental conditions and provide clients with important information regarding the overall well-being of their horses. Acknowledgments The author acknowledges the following individuals at the College of Veterinary Medicine at Texas A&M University for their assistance in preparing this article: Michael Walker, DVM, Department of Large Animal Clinical Sciences; Kyle Westfall, veterinary technician, Veterinary Medical Teaching Hospital; and Betsy McCauley, veterinary radiologic technologist, Veterinary Medical Teaching Hospital.

FIGURE 20 Radiography of eruption cysts.

A

B

This lateral radiograph of the mandible and maxilla of a 2-year-old Quarter horse shows caps on premolars 2, 3, and 4 (Triadan ’06, ’07, and ’08) in the upper and lower jaws and mild cortical thickening of the mandible ventral to premolar 3 (Triadan ’07).

414

This oblique lateral radiograph of the right mandible shows smooth-bordered periapical lucency and cortical bony enlargement involving premolar 3 (Triadan 307) due to a slight eruption cyst.

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Dentistry in Juvenile Performance Horses CE References 1. Nickel R, Schummer A, Seiferle E. The Viscera of Domestic Mammals. 2nd ed. Philadelphia: Springer-Verlag; 1979:95. 2. Sisson S, Grossman JD. Anatomy of Domestic Animals. 4th ed. Philadelphia: WB Saunders; 1953. 3. Floyd MR. The modified Triadan system nomenclature for veterinary dentistry. J Vet Dent 1991;8(4):18-19. 4. Martin MT. Guide for Determining the Age of the Horse. 7th ed. Lexington, KY: AAEP; 2007. 5. Dixon PM. Dental anatomy. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:25-48. 6. Easley KJ. Equine canine and first premolar (wolf) teeth. Proc AAEP 2004;50:13-18. 7. Dixon PM, Dacre I. A review of equine dental disorders. Vet J 2005;169:165-187. 8. Easley KJ. Corrective dental procedures. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:221-248. 9. Brown SL, Shaw DJ, Dixon PM, Arkins S. Occlusal angles of cheek teeth in normal horses and horses with dental disease. Vet Rec 2008;162:807-810. 10. Scrutchfield L, Schumacher J. Examination of the oral cavity and routine dental care. Vet Clin North Am 1993;9(1):123-131. 11. Baker GJ, Allen ML. The use of power equipment in equine dentistry. Proc AAEP 2002:438-442. 12. Glossary of equine dental terminology. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:329-346. 13. Johnson TJ, Porter CM. Common disorders of incisor teeth and treatment. Focus Dent Proc AAEP 2006:32-38. 14. Easley J. Basic equine orthodontics. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:249-266. 15. Dixon PM, Tremaine WH, Pickles K, et al. Equine dental disease part 1: a long-term study of 400 cases: disorders of incisor, canine and first premolar teeth. Equine Vet J 1999;31(5):369-377. 16. Tremaine WH, Lane JG. Exodontia. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:267-294.

17. Caldwell LA. Canine teeth in the equine patient. Focus Dent Proc AAEP 2006:47-55. 18. Allen TE. Incidence and severity of abrasions on the buccal mucosa adjacent to the cheek teeth in 199 horses. Proc AAEP 2004:31-36. 19. Tell A, Egenvall A, Lundström T, Wattle O. The prevalence of oral ulceration in Swedish horses when ridden with bit and bridle and when unridden. Vet J 2008;178(3):405-410. 20. Manfredi J, Clayton HJ, Rosenstein D. Radiographic study of bit position within the horse’s oral cavity. Equine Comp Exerc Physiol 2005;3:195-201. 21. Bennet DG. An overview of bits and bitting. Focus Dent Proc AAEP 2006:181-195. 22. Orsini PG. Oral cavity. In: Auer JA, ed. Equine Surgery. Philadelphia: WB Saunders; 1992:218-305. 23. Stubbs RC. Dentistry of equine cheek teeth. Proc AAEP 2004; 50:1-6. 24. Dixon PM, Tremaine WH, Pickles K, et al. Equine dental disease part 2: a long-term study of 400 cases: disorders of development and eruption and variations in position of the cheek teeth. Equine Vet J 1999;31(6):519-528. 25. Carmalt JL. Evidence-based equine dentistry: preventive medicine. Vet Clin Equine 2007;23:519-524. 26. Linkous MB. Dental conditions affecting juvenile performance horses. Proc AAEP Dent Focus 2006:212-220. 27. Dixon PM. Dental anatomy. In: Baker GJ, Easley KJ, eds. Equine Dentistry. Philadelphia: WB Saunders; 1999:3-28. 28. Dacre IT. Equine dental pathology. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:91-109. 29. Gerard MP, Wotman KL, Komaromy AM. Infections of the head and ocular structures in the horse. Vet Clin Equine 2006;22:591-631. 30. Dixon PM, Tremaine WH, Pickles K, et al. Equine dental disease part 4: a long-term study of 400 cases: apical infections of cheek teeth. Equine Vet J 2000;32(3):182-194.

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 CompendiumEquine.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. When do the deciduous premolars normally erupt in horses? a. at birth or shortly thereafter b. at 2 years of age c. at 3 years of age d. at 4 years of age 2. The difference in width between the upper and lower jaws is called a. isognathia. b. brachygnathia. c. prognathia. d. anisognathia. 3. Brachygnathia is also known as a. sow mouth. b. monkey mouth. c. parrot mouth. d. none of the above 4. Retained deciduous incisors a. may be associated with discomfort. b. cause caudal displacement of the erupting permanent incisors.

c. can be removed in a standing patient. d. all of the above 5. Canine teeth a. are usually problematic in mares and should be removed. b. may irritate the eruption site. c. are synonymous with wolf teeth. d. none of the above 6. In regard to the cheek teeth, sharp dental points and overgrowths a. may traumatize the cheeks or tongue. b. have been associated with bitting problems. c. require floating. d. all of the above 7. Deciduous premolar caps a. may cause discomfort. b. do not occur in fillies and mares. c. are also known as wolf teeth. d. none of the above

8. Eruption cysts a. are not detectable with radiography. b. are associated with eruption of permanent premolars. c. do not occur on the maxilla. d. all of the above 9. Wolf teeth may a. cause pain due to bit contact. b. not be present in all of the dental arcades. c. not erupt. d. all of the above 10. In regard to dental examination, a. wetting the hands and instruments can reduce irritation to the horse’s mouth. b. wearing examination gloves helps minimize contamination of the clinician’s skin. c. a bright light source facilitates most procedures. d. all of the above

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3 CE CREDITS

CE Article 2

Treating Acute Colitis* ❯❯ R. P. Atherton, BVSc, MSc, DACVIM, MRCVS Lingfield Equine Vets, Chester Lodge, Felbridge, Surrey, United Kingdom

❯❯ H. C. McKenzie III, DVM, MS, DACVIM ❯❯ M. O. Furr, DVM, PhD, DACVIM Marion duPont Scott Equine Medical Center, VirginiaMaryland Regional College of Veterinary Medicine

At a Glance Fluid Therapy Page 416

Electrolyte Supplementation and Correction of Acid–Base Derangements Page 418

Colloidal Support

Abstract: Acute colitis is a therapeutic challenge for equine veterinarians. A plethora of therapies are available, but treatment may vary because a definitive diagnosis may be elusive. In addition, treatment of horses with acute colitis is intensive and often costly. This article discusses (1) a logical approach to treatment and (2) the therapeutic options available to equine clinicians. The prevention and treatment of complicating sequelae, such as laminitis and endotoxemia, are discussed and must be considered in the patient’s prognosis.

F

or many equine diseases, the goal of treatment is to target the underlying etiology; however, in cases of acute colitis, a definitive diagnosis may not be determined and was made in only 35% of cases in one report.1 Appropriate diagnostic tests may identify specific infectious organisms, but often not in a timely manner. Because the condition can be fatal, treatment must be initiated before results are obtained. The primary treatment goals for acute colitis are as follows:

Fluid Therapy When the integrity of the gastrointestinal (GI) barrier is compromised, fluid shifts from the intravascular compartment to the interstitial compartment, which can have catastrophic effects. Depending on time to clinical assessment and the severity of disease, signs of hypovolemia may be apparent only within the intravascular space (i.e., poor systemic perfusion and pulse quality) or may manifest as clinical hypovolemia (TABLE 1). In cases of mild to moderate hypovolemia of short duration

Page 419

Antiinflammatory Therapy Page 420

Analgesic Therapy Page 420

Antidiarrheal Therapy Page 421

Probiotics Page 421

Antimicrobial Therapy Page 421

Treating Common Sequelae of Acute Colitis Page 422

Nursing Care and Nutrition Page 424

Response to Therapy Page 424

Prognosis and Outcome Page 425

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Maintenance of fluid and electrolyte balance Preservation of colloid oncotic pressure and replacement of plasma protein Control of local and systemic inflammation Promotion of tissue perfusion Promotion of mucosal repair Nutritional management All patients with acute colitis require intensive care, and even if the primary treatment is effective, sequelae associated with the disease can limit a horse’s future performance or can be severe enough to require euthanasia. The cost of treatment can rise quickly, and the total bill may easily approach that for colic surgery. *Companion articles on the pathophysiology and noninfectious causes as well as the infectious causes appeared in the October 2009 issue.

