Compendium Equine | March 2009

6 CE Contact Hours | CompendiumEquine.com | Peer Reviewed

Vol 4(2) March 2009

From the NEW Horse’s Mouth

Hemostasis H

se as e

Managing Your Practice and Life A Talk with Dr. Bob Emery Pa ge and atri 66 D x i i n

FREE

CE

The First Premolar Teeth

Jo Ex in tra t H ce ea llul lth ar M

FREE

CE

We’re for innovation.

Only PreveNile ® West Nile Virus vaccine has chimera technology for one-dose protection.

Only PreveNile® West Nile Virus vaccine utilizes chimera technology. Which is why PreveNile requires just one dose for primary immunization – making it the perfect choice for foals and horses with unknown vaccination history as well as horses previously vaccinated with other West Nile vaccines.

PreveNile starts strong. It was proven efficacious in a severe intrathecal challenge study and has the most comprehensive label claim of all West Nile vaccines available. And PreveNile lasts long. Just one dose safely protects against viremia and aids in prevention of disease and encephalitis caused

by West Nile Virus infection in yearlings or older horses for a full 12 months.

Choose PreveNile, the superior single-shot solution.

We’re for the horse.

P.O. Box 318 • 29160 Intervet Lane • Millsboro, Delaware 19966 • intervetusa.com • 800.521.5767 PreveNile is a registered trademark of Intervet Inc. or an affiliate. ©2009 Intervet Inc. All rights reserved.

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March 2009 Vol 4(2)

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).

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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 EDITORIAL ASSISTANT 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 SENIOR ART DIRECTOR Michelle Taylor 267-685-2474 | mtaylor@vetlearn.com ART DIRECTOR David Beagin 267-685-2461 | dbeagin@vetlearn.com OPERATIONS Marissa DiCindio, Director of Operations 267-685-2405 | mdicindio@vetlearn.com Elizabeth Ward, Associate Production Manager–Journals 267-685-2458 | eward@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 Lisa Siebert, Account Manager 913-422-3974 | Cell 215-589-9457 | lsiebert@vetlearn.com CLASSIFIED ADVERTISING Liese Dixon, Classified Advertising Specialist 800-920-1695 | classifieds@vetlearn.com | www.vetclassifieds.com

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March 2009 Vol 4(2)

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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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.

Platinum Performance_USE.qxp:1

3/4/09

10:40 AM

This is my horse

Page 1

™

Ever since my Grandpa used to take me out to see the cows and horses, I've been a horse lover. As far back as I can remember - even my early days spent riding in the saddle in front of my dad - I've taken pride in the care of horses.

By that I mean, providing the best training, the best care and the best nutrition. After breeding horses for the past 25 years, I understand just how important proper nutrition is. That's why I use Platinum. It works at a cel lular level, and that makes a lot of sense to me. If the cel ls are healthy, then the whole horse is healthy and performing at its best. Just like Dash, here.

I'm in the music business because I love music and I'm in the horse business because I love horses. Life is too short to not spend it doing what you love.

Lyle Lovett 4-time Grammy Award winning Recording Artist, American Quarter Horse breeder, Platinum Performance Client since 2005

First Down Shine, 4-year-old American Quarter Horse

Platinum Performance™ Improves • Joint function • Hoof health • Skin and coat health • Performance recovery • Digestive health • Bone and skeletal health • Healing

Find the solution to your horse’s needs – discover your Platinum!

To find the right Platinum Performance™ nutritional solution, and to learn about the science behind the supplements call 1-800-553-2400, visit ThisIsMyPlatinum.com or speak with your equine veterinarian.

Platinum Performance CJ™ = Platinum Performance™ + Ortho-Chon II HA + ASU.

For horses that require additional joint support.

21518_Lyle_8.25x11.indd 1

Lyle feeds some of his horses Platinum Performance and for the ones that need additional joint support, he feeds Platinum Performance CJ.

© 2009 platinum performance, inc.

3/2/09 1:30:42 PM

March 2009 Vol 4(2)

Features 63

❯❯ C. Lyon Dr. Emery specializes in performance horse medicine and does some competing of his own … in triathlons. We talked to him about how he maintains his work–life balance.

CompendiumEquine.com | Peer Reviewed | Free CE

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CE

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

Managing Your Practice and Life A Workhorse at Play: A Talk with Dr. Bob Emery

FREE

From the Horse’s Mouth NEW TThe First Premolar Teeth

CE

❯❯ Cleet Griffin ❯ Equine practitioners E should know the basics regarding the first premolar teeth (wolf teeth) and the problems they can cause. This article reviews the history, anatomy, and eruption of wolf teeth as well as the rationale for removing them.

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CE Feature Hemostasis H

FREE

CE

❯❯ Cody Alcott, David M. Wong, ❯ Charles Brockus, and Brett Sponseller A basic knowledge of hemostasis is necessary to evaluate various disease processes in horses. This article reviews coagulation and fibrinolysis as well as diagnostic testing to evaluate these systems in horses.

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The Final Diagnosis I’ve Been Practicing Long Enough … ❯❯ Ronald E. Gill In his 34 years as a mixed animal practitioner, Dr. Gill has learned and seen a few things that might surprise you.

Departments 54 CompendiumEquine.com 56 The Editor’s Desk Meet Our New Online CE “Sister” Cover image © 2009 Marilyn Barbone/Shutterstock.com.

A wild Welsh Mountain pony foal in Brecon Beacons National Park, Wales, United Kingdom.

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.

52

❯❯ Kirk McKay

Clinical Snapshot 58 Colic in a WarmbloodCross Gelding ❯❯ Gal Kelmer

60 Seizures in a 2-HourOld Thoroughbred Colt ❯❯ Balazs Toth and Katherine C. MacGillivray

66 Abstract Thoughts Extracellular Matrix in Equine Joint Health and Disease ❯❯ David J. Hurley and James N. Moore

76 Index to Advertisers 933

CE

Calendar C

94 Market Showcase 94 Classified Advertising

Merial-Recombitek.qxp:Sound Technologies_USE

2/19/09

11:33 AM

Page 1

RECOMBITEK®. Fast-acting, long-lasting West Nile virus protection from a brilliant bit of technology.

Protection against viremia, natural challenge.1 Two weeks after vaccination RECOMBITEK Equine WNV vaccine = 100% Nonvaccinates = 20%

345 days after vaccination RECOMBITEK Equine WNV vaccine = 90% Nonvaccinates = 16%

1 2 3

We’ve got to give credit to the canary. RECOMBITEK® Equine West Nile Virus vaccine is made using recombinant canarypox-vectored technology, developed by Merial scientists from a canary vaccine. It provides a fast-acting immune response that lasts throughout the season.1 One study even showed onset of immunity just 26 days after the initial dose.2,3 RECOMBITEK Equine WNV vaccine is proven against a natural mosquito-borne infection, and is approved for use in young foals.

In fact, our recombinant canarypox-vectored vaccines have helped protect dogs against distemper and cats against rabies and feline leukemia safely and effectively for years. Be confident with RECOMBITEK brand products.

Minke JM, et al. Recombinant canarypox virus vaccine carrying the prM/E genes of West Nile virus protects horses against a West Nile virus-mosquito challenge, Arch of Vir 2004;18[Supp]:221-230.

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. Am J Vet Res 2004;65:1459-1462.

For primary vaccination, the product label recommends a two-dose series including a second dose 4 to 6 weeks after the first, and annual revaccination.

www.equinewnv.com 1-888-MERIAL-1 Merial Family of Brands

®RECOMBITEK, ZIMECTERIN, EQUIOXX, HEARTGARD, the DOG & HAND LOGO and FRONTLINE are registered trademarks, and ™the HORSE HEAD LOGO is a trademark, of Merial. ®GASTROGARD and ULCERGARD are registered trademarks, of the AstraZeneca Group of Companies. ©2007 Merial Limited. Duluth, GA. All rights reserved. EVXADS7WNVVETAD

March

CompendiumEquine.com

2009 Vol 4(2)

WEB EXCLUSIVES

CE ARTICLES WEB EXCLUSIVE

VIDEOS

Earn 3 free contact hours for each CE article.

SEARCHABLE ARCHIVES

Search all content since Compendium Equine’s launch in 2005.

CE CONFERENCE CALENDAR

❯❯ Head Shaking Videos os Head shaking is one of the most difficult problems to diagnosee because of the great diversity of causes.

Watch videos of typical and photic head shaking.

Check the online version to find events that aren’t listed in the journal.

NEWS BITS

❯❯ Using a Bitless Bridle ❯❯ Improved GET-A-DVM Online Locator Service Launched ❯❯ AAEP Releases Recommendations for Protecting Racehorses

54

E-NEWSLETTERS

❯❯ EquineMail helps you prepare for questions from your clients by highlighting the latest topics from popular publications for horse owners. In addition, links to related content in Compendium Equine are provided. ❯❯ Compendium Equine EXTRA provides a preview of, and access to, the latest issue of Compendium Equine. Breaking news and Web-exclusive content is included.

For both monthly e-newsletters, sign up for free at CompendiumEquine.com.

CONTACT US

❯❯ Email your questions, suggestions, comments, or letters to the editor: editor@CompendiumEquine.com

Purina Mills_USE.qxp:Sound Technologies_USE

2/19/09

11:35 AM

Page 1

NEW

Losing weight

doesn’t have to mean eating less.

Many horse owners simply can’t stand to feed their horses small portions, even when their animals are obese. That’s why Purina Mills created WellSolve W/C® horse feed. Its Full-Scoop™ Formula uses a first-of-its-kind extruded pellet that lets horse owners feed full-sized meals that aren’t filled with excess carbs and calories. For the horse, that means a generous, satisfying meal packed with all the nutrients he needs yet still allowing him to lose weight. For you, it means greater owner compliance, because your clients won’t feel like they’re “starving” their horses.

To see the abstract behind this new weight control diet, proven in thousands of feeding trials, visit wellsolveequine.com. Chances are, this could be the easiest way you’ll find to help your clients get unwanted weight off their horses.

Introducing wellsolveequine.com ©2008 Purina Mills, LLC

horse feeds. New from

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

Kirk McKay

Meet Our New Online CE “Sister”

A

s your trusted source for continuing education (CE) for more than 30 years, Veterinary Learning Systems is pleased to announce the launch of Compendium Equine’s new online CE “sister”: CECenter.com.

CECenter.com is a companion site to VetLearn. com, which comprises CompendiumEquine.com, CompendiumVet.com, VetTechJournal.com, VeterinaryTherapeutics.com, and ForumVet.com.

However, CECenter.com is devoted exclusively to providing interactive CE to veterinarians and veterinary technicians through a wide array of new and timely CE activities—information you need to know now and incorporate into practice today.

The need and vision for a dedicated veterinary CE Web site developed with the increasing number of veterinary practitioners using VetLearn. com and CompendiumEquine.com to meet their CE requirements. The monthly visitor profile for VetLearn.com comprises approximately 145,000 registered users (43.3% of whom are practicing veterinarians; 47.7%, veterinary technicians; 3%, veterinary technician students; and 1.2%, veterinary students). Approximately 10% of the CE we

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deliver is equine related. VetLearn.com’s monthly average of 2000 CE credits delivered and 200,000 page views (40,000 of which are clinical CE review articles) demonstrated a clear need to expand our CE offerings by creating a companion Web site dedicated to CE. CECenter.com allows veterinarians and veterinary technicians to search for and participate in CE activities in a central location. In addition to archiving peer-reviewed CE content from Compendium Equine, Compendium, and our sister publication Veterinary Technician, CECenter.com offers exclusive, interactive, sponsored courses accredited by the Registry of Approved Continuing Education as well as a list of CE from other respected sources, such as the American Veterinary Medical Association, the American Animal Hospital Association, and accredited universities and institutions. As a convenience, CECenter.com maintains individual CE accounts for users so they have a permanent online record of their CE history and can reprint any CE certificate at any time. Other features of CECenter.com include a complete listing of CE requirements by state and a preview of upcoming courses and activities. And plans call for more CE opportunities as CECenter.com grows throughout 2009.

