Compendium Equine | April 2009

VOLUME 4 NUMBER 3 APRIL 2009

3 CE Contact Hours | CompendiumEquine.com | Peer Reviewed

Vol 4(3) April 2009

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Clinical Forum

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Imaging Is Believing Stifle Ultrasonography: A Case Study

Cu Ur ttin o g

Shock-Wave Sh kW Therapy

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COMPENDIUM EQUINE CONTINUING EDUCATION FOR VETERINARIANS®

Perinatal Asphyxia Syndrome in Foals

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

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

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

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

The benefits of POTOMAVAC also are available in Equine POTOMAVAC + IMRAB®, a combination vaccine that helps protect against rabies and Potomac horse fever. Best of all, both are backed

by Merial, a trusted leader in equine health.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Winning Gold is without a doubt the highlight of my 35 years of professional riding, a moment that wouldn't have happened without Carlsson. When I first saw him, I thought to myself: there's a horse with "a lot of blood." I knew we would pair well.

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Nothing more. Nothing less. © 2009 platinum performance, inc.

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April 2009 Vol 4(3)

Features 110

❯❯ Scott R. McClure Learn how to use shock-wave therapy for treating suspensory desmitis, damaged tendons and ligaments, musculoskeletal disorders, inflammation, and soft tissue disorders.

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CE

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

Clinical Forum Shock-Wave Therapy: How It Has Shocked or Bored Us

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Imaging Is Believing Stifle Ultrasonography: A Case Study ❯❯ Elizabeth Charles, Natasha Werpy, and Norman Rantanen Learn how ultrasonography can improve the likelihood of correctly diagnosing stifle injuries.

125 FREE

CE

134

Cutting to Cure Urolithiasis

NEW SERIES

❯❯ Alicia Foley, Sabrina H. Brounts, and Jan F. Hawkins This article reviews the diagnosis, treatment, and prognosis of urolithiasis in horses.

Feature Perinatal Asphyxia Syndrome in Foals ❯❯ Wendy E. Vaala With proper support, 70% to 80% of foals with this condition recover. This article can help you achieve the best results.

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The Final Diagnosis You Might Be a Mixed Animal Practitioner If … ❯❯ Ronald E. Gill If you show these signs of being a mixed animal practitioner, Dr. Gill considers you fortunate.

Departments 102 CompendiumEquine.com Cover image © 2009 R/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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Compendium Equine: Continuing Education for Veterinarians®

104 Editorial Keeping PACE: Positive Attitude Changes Everything ❯❯ P. O. Eric Mueller

106

Calendar C

❯❯ Amber L. Labelle and Ralph E. Hamor

116 Abstract Thoughts How Cell Membranes Work: Smoke on the Water ❯❯ David J. Hurley and James N. Moore

141 Product Forum Clinical Snapshot 107 A Quarter Horse Mare with a Cataract

142 Index to Advertisers 142 Classified Advertising

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FPO The best treatment for EGUS may be a dose of reality.

Equine Gastric Ulcer Syndrome (EGUS) caan easily become a reality for today’s horse. In fact, the majority of your clients’ racing and non-racing competittive horses could already be sufffering in silence with gastric ulcers.1,2 Clients come to o you for knowledge and tools they can’t get anywhere else. Training.

Experience. Diagnosis. Approved treatment. You havee the power to make the solution n for EGUS this simple.

Unique respon nse. Only GASTROGARD® (omeprazole) is FDA-approved to treeat gastric ulcers.

Unique ability.. Only you have the ability to prrovide diagnoses and GASTTROGARD. For information and EGUS educational tools, taalk with your Merial Sales Represeentative today. Or call 1-888--MERIAL-1.

Response.Ability.

CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian. GASTROGARD is indicated for the treatment and prevention of recurrence of gastric ulcers in horses and foals 4 weeks and older. In efficacy trials, no adverse reactions were observed. Safety in pregnant or lactating mares has not been determined. DO NOT USE IN HORSES INTENDED FOR HUMAN CONSUMPTION. KEEP THIS AND ALL DRUGS OUT OF THE REACH OF CHILDREN. Mitchell RD. Prevalence of gastric ulcers in hunter/jumper and dressage horses evaluated for poor performance. Association for Equine Sports Medicine. September 2001.