TO LEARN MORE

Consultant’s Corner: How Do I Diagnose and Manage Right Dorsal Colitis? (Winter 2006) Related content on

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Treating Acute Colitis CE TABLE 1

Clinical Assessment of Hypovolemia Degree of Hypovolemia

Parameter

Mild

Moderate

Severe

Skin turgor

Good to fair

Fair

Poor

Mucous membrane moisture

Good to fair

Tacky

Dry

Capillary refill time

1–2 sec

2–4 sec

>4 sec

PCVa

40%–50%

50%–65%

>65%

Total plasma proteina

6.5–7.5 g/dL

7.5–8.5 g/dL

>8.5 g/dL

Heart rateb

40–60 bpm

60–80 bpm

>80 bpm

Pulse quality

Good (easily palpated and turgid)

Fair (slightly weak with decreased tone)

Poor (weak/thready and difficult to palpate)

a Normal packed cell volume (PCV) depends on the horse’s breed and level of athletic training. Thoroughbreds and

Standardbreds in training have normal PCVs up to 45%. The normal PCV of draft breeds can be 25%–30%. Splenic contraction and hypoproteinemia may affect PCV and total protein, respectively.

bHeart rate is also affected by the horse’s pain level.

without continued GI dysfunction and ongoing losses, simple replacement of the calculated fluid deficit with an isotonic crystalloid solution may be adequate to restore fluid and electrolyte homeostasis (BOX 1). Typically, a polyionic, isotonic, crystalloid fluid (e.g., Normosol-R [Baxter Healthcare], lactated Ringer’s solution) can be used as an initial replacement fluid.2 The volume of fluid to administer should be estimated based on the replacement deficit/ degree of hypovolemia, maintenance requirements, and anticipated ongoing losses. A general guide for fluid replacement during initial resuscitation is 10 to 20 mL/kg/h, but rates of 20 to 45 mL/kg/h might be indicated in a profoundly hypovolemic patient. These high rates of fluid administration should be used only for the first 2 to 3 hours of treatment, during which the goal is to replace the calculated fluid deficit. Once a fluid volume equal to the calculated fluid deficit has been administered, ongoing fluid losses must be assessed and the fluid rate switched to a maintenance rate that accounts for the patient’s basal metabolic needs and ongoing losses. Prolonged fluid administration at a rate above 10 to 20 mL/kg in a patient without substantial fluid losses may result in edema, especially because many colitis patients have hypoproteinemia and diminished colloidal oncotic pressure. During colitis, fluid is lost into the colon wall and the GI lumen, so there is no

quantitative means of accurately determining ongoing fluid losses, which can be as high as 150 mL/kg/d.3 Frequency, consistency, and volume of diarrhea per episode are useful subjective indicators; high-volume, high-frequency, watery diarrhea indicates that a large volume of fluid has been lost from the colon. Most cases of acute colitis require a fluid rate two to three times the maintenance rate once the deficit has been replaced due to ongoing water loss through diarrhea; however, this rate varies from patient to patient and can be reduced with clinical improvement. Close monitoring of the patient’s hydration status by assessing capillary refill time and cardioBOX 1

Calculating Fluid Deficit and Formulating a Fluid Replacement Plan Replacement fluid volume (L) = Body weight (kg) × % Hypovolemia ÷ 100 (L/kg) Replacement fluid rate = 10–20 mL/kg/hr Maintenance fluid volume = 50–100 mL/kg/day Rate of maintenance fluid administration = 2–4 mL/kg/hr Example: A 500-kg horse is 5% hypovolemic. Replacement fluid volume (L) = 500 kg × 5% Hypovolemia ÷ 100 = 25 L Replacement fluid rate (hr) = 10–20 mL/kg/hr × 500 kg/1000 mL/L = 5–10 L/hr for 2.5–5 hr Maintenance fluid volume (L/day) = 50–100 mL/kg/24 hr × 500 kg/1000 mL/L = 25–50 L/day Maintenance rate (L/hr) = 2–4 mL/kg/hr × 500 kg/1000 mL/L = 1–2 L/hr

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FREE CE Treating Acute Colitis

CriticalPo nt Fluid therapy is the most important treatment for acute equine colitis.

vascular parameters (e.g., heart rate, pulse quality) is essential to ensure an appropriate fluid rate. Indirect blood pressure monitoring is also useful for assessing response to treatment. Measurement of packed cell volume (PCV) and total protein concentration (TP) is quick, inexpensive, and clinically useful for monitoring hydration status. However, while increased PCV and TP suggest hypovolemia, these values may be lower than expected due to intravenous fluid therapy and hypoproteinemia secondary to colitis. In very mild cases of acute equine colitis, the volume of each fecal episode and the frequency (e.g., five to six times per day) of diarrhea are only moderate, so the patient can maintain an acceptable hydration state without supplementary intravenous crystalloid fluid therapy. When a fluid therapy plan is designed, it is important to remember that sodium-containing fluids rapidly exit the vasculature to equilibrate with extracellular fluid, and only 25% of these fluids remain in the intravascular space. Therefore, if ongoing fluid losses are significant, adequate colloidal support (e.g., plasma) and electrolyte supplementation must be provided.2 In severely hypovolemic equine patients, hypertonic saline (1 to 2 L of 7% sodium chloride [NaCl]) can expand intravascular blood volume, increasing systemic blood pressure and cardiac output. Circulating fluid volume can be rapidly increased as fluid moves from the extracellular space into the vascular compartment in response to hypertonic solution in the vascular space.4 However, after administration of hypertonic saline, it is imperative to quickly administer crystalloid fluids to replenish fluid from the extracellular space and maintain intravascular fluid volume.

Electrolyte Supplementation and Correction of Acid–Base Derangements Horses with colitis often have marked electrolyte deficiencies, which can be exacerbated by aggressive fluid therapy. Diminished absorption and increased secretion via the GI tract lead to a net loss of serum sodium, chloride, potassium, calcium, and bicarbonate into the colonic lumen. Clinical signs do not adequately predict the patient’s need for electrolyte supplementation, so this should be determined from measured plasma concentrations.

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Ongoing monitoring throughout the course of the disease is also essential. The recommended supplementation rate differs for each ion. Potassium is typically supplemented using potassium chloride (KCl). The starting supplementation rate should be determined from the serum potassium concentration after clinical rehydration of the patient, and the clinician should be careful to account for the ongoing loss of potassium, especially in an inappetent patient. In most cases, adding KCl to intravenous fluids at a concentration of 20 mEq/L is appropriate for replacement therapy. More severe hypokalemia can be treated by increasing the KCl concentration to 40 mEq/L, but care must be taken not to exceed an administration rate greater than 0.5 mEq/kg/h.5 Hypocalcemia is usually treated with intravenous administration of 23% calcium gluconate solution. Daily administration of 100 to 300 mL (2.14 to 6.42 g) is typically required in equine patients with ongoing GI losses, but the amount depends on the severity of disease and the patient’s nutritional intake.6 The calcium gluconate solution is typically added to the intravenous fluids that the patient is already receiving, but calcium-containing solutions cannot be used concurrently with bicarbonate-containing solutions because this results in formation of calcium carbonate precipitate. Some horses with severe colitis remain hypocalcemic despite aggressive calcium supplementation, so ongoing monitoring of the ionized calcium concentration is indicated. Excessively rapid calcium administration may result in cardiovascular complications, particularly in septic horses, which may be more vulnerable to toxic effects of calcium. However, a calcium dose of 1 to 2 mg/kg/h is considered safe, and Toribio et al7 have induced hypercalcemia in horses with rapid administration of calcium gluconate with no obvious complications. Concurrent administration of fresh-frozen plasma or blood results in a transient fall in the number of divalent cations as a result of chelation by citrate.8 Magnesium is typically supplemented using magnesium sulfate (MgSO4). A recommended dosage of intravenous MgSO4 in adult horses is 25 to 150 mg/kg/d (12.5 to 75 g/d for a 1100-lb [500-kg] horse), and MgSO4 can be added to the crystalloid fluids that the horse is already receiving.9 Magnesium is already added to some

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Treating Acute Colitis CE crystalloid fluids (e.g., Normosol-R), so this must be considered when calculating the rate of magnesium supplementation. When sodium is supplemented beyond what is contained in primary resuscitation fluids, it is important to remember that in other species, rapid correction of sodium deficits has been shown to cause demyelination of pontine and extrapontine neurons, resulting in severe neurologic dysfunction.10 This concern is greatest when the patient is profoundly hyponatremic (serum Na+ concentration: ≤120 mEq/L). A simple guideline for clinical use is to calculate the sodium deficit using the following equation: Normal serum sodium concentration – Actual serum sodium concentration = Sodium deficit (mEq/L) The result can be used as a guideline; for example, a deficit of 20 mEq/L should be replaced over no fewer than 20 hours and a deficit of 15 mEq/L over no fewer than 15 hours. Hypertonic saline (5%) or sodium bicarbonate (5% or 8.5%) solutions are used for sodium supplementation; NaCl may be used when hyponatremia is accompanied by hypochloremia, and sodium bicarbonate may be used when the serum chloride concentration is normal or increased. To avoid excessive or overly rapid correction of the serum sodium concentration, the plasma sodium concentration should be carefully monitored. We recommend taking a repeat blood sample 6 to 8 hours after initiating corrective fluid therapy and every 12 hours thereafter until the sodium concentration is within normal limits. Acid–base disturbances in colitis patients are primarily corrected by addressing the primary disease process and the associated sequelae, such as hypovolemia. Metabolic acidosis frequently accompanies acute colitis due to (1) the colon’s failure to resorb bicarbonate and (2) lactate buildup in the tissues secondary to poor tissue perfusion and anaerobic metabolism associated with endotoxemia. Correction of hypovolemia is an important component of therapy for acid–base disorders in diarrheic patients. If correction of hypovolemia is not accompanied by correction of acid–base abnormalities, additional therapy will be required to correct plasma imbalances.

