Compendium Equine | June 2009

VOLUME 4 NUMBER 5 JUNE 2009

6 CE Contact Hours | CompendiumEquine.com | Peer Reviewed

Voll 4(5) V June 2009

Refereed Peer Review

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CE

Treating Thoracic Injuries

PAGES 193–240

Modifying the M Coagulation Cascade: C Available Medications

Pr Man ac a tic gin Pa e g ge an Yo 20 d ur 4 Li fe

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POTOMAVAC™. As the face of PHF changes, trusted protection remains the same.

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

Potomac horse fever (PHF) has been around since 1979. But its epidemiology has only recently been defined, and clinical cases have now been reported in more than 40 states1 — far from the Potomac valley — and into many nontraditional areas.2 Changing weather patterns and improved diagnosis suggest this trend will continue, and PHF may become even more widespread.

Equine POTOMAVAC is a trusted vaccine for aiding the prevention of PHF — even in foals as young as 3 months. Early and regular vaccination helps protect horses in your care against the effects of PHF, including fever, dehydration, colic, late-term abortions and laminitis.

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by Merial, a trusted leader in equine health.

Madigan J and Pusterla N. Life Cycle of Potomac Horse Fever – Implications for Diagnosis, Treatment, and Control: A Review. AAEP Proceedings 2005;51:158-162.

Hamende V. Potomac horse fever cases confirmed in northern Wyoming. University of Wyoming Cooperative Extension Service. Press Release, September 13, 2002.

Available at http://wyovet.uwyo.edu/Diseases/2002/PotomacConf.pdf. Accessed February 18, 2008.

3 Merck Veterinary Manual. Ninth Edition. 2005:236-237.

4 Ryder E. Potomac Horse Fever Cases Popping Up in Ohio. TheHorse.com. Article #10013. July 15, 2007.

5 Marcella K. Conditions collide to propel PHF/Potomac horse fever must be treated rapidly to dodge fatalities. DVM, January 15, 2005.

Available at http://www.dvmnews.com/dvm/article/articleDetail.jsp?id=144082&pageID=1&sk=&date=. Accessed February 18, 2008.

6 Potomac Horse Fever. AAEP.org. Available at http://www.aaep.org/potomac_fever.htm. Accessed February 6, 2008.

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June 2009 Vol 4(5)

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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.

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June 2009 Vol 4(5)

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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.

194

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.

5/13/09

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Pfizer_Dormosedan_USE.qxp:Sound Technologies_USE

Hence, the need for a predictable sedative.

DORMOSEDAN® (detomidine hydrochloride). Sedation and pain management in one.

DORMOSEDAN is an alpha 2 (α2) adrenoceptor agonist that interrupts the nervous system to provide both sedation and analgesia. No drug combining is necessary. Administered IV or IM, DORMOSEDAN is safe at full label dose and allows f lexible dosing to regulate length and depth of sedation and analgesia.

(Additional dosing prolongs not deepens sedation.) DORMOSEDAN. Innovation you’d expect from a leader in equine health. To learn more, contact your Pfizer representative or visit safeandpredictable.com.

As with other α2 agonists, bradycardia and partial AV and SA blocks can occur with decreased respiratory rates.

Occasional reports of anaphylactic-like reactions have been observed. The use of epinephrine should be avoided since epinephrine may potentiate the effects of α2 agonists. Please see full prescribing information for more information.

DORMOSEDAN is a registered trademark of Orion Corporation and is distributed by Pfizer Animal Health. ©2008 Pfizer Inc. All rights reserved. DOR08032

See Page 196 for Product Information Summary

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Pfizer_Dormosedan_LEGAL.qxp:Sound Technologies_USE

6/18/08

Sedative and Analgesic For Use in Horses Only Sterile Solution 10 mg/mL CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian.

DESCRIPTION: Dormosedan® is a synthetic alpha-2 adrenoreceptor agonist with sedative and analgesic properties. The chemical name is 1H imidazole, 4-[(2,3-dimethylphenyl) methyl]-hydrochloride and the generic name is detomidine hydrochloride. It is a white, crystalline,water-soluble substance having a molecular weight of 222.7. The molecular formula is C12H14N2•HCl. CHEMICAL STRUCTURE:

Each mL of Dormosedan® contains 10.0 mg detomidine hydrochloride, 1.0 mg methyl paraben,5.9 mg sodium chloride, and water for injection, q.s.

CLINICAL PHARMACOLOGY: Dormosedan®, a non-narcotic sedative and analgesic, is a potent _2 -adrenoreceptor agonist which produces sedation and superficial and visceral analgesia which is dose dependent in its depth and duration. Profound lethargy and a characteristic lowering of the head with reduced sensitivity to environmental stimuli (sounds, etc.) are seen with detomidine. A short period of incoordination is characteristically followed by immobility and a firm stance with front legs well spread. The analgesic effect is most readily seen as an increase in the pain threshold at the body surface. Sensitivity to touch is little affected and in some cases may actually be enhanced.

With detomidine administration, heart rate is markedly decreased, blood pressure is initially elevated, and then a steady decline to normal is seen. A transient change in the conductivity of the cardiac muscle may occur, as evidenced by partial atrioventricular (AV) and sinoauricular(SA) blocks. This change in the conductivity of the cardiac muscle may be prevented by IV administration of atropine at 0.02 mg/kg of body weight.

No effect on blood clotting time or other hematological parameters was encountered at dosages of 20 or 40 mcg/kg of body weight. Respiratory responses include an initial slowing of respiration within a few seconds to 1–2 minutes after administration, increasing to normal within 5 minutes. An initial decrease in tidal volume is followed by an increase.

INDICATIONS: Dormosedan® is indicated for use as a sedative and analgesic to facilitateminor surgical and diagnostic procedures in mature horses and yearlings. It has been used successfully for the following: to calm fractious horses, to provide relief from abdominal pain, to facilitate bronchoscopy, bronchoalveolar lavage, nasogastric intubation, non reproductive rectal palpations, suturing of skin lacerations, and castrations. Additionally, an approved, local infiltration anesthetic is indicated for castration.

CONTRAINDICATIONS: Dormosedan® should not be used in horses with pre-existing AV or SA block, with severe coronary insufficiency, cerebrovascular disease, respiratory disease, or chronic renal failure. Intravenous potentiated sulfonamides should not be used in anesthetized or sedated horses as potentially fatal dysrhythmias may occur. Information on the possible effects of detomidine hydrochloride in breeding horses is limited to uncontrolled clinical reports; therefore, this drug is not recommended for use in breeding animals.

WARNINGS: Not for use in horses intended for food. Not for human use. Keep out of reach of children.

HUMAN SAFETY INFORMATION: Care should be taken to assure that detomidine hydrochloride is not inadvertently ingested as safety studies have indicated that the drug is well absorbed when administered orally. Standard ocular irritation tests in rabbits using the proposed market formulation have shown detomidine hydrochloride to be nonirritating to eyes. Primary dermal irritation tests in guinea pigs using up to 5 times the proposed market concentration of detomidine hydrochloride on intact and abraded skin have demonstrated that the drug is nonirritating to skin and is apparently poorly absorbed dermally. However, in accordance with prudent clinical procedures, exposure of eyes or skin should be avoided and affected areas should be washed immediately if exposure does occur. As with all injectable drugs causing profound physiological effects, routine precautions should be employed by practitioners when handlingand using loaded syringes to prevent accidental self-injection.

11:23 AM

PRECAUTIONS: Before administration, careful consideration should be given to administering Dormosedan® to horses approaching or in endotoxic or traumatic shock, to horses withadvanced liver or kidney disease, or to horses under stress from extreme heat, cold, fatigue, or high altitude. Protect treated horses from temperature extremes. Some horses, although apparently deeply sedated, may still respond to external stimuli. Routine safety measures should be employed to protect practitioners and handlers. Allowing the horse to stand quietly for 5 minutes before administration and for 10–15 minutes after injection may improve the response to Dormosedan®.

Dormosedan® is a potent _2-agonist, and extreme caution should be exercised in its use with other sedative or analgesic drugs for they may produce additive effects.

When using any analgesic to help alleviate abdominal pain, a complete physical examination and diagnostic work-up are necessary to determine the etiology of the pain.

Food and water should be withheld until the sedative effect of Dormosedan® has worn off.

ADVERSE REACTIONS: Occasional reports of anaphylactic-like reactions have been received, including 1 or more of the following: urticaria, skin plaques, dyspnea, edema of the upper airways, trembling, recumbency, and death. The use of epinephrine should be avoided sinceepinephrine may potentiate the effects of _2 - agonists. Reports of mild adverse reactions haveresolved uneventfully without treatment. Severe adverse reactions should be treated symptomatically. As with all _2 -agonists, the potential for isolated cases of hypersensitivity exist,including paradoxical response (excitation).

SIDE EFFECTS: Horses treated with Dormosedan® exhibit hypertension.

Bradycardia routinely occurs 1 minute after injection. The relationship between hypertension and bradycardia is consistent with an adaptive baroreceptor response to the increased pressure and inconsistent with a primary drug-induced bradycardia. Piloerection, sweating, salivation, and slight muscle tremors are frequently seen after administration. Partial transient penis prolapse may be seen.Partial AV and SA blocks may occur with decreased heart and respiratory rates. Urination typically occurs during recovery at about 45–60 minutes posttreatment, depending on dosage. Incoordination or staggering is usually seen only during the first 3–5 minutes after injection,until animals have secured a firm footing.

Because of continued lowering of the head during sedation, mucus discharges from the nose and, occasionally, edema of the head and face may be seen.

Holding the head in a slightly elevated position generally prevents these effects.

OVERDOSAGE: Detomidine hydrochloride is tolerated in horses at up to 200 mcg/kg of bodyweight (10 times the low dosage and 5 times the high dosage). In safety studies in horses,detomidine hydrochloride at 400 mcg/kg of body weight administered daily for 3 consecutive days produced microscopic foci of myocardial necrosis in 1 of 8 horses.

DOSAGE AND ADMINISTRATION: For Sedation: Administer Dormosedan® IV or IM at the rates of 20 or 40 mcg detomidine hydrochloride per kg of body weight (0.2 or 0.4 mL of Dormosedan® per 100 kg or 220 lb), depending on the depth and duration of sedation required.

Onset of sedative effects should be reached within 2–4 minutes after IV administration and 3–5 minutes after IM administration.Twenty mcg/kg will provide 30–90 minutes of sedation and 40 mcg/kg will provide approximately 90 minutes to 2 hours of sedation.

For Analgesia: Administer Dormosedan® IV at the rates of 20 or 40 mcg detomidine hydrocloride per kg of body weight (0.2 or 0.4 mL of Dormosedan® per 100 kg or 220 lb), depending on the depth and duration of analgesia required. Twenty mcg/kg will usually begin to take effect in 2–4 minutes and provide 30–45 minutes of analgesia. The 40 mcg/kg dose will alsobegin to take effect in 2–4 minutes and provide 45–75 minutes of analgesia.

For Both Sedation and Analgesia: Administer Dormosedan® IV at the rates of 20 or 40 mcg detomidine hydrochloride per kg of body weight (0.2 or 0.4 mL of Dormosedan® per 100 kg or 220 lb), depending on the depth and duration of sedation and analgesia required.

Before and after injection, the animal should be allowed to rest quietly.

STORAGE: Store at controlled room temperature 15°–30°C (59°–86°F) in the absence of light.

HOW SUPPLIED: Dormosedan® is supplied in 5- and 20-mL multidose vials.

U.S. Patent Nos. 4,443,466 and 4,584,383 NADA #140-862, Approved by FDA Manufactured by: Distributed by:

Animal Health Exton, PA 19341, USA Div. of Pfizer Inc NY, NY 10017

107224US-8 Made in Finland

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June 2009 Vol 4(5)

Features 204

Managing Your Practice and Life Living Up to an Image: A Talk With Dr. Alexia McKnight ❯❯ C. Lyon Radiologist and equine magnetic resonance imaging specialist Alexia McKnight has found a way to have a rewarding career in veterinary medicine, make time for her family, and pursue her interest in gardening.

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CE Feature Treating Thoracic Injuries

CompendiumEquine.com | Peer Reviewed | Free CE

CE

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

❯❯ Rolfe M. Radcliffe, Norm G. Ducharme, Thomas J. Divers, FREE and Robin D. Gleed CE Learn how to manage thoracic injuries through emergency first aid; shock therapy; surgery; and wound treatment, reconstruction, and closure.

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CE Feature Modifying the Coagulation Cascade: Available Medications ❯❯ David M. Wong, Charles Brockus, Cody Alcott, and Brett Sponseller This article summarizes the mechanism of action and potential applications of some of the more commonly used anti- and d procoagulant medications in horses. FREE

CE

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The Final Diagnosis Face it, We’re Aneuronal ❯❯ James N. Moore Dr. Moore presents evidence that he’s not the only one missing some “marbles.”

Departments 198 CompendiumEquine.com

203 In Memory: Anna Worth

200 Guest Editorial Clean Your Own House, Veterinarians!

239 Index to Advertisers

❯❯ Scott E. Palmer

239 Market Showcase

Cover image © 2009 E.G. Pors/Shutterstock.com

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.

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

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Guest Editorial ❯❯ Scott E. Palmer, VMD* | New Jersey Equine Clinic | Millstone Township, New Jersey

Clean Your Own House, Veterinarians!

M

edication is the root of all evil at the racetrack, and veterinarians are the ones sticking needles into racehorses, right?

This isn’t a pretty picture, but it’s a common paradigm in which the general public and even some of our own small animal colleagues paint a broadbrush portrait of veterinarians who’ve dedicated their careers to serving the needs of racehorses … guilt by implication and association.

This is not to say that veterinarians do not have ownership in the problems of horse racing. We certainly do. What industry or profession does not have its share of “bad apples?” We only have to look at the US banking industry or political offices to find examples of individuals who made bad choices. Finger-pointing has become a national pastime, and blogs provide a public forum to define the truth without the cumbersome burden of peer review.

*Dr. Palmer is chair of the AAEP Racing Committee, which created the white paper titled “Putting the Horse First: Veterinary Recommendations for the Safety and Welfare of the Thoroughbred Racehorse.” a To read the white paper, search for “racehorse white paper” at aaep.org or go to www.aaep.org/images/files/ Racing%20Industry%20White%20Paper%20Final.pdf.

200

The AAEP recently released a white paper titled “Putting the Horse First: Veterinary Recommendations for the Safety and Welfare of the Thoroughbred Racehorse.”a It provoked more than a few cynical responses: “An overworked subject. Naïve, but well-intentioned. Kumbaya around the campfire.”

“Why don’t the vets make recommendations about things they know rather than blame jockeys and trainers?” asked one individual. In fact, those who take the time to read the white paper will find that it isn’t about blaming; it’s about reducing injury and establishing a culture of integrity.

Racetrack veterinarians practice medicine in the larger context of society’s perception of horses as companion animals, the business model of horse racing, and the veterinarian–trainer–owner relationship. We endorse the current Racing Medication & Testing Consortium (rmtcnet.com) recommendations for uniform medication guidelines that limit race-day medication to furosemide. We call for increased racetrack security and significant uniform penalties for violators of medication rules, including veterinarians. We all need to accept personal responsibility for equine welfare.

The AAEP Racing Committee is currently drafting specific “best-practice” guidelines for racetrack

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

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Guest Editorial

CriticalPo nt We feel strongly that a horse suffering from a catastrophic injury or having a positive test result following a race should remain the property of the owner who entered the horse rather than be handed over to the new owner at the finish.