CECenter.com is free and accessible to all registered CompendiumEquine.com users. We invite you to go online today to experience this powerful new career and education tool for yourself.

Along with CompendiumEquine.com, we are confident that CECenter.com will become the preferred and trusted online CE source for you and your staff.

As always, we welcome your comments and suggestions regarding VetLearn.com, CompendiumEquine.com, and CECenter.com. Please feel free to email me at kmckay@vetlearn.com, and enjoy your learning (and CE-credit earning) experience!

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

FPO 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 Represeentative today. Or call 1-888--MERIAL-1.

Response.Ability.

CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian. GASTROGARD is indicated for the treatment and prevention of recurrence of gastric ulcers in horses and foals 4 weeks and older. In efficacy trials, no adverse reactions were observed. Safety in pregnant or lactating mares has not been determined. DO NOT USE IN HORSES INTENDED FOR HUMAN CONSUMPTION. KEEP THIS AND 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.

1

2

®GASTROGARD is a registered trademark of the AstraZeneca Group of Companies. ©2008 Merial Limited. Duluth, GA. All rights reserved. EQUIGGD901-A (10/08)

See Page 58 for Product Information Summary

Clinical Snapshot 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

OCH3 CH3 O

Particularly intriguing or difficult cases

Case Presentation #1 ❯❯ Gal Kelmer, DVM, MS, DACVS, Koret Veterinary Teaching Hospital, University of Jerusalem, Israel*

OCH3 H

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.

*Dr. Kelmer was affiliated with the University of Tennessee when he saw this case.

A

A 15-year-old Warmblood-cross gelding with colic was referred as an emergency due to continued pain despite administration of analgesics in the field. At presentation, the horse appeared to be in pain, and 8 L of reflux were obtained by nasogastric intubation. Rectal palpation did not reveal any specific abnormalities; however, several distended loops of small intestine were noted on ultrasonographic evaluation of the abdomen.

Abdominocentesis yielded red-tinged fluid with a normal leukocyte count and normal total protein and lactate concentrations. Because of the gelding’s recurrent pain and small intestinal dysfunction, surgery was recommended, but the owners declined it. Medical treatment was initiated by intermit-

58

tently decompressing the stomach, administering replacement fluids intravenously, and providing analgesia as needed. The horse responded initially but became more painful over the next 24 hours. Surgery was again declined by the owners, and euthanasia was performed. The major finding from the gross necropsy examination is shown (A).

1. What is your diagnosis?

2. What clinical condition may lead to this lesion?

3. What is the appropriate surgical procedure to treat this lesion?

4. If surgery had been performed, which potential complications regarding this lesion should have been discussed with the owners?

SEE PAGE 61 FOR ANSWERS AND EXPLANATIONS.

Compendium Equine: Continuing Education for Veterinarians® | March 2009

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Clinical Snapshot Particularly intriguing or difficult cases

Case Presentation #2 ❯❯ Balazs Toth, DVM, and Katherine C. MacGillivray, VMD, DACVIM, Hagyard Equine Medical Institute

A 2-hour-old Thoroughbred colt presented to the clinic with a history of seizures since birth. The mare had placentitis and was treated with antimicrobials, NSAIDs, altrenogest, and pentoxifylline during the last few weeks of gestation. The foal was full-term, weighed 90.2 lb (41 kg), and was in poor body condition (2 of 9). There were no signs of prematurity.

On initial clinical examination, the neonate had abnormal mentation, a heart rate of 150 beats/min, a respiratory rate of 56 breaths/min, and a rectal temperature of 98.1°F (36.7°C).

The mucous membranes were pale and injected. There were no palpable peripheral pulses, and the extremities were cold.

The indirect blood pressure was 88/56 mm Hg, the arterial oxygen saturation was 81%, and the PCO2 was 44 mm Hg. The complete blood count and serum chemistry profile revealed leukopenia (2800 leukocytes/μL), hypoglycemia (54 mg/dL), and a low serum IgG concentration (<100 mg/dL). The foal

exhibited seizure activity (i.e., severe extensor rigidity that was more pronounced in the forelimbs, opisthotonus, nystagmus) and could not sit in a sternal position or rise. The foal continued to exhibit seizures despite aggressive medical therapy and was euthanized due to progression of the seizures. A necropsy was performed.

1. What is your differential diagnosis based on the foal’s history and the clinical findings?

2. How would you have treated this neonate?

3. How would you have proceeded if the seizure activity had continued despite treatment and the owner had wanted to proceed?

4. Based on your diagnosis, what central nervous system abnormalities would you expect on the postmortem examination?

SEE PAGE 62 FOR ANSWERS AND EXPLANATIONS.

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Compendium Equine: Continuing Education for Veterinarians® | March 2009

Clinical Snapshot Answers and Explanations Case Presentation #1 SEE PAGE 58 FOR CASE PRESENTATION.

1. Thrombosis of the iliac vein leading

to infarction. A clear line of demarcation (B) separates the apparently healthy ileum from the segment of the ileum affected by the thrombus.

2. Parasitism such as worm migration is often implicated in thrombus formation and intestinal infarction.1 Although there was no evidence of parasites during histologic examination of the lesion, Eimeria spp were found in other parts of the small intestine wall, and the colonic wall was infiltrated with eosinophils.

3. The surgical procedure indicated in this case is small intestinal resec-

tion and anastomosis. This can be performed by jejunocecostomy or, preferably, jejunoileostomy, depending on how much healthy ileum is available.

4. Because the cause of this condition is unknown, the owners should have been advised that in addition to common potential complications related to small intestinal surgery (e.g., endotoxemia, intestinal adhesions), recurrence is a possibility anywhere along the gastrointestinal tract.

Reference 1. Mair TS, Pearson GR. Multifocal non-strangulating intestinal infarction associated with larval cyathostomiasis in a pony. Equine Vet J 1995;27:154-155.

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March 2009 | Compendium Equine: Continuing Education for Veterinarians®

61

Clinical Snapshot Answers and Explanations Case Presentation #2 SEE PAGE 60 FOR CASE PRESENTATION.

1. Differential diagnosis: septicemia; hypoxic ischemic enceph-

alopathy, neonatal encephalopathy, or perinatal asphyxia; metabolic abnormalities; central nervous system trauma; developmental anomalies; and toxicosis.

2. The foal was treated with the following:

Intravenous bolus of Normosol R (40 mL/kg) Intravenous polyionic crystalloids with 2.5% dextrose (4 mL/kg/hr) Hyperimmune plasma (20 mL/kg IV) Antioxidants: dimethyl sulfoxide (0.8 g/kg IV) and allopurinol (45 mg/kg per nasogastric tube) Vitamins: ascorbic acid (5 g) and thiamine (500 mg) IV (added to crystalloids) Antimicrobials: amikacin (25 mg/kg IV q24h) and potassium penicillin (20,000 U/kg IV q6h) Anticonvulsants: magnesium sulfate (0.025 g/kg/hr); diazepam (0.1 mg/kg twice in the ďŹ rst 2 hours); and midazolam (0.04 mg/kg/hr via constant-rate infusion), which was increased to 0.08 mg/kg/hr after 2 hours and 0.12 mg/kg/hr after another 2 hours Intranasal oxygen insufďŹ&#x201A;ation (6 L/min) 3. If seizure activity had continued despite treatment, rea-

sonable options would have included skull radiography,

ultrasonography of the cisterna magna, cerebrospinal ďŹ&#x201A;uid collection, computed tomography, magnetic resonance imaging, and electroencephalography.

4. In this case, postmortem examination revealed severe

cerebellar hypoplasia. While this is a rare ďŹ nding in this type of presentation, antemortem diagnosis could have been made using magnetic resonance imaging.

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Compendium Equine: Continuing Education for VeterinariansÂŽ | March 2009 | CompendiumEquine.com

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

A Workhorse at Play A Talk with Dr. Bob Emery Equine practitioner Robert Emery, DVM, specializes in performance horse medicine and does some competing of his own … in triathlons! We talked to him about his practice (Beadle Lake Large Animal Clinic in Battle Creek, Michigan), his triathlon training, his family, and how he maintains his work–life balance.

How long have you been practicing veterinary medicine?

Describe your practice setup. How many vets work with you?

I graduated in 1990, so almost 20 years now.

Our practice is an exclusively large animal practice with an outpatient clinic. On a daily basis, the practice works best with one veterinarian in the clinic and the rest of the veterinarians driving around the country working on farms. We have four veterinarians—two full-time and two associates. The associates are part-time and kind of job-share, which I think could be a niche for the future.

Do you practice equine medicine exclusively, or do you treat other species on a regular basis?

When I came out of school, I didn’t know what I wanted to do. I worked with everything: dogs, cats, gerbils, horses, cows, goats, llamas.

As time went on, I developed into a performance equine vet. I really love performance work (chiropractic, acupuncture, lameness) and dentistry. That’s pretty much what I do now— exclusively performance equine medicine. I don’t work with one particular group of horses.

I work with racehorses, dressage horses, a little bit of everything.

What do you enjoy most about your job?

There is always a challenge. There is always a better, more efficient way to do things. It’s really the challenge I enjoy most. It’s never the same thing. There’s always more to learn.

What do you enjoy least?

The hardest part of being an equine vet is being on call—late night call. I don’t mind the emergencies. I actually enjoy doing emergencies if I can help my patients. However, I like working hard from 8:00 am to 5:00 pm and then going home and being done. Managing the practice and all the different personalities in it can also be challenging.

Have you struggled to find and maintain a balance between your work and personal life?

I think I’ve always made it a very high priority to try to maintain a balance. Honestly, my family is always the most important. I’ve learned that if I do the things that I really love fi rst, early in There is always the morning, nobody really a challenge. There misses me. Our town has the greatest group of people who is always a better, love to play in the morning more efficient way before work. Some are swimmers, some are runners, some to do things. are cyclists. As long as I train early in the morning, before work, my training gets done. If I try to train after work, I fi nd that I’m tired, I’ve got lots of family commitments, etc. I’ve got three children, and they’re all teenagers now. They don’t miss me early in the morning…especially on the weekend!

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

63

Managing Your Practice and Life

You are a competitive triathlete. How long have you been competing in triathlons?

For about 9 years.

Tell us a little about your involvement in this sport.

I started mountain biking first and could not believe how much fun I had. Everything was a challenge. At first, I couldn’t get up that hill, I couldn’t get over that log, and then the next time out, I could get up that hill, I could get over that log. One particular Saturday, I had had a pretty stressful week and I really needed the ride. I was on the mountain, and all the trails were closed because of a big race. So I said, “Well, how much does it cost to enter the race?” And the answer was $25.

I actually had $25 with me, so I entered. There were about 300 or 400 people in the race, and I came in 10th in my age group. So, I did well and could not believe how much fun I had competing again (I played sports in high school and college). And then I found out that the really good mountain bikers train on road bikes 4 days a week. I realized that I Because of a staggered start in this race, could get a great workout on Dr. Emery was actually an hour faster than the time shown on the clock. my road bike from home in an hour or 2, whereas with my mountain bike, I had to drive to trails and then ride, so road biking was a lot faster.