For example, hyponatremia leads to metabolic acidosis, so sodium supplementation should help resolve acidosis. Similarly, albumin is a weak acid, so severe hypoalbuminemia may contribute to metabolic alkalosis or mask concurrent metabolic acidosis; therefore, protein supplementation should correct the acid–base imbalance.11 Persistence of acidosis despite correction of oral or intravenous supplementation should prompt the clinician to reassess the source of the pH abnormality (i.e., Is it respiratory or metabolic acidosis?). In addition, the clinician should address the underlying cause of this physiologic imbalance by treating the primary disease process. Oral administration of fluids is an effective and economical adjunct to intravenous fluid administration. Once severe electrolyte or acid– base disturbances have been corrected, horses, if given a choice, often elect to drink a solution containing the electrolyte in which they are deficient. The following “water buffet,” including an assortment of electrolyte-supplemented water solutions, can be offered free choice: Plain water Water with 6 to 10 g/L Lite Salt (iodized NaCl and KCl; Morton) Water with 10 g/L baking soda (sodium bicarbonate) Water with 6 to 10 g/L plain salt (NaCl)

CriticalPo nt Many adjunctive anecdotal therapies are available for treating acute colitis, but clinical evidence supporting their use is limited.

Colloidal Support Because of GI losses and serum albumin catabolism, many horses with acute colitis are hypoproteinemic. Additionally, absorption of bacterial products may induce systemic inflammatory response syndrome (SIRS), leading to increased vascular permeability and low plasma oncotic pressure. A large volume of crystalloid fluids causes hemodilution, contributing to decreased plasma oncotic pressure.12 In contrast, colloids preserve colloidal oncotic pressure, resulting in more effective volume expansion.2 Commercial colloids include plasma, dextran 40, dextran 70, hydroxyethyl starch (hetastarch), and polymerized bovine hemoglobin. The duration of oncotic support provided by a colloid is affected by the severity of inflammation in the colon and by resultant molecular loss from the circulation. Hetastarch (up to 10 mL/kg/d) has been shown to increase colloidal oncotic pressure for up to 24 hours in

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FREE CE Treating Acute Colitis

CriticalPo nt Prevention and treatment of the devastating sequelae of acute colitis are crucial to optimizing a patient’s chance of survival.

hypoproteinemic horses. Experimental studies suggest hetastarch may be superior to plasma in stopping endotoxin-induced increases in vascular permeability.2 This is due to the larger molecular size of polymers in hetastarch and, perhaps, to its ability to attenuate permeability dysfunction associated with endotoxemia. Caution is indicated, as higher doses of hetastarch (>20 mL/kg total cumulative dose) may prolong bleeding by altering von Willebrand’s factor function.2 Intravenous administration of plasma provides protein (albumin and globulins) as well as other beneficial elements, such as coagulation factors. Acute colitis is probably the most common disease associated with disseminated intravascular coagulation (DIC) in horses. In one study, the 1-year incidence of subclinical DIC in horses with acute colitis was 32%.13 There is no published dose of plasma for correction of hypoproteinemia in adult horses; however, as a guideline, equine patients with acute colitis require 10 to 15 mL/kg of plasma to raise their TP approximately 1 g/L. Close monitoring of the patient’s plasma protein is essential, as ongoing GI losses may require repeated doses of plasma. Fresh-frozen commercial equine plasma is readily available from various sources. Adverse effects of plasma administration in horses are uncommon but may include immune-mediated reactions and changes in hemostatic variables.14

Antiinflammatory Therapy The NSAIDs typically used in equine patients inhibit cyclooxygenase (COX) 1 and 2, which are responsible for producing vasoactive and proinflammatory prostanoid compounds, such as prostaglandin I2 (PGI2), prostaglandin E2 (PGE2), and thromboxane. Suppression of this process can help break the self-perpetuating inflammatory cycle within inflamed colonic mucosa and allow GI mucosa to heal. However, evidence suggests that certain prostaglandins, such as PGI2 and PGE2, are cytoprotective to GI mucosa and critical for mucosal repair; therefore, using COX inhibitors to block prostaglandin production in these tissues may exacerbate GI pathology.15 It is unclear whether the benefits of NSAID therapy outweigh the limitations; however, many horses with colitis may initially require analgesia. Similar to the standard dose of flunixin meglumine (1.1 mg/

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kg IV q12h), the low dose (0.25 mg/kg IV q8h) has been shown to decrease eicosanoid production and ameliorate some clinical signs of systemic inflammation following exposure to intravenous endotoxin. The low dose is also thought to be less likely to impair tissue blood flow in the GI mucosa; therefore, the low dose may be safer than the standard dose.16 Other antiinflammatory therapies for equine acute colitis include the free radical scavenger dimethyl sulfoxide (DMSO; 1 g/kg IV q12–24h as a 10% solution), the antimicrobial metronidazole (20 mg/kg PO q8h; 10–25 mg/kg PO q6–12ha; 15–25 mg/kg PO q6hb),17,18 the prokinetic and analgesic lidocaine (1.3 mg/ kg over 15 min, then 0.05 mg/kg/min), and the PGE1 analogue misoprostol (5 μg/kg q8h). Experimental evidence for these therapies is limited, but they may be of clinical value.

Analgesic Therapy Many horses with acute colitis develop mild to severe signs of abdominal discomfort from gas and fluid distention of the colon, colonic ischemia, and infarction. NSAIDs are commonly used, particularly flunixin meglumine (1.1 mg/kg IV or PO q12h) because of its antiinflammatory effects compared with the effects of phenylbutazone or ketoprofen.16,19 However, NSAIDs impair prostaglandin production by the kidneys, inhibiting normal renal blood flow. Overdosage or misuse of NSAIDs, especially in hypovolemic patients, can lead to renal crest necrosis and may increase the risk of acute tubular nephrosis during hypovolemia or aminoglycoside administration. Therefore, low-dose flunixin meglumine may be better to use than the standard dose in some patients. Alternative analgesics include lidocaine, α2-agonists (e.g., xylazine, detomidine), and opioids (e.g., butorphanol). These are all considered to be short acting, but constant-rate in fusion may be used to provide sustained clinical analgesia. However, opioids and α2-agonists decrease GI motility, so patient comfort and fecal output should be monitored. aIn: Robinson NE, Sprayberry K, eds. Current Therapy in Equine Medicine. 6th ed. Philadelphia: WB Saunders; 2008. bSweeney RW, Soma LR, Woodward CB, Charlton CB. Pharmacokinetics of metronidazole given to horses by intravenous and oral routes. Am J Vet Res 1986;47(8):1726-1729.

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Treating Acute Colitis CE Antidiarrheal Therapy Bismuth Subsalicylate Bismuth subsalicylate is commonly administered orally to equine patients with colitis to decrease inflammation and secretion in the colon. In a double-blind, placebo-controlled study in children with acute diarrhea, this drug was shown to significantly decrease the time to the last watery stool.20 The precise mechanism of action of bismuth subsalicylate in any species is unclear, but the salicylate moiety may have an antisecretory action in the large colon, where it stimulates fluid and electrolyte absorption.21 In addition, salicylic acid inhibits prostaglandin synthesis, which is responsible for intestinal inflammation and hypermotility, and modulates oxidative stress in colonic mucosal cells.22 Furthermore, the drug and its intestinal reaction products, bismuth oxychloride and bismuth hydroxide, appear to be bacteriocidal in vivo and in vitro.21 Based on extrapolation from human medicine, the dose required in adult horses is large (3 to 4 L by stomach tube q4–6h)20; however, the drug is also available as a concentrated paste. In humans, bismuth subsalicylate is considered extremely safe. A feeding trial in which mice were fed 60 times the maximal recommended human dose did not result in adverse effects, and no histopathologic lesions were noted in the brains on postmortem examination.23 Bismuth subsalicylate toxicosis in horses has not been reported.

Di-Tri-Octahedral Smectite Di-tri-octahedral smectite is a natural hydrated aluminomagnesium silicate with a lamellar structure. It binds to digestive mucus and increases intestinal resistance to bacterial damage.24 The drug has been shown to increase water and electrolyte absorption in rabbit intestinal loops in the presence of Escherichia coli infection; a preliminary study in horses reported that administration of di-tri-octahedral smectite prevented lincomycin-induced colitis in four horses, whereas four untreated horses died or were euthanized due to severe colitis.24,25 In vitro studies have shown that ditri-octahedral smectite can bind Clostridium difficile toxins A and B as well as Clostridium perfringens enterotoxin and endotoxin.26 The current recommendation for a 1000-lb (454.5kg) horse is administration of a solution of 1 lb

of Bio-Sponge (Platinum Performance) and 3 L of water via nasogastric tube q6–12h.

Probiotics Restoring the microbial ecology of the colon has recently attracted experimental interest, leading to the use of many different agents (e.g., commercial probiotic pastes, live-culture yogurt) and techniques (e.g., transfaunation). In transfaunation, freshly harvested colonic or cecal contents (5 to 6 L) or a slurry of fresh feces from a healthy horse is administered via nasogastric tube to the patient to restore normal GI flora. Transfaunation has had reported clinical success in cattle but has not been reported in diarrheic horses.27 There is little supportive evidence for the use of commercial probiotic pastes in horses, and one study in foals found the pastes to be detrimental.28 In comparison, Saccharomyces boulardii is a nonpathogenic yeast that has been used prophylactically and therapeutically as an antidiarrheic agent in humans since 1962.29 Experimentally, the yeast has been found to survive within the equine GI tract, and the severity and duration of acute enterocolitis were significantly decreased in horses that received S. boulardii compared with horses that received a placebo.29 S. boulardii has been found to release a protease that can digest C. difficile toxins A and B; additional mechanisms of action include an immunoprotective effect attributed to promoting the release of secretory immunoglobulins within the intestine or activation of the reticuloendothelial and complement systems.30,31 Because pharmacokinetic studies with S. boulardii have not been performed in horses, the equine dose is extrapolated from the human literature. One study reported the use of an S. boulardii dose of 25 g (10 × 109 yeast cells) PO q12h for 14 days in horses with acute colitis, resulting in no clinical adverse effects and in significant improvement in the severity and duration of GI disease compared with a placebo group of horses.29

CriticalPo nt In a double-blind, placebo-controlled study in children with acute diarrhea, this drug was shown to significantly decrease the time to the last watery stool.