202

practitioners and regulatory veterinarians that racing industry? Absolutely. If the objectives will be used to “put the horse first” in the back- are to improve the safety and integrity of stretch. The practitioner best-practice document horse racing, recommendations from a veteriwill include recommendations on handling nary perspective are relevant, appropriate, and and administering medication, a change in intended to be supportive. While numerous emphasis from billing for medication (admin- organizations are focused on “fi xing” the indusistered or dispensed) to billing for professional try, the AAEP Racing Committee feels that it is services, and transparency in the veterinarian– critical for someone to speak for horses in the trainer–owner relationship. process. The white paper’s unique veterinary In the past year, the winds of change have viewpoint offers recommendations designed been sweeping out the status quo in horse rac- to encourage decision makers in the industry ing. Diverse stakeholders are joining forces to to put horses first. Are the recommendations implement changes that will make horse rac- broad in scope? Certainly; as are the problems ing safer and help restore integrity to the sport. that confront us. Controversial? Absolutely; This is no easy task, and meaningful results the diversity of stakeholders mandates that will not happen overnight. Principal obstacles no single perspective will please everyone. to change include financial pressures made Ambitious and expensive? You bet; but mainmore acute by the economic downturn, the taining the status quo will be far more costly existence of 38 individual horse-racing jurisdic- for the industry. tions with unique challenges and opinions on A white paper on such a broad topic is, by how to best regulate the industry, and a natu- its nature, superficial to some degree, and ral reluctance by some to embrace change. the “devil” is always in the details. The ComThere seems to be a tendency to compart- mittee’s claiming recommendations have been mentalize individual stakeholders in the horse- particularly controversial. We feel strongly that racing industry. For example, the perception a horse suffering from a catastrophic injury or is that veterinarians should stay focused on having a positive test result following a race medication issues, which are, after all, our area should remain the property of the owner who of expertise. We should stick to what we know. entered the horse rather than be handed over However, the AAEP white paper does exactly to the new owner at the finish. We feel that that. The Thoroughbred industry is facing this change will encourage more responsible enormous challenges that are broad in scope care of claiming horses. But what if a horse just and cannot be solved with simplistic or com- clips its heels in the race? Or what if a rider partmentalized recommendations. Simplistic pulls up the horse to prevent the claim? We are approaches provide catchy sound bites for the working with our industry partners, such as the media but divert attention from real solutions.

National Horsemen’s Benevolence & Protective The AAEP white paper is partly a response Association, to address these concerns. Noneto crisis management by the Thoroughbred theless, our eyes are on the prize. Our goal is to industry. A recent survey of horse-racing protect horses in a racing environment. and general sports fans identified two fundaVeterinarians will continue to work with indusmental factors now considered to be the root try stakeholders to put horses first. The AAEP cause of horse racing’s downturn: (1) high- white paper is not perfect, but the Committee’s profile injuries of horses and riders and (2) vision is clear: if we do what is best for horses a perception that medication has tilted the in all aspects of the industry, everybody wins. playing field in favor of cheaters. The National The alternatives are simply unacceptable.

Thoroughbred Racing Association has identified five areas of reform to address these conSHARE YOUR COMMENTS cerns: medication and testing, injury reporting Have something to say about this and prevention, safety research, improvement editorial or topic? Let us know: of safety in the horse-racing environment, and care of retired racehorses. Interestingly, all of E-MAIL editor@CompendiumEquine.com these reforms are veterinary medical issues. So FAX 800-556-3288 is it appropriate for veterinarians to comment on the myriad problems of the Thoroughbred

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

In Memory

Anna Worth Past President of AAHA Anna Elizabeth Worth, VMD, died on Saturday, May 16, after a valiant battle with cancer. She was 55 years old.

“It is with heavy hearts and deep sadness that we say goodbye to such a compassionate and talented individual,” said John Albers, DVM, executive director of AAHA. “AAHA will forever be indebted to Anna’s unwavering devotion and leadership to the association and to our profession.”

A 1978 graduate of the University of Pennsylvania School of Veterinary Medicine, Worth, with her husband, Bob Bergman, VMD, served as a director and owner of West Mountain Animal Hospital, an AAHA-accredited practice in Shaftsbury, Vermont, for more than 25 years.

Worth was AAHA president from 2008 to 2009 and had served on the association’s board of directors since 2002. She was instrumental in creating the AAHA Helping Pets Fund.

Worth had an active interest in animal welfare and was a past president of the Society for Veterinary Medical Ethics. The Massachusetts Society for the Prevention of Cruelty to Animals presented her with the Veterinarian of the Year Award in 1992.

In lieu of flowers, contributions in memory of Anna Worth can be made to the AAHA Helping Pets Fund (www.aahahelpingpets.org) or the Southwestern Vermont Regional Cancer Center.

Adapted with permission from AAHA.

CompendiumEquine.com | June 2009

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Only Adequan® i.m. (polysulfated glycosaminoglycan)

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Within 48 hours the hyaluronic acid (HA) in the synovial fluid nearly doubles after a single injection.* Recommended dose: 5 mL every 4 days for 7 treatments intramuscularly.

To learn about the wear-and-repair of joints go to www.adequan.com.

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Keep joints in healthy balance There are no known contraindications to the use of intramuscular PSGAG in horses. Studies have not been conducted to establish safety in breeding horses. WARNING: Do not use in horses intended for human consumption. Adequan® i.m. brand Polysulfated Glycosaminoglycan (PSGAG). Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian. Each 5 mL contains 500 mg Polysulfated Glycosaminoglycan. Brief Summary Indications: For the intramuscular treatment of non-infectious degenerative and/or traumatic joint dysfunction and associated lameness of the carpal and hock joints in horses.

LUITPOLD PHARMACEUTICALS, INC. Animal Health Division, Shirley, NY 11967.

See product package insert for full prescribing information. *Burba DJ, Collier MA, Default LE, Hanson-Painton O, Thompson HC, Holder CL: IN VIVO KINETIC STUDY ON UPTAKE AND DISTRIBUTION OF INTRAMUSCULAR TRITIUM-LABELED POLYSULFATED GLYCOSAMINOGLYCAN IN EQUINE BODY FLUID COMPARTMENTS AND ARTICULAR CARTILAGE IN AN OSTEOCHONDRAL DEFECT MODEL. The Journal of Equine Veterinary Science 1993; 696-703. Concentrations of Adequan i.m. in the synovial fluid begin to decline after peak levels are reached at 2 hours; then remain constant from 24 hours post injection through 96 hours. © 2008 Luitpold Animal Health. Adequan® is a registered trademark of Luitpold Pharmaceuticals, Inc. AHD 85201, Iss. 2/08 CE

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

Dr. McKnight at work.

Living Up to an Image: A Talk With Dr. Alexia McKnight

Radiologist and equine magnetic resonance imaging (MRI) specialist Alexia McKnight, DVM, DACVR, has found a way to have a rewarding career in veterinary medicine, make time for her family, and pursue her interest in gardening. We talked to her about her practice (McKnight Insight, LLC, Chadds Ford, Pennsylvania), family, and horticultural endeavors.

You graduated from veterinary school in 1997. Tell me about your path to establishing McKnight Insight, LLC. After veterinary school, I finished a 2-year fellowship in an MRI research laboratory at Mayo Clinic in Rochester, Minnesota. This outstanding opportunity gave me a much deeper understanding of the physics and clinical applications of MRI. I began my radiology residency at the University of Pennsylvania in 1999 and finished in 2002. I stayed on as a faculty member at New Bolton Center until 2006, when I started my consultation practice, which has allowed me to pursue my long-term passion for veterinary MRI.

What services does McKnight Insight provide?

I’m primarily a teleradiologist with a strong focus on veterinary MRI, especially equine MRI. I’m also a consultant for practices that are interested in an MRI system or have recently installed a system and need help training staff. When possible, I’m available for real-time reviews to ensure that special sequences and planes have been acquired to complete an animal’s examination.

Do you consult exclusively on equine cases?

I began consulting exclusively on equine cases because that had been my focus and interest since college, but I agreed to help a few small animal imaging centers in the past year. Since then, I’ve thoroughly enjoyed those clients and their small animal cases.

What do you enjoy most about your job?

I can focus on the cases, the animals, my clients, my friends, and my family without the red tape

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that plagues a lot of larger businesses. I’m enjoying the personal interactions with my colleagues and the ability to make a significant difference in many of their cases. My 11-second commute is also quite nice, as is the ability to spend time with my daughter.

What do you enjoy least?

Keeping the books and paying taxes!

Tell me about your child.

My 3-year-old daughter is amazing … a pure delight. My second child is in the “oven” and is expected to “hit the ground” in a few months.

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

It used to be difficult for me to get out of my dark office because I really enjoy my work. But when the weather warms up and the sun starts shining, it gets easier to leave the monitors and make some vitamin D outdoors.

What changes have you made in your professional life to achieve a better work–life balance?

Starting my own business! My equine specialty makes maintaining a work–life balance easier than most other equine specialties. Some days, I can put out the work “fires,” take time to do some gardening, and finish my work in the evening. When I graduated, I recognized that working at home interested me and that pursuing veterinary radiology might make this a reality. I envisioned my current work–life situation a long time ago and planned ahead.

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

Managing Your Practice and Life Dr. McKnight at “work” in her garden.

Do you have any advice for veterinarians interested in adjusting their work schedules or in changing practices to improve their work–life balance?

The standard veterinary work hours make it very difficult to achieve a work–life balance.

Long hours, weekend availability, and on-call work cut into time for life’s other activities.

Something has to give. The mentality of the profession has to allow for more normal work hours and job sharing for individuals who need more time for themselves or their families without labeling these individuals as “not working hard.” Sixty- to 100-hour workweeks aren’t a good idea for achieving a work–life balance.

The profession needs to recognize the benefits of a work–life balance and adapt accordingly rather than focus on the workaholic mentality.

fruits such as blueberries, raspberries, and cherries and vegetables such as tomatoes, beans, and kale. I’d love to add some fruit trees as well.

However, what I do this season might be limited to what I can safely manage in my last trimester of pregnancy.

I’ve never taken horticulture courses. If I have questions, I ask my good friend Google or my phenomenal maternal encyclopedia— my mother!

How have your horticultural pursuits affected your work and professional life?

It is unbelievably refreshing to get out of a dark office with computers and go outside for some fresh air, exercise, and sunlight. This does wonders to reset my system.

Do you have any other hobbies?

I hear that you’re an avid gardener. Tell me about this hobby. When did you begin pursuing it?

As soon as I had land and time to do so! The enormous number of weeds and invasive shrubs around my property was also a motivating force.

My interest in gardening long preceded my time in the garden. I’ve been actively exploring horticulture since I moved into my house a couple of years ago.

I enjoy ornamental gardens as well as organic fruit and vegetable gardens. After I moved into my house, my first task was to remove the invasive weeds and reestablish an evergreen screen on certain parts of the property. Then I touched it up with some native plants and a few ornamental and exotic species. Now I’m focusing on

I used to do more horseback riding, bicycling, and karate. I’d love to do more of them again, particularly horseback riding. I’m hoping that when my daughter gets older, we’ll go riding together.

Dr. McKnight with her family.

What advice would you give practitioners who are having trouble making time to pursue interests outside of work?

Job sharing is a good idea. Working for yourself or from home may help.

Employers need to recognize the value of having sound-minded, physically fit, happy employees and allow more part-time employment opportunities.

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

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P.O. Box 318 29160 Intervet Lane Millsboro, Delaware 19966 www.intervetusa.com 800.521.5767 Panacur, Prestige, PreveNile, Banamine, and Regu-Mate are registered trademarks, EquiRab is a trademark, Partners In Practice is a registered service mark, and Intervet Foal Care is a service mark of Intervet/Schering-Plough Animal Health or an affiliate. Š 2009 Intervet Inc. All rights reserved. 35968-PortfolioVet-03/09-Spread-CE-REVISED

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Because at Intervet/Schering-Plough, we’re for the same things you are – the health and welfare of the horse.

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3 CE CREDITS

CE Article 1

Treating Thoracic Injuries ❯❯ Rolfe M. Radcliffe, DVM, DACVS ❯❯ Norm G. Ducharme, DVM, MS, DACVS ❯❯ Thomas J. Divers, DVM, DACVIM, DACVECC ❯❯ Robin D. Gleed, BVS, MRCVS, DACVA Cornell University

At a Glance Clinical Signs Page 208

Emergency Management Page 210

Thoracic Injury Evaluation Page 216

Specific Thoracic Injury Page 217

Conservative Versus Surgical Management Page 219

Prognosis Page 220

Abstract: The treatment of equine thoracic trauma often requires rapid emergency measures to save horses from life-threatening sequelae. Complications of thoracic trauma include pneumothorax, pneumomediastinum, hemothorax, pleuritis, diaphragmatic hernia, and damage to the lungs, heart, blood vessels, or abdomen. Patient stabilization is the primary objective before conservative or surgical treatment. Deciding how to manage each case depends on many factors, such as the location, type, and extent of the injury; anesthetic concerns; and response to initial treatment.

T

horacic injuries are relatively uncommon in horses and may follow blunt or penetrating trauma1 (FIGURE 1).

Because these injuries may be life threatening, efficient management of affected patients is necessary to optimize the chance for survival.1 A review of penetrating thoracic wounds in horses identified collision with an object as the most common cause of trauma.2 The many reported sequelae of thoracic injury in horses include subcutaneous emphysema, pneumothorax, pneumomediastinum, hemothorax, pleuritis, diaphragmatic hernia, and damage to the lungs, heart, and blood vessels.

Abdominal and spinal injury may also occur in association with thoracic trauma.

Additional extrathoracic trauma indicated a grave prognosis, with all affected horses requiring euthanasia.2 However, an overall satisfactory outcome was reported when thoracic injury occurred alone.

Clinical Signs Clinical signs may be attributed to damage to internal or external thoracic structures.2 External injury may cause soft tissue or muscle damage, blood vessel laceration, and rib fracture, with systemic consequences including pain and shock. Horses with internal thoracic trauma, such as pneumothorax or hemothorax, often present in respiratory distress. Common clinical signs include nostril flaring; dyspnea;

FIGURE 1

A thorough evaluation of the abdomen is indicated when penetrating thoracic injury occurs caudal to the sixth rib. In this case, the stake did not enter the thoracic or abdominal cavities, and conservative treatment with antimicrobials and local wound therapy resulted in complete healing without complications.

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

Courtesy of Dr. Ed Earley

Deep penetrating injury near the cranial thoracic cavity caused by a large wooden stake.

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Siger L, et al. Assessment of the efficacy of a single dose of a recombinant vaccine against West Nile virus in response to natural challenge with West Nile virus-infected mosquitoes in horses. American Journal of Veterinary Research 2004;65(11):1459-1462.

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Siger L, Bowen R, et al. Evaluation of the efficacy provided by a recombinant canarypox-vectored equine West Nile virus vaccine against an experimental West Nile virus intrathecal challenge in horses. Veterinary Therapeutics 2006;7(3):249-256.

4 Data on file at Merial. Study 02-067.

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tachypnea; accentuated respiratory excursions; and cyanotic mucous membranes.1 Horses with abdominal trauma may develop colic associated with damage to, or rupture of, abdominal viscera; diaphragmatic hernias; or other organ injury. Determining the location and depth of trauma can guide management decisions regarding thoracic or abdominal involvement; deep wounds and those caudal to the sixth rib are more likely to involve the abdomen.1,2 Neurologic signs arising from other extrathoracic injury, such as spinal trauma, have also been reported.2

Emergency Management

CriticalPo nt Determining the location and depth of trauma can guide management decisions regarding thoracic or abdominal involvement; deep wounds and those caudal to the sixth rib are more likely to involve the abdomen.

Patient stabilization through rapid evaluation and treatment is the cornerstone of effective emergency management. Immediate emergency treatment must be administered during the initial patient evaluation before a more thorough diagnostic evaluation. As with cardiopulmonary resuscitation in humans, emergency triage treatment of equine patients should follow the ABC protocol: Airway, Breathing, and Circulation. Initial treatment should be directed at restoring alveolar ventilation and oxygenation as well as managing shock. In small animal patients with acute thoracic injury, six conditions are immediately addressed: airway obstruction, open and tension pneumothorax, flail chest, massive hemothorax, and cardiac tamponade.3 Pneumothorax, flail chest, hemothorax, hemorrhagic shock, and abdominal injury are the primary complications in horses, requiring immediate action.

Pneumothorax Chest wounds should be sealed with a sterile, airtight dressing to prevent further movement of air into the thorax. Temporary wound closure or packing, application of petrolatum dressings, or application of plastic wrap over sterile dressings can create an airtight “membrane.” Next, stent bandages or standard bandage materials should be placed fully around the thorax, except in flail chest patients, in which bandaging is contraindicated.3 Severe pain often accompanies trauma to the pleural cavity, ribs, and intercostal nerves, leading to abnormal ventilation (i.e., shallow breathing, tachypnea, hypoventilation) and hypoxemia (PaO2: <80 mm Hg).1,2 Nasal or tracheal insufflation of oxygen (15 L/min) is indicated in

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cyanotic or hypoxemic adult equine patients.1,4,5 Intratracheal oxygen insufflation improves PaO2 compared with nasal oxygen by providing higher inspired concentrations of oxygen; however, tracheal oxygen delivery may cause coughing, which may be counterproductive.