It was fun and a great workout. A client of mine introduced me to a lot of people who got me doing triathlons and other races.

How many triathlons do you do per year?

This year, I only did three, but one of them was an ironman (a 2.4-mile swim, 26.2-mile run, and 112-mile bike ride). I’m really glad I did the ironman, but I seriously doubt I’ll do something that big again for 4 or 5 years. It got very, very challenging the last 2 months to hold it all together: the family, work, and

64

training. I usually do about four or five triathlons per year. I’d really like to do more Xterra triathlons (mountain biking and trail running).

Do you find that your colleagues are supportive of your training and competitions?

They are. I actually made sure my business partner was supportive before he became my partner. And he has been extremely supportive. He covers call for me, etc. If you’re ever going to do something like this, you’ve got to have your family 100% behind you. Your partners at work have to support you, too.

How would you describe the effect of triathlon training and competitions on your work?

I’m not quite as nice to be around if I don’t exercise in the morning. I am on a higher plane all day if I work out early in the morning. I just function better if I get up and train.

When I’m training for a big race, I am more efficient at work. I work fewer hours, but my productivity goes up. It’s not sustainable, of course, but it is surprising.

Also, I have learned a lot about equine performance injuries and other issues from my own ailments during training—things like rest and recovery, nutrition, footwear, etc.

What advice, if any, would you give to practitioners who are having trouble finding the time to pursue interests outside of work?

You have to look at what’s important to you.

You need to keep enough staff so you don’t have to work 70 hours a week. Keep your prices competitive. If it interests you, figure out ways to job share. Have a great staff that you really trust and be a good delegator.

SHARE YOUR COMMENTS Have a question or comment about this article? Let us know: E-MAIL editor@CompendiumEquine.com FAX 800-556-3288 WEB CompendiumEquine.com

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

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Abstract Thoughts Highlighting scientific articles with important information relating to equine diseases

Extracellular Matrix in Equine Joint Health and Disease Column Editors ❯❯ David J. Hurley, PhD The University of Georgia ❯ email djhurley@uga.edu ❯❯ James N. Moore, DVM, PhD The University of Georgia

ABSTR ACT

Biologic scaffolds composed of naturally occurring extracellular matrix (ECM) have received significant attention for their potential therapeutic applications. The full potential of the ability of ECM scaffolds to promote constructive remodeling will not be realized, however, until an understanding of the biology and the external influences that affect biology are better achieved. The factors that appear important for the constructive remodeling of ECM biologic scaffolds are its ability to be rapidly and completely degraded with the generation of downstream bioactive molecules, the bioinductive properties of the functional molecules that compose native ECM material, and the ability to engineer its mechanical properties at the time of implantation through an understanding of its collagen fiber microstructure.

❯❯ This abstract has been reprinted from Badylak SF. The extracellular matrix as a biologic scaffold material. Biomaterials 2007;28(25):3587-3593; with permission from Elsevier.

COMMENTARY

SHARE YOUR COMMENTS Have a question or comment about this abstract? Let us know: E-MAIL editor@CompendiumEquine.com FAX 800-556-3288 WEB CompendiumEquine.com

66

Ever think you’d have something in common with Keanu Reeves? Well, you do now. About 10 years ago in The Matrix, he asked Carrie-Anne Moss the same question you might be pondering: “What is the Matrix?” Rather than repeat her reply that “the Matrix is looking for you and will find you if you want it to,” our approach is more scientific.

Of the parts of joints, tendons, and ligaments, the one that is least understood by most veterinarians is the ECM. This is for good reason, as the veterinarian’s focus is most often on the parts that can be evaluated by radiography or ultrasonography. However, the ECM may be equally important, which is why we have recommended the article by Dr. Badylak in this column. While Dr. Badylak’s article is somewhat “tougher sledding” than most we have recommended, a PhD in organic chemistry and instrumental analysis is not needed to follow it. However, a basic understanding of engineering might prove useful.

ECM is a space-defining family of protein–sugar complexes that provide a “cushion” and “conduit” for the organization of tissues. While it appears to play a critical role in organ formation, the ECM is most important in connective tissues. This protein–sugar construct is a three-dimensional complex that organizes space to allow connective tissues to resist weight bearing and stress, a process that appears to be regulated by this complex’s hydration state (i.e., the amount of water it has bound). Consequently, the ECM helps make connective tissues strong and flexible and allows movement of part upon part.

ECM complexes are composed of a limited number of proteins and sugars that can be arranged in an almost limitless set of combinations. This is one reason why ECM is so hard to describe and so difficult to reduce to gen-

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

Abstract Thoughts

eralizations. The mix of proteins and that fragment as a potential early diagsugars and the differential level and nostic test for osteoarthritis because it position of sulfur or uronic acid on appeared with equal clarity in both the sugars in the complex determine mild and severe cases. the form and function of the specific Exercise in foals also appears to composite of ECM at any body site.1 have an impact on the composition Alterations in the composition of this and structure of the ECM complex. material or its hydration state can lead In a study of foals aged 10 days to to trouble, as is evident in degen- 18 months, one group of foals was erative suspensory desmitis, which subjected to a training program that commonly affects Peruvian Paso increased the average exercise load horses and is being recognized with by 30% over that of pasture-reared increasing frequency in Warmbloods, control foals.4 Early training did not Thoroughbreds, and Quarter horses. appear to induce clear degradation of This disease has been characterized cartilage but did appear to increase by the expression of a defect in the the density of cross-linkage of protein ECM where the sulfur group nor- components and sugars, the distribumally found in the “4-position” in tion of specific glycosaminoglycans, decorin proteoglycan has shifted to and hydroxylysine conjugation in the the “6-position.”2 This change in the joints of these foals. While the effects sulfur position in the proteoglycan of increasing the density of ECM in the leads to functional changes in the tis- joints of foals are not completely clear, sue that are characterized by chronic it appears that a small (30%) increase inflammation. This ongoing inflam- in weight-bearing exercise can signifimation ultimately leads to failure of cantly affect the structure of the ECM. the ligament.

In summary, it is important to note Joint disease in most species is that the strength of connective tisassociated with the development of sue is based on the composition and chronic inflammation and changes in three-dimensional organization of its the ECM. This also appears to be true surrounding ECM. The composition of in horses with osteoarthritis, in which the matrix complex is driven by enzylevels of oligomeric matrix protein matic reactions directed by the cells in complex and hyaluronan in synovial the tissues the ECM surrounds. Small fluid are lower than in horses with no changes in ECM composition lead to signs of osteoarthritis.3 In this study, big changes in function. These are a change in the composition of the partly mediated by a change in the ECM complex was demonstrated by amount of water bound to the matrix the presence of a small fragment of complex. A healthy mix yields functhe ECM on an electrophoresis gel tion and flexibility; an unhealthy mix that did not appear on gels from nor- leads to inflammation and pain. We mal horses. These authors proposed a bet Keanu wouldn’t like the latter— study exploring the use of an assay for would you?

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References 1. Hitchcock AM, Yates KE, Costello CE, Zaia J. Comparative glycomics of connective tissue glycosaminoglycans. Proteomics 2008;8(7):1384-1397.

2. Halper J, Kim B, Khan A, et al. Degenerative suspensory ligament desmitis as a systemic disorder characterized by a proteoglycan accumulation. Biomed Central Vet Res 2006;2:12.

3. Taylor SE, Weaver MP, Pitsillides AA, et al. Cartilage

oligomeric matrix protein and hyaluronan levels in synovial fluid from horses with osteoarthritis of the tarsometatarsal joint compared to a control population.

Equine Vet J 2006;38(6):502-507.

4. van Weeren PR, Firth EC, Brommer B, et al. Early exercise advances the maturation of glycosaminoglycans and collagen in the extracellular matrix of articular cartilage in the horse. Equine Vet J 2008;40(2):128-135.

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

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For more information, call 866-374-0242 or visit www.meridiananimalhealth.com

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The First Premolar Teeth ❯❯ Cleet Griffin, DVM, DABVP Texas A&M University

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Abstract: The first premolar teeth (wolf teeth) of horses are considered a component of the permanent dentition and may be identified as Triadan ‘05. Through study of the fossil record, it has been determined that wolf teeth are dental vestiges from ancestors of the modern horse.

Although wolf teeth may not be problematic for the horse, many believe that harm arising from the presence of wolf teeth in some horses may account for oral discomfort, abnormal behaviors during performance, and bitting problems. Rationale exists for veterinarians to remove wolf teeth when necessary to alleviate discomfort and bitting problems.

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orphologic features of the modern horse’s teeth represent adaptations to ecologic changes.1 In the Eocene period, the first ancestor of the horse—a small, leaf-eating mammal called Hyracotherium—had four toes on each front foot and three toes on each hind foot2 and bore little resemblance to modern horses. Fossils show that Hyracotherium had three incisors; one canine tooth; and seven primitive, short-crowned cheek teeth (four premolars and three molars) in each side of the

upper and lower jaws.3 Over time, the second, third, and fourth premolars as well as the three molars progressively became (through “molarization”) long-crowned, complex, well-developed grinders as the horse adapted to prolonged periods of grazing.1,3 The first premolar progressively became smaller and is now small, cone shaped, and usually situated just rostrally to the first well-developed cheek tooth3–5 (FIGURE 1). Thus, the first premolar (wolf tooth) is a functionless remnant from ancestors of the modern horse.1–5

FIGURE 1

At a Glance Triadan Tooth Numbering System Page 70

Anatomy and Eruption Page 71

Rationale for Removing Wolf Teeth Page 75

The maxillary dental arcades. Upper wolf teeth (arrows; Triadan 105 and Triadan 205) are just rostral to each row of the upper cheek teeth.

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

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FREE CE From the Horse’s Mouth

There are several possible origins of the term wolf tooth, some of which appear to be based on superstition. In one publication from the 1700s, the term wolves’ teeth was used as a general description of teeth with sharp edges that could prick and wound the oral mucosa or tongue while eating.6 At about the same time, Daubenton7 described the horse’s first premolars as “supplementary premolars,”8 and some early 20th-century texts suggested that the term wolf teeth may have originated from the resemblance of these teeth to the incisors of carnivores.8,9 Merrillat10 used the terms remnant teeth and supernumerary teeth as synonyms for wolf teeth. He suggested that these BOX 1.

CriticalPo nt Wolf teeth are functionless dental remnants from ancestors of the modern horse.

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 numbering 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)21,22 (FIGURE 2).

teeth were retrogressive representatives of prehistoric horses’ premolars that were degenerating under the influence of selection. He further theorized that the use of the bit over many generations had rid the interdental space of premolars.10 Easley11 retold a remarkable story about a 16th-century military general’s horse that had turned and reared, refusing to move forward into a battle. According to the story, removal of a small tooth in the area of bit contact alleviated the embarrassing behavior of the general’s horse, which became a favorite mount for battle. Unable to leave well enough alone, the general’s horseman concluded that the horse had sensed the presence of wolves when the bit was worked against the tooth, which instinctively caused the horse to shy in order to protect the general.11 In some older publications, the first premolar teeth were blamed for eye problems, including excessive watering, inflammation, and blindness.12,13 It was even speculated that wolf teeth adversely influenced ophthalmic branches of the fifth cranial nerve.12 Therefore, wolf teeth were commonly removed from horses to alleviate eye ailments, resulting in use of the synonym eye tooth.5,10,12,13 Apart from these myths and misconceptions, the presence of wolf teeth in horses remains an area of importance and interest to veterinarians. In general, wolf teeth are not considered to serve a useful purpose. Although wolf teeth may not be problematic for the horse, many horsemen and horsewomen believe that harm caused by the presence of wolf teeth

FIGURE 2

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)

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The First Premolar Teeth CE FIGURE 3

The upper wolf tooth (green arrow; Triadan 205) is near the erupting second premolar (black arrow; Triadan 206). A deciduous premolar cap (blue arrow; Triadan 606) is present. A small lower wolf tooth (yellow arrow; Triadan 305) is present. (Skull specimen.)

may account for oral discomfort, problems with the bit, and abnormal behavior of some horses at work.11,14–20

Anatomy and Eruption Anatomically, the wolf tooth is a component of the permanent dental formula of the horse and is designated as Triadan ’05. Because practitioners are using the modified Triadan tooth numbering system more frequently to identify specific teeth, a review of the numbering system is provided21,22 (BOX 1 and FIGURE 2).