Antimicrobial Therapy Antimicrobial therapy is hotly debated in many cases of acute colitis. In cases with concurrent neutropenia, it is thought that the host’s defenses may be weakened sufficiently to render the horse susceptible to organisms

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CriticalPo nt Experimentally, the yeast has been found to survive within the equine GI tract, and the severity and duration of acute enterocolitis were significantly decreased in horses that received S. boulardii compared with horses that received a placebo.

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that breach the mucosal barrier; therefore, some clinicians recommend broad-spectrum antimicrobial coverage. However, antimicrobials can have adverse GI effects in horses.32 Antimicrobial administration has been reported to prolong shedding of Salmonella spp in experimentally infected ponies, and there are many reports of antimicrobial-induced diarrhea in horses.32 For certain infectious causes of acute colitis in horses, such as Potomac horse fever (equine monocytic ehrlichiosis) and Clostridium infections, antimicrobial therapy is required to address the underlying cause. Neorickettsia risticii, which causes Potomac horse fever, is highly sensitive to tetracyclines (e.g., oxytetracycline dosed at 6.6 mg/kg IV q24h for 5 days).33 Clostridium spp, namely C. difficile and C. perfringens, have been shown to be eradicated using metronidazole (minimum inhibitory concentration: ≤4 mg/mL34; commonly used dosage: 20 mg/kg PO q8h), and in vitro evidence suggests efficacy of chloramphenicol (50 mg/kg PO q6h).35 Antimicrobial use must be decided on a case-specific basis, with consideration for the most likely etiology, including the most common agents in the area, the season of the year, and the history and clinical presentation.

Treating Common Sequelae of Acute Colitis Because of the severity of systemic illness associated with acute colitis, complicating issues are frequently encountered, the most common of which are endotoxemia, thrombophlebitis, and laminitis. Preventive or therapeutic measures must address these sequelae to optimize the patient’s chance of survival. Endotoxemia is a well-recognized complication of GI disease, particularly diseases involving GI inflammation or ischemia, such as acute colitis. A horse’s intestinal tract normally contains a large number of gram-negative bacteria that release endotoxin when they die or multiply rapidly. The endotoxin is normally restricted to the intestinal lumen by an efficient intestinal mucosal barrier; however, if some endotoxin crosses the mucosal barrier, it enters the portal system and is removed by hepatic mononuclear phagocytes without initiating systemic signs in the horse.36 If the intestinal barrier is impaired (e.g., inflammation, ischemia), endotoxin translocates more sig-

nificantly into the circulation, and the hepatic clearance mechanism becomes overwhelmed, leading to endotoxemia as well as synthesis and release of inflammatory mediators. Four therapeutic approaches should be considered when addressing endotoxemia. The first approach is to prevent absorption of endotoxin into the circulation by treating the primary cause of the GI disease. The second approach is neutralization of endotoxin before it interacts with inflammatory cells. Polymyxin B has shown some promising endotoxin-neutralization effects in vitro and in vivo, appearing to be clinically useful in decreasing the inflammatory response to endotoxin exposure.37 However, polymyxin B must be used judiciously due to its inherent toxic effects on neural and renal tissues.38 Polymyxin B is administered at a rate of 1 mg (6000 U)/ kg diluted in 1 L of sterile saline solution IV q8h and is typically discontinued after 1 or 2 days of therapy39; however, many clinicians administer the drug every 12 hours to prevent adverse effects. Doses below 6000 U/kg may be effective and less nephrotoxic.40 Although few experimental data are available to support the in vivo use of antilipopolysaccharide (anti-LPS) hyperimmune equine plasma, it provides antibodies that target the endotoxin and appears to have bacteriocidal activity.40,41 The third approach is prevention of the synthesis, release, or action of inflammatory mediators that follow endotoxin exposure and are responsible for SIRS. This approach has included the use of NSAIDs, corticosteroids, monoclonal antibodies directed against cytokines, platelet-activating factor receptor antagonists, pentoxifylline, and naturally occurring nontoxic endotoxins. However, all of these interventions have demonstrated only limited efficacy,42 and only flunixin meglumine has become clinically accepted. The fourth and most clinically important approach to endotoxemia is appropriate supportive care. This helps minimize organ dysfunction secondary to severe SIRS, which is characteristic of endotoxemia. Abdominal pain associated with colitis may result in stall rolling, excessive catheter movement, and contamination or disconnection of the intravenous line. Patients with acute colitis can be at high risk for thrombophlebitis (inflammation of the vein with thrombus for-

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Treating Acute Colitis CE mation) because of associated general debilitation, lowering of the head for prolonged periods, and placement of an indwelling catheter for several days or weeks.43 In addition, a large volume of intravenous uids and intravenously administered drugs can cause turbulent blood ow and irritate vascular endothelium at the catheter tip. Patients with colitis may be predisposed to venous thrombosis because of endotoxemia-associated loss of anticoagulants in the bloodstream and systemic activation of procoagulants.44 No studies have proven that type of catheter material is a risk factor for thrombophlebitis in horses, but polyurethane, over-the-wire catheters are assumed to have less risk. If thrombophlebitis develops, the use of topical antiinammatory therapies (e.g., DMSO), systemic anticoagulants (e.g., aspirin), and antimicrobials is advisable but has not been experimentally conďŹ rmed to be beneďŹ cial. Laminitis is the primary reason for euthanasia in many colitis cases.44 Prevention and treatment of laminitis are controversial, pri-

marily because the exact pathophysiology of the condition is unclear. To effectively prevent laminitis, clinicians must be aware that patients with colitis are at high risk of developing it. Preventives include vasodilator administration, corrective hoof trimming and shoeing, deeply bedded stalls, and frog support. Many of these measures are also used therapeutically. Venodilatory therapy, namely low-dose acepromazine (0.03 to 0.06 mg/kg IM q6–8h), isoxsuprine hydrochloride (1.2 mg/kg PO q12h), or topical glyceryl trinitrate cream (2-cm strip applied to the back of the pastern of the affected feet q6–8h), should theoretically reduce venous resistance in the feet, decrease capillary pressure, and diminish abnormal uid movement within laminar tissue.45 Conversely, blood ow to the feet can be decreased or altered by dramatically cooling the feet with ice-packed boots. The associated mechanism of action is thought to be induction of hypometabolism of laminar tissue, thereby decreasing proteolytic and neutrophil enzyme activities, inammatory

CriticalPo nt For certain infectious causes of acute colitis in horses, such as Potomac horse fever (equine monocytic ehrlichiosis) and Clostridium infections, antimicrobial therapy is required to address the underlying cause.

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BOX 2

Technician Tips Many hospitals provide frequent supportive care and intensive care unit checks. Examples of supportive care checks Is the patient eating well? Are there signs of deterioration? Examples of intensive care unit checks Are there signs of colic (pawing, rolling)? How much is the patient drinking? Is there fever? Is the heart rate or respiratory rate increased? Are there signs of inflammation or infection at the intravenous catheter site? What is the frequency and consistency of diarrhea? Are there signs of laminitis?

CriticalPo nt Because of the severity of systemic illness associated with acute colitis, complicating issues are frequently encountered, the most common of which are endotoxemia, thrombophlebitis, and laminitis.

cytokine activity, and metalloproteinase activity, which have been found to be increased in laminitic feet.46 Applying supportive pads to the feet, trimming the hooves, and using soft bedding may decrease mechanical shear forces on the laminae, limiting the predisposition to or exacerbation of laminitis. Inhibiting neutrophil adhesion to endothelial cells with the use of pentoxifylline, lidocaine, or flunixin meglumine could also have some prophylactic value.47,48 If a horse with acute colitis develops laminitis, treatment should be directed at pain control and ongoing correction of the underlying cause. Historically, phenylbutazone (2.2 to 4.4 mg/kg IV or PO q12h) has been regarded as the best NSAID for treating pain and inflammation associated with laminitis; however, it is important to consider using available COX-2– selective NSAIDs such as firocoxib (Equioxx, Merial) and meloxicam (Metacam, Boehringer Ingelheim). Further research may show COX-2 inhibitors to be superior and safer.49 Lateral radiographs of the feet illustrating rotation or sinking of the pedal bone in addition to response to analgesic therapy are key prognostic indicators in laminitic cases.

Nursing Care and Nutrition Good nursing care and nutrition are essential to a successful outcome for equine patients with acute colitis (BOX 2). The goal of enteral

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nutrition should be to avoid overloading the poorly functioning colon; this can be achieved by feeding small, frequent meals with a predominantly pellet base. Feeds with greater digestibility decrease the amount of undigested concentrate that reaches the cecum, where fermentation may exacerbate diarrhea. Hay can be fed but should be high-quality grass hay. Feeding hay may help produce volatile fatty acids (propionate, butyrate, acetate) within the colon; these compounds are important for normal functioning of colonic mucosa. Because many colitis patients are anorectic and the severity of the disease can result in catabolism, corn oil can be added to the diet to increase caloric intake. If a patient remains anorectic for longer than 3 to 4 days despite therapy, parenteral nutrition should be provided. In addition, gastroprotectants such as sucralfate (1 g/45.5 kg PO q6–8h) and omeprazole (4 mg/kg PO q24h) are useful for improving appetite and treating gastric ulcers, if present, due to inappetence.