Emergency evacuation of pleural air should be performed after wound bandage or closure. When tension pneumothorax is suspected, immediate opening of the thorax or placement of a cannula allows supra-atmospheric pressure to return to atmospheric pressure, converting tension pneumothorax to open pneumothorax—a less life-threatening complication of thoracic injury.1 Immediate removal of air from the thorax is then indicated. Pulmonary reexpansion improves ventilation and helps control hemorrhage from the low-pressure pulmonary vessels. A sterile teat cannula, 14-gauge catheter, or thoracostomy tube is inserted into the dorsal thorax at the 11th to 15th intercostal space1,4 (FIGURE 2). A thoracostomy tube (24–36 French) placed ventrally is indicated to provide complete drainage if large volumes of pleural fluid or blood clots are present. Cannula placement directly in front of a rib avoids the intercostal blood vessels located caudal to the ribs. An extension line and three-way stopcock are attached to facilitate active suction via a 60-mL syringe or suction device. A Heimlich or other oneway valve allows continuous exiting flow1,4 but must be attached firmly and monitored closely because pneumothorax will worsen if the valve becomes dislodged. A continuous flow evacuation device has also been used successfully in cattle to treat pneumothorax secondary to infectious lower airway disease.6 These authors reported continuous-flow chest evacuation to be superior to traditional one-time air removal because it avoids the high recurrence rate common in closed pneumothorax, in which air leakage continues from ruptured bullae.

Flail Chest Flail chest results when two or more adjacent ribs are fractured in multiple planes.2,3 Blunt trauma is frequently the cause, with fractures occurring on either side of the point of impact.

This creates a flail segment of chest wall that exhibits paradoxical respiratory movement.

Such abnormal motion prevents development

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

©2009 Purina Mills, LLC

Thomas Kellerman, DVM Pacific, MO AAEP Practitioner

Lowering starch raise hopes could

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No two cases are alike. And every step you take requires a delicate balance. Fortunately, help has arrived. Introducing Purina® WellSolve L/S® horse feed. This veterinary-researched, nutritional solution for wellness delivers a guaranteed level of 4% sugar and 7% starch. The culmination of thousands of tests and field trials, the research behind WellSolve L/S® horse feed is peer reviewed and published in the Journal of Equine Veterinary Science. So if you’re facing a delicate situation with a carbohydrate-sensitive horse, your good care and WellSolve LS® horse feed can help give hope to your clients. For more details, call 1-877-454-7109, talk to your certified Purina® Dealer, or visit wellsolveequine.com.

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FIGURE 2

CriticalPo nt Patient stabilization is the primary goal of initial therapy. Treatment is directed at removal of pleural air, closure or bandaging of thoracic wounds, control of hemorrhage, and treatment of shock.

212

Diagram showing placement of a thoracostomy tube (a) with a continuous-flow evacuation system (b) and tube attachment via a Chinese locking pattern (c).

(Reprinted with permission from Chevalier H, Divers TJ. Pulmonary dysfunction in adult horses in the intensive care unit. Clin Tech Equine Pract 2003;2[2]:165-177)

of the pressure gradient necessary for normal air exchange, leading to severe ventilatory compromise.3 Stabilization of the flail chest segment is required to restore ventilation.

Application of an external splint is recommended in small animals with an intact flail segment with little soft tissue damage; this may prove useful in equine patients as well2,3 (FIGURE 3). The splint, which is constructed of aluminum rods and a metal or plastic stent, is secured to the ribs with orthopedic wire, providing stability for fracture healing. Septic pleuritis, possibly associated with an orthopedic wire, was a reported complication in one repair.2 Flail chest characterized by severe fractures or extensive soft tissue damage usually requires surgical debridement, fracture stabilization, and reconstructive procedures of the chest wall.3 Bandaging of the thorax is contraindicated for patients with flail chest, as inward stabilization of the flail segment results

in decreased ventilation and further pulmonary injury. Attendant pulmonary contusion, which is significant with flail chest patients, causes decreased alveolar volume, decreased compliance, and impeded diffusion at the blood–air interface.

Hemothorax and Hemorrhagic Shock Hemorrhagic shock results from the pathologic loss of blood from many causes, including trauma, and leads to hypovolemia.7 Hemorrhagic shock may occur in horses with thoracic trauma when damage to the heart, great vessels, and intercostal and pulmonary vasculature results in hemothorax and significant blood volume loss. Clinical signs associated with hemorrhagic shock include tachycardia, tachypnea, pale mucous membranes, trembling, sweating, distress, and, possibly, a systolic heart murmur.8,9 These signs vary with the severity of blood loss, acute or chronic hemorrhage, and

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

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CriticalPo nt The need for a transfusion in patients with acute hemorrhage should be based on clinical signs (i.e., heart rate, pulse quality, mucous membrane color, temperature of extremities, attitude, degree of weakness) and not on the PCV.

the underlying lesion.9 In equine patients with trauma and acute hemorrhage into the thorax or abdomen, the degree of tachycardia may not correlate with the severity of pain. For example, moderate to severe tachycardia (80 to 140 bpm) in a horse with mild or intermittent pain may indicate severe blood loss.

Immediate treatment of equine patients with thoracic hemorrhage includes fluid therapy, stopping the hemorrhage if possible, and whole blood transfusion when indicated.10–12 The goal of fluid support in treating acute circulatory failure is rapid restoration of the circulating vascular volume, cardiac output, and tissue perfusion.10,13 The administration of balanced, polyionic intravenous crystalloid fluids is indicated at a rate of 20 to 80 mL/kg over several hours, depending on the degree of hypovolemia and blood pressure. Normal to low blood pressure (permissive hypotension) is the goal of therapy if the hemorrhage can be stopped.8 Hypertonic (7.2%) sodium chloride solution (4 mL/kg; 1 to 2 L in an adult horse) has also been used successfully in treating hemorrhagic shock in horses and other species,13 but its use in uncontrolled hemorrhage may be detrimental because rapid increases in blood pressure could disrupt clot formation.

Hypertonic saline exerts its effect via osmotic extracellular plasma expan sion, increased plasma volume, and increased vasopressin levels.13,14 When hypertonic saline is used in horses for shock management, isotonic

fluid therapy should follow immediately. The use of a large amount of hetastarch is likely contraindicated in patients with acute hemorrhage because of possible coagulopathy or coagulopathic effects. 8,11 Fresh-frozen plasma is indicated to replace clotting factors when hemorrhage leads to abnormal clotting factor loss or consumption, a problem further exacerbated by additional crystalloid therapy.8,11 Aminocaproic acid (10 to 20 mg/ kg) may help prevent fatal hemorrhage when surgery is not an option; it should be administered slowly, mixed in intravenous fluids.8,15 Blood transfusions should be considered when signs of hypotension and severe bleeding persist despite initial fluid therapy. Horses can lose approximately 20% of their blood volume (8% to 10% of their body weight; approximately 8 to 10 L in an 1100-lb [500–kg] adult horse) without changes in their blood pressure.

In peracute cases, death from hemorrhage may occur without a marked decrease in the packed cell volume (PCV).8,12 Therefore, the need for a transfusion in patients with acute hemorrhage should be based on clinical signs (i.e., heart rate, pulse quality, mucous membrane color, temperature of extremities, attitude, degree of weakness) and not on the PCV. Several measurements that may be helpful when determining the need to transfuse include blood lactate, arterial or venous oxygen tension or saturation, and blood pressure.12 The recommended volume of blood to transfuse is approximately

FIGURE 3

Application of orthopedic wires.

214

An external splint.

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

Courtesy of Norm G. Ducharme

Managing rib fractures that create flail chest. Septic pleuritis is a reported complication of this technique if the wires that stabilize the ribs enter the thoracic cavity and act as a conduit for bacteria.

THE WORLD’S FIRST LOW STARCH FEED COULD GIVE NEW MEANING TO “HEALTHY AS A HORSE.” Leading equine nutritionists agree – Triple Crown® Low Starch is the first feed to truly be considered low carb. The carbohydrate content is below 15% and contains no molasses, grains or alfalfa. This pelleted feed is ideal for horses prone to laminitis, as well as horses with insulin problems, colic and grain-related temperament issues. The good digestible fiber and higher fat level provide the right amount of calories and can replace all, or a portion, of your hay. For more information or to find a dealer near you, visit us online at www.triplecrownfeed.com or call 800-267-7198.

Triple Crown® is a registered trademark of Triple Crown Nutrition Inc., Wayzata, MN. © 2009 Equine Specialty Feed Company

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6 to 8 L in adult horses or 30% to 40% of the estimated or calculated blood loss8 (BOX 1).

Autotransfusion may be attempted when a large volume of blood is present in the thorax and when bleeding is unassociated with sepsis or bacterial contamination.8,16,17 We agree with the cited authors that the blood must be collected from a sterile thorax via aseptic technique to avoid bacterial contamination.

After insertion of a thoracic teat cannula or chest tube, blood is collected in a container BOX 1.

A Practical Example of Transfusion in an Equine Patienta The amount of lost blood can be estimated from the following formula (packed cell volume [PCV] can be used in this formula once blood volume is reestablished with fluid administration or after 8–12 hr of compensation): Liters of blood lost =

Normal PCV – Patient PCV Normal PCV

× 0.08 × Patient weight (kg)

As a rule of thumb, if a PCV of 40% is assumed for the donor, 2.2 mL of whole blood per kilogram of patient weight will increase the PCV by approximately 1% in most horses. For example, 1100 mL of whole blood will raise the PCV from 15% to 16% in a 500-kg (1100-lb) horse. The administration rate of blood varies with the patient’s clinical status. For horses with severe hypotension and hemorrhage, blood can be administered as a rapid bolus along with (but not in place of) crystalloids and colloids because the benefits outweigh the risks of reactions. More often, crystalloids and colloids are given as boluses first and then followed with blood administration. When possible, it is advisable to initially administer blood slowly (approximately 0.1 mL/kg over 10–15 min) to ensure tolerance. After that period, rates of up to 20–30 mL/kg/hr can be used. To remove fibrin and debris, plasma filtration sets should be used for blood administration.

Case Example: A 450-kg (990-lb) Thoroughbred racehorse was impaled on a fence, resulting in acute thoracic trauma and a PCV of 10%.

Blood loss (liters) = (40% – 10%) ÷ 40% × (0.08 × 450 kg) = 30% ÷ 40% × 36 = 27 L Typically, the goal is to replace 30% to 40% of the calculated blood loss: 27 L × 0.30 = 8.1 L of whole blood administered as a transfusion a Adapted from Magdesian KG. Therapeutics in practice: acute blood loss. Compend Equine Contin Educ Vet 2008;3(2):80-90.

216

with small amounts of an anticoagulant (e.g., approximately one part acid citrate dextrose per 15 parts blood).

Abdominal Injury Thorough evaluation of the abdominal cavity is also important in equine patients with thoracic trauma.1,2 The cupula of the diaphragm extends to the sixth rib during expiration, making it essential to evaluate the abdomen of an equine patient with a deep, penetrating thoracic injury caudal to this location.1 A complete evaluation of the abdomen includes peritoneal paracentesis, ultrasonography, wound exploration, laparoscopy, or exploratory celiotomy.

Diaphragmatic hernias occur infrequently in horses but have been reported secondary to trauma.18 Thoracic radiography and ultrasonography are indicated for preoperative diagnosis (FIGURE 4). In one study, although two horses with penetrating thoracic injury were euthanized due to abdominal perforation and bowel rupture, only one had a diaphragmatic hernia.2 Large defects with secondary colon displacement into the thorax may cause pulmonary compression and dyspnea, whereas small defects are more likely to incarcerate bowel and cause colic.18 Successful repairs of diaphragmatic hernias in horses have been reported18–20; however, the prognosis is less favorable with large defects and in horses showing clinical signs.21

Thoracic Injury Evaluation Examination of equine patients with thoracic trauma includes thoracic auscultation and percussion, diagnostic thoracocentesis, chest wall palpation, wound evaluation, blood gas analysis, radiography, and ultrasonography.1,2 Auscultation and percussion of the chest wall in equine patients may help identify pneumothorax or hemothorax. In patients with pneumothorax, lung sounds are absent, but increased resonance is percussed dorsally. Diminished lung sounds ventrally and percussion of a fluid line are characteristic of hemothorax. Diagnostic thoracocentesis can be used to confirm pneumothorax or hemothorax.22 A needle, catheter, or teat cannula is placed into the thorax as previously described, and a fluid extension line is attached. Pneumothorax is confirmed when fluid bubbles out of the extension; however, if the fluid is aspirated into the chest,

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Treating Thoracic Injuries CE pneumothorax is unlikely. Chest wall and wound palpation may help identify rib fractures, thoracic wall penetration, foreign bodies, or other injury. Arterial blood gas analysis provides information on lung ventilation, lung perfusion, and acid–base status, while arterial and venous samples together provide information on tissue oxygenation.12 Serial samples are indicated to help evaluate the response to therapy. Thoracic radiography (FIGURE 5) and ultrasonography are becoming more practical in the field. These diagnostics can help detect rib fractures, pneumothorax, pneumomediastinum, hemothorax, diaphragmatic hernias, and foreign bodies.1 Ultrasonographic evaluation is also useful for determining the amount of blood or air in the thorax, guiding pleurocentesis, and inserting chest tubes.

Specific Thoracic Injury Pneumothorax In a review of 40 cases of pneumothorax in horses, the reported causes were pleuropneumonia, open and closed thoracic trauma, and surgery of the upper and lower respiratory tract.23 In this study, pleuropneumonia was the most common cause of pneumothorax; affected horses had a significantly worse prognosis for survival compared with horses with pneumothorax due to other causes. There are three types of pneumothorax. Open pneumothorax occurs with penetrating, open chest wounds when air moves freely during inspiration and expiration.1,2 Damage to the lung parenchyma by displaced rib fractures or a ruptured lung bulla permits air to enter the pleural space, creating a closed pneumothorax.

Tension pneumothorax occurs when intrapleural pressure exceeds atmospheric pressure. This life-threatening condition usually follows the formation of a pleurocutaneous fistula, in which air enters the pleural space during inspiration but is blocked from exiting during expiration. Thoracic pressure builds on the affected side, forcing air across the mediastinal cavity and/or decreasing compliance of the opposite lung. Severe hypoxemia with PaO2 levels as low as 22 mm Hg has been reported in humans with tension pneumothorax.1 Unilateral pneumothorax, except for tension pneumothorax, is well tolerated in horses.

However, a thin, fenestrated caudal mediastinum in some horses may predispose them to

FIGURE 4

Thoracic ultrasonogram of an equine patient with diaphragmatic hernia involving the liver and small intestine. Note the distended loops of small intestine (large arrow) and region of the liver (small arrow) within the thoracic cavity.

bilateral pneumothorax—a potentially fatal complication. Based on radiographic examination, nine of 15 horses with penetrating thoracic injury had pneumothorax, six cases of which were bilateral.2

CriticalPo nt Hemothorax Hemothorax, hemorrhagic shock, and death may result from severe thoracic injury involving the heart or great vessels. Most horses with massive hemothorax from thoracic injury do not survive.1 However, in six of 15 horses with a penetrating thoracic injury, hemothorax (possibly originating from the intercostal artery or pulmonary laceration) was not life threatening.2 Removing blood from the thorax improves pulmonary ventilation and avoids the formation of septic pleural effusion, pleural adhesions, and constricting fibrothorax.1,2 Patient stabilization through restoration of circulating blood volume is recommended before thoracic drainage.

Progressive subcutaneous emphysema with secondary pneumomediastinum or, less commonly, pneumothorax is a reported complication of axillary wounds in horses.