Murray MJ. Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc 1989;195(8):1135-1141.

1

2

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

See Page 105 for Product Information Summary

Editorial ❯❯ P. O. Eric Mueller, DVM, PhD, DACVS, The University of Georgia

P. O. Eric Mueller

Keeping PACE: Positive Attitude Changes Everything

I

f you’re like me, you’re getting tired of negative news regarding the economy. It’s amazing how many different business news analysts are required to tell us the economy is in a downturn with little evidence of recovery in the near future. In the Veterinary Medical Teaching Hospital at The University of Georgia, we have our own economic indicator called the Colic Surgery Standard and Poor Index (CSSPI).

A common thread among veterinary practices that prosper during economic downturns is particular attention to exemplary client service by doctors and staff.

During economic growth and prosperity, for every 10 horses admitted to the hospital requiring surgery to correct a gastrointestinal lesion, nine have surgery (CSSPI = 0.9 or 90%). During economic downturns, five or six of every 10 horses have surgery (CSSPI = 0.5 to 0.6 or 50% to 60%).

In this current downturn, it’s interesting that the number of horses admitted to our hospital for colic has not declined. It appears that owners are willing to have their horses evaluated and treated medically but aren’t willing to incur the

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additional expense of surgery ($4000 to $6000).

I’ve learned from colleagues across the country that this pattern is fairly representative of most academic and private veterinary referral institutions. Our CSSPI will likely remain low for the coming months.

I’m sure that as you make your calls, many horse owners mention the depressed economy.

This is where we can make a difference. There are several ways we can do our part to help turn around the economy. The first is our attitude. Some veterinarians can be pessimistic about the benefits of their career choice. How many times have you heard a veterinarian say the following to a potential veterinary student? “Have you thought about human medicine? You will make more money and have more time to yourself.” As a student, I considered a career in human medicine, but after a few summers working in a human hospital, I realized that most patients were cranky and the physicians constantly grumbled about the intricacies of insurance claims and copayments … not the most pleasant working environment. Therefore, more than 20 years ago, I chose a career in veterinary medicine, and I’ve never regretted it. I’ll bet if you honestly evaluate your lifestyle, accomplishments, and compensation, you’ll agree that you also made the right decision. As I learned from my children’s

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

Editorial first-grade teacher, Mrs. Telefson, ment, such as a digital radiography PACE: positive attitude changes every- unit, ultrasonography machine, or thing. So whether you’re talking to endoscope, now is the time to do a prospective veterinary student in it. Interest rates are low, financing your truck while making calls or to plans flexible, and prices favorable. If a client, try to emphasize the positive you’ve been considering renovating aspects of your career and current or expanding your clinic or building events. or buying a new hospital, now is the The most important aspect of any time to start. Service businesses such service-based business is service as veterinary medicine are perceived itself. In times of economic difficulty, favorably by lending institutions, clients spend money on goods and building material and labor costs are services that are valuable to them at 5-year lows, and interest rates for and reduce or eliminate expenses qualified customers are extremely they consider less valuable. A com- competitive. If all of us do our part mon thread among veterinary prac- to promote and maintain a positive tices that prosper during economic outlook, invest in our future, and downturns is particular attention to resist temptation to thoughtlessly folexemplary client service by doctors low the media’s negativity, we can at and staff. I often reiterate to veteri- least feel good about our efforts and nary students and house officers the assist in jumpstarting the recovery. following pillar of client service: Here’s some more good news: an although clients can be demanding informal survey of regional equine and occasionally irrational, they are practices that regularly refer cases always right (as long as fulfilling to our hospital indicates that most their requests does not compromise practices are as busy as ever. Sure, your moral principles), so “kill them” they had the usual decrease in calls with kindness and service. in the late fall and early winter, but When the economy begins to with spring here, business is on the recover, it will likely not be the direct upswing. Some veterinarians indiresult of any one stimulus package or cate that practice growth may not bailout. Recovery will happen when have been as robust in 2008 as in individuals with money to spend on previous years, but it didn’t decline. goods and services have the confi- I hope your practice is following a dence to spend it. History tells us that similar positive trend. We veterinarthe economy and financial markets ians are fortunate that we’ll always will bounce back. We just don’t know be gainfully employed unless we when. But it seems obvious that we’ll choose otherwise. So the next be waiting a long time if we do noth- time someone dwells on the ecoing and just wait for things to improve. nomic downturn, be grateful for Stimulus packages may help, but we all the good things in your life and must have a positive attitude and an remember Mrs. Telefson’s encouragoptimistic outlook for such pack- ing words: “PACE: positive attitude ages to have significant long-term changes everything.” effects. Therefore, those who can invest in goods SHARE YOUR COMMENTS and services should do so now. This may mean Have something to say about this hiring an additional techeditorial or topic? Let us know: nician, receptionist, or EMAIL editor@CompendiumEquine.com animal handler. If you’ve FAX 800-556-3288 been thinking about purchasing new equipApril 2009 | Compendium Equine: Continuing Education for Veterinarians®