Response to Therapy Response to therapy is determined by frequent monitoring of clinical signs, clinicopathologic data, and fecal water content. Signs of improvement are decreased fever, stability of serum electrolyte concentrations, acid–base balance, and improved appetite. Clinicopathologically, one of the earliest signs of improvement can be a decreased number of morphologically “toxic” neutrophils. Decreases in fecal water content and frequency of diarrhea suggest clinical improvement. Acute colitis can have an infectious cause, so equine patients may continue shedding the infectious agent even when diarrhea has resolved, thereby putting other horses at risk.50 Repeated diagnostic testing should be considered before removing a horse from isolation. Because salmonellosis patients shed Salmonella spp intermittently, a series of five fecal cultures obtained on different days should have negative results before isolation protocols are discontinued.50 Alternatively, three consecutive fecal samples can be obtained 24 hours apart and submitted for polymerase chain reaction (PCR) testing to test for Salmonella spp. This method can provide a level of confidence similar to that obtained by testing five samples by culture.51 Because watery feces are difficult to culture

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Treating Acute Colitis CE for Salmonella spp due to a dilutional effect, samples for culture or PCR testing should contain at least 5 to 10 g of feces. The usefulness of repeat testing in clostridiosis cases has not been critically evaluated, but obtaining negative results from a fecal sample following resolution of diarrhea helps ensure that the risk of shedding has decreased. Because salmonellosis is highly contagious, many hospitals have an infectious disease, environmental monitoring protocol.

Prognosis and Outcome The substantial mortality rate and treatment expense associated with acute enterocolitis underscore the importance of identifying equine patients with a poor prognosis for survival. Patients that recover from acute colitis typically show clinical improvement within 3 to 6 days after treatment begins.5,52 The following clinical signs suggest a guarded prognosis: azotemia, clinicopathologic findings consistent with hemoconcentration and

hypoproteinemia (e.g., a persistent PCV >50% and TP <6.2 g/dL), and failure to show demonstrable signs of improvement after 10 days of therapy.5,52 Certain types of colitis, including necrotizing enterocolitis and antimicrobialassociated diarrhea, have been associated with low survival rates.52 If a horse survives acute colitis without developing sequelae such as laminitis, ongoing health issues are unlikely.

Conclusion Managing equine patients with acute colitis can be challenging due to the intensity of care involved and the concerns regarding disease transmission. Many different treatments are available for this condition; although the efficacy of some treatments is unclear, clinicians have the opportunity to explore different therapeutic approaches, making acute colitis rewarding to treat. It is important to remember that if the patient responds to therapy in the first few days, the prognosis for a full recovery is favorable.

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References 1. Mair TS, de Westerlaken LV, Cripps PJ, et al. Diarrhoea in adult horses: a survey of clinical cases and an assessment of some prognostic indices. Vet Rec 1990;126:479-481. 2. Seahorn JL, Seahorn TL. Fluid therapy in horses with gastrointestinal disease. Vet Clin North Am Equine Pract 2003;19:665-679. 3. McConnico R. Acute equine colitis. Compend Contin Educ Pract Vet 2003;25:625-631. 4. Schmall LM, Muir WW, Robertson JT. Haemodynamic effects of small volume hypertonic saline in experimentally induced haemorrhagic shock. Equine Vet J 1990;22:273-277. 5. Murray MJ. Therapeutic procedures for horses with colitis. Vet Med 1990:510-518. 6. Dart AJ, Snyder JR, Spier SJ, et al. Ionized calcium concentration in horses with surgically managed gastrointestinal disease: 147 cases (1988-1990). JAVMA 1992;201:1244-1248. 7. Toribio RE, Kohn CW, Rourke KM, et al. Effects of hypercalcemia on serum concentrations of magnesium, potassium, and phosphate and urinary excretion of electrolytes in horses. Am J Vet Res 2007;68:543-554. 8. Krishnan RG, Coulthard MG. Minimising changes in plasma calcium and magnesium concentrations during plasmapheresis. Pediatr Nephrol 2007;22:1763-1766. 9. Borer KE, Corley KTT. Electrolyte disorders in horses with colic. Part 1: potassium and magnesium. Equine Vet Educ 2006;18:266-271. 10. O’Brien DP, Kroll RA, Johnson GC, et al. Myelinolysis after correction of hyponatremia in two dogs. J Vet Intern Med 1994;8:40-48. 11. Corley KTT, Marr CM. Pathophysiology, assessment and treatment of acid-base disturbances in the horse. Equine Vet Educ 1998;10:255-265. 12. Jones PA, Bain FT, Byars TD, et al. Effect of hydroxyethyl starch infusion on colloid oncotic pressure in hypoproteinemic horses. JAVMA 2001;218:1130-1135. 13. Dolente BA, Wilkins PA, Boston RC. Clinicopathological evidence of disseminated intravascular coagulation in horses with acute colitis. JAVMA 2002;220:1034-1038. 14. Jones PA, Tomasic M, Gentry PA. Oncotic, hemodilutional, and hemostatic effects of isotonic saline and hydroxyethyl starch solutions in clinically normal ponies. Am J Vet Res 1997;58:541-548. 15. Blikslager AT, Roberts MC. Mechanisms of intestinal mucosal repair. JAVMA 1997;211:1437-1441. 16. Semrad SD, Hardee GE, Hardee MM, et al. Low dose flunixin meglumine: effects on eicosanoid production and clinical signs induced by experimental endotoxaemia in horses. Equine Vet J 1987;19:201-206. 17. Yamada T, Deitch E, Specian RD, et al. Mechanisms of acute and chronic intestinal inflammation induced by indomethacin. Inflammation 1993;17:641-662. 18. Leite AZ, Sipahi AM, Damião AO, et al. Protective effect of metronidazole on uncoupling mitochondrial oxidative phosphorylation induced by NSAID: a new mechanism. Gut 2001;48:163-167. 19. Semrad SD, Moore JN. Effects of multiple low doses of flunixin meglumine on repeated endotoxin challenge in the horse. Prostaglandins Leukot Med 1987;27:169-181. 20. Soriano-Brucher H, Avendano P, O’Ryan M, et al. Bismuth subsalicylate in the treatment of acute diarrhea in children: a clinical study. Pediatrics 1991;87:18-27. 21. Ericsson CD, Evans DG, DuPont HL, et al. Bismuth subsalicylate inhibits activity of crude toxins of Escherichia coli and Vibrio cholerae. J Infect Dis 1977;136:693-696. 22. Drew JE, Arthur JR, Farquharson AJ, et al. Salicylic acid modulates oxidative stress and glutathione peroxidase activity in the rat colon. Biochem Pharmacol 2005;70:888-893. 23. Bierer DW. Bismuth subsalicylate: history, chemistry, and safety. Rev Infect Dis 1990;12(suppl 1):S3-S8. 24. Rateau JG, Morgant G, Droy-Priot MT, et al. A histological, enzymatic and water-electrolyte study of the action of smectite, a mucoprotective clay, on experimental infectious diarrhoea in the rabbit. Curr Med Res Opin 1982;8:233-241. 25. Herthel D. Treatment of clostridial colitis with smectite. Proc 6th Annu Colic Res Symp 1998:12. 26. Weese JS, Cote NM, deGannes RV. Evaluation of in vitro properties of di-tri-octahedral smectite on clostridial toxins and growth.

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Equine Vet J 2003;35:638-641. 27. Rager KD, George LW, House JK, et al. Evaluation of rumen transfaunation after surgical correction of left-sided displacement of the abomasum in cows. JAVMA 2004;225:915-920. 28. Weese JS, Rousseau J. Evaluation of Lactobacillus pentosus WE7 for prevention of diarrhea in neonatal foals. JAVMA 2005;226:2031-2034. 29. Desrochers AM, Dolente BA, Roy MF, et al. Efficacy of Saccharomyces boulardii for treatment of horses with acute enterocolitis. JAVMA 2005;227:954-959. 30. Castagliuolo I, Riegler MF, Valenick L, et al. Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa. Infect Immun 1999;67:302-307. 31. Buts JP, Bernasconi P, Vaerman JP, et al. Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii. Dig Dis Sci 1990;35:251-256. 32. Papich MG. Antimicrobial therapy for gastrointestinal diseases. Vet Clin North Am Equine Pract 2003;19:645-663, vi. 33. Palmer JE, Benson CE, Whitlock RH. Effect of treatment with oxytetracycline during the acute stages of experimentally induced equine ehrlichial colitis in ponies. Am J Vet Res 1992;53:2300-2304. 34. Båverud V, Gustafsson A, Franklin A. Clostridium difficile: prevalence in horses and environment, and antimicrobial susceptibility. Equine Vet J 2003;35:465-471. 35. Baverud V, Gunnarsson A, Karlsson M, et al. Antimicrobial susceptibility of equine and environmental isolates of Clostridium difficile. Microb Drug Resist 2004;10:57-63. 36. Moore JN. Introduction to endotoxemia. Proc Annu Conv AAEP 1995;41:100-102. 37. Barton MH, Parviainen A, Norton N. Polymyxin B protects horses against induced endotoxaemia in vivo. Equine Vet J 2004;36:397-401. 38. MacKay RJ, Clark CK, Logdberg L, et al. Effect of a conjugate of polymyxin B–dextran 70 in horses with experimentally induced endotoxemia. Am J Vet Res 1999;60:68-75. 39. Morresey PR, Mackay RJ. Endotoxin-neutralizing activity of polymyxin B in blood after IV administration in horses. Am J Vet Res 2006;67:642-647. 40. Parviainen AK, Barton MH, Norton NN. Evaluation of polymyxin B in an ex vivo model of endotoxemia in horses. Am J Vet Res 2001;62:72-76. 41. Gaffin SL, Wells MT. A morphological study of the action of equine anti-lipopolysaccharide plasma on gram-negative bacteria. J Med Microbiol 1987;24:165-168. 42. Moore JN, Barton MH. Treatment of endotoxemia. Vet Clin North Am Equine Pract 2003;19:681-695. 43. Traub-Dargatz JL, Dargatz DA. A retrospective study of vein thrombosis in horses treated with intravenous fluids in a veterinary teaching hospital. J Vet Intern Med 1994;8:264-266. 44. Divers TJ. Prevention and treatment of thrombosis, phlebitis, and laminitis in horses with gastrointestinal diseases. Vet Clin North Am Equine Pract 2003;19:779-790. 45. Hinckley KA, Fearn S, Howard BR, et al. Glyceryl trinitrate enhances nitric oxide mediated perfusion within the equine hoof. J Endocrinol 1996;151:R1-8. 46. van Eps AW, Pollitt CC. Equine laminitis: cryotherapy reduces the severity of the acute lesion. Equine Vet J 2004;36:255-260. 47. Weiss DJ, Evanson OA, McClenahan D, et al. Effect of a competitive inhibitor of platelet aggregation on experimentally induced laminitis in ponies. Am J Vet Res 1998;59:814-817. 48. Weiss DJ, Evanson OA. Evaluation of lipopolysaccharide-induced activation of equine neutrophils. Am J Vet Res 2002;63:811-815. 49. Divers TJ. COX inhibitors: making the best choice for the laminitic case. J Equine Vet Sci 2008;28:367-369. 50. Kim LM, Morley PS, Traub-Dargatz JL, et al. Factors associated with Salmonella shedding among equine colic patients at a veterinary teaching hospital. JAVMA 2001;218:740-748. 51. Cohen ND, Martin LJ, Simpson RB, et al. Comparison of polymerase chain reaction and microbiological culture for detection of salmonellae in equine feces and environmental samples. Am J Vet Res 1996;57:780-786. 52. Cohen ND, Woods AM. Characteristics and risk factors for failure of horses with acute diarrhea to survive: 122 cases (19901996). JAVMA 1999;214:382-390.