Rib Fractures Most rib fractures in equine patients occur in foals during parturition, and their management is described in the literature.1,24–27 Rib fractures in foals are reported to be a significant cause of morbidity and mortality but may not be clinically apparent.24–27 Ultrasonography was found

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Lung Lacerations

FIGURE 5

Thoracic radiograph depicting bilateral pneumothorax in an equine patient with thoracic trauma. Note the dorsal margin of the collapsed lungs (large arrow), the fractured rib (small arrow), and the chest tubes (arrowheads).

to be superior to radiography for evaluating thoracic trauma in foals, even for identifying nondisplaced fractures.27 Surgical stabilization may be recommended to reduce the reported 25% mortality rate associated with direct complications from rib fractures.24,26,27 Rib fractures are also common in adult horses following blunt or penetrating thoracic injury.1 Five of 15 horses sustained rib fractures in a review of penetrating thoracic trauma.2 Although some fractured ribs can be identified on physical or radiographic examination, many fractures may not be palpable or visible and may be missed. Most rib fractures in adult horses are reported to heal without fi xation.1 Displaced rib fractures may lacerate the lungs, heart, blood vessels, diaphragm, or other deep structures. In such cases, surgical rib fi xation is indicated to minimize continued thoracic injury.3 One possible complication is a closed pneumothorax, resulting from closed chest wounds in which rib fractures cause pulmonary parenchymal damage. The reported techniques for stabilizing rib fractures include the use of quill sutures, external splints, pins, wires, and plate application.3,28 When severe rib damage prevents realignment, the remaining bone and fragments should be removed.

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Lung trauma is a rare manifestation of thoracic injury in horses. Few reports in the large animal literature describe how to manage lacerations involving the lung following thoracic trauma, although one report summarizes intrathoracic surgery in large animals.28 Partial or complete lung lobectomy is recommended for severe lacerations, cysts, bullae, abscesses, or tumors.29 Conventional excision and closure by suture or staple techniques are described in small animals and may be applied to equine patients.29,30 Bronchial involvement is identified via application of warm saline to the site of injury and followed by bronchial closure.28 Overlapping horizontal mattress sutures are placed to seal the lung stump after an amputation and to repair lacerations to the lung margin. The edge of the excision line is oversewn with a simple continuous pattern to avoid leakage.30 Injury to the central lung parenchyma may also be closed via a simple continuous suture pattern following identification of bronchial damage and ligation. Monofilament, absorbable suture material with swaged-on, atraumatic needles is currently recommended for lung and bronchial closure.28,30 Minor alveolar leakage does not require closure and generally seals quickly.

Axillary Wounds Axillary wounds often extend deep into the tissues and function as one-way valves, producing marked, progressive subcutaneous emphysema.

Most clinicians recommend packing these wounds with gauze and closing the skin or using stent bandages to limit further air penetration into the tissue.22 Packing material should be replaced every 24 to 48 hours until the wound bed has completely granulated. Equine patients should be confined to a stall and cross-tied to minimize limb movement. However, despite various treatments, axillary wounds in horses may lead to severe subcutaneous emphysema that may progress to secondary pneumomediastinum (and, occasionally, pneumothorax), which may become apparent weeks after the initial injury. In affected patients, reports document respiratory distress that occurred as late as 16 days after injury, necessitating patient confinement and observation for an extended period of time.2,31 In six of 15 horses in one study, pneumomediastinum was identified; five of the six horses had axillary wounds.2

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Treating Thoracic Injuries CE Conservative Versus Surgical Management

Anesthesia and Surgical Approach

Thoracic injury may be successfully managed with conservative and surgical treatment strategies.1,2,22,32 However, patient stabilization is the primary objective before either method of treatment.1,22,32 Horses with simple rib fractures, small chest wounds, or modest degrees of pneumothorax or hemothorax and without severe lung lacerations, rib fractures, deep penetration, or contamination are candidates for conservative management. Medical therapy includes antimicrobials and NSAIDs, thoracocentesis or thoracostomy tube placement, second-intention wound healing, bandaging, and the supportive care measures described in this article. Surgical therapy may be indicated for more severe injury.32 Surgery allows improved exploration and lavage of the wound and pleural or abdominal cavities, control of hemorrhage, complete removal of foreign bodies, repair of lung lacerations and rib fractures, and the stabilization of flail chest.

Selecting the appropriate type of anesthesia and surgical approach for treating thoracic injury requires careful consideration of several factors, specifically patient stability; anesthetic concerns; location, type, and extent of the injury; clinician experience; and response to initial treatment.28 General anesthesia should be used with caution in thoracic trauma patients until they have been initially stabilized.1,22 Anesthetic risks must be weighed against the benefits of standing versus recumbent procedures. To avoid further respiratory and cardiovascular compromise of patients, clinicians should select standing wound exploration and treatment when possible.1,22 Intercostal perineural anesthesia is recommended for standing procedures to facilitate repair and help control postoperative pain.

Thorough wound exploration, debridement, and lavage are necessary to remove bacteria, foreign bodies, rib fragments, and other debris.1 Many of these treatments may be used in standing horses. However, tension or bilateral pneu-

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mothorax, which is difficult to manage without the ability to provide mechanical ventilation, may develop during standing surgery, resulting in severe cardiopulmonary deterioration.1,2 General anesthesia is indicated in horses with severe chest wall disruption, deep penetrating wounds, foreign bodies, abdominal cavity involvement, complicated rib fractures, extensive lung lacerations, or severe contamination that requires aggressive thoracic lavage.32 The use of controlled positive-pressure ventilation is essential in equine patients with open pneumothorax.2 In addition, patients in which hemorrhage, pneumothorax, or hypoxemia persists despite conservative treatment may require wound exploration or wound closure techniques that necessitate mechanical ventilation and general anesthesia.2 Most thoracic approaches in equine patients simply involve enlarging the existing traumatic wound. However, several surgical approaches to the equine thorax have been reported, including lateral thoracotomy via the intercostal technique or rib resection and thoracoscopy.28,30,33–35 In small animals, a median sternotomy has also been described for gaining access to both sides of the thorax30; this approach may be useful in calves or foals.28 In general, the thoracotomy incision is centered over the site of the thoracic injury, and in most cases, the wound is simply enlarged to obtain adequate exposure of the ribs, heart, lungs, diaphragm, and pleura.1,28 Various retractors, including the Finochietto rib retractor, are also useful for gaining surgical exposure.

Thoracoscopy provides several advantages over thoracotomy for evaluating and treating thoracic injury in equine patients.33–35 Thoracoscopy allows detailed exploration of the thoracic cavity in patients with minimal morbidity, whereas thoracotomy is more invasive and is limited by difficult exposure.33–36 Standing thoracoscopy provides excellent access to the dorsal and lateral aspects of the thorax, while the cranial and ventral portions are best viewed with a lateral, a dorsal, or an oblique recumbency technique.35 The specific identification of the organ injury can help direct treatment and improve planning for thoracotomy or abdominal procedures.33 With thoracoscopy, foreign bodies within accessible regions of the thorax may be identified and removed.1 Thoracoscopy can also help effectively evaluate

220

and treat many postoperative complications of thoracic injury, including pleuritis, pericarditis, abscesses, pleural adhesions, and diaphragmatic hernias.33–35 Currently, thoracoscopy alone does not allow closure of diaphragmatic defects because of nonreducible omental adhesions and the limitations of available instrumentation.33

Wound Closure Primary wound closure is recommended, when possible, after thoracic injury in horses.1,2,22 For small uncomplicated wounds, the thoracic muscles and soft tissues are apposed over the defect. For large chest wounds, or those otherwise unsuitable for routine closure, two thoracic reconstructive techniques have been described in large animals: primary muscle flap and prosthetic mesh repairs.1,3,22 Rotating muscle pedicle flaps of the longissimus dorsi and external abdominal oblique muscles, transposed via a Z-plasty technique, were used to close a caudal lateral thoracic wound in a horse.37 Polypropylene mesh, although useful for closing large defects in animals, should be used with caution to avoid complications related to infection. We recommend closing as much of the wound as possible at the initial surgery. Mesh implants should be reserved for subsequent procedures, when necessary, and only after infection has resolved. Delayed primary closure and second-intention healing may also be selected, especially with large or highly contaminated wounds.1,22 Closed suction drains placed into the wound can help prevent seroma formation and secondary incisional infection. Mesh expansion and various tension-relieving suture patterns are most commonly used in horses to reduce tension during closure of extensive thoracic or abdominal wounds.1 Close postoperative monitoring is essential. When infection persists, aggressive retreatment via debridement, drainage, lavage, and appropriate antimicrobial selection based on culture and sensitivity is recommended to prevent secondary pleuritis.22

Prognosis In a review of 15 cases, a satisfactory outcome was reported following penetrating thoracic trauma without extrathoracic injury.2 Eleven horses, representing a 73% survival rate, were discharged from the hospital. The other four horses were euthanized due to complications

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Treating Thoracic Injuries CE of extrathoracic injury, including colon perforation, renal trauma, and spinal luxation.2 While horses that develop secondary pleuritis often have a guarded prognosis,38,39 it is important to note that only one horse developed pleuritis, indicating a low incidence of this complication.2 A mortality rate of approximately 50% has been reported in horses that develop pleuritis or acute pleuropneumonia.1,2,22,38,39

Conclusion The emergency evaluation and treatment of horses with thoracic injury primarily involves cardiovascular and respiratory function assessment and provision of appropriate support. An understanding of emergency first-aid steps; shock therapy; anesthetic concerns; standard surgical approaches to the thorax; methods of wound treatment, reconstruction, and closure; and potential complications can help clinicians manage these difficult cases.

We recommend a thorough evaluation of the abdomen in all cases of thoracic trauma,

especially for injuries caudal to the sixth rib.

Frequent, extended monitoring for respiratory distress in equine patients with axillary wounds is advised to detect secondary pneumomediastinum and pneumothorax and to provide appropriate therapy. A low occurrence of thoracic empyema has been reported in cases of penetrating thoracic injury in horses; however, if septic pleuritis develops, it has a poor prognosis and a mortality rate of approximately 50%.1,2,22,38,39 Without extrathoracic injury or severe complications, as discussed in this article, the prognosis for equine patients with thoracic injury should be favorable.2

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REFERENCES

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1. Holcombe SJ, Laverty S. Thoracic trauma. In: Auer JA, Stick JA, eds. Equine Surgery. Philadelphia: WB Saunders; 1999:382-385.

2. Laverty S, Lavoie JP, Pascoe JR, Ducharme NG. Penetrating wounds of the thorax in 15 horses. Equine Vet J 1996;28(3):220-224.

3. Spackman CJA, Caywood DD. Management of thoracic trauma and chest wall reconstruction. Vet Clin North Am Small Anim Pract 1987;17(2):431-447.

4. Chevalier H, Divers TJ. Pulmonary dysfunction in adult horses in the intensive care unit. Clin Tech Equine Pract 2003;2(2):165-177.

5. Mason DE, Ainsworth DM, Robertson JT. Respiratory emergencies in the adult horse. Vet Clin North Am Equine Pract 1994;10(3):685-702.

6. Peek SF, Slack JA, McGuirk SM. Management of pneumothorax in cattle by continuous-ďŹ&#x201A;ow evacuation. J Vet Intern Med 2003;17(1):119-122.

7. Allen DA, Schertel ER. Pathogenic aspects of circulatory shock.

Vet Clin North Am Equine Pract 1994;10(3):495-501.

8. Divers TJ. Liver failure and hemolytic anemia. In: Orsini JA, Divers TJ, eds. Manual of Equine Emergencies: Treatment and Procedures. Philadelphia: WB Saunders; 2003:315-338.

9. Edens LM. Abdominal hemorrhage. In: Robinson NE, ed. Current Therapy in Equine Medicine, ed 4. Philadelphia: WB Saunders; 1997:211-214.

10. Cook VL, Bain FT. Volume (crystalloid) replacement in the ICU patient. Clin Tech Equine Pract 2003;2(2):122-129.

11. Magdesian KG. Colloid replacement in the ICU. Clin Tech Equine Pract 2003;2(2):130-137.

12. Divers TJ. Monitoring tissue oxygenation in the ICU patient. Clin Tech Equine Pract 2003;2(2):138-144.

13. Bertone JJ. Hypertonic saline in management of shock. In: Reed SM, Bayly WM, eds. Equine Internal Medicine. Philadelphia: WB Saunders; 1998:198-201.

14. Irvine CH, Alexander SL, Donald RA. Effect of an osmotic stimulus on the secretion of arginine vasopressin and adrenocorticotropin in the horse. Endocrinology 2005;124(6):3102-3108.

15. Kikura M, Levy JH, Tanaka KA, Ramsay JG. A double-blind, placebo-controlled trial of epsilon-aminocaproic acid for reducing blood loss in coronary artery bypass grafting surgery. J Am Coll Surg 2006;202(2):216-222.

16. Beadle RE. Hemothorax. In: Colahan PT, Mayhew IG, Merritt AM, Moore JN, eds. Equine Medicine and Surgery. St. Louis: Mosby; 1999:555-556.

17. Baldan M, Giannou CP, Rizzardi G, et al. Autotransfusion from haemothorax after penetrating chest trauma: a simple, life-saving procedure. Trop Doct 2006;36(1):21-22.

18. Freeman DE. Small intestine. In: Auer JA, Stick JA, eds. Equine Surgery. Philadelphia: WB Saunders; 1999:232-256.

19. Malone ED, Farnsworth K, Lennox T, et al. Thoracoscopic-assisted diaphragmatic hernia repair using a thoracic rib resection.

Vet Surg 2001;30(2):175-178.

20. Santschi EM, Juzwiak JS, Moll HD, et al. Diaphragmatic hernia repair in three young horses. Vet Surg 1997;26(3):242-245.

21. Beadle RE. Diaphragmatic hernia. In: Colahan PT, Mayhew IG, Merritt AM, Moore JN, eds. Equine Medicine and Surgery. St. Louis: Mosby; 1999:554.

22. Hendrix SM, Baxter GM. Management of complicated wounds.

Vet Clin North Am Equine Pract 2005;21(1):217-230.

23. Boy MG, Sweeney CR. Pneumothorax in horses: 40 cases (1980-1997). JAVMA 2000;216(12):1955-1959.

24. Bellezzo F, Hunt RJ, Provost P, et al. Surgical repair of rib fractures in 14 neonatal foals: case selection, surgical technique and results. Equine Vet J 2004;36(7):557-562.

25. Jean D, Laverty S, Halley J, et al. Thoracic trauma in newborn

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Treating Thoracic Injuries CE foals. Equine Vet J 1999;31(2):149-152.

26. Kraus BM, Richardson DW, Sheridan G, Wilkins PA. Multiple rib fracture in a neonatal foal using a nylon strand suture repair technique. Vet Surg 2005;34(4):399-404.

27. Sprayberry KA, Bain FT, Seahorn TL, et al. 56 cases of rib fractures in neonatal foals hospitalized in a referral center intensive care unit from 1997-2001. Proc AAEP 2001:395-399.

28. Fowler ME. Intrathoracic surgery in large animals. JAVMA 1973;162(11):967-973.

29. Facemire PR, Chilcoat CD, Sojka JE, et al. Treatment of granular cell tumor via complete right lung resection in a horse. JAVMA 2000;217(10):1522-1525.

30. Caywood DD, Lipowitz AJ. Surgical approaches and techniques for managing pulmonary disease. Vet Clin North Am Small Anim Pract 1987;17(2):449-467.

31. Hance SR, Robertson JT. Subcutaneous emphysema from an axillary wound that resulted in pneumomediastinum and bilateral pneumothorax in a horse. JAVMA 1992;200(8):1107-1110.

32. Beadle RE. Thoracic wall trauma. In: Colahan PT, Mayhew IG, Merritt AM, Moore JN, eds. Equine Medicine and Surgery. St. Louis: Mosby; 1999:553-554.

33. Fischer Jr AT, Vachon AM. Thoracoscopy and thoracoscopic surgery in horses. In: Fischer Jr AT, ed. Equine Diagnostic & Surgical Laparoscopy. Philadelphia: WB Saunders; 2002:255-264.

34. Peroni JF, Horner NT, Robinson NE, Stick JA. Equine thoracoscopy: normal anatomy and surgical technique. Equine Vet J 2001;33(3):231237.

35. Vachon AM, Fischer Jr AT. Thoracoscopy in the horse: diagnostic and therapeutic indications in 28 cases. Equine Vet J 1998;30(6):467-475.

36. Peroni JF, Robinson NE, Stick JA, Derksen FJ. Pleuropulmonary and cardiovascular consequences of thoracoscopy performed in healthy standing horses. Equine Vet J 2000;32(4):280-286.

37. Stone WC, Trostle SS, Gerros TC. Use of a primary muscle pedicle flap to repair a caudal thoracic wound in a horse. JAVMA 1994;205(6):828-830.

38. Mair TS, Lane JG. Pneumonia, lung abscesses and pleuritis in adult horses: a review of 51 cases. Equine Vet J 1989;21(3):175-180.