The first premolars have a simple shortcrown (brachyodont) structure22 and are composed of enamel, dentine, cementum, and a pulp chamber.23 These teeth usually erupt between 6 and 12 months of age and may be present in up to 90% of yearlings.11,22 When horses are approximately 3 years of age, supporting structures of the wolf tooth become sclerosed and calcified and the pulp chamber starts to obliterate with secondary dentine.23 Wolf teeth are usually no more than 1 to 2 cm in length and have a single root of variable length and substance, ranging from short, loose attachments to the gingiva to 30 mm in length.4,14,22 During eruption of the adjacent second premolar (which occurs at approxi-

mately 30 months of age), some wolf teeth may undergo root resorption or be shed.4,24,25 This normal shedding process may account, in part, for the 13% to 32% reported incidence of wolf teeth in mature horses22,25,26 (FIGURE 3).

In my experience, the incidence of mandibular wolf teeth (Triadan 305 and Triadan 405) is very low; however, it has been reported that these teeth may be more common in some lines of Standardbred horses.27 Lower wolf teeth are usually very small but can be

CriticalPo nt Wolf teeth were once superstitiously and incorrectly associated with a variety of conditions.

FIGURE 4

An erupted lower wolf tooth (arrow; Triadan 305).

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FREE CE From the Horse’s Mouth

FIGURE 5

FIGURE 6

The upper left interdental space of a 3-year-old Quarter horse gelding. The commissure of the lips is retracted by the clinician to demonstrate the location of a nodular submucosal enlargement (arrow) that was detected by palpation of the interdental space.

FIGURE 7

A small, lower wolf tooth (arrow) is adjacent to the first cheek tooth. (Skull specimen.)

CriticalPo nt It is generally accepted that wolf teeth probably do not cause problems for most horses; however, in some cases, discomfort due to the presence of wolf teeth may cause bitting problems and affect the horse’s performance.

74

large with a sharp point25 (FIGURE 4). Careful examination is required to detect short, small, splinter-like lower wolf teeth because they can be positioned close to the second premolar and may be partially concealed by the mucosa of the cheek and gingiva (FIGURE 5).

The upper wolf teeth usually erupt in a vertical plane close to the first cheek tooth.

Occasionally, the crown of the upper wolf tooth may be positioned further rostral to or palatal or buccal to the second premolar. The crown may also be angled slightly in some instances.22 Wolf teeth have been reported to be quite large and even “molarized” in Clydesdale horses or other draft breeds.16,25 In some horses, a wolf tooth can be large, rostrally displaced, and mistaken for a supernumerary canine tooth.28 Supernumerary wolf teeth are reported to be rare; however, small, superficial remnant portions of the deciduous second premolar may occasionally be found just rostral to the first cheek tooth and may be erroneously identified as a supernumerary wolf tooth.14,19,28 Unerupted wolf teeth are occasionally detected in the upper arcades. Synonyms for unerupted wolf teeth include blind or impacted wolf teeth.27 An unerupted wolf tooth is positioned along the maxilla several centimeters rostral to the first cheek tooth in a relatively horizon-

Oblique radiograph of the upper left interdental space (of the same horse in FIGURE 6).

An unerupted wolf tooth is situated at an angle (within the white circle) just rostral to the larger first cheek tooth.

tal orientation within the submucosa of the interdental space. Because of this orientation, the crown fails to erupt vertically through the mucosa. With careful palpation, a blind wolf tooth can usually be detected as a firm, nodular, submucosal enlargement. These teeth are generally small, so radiography can be useful for confirming their presence25 (FIGURES 6 AND 7). Unerupted wolf teeth of the mandible are reported to be rare and are probably very difficult to detect without the use of radiography.22

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The First Premolar Teeth CE Rationale for Removing Wolf Teeth Horses may experience oral pain as a result of pressure from the bit forcing the cheeks against sharp dental points.29 In some horses, a wolf tooth may cause discomfort as a result of the bit working against the tooth and forcing cheek mucosa into the sharp point of the tooth.14,16,17 Behaviors associated with oral discomfort caused by wolf teeth include bitting problems, head tossing, and head shaking.14,30 The presence of a wolf tooth also makes it difficult to adequately float and bevel the rostral portion of the second premolar (i.e., creating “bit seats”).

Wolf teeth that are enlarged, displaced, loose, fractured, or diseased are considered to be a source of pain.14,18,25,30 Blind wolf teeth may cause discomfort when the mucosa is hit and compressed against the tooth by the bit.27 Erupted and unerupted lower wolf teeth have also been associated with bitting problems in horses.14,22 Therefore, I prefer to remove wolf teeth from young riding horses and from horses of any age with a history of performance problems that may be related to oral discomfort. On occasion, erupted upper wolf teeth may be pres-

ent in mature horses that are being ridden successfully with a bit and have no history of oral discomfort.14,31 If wolf teeth are detected during examination of this type of horse, the owner should be made aware of potential behavioral problems related to the teeth. Extraction is not recommended in these horses unless the wolf teeth begin to cause a problem.

Acknowledgment The author acknowledges the following individuals at Texas A&M University’s College of Veterinary Medicine for their assistance in preparing this article: Kathrin R. Burke, DrMedVet, Department of Veterinary Pathobiology; Kyle Westfall, veterinary technician, Veterinary Medical Teaching Hospital; Betsy McCauley, veterinary radiologic technologist, Veterinary Medical Teaching Hospital; and Larry Wadsworth, medical photographer, College of Veterinary Medicine Media Resources.

TO LEARN MORE Watch for an upcoming article on extraction of the first premolar teeth.

CriticalPo nt Upper and lower wolf teeth can be removed by a veterinarian to help the horse perform more comfortably.

References 1. Soana S, Gnudi G, Bertoni G. The teeth of the horse: evolution and anatomo-morphological and radiographic study of their development in the foetus. Anat Histol Embryol 1999;28:273-280.

2. Matthew WD. Evolution of the Horse. New York: Guide Leaflet Series; 1932:36.

3. MacFadden BJ. Equine dental evolution: perspective from the fossil. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:1-8.

4. Sisson S, Grossman JD. Anatomy of Domestic Animals. 4th ed.

Philadelphia and London: WB Saunders; 1953.

5. Jones WE. The Teeth of the Horse. Fort Collins, CO: Caballus Publishers; 1972:31.

6. Bartlet J. The Gentleman’s Farriery: or, a Practical Treatise on the Diseases of Horses. 8th ed. London; 1773:283-284. Based on information from English Short Title Catalogue. Eighteenth Century Collections Online. Accessed May 2008 at http://galenet.galegroup.com/servlet/ECCO. 7. Daubenton LJM. Histoire Naturelle, Générale et Particulière, avec la Description du Cabinet du Roi. Paris: Imprimerie Royale; 1763:344.

8. Huidekoper RS. Age of the Domestic Animals. Chicago: Alexander Eger; 1903:33.

9. Goubaux A, Gustave B. The Exterior of the Horse. 2nd ed. London: JB Lippincott; 1904:621-622.

10. Merrillat LA. Animal Dentistry and Diseases of the Mouth. Chicago: Alexander Eger; 1905:202-204.

11. Easley KJ. Equine canine and first premolar (wolf) teeth. Proc AAEP 2004;50:13-18.

12. Korinek CJ. The Veterinarian. 2nd ed. Cedar Rapids, IA: The Veterinarian Publishing Company; 1916:85.

13. Baker AH. Livestock and Complete Stock Doctor, A Cyclopedia.

St. Louis: ND Thompson Publishing Company; 1916:116.

14. Dixon PM, Dacre I. A review of equine dental disorders. Vet J 2005;169:165-187.

15. Lane JG. A review of dental disorders of the horse, their treatment and possible fresh approaches to management. Equine Vet Educ 1994;6:13-21.

16. Linkous MB. Performance dentistry and equilibration. Clin Techniques Equine Pract 2005;4(2):124-134.

17. Easley J. Guidelines to extracting wolf teeth. Vet Pract News 2002:39-40.

18. Gaughn EM. Dental surgery in horses. Vet Clin North Am 1998;14(2):381-397.

19. Dixon PM. Equine dental disease, part 1: a long term study of 400 cases: disorders of incisor, canine, and first premolar teeth.

Equine Vet J 1999;31:369-377.

20. Scrutchfield L, Schumacher J. Examination of the oral cavity and routine dental care. Vet Clin North Am 1993;9(1):123-131.

21. Easley KJ. Dental and oral examination. In: Baker GJ, Easley J, eds.

Equine Dentistry. Philadelphia: WB Saunders; 1999;(1):151-169.

22. Dixon PM. Dental anatomy. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005:25-48.

23. Stelzer P. Die Extraktion des Wolfszahnes beim Pferd (Extraction of the wolf tooth in horses). Der Praktische Tiearzt 2004;85(3):188-189.

24. Nickel R, Schummer A, Seiferle E. The Viscera of Domestic Mammals. New York: Springer-Verlag; 1979;2:95.

25. Easley KJ. Corrective dental procedures. In: Baker GJ, Easley J, eds. Equine Dentistry. 2nd ed. Philadelphia: Elsevier; 2005;2:221-248.

26. Dixon PM. The gross, histological, and ultrastructural anatomy of equine teeth and their relationship to disease. Proc AAEP 2002;48:421-437.

27. Scrutchfield WL. Dental prophylaxis. In: Baker GJ, Easley J, eds.

Equine Dentistry. Philadelphia: WB Saunders; 1999;1:185-205.

28. Dixon PM, Easley J, Ekmann A. Supernumerary teeth in the horse.

Clin Techniques Equine Pract. Philadelphia: Elsevier; 2005;4:155-161.

29. 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.

30. Lowder M. Dental conditions affecting the young horse birth to 2 years. Focus Dent Proc AAEP 2006:203-205.

31. Scrutchfield WL. Wolf teeth: how to safely and effectively extract and is it necessary. Focus Dent Proc AAEP 2006:56-60.

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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. Lower wolf teeth are reported to a. never cause bitting problems and should not be removed. b. be important for proper mastication of roughage. c. occur more frequently in some lines of Standardbred horses. d. none of the above 2. Which of the following has been associated with the presence of unerupted upper wolf teeth? a. nasal discharge b. behavioral problems when a bit is used c. lingual ulcers d. unilateral epistaxis

b. in 100% of yearlings. c. only in some lines of Standardbred horses. d. none of the above 5. Unerupted upper wolf teeth are also called a. canine teeth. b. impacted wolf teeth. c. blind wolf teeth. d. b and c 6. Abnormal bitting behavior associated with the presence of wolf teeth in some horses includes a. head tossing. b. head shaking. c. vision problems. d. a and b

3. Which statement regarding wolf teeth in horses is correct? a. The terms wolf teeth and canine teeth are synonymous. b. Wolf teeth are functionless structures. c. Wolf teeth are necessary for proper mastication. d. Wolf teeth are composed entirely of enamel.