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Treating Acute Colitis CE

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 CompendiumEquine.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 fluid would not be appropriate to administer to a hypovolemic equine patient? a. hypertonic saline b. lactated Ringer’s solution c. plasma d. dextrose 50% e. 0.9% saline 2. Which serum level is not typically low in an equine patient with acute colitis? a. sodium d. potassium b. chloride e. bicarbonate c. lactate 3. Which statement regarding equine acute colitis is false? a. Prostaglandins such as PGI2 and PGE2 may be cytoprotective to GI mucosa. b. Flunixin meglumine must be administered at 1.1 mg/kg IV q12h to decrease production of tumor necrosis factor and other inflammatory cytokines in the GI mucosa. c. Horses with severe colitis have profound hypoproteinemia. d. Metronidazole use is indicated in cases of C. difficile infection. e. DMSO and lidocaine may be used as antiinflammatories in horses with acute colitis. 4. Which statement regarding bismuth subsalicylate is true? a. The anecdotal dose of liquid bismuth subsalicylate for horses is large, requiring passage of a stomach tube every 6 to 8 hours. Alternatively, a concentrated paste can be administered. b. Several cases of associated toxicosis in horses have been reported. c. Adverse cardiac signs were reported in a person with suspected bismuth subsalicylate toxicosis. d. It has a prokinetic mechanism of action. e. No studies support its use in humans. 5. Which commonly used therapy lacks experimental support as a beneficial treatment of equine acute colitis? a. bismuth subsalicylate b. metronidazole c. di-tri-octahedral smectite d. S. boulardii e. probiotic pastes 6. Which disease and treatment combination for equine patients is incorrect? a. C. difficile infection; metronidazole b. Potomac horse fever; oxytetracycline c. C. difficile infection; S. boulardii d. antimicrobial-associated colitis; ceftiofur sodium e. right dorsal colitis; misoprostol

7. Which statement regarding colloid therapy in equine patients is true? a. Administering plasma is beneficial only if the volume is adequate to replace all protein loss. b. Hydroxyethyl starch should not be administered to horses with diarrhea. c. Hypertonic saline has short-term colloidal action. d. Plasma administration reduces the chance of developing laminitis. e. Colloid administration decreases plasma oncotic pressure. 8. Which statement regarding fluid therapy for equine acute colitis is false? a. Fluids should not be administered until clinicopathologic test results are available. b. Calcium supplementation is often required due to reduced feed intake and increased GI loss. c. Ongoing fluid losses must be considered in addition to maintenance requirements and replacement of lost fluid when determining an appropriate fluid plan. d. Potassium should be supplemented carefully. e. Sodium bicarbonate administration is appropriate for correcting hyponatremia in some cases. 9. Which statement regarding equine acute colitis is false? a. Many components of treatment are the same regardless of etiology. b. Fluid therapy is crucial to all treatment plans. c. Antimicrobial therapy should not be routinely administered in colitis cases. d. If complications do not occur and diarrhea resolves, the patient should have no longterm effects. e. Laminitis is an uncommon sequela of acute colitis. 10. Which statement regarding treatment of equine acute colitis is false? a. Treatment with COX inhibitors should be routine because they limit the chance of developing intestinal ulceration. b. The volume and frequency of diarrhea are good subjective indicators of fluid loss and should be considered when devising a fluid therapy plan. c. There is limited evidence to support the use of transfaunation. d. Antimicrobial therapy may prolong bacterial shedding in salmonellosis cases. e. Oxytetracycline is an appropriate therapy for Potomac horse fever.

November/December 2009 | Compendium Equine: Continuing Education for Veterinarians®

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2009 Annual Index Aut Authors

G

A Alcott C: Hemostasis; Mar, 78–89; Modifying the Coagulation Cascade: Available Medications; Jun, 224–236 Atherton RP: Acute Colitis: Pathophysiology and Noninfectious Etiologies; Oct, 366–374; Acute Colitis: Infectious Causes; Oct, 375–380; Treating Acute Colitis; Nov/Dec, 416–427

B Bach C: Fare Thee Well: How to Help Owners (and Yourself) Deal With the Death of a Horse; Jul/Aug, 267–273 Beard L: Therapeutics in Practice: Managing Foal Diarrhea; Jan/Feb, 16–26 Bentz AI: Fare Thee Well: How to Help Owners (and Yourself) Deal With the Death of a Horse; Jul/Aug, 267–273; The Final Diagnosis: Nala and Me; Sep, 335–336; Editorial: How Did I Get Here?; Oct, 344 Breaux CB: Clinical Snapshot: Blepharospasm in a Paint Horse Gelding; May, 185–186 Breshears M: Clinical Snapshot: A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348 Brock B: The Final Diagnosis: My Buddy Mahoot; May, 188–189; The Final Diagnosis: Through the Eyes, and Ears, of a Child; Jul/Aug, 288 Brockus C: Hemostasis; Mar, 78–89; Modifying the Coagulation Cascade: Available Medications; Jun, 224–236 Brounts SH: Cutting to Cure: Urolithiasis; Apr, 125–133 Buffi ngton CAT: Guest Editorial: Some People Use Data Like Drunks Use Lampposts: More for Support Than Illumination; May, 152–154

C Carmona JU: Pathophysiology of Osteoarthritis; Jan/Feb, 28–40 Charles E: Imaging Is Believing: Stifle Ultrasonography: A Case Study; Apr, 119–124

D Divers TJ: Treating Thoracic Injuries; Jun, 208–223 Ducharme NG: Treating Thoracic Injuries; Jun, 208–223

F Foley A: Cutting to Cure: Urolithiasis; Apr, 125–133 Fontenot R: Clinical Snapshot: A Rapidly Growing Mass on a Quarter Horse Mare; May, 162, 164 Frazer M: Clinical Snapshot: Tachycardia and Tachypnea in a 2-Day-Old Thoroughbred; Jan/Feb, 40, 42 Furr MO: Acute Colitis: Pathophysiology and Noninfectious Etiologies; Oct, 366–374; Acute Colitis: Infectious Causes; Oct, 375–380; Treating Acute Colitis; Nov/Dec, 416–427

Gill RE: The Final Diagnosis: Just Another Unusual Day; Jan/Feb, 48; The Final Diagnosis: I’ve Been Practicing Long Enough…; Mar, 96; The Final Diagnosis: You Might Be a Mixed Animal Practitioner If…; Apr, 144 Gleed RD: Treating Thoracic Injuries; Jun, 208–223 Grady JA: Vestibular Disease: Temporohyoid Osteoarthropathy; Jul/Aug, 278–282; Photic Head Shaking; Sep, 327–331 Griffi n C: From the Horse’s Mouth: The First Premolar Teeth; Mar, 68–76; From the Horse’s Mouth: Extraction of the First Premolar Teeth; Jul/Aug, 254–266; From the Horse’s Mouth: Routine Dentistry in Juvenile Performance Horses; Nov/Dec, 402–415

H Hamor RE: Clinical Snapshot: A Quarter Horse Mare with a Cataract; Apr, 107–108 Hawkins JF: Cutting to Cure: Urolithiasis; Apr, 125–133 Holbrook TC: Therapeutics in Practice: Treating Cantharidin Toxicosis; Oct, 353–357 Hurley DJ: Abstract Thoughts: Extracellular Matrix in Equine Joint Health and Disease; Mar, 66–67; Abstract Thoughts: How Cell Membranes Work: Smoke on the Water; Apr, 116–118; Abstract Thoughts: Infl ammation and Infertility in Mares: How Irritating!; May, 158–160; Abstract Thoughts: Infl ammation and Male Infertility: A Break in Immune Privilege Affects “Mojo”; Jul/Aug, 283–285; Abstract Thoughts: Cells Arising From Monocytes: Nature’s Transformers; Sep, 321–323

K Kelly G: Cutting to Cure: Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318 Kelmer G: Clinical Snapshot: Colic in a Quarter Horse; Jan/Feb, 12–14; Clinical Snapshot: Severe Forelimb Lameness in a Quarter Horse; Jan/Feb, 41, 43; Clinical Snapshot: Colic in a Warmblood-Cross Gelding; Mar, 58, 61

L Labelle AL: Clinical Snapshot: A Quarter Horse Mare with a Cataract; Apr, 107–108; Clinical Snapshot: Blepharospasm in a Paint Horse Gelding; May, 185–186 Lamm C: Clinical Snapshot: A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348 Linford RL: Clinical Snapshot: Puncture Wound in a Thoroughbred Filly; Sep, 302–304 Lowder M: Clinical Snapshot: Oral Bleeding and Swelling in a Quarter Horse Gelding; Sep, 319–320