39. Collins MB, Hodgson DR, Hutchins DR. Pleural effusion associated with acute and chronic pleuropneumonia and pleuritis secondary to thoracic wounds in horses: 43 cases (1982-1992). JAVMA 1994;205(12):1753-1758.

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. Which condition does not require immediate emergency treatment in horses with acute thoracic injury? a. airway obstruction b. tension pneumothorax c. nondisplaced rib fracture d. massive hemothorax

5. Of the following sequelae reported with thoracic injury in horses, which one has been associated with axillary wounds? a. hemothorax b. pleuritis c. pneumomediastinum d. rib fracture

2. In a retrospective study23 in horses, which problem was identified as the most common cause of pneumothorax and was associated with decreased survival? a. open thoracic trauma b. closed thoracic trauma c. pleuropneumonia d. lower respiratory surgery

6. A horse presents to your clinic with a history of acute thoracic injury and clinical signs of hemorrhagic shock. On what clinical evidence should you base the need for a whole blood transfusion? a. PCV b. total plasma protein level c. platelet count d. clinical signs

3. Overlapping ___________ sutures are placed to seal the lung stump after amputation or to repair lacerations to the lung margin. a. horizontal mattress b. vertical mattress c. simple interrupted d. cruciate 4. Following wound bandaging or closure in equine patients with pneumothorax secondary to thoracic trauma, which emergency procedure is indicated? a. intravenous fluid therapy b. whole blood transfusion c. removal of a foreign body d. removal of pleural air

7. In patients with acute hemorrhage, a large amount of ___________ is contraindicated because of possible coagulopathic effects. a. hetastarch b. hypertonic saline c. whole blood d. plasma 8. A 5-year-old Standardbred gelding suffers blunt trauma during race training. On presentation, you note the following: severe respiratory distress, an open chest wound, flail chest, tachycardia, pale mucous membranes, and colic. You diagnose pneumothorax, hemothorax, diaphragmatic hernia, and multiple rib fractures.

Following patient stabilization, which treatment strategy do you recommend?

a. standing surgery to stabilize the flail chest with a thoracic bandage b. standing surgery to stabilize the flail chest with an external splint c. standing surgery to explore the wound and stabilize rib fractures d. surgery with the patient under general anesthesia to explore the wound; evaluate the thoracic and abdominal cavities; repair the diaphragmatic hernia; stabilize the rib fractures; remove foreign bodies; place thoracic drains; and debride, lavage, and close the wound 9. Flail chest results from a. the fracture of two or more adjacent ribs in one plane. b. the fracture of two or more adjacent ribs in multiple planes. c. two or more fractures involving a single rib. d. rib fracture with secondary pulmonary laceration.

10. Which statement regarding pneumothorax is true? a. Open pneumothorax involves lung perforation. b. Closed pneumothorax does not involve lung perforation. c. Tension pneumothorax occurs when intrapleural pressure exceeds atmospheric pressure. d. Tension pneumothorax occurs when atmospheric pressure exceeds intrapleural pressure.

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CE Article 2

Modifying the Coagulation Cascade: Available Medications* ❯❯ David M. Wong, DVM, MS, DACVIM Iowa State University

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

❯❯ Cody Alcott, DVM ❯❯ Brett Sponseller, DVM, PhD, DACVIM Iowa State University

At a Glance Anticoagulants Page 225

Clinical Signs of Coagulopathy Page 225

Fibrinolytic Medications Page 230

Procoagulant Medications in Treating Severe Hemorrhage Page 231

Suggested Medications and Doses for Modifying the Coagulation Cascade in Equine Patients Page 232

*A companion article titled “Hemostasis” was published in the March 2009 issue.

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Abstract: Equine practitioners require a basic knowledge of the coagulation cascade to effectively diagnose and treat many primary diseases. With this knowledge, practitioners can administer adjunctive medications to horses to promote an anti- or procoagulant state. Among the anticoagulants, heparin has received the greatest attention in equine medicine. However, other anticoagulants, such as aspirin and warfarin, have also been used in horses. Alternatively, medications such as tissue plasminogen activator and urokinase have been administered to foals with thromboembolism. In addition, medications such as aminocaproic acid and formalin have been administered to horses to promote hemostasis. While the benefits of many of the medications used for these purposes in horses remain unsubstantiated, numerous case reports and reviews have recommended these therapeutic options in horses. Thus, appropriately administered medications that modify the coagulation cascade may be beneficial prophylactic or therapeutic choices in certain instances.

C

oagulopathies are occasionally encountered secondary to various disease processes in equine medicine, especially in critically ill equine patients (BOX 1). At times, coagulopathies can result in performance-limiting (e.g., laminitis) or lifethreatening (e.g., disseminated intravascular coagulation [DIC]) conditions. Although no single medication is likely to eliminate these complications, various medications are available to modify the coagulation system to promote or retard hemostasis in horses.

Many of the medications discussed in this article have limited experimental evidence to support positive clinical efficacy and use in horses. However, these medications have been used in an attempt to treat various disease processes in multiple anecdotal reports.

This article summarizes the mechanism of action and potential applications of some of the more commonly used anti- and procoagulant medications in horses.

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

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Modifying the Coagulation Cascade: Available Medications CE Anticoagulants Among the anticoagulants, heparin has been used most widely in equine medicine in an attempt to prevent or control the progression of many diseases, such as postceliotomy intestinal adhesion formation, DIC, acute laminitis, and vessel thrombosis.

Unfractionated Heparin Unfractionated heparin (UFH) is a heterogenous mixture of glycosaminoglycan chains that vary in molecular weight from 3000 to 40,000 daltons.1,2 The mechanism of action of heparin includes its ability to bind to antithrombin, resulting in a conformational change of the reactive center of antithrombin and acceleration of the interaction between antithrombin and activated factor X (Xa) or thrombin by approximately 1000 times.1 Subsequently, inactivation of factor Xa and thrombin occurs, inactivating various stages of the coagulation cascade. The interaction between heparin and antithrombin is mediated by a pentasaccharide sequence in the heparin chain.1 To inhibit thrombin, the heparin chain must be long enough (at least 18 saccharide units) to bind and form a complex with antithrombin and thrombin (FIGURE 1).1,2 Heparin also inactivates factors IX, XI, and XII and stimulates plasminogen activator activity.

After inactivation of factor Xa and thrombin, BOX 1.

Clinical Signs of Coagulopathy When performing venipuncture or inspecting indwelling intravenous catheters, clinicians or technicians should examine the patient for the following clinical signs of coagulopathy: Hematoma formation Prolonged or excessive bleeding at venipuncture site Thrombophlebitis Petechial or ecchymotic hemorrhage of mucous membranes (oral, vulvar) Epistaxis Thrombosis of veins or arteries (digital, brachial, aortoiliac) Hemarthrosis Intracavitary bleeding (abdominal or thoracic cavity) Soft tissue bruising Melena

heparin dissociates from the complex and is again biologically available.2,3 Endogenous heparin is produced by mast cells in most mammalian tissues, with the highest concentrations produced in the lungs, liver, and intestine.2 In addition, heparan sulfate is located on endothelial cell surfaces and promotes activation of antithrombin.

UFH is highly bound to plasma proteins, macrophages, and endothelial cells, which act as storage pools. When these pools become saturated, free heparin is available in plasma.2,3 Because of these pharmacokinetic variables, individual and dose-related variations in efficacy may occur with the use of UFH. Adverse effects of UFH administration in horses include thrombocytopenia and heparininduced agglutination of erythrocytes.2 Less frequent complications reported in horses include hemorrhage and pain at injection sites. 2,4 Protamine sulfate is a heparin antagonist and has been used in people (1 mg of protamine sulfate per 100 to 150 IU of heparin) to ameliorate untoward effects of heparin therapy.2,5 Protamine competes with antithrombin for binding to heparin; because protamine has a stronger affinity for heparin, antithrombin is dissociated from the heparin–antithrombin complex, which reverses the anticoagulant function of heparin.5 Protamine has additional effects, such as inhibition of factor VII activation of the extrinsic pathway, but its use should be judicious because profound hypotension, vasodilation, reflex tachycardia, and idiosyncratic fatal reactions have been reported in people.2,5,6 Heparin therapy has been used to treat various disease processes in equine medicine, but its true efficacy in clinical situations is unknown. Heparin has been administered intraperitoneally and systemically to prevent intestinal adhesion formation in horses—a complication that may increase morbidity and mortality after abdominal surgery.7 Adhesion formation results from an imbalance between fibrin deposition and fibrinolysis.7 The normal response to intraabdominal injury and inflammation involves the production of serofibrinous exudate by peritoneal mesothelium, deposition of a fibrin matrix, and release of tissue factor, thereby activating the extrinsic pathway of coagulation.7–9 Cross-linked fibrin forms fibrinous adhesions; fibroblasts and endothelial cells subsequently infiltrate

CriticalPo nt Heparin therapy has been used to treat various disease processes in equine medicine, but its true efficacy in clinical situations is unknown.

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FIGURE 1

The pentasaccharide sequences of unfractionated heparin (upper image) and low-molecular-weight heparin (LMWH; lower image) bind to antithrombin, resulting in a conformational change in the reactive center of antithrombin. This conformational change accelerates the interaction of antithrombin with, and the inactivation of, factor Xa. In contrast, accelerated inactivation of thrombin by antithrombin requires the formation of a ternary heparin– antithrombin–thrombin complex, which can be formed only by chains that have at least 18 saccharide units. This explains the limited inhibitory activity of LMWH against thrombin compared with that of unfractionated heparin. (Adapted with permission.1)

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these adhesions, forming granulation tissue in response to the original mesothelial defect.8 Under normal conditions, fibrin strands and fibrinous adhesions are lysed via local peritoneal fibrinolytic activity before fibrous maturation occurs.7–9 More specifically, peritoneal mesothelial cells release tissue plasminogen activator (TPA), which subsequently activates plasminogen to plasmin, a natural fibrinolytic.10 Intestinal ischemia, inflammation, distention, and trauma may suppress normal peritoneal fibrinolytic activity, thus predisposing a horse to adhesion formation following intestinal injury (colic) and abdominal surgery.7 Heparin therapy may facilitate decreased thrombin formation and the conversion of fibrin to fibrinogen, thereby decreasing fibrous adhesion formation. In addition, stimulation of TPA activity by heparin may enhance fibrinolysis.7 Positive results of heparin therapy have been experimentally demonstrated in an ischemia–reperfusion model in ponies, but clinical studies have produced mixed results.9,11 In the experimental ischemic bowel model, three of four control ponies developed multiple intestinal adhesions in response to ischemia, whereas only one of four heparin-treated (40 U/kg IV once at surgery, then 40 U/kg SC q12h for 48 hr) ponies developed a single adhesion.

The results of this study have been used to suggest the use of low-dose heparin to prevent intestinal adhesions.9 In another study involving 33 horses that underwent exploratory celiotomy, no significant differences were detected between the control group and heparin-treated (66 U/kg SC q12h for 72 hr) group regarding complications (fever, ileus, jugular vein phlebitis, acute laminitis) or survival rates.11 Because of the variety of intestinal lesions reported, the cases selected may have had insufficient intestinal injury or peritoneal inflammation to benefit from heparin therapy.

Therefore, the study was unable to evaluate the effect of heparin administration on intestinal adhesion formation. A more recent investigation in foals demonstrated intestinal adhesion formation in three of four foals treated with heparin (80 U/kg SC q12h for 72 hr), while adhesions were not observed in foals treated with dimethyl sulfoxide or the combination of flunixin meglumine and antimicrobials.

These results suggest that heparin provides no benefit in preventing intestinal adhesions

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Modifying the Coagulation Cascade: Available Medications CE also contributes to DIC and delayed fibrinolysis.13 Decreased plasma Heparin has been administered antithrombin, a major anticoaguin an attempt to reduce multiple lant, is observed in people13 and horses14 during DIC, resulting from complications in horses, including impaired synthesis of antithrombin and degradation by elastase intestinal adhesions, disseminated released from activated neutrophils. intravascular coagulation, laminitis, Simultaneously, spontaneous hemorrhage may occur, resulting from and thrombophlebitis. The use the consumption and depletion of of low-molecular-weight heparin platelets and coagulation proteins.

DIC has been well documented in may be associated with fewer horses; the most common initiators are acute GI disease, such as stranguadverse affects than the use lating intestinal obstruction, enteritis, of unfractionated heparin. colitis, and bacterial septicemia.14–16 Endotoxemia is a common underlying pathophysiologic trigger of the in foals.12 Heparin (30,000 to 50,000 U) has inflammatory and coagulation cascade in both also been added to 10 L of lavage fluid and instances.17,18 Addressing the primary disorder administered intraabdominally after celiotomy is crucial to treating DIC. Because obstruction to prevent intestinal adhesion formation, but of the microvasculature by microthrombi may the true efficacy of heparin in this situation is result in organ (e.g., GI, renal) dysfunction or failure, the use of heparin has been suggested unknown.10 Heparin therapy may also be warranted as a preventive therapy to decrease the incifor treating DIC. A brief review of the patho- dence of thrombus formation. Controversial genesis of DIC follows; more information is in human and veterinary medicine, the ratioavailable elsewhere.13 DIC can be described nale for heparin therapy for DIC is based on as widespread activation of the coagulation inactivation of thrombin and factors Xa and system, resulting in a procoagulant state with XIa, which may prevent further conversion systemic thromboses and secondar y dif- of fibrinogen to fibrin, thus reducing microfuse hemorrhage throughout the body. DIC thrombus formation.19 To date, controlled prospective studies that is not a primary disease but is secondary to pathologic conditions such as sepsis, local- demonstrate efficacy of heparin in treating ized infections, acute gastrointestinal (GI) DIC in horses are lacking. In one study involvdisease (colic), colitis, neoplasia, trauma, ing 23 horses with colic and DIC, a greater hemolysis, hepatic or renal failure, vasculi- proportion of survivors (seven of eight) were tis, and endotoxemia in horses.14,15 While DIC administered heparin (40 to 90 U/kg SC q8h) is not always associated with these disease compared with horses that died (nine of 15), processes, in certain situations, the primary but this finding was not statistically signifidisease causes inappropriate overactivation cant.14 Heparin therapy used in conjunction of the coagulation cascade with subsequent with plasma therapy has been suggested if production of fibrin and, ultimately, throm- antithrombin activity is progressively decreasbotic occlusion of small and midsize vessels.13 ing or is less than 60% of normal values.14,20 Thrombosis causes varying degrees of organ The addition of 400 U of heparin per liter of dysfunction or failure. Clinical manifestations fresh-frozen plasma may activate antithrombin of DIC in an individual horse depend, in part, and inhibit coagulation protein activation when on the nature, intensity, and duration of the administered to horses in a hypercoagulable initial stimulus and concentration of endog- state.20 However, studies in septic people have enous anticoagulants.14,15 Concurrent suppres- found that antithrombin therapy improved sursion of anticoagulants such as antithrombin, vival, whereas the combination of antithromprotein C, and tissue factor–pathway inhibitor bin and heparin had no benefit in terms of

CriticalPo nt Decreased plasma antithrombin, a major anticoagulant, is observed in people and horses during DIC, resulting from impaired synthesis of antithrombin and degradation by elastase released from activated neutrophils. Addressing the primary disorder is crucial to treating DIC.

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CriticalPo nt The use of lowmolecular-weight heparin has gained popularity in human and veterinary medicine because the drug has better bioavailability, a longer plasma halflife, a more predictable response, and decreased adverse effects compared with unfractionated heparin.

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survival.21 Furthermore, heparin may partially interfere with some of the antiinflammatory effects of antithrombin.22 Additional studies in horses and people are needed before the effects of concomitant administration of heparin and antithrombin are fully understood.

Laminitis is another serious and debilitating disease with multiple causes and severities.

Although the pathogenesis of equine laminitis is incompletely understood, coagulopathy and occlusion of digital vessels by microthrombi may play a role in the development of some cases of acute laminitis.17,23 As noted above, conditions such as enterocolitis, colic, DIC, and other disorders involving endotoxemia may increase the incidence of thromboembolism in horses.17 Thus, heparin has been used in efforts to prevent the development of thrombus formation and decrease the incidence of laminitis in certain clinical settings.