105

Oral Paste for Horses and Foals NADA 141-123, Approved by FDA Caution Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

Description Chemical name: 5-Methoxy-2-[[(4-methoxy-3,5-dimethyl-2-pyridinyl) methyl]sulfinyl]-1H-benzimidazole.

Empirical formula: C17H19N3O3S. Molecular weight: 345.42. Structural formula: H3C

OCH3 CH3 O

OCH3 H

How Supplied GASTROGARD® (omeprazole) Paste for horses contains 37% w/w omeprazole and is available in an adjustable-dose syringe. Each syringe contains 2.28 g of omeprazole. Syringes are calibrated according to body weight and are available in boxes of 7 units or 72 units.

Storage Conditions Store at 68°F – 77°F (20-25°C). Excursions between 59°F – 86°F (15-30°C) are permitted.

Indications For treatment and prevention of recurrence of gastric ulcers in horses and foals 4 weeks of age and older.

Dosage Regimen For treatment of gastric ulcers, GASTROGARD Paste should be administered orally once-a-day for 4 weeks at the recommended dosage of 1.8 mg omeprazole/lb body weight (4 mg/kg). For the prevention of recurrence of gastric ulcers, continue treatment for at least an additional 4 weeks by administering GASTROGARD Paste at the recommended daily maintenance dose of 0.9 mg/lb (2 mg/kg).

Directions For Use • GASTROGARD Paste for horses is recommended for use in horses and foals 4 weeks of age and older. The contents of one syringe will dose a 1250 lb (568 kg) horse at the rate of 1.8 mg omeprazole/lb body weight (4 mg/kg). For treatment of gastric ulcers, each weight marking on the syringe plunger will deliver sufficient omeprazole to treat 250 lb (114 kg) body weight. For prevention of recurrence of gastric ulcers, each weight marking will deliver sufficient omeprazole to dose 500 lb (227 kg) body weight.

• To deliver GASTROGARD Paste at the treatment dose rate of 1.8 mg omeprazole/lb body weight (4 mg/kg), set the syringe plunger to the appropriate weight marking according to the horse’s weight in pounds.

• To deliver GASTROGARD Paste at the dose rate of 0.9 mg/lb (2 mg/kg) to prevent recurrence of ulcers, set the syringe plunger to the weight marking corresponding to half of the horse’s weight in pounds.

• To set the syringe plunger, unlock the knurled ring by rotating it 1/4 turn. Slide the knurled ring along the plunger shaft so that the side nearest the barrel is at the appropriate notch. Rotate the plunger ring 1/4 turn to lock it in place and ensure it is locked. Make sure the horse’s mouth contains no feed. Remove the cover from the tip of the syringe, and insert the syringe into the horse’s mouth at the interdental space. Depress the plunger until stopped by the knurled ring. The dose should be deposited on the back of the tongue or deep into the cheek pouch. Care should be taken to ensure that the horse consumes the complete dose. Treated animals should be observed briefly after administration to ensure that part of the dose is not lost or rejected. If any of the dose is lost, redosing is recommended.