7. According to the modified Triadan system of dental nomenclature for horses, the first premolar of the left maxillary dental arcade is designated Triadan a. 105. c. 505. b. 205. d. 705.

4. Upper wolf teeth usually erupt a. during the first year of life.

8. A veterinarian detects a firm, nodular, submucosal enlargement in the interden-

tal space of the right side of the maxilla during examination of a 3-year-old Thoroughbred mare with bitting problems. The enlargement is 2 cm rostral to the first cheek tooth (Triadan 106). Which statement(s) is/are correct? a. An unerupted or blind wolf tooth should be suspected. b. Blind wolf teeth cannot cause bitting problems because they are padded by the gingiva. c. Radiography can be useful for confirming the presence of a blind wolf tooth. d. a and c 9. Lower wolf teeth (Triadan 305 and Triadan 405) may be a. associated with bitting problems. b. present in horses. c. very small. d. all of the above 10. During eruption of the permanent second premolar, some wolf teeth may a. undergo root resorption. b. be shed. c. a and b d. none of the above

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3 CE E CREDITTS CREDITS

CE Article 2

Hemostasis At a Glance Response to initial vascular injury Page 78

Platelet plug formation and primary hemostasis Page 79

Endothelial cell reactions Page 80

Secondary hemostasis Page 80

The coagulation cascade: the extrinsic pathway Page 80

The coagulation cascade: the intrinsic pathway Page 81

Common pathway Page 81

Clot formation Page 82

Thrombin Page 82

Clot prevention Page 82

Fibrinolysis Page 83

Diagnostic testing of coagulation Page 83

Adult versus neonatal differences in diagnostic tests Page 86

❯❯ Cody Alcott, DVM David M. Wong, DVM, MS, DACVIM Iowa State University

❯❯ Charles Brockus, DVM, PhD, DACVIM, DACVP Charles River Labs Sparks, Nevada

Iowa State University

Abstract: Hemostasis, the coagulation cascade, and clot formation present a daunting list of factors, pathways, and interactions to equine clinicians. A basic knowledge of hemostasis is necessary to evaluate various disease processes in horses. Initial injury to the vascular endothelium results in local vasoconstriction and formation of a platelet plug. This initial response reduces blood loss from the damaged vessel but may be inadequate at maintaining hemostasis alone. Therefore, the intrinsic, extrinsic, and common coagulation pathways interact with one another to form thrombin and ultimately stabilize the platelet plug. Thrombin accomplishes this by converting soluble fibrinogen to insoluble fibrin, resulting in clot stabilization. Alternatively, fibrinolysis promotes resolution of clot formation. Because of multiple positive and negative feedback interactions as well as multiple circulating mediators and inhibitors, coagulation and fibrinolysis are finely controlled systems in healthy patients. However, perturbations of the coagulation cascade in disease states can result in severe complications or death.

A

lterations in coagulation and fibrinolysis are relatively uncommon in horses, but when they occur, especially in critically ill patients, general knowledge of the associated pathways is vital to equine clinicians to properly diagnose, monitor, and treat primary or secondary disease processes involving these systems (TABLE 1 lists coagulation factor synonyms). Clinicians must also be able to interpret and understand the available diagnostic tests used to evaluate these systems. This article reviews coagulation, fibrinolysis, and diagnostic testing to evaluate these systems in horses.

Response to Initial Vascular Injury The main function of the coagulation system is to control hemorrhage from the vascular endothelium when it has been damaged by trauma or inflammation.

Conversely, anticoagulants and fibrinolytic mechanisms maintain patency and adequate blood flow. The regulation of these mechanisms is a tightly knit system of local and systemic feedback control pathways that maintains a delicate balance between pro- and anticoagulant processes.

Hemostasis is defined as the arrest of bleeding by vasoconstriction and coagulation and is an essential part of normal functioning of the cardiovascular system.

FIGURE 1

Primary and secondary hemostasis. (A) Initial vessel injury results in local vasoconstriction via reflex myogenic spasm and release of endothelin and thromboxane. (B) Formation of the platelet plug results from platelet adhesion, activation, recruitment, and aggregation. (vWF = von Willebrand’s factor)

78

❯❯ Brett Sponseller, DVM, PhD, DACVIM

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Hemostasis CE CE TABLE 1

Coagulation Factor Synonyms

FACTOR

SYNONYM

I

Fibrinogen

II

Prothrombin

III

Tissue factor, thromboplastin

IV

Calcium

V

Proaccelerin, labile factor

VI

—

VII

Proconvertin, stable factor

VIII

Antihemophilic factor

IX

Christmas factor

X

Stuart-Prower factor

XI

Plasma thromboplastin antecedent

XII

Hageman factor

XIII

Fibrin-stabilizing factor, transglutaminase

and initiator of platelet adherence and formation of the platelet plug, known as primary hemostasis. Likewise, damaged endothelium activates the extrinsic and intrinsic coagulation enzyme cascades via tissue factor and collagen fiber exposure. The direct result of activating either or both coagulation cascades is conversion of prothrombin to thrombin; this subsequently results in the conversion of soluble fibrinogen to insoluble fibrin and stabilization of the clot (secondary hemostasis).

Platelet adherence and activation combined with activation of the coagulation cascades result in a blood clot or thrombus formation to stop hemorrhage.

Platelet Plug Formation and Primary Hemostasis

Hemostasis is usually initiated by vascular trauma but can be induced by inflammation or sepsis.1 Smooth muscle contraction marks the beginning of the hemostatic process and begins instantaneously after endothelial damage (FIGURE 1). Myogenic spasm of smooth muscle is followed by endothelial and platelet release of autocoid vasoconstrictive substances—endothelin and thromboxane, respectively.2,3 Further vasoconstriction caused by sensory nerve impulses results in a neurogenic contractile reflex of smooth muscle.2 Damaged endothelium serves as a mediator

Essential to progression of the clotting process is the development of a platelet plug via platelet adhesion, activation, recruitment, and aggregation (FIGURE 1). Platelets are circulating cytoplasmic fragments of megakaryocyte pseudopods. They contain actin–myosin molecules and thrombosthenin for platelet contraction, an endoplasmic reticulum and Golgi apparatus for enzyme production and calcium storage, and a variety of enzymatic systems and secretory granules.2 Glycoproteins on the platelet surface and within platelet granules help mediate adherence to the vascular endothelium and serve as a means of communication and activation among platelets. After vascular injury, adherence is initiated largely by the binding of platelets to exposed subendothelial matrix via von Willebrand’s factor (vWF).4 Fibrinogen binding to platelet glycoprotein complexes enhances the activation of additional platelets.5 Platelet aggregation ensues with further

(C) Secondary hemostasis involves activation of the intrinsic and extrinsic pathways, culminating in the activation of prothrombin to thrombin via the common pathway of coagulation. (D) Clot stabilization occurs via fibrin fiber formation within the clot and subsequent clot stabilization by fibrin stabilizing factor (XIII).

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FREE FREE CE Hemostasis CE

CriticalPo nt The hemostatic process begins immediately following vascular endothelial damage.

platelet activation, forming the platelet plug.

Prothrombin attaches to platelet surface receptors as well, accumulating within the newly formed platelet plug. Platelet activation results in platelet swelling and the development of membrane surface pseudopods containing alpha granules and dense bodies. Alpha granules contain substances essential to hemostasis, including adhesive proteins for vWF, fibrinogen, plasminogen, fibronectin, and thrombospondin; plasma proteins IgG and albumin; cellular mitogens of platelet-derived growth factor; coagulation factors V and VIII; and protease inhibitors α2-macroglobulin and α2-antiplasmin.6 Dense bodies activate and recruit locally circulating platelets via release of ADP, ATP, serotonin, ionized calcium, histamine, epinephrine, and pyrophosphate.7 Fibronectin and thrombospondin help reinforce and stabilize aggregated platelets. Platelet-derived growth factor increases smooth muscle growth while controlling tissue repair. These factors facilitate and regulate the continual adherence, activation, and aggregation of platelets until a loose but reversible plug forms. Further platelet plug stabilization is attained through the activation of coagulation pathways and the generation of thrombin.

Endothelial Cell Reactions Endothelial cells are responsible for initiating coagulation in response to local vascular injury or systemic inflammation.8 Intact endothelium maintains normal function and limits activation of coagulation by maintaining the smooth luminal surface of vessels. Endothelial production of the glycocalyx, a mucopolysaccharide, limits platelet adherence to the endothelium and platelet activation. Vessel trauma and resulting endothe-

TO LEARN MORE Therapeutics in Practice: Acute Blood Loss (March 2008) Therapeutics in Practice: Treating Disseminated Intravascular Coagulation (July/August 2008) Related content on

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lial damage lead to exposure of subendothelial matrix, which is largely composed of collagen.

The combined endothelial expression of vWF and tissue factor, in addition to subendothelial collagen exposure, activates the coagulation cascade and supports platelet adhesion and activation.5 vWF mediates the adhesion of platelets to exposed collagen fibrils while stabilizing factor VIII; the latter plays a role in secondary hemostasis. Tissue factor initiates secondary hemostasis via the extrinsic pathway. Collagen exposure simultaneously causes a change in configuration of the proteolytic enzyme factor XII, which signals the activation of the intrinsic pathway. In summary, the endothelium plays a key role in initiating, amplifying, and modulating the coagulation process in response to many conditions, including trauma, inflammation, sepsis, and endotoxemia.9,10

Secondary Hemostasis Secondary hemostasis begins with the activation of the extrinsic and intrinsic pathways immediately after vessel damage. These pathways converge to form prothrombin activator, which catalyzes the formation of thrombin from prothrombin. Thrombin converts soluble fibrinogen to insoluble fibrin fibers that interact with platelets, blood cells, and plasma for final formation of a stable clot.

The Coagulation Cascade: the Extrinsic Pathway Activation of the extrinsic pathway occurs via expression of tissue factor, a cellular lipoprotein, resulting from endothelial damage and subsequent subendothelial matrix exposure (FIGURE 1). Activated factor VII (VIIa), alone or in combination with calcium and tissue factor, forms a proteolytic complex composed of phospholipids and lipoproteins that enzymatically activates factor X.11 In addition to tissue factor, factor VII can be activated by factor IXa, Xa, XIIa, or XIIIa or thrombin and, when activated, catalyzes the activation of additional factor X.12 The common pathway proceeds with the activation of factor X to produce thrombin and, subsequently, fibrin. Thrombin’s activation of factor VII is concentration dependent, with activation and inactivation occurring at lower and higher concentrations, respectively.13 Thrombin production is further regulated by the production of tissue factor pathway inhibi-

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Hemostasis CE CE tor by the vascular endothelium when factor Xa is formed via the extrinsic pathway.8 Tissue factor pathway inhibitor inhibits the extrinsic pathway through binding of the tissue factor/ calcium/factors VIIa and Xa complex. The small amount of thrombin that is produced rapidly catalyzes its own formation via activation of factor V and interacts with the intrinsic pathway by activating factor VIII. An interconnection between the extrinsic and intrinsic pathways exists through the activation of factor IX of the intrinsic pathway by a tissue factor–factor VIIa complex.14 Factor VII, which is produced by the liver, has the shortest halflife of the coagulation factors and is, therefore, significant during diagnostic evaluation of the extrinsic pathway and of liver function.15

The Coagulation Cascade: the Intrinsic Pathway Coagulation factors VIII, IX, XI, and XII are essential for proper function of the intrinsic pathway (FIGURE 1). Calcium ions, platelet phospholipids, and the proteins prekallikrein and high-molecular-weight kininogen (HMWK) are cofactors necessary for coagulation factor activation and positive feedback. Contact between factor XII and collagen fibers exposed by endothelium damage is the primary initiator of the intrinsic pathway. This stimulates a conformational change and activation of the proteolytic enzyme to factor XIIa. Conversion of prekallikrein to kallikrein by factor XIIa can also activate factor XII, and additional factor XIIa results in further conversion of prekallikrein to kallikrein. This positive feedback mechanism results in amplification of the intrinsic pathway. In the presence of HMWK, factor XIIa converts factor XI; and this process is accelerated by prekallikrein. Bradykinin is released from HMWK in this process, acting as a potent vasodilator, and counterbalances other vasoconstrictive substances released with vessel damage. The enzymatic action of factor XIa activates factor IX. Factor IX contains vitamin K–dependent γ-carboxyglutamate (Gla) and is calcium dependent (calcium binds and activates Gla). Vitamin K is a cofactor in the carboxylation of glutamate of coagulation proteins; it is essential for the conformational change and calcium chelation that occur with factor activation, specifically factors II (prothrombin), VII, IX, and X.16 Coumarin-type anticoagulants inhibit

vitamin K–dependent epoxide reductase and carboxylation of coagulation factors, thus limiting factor synthesis in the liver and activation at the site of vascular injury.15 The combination of factor IXa, factor VIIIa, platelet phospholipid, tissue factor, and calcium ions completes the intrinsic pathway process through activation of factor X. The complex of calcium and factors VIIIa, IXa, and X is found on the surface of platelets and is known as the tenase complex.