An early study demonstrated a decreased incidence of lameness and rotation of the third phalanx in horses with carbohydrate-induced laminitis that were treated with heparin.24 However, in another retrospective study of 71 horses that required abdominal surgery for small intestinal disorders, no difference in the incidence of laminitis was detected between untreated horses and horses treated with heparin.25 However, a further retrospective study demonstrated a decreased incidence of laminitis associated with proximal enteritis in horses treated with heparin (0% [none of 12] developed laminitis) compared with horses that were not treated with heparin (29.8% [31 of 104] developed laminitis).26 Differences in disease processes, heparin dose, and timing of administration; concurrently administered medications; and small sample size may explain some of the differences noted between these studies.

Phlebitis or thrombophlebitis can occur secondary to neonatal septicemia or as a sequela of severe GI, pulmonary, or systemic disease in horses.27,28 Systemic coagulopathies, injury to the vessel wall (e.g., an indwelling intravenous catheter, repeated venipuncture), type of catheter material, type(s) of intravenous medications administered, and blood stasis may predispose horses to thrombophlebitis. 27,29 Prompt removal of intravenous catheters, avoidance of venipuncture, hydrotherapy, and topical antiinflammatory salves (e.g., dimethyl

sulfoxide gel; 1% diclofenac sodium [SURPASS, IDEXX Laboratories]) frequently halt the progression of thrombophlebitis, particularly when instituted at the onset of clinical signs of blood vessel irritation and inflammation (palpable thickening of the vein, pain, swelling, exudation, increased resistance to catheter flow).29 The clinician can also consider the use of anticoagulants, such as heparin, in equine patients in a hypercoagulable state.

Heparin is ineffective at dissolving existing thrombi but may prevent thrombophlebitis or further extension of existing thrombi.17,29 Although low-dose heparinized saline (10 U/ mL of saline) is routinely used to flush catheters, clinicians may consider using systemic doses of heparin (20 to 40 U/kg SC q12h) to help prevent or treat thrombophlebitis.17 Thrombosis of central and peripheral vessels is a possible complication of sepsis in foals and severe infectious diseases in adult horses and warrants a guarded to poor prognosis.27,30 Thrombosis of the bowel wall subsequent to severe infectious colitis and pulmonary thromboembolism as a sequela of necrotizing pneumonia have also been reported in horses.27,31 Thrombolytic agents have been used in a foal with vessel thrombosis.32 Aggressive treatment of the primary disease coupled with prophylactic administration of anticoagulants such as aspirin or heparin may help prevent vessel thrombosis, but prospective clinical trials are needed. Heparin therapy has been used in septic humans and a foal and may decrease the incidence of thromboembolic disease in humans.32,33 In addition, adult horses with low antithrombin activity may be administered heparin (40 U/kg) preincubated with fresh-frozen plasma to provide anticoagulant proteins, and this treatment has been suggested to help prevent GI thrombosis secondary to systemic coagulopathies.27

Low-Molecular-Weight Heparin The use of low-molecular-weight heparin (LMWH) has gained popularity in human and veterinary medicine because the drug has better bioavailability, a longer plasma half-life, a more predictable response, and decreased adverse effects compared with UFH.4,34 LMWH has the ability to bind with antithrombin and inhibit factor Xa, but because of the small molecular size of the drug, fewer than half

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Modifying the Coagulation Cascade: Available Medications CE of LMWHs have molehorses administered hirucules that are of sufficient din.36 For prophylaxis and Limited information treatment of thrombotic length to bind to both antion the use of disease in horses, doses thrombin and thrombin; of 0.5 and 1 mg/kg SC therefore, these LMWHs thrombolytic q12h, respectively, of hiruhave lower activity against din were recommended.36 thrombin (FIGURE 1).1 medications (e.g., LMWH has been invesHowever, the use of hirutissue plasminogen tigated in horses at a dose din in clinical cases needs of 50 U/kg SC q24h and further investigation. activator) is available has demonstrated adequate in horses. However, Aspirin therapeutic/prophylactic The NSAID aspirin has plasma concentrations after thrombosis of major been used for its antipyretic, the first administration.4 In addition, no agglutination analgesic, antiinflammavessels in foals has of erythrocytes and no sigtory, and antithrombotic been associated nificant change in packed properties for many years. cell volume, hemoglobin Aspirin inhibits the enzyme with a poor outcome. concentration, or platelet cyclooxygenase, thereby counts occurred in the reducing the production of LMWH group compared prostaglandins and thromwith the UFH group.4 One study that compared boxanes. Platelets are responsible for primary the use of UFH versus LMWH in horses with hemostasis by interacting with subendothelial colic demonstrated a decreased incidence of collagen, releasing various mediators, and formjugular vein changes (partial thrombosis or ing a platelet plug. Thromboxane A2, a significant thickening of the wall of the jugular vein) in product of platelet activation, stimulates vasohorses administered LMWH (four of 16 [25%]) constriction and aggregation of platelets, concompared with those administered UFH (eight tributing to platelet plug formation. Inhibition of of 13 [61.5%]) after surgery.34 Another equine platelet-derived thromboxane, therefore, thwarts study investigated the pharmacokinetic prop- these responses and potentially decreases the erties of two LMWH preparations (dalteparin propensity for thrombus formation. While most and enoxaparin) and suggested doses of 50 U/ cells can synthesize cyclooxygenase de novo, kg SC q24h of dalteparin or 40 U/kg SC q24h platelets cannot, once they are inhibited by aspiof enoxaparin as a prophylactic anticoagulant rin. Therefore, aspirin inhibits platelet aggregatreatment.35 Higher doses (100 U/kg SC q24h of tion for the life of the platelet (3 to 5 days in dalteparin or 80 U/kg SC q24h of enoxaparin) horses), and establishment of normal platelet were suggested for treating horses considered function requires production of new platelets. to be at high risk for developing thrombotic Aspirin is used infrequently for analgesia disease.35 Furthermore, a clinical study that in horses because of its relatively short halfused 50 U/kg SC q24h of dalteparin in horses life and lower potency compared with other being treated medically or surgically for colic NSAIDs, such as flunixin meglumine and demonstrated fewer adverse effects compared phenylbutazone. However, the antithrombotic with the use of UFH.34 effects of aspirin are prolonged; thus intermitA recent study has investigated the use of tent administration of low-dose aspirin (5 to 30 another anticoagulant medication, recombinant mg/kg PO q24–48h) may help prevent thromhirudin, in healthy horses.36 In people, hirudin bus formation related to DIC, endotoxemia, is primarily used to prevent or treat arterial or and thromboembolic diseases such as acute venous thrombosis. Hirudin directly and irre- laminitis and vascular occlusion.3,18,37 While versibly inhibits free and fibrin-bound thrombin, human studies have suggested that aspirin independent of antithrombin activity. No adverse is beneficial for preventing thromboembolicreactions or significant changes were noted in related disorders, there is a lack of evidence general behavior, bleeding tendency, or hema- demonstrating the efficacy of aspirin as a protologic or biochemical parameters in healthy phylactic medication in equine patients pre-

CriticalPo nt Thromboxane A2, a significant product of platelet activation, stimulates vasoconstriction and aggregation of platelets, contributing to platelet plug formation.

Inhibition of plateletderived thromboxane, therefore, thwarts these responses and potentially decreases the propensity for thrombus formation.

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FREE CE Modifying the Coagulation Cascade: Available Medications

disposed to thrombus formation.38 One equine study suggested that thromboxane A 2 plays a minor role in aggregation of equine platelets and that aspirin is not an effective antithrombotic medication in horses compared with other species.3,27,39 Controlled equine studies investigating the role of aspirin as an antithrombotic medication in clinical situations are needed.

CriticalPo nt Fibrinolytic medications, such as TPA, urokinase, and streptokinase, dissolve thrombi by promoting the conversion of plasminogen to plasmin.

FIGURE 2

Warfarin Warfarin is a coumarin-derivative anticoagulant that has been used to prevent or treat laminitis, thrombophlebitis, and navicular syndrome in horses.3,40,41 As with other coumarins, the anticoagulant effects of warfarin are indirect via interference with the action of vitamin K1 in the hepatic synthesis of coagulation factors II, VII, IX, and X. Initial study of warfarin therapy in horses with navicular syndrome proved favorable: 17 of 20 horses became sound after warfarin therapy.41 A starting dose of 0.018 mg/kg PO q24h was increased by 20% until a 2- to 4-second increase in one-stage prothrombin time was achieved.41 However,

Fibrinolytic Medications The fibrinolytic system dissolves intravascular clots via the enzyme plasmin, which digests fibrin and fibrinogen. Plasminogen is the inactive precursor of plasmin, and conversion to the active form results from the interaction of fibrinbound plasminogen with TPA (FIGURE 2).

Fibrinolytic medications, such as TPA, urokinase, and streptokinase, dissolve thrombi by promoting the conversion of plasminogen to plasmin. Under normal circumstances, circulating TPA has minimal effect on circulating plasminogen because it is either rapidly cleared from the blood or inhibited by the circulating inhibitors plasminogen activator inhibitor-1 and -2. A distinct disadvantage of thrombolytic medication administration is that

Mechanism of activation and inhibition of plasminogen.

A Normal fibrinolysis occurs by binding of plasminogen to fibrin and subsequent activation to plasmin via the interaction with plasminogen activator. Plasmin bound to fibrin results in degradation of fibrin into fibrin degradation products.

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with the advent of newer therapies for navicular syndrome, the adverse effects of warfarin therapy (hemorrhage, hematoma formation, hemarthrosis), and the need for close monitoring of therapy (one-stage prothrombin time), warfarin has been relegated to infrequent use in equine practice.40,41

B Antifibrinolytic medications such as aminocaproic acid and tranexamic acid bind to the site where plasminogen binds to fibrin, thereby preventing activation of plasminogen on the surface of fibrin. Fibrinolysis is therefore blocked.

(Adapted with permission.48)

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Modifying the Coagulation Cascade: Available Medications CE natural inhibitors of plasminogen activators Procoagulant Medications may become overwhelmed, resulting in gen- in Treating Severe Hemorrhage Severe acute hemorrhage from conditions such eralized fibrinolysis and hemorrhage.

As noted above, vessel thrombosis can occur as trauma, uterine artery rupture, hemothorax, during sepsis in neonates as a result of bacteria or hemoperitoneum, and guttural pouch mycoendotoxin altering or activating the coagulation sis occurs occasionally in equine medicine. cascade. In addition, neonatal foals have a lower Adjunctive medications such as formalin, protein C concentration and decreased activities aminocaproic acid, tranexamic acid, and conof antithrombin and plasminogen during the jugated estrogens have been used to facilitate first month of life, which may contribute hemostasis. While these drugs may help proto the increased incidence off coagulopathies such as vessel thrombosis in septic foals.15,42,43 Procoagulant medications (e.g., formalin, Clinical signs of vessel thrombosis aminocaproic and tranexamic acid, include lameness, cool extremities and tissue edema distal to conjugated estrogens) may facilitate thrombosis, a lack of a palpable hemostasis in hemorrhaging horses. arterial pulse, and sloughing or separation of the skin or hooves.

Thrombolytic agents can be administered systemically or regionally (catheter mote hemostasis, clinicians should not ignore directed); the latter results in better clot resolu- obvious and potentially lifesaving therapies, tion in people with peripheral artery thrombi as such as blood transfusions, fluid therapy a result of more direct and localized effects.44 with crystalloids and/or colloids, and direct The published use of thrombolytic medica- mechanical pressure to control hemorrhage. tions is limited in equine medicine. One report One proposed mechanism by which formadetailed the use of a constant-rate infusion of lin enhances primary hemostasis is through urokinase (4000 U/min for 60 minutes) into the enhanced endothelial or platelet activation.48 right hindlimb of a 6-day-old Quarter horse Ten to 150 mL of 10% buffered formalin diluted filly with thromboembolism of the hindlimbs. in 1 L of isotonic fluid has been suggested to Angiography did not show reperfusion of the control hemorrhage in horses.48–50 However, right hindlimb, and the foal was subsequently adverse effects such as muscle tremors, tachyeuthanized.45 In another instance, TPA was cardia, tachypnea, serous ocular and nasal administered (2 mg IV) in an attempt to dissolve discharge, agitation, and restlessness have an aortoiliac thrombus in a 5-day-old Quarter been observed with doses greater than 4000 horse filly. The foal was subsequently euthanized mg of formalin (>40 mL of 10% formalin) in due to deterioration of its condition and the lack experimental studies.50 These signs abated after of reperfusion of the hindlimbs.43 Streptokinase discontinuation of administration. Although does not activate equine plasminogen, thus limit- anecdotal reports have suggested positive ing its use in horses.29 results with the use of formalin, one study Based on a review of case reports involv- found no difference in coagulation profi les ing vascular thrombosis, a poor prognosis is between healthy horses administered IV forwarranted once arterial thrombosis occurs, as malin and the control group.49,50 It was sugno resolution of vessel thrombosis has been gested that the vasoconstrictive response to documented and all horses died or were eutha- hypovolemia along with cytokines and inflamnized.30,32,43,45–47 Poor resolution of thromboembo- matory mediators present in hemorrhaging lic disease in horses may be due to the delayed horses may enhance the effects of formalin recognition and treatment of thrombosis, inap- administration. This may explain the lack of propriate dosing and frequency of thrombolytic response in healthy horses.50 Aminocaproic acid and tranexamic acid medications, inappropriate delivery methods, and a lack of adjunctive therapies, such as inter- are synthetic derivatives of lysine that inhibit ventional (mechanical thrombectomy) and surgi- fibrinolysis primarily by binding and inhibiting plasminogen activation and, to a lesser cal procedures.

CriticalPo nt While numerous medications have been used as anticoagulants or antifibrinolytics in horses in various clinical situations, the efficacy of these efforts is largely undefined.

Despite this, theoretical benefits of these medications may justify their use until controlled studies can be completed.

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FREE CE Modifying the Coagulation Cascade: Available Medications

TABLE 1

Suggested Medications and Doses for Modifying the Coagulation Cascade in Equine Patients

Medication

Uses/Indications

Suggested Dose

Reference

UFH

Prevention of abdominal adhesions

20–120 U/kg q6–24h systemic or 15,000–50,000 U intraperitoneal

Southwood and Baxter7

40 U/kg IV during surgery, SC immediately after surgery, then q12h for 48 hr after surgery

Parker et al9

80 U/kg SC q12h for 72 hr (foals)

Sullins et al12

66 U/kg SC q12h for 72 hr

Young et al11

30,000–50,000 U in 10 L lavage fluid, intraperitoneal

Eggleston and Mueller10

Prevention or treatment of DIC

40–90 U/kg SC q8h

Welch et al14

Prevention or treatment of hypercoagulable disease or DIC

400 U/L IV of equine plasma

Darien20

Prevention of laminitis associated with proximal enteritis

40–110 U/kg q8–12h systemic

Cohen et al26

Prevention of thrombophlebitis or further extension of existing thrombi

20–40 U/kg SC q12h

Morris17

Prevention of organ thrombosis (secondary to severe infectious colitis)

40 U/kg preincubated with equine plasma, IV

Divers27

Prophylactic anticoagulant therapy

Dalteparin: 50 U/kg SC q24h

Feige et al34

Enoxaparin: 40 U/kg SC q24h

Schwarzwald et al35

Prophylactic therapy in patients at high risk of thrombotic disease

Dalteparin: 100 U/kg SC q24h Enoxaparin: 80 U/kg SC q24h

Schwarzwald et al35

Hirudin

Prophylaxis and treatment of thrombotic disease

0.5–1 mg/kg SC q12h

Feige et al36

Aspirin

Prevention or treatment of DIC

15–100 mg/kg PO q8–12h or 30 mg/kg PO q24–48h

Dallap18

20 mg/kg per rectum

Broome et ala

17 mg/kg PO q24–48h

Morris17

5–10 mg/kg PO q24–48h

Brumbaugh et al3

20 mg/kg PO every 4–5 days

Brumbaugh et al3

Prevention or treatment of laminitis

0.0198 mg/kg PO q24h Monitor one-step prothrombin time until prolonged 2–4 sec beyond baseline

Brumbaugh et al3

Prevention or treatment of navicular syndrome

0.018 mg/kg PO q24h Increase dose by 20% until 2–4 sec increase in one-step prothrombin time

Colles41

Urokinase

Thrombolysis

4000 U/min IV for 60 min

Forrest el al45

Tissue plasminogen activator

Thrombolysis

2 mg IV

Duggan et al43

Formalin

Control of hemorrhage

10–150 mL of 10% buffered formalin diluted in 1 L of isotonic fluids, IV

Jones,49 Taylor et al50

Aminocaproic acid

Control of hemorrhage

100 mg/kg IV

Heidmann et al52

Tranexamic acid

Control of hemorrhage

5 g IV q12h 10 g PO q6h

Dechantb

Conjugated estrogens

Control of hemorrhage

3 mg/kg divided over 5 consecutive days, IV or 0.6 mg/kg IV q24h for 5 days (dose used in people)

Livio et al56

25–50 mg IV or IM

Dechantb

LMWH

Treatment of acute laminitis Warfarin

a

Broome TA, Brown MP, Gronwall RR, et al. Pharmacokinetics and plasma concentrations of acetylsalicylic acid after intravenous, rectal, and intragastric administration to horses.