Lyon C: Managing Your Practice and Life: A Workhorse at Play: A Talk with Dr. Bob Emery; Mar, 63–64; Managing Your Practice and Life: Living Up to an Image: A Talk With Dr. Alexia McKnight; Jun, 204–205; Managing Your Practice and Life: The Upside of Weekend Work: A Talk With Dr. Claudia Sandoval; Sep, 298–300; Managing Your Practice and Life: Music and Medicine: An Inspiring “Duet” for Dr. Lynsey Makkreel; Nov/Dec, 394–397

M MacGillivray KC: Clinical Snapshot: Seizures in a 2-Hour-Old Thoroughbred Colt; Mar, 60, 62 McClure SR: Clinical Forum: Shock-Wave Therapy: How It Has Shocked or Bored Us; Apr, 110–114 McCoy P: Clinical Snapshot: A Rapidly Growing Mass on a Quarter Horse Mare; May, 162, 164 McKay K: The Editor’s Desk: Meet Our New Online CE “Sister”; Mar, 56; The Editor’s Desk: Your Journal, Your Success; Jul/Aug, 248; The Editor’s Desk: Practicing Compassion; Nov/Dec, 390 McKenzie III HC: Acute Colitis: Pathophysiology and Noninfectious Etiologies; Oct, 366–374; Acute Colitis: Infectious Causes; Oct, 375–380; Treating Acute Colitis; Nov/Dec, 416–427 McNeil JG: Clinical Snapshot: Puncture Wound in a Thoroughbred Filly; Sep, 302–304 Moore JN: The Editor’s Desk: The New World Disorder and the New Year; Jan/Feb, 8; Abstract Thoughts: Extracellular Matrix in Equine Joint Health and Disease; Mar, 66–67; Abstract Thoughts: How Cell Membranes Work: Smoke on the Water; Apr, 116–118; Abstract Thoughts: Inflammation and Infertility in Mares: How Irritating!; May, 158–160; The Final Diagnosis: Face it, We’re Aneuronal; Jun, 240; Abstract Thoughts: Inflammation and Male Infertility: A Break in Immune Privilege Affects “Mojo”; Jul/Aug, 283–285; Abstract Thoughts: Cells Arising From Monocytes: Nature’s Transformers; Sep, 321–323; The Final Diagnosis: The Grada Haus; Oct, 383–384 Moore RM: Editorial: Cutting to Cure: A New Partnership With the ACVS; Sep, 296 Mueller POE: Editorial: Keeping PACE: Positive Attitude Changes Everything; Apr, 104–105

N Nogradi N: Clinical Snapshot: Tachycardia and Tachypnea in a 2-Day-Old Thoroughbred; Jan/Feb, 40, 42

O Oke S: Oral Joint Health Supplements: Chemistry, Pharmacology, and Administration; May, 177–185

P Palmer SE: Guest Editorial: Clean Your Own House, Veterinarians!; Jun, 200–202 Prades M: Pathophysiology of Osteoarthritis; Jan/Feb, 28–40

CompendiumEquine.com | November/December 2009 | Compendium Equine: Continuing Education for Veterinarians®

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2009 Annual Index

Subjects

R Radcliffe RM: Treating Thoracic Injuries; Jun, 208–223 Rantanen N: Imaging Is Believing: Stifle Ultrasonography: A Case Study; Apr, 119–124 Rashmir-Raven A: Clinical Snapshot: A Rapidly Growing Mass on a Quarter Horse Mare; May, 162, 164; Clinical Snapshot: Puncture Wound in a Thoroughbred Filly; Sep, 302–304 Rezabek G: Clinical Snapshot: A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348 Rodgers LL: Clinical Snapshot: A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348 Rush BR: Vestibular Disease: Temporohyoid Osteoarthropathy; Jul/Aug, 278–282; Photic Head Shaking; Sep, 327–331

S

Cardiology Clinical Snapshot: Tachycardia and Tachypnea in a 2-Day-Old Thoroughbred; Jan/Feb, 40, 42

Dentistry From the Horse’s Mouth: The First Premolar Teeth; Mar, 68–76 From the Horse’s Mouth: Extraction of the First Premolar Teeth; Jul/Aug, 254–266 Clinical Snapshot: Oral Bleeding and Swelling in a Quarter Horse Gelding; Sep, 319–320 From the Horse’s Mouth: Routine Dentistry in Juvenile Performance Horses; Nov/Dec, 402–415

Dermatology

Schramme M: Cutting to Cure: Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318 Schumacher J: Cutting to Cure: Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318 Smith H: Clinical Snapshot: Weight Loss and Acute Colic in a Thoroughbred Gelding; Oct, 363–365 Smith S: Clinical Snapshot: Dysphagia and Nasal Discharge in a Quarter Horse Gelding; Sep, 325–326 Snider T: Clinical Snapshot: Flaking and Crusting Skin on an American Paint Gelding; May, 156, 163 Sponseller B: Hemostasis; Mar, 78–89; Modifying the Coagulation Cascade: Available Medications; Jun, 224–236 Sprayberry KA: Pleuropneumonia; May, 166–176 Stern A: Clinical Snapshot: Flaking and Crusting Skin on an American Paint Gelding; May, 156, 163; Clinical Snapshot: Recurrent Epistaxis in a Thoroughbred Mare; Jul/Aug, 250–252; Clinical Snapshot: Dysphagia and Nasal Discharge in a Quarter Horse Gelding; Sep, 325–326; Clinical Snapshot: A Large Growth on a Quarter Horse Gelding; Oct, 350–352; Clinical Snapshot: Acute Colic in a Quarter Horse Mare; Nov/Dec, 398–400 Swiderski C: Clinical Snapshot: Weight Loss and Acute Colic in a Thoroughbred Gelding; Oct, 363–365

T Toth B: Clinical Snapshot: Seizures in a 2-Hour-Old Thoroughbred Colt; Mar, 60, 62 Tóth F: Cutting to Cure: Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318

V Vaala WE: Perinatal Asphyxia Syndrome in Foals; Apr, 134–140

W

Clinical Snapshot: Flaking and Crusting Skin on an American Paint Gelding; May, 156, 163 Clinical Snapshot: Recurrent Epistaxis in a Thoroughbred Mare; Jul/Aug, 250–252 Clinical Snapshot: A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348

Emergency Medicine Treating Thoracic Injuries; Jun, 208–223

Euthanasia Fare Thee Well: How to Help Owners (and Yourself) Deal With the Death of a Horse; Jul/Aug, 267–273

Gastroenterology Clinical Snapshot: Colic in a Quarter Horse; Jan/Feb, 12–14 Therapeutics in Practice: Managing Foal Diarrhea; Jan/Feb, 16–26 Clinical Snapshot: Colic in a Warmblood-Cross Gelding; Mar, 58, 61 Clinical Snapshot: Dysphagia and Nasal Discharge in a Quarter Horse Gelding; Sep, 325–326 Clinical Snapshot: Weight Loss and Acute Colic in a Thoroughbred Gelding; Oct, 363–365 Acute Colitis: Pathophysiology and Noninfectious Etiologies; Oct, 366–374 Acute Colitis: Infectious Causes; Oct, 375–380 Clinical Snapshot: Acute Colic in a Quarter Horse Mare; Nov/Dec, 398–400 Treating Acute Colitis; Nov/Dec, 416–427

Hematology Hemostasis; Mar, 78–89 Modifying the Coagulation Cascade: Available Medications; Jun, 224–236

Horse Racing Guest Editorial: Clean Your Own House, Veterinarians!; Jun, 200–202

Imaging

Weese JS: Therapeutics in Practice: Treating Methicillin-Resistant Staphylococcus aureus Infection; Jul/Aug, 274–277 Weisler S: Clinical Snapshot: Severe Forelimb Lameness in a Quarter Horse; Jan/Feb, 41, 43 Welsh RD: Clinical Snapshot: A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348 Werpy N: Imaging Is Believing: Stifle Ultrasonography: A Case Study; Apr, 119–124 Wong DM: Hemostasis; Mar, 78–89; Modifying the Coagulation Cascade: Available Medications; Jun, 224–236

430

Behavior Photic Head Shaking; Sep, 327–331

Imaging Is Believing: Stifle Ultrasonography: A Case Study; Apr, 119–124

Immunology Abstract Thoughts: Cells Arising From Monocytes: Nature’s Transformers; Sep, 321–323

Infectious Disease Pleuropneumonia; May, 166–176 Clinical Snapshot: Recurrent Epistaxis in a Thoroughbred Mare; Jul/Aug, 250–252 Therapeutics in Practice: Treating Methicillin-Resistant Staphylococcus aureus Infection; Jul/Aug, 274–277

Clinical Snapshot: Dysphagia and Nasal Discharge in a Quarter Horse Gelding; Sep, 325–326

Neurology Clinical Snapshot: Seizures in a 2-Hour-Old Thoroughbred Colt; Mar, 60, 62 Perinatal Asphyxia Syndrome in Foals; Apr, 134–140 Vestibular Disease: Temporohyoid Osteoarthropathy; Jul/Aug, 278–282 Photic Head Shaking; Sep, 327–331

Nutrition Oral Joint Health Supplements: Chemistry, Pharmacology, and Administration; May, 177–185

Oncology Clinical Snapshot: A Rapidly Growing Mass on a Quarter Horse Mare; May, 162, 164 Clinical Snapshot: Oral Bleeding and Swelling in a Quarter Horse Gelding; Sep, 319–320 Clinical Snapshot: A Large Growth on a Quarter Horse Gelding; Oct, 350–352

Ophthalmology Clinical Snapshot: A Quarter Horse Mare with a Cataract; Apr, 107–108 Clinical Snapshot: Blepharospasm in a Paint Horse Gelding; May, 185–186