• If, after dosing, the syringe is not completely empty, it may be reused on following days until emptied.

Replace the cap after each use.

Warning Do not use in horses intended for human consumption. Keep this and all drugs out of the reach of children. In case of ingestion, contact a physician. Physicians may contact a poison control center for advice concerning accidental ingestion.

Adverse Reactions In efficacy trials, when the drug was administered at 1.8 mg omeprazole/lb (4 mg/kg) body weight daily for 28 days and 0.9 mg omeprazole/lb (2 mg/kg) body weight daily for 30 additional days, no adverse reactions were observed.

Precautions The safety of GASTROGARD Paste has not been determined in pregnant or lactating mares.

Clinical Pharmacology Mechanism of Action: Omeprazole is a gastric acid pump inhibitor that regulates the final step in hydrogen ion production and blocks gastric acid secretion regardless of the stimulus. Omeprazole irreversibly binds to the gastric parietal cell’s H+, K+ ATPase enzyme which pumps hydrogen ions into the lumen of the stomach in exchange for potassium ions. Since omeprazole accumulates in the cell canaliculi and is irreversibly bound to the effect site, the plasma concentration at steady state is not directly related to the amount that is bound to the enzyme. The relationship between omeprazole action and plasma concentration is a function of the rate-limiting process of H+, K+ ATPase activity/turnover. Once all of the enzyme becomes bound, acid secretion resumes only after new H+, K+ ATPase is synthesized in the parietal cell (i.e., the rate of new enzyme synthesis exceeds the rate of inhibition).

Pharmacodynamics: In a study of pharmacodynamic effects using horses with gastric cannulae, secretion of gastric acid was inhibited in horses given 4 mg omeprazole/kg/day. After the expected maximum suppression of gastric acid secretion was reached (5 days), the actual secretion of gastric acid was reduced by 99%, 95% and 90% at 8, 16, and 24 hours, respectively.

Pharmacokinetics: In a pharmacokinetic study involving thirteen healthy, mixed breed horses (8 female, 5 male) receiving multiple doses of omeprazole paste (1.8 mg/lb once daily for fifteen days) in either a fed or fasted state, there was no evidence of drug accumulation in the plasma when comparing the extent of systemic exposure (AUC0-∞). When comparing the individual bioavailability data (AUC0-∞, Cmax, and Tmax measurements) across the study days, there was great inter- and intrasubject variability in the rate and extent of product absorption. Also, the extent of omeprazole absorption in horses was reduced by approximately 67% in the presence of food. This is evidenced by the observation that the mean AUC0-∞ values measured during the fifth day of omeprazole therapy when the animals were fasted for 24 hours was approximately three times greater than the AUC estimated after the first and fifteenth doses when the horses were fed hay ad libitum and sweet feed (grain) twice daily. Prandial status did not affect the rate of drug elimination. The terminal half-life estimates (N=38) ranged from approximately one-half to eight hours.

Efficacy Dose Confirmation: GASTROGARD® (omeprazole) Paste, administered to provide omeprazole at 1.8 mg/lb (4 mg/kg) daily for 28 days, effectively healed or reduced the severity of gastric ulcers in 92% of omeprazole-treated horses. In comparison, 32% of controls exhibited healed or less severe ulcers. Horses enrolled in this study were healthy animals confirmed to have gastric ulcers by gastroscopy. Subsequent daily administration of GASTROGARD Paste to provide omeprazole at 0.9 mg/lb (2 mg/kg) for 30 days prevented recurrence of gastric ulcers in 84% of treated horses, whereas ulcers recurred or became more severe in horses removed from omeprazole treatment.