Can J Vet Res 2003;67:297-302.

b

Personal communication, Dr. Julie Dechant, School of Veterinary Medicine, University of California, Davis (September 2006).

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CriticalPo nt Hemorrhage from smaller vessels may be minimized by the administration of aminocaproic or tranexamic acid, particularly when a patient is in a hypotensive state and/or direct mechanical control of bleeding can be instituted.

degree, by enhancing α2-antiplasmin activity51,52 (FIGURE 2). Antifibrinolytic activity is believed to be limited to clot maintenance and stabilization, with no major effect on promoting clot formation through the intrinsic or extrinsic coagulation pathways. In the human literature, there are mixed reviews on the efficacy of aminocaproic acid for minimizing bleeding, but beneficial effects have been demonstrated in controlling intra- or postoperative bleeding and traumatic hyphema.53,54 No controlled clinical studies have investigated the efficacy of aminocaproic acid and tranexamic acid in hemorrhaging horses. It is unlikely that either medication alone could control blood loss from large vessels in normotensive horses.

However, hemorrhage from smaller vessels may be minimized by the administration of aminocaproic or tranexamic acid, particularly when a patient is in a hypotensive state and/ or direct mechanical control of bleeding can be instituted.52 In one study involving healthy horses, aminocaproic acid was administered once at 30 or 100 mg/kg IV; the results demonstrated modest but significantly higher α2-antiplasmin activity and lower fibrinogen concentrations compared with baseline values at the 100-mg/kg dose.52 Drug administration was well tolerated, and the effects lasted up to 5 hours after administration. These findings were consistent with the antifibrinolytic effects of aminocaproic acid, and the authors stated that clinical use may benefit some horses.52 Tranexamic acid is approximately 10 times more potent and has a longer half-life than aminocaproic acid, but it has been used too infrequently in horses with hemoperitoneum to confirm its possible advantages.51,55 Bleeding is a common complication in uremic people, but the cause remains unclear.56 Conjugated estrogens have been used perioperatively and in uremic people to shorten prolonged bleeding times and reduce or stop bleeding, but the exact mechanism of action is unknown. Conjugated estrogens may facilitate hemostasis by reducing capillary and arteriolar permeability through polymerization of mucopolysaccharides in vessel walls

and/or by possibly decreasing antithrombin activity.57 Studies have documented shortened bleeding times in uremic people administered conjugated estrogens, with onset of action noted within 6 hours of administration and a maximum effect between 5 and 7 days (total duration of action: 14 days).56 The prolonged effects of conjugated estrogens make these agents attractive for situations in which long-lasting hemostasis is required (i.e., reduction of bleeding during elective surgery, recurrent episodes of bleeding).51 One human study demonstrated decreased need for intraoperative administration of erythrocytes, plasma, and platelets in liver transplant recipients treated with conjugated estrogens at the beginning of surgery compared with the control group.57 These results suggested a possible benefit of the administration of conjugated estrogens in patients who undergo surgery in which significant blood loss is anticipated.

Similar to tranexamic acid, conjugated estrogens have been used to facilitate hemostasis in horses with hemoperitoneum, but the efficacy is unknown.55

Conclusion Many clinical situations in equine practice warrant the use of adjunctive medications to promote or inhibit the coagulation cascade.

While numerous medications have been used as anticoagulants or antifibrinolytics in horses in various clinical situations, the efficacy of these efforts is largely undefined. Despite this, theoretical benefits of these medications may justify their use until controlled studies can be completed. TABLE 1 provides a summary of the drugs, dosages, and indications of the medications discussed in this article.

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References 1. Weitz JI. Low-molecular-weight heparins. N Engl J Med 1997; 337:688-698.

2. Moore BR, Hinchcliff KW. Heparin: a review of its pharmacology

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and therapeutic use in horses. J Vet Intern Med 1994;8:26-35.

3. Brumbaugh G, Lopez H, Sepulveda M. The pharmacologic basis for the treatment of developmental and acute laminitis. Vet Clin

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Modifying the Coagulation Cascade: Available Medications CE North Am Equine Pract 1999;15:345-362.

4. Monreal L, Villatoro AJ, Monreal M, et al. Comparison of the effects of low-molecular-weight and unfractionated heparin in horses. Am J Vet Res 1995;56:1281-1285.

5. Byun Y, Singh VK, Yang VC. Low molecular weight protamine: a potential nontoxic heparin antagonist. Thromb Res 1999;94:53-61.

6. Chu AJ, Wang ZG, Raicu M, et al. Protamine inhibits tissue factor– initiated extrinsic coagulation. Br J Haematol 2001;115:392-399.

7. Southwood LL, Baxter GM. Current concepts in management of abdominal adhesions. Vet Clin North Am Equine Pract 1997;13:415-435.

8. Thompson J. Pathogenesis and prevention of adhesion formation. Dig Surg 1998;15:153-157.

9. Parker JE, Fibini SL, Car BD, et al. Prevention of intraabdominal adhesions in ponies by low-dose heparin therapy. Vet Surg 1987;16: 459-462.

10. Eggleston RB, Mueller PO. Prevention and treatment of gastrointestinal adhesions. Vet Clin North Am Equine Pract 2003;19:741-763.

11. Young DR, Richardson DW, Markel MD. The effect of low dose heparin therapy on complication and survival rates in horses following exploratory celiotomy. Equine Vet J Suppl 1989;(7):91-93.

12. Sullins KE, White NA, Lundin CS, et al. Prevention of ischaemiainduced small intestinal adhesions in foals. Equine Vet J 2004;36: 370-375.

13. Levi M, Ten Cate H. Disseminated intravascular coagulation. N Engl J Med 1999;341:586-592.

14. Welch RD, Watkins JP, Taylor TS, et al. Disseminated intravascular coagulation associated with colic in 23 horses (1984-1989). J Vet Intern Med 1992;6:29-35.

15. Barton MH, Morris DD, Norton N, et al. Hemostatic and fibrinolytic indices in neonatal foals with presumed septicemia. J Vet Intern Med 1998;12:26-35.

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

17. Morris DD. Recognition and management of disseminated intravascular coagulation in horses. Vet Clin North Am Equine Pract 1988;4:115-143.

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

19. Zhang Y, Scandura JM, Van Nostrand WE, et al. The mechanism by which heparin promotes the inhibition of coagulation factor XIa by protease nexin-2. J Biol Chem 1997;272:26139-26144.

20. Darien BJ. Heparin therapy: rationale and clinical indications.

Compend Contin Educ Pract Vet 1993;15:1273-1276.

21. Kienast J, Juers M, Wiedermann CJ, et al. Treatment effects of high-dose antithrombin without concomitant heparin in patients with severe sepsis with or without disseminated intravascular coagulation.

J Thromb Haemost 2006;4:90-97.

22. Iba T, Kidokoro A, Fukunaga M, et al. Antithrombin ameliorates endotoxin-induced organ dysfunction more efficiently when combined with danaparoid sodium than with unfractionated heparin. Intensive Care Med 2005;31:1101-1108.

23. Weiss DJ, Evanson OA, McClenahan D, et al. Effect of a competitive inhibitor of platelet aggregation on experimentally induced laminitis in ponies. Am J Vet Res 1998;59:814-817.

24. Stashak T. The foot. In: Stashak T, ed. Adam’s Lameness in Horses.

5th ed. Philadelphia: Lippincott Williams & Wilkins; 2002:645-664.

25. Belknap JK, Moore JN. Evaluation of heparin for prophylaxis of equine laminitis: 71 cases (1980-1986). JAVMA 1989;195:505-507.

26. Cohen ND, Parson EM, Seahorn TL, et al. Prevalence and factors associated with development of laminitis in horses with duodenitis/ proximal jejunitis: 33 cases (1985-1991). JAVMA 1994;204:250-254.

27. Divers TJ. Prevention and treatment of thrombosis, phlebitis, and laminitis in horses with gastrointestinal diseases. Vet Clin North Am Equine Pract 2003;19:779-790.

28. Morris DD, Beech J. Disseminated intravascular coagulation in six horses. JAVMA 1983;183:1067-1072.

29. Morris D. Thrombophlebitis in horses: the contribution of hemostatic dysfunction to pathogenesis. Compend Contin Educ Pract Vet 1989;11:1386-1395.

30. Brianceau P, Divers TJ. Acute thrombosis of limb arteries in horses with sepsis: five cases (1988-1998). Equine Vet J

2001;33:105-109.

31. Carr EA, Carlson GP, Wilson WD, et al. Acute hemorrhagic pulmonary infarction and necrotizing pneumonia in horses: 21 cases (1967-1993). JAVMA 1997;210:1774-1778.

32. Triplett EA, O’Brien RT, Wilson DG, et al. Thrombosis of the brachial artery in a foal. J Vet Intern Med 1996;10:330-332.

33. Davidson BL. Risk assessment and prophylaxis of venous thromboembolism in acutely and/or critically ill patients. Haemostasis 2000;30(suppl 2):77-81.

34. Feige K, Schwarzwald CC, Bombeli T. Comparison of unfractioned and low molecular weight heparin for prophylaxis of coagulopathies in 52 horses with colic: a randomised double-blind clinical trial. Equine Vet J 2003;35:506-513.

35. Schwarzwald CC, Feige K, Wunderli-Allenspach H, et al. Comparison of pharmacokinetic variables for two low-molecular-weight heparins after subcutaneous administration of a single dose to horses.

Am J Vet Res 2002;63:868-873.

36. Feige K, Dennler M, Kastner SB, et al. Pharmacokinetics of recombinant hirudin in healthy horses. Equine Vet J 2004;36:135-141.

37. Cambridge H, Lees P, Hooke RE, et al. Antithrombotic actions of aspirin in the horse. Equine Vet J 1991;23:123-127.

38. Hovens MM, Snoep JD, Tamsma JT, et al. Aspirin in the prevention and treatment of venous thromboembolism. J Thromb Haemost 2006;4:1470-1475.

39. Heath MF, Evans RJ, Poole AW, et al. The effects of aspirin and paracetamol on the aggregation of equine blood platelets. J Vet Pharmacol Ther 1994;17:374-378.

40. Scott EA, Byars TD, Lamar AM. Warfarin anticoagulation in the horse. JAVMA 1980;177:1146-1151.

41. Colles CM. A preliminary report on the use of warfarin in the treatment of navicular disease. Equine Vet J 1979;11:187-190.

42. 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;7:380-385.

43. Duggan VE, Holbrook TC, Dechant JE, et al. Diagnosis of aortoiliac thrombosis in a Quarter horse foal using Doppler ultrasound and nuclear scintigraphy. J Vet Intern Med 2004;18:753-756.

44. Razavi MK, Lee DS, Hofmann LV. Catheter-directed thrombolytic therapy for limb ischemia: current status and controversies. J Vasc Interv Radiol 2003;14:1491-1501.

45. Forrest LJ, Cooley AJ, Darien BJ. Digital arterial thrombosis in a septicemic foal. J Vet Intern Med 1999;13:382-385.

46. Moore LA, Johnson PJ, Bailey KL. Aorto-iliac thrombosis in a foal. Vet Rec 1998;142:459-462.

47. Spier S. Arterial thrombosis as the cause of lameness in a foal.

JAVMA 1985;187:164-165.

48. Doyle AJ, Freeman DE, Rapp H, et al. Life-threatening hemorrhage from enterotomies and anastomoses in 7 horses. Vet Surg 2003;32:553-558.

49. Jones W. IV formalin to control hemorrhage. J Equine Vet Sci 1998;18:581.

50. Taylor EL, Sellon DC, Wardrop KJ, et al. Effects of intravenous administration of formaldehyde on platelet and coagulation variables in healthy horses. Am J Vet Res 2000;61:1191-1196.

51. Mannucci PM. Hemostatic drugs. N Engl J Med 1998;339:245-253.

52. Heidmann P, Tornquist SJ, Qu A, et al. Laboratory measures of hemostasis and fibrinolysis after intravenous administration of epsilon-aminocaproic acid in clinically normal horses and ponies.

Am J Vet Res 2005;66:313-318.

53. Pieramici DJ, Goldberg MF, Melia M, et al. A phase III, multicenter, randomized, placebo-controlled clinical trial of topical aminocaproic acid (Caprogel) in the management of traumatic hyphema. Ophthalmology 2003;110:2106-2112.

54. Tobias JD. Strategies for minimizing blood loss in orthopedic surgery. Semin Hematol 2004;41:145-156.

55. Dechant JE, Nieto JE, Le Jeune SS. Hemoperitoneum in horses: 67 cases (1989-2004). JAVMA 2006;229:253-258.

56. Livio M, Mannucci PM, Vigano G, et al. Conjugated estrogens for the management of bleeding associated with renal failure. N Engl J Med 1986;315:731-735.

57. Erstad BL. Systemic hemostatic medications for reducing surgical blood loss. Ann Pharmacother 2001;35:925-934.

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FREE CE Modifying the Coagulation Cascade

3 CE

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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.

CREDITS

1. The primary mechanism of action of heparin is a. to block interaction of plasminogen with TPA. b. inactivation of thrombin and factor Xa. c. inactivation of factor VII. d. suppression of antithrombin.

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2. A common adverse effect of heparin administration in horses is a. leukopenia. b. leukocytosis. c. hypofibrinogenemia. d. anemia.

3. LMWH combines with antithrombin; together, the complex has the greatest affinity to bind to a. factor VIa. b. thrombin. c. factor Xa. d. factor XII. 4. The anticoagulant activity of hirudin results from direct inhibition of a. factor X. b. plasminogen. c. antithrombin. d. thrombin.

5. Aspirin a. inhibits cyclooxygenase and lipoxygenase. b. has profound analgesic properties at low doses. c. inhibits platelet aggregation. d. has a long half-life in horses.

6. Which coagulation factor is not blocked by the actions of warfarin? a. VI b. VII c. IX d. X 7. Fibrinolytic medications such as urokinase promote clot resolution by facilitating conversion of a. prothrombin to thrombin. b. fibrinogen to fibrin. c. plasminogen to plasmin. d. antithrombin to thrombin.

8. Which adverse effect is not associated with the administration of formalin? a. tachycardia b. serous ocular and nasal discharge c. muscle tremors d. petechiae 9. Aminocaproic acid and tranexamic acid inhibit fibrinolysis by a. inhibiting plasminogen activation. b. inhibiting α2-antiplasmin activity. c. promoting plasminogen activation. d. promoting thrombin formation.

10. The procoagulant activity of conjugated estrogens arises from a. inhibition of TPA activity. b. blockage of fibrin from the plasminogen binding site. c. inhibition of antithrombin activity. d. none of the above; the exact mechanism is unknown.

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JOINT HEALTH

MANAGEMENT

RUB.

INJECT.

RELIEVE.

THE CHOICE IS UP TO YOU.

SURPASS® is a trusted name for effective FRQWURO RI SDLQ DQG LQÁDPPDWLRQ DVVRFLDWHG with osteoarthritis in hock, knee, fetlock and pastern joints in horses.

i ® combines Hyvisc bi hi high h molecular l l weight i ht with extremely low levels of extraneous protein, offering your horse a pure, dependable treatment for joint dysfunction.

Boehringer Ingelheim Vetmedica Inc. is proud to provide the veterinarian with these two distinct Joint Health Management products.

1-866-638-2226 WWW.BI-VETMEDICA.COM

As with any prescription medication, prior to use, a veterinarian should review the medical history of the horse and perform a physical examination. Observe for signs of potential drug toxicity. As a class, nonsteroidal anti-inflammatory drugs may be associated with gastrointestinal and renal toxicity. Consult full package insert for information regarding use.

In the clinical trial, as is common with intra-articular injection, a mild inflammatory response was observed post-injection. Care should be taken to ensure aseptic technique. There are no known contraindications to the use of Hyvisc.