Orthopedics Pathophysiology of Osteoarthritis; Jan/Feb, 28–40 Clinical Snapshot: Severe Forelimb Lameness in a Quarter Horse; Jan/Feb, 41, 43 Abstract Thoughts: Extracellular Matrix in Equine Joint Health and Disease; Mar, 66–67 Clinical Forum: Shock-Wave Therapy: How It Has Shocked or Bored Us; Apr, 110–114 Imaging Is Believing: Stifle Ultrasonography: A Case Study; Apr, 119–124 Vestibular Disease: Temporohyoid Osteoarthropathy; Jul/Aug, 278–282 Cutting to Cure: Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318

Pharmacology Oral Joint Health Supplements: Chemistry, Pharmacology, and Administration; May, 177–185 Modifying the Coagulation Cascade: Available Medications; Jun, 224–236 Therapeutics in Practice: Treating Methicillin-Resistant Staphylococcus aureus Infection; Jul/Aug, 274–277 Therapeutics in Practice: Treating Cantharidin Toxicosis; Oct, 353–357

Practice Management Managing Your Practice and Life: A Workhorse at Play: A Talk with Dr. Bob Emery; Mar, 63–64 The Final Diagnosis: I’ve Been Practicing Long Enough…; Mar, 96 Editorial: Keeping PACE: Positive Attitude Changes Everything; Apr, 104–105 The Final Diagnosis: You Might Be a Mixed Animal Practitioner If…; Apr, 144 Managing Your Practice and Life: Living Up to an Image: A Talk With Dr. Alexia McKnight; Jun, 204–205 Fare Thee Well: How to Help Owners (and Yourself) Deal With the Death of a Horse; Jul/Aug, 267–273 Managing Your Practice and Life: The Upside of Weekend Work: A Talk With Dr. Claudia Sandoval; Sep, 298–300 Managing Your Practice and Life: Music and Medicine: An Inspiring “Duet” for Dr. Lynsey Makkreel; Nov/Dec, 394–397

Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com


2009 Annual Index Reproduction Abstract Thoughts: Inflammation and Infertility in Mares: How Irritating!; May, 158–160 Abstract Thoughts: Inflammation and Male Infertility: A Break in Immune Privilege Affects “Mojo”; Jul/Aug, 283–285

Respiratory Medicine Perinatal Asphyxia Syndrome in Foals; Apr, 134–140 Pleuropneumonia; May, 166–176

Surgery Cutting to Cure: Urolithiasis; Apr, 125–133 Editorial: Cutting to Cure: A New Partnership With the ACVS; Sep, 296 Cutting to Cure: Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318

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

Product

Page #

Alberts

Carbide Blades

397

American Association of Equine Practitioners

12th Annual Resort Symposium

392

Bayer HealthCare Animal Health

Legend

387

Dandy Products, Inc

Padding and Flooring

423

Equine Oxygen Therapy, LLC

Hyperbaric Treatment

427

GLC Direct

GLC 5500 RX with Actistatin

403

Intervet/Schering-Plough Animal Health

EquiRab

428

Luitpold Pharmaceuticals, Inc

Adequan i.m.

393

Meds for Vets

Compounding Pharmacy

425

Merial

Equioxx

399, 400

Toxicology Therapeutics in Practice: Treating Cantharidin Toxicosis; Oct, 353–357

Urology Cutting to Cure: Urolithiasis; Apr, 125–133

Wound Care The Final Diagnosis: Just Another Unusual Day; Jan/ Feb, 48 Treating Thoracic Injuries; Jun, 208–223 Clinical Snapshot: Puncture Wound in a Thoroughbred Filly; Sep, 302–304

Series and Departments Abstract Thoughts Extracellular Matrix in Equine Joint Health and Disease; Mar, 66–67 How Cell Membranes Work: Smoke on the Water; Apr, 116–118 Inflammation and Infertility in Mares: How Irritating!; May, 158–160 Inflammation and Male Infertility: A Break in Immune Privilege Affects “Mojo”; Jul/Aug, 283–285 Cells Arising From Monocytes: Nature’s Transformers; Sep, 321–323

Clinical Forum Shock-Wave Therapy: How It Has Shocked or Bored Us; Apr, 110–114

Clinical Snapshot Colic in a Quarter Horse; Jan/Feb, 12–14 Tachycardia and Tachypnea in a 2-Day-Old Thoroughbred; Jan/Feb, 40, 42 Severe Forelimb Lameness in a Quarter Horse; Jan/ Feb, 41, 43 Colic in a Warmblood-Cross Gelding; Mar, 58, 61 Seizures in a 2-Hour-Old Thoroughbred Colt; Mar, 60, 62 A Quarter Horse Mare with a Cataract; Apr, 107–108 Flaking and Crusting Skin on an American Paint Gelding; May, 156, 163 A Rapidly Growing Mass on a Quarter Horse Mare; May, 162, 164 Blepharospasm in a Paint Horse Gelding; May, 185–186 Recurrent Epistaxis in a Thoroughbred Mare; Jul/Aug, 250–252 Puncture Wound in a Thoroughbred Filly; Sep, 302–304 Oral Bleeding and Swelling in a Quarter Horse Gelding; Sep, 319–320

GastroGard

395, 396

IMRAB

407

Potomavac

Inside front cover

RECOMBITEK

405

Platinum Performance, Inc

Platinum Performance

389

Purina

Equine Senior

401

Shank’s Veterinary Equipment

Surgery Tables

432

Triple Crown Nutrition, Inc

Triple Crown Senior

Back cover

Universal Ultrasound

MYLAB Ultrasound, UMS 900, TERAVET T3000

391

Veterinary Learning Systems

VetLearn.com

398

Western Veterinary Conference

82nd Annual Conference

Inside back cover

Dysphagia and Nasal Discharge in a Quarter Horse Gelding; Sep, 325–326 A Severe Dermatologic Condition in a Paint Gelding; Oct, 346–348 A Large Growth on a Quarter Horse Gelding; Oct, 350–352 Weight Loss and Acute Colic in a Thoroughbred Gelding; Oct, 363–365 Acute Colic in a Quarter Horse Mare; Nov/Dec, 398–400

Cutting to Cure Urolithiasis; Apr, 125–133 Proximal Suspensory Desmitis of the Hindlimbs; Sep, 308–318

Editorial Keeping PACE: Positive Attitude Changes Everything; Apr, 104–105 Cutting to Cure: A New Partnership With the ACVS; Sep, 296 How Did I Get Here?; Oct, 344

From the Horse’s Mouth The First Premolar Teeth; Mar, 68–76 Extraction of the First Premolar Teeth; Jul/Aug, 254–266 Routine Dentistry in Juvenile Performance Horses; Nov/Dec, 402–415

Guest Editorial Some People Use Data Like Drunks Use Lampposts: More for Support Than Illumination; May, 152–154 Clean Your Own House, Veterinarians!; Jun, 200–202

Imaging Is Believing Stifle Ultrasonography: A Case Study; Apr, 119–124

Managing Your Practice and Life A Workhorse at Play: A Talk with Dr. Bob Emery; Mar, 63–64 Living Up to an Image: A Talk With Dr. Alexia McKnight; Jun, 204–205

The Upside of Weekend Work: A Talk With Dr. Claudia Sandoval; Sep, 298–300 Music and Medicine: An Inspiring “Duet” for Dr. Lynsey Makkreel; Nov/Dec, 394–397

Reading Room Technical Large Animal Emergency Rescue; Jan/Feb, 10 Blackwell’s Five-Minute Veterinary Consult: Equine, 2nd ed.; Sep, 306 Natural Methods for Equine Health and Performance, 2nd ed.; Oct, 358 Vault Guide to Veterinary and Animal Careers; Oct, 360

The Editor’s Desk The New World Disorder and the New Year; Jan/Feb, 8 Meet Our New Online CE “Sister”; Mar, 56 Your Journal, Your Success; Jul/Aug, 248 Practicing Compassion; Nov/Dec, 390

The Final Diagnosis Just Another Unusual Day; Jan/Feb, 48 I’ve Been Practicing Long Enough…; Mar, 96 You Might Be a Mixed Animal Practitioner If…; Apr, 144 My Buddy Mahoot; May, 188–189 Face it, We’re Aneuronal; Jun, 240 Through the Eyes, and Ears, of a Child; Jul/Aug, 288 Nala and Me; Sep, 335–336 The Grada Haus; Oct, 383–384

Therapeutics in Practice Managing Foal Diarrhea; Jan/Feb, 16–26 Treating Methicillin-Resistant Staphylococcus aureus Infection; Jul/Aug, 274–277 Treating Cantharidin Toxicosis; Oct, 353–357

2009 Supplements to Compendium Equine Equine Medical Review; Sep, Suppl 7A; Nov/Dec Suppl 9A

CompendiumEquine.com | November/December 2009 | Compendium Equine: Continuing Education for Veterinarians®

431


MARKET SHOWCASE

CLASSIFIED ADVERTISING PRACTICES FOR SALE

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.

FLORIDA – Only practice in Fort Meade. FL40. GEORGIA – Gross up 9% through August 2009. New Heska Lab! GA8. UPSTATE NEW YORK – Gorgeous equine practice. NY4. SOUTHERN TEXAS - Profitable, up-to-date practice. New laser! TX1. OTHER AVAILABLE PRACTICES: FLORIDA, GEORGIA, NEW HAMPSHIRE, NEW JERSEY

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HAVE YOU HEARD THE NEWS? Compendium Equine Market Showcase and Classified Advertising sections deliver your product, service, or opportunity to thousands of potential buyers and responders each issue. Every ad is also featured on vetclassifieds.com for even greater marketing exposure. Contact Trish O'Brien to create a marketing plan or to schedule your classified ad–we are here to assist! Call: 800-237-9851, ext. 237 or e-mail: compeq@rja-ads.com 432

Compendium Equine: Continuing Education for Veterinarians® | November/December 2009 | CompendiumEquine.com


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