Exposure of platelet phospholipids allows the tenase complex to form. The entire complex is then regulated by activation of factor VIII by thrombin. Assembly of the tenase complex on a platelet phospholipid foundation in the presence of calcium allows clot formation to remain localized.

Factor VIII is considered a cofactor in the coagulation cascade and is activated by the presence of thrombin. Factor VIII works as a receptor for factors IXa and X. As described above, the conversion of factor VIII to VIIIa depends on the thrombin concentration, with a high concentration resulting in factor VIIIa cleavage and inactivation. This inherent mechanism serves as a local means of coagulation regulation.

Common Pathway

CriticalPo nt

The intrinsic and extrinsic pathways converge at the common pathway, resulting in prothrombin activation, which occurs on platelet surfaces and requires formation of the prothrombinase complex. Components of the prothrombinase complex include phosphatidylinositol and phosphatidylserine (procoagulant platelet phospholipids), tissue phospholipids (from tissue factor), calcium ions, factors Va and Xa, and prothrombin.12 Within a few seconds, prothrombinase catalyzes the conversion of prothrombin to thrombin in the presence of calcium. Factor Va functions as a cofactor in prothrombinase complex formation and is bound to the surface of platelets. Factor X represents the actual protease responsible for the conversion of prothrombin to thrombin, which can be accelerated by factor Va and platelet phospholipid. The proteolytic action of thrombin to form factor Va catalyzes the formation of additional thrombin. Factor V is activated by a low thrombin concentration and is gradually inactivated as the thrombin concentration increases. This demonstrates a local feedback mechanism of coagulation.

Platelet adhesion and aggregation at the site of initial vascular injury form the platelet plug, which marks the beginning of primary hemostasis.

This is essential for the coagulation process to proceed.

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CriticalPo nt Secondary hemostasis further stabilizes the platelet plug via thrombin’s conversion of fibrinogen to insoluble fibrin fibers.

Clot Formation

Thrombin

The final phases of clot formation are characterized by the conversion of fibrinogen to fibrin by thrombin. Thrombin acts through proteolytic cleavage of fibrinogen to a fibrin monomer. The polymerization of fibrin monomers leads to fibrin fiber formation. Initially, weak fibrin bonds progress to form the long fibers of the clot reticulum. The conversion and activation of factor XIII (fibrin-stabilizing factor) by thrombin help develop covalent bonds between fibrin fibers to further strengthen the clot (FIGURE 1). Fibrin-stabilizing factor is supplied by platelets and circulating plasma globulins in the clot reticulum.

As the meshwork of fibrin fibers grows, circulating red blood cells, platelets, and plasma become trapped in damaged areas. This combination leads to the recruitment of platelets and coagulation factors necessary for clot expansion and aggregation, eventually stopping vessel hemorrhage. Clot retraction begins within 20 to 60 minutes after formation.2 Platelet release of procoagulants from alpha granules, as well as factor XIII, further stabilizes the bonding of fibrin fibers. Platelet contractile proteins thrombosthenin, actin, and myosin are stimulated to contract platelet spicules attached to adjacent fibrin fibers. Calcium ions from platelet stores and thrombin production facilitate further clot contraction. This process continues as the edges of the damaged vessel are pulled together in conjunction with smooth muscle contraction until hemorrhage ceases and hemostasis is achieved.

Thrombin plays a pivotal role in all aspects of hemostasis. Thrombin has multiple “avenues” of positive feedback to accelerate further thrombin production. The catalysis of factors V, VII, VIII, and XI drives the extrinsic and intrinsic coagulation pathways. Other functions of thrombin include platelet activation, aggregation and secretion, and smooth muscle contraction.13,17 The ability of thrombin to influence these reactions is concentration dependent, as described above, and serves as a mechanism of local feedback to control clot formation. As the formation of thrombin accelerates, so does the production of anticoagulant reactions necessary for clot dissolution. The binding of thrombin to thrombomodulin, tissue plasminogen activator (TPA), and activated protein C are examples of thrombin’s ability to initiate clot breakdown.18

Clot Prevention Endogenous anticoagulants maintain vessel patency by limiting intravascular coagulation caused by daily trauma to the vascular endothelium. Induction of the contact phase and tissue factor pathway of the intrinsic and extrinsic pathways, respectively, is limited by the endothelial production of the glycocalyx, which lines the endothelium to produce a smooth surface. Tissue factor pathway inhibitor serves as an important endogenous mechanism of controlling hemostasis by directly inhibiting the formation of the factor Xa–factor

FIGURE 2

Inhibition of thrombosis occurs via multiple mechanisms. Thrombin can bind thrombomodulin, resulting in activation of protein C and proteolysis of factors Va and VIIIa. In addition, antithrombin inhibits thrombin and factors XIIa, XIa, Xa, and IXa. Antithrombin also binds heparin-like molecules (i.e., heparin sulfate) that are expressed on endothelial surfaces, which subsequently inhibits thrombin and factors Xa and IXa.

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Hemostasis CE CE VIIa–tissue factor complex.14 The removal of thrombin can also control coagulation. Fibrin fibers themselves incorporate large amounts of thrombin within the clot reticulum.13 In addition, the binding of free thrombin by thrombomodulin activates plasma protein C, which inactivates factors Va and VIIIa via proteolysis, representing another aspect of negative feedback control of coagulation and downregulation of thrombin19 (FIGURE 2). Protein C has many anticoagulant, profibrinolytic, and antiinflammatory actions and has been shown to decline during periods of sepsis.20 Antithrombin inactivates the remaining thrombin in the immediate area of clot formation.

Antithrombin is responsible for inactivation of factors IXa, Xa, XIa, and XIIa through thrombin binding. Endogenous or exogenous heparin binding to antithrombin results in a conformational change of the globulin and heightened affinity for thrombin. Further thrombin activity can also be limited by α2-macroglobulin, heparin cofactor II, and α1-antitrypsin.21

Fibrinolysis Hemostasis is followed by the return to normal vascular flow around, or adjacent to, the newly formed clot. Returning the damaged vessel to normal function requires the dissolution of the clot by fibrinolysis. Circulating plasminogen (profibrinolysin) becomes ensnared within the newly formed clot, binding to fibrin and fibrinogen. Trapped plasminogen is activated by endothelially synthesized TPA to form plas-

min (FIGURE 3). Binding of TPA to fibrin is inhibited by plasminogen–activator inhibitors types 1 and 2. Urokinase, which is produced by epithelial cells lining excretory ducts, is also responsible for plasmin activation, to a lesser degree, and assists in dissolution of fibrin clots that may form in these ducts.22 Plasmin causes proteolytic digestion of fibrin fibers, fibrinogen, prothrombin, and factors V, VIII, and XII. The digestion of fibrinogen and fibrin fibers results in the release of soluble fibrin degradation products (FDPs). The digestion by plasmin of insoluble cross-linked fibrin fibers during fibrinolysis causes the release of D-fragments or cross-link remnants, known as D-dimers. The action of plasmin is the final step in clot dissolution and can reopen previously blocked vessels. Renal and hepatic production of α2-antiplasmin inactivates free plasmin.23

Diagnostic Testing of Coagulation Cytology Examination of a peripheral blood smear or automated quantification of platelet numbers is one avenue of assessing primary hemostasis (TABLE 2). Reported and established reference intervals for platelet concentration in an adult horse generally range from 100,000 to 300,000 platelets/μL. Six to 20 platelets per high-powered field (magnification: ×1000) is considered adequate when examining a peripheral blood smear, if clumping of platelets is not observed.

Ten different fields must be examined and the

CriticalPo nt Endogenous anticoagulants antithrombin and protein C limit intravascular coagulation from daily vascular trauma.

FIGURE 3

Fibrinolysis occurs through the conversion of plasminogen to plasmin by tissue plasminogen activator, which is released from damaged endothelial cells. This conversion results in proteolytic digestion of fibrin fibers within the clot and the production of fibrin degradation products. Circulating plasmin is neutralized by α2-antiplasmin. (TPA = tissue plasminogen activator) CompendiumEquine.com | March 2009 | Compendium Equine: Continuing Education for Veterinarians®

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average number of platelets per field determined to adequately evaluate platelet concentration by this method. Platelet numbers must be interpreted carefully in horses because of the effects of splenic sequestration and collection methods. Splenic contraction can mildly increase circulating platelets. Also, the use of EDTA anticoagulant has been shown to falsely lower the platelet concentration.24,25 Therefore, the use of a sodium ion citrate blood tube (light blue–top tube) is recommended.

Thrombocytopenia is classified as platelet concentration below 100,000/μL, and clinical bleeding has been associated with platelet concentrations below 30,000/μL.24 Platelet characteristics, granularity, size, shape, and clumping can also be evaluated on peripheral blood smear examination. However, granules in equine platelets are very faint compared with those of other species, making platelets more difficult to identify and granularity difficult to assess in horses. In addition, even if the platelet count is within normal limits, plateTABLE 2

let function may not be normal, and platelet function testing is currently being evaluated in equine patients.