Surpass® is a registered trademark of Boehringer Ingelheim Vetmedica, Inc. © 2008 Boehringer Ingelheim Vetmedica, Inc. All rights reserved

See Page 238 for Product Information Summary

NADA 141-186, Approved by FDA Veterinary Package Insert

Surpass® (1% diclofenac sodium) Topical Anti-Inflammatory Cream For Use in Horses Caution: Federal law restricts this drug to use by or on the order of a licensed veterinarian.

Description: Surpass® topical cream contains 1% diclofenac sodium. Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) of the phenylacetic acid class. The chemical name for diclofenac is sodium [o- (2,6-dichloroanilino)phenyl]acetate. The empirical formula is C14H10Cl2NNaO2 and the molecular weight is 318.13. Surpass topical cream contains 1% diclofenac sodium in a base composed of Phospholipon 90H, propylene glycol, alcohol (5.94%), vitamin E acetate, benzethonium chloride and purified water in the Wisdom® liposomal formulation.

Indications: Surpass topical cream is indicated for the control of pain and inflammation associated with osteoarthritis (OA) in tarsal, carpal, metacarpophalangeal, metatarsophalangeal and proximal interphalangeal (hock, knee, fetlock and pastern) joints in horses.

Dosage and Administration: Always provide the Client Information Sheet with the prescription.

Dosage: Apply a five-inch (5”) ribbon of Surpass topical cream twice daily over the affected joint for up to ten days.

Administration: Wear rubber gloves to prevent absorption into the hands. Rub the cream thoroughly into the hair covering the joint until it disappears.

Contraindications: Surpass topical cream is contraindicated in animals with known hypersensitivity to diclofenac.

Warnings: Not for horses intended for human consumption.

User Safety: Keep out of reach of children. Not for human use. Consult a physician in case of accidental ingestion by humans.

Wear gloves to prevent absorption into the hands. Direct contact with the skin should be avoided. If contact occurs, the skin should be washed immediately with soap and water.

Animal Safety: For topical use in horses only. Owners should be advised to observe for signs of potential drug toxicity (see Information for Owner or Person Treating Animal and Adverse Reactions).

Precautions: Exceeding the recommended dosage or treating multiple joints may increase plasma concentrations of diclofenac (see Animal Safety). The systemic effects of excess diclofenac doses that exceed the recommended label amount and duration have not been evaluated.

Horses should undergo a thorough history and physical examination before initiation of NSAID therapy. Appropriate laboratory tests should be conducted to establish hematological and serum biochemical baseline data before and periodically during administration of any NSAID. Owners should be advised to observe for signs of potential drug toxicity (see Information for Owner or Person Treating Animal).

Treatment with Surpass cream should be terminated if signs such as inappetence, colic, fecal abnormalities, anemia or depression are observed.

As a class, NSAIDs may be associated with gastrointestinal and renal toxicity. When NSAIDs inhibit prostaglandins that cause inflammation, they may also inhibit prostaglandins that maintain normal homeostatic function. These anti-prostaglandin effects may result in clinically significant disease in patients with underlying or preexisting disease more often than in healthy patients. Patients at greatest risk for renal toxicity are those that are dehydrated, on concomitant diuretic therapy, or those with renal, cardiovascular and/or hepatic dysfunction.

Studies to determine the effect of Surpass topical cream when administered concomitantly with other drugs have not been conducted.

Since many NSAIDs possess the potential to induce gastric ulceration, concomitant use of Surpass cream with any other anti-inflammatory drugs, such as other NSAIDs and corticosteroids, should be avoided. Drug compatibility should be monitored closely in patients receiving adjunctive therapy.

The safety of Surpass cream has not been investigated in breeding, pregnant or lactating horses, or in horses under one year of age.

Adverse Reactions: During the field study, one diclofenac-treated horse developed colic on day four of the study and responded to symptomatic treatment. One placebo-treated horse exhibited mildly jaundiced mucous membranes on day five. Adverse reactions during the safety study included a gastric ulcer in one horse that received 5.6X the recommended dosage, diarrhea and uterine discharge in one horse that received 2.8X the recommended dosage, and weight loss in four of the six horses in the 5.6X dosage group.

To report suspected adverse reactions, to obtain a Material Safety Data Sheet or for technical assistance, call 1-866-638-2226.

Information for Owner or Person Treating Animal: Owners should be advised of the potential for adverse reactions and be informed of the clinical signs associated with NSAID intolerance. Adverse reactions may include: weight loss, colic, diarrhea, or icterus. Serious adverse reactions associated with this drug class can occur without warning and, in rare situations, result in death. Owners should be advised to discontinue NSAID therapy and contact their veterinarian immediately if signs of intolerance are observed. The majority of patients with drug-related adverse reactions recover when the signs are recognized, drug administration is stopped, and veterinary care is initiated.

Clinical Pharmacology: Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) with analgesic properties. The mechanism of action of diclofenac, like other NSAIDs, is believed to be associated with the inhibition of cyclooxygenase activity.

Effectiveness: In a controlled field study, 82 horses with osteoarthritis were treated with Surpass topical cream (42 horses) or placebo (40 horses). Lameness examinations were performed in horses with osteoarthritis associated with the tarsal, carpal, metacarpophalangeal, metatarsophalangeal and proximal interphalangeal joints. Investigators were masked to treatment. Investigators and owners were instructed to apply the test article over the affected joint twice daily (BID) for five days. Actual doses received by individual horses were calculated using tube weight measurements. The mean dose applied during the study was 73 mg per application. Average lameness scores showed statistically significant improvement following treatment with Surpass topical cream.

One diclofenac-treated horse developed colic and responded to symptomatic treatment on day four of the study. Day five bloodwork for the horse that colicked showed decreases in RBC, Hb and HCT, with an increase in PMNs, compared to pretreatment values. One placebotreated horse exhibited mildly jaundiced mucous membranes on day five. No other adverse reactions were noted during the study.

Animal Safety: A controlled safety study was conducted with Surpass topical cream. Four groups of six healthy adult horses received 0, 0.6, 1.7 or 2.8X the recommended daily dose for twenty-eight days. The daily dose was divided into two applications on day one of the study. For the remainder of the study, the entire daily dose was given at one time on 0, 1, 3 or 5 joints (tarsal, carpal, metacarpophalangeal, metatarsophalangeal, and proximal interphalangeal joints), depending on the dosage group. The control group of six horses was shamdosed by rubbing the joints daily for twenty-eight days. An additional study group evaluated six horses that received 5.6X the recommended daily dose of Surpass topical cream distributed over five joints on a single day. This dose group was observed for fourteen days without additional treatment.

Clinical examinations, hematology, serum chemistry, synovial fluid analyses, gross necropsy and histopathology were performed. At necropsy, one horse in the 5.6X group had a glandular gastric ulcer. A horse in the 2.8X group had diarrhea and uterine discharge throughout the study.

Four of the six horses in the 5.6X group lost weight during the study.

Dose-dependent increases in diclofenac plasma concentrations were detected in horses in the 1.7X and 2.8X treatment groups.

Storage Information: Store at up to 25°C (77°F). Protect from freezing.

How Supplied: Surpass topical cream is white to pinkish-white and is packaged in 124-gram trilaminate tubes.

Surpass and Wisdom are registered trademarks of Boehringer Ingelheim Vetmedica, Inc. Manufactured for: Boehringer Ingelheim Vetmedica, Inc., St. Joseph, MO 64506 U.S.A. Manufactured under U.S. Patent Nos. 4,937,078 and 6,936,273. © 2009 Boehringer Ingelheim Vetmedica, Inc. All Rights Reserved.

449801L-00-0901 Revised 01/2009 Code 449811

+\YLVF

11 mg/mL (hyaluronate sodium) STERILE INJECTION For intra-articular injection in horses only.

DESCRIPTION: Hyvisc® (hyaluronate sodium) is a clear, colorless, viscous fluid contained in a 5 mL disposable syringe, as a single 2 mL dose. Chemically, hyaluronic acid is a high molecular weight mucopolysaccharide composed of repeating di-saccharide units, each unit consisting of D-glucuronic acid and N-acetylD-glucosamine. Each mL of Hyvisc® Injection contains 11 mg of hyaluronate sodium and 8.47 mg of sodium chloride, U.S.P., in sterile water for injection, U.S.P., q.s.

ACTIONS: Hyaluronate sodium is a natural constituent of connective tissue and synovial fluid in both man and animals. In synovial fluid, hyaluronate sodium confers viscoelastic as well as lubricating properties (1-2). In connective tissue, hyaluronate sodium specifically interacts with cartilage proteoglycans to form stable aggregates (3-5). The mechanism of action by which exogenous hyaluronate sodium exerts its therapeutic effect in arthritic joints is not known at this time.

INDICATIONS: Hyvisc® (hyaluronate sodium) Injection is recommended for the treatment of joint dysfunction in horses due to non-infectious synovitis associated with equine osteoarthritis.

CONTRAINDICATIONS: There are no known contraindications to the use of Hyvisc® (hyaluronate sodium) Injection.

WARNINGS: Not for use in horses intended for food. Hyvisc® (hyaluronate sodium) Injection must not be administered intravascularly.

ADVERSE REACTIONS: In the clinical trial with Hyvisc® (hyaluronate sodium) Injection, a mild, transient post-injection inflammatory response in the joint was reported in 12% of the cases treated. There were no other side effects.

DOSAGE AND ADMINISTRATION: The recommended dose of Hyvisc® (hyaluronate sodium) Injection is 2 mL (22 mg) given to horses intra-articularly in small and medium-sized joints (carpal, fetlock). In larger joints (hock), the dosage is 4 mL (44 mg).

Treatment may be repeated at weekly intervals for a total of three treatments. As with any intra-articular injection, aseptic technique is used. The following are suggested use directions regardless of the type of joint to be treated.

1. Carefully diagnose each case using routine methods. The origin of lameness should be pinpointed to be within a specific joint or joints (e.g., lameness is localized to a specific joint using intra-articular anesthesia). Radiographs or other diagnostic aids should not reveal recent fractures or other serious abnormalities which would suggest a poor prognosis.

2. Aseptically remove as much synovial fluid from the afflicted joint as can be easily withdrawn.

3. Remove tip cap from the Hyvisc® syringe and inject through a sterile needle, 20 gauge or larger.

4. Inject a single 2 mL dose (one syringe) of Hyvisc® into each joint to be treated; if the joint being treated is the hock joint, inject 4 mL (two syringes). Since Hyvisc® is a viscous fluid, care should be exercised on injection so as not to dislodge the needle from the syringe.

5. Two or four days of rest or light exercise is recommended before resumption of normal activity. Improvement of joint function should be seen within one to two weeks after Hyvisc® Injection.

As with any intra-articular injection, a mild inflammatory response (tenderness, heat and swelling) may be seen in the joint following the Hyvisc® Injection. This response is self-limiting, but may last from two to five days after treatment. If inflammation is excessive or severe, the possibility of infection should be considered and appropriate antibiotic therapy instituted.

CAUTION: Federal Law restricts this drug to use by or on the order of a licensed veterinarian.

Used or partially used syringes should be crushed and disposed of in an appropriate landfill.

Do not use if numerous small air bubbles are present throughout the solution.

STORAGE: Store under refrigerated conditions. Protect from freezing and avoid excessive heat.

HOW SUPPLIED: Hyvisc® (hyaluronate sodium) Injection, 11 mg/mL, is available in 2 mL prefilled, disposable syringes individually packaged.

SAFETY MARGIN IN HORSES: In toxicity studies of Hyvisc® (hyaluronate sodium) Injection in horses, intra-articular doses at one, three, and five times the recommended dose once weekly for three consecutive weeks did not result in any drug related local or systemic toxic effects. The mild transient post-injection inflammatory response observed within the joints of some horses was qualitatively and quantitatively similar to that detected in the physiologic saline injected controls. In a reproductive study in mares, 16 mL of Hyvisc® (10 mg/mL) injected intramuscularly or subcutaneously once or twice during the second or third stage of pregnancy resulted in no adverse effects on the mares or newborn foals.

REFERENCES: 1. Radin, E.L. et al: Annals of the Rheumatic Diseases, 30: 322325, (1971).

2. Swann, D.A. et al: Annals of the Rheumatic Diseases, 33: 318326, (1974).

3. Hardingham, T.E. and H. Muir: Biochemical et Biophysica Acta, 279: 401-405, (1972).

4. Hascall, V.C. and D. Heingard: Journal of Biological Chemistry, 249: 423-433, (1974).

5. Brandt, K.D. et al: Arthritis and Rheumatism, 19: 1308-1314, (1976).

Hyvisc® registered trademark of Anika Therapeutics, Inc. Manufactured by: Anika Therapeutics, Inc. Woburn, Massachusetts 01801 U.S.A. Distributed by: Boehringer Ingelheim Vetmedica, Inc. St. Joseph, MO 64506 U.S.A.

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We invite the submission of clinical and laboratory research manuscripts in small animal, large animal, and comparative medicine, including pathophysiology, diagnosis, treatment, and prognosis.

Prospective, retrospective, and corroborative studies are all welcome. Submitted articles are scheduled to be published 90 to 120 days after acceptance.

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Compounding Pharmacy Potomavac Recombitek Dormosedan Platinum Performance Complete Joint WellSolve L/S Horse Feed Surgery Tables Triple Crown Low Starch MYLAB Ultrasound, UMS 900, TERAVET T3000 Veterinary Therapeutics

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The Final Diagnosis ❯❯ James N. Moore, DVM, PhD, The University of Georgia

Face it, We’re Aneuronal

O

kay, I freely admit it—I’m an idiot.

But it appears that I’m not alone.

Not by a long shot.

Take, for instance, my recent habit of spending four bucks for a cup of warmed skim milk laced with a bit of decaffeinated coffee and a packet or two of sweetener. When did we switch from “small, medium, and large” to “tall, venti, and grande”? Is the exorbitant cost somehow offset by using two languages to order these things, or does this finally make Americans multilingual? I’d prefer to believe the latter. Prego.

If you’re still unconvinced that, collectively, we’re missing some marbles, all you have to do is fly somewhere.

Okay, I freely admit it—I’m an idiot.

But it appears that I’m not alone.

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

CompendiumEquine.com

240

Anywhere. Arrive at your gate a couple of minutes early, as I usually do, and watch what happens when the person at the counter announces, “Now boarding zone one. Passengers with boarding passes for zone one only.” What happens?

Every knucklehead in zones two through seven immediately gets up and moves zombie-like, dragging suitcases and children until they’ve formed an impenetrable semicircle at the gate. Clearly, we’re convinced that Delta is somehow going to sneak away its plane with only the zone-one elite on board, leaving us to wander about, buying rolls of Mentos we don’t want and magazines we’ll never read. Then, at our destination, what do we do as soon as the plane arrives at the gate, before the flight attendant even has a chance to crack the door? You bet—we stand up. All 48 rows of us ... with absolutely no way out until the first 100 people or so have made it past the “Good-bye …

Good-bye … Good-bye” crew. Sheesh!

The final nail in the stupidity coffin was driven home for me this past fall on a trip to Oklahoma. Because I arrived earlier than expected at the Oklahoma City Airport, I had time to look around before my nephew Troy picked me up. Wandering out of the airport, I was immediately taken by the immenseness of the prairie, stretching horizon to horizon. Seeing this, I realized I’d never read The Grapes of Wrath, the American novel, the one that defined Oklahoma and the Great Depression. So I vowed to buy a copy in Stillwater and begin to fill that void in my life while I was right there where it all started.

The next day, while Troy was in class, I headed downtown to locate the book.

After the obligatory trek to Eskimo Joe’s, I found the off-campus bookstore—a large, two-room establishment populated by stacks and stacks of textbooks.

Concluding that I was probably wasting my time, I turned for the door.

“Can I help you, sir?” said a guy in his late twenties, coming out of an office behind me.

“Looks like you probably don’t have what I’m after,” I said, based on the lack of anything that looked like a novel.

“No harm in trying,” he replied, as he headed toward the cash register. “What are you after?”

“The Grapes of Wrath, but it doesn’t look like you’re going to have it.”

“You never know. Someone might be using it in a class this semester,” he offered as he booted up the computer to search his inventory. Having successfully logged onto his search engine, he looked me right in the eye and floored me with, “Author?”

Yep, there are a lot of us. But it isn’t all bad. The next time someone I haven’t met asks me to describe myself over the phone, I’m going to take a sip of my latte and say, “Well … I’m tall.”

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

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