Template Bleeding Time Template bleeding time evaluates endothelial interaction with circulating platelets. Template bleeding time is a cost-effective and easily performed evaluation of primary hemostasis, whereas other functional tests are specific to secondary hemostasis. Hair is clipped over the skin distolateral to the accessory carpal bone, and a template bleeding device is placed and discharged. Filter paper is used to absorb blood that is discharged from the incision 1 to 2 mm below the incision site. Timing starts when the incision is made and ends when the bleeding stops. The reported reference range for template bleeding time in healthy horses is 2 to 6 minutes.26 Thrombocytopenia and the functional platelet disorders von Willebrand’s disease and Glanzmann’s thrombasthenia can be screened using this test.24,26

Diagnostic Testing of Hemostasis PATIENT AGE

DIAGNOSTIC TEST*

< 24 HOURS

4–7 DAYS

10–14 DAYS

25–30 DAYS

ADULT

FACTORS EVALUATED

PT (sec)

10.9 ± 0.6

9.6 ± 0.6

9.5 ± 0.4

9.4 ± 0.4

9.5 ± 0.3

Extrinsic and common39

aPTT (sec)

56.8 ± 6.3

39.8 ± 4.0

39.9 ± 4.8

40.8 ± 6.0

42.0 ± 8.9

Intrinsic and common39

Fibrinogen (mg/dL)

116.8 ± 39.1

196.8 ± 26.6

199.6 ± 50.0

221.1 ± 48.0

195 ± 54

Quantification of fibrinogen39

Platelet count (103/μL)

243 ± 170

181 ± 60

218 ± 57

245 ± 59

153 ± 49

Quantification of platelet numbers39

FDPs (μg/mL +1)1/2

8.2 ± 2.7

5.6 ± 3.4

4.5 ± 3.1

3.5 ± 2.6

1.8 ± 0.6

Presence of fibrin from action of plasmin on fibrin or fibrinogen39

Antithrombin activity (%)

107 ± 41

164 ± 35

170.9 ± 40.9

166.5 ± 40.6

202 ± 82

Evaluates antithrombin activity39

D-dimers (ng/mL)

N/A

N/A

N/A

N/A

677 ± 119

Specific evaluation for plasmin degradation of cross-linked fibrin1

Template bleeding time (min)

4±2

4±2

4±2

4±2

4±2

Hemostatic plug formation25,a

Activated clotting time (min)

5.8 ± 1.3

5.8 ± 1.3

5.8 ± 1.3

5.8 ± 1.3

2.6 ± 0.5

Secondary hemostasisa,26

Thrombin time (sec)

N/A

N/A

N/A

N/A

19.5 ± 5.5

Conversion time of fibrinogen to fibrinb

*Listed in order of most used to least used. a

Knottenbelt D, Holdstock N, Madigan J. Equine Neonatology Medicine and Surgery. Philadelphia: Elsevier Science; 2004.

b

Feige K, Ehrat FB, Kastner SBR, et al. The effects of automated plasmapheresis on clinical, haematological, biochemical and coagulation variables in horses. Vet J 2004;169:102-107.

aPTT = activated partial thromboplastin time; FDPs = fibrin degradation products; N/A = reference intervals for a horse of this age are not available; PT = prothrombin time.

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Hemostasis CE CE Activated Clotting Time Secondary hemostasis can be functionally assessed using the activated clotting time (ACT). A deficiency in factors V, VIII, IX, X, XI, and XII; prothrombin (factor II); and fibrinogen prolongs the ACT. The ACT is not affected by the blood concentration of factor VII or the blood platelet concentration and thus evaluates the intrinsic and common pathways.27 However, severe thrombocytopenia can result in a prolonged ACT because of decreased availability of phospholipid. The test is conducted by mixing whole blood directly with diatomaceous earth, incubating it at 98.6°F (37°C), tilting the sample back and forth, and recording the time to clot formation. The reference time for clot formation has been reported as 2 minutes and 38 seconds (± 29 seconds).27 Variations in the testing protocol, including syringe versus vacuum collection, incubation period and temperature, and frequency of monitoring for clot formation, account for the general low sensitivity of this test.

Partial Thromboplastin Time Evaluation of the intrinsic and common pathways via the partial thromboplastin time (PTT) is similar to evaluation by the ACT, but the PTT has a higher sensitivity. Deficiency of factors V, VIII, IX, X, XI, and XII; prothrombin; and fibrinogen causes prolongation of the PTT. The test is conducted by adding citrated plasma to a glass tube with a phospholipid and calcium chloride substrate. The time until clot formation is then determined.

Activated Partial Thromboplastin Time The activated partial thromboplastin time (aPTT) test is similar to that for the PTT, except that a contact activator (e.g., kaolin, silicates, ellagic acid) is added to the specimen when determining the aPTT. The aPTT is most commonly used to evaluate the intrinsic and common pathways. Prolongation of the PTT and aPTT in horses has been associated with hemophilia A (factor VIII deficiency) and plasma prekallikrein deficiency.28

Prothrombin Time The prothrombin time (PT) or one-stage PT test is an analysis of the extrinsic and common pathways, specifically their ability to convert fibrinogen to fibrin. Deficiencies of tissue fac-

tor (III); coagulation factors V, VII, and X; prothrombin; and fibrinogen result in prolongation of PT. The test is conducted by mixing citrated plasma with tissue factor and calcium.

The time until fibrin fiber or clot formation is calculated automatically. Citrated whole blood or plasma can be used up to 3 days after collection with the concurrent submission of a control sample from a normal horse.29 Prolongation of PT occurs when the fibrinogen concentration decreases below 100 mg/dL, the coagulation factors listed above are reduced more than 50%,30 prothrombin decreases 30%,30 or vitamin K deficiency is present. Clinically relevant prolongation has been described as a 20% increase in clotting time compared with that of healthy horses.30

Thrombin Time The thrombin time test is an assessment of the terminal common pathway of secondary hemostasis and is a direct assessment of fibrinogen quality and quantity. FDPs interfere with fibrin polymerization and can prolong thrombin time.

Hypofibrinogenemia also prolongs thrombin time. The test is conducted by the addition of thrombin to citrated plasma and is interpreted by the time interval for clot formation.

CriticalPo nt Partial thromboplastin time is used to evaluate the intrinsic and common pathways.

Proteins Induced by Vitamin K Absence or Antagonism The proteins induced by vitamin K absence or antagonism (PIVKA) test is an evaluation of the proteins awaiting conversion to coagulation factors as well as proteins that inhibit coagulation. Factors II, VII, IX, and X and the anticoagulant proteins C and S depend on vitamin K carboxylation of glutamate from their protein precursor for normal hemostatic function. In the absence of vitamin K, continual synthesis of protein precursors causes a buildup within hepatocytes and a decline of functional coagulation factor production.

The leakage of PIVKA into the peripheral circulation is quantified through the PIVKA test, which determines the clotting time with the addition of thromboplastin to the sample. Deficiencies in prothrombin and factors VII, IX, and X as well as anticoagulant poisoning can cause prolongation of the PIVKA test. The PIVKA test, in conjunction with the PT, has been widely used in diagnosing and confirming anticoagulant poisoning in dogs

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when results exceed 150 seconds.31 The use of the PIVKA test in horses has been limited to suspected cases of anticoagulant toxicity but could also be indicated in cases of feed toxicity (moldy sweet clover).32

Fibrinogen

CriticalPo nt Prothrombin time is used to evaluate the extrinsic and common pathways.

Evaluation of the fibrinolytic system through the fibrinogen concentration is less sensitive in horses than in other species.30 A decreased fibrinogen concentration can indicate disseminated intravascular coagulation (DIC), but given the capacity of the equine liver to produce large amounts of acute-phase proteins (fibrinogen) in response to inflammation, the fibrinogen level may be increased or remain unaltered despite profound inflammation.26,33 The fibrinogen concentration can be determined by a heat precipitation test that compares the plasma protein concentration before and after heating. A more sensitive mechanical method can be conducted by many coagulation analyzers.

Fibrin Degradation Products FDPs are the result of the consumption of fibrinogen or cross-linked fibrin fibers by plasmin. Fibrin fragments are detected by mixing a blood sample with thrombin and a protease inhibitor. An increased FDP concentration suggests increased activities of fibrinolysis or fibrinogenolysis. Increased serum FDPs can occur when fibrin deposition exceeds normal clearance mechanisms, and they have been linked to DIC, severe inflammatory processes, hemorrhagic disorders, and postoperative states.1

D-dimers D-dimer production is the end result of fibrinolysis caused by plasmin activity. Specifically, it is the breaking of thrombin-induced fibrin fiber bonds with the release of D-fragments (dimers). D-dimer identification differs from testing for FDPs in that it is specific for dissolution, by plasmin, of fibrin generated from active thrombin production, whereas FDPs indicate general fibrinolysis and fibrinogenolysis. D-dimer testing in conjunction with FDP analysis has been used in assessing DIC in horses,34 but it is important to note that the D-dimer concentration alone is not specific for the process or diagnosis of DIC35 and, therefore, should not be overinterpreted.

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Antithrombin The hepatocyte-produced α-globulin antithrombin is considered one of the most important endogenous inhibitors of coagulation. The function of antithrombin is the neutralization of thrombin; activated factors IX, X, XI, and XII; kallikrein; and plasmin. A functional assay of antithrombin (chromogenic assay) is preferred to simply detecting its presence (immunoassay) in plasma.24 Chromogenic assays determine the amount of functional antithrombin present by adding the test plasma to a reagent containing heparin and excess thrombin or factor Xa, which also contains the chromogen-labeled substrate for thrombin or factor Xa.36 The more antithrombin present in the test specimen, the less activity of thrombin or factor Xa and thus less color, which is measured spectrophotometrically. A decreased plasma concentration of antithrombin can be caused by widespread coagulation or DIC,1 decreased hepatic function,37 or protein-losing enteropathies and nephropathies.33 Increased antithrombin production has been implicated with acute-phase protein production in cases of acute inflammation24 and has been suggested to be one of the most accurate prognostic indicators in horses with colic.30 Antithrombin I complexes in a 1:1 ratio with thrombin, and thrombin–antithrombin complex has been used as an indirect means to evaluate thrombin production/activation during hypercoagulable states.38

Adult Versus Neonatal Differences in Diagnostic Tests Clear differences in the reference intervals between adult horses and neonatal foals are present as demonstrated in TABLE 2. The most striking differences are noted when comparing coagulation times of foals younger than 24 hours of age with those of adults. Differences include higher platelet concentrations, increased FDPs, prolonged PT and aPTT, and lower fibrinogen concentrations. With the exception of the platelet concentration, hemostatic parameters in foals are indistinguishable from healthy adult horse values by 1 month of age.39

Conclusion Clot formation and dissolution is a dynamic balance of procoagulant and anticoagulant processes necessary in establishing hemostasis while preserving normal tissue perfusion.

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Hemostasis CE CE Calcium, an essential ion for hemostasis, is used in all reactions of clotting factors, except the first two steps of the intrinsic pathway.

The separation of the intrinsic and extrinsic coagulation pathways has greatly facilitated the understanding of secondary hemostasis.

However, it is apparent that these two systems function simultaneously to produce thrombin.

Tissue factor stimulates the induction of the extrinsic pathway, while factor XII interacts with exposed collagen fibers to initiate the intrinsic pathway. The extrinsic pathway is very rapid, while the intrinsic pathway proceeds at a slightly slower rate. Along with clot formation, activation of fibrinolysis occurs, serving as a “check and balance” to limit detrimental

extension of vessel clotting. Normal function of this dynamic process leads to maintenance of vessel patency while simultaneously controlling excessive blood loss. Knowledge of these basic mechanisms of clot formation and the diagnostic means to evaluate coagulation should aid equine clinicians.

TO LEARN MORE Watch for a related article titled “Modification of the Coagulation Cascade: Available Medications” in an upcoming issue.

References 1. Monreal L, Angles A, Espada Y, et al. Hypercoagulation and hypofibrinolysis in horses with colic and DIC. Equine Vet J Suppl 2000;32:19-25.

2. Guyton AHJ. Textbook of Medical Physiology. 11th ed. Philadelphia: Elsevier; 2006.

3. Turk JR. Physiologic and pathophysiologic effects of endothelin: implications in cardiopulmonary disease. JAVMA 1998;212(2):265-270.

4. Nakamura F, Pudas R, Heikkinen O, et al. The structure of the GPIb-filamin A complex. Blood 2006;107(5):1925-1932.

5. Nakamura T, Kambayashi J, Okuma M, et al. Activation of the GP IIb-IIIa complex induced by platelet adhesion to collagen is mediated by both alpha2beta1 integrin and GP VI. J Biol Chem 1999;274(17):11897-11903.

6. Harrison P, Cramer EM. Platelet alpha-granules. Blood Rev

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1993;7(1):52-62.

7. McNicol A, Israels SJ. Platelet dense granules: structure, function and implications for haemostasis. Thromb Res 1999;95(1):1-18.

8. Levi M, ten Cate H, van der Poll T. Endothelium: interface between coagulation and inflammation. Crit Care Med 2002;30(5 suppl):S220-S224.

9. Aird WC. Vascular bed-specific hemostasis: role of endothelium in sepsis pathogenesis. Crit Care Med 2001;29(7 suppl):S28-S34.

10. Marshall JC. Inflammation, coagulopathy, and the pathogenesis of multiple organ dysfunction syndrome. Crit Care Med 2001;29(7 suppl):S99-S106.

11. Bom VJ, Bertina RM. The contributions of Ca2+, phospholipids and tissue-factor apoprotein to the activation of human blood-coagulation factor X by activated factor VII. Biochem J 1990;265(2):327336.

12. Roncales FJ. Schalm’s Veterinary Hematology. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2000.

13. Fenton 2nd JW, Ofosu FA, Brezniak DV, et al. Understanding thrombin and hemostasis. Hematol Oncol Clin North Am 1993;7(6):1107-1119.

14. Hack CE. Tissue factor pathway of coagulation in sepsis. Crit Care Med 2000;28(9 suppl):S25-S30.

15. Sheafor SE, Couto CG. Anticoagulant rodenticide toxicity in 21 dogs. JAAHA 1999;35(1):38-46.

16. Vermeer C. Gamma-carboxyglutamate-containing proteins and the vitamin K–dependent carboxylase. Biochem J 1990;266(3):625636.

17. Walz DA, Anderson GF, Ciaglowski RE, et al. Thrombin-elicited contractile responses of aortic smooth muscle. Proc Soc Exp Biol Med 1985;180(3):518-526.

18. Mann KG. Thrombin formation. Chest 2003;124(3 suppl):4S10S. 19. Good LI. Thromboembolic disease: physiology of hemostasis and pathophysiology of thrombosis. Compend Contin Educ Vet 2003;25(9):650-659.

20. Esmon CT. The protein C pathway. Chest 2003;124(3 suppl): 26S-32S. 21. Lau A, Berry LR, Mitchell LG, et al. Effect of substrate and fibrin polymerization inhibitor on determination of plasma thrombin generation in vitro. Thromb Res 2007;119(6):667-677.

22. Sappino AP, Huarte J, Vassalli JD, et al. Sites of synthesis of urokinase and tissue-type plasminogen activators in the murine kidney. J Clin Invest 1991;87(3):962-970.

23. Menoud PA, Sappino N, Boudal-Khoshbeen M, et al. The kidney is a major site of alpha(2)-antiplasmin production. J Clin Invest 1996;97(11):2478-2484.

24. Reed SMW, Bayly M, Sellon DC. Equine Internal Medicine. 2nd ed. Philadelphia: Elsevier; 2004.

25. Hinchcliff KW, Kociba GJ, Mitten LA. Diagnosis of EDTA-dependent pseudothrombocytopenia in a horse. JAVMA 1993;203(12): 1715-1716.

26. Lassen ED, Swardson CJ. Hematology and hemostasis in the horse: normal functions and common abnormalities. Vet Clin North Am Equine Pract 1995;11(3):351-389.

27. Rawlings CA, Byars TD, Van Noy MK, et al. Activated coagulation test in normal and heparinized ponies and horses. Am J Vet Res 1975;36(5):711-713.

28. Zimmel DN. Current Therapy in Equine Medicine. 5th ed. St. Louis: Elsevier Science; 2003.

29. Wagner AE. Transport of plasma for prothrombin time testing in monitoring warfarin therapy in the horse. JAVMA 1981;178(3):306.

30. Dallap BL. Coagulopathy in the equine critical care patient. Vet Clin North Am Equine Pract 2004;20(1):231-251.

31. Mount ME, Kim BU, Kass PH. Use of a test for proteins induced by vitamin K absence or antagonism in diagnosis of anticoagulant poisoning in dogs: 325 cases (1987-1997). JAVMA 2003;222(2):194-198.

32. Beasley V. Toxicants that interfere with the function of vitamin K. Veterinary Toxicology. Ithaca, NY: International Veterinary Information Service (www.ivis.org); 1999.

33. Dolente BA, Wilkins PA, Boston RC. Clinicopathologic evidence of disseminated intravascular coagulation in horses with acute colitis. JAVMA 2002;220(7):1034-1038.

34. Stokol T, Erb HN, De Wilde L, et al. Evaluation of latex agglutination kits for detection of fibrin(ogen) degradation products and D-dimer in healthy horses and horses with severe colic. Vet Clin Pathol 2005;34(4):375-382.

35. Stokol T, Brooks MB, Erb HN, et al. D-dimer concentrations in healthy dogs and dogs with disseminated intravascular coagulation. Am J Vet Res 2000;61(4):393-398.

36. Stockham SL, Scott MA. Fundamentals of Veterinary Clinical Pathology. Ames: Iowa State University Press; 2002.

37. Johnstone IB, Petersen D, Crane S. Antithrombin III (ATIII) activity in plasmas from normal and diseased horses, and in normal canine, bovine and human plasmas. Vet Clin Pathol 1987;16(1):14-18.

38. Topper MJ, Prasse KW, Morris MJ, et al. Enzyme-linked immunosorbent assay for thrombin-antithrombin III complexes in horses. Am J Vet Res 1996;57(4):427-431.

39. Barton MH, Morris DD, Crowe N, et al. Hemostatic indices in healthy foals from birth to one month of age. J Vet Diagn Invest 1995;7(3):380-385.

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. Platelet adherence to the vascular endothelium during primary hemostasis is initiated via a. platelet glycoprotein. b. IgG. c. vWF. d. thrombosthenin.

2. How does the vascular endothelium prevent platelet adherence in healthy vessels? a. exposure of subendothelial collagen b. production of the glycocalyx

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c. production of tissue factor d. antithrombin release 3. Tissue factor combines with factor __________ of the extrinsic pathway to activate factor X, thereby initiating the common pathway. a. IXa c. XII b. II d. VIIa 4. Vitamin K is an essential cofactor in the carboxylation of glutamate during the activation of factors

a. V, X, IX, and XII. b. II, VII, IX, and X. c. VII, VIII, IX, and XI. d. II, VIII, X, and XII. 5. The ability of antithrombin to bind thrombin, thus controlling the rate of clot formation, can be greatly enhanced by a. endogenous or exogenous heparin. b. TPA. c. plasmin. d. thrombomodulin.

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Hemostasis CE

6. During fibrinolysis, plasmin is responsible for the proteolytic digestion of a. factors IX, X, XI, and XII and thrombin. b. factors V, VIII, and XII; fibrin; and prothrombin. c. TPA and factors V, VII, IX, and X. d. plasma proteins C and S, TPA, and factors II, VIII, and XII. 7. What are the two most important endogenous anticoagulants? a. protein C and antithrombin b. fibrinogen and plasmin c. thrombin and Christmas factor d. factor VII and vWF 8. Functional assessment of the intrinsic and common pathways of secondary hemostasis is

best determined by a. PT and ACT. b. ACT and PTT. c. thrombin time and PT. d. PTT and aPTT. 9. During clot dissolution, which of the following tests best quantifies the activity of plasmin? a. D-dimer b. FDP c. PTT d. antithrombin 10. A deficiency of vWF, resulting in coagulopathy with a normal platelet concentration, PT, and aPTT, can be attributed to a. factor VIII deficiency. b. prekallikrein deficiency. c. platelet adhesion. d. vitamin K deficiency.

Call for Papers Are you involved in research?

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AQHA SuperHorse 2005, With All Probability

The number one health concern of equine veterinarians met its match more than 15 years Ago.1

There is still no better way to defeat acute equine joint disease than with LegendÂŽ (hyaluronate sodium). The only FDA-approved I.V. and I.A. joint therapy, Legend safely lubricates and relieves inflamed equine joints with exceptional results more than 90 percent of the time.2,3 With more than 15 years and over 2.5 million successful doses* under its belt, Legend is not about to back down now.

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Legend 2 mL is approved for I.V. and I.A. use. The intra-articular safety of Legend Multi Dose with benzyl alcohol has not been determined.

*Data on file.

1

Brakke Equine Market Study, May 2004.

Kawcak CE, Frisbee DD, Trotter GW, McIlwraith CW, Gillette SM, Powers BE, Walton RM: Effects of intravenous administration of hyaluronate sodium on carpal joints in exercising horse after arthroscopic surgery and osteochondral fragmentation. AJVR, Vol. 58, No. 110, October 1997.

3 96% effective when administered I.A.; 90% effective when administered I.V. Freedom of Information Summary for Legend (hyaluronate sodium) Injectable Solution: NADA 140-883. Š 2008 Bayer HealthCare LLC, Animal Health Division, Shawnee Mission, Kansas 66201. Bayer, the Bayer Cross and Legend are trademarks of Bayer.

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May 8–9 Annual European Equine Basic Arthroscopy Course Newmarket Equine Hospital Newmarket, United Kingdom Web tierklinik-telgte.com/telgte-ce

June 4 Basic Arthroscopy Colorado State College of Veterinary Medicine and Biomedical Sciences Fort Collins, Colorado Phone 970-297-1273 Web www.cvmbs.colostate.edu/clinsci/ce

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The Final Diagnosis ❯❯ Ronald E. Gill, DVM, Gill Veterinary Clinic, West Salem, Illinois

I’ve Been Practicing Long Enough …*

“H

ow long have you been working, Dr. Gill?” my clients ask.

I celebrated 33 years as a mixed animal practitioner on May 18, 2008. This sounds like a long time, and I guess it is. Just how long is it? I’ve been practicing long enough … … to know that the miracle of life and birth never grows old. … to know that the 300-lb gorilla of a man with a shaved head, tattoos, and a biker jacket will sob like a baby at the death of his 6-lb ball of fluff. … to know that despite everything I do, some patients will survive. … to know that despite everything I do, some patients won’t survive.

… to know that when once-in-a-career cases come along, I’ll remember them forever.

*Adapted with permission from the Iowa Veterinary Medical Association and the Illinois Veterinary Medical Association.

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… to know that a little youthful exuberance mixed with some seasoned experience is a good combination. … that I’m now serving the third generation of some clients. … that I can identify many of my clients by their vehicles. … that my clients can identify me by my vehicle. … to know that my clients know where I’ll be on Sunday morning or any other time during the week. … to know that some clients will ask me about their own symptoms before contacting their physician. … to see the glint of optimism in the eyes of a 90-year-old horse trainer.

… to see the stoicism of a young dairy farmer who watched his best cow suffer from a severe case of gangrenous mastitis. … to see a seasoned cattleman who knew that his current calf crop might be the last one he sees playing in the pasture. … to know that when once-in-a-career cases come along, I’ll remember them forever. … to know that my clients are my friends and family. … to know that when friends and family call me Doc, it’s with genuine admiration for the veterinary profession and what I can do for the community. … to understand why we call it practice. … to know that if I could do it all over again, I would still want to be a veterinarian. … to know that I have thoroughly enjoyed my 33 years as a mixed animal practitioner in rural areas and small towns of Illinois.

TO LEARN MORE The Final Diagnosis gives readers a chance to share their wondrous, weird, or legendary cases. Email submissions (no more than 1500 words) to jmoore@uga.edu.

CompendiumEquine.com

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

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Century s BudDee: 9 year old Western Pleasure and Halter horse, stem cell user, and advocate since April of 07

Four Hooves Up for Vet-Stem

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