Clinical Field Trials: GASTROGARD Paste administered at 1.8 mg/lb (4 mg/kg) daily for 28 days healed or reduced the severity of gastric ulcers in 99% of omeprazoletreated horses. In comparison, 32.4% of control horses had healed ulcers or ulcers which were reduced in severity. These trials included horses of various breeds and under different management conditions, and included horses in race or show training, pleasure horses, and foals as young as one month. Horses enrolled in the efficacy trials were healthy animals confirmed to have gastric ulcers by gastroscopy. In these field trials, horses readily accepted GASTROGARD Paste. There were no drug related adverse reactions. In the clinical trials, GASTROGARD Paste was used concomitantly with other therapies, which included: anthelmintics, antibiotics, non-steroidal and steroidal anti-inflammatory agents, diuretics, tranquilizers and vaccines.

Diagnostic and Management Considerations: The following clinical signs may be associated with gastric ulceration in adult horses: inappetence or decreased appetite, recurrent colic, intermittent loose stools or chronic diarrhea, poor hair coat, poor body condition, or poor performance.

Clinical signs in foals may include: bruxism (grinding of teeth), excessive salivation, colic, cranial abdominal tenderness, anorexia, diarrhea, sternal recumbency or weakness. A more accurate diagnosis of gastric ulceration in horses and foals may be made if ulcers are visualized directly by endoscopic examination of the gastric mucosa.

Gastric ulcers may recur in horses if therapy to prevent recurrence is not administered after the initial treatment is completed. Use GASTROGARD Paste at 0.9 mg omeprazole/lb body weight (2 mg/kg) for control of gastric ulcers following treatment. The safety of administration of GASTROGARD Paste for longer than 91 days has not been determined.

Maximal acid suppression occurs after three to five days of treatment with omeprazole.

Safety • GASTROGARD Paste was well tolerated in the following controlled efficacy and safety studies.

• In field trials involving 139 horses, including foals as young as one month of age, no adverse reactions attributable to omeprazole treatment were noted.

• In a placebo controlled adult horse safety study, horses received 20 mg/kg/day omeprazole (5x the recommended dose) for 90 days. No treatment related adverse effects were observed.

• In a placebo controlled tolerance study, adult horses were treated with GASTROGARD Paste at a dosage of 40 mg/kg/day (10x the recommended dose) for 21 days. No treatment related adverse effects were observed.

• A placebo controlled foal safety study evaluated the safety of omeprazole at doses of 4, 12 or 20 mg/kg (1, 3 or 5x) once daily for 91 days. Foals ranged in age from 66 to 110 days at study initiation. Gamma glutamyltransferase (GGT) levels were significantly elevated in horses treated at exaggerated doses of 20 mg/kg (5x the recommended dose). Mean stomach to body weight ratio was higher for foals in the 3x and 5x groups than for controls; however, no abnormalities of the stomach were evident on histological examination.

Reproductive Safety In a male reproductive safety study, 10 stallions received GastroGard Paste at 12 mg/kg/day (3x the recommended dose) for 70 days. No treatment related adverse effects on semen quality or breeding behavior were observed. A safety study in breeding mares has not been conducted.

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All rights reserved. Rev. 08-2005 ®GASTROGARD is a registered trademark of the AstraZeneca Group of Companies.

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

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

June 5–6 Advanced Arthroscopy Colorado State College of Veterinary Medicine and Biomedical Sciences Fort Collins, Colorado Phone 970-297-1273 Web www.cvmbs.colostate.edu/clinsci/ce

June 23–July 3 Equine Practitioners Conference 2009

Only Adequan® i.m. (polysulfated glycosaminoglycan)

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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

Victoria, Australia Phone (03) 5829 9566 Email conference@gvequine.com.au Web gvequine.com.au

July 18–24 31st Bain Fallon Memorial Lectures Twin Waters Resort Sunshine Coast, Queensland, Australia Phone (02) 9280 0922 Fax (02) 9211 7601 Email eva@infosalons.com.au Web eva.org.au

July 19–21 AAEP Focus on the Foot and Practice Management Seminar Columbus, Ohio Web aaep.org

August 6 Hambletonian Continuing Education Wet Labs for Equine Veterinarians Meadowlands Racetrack East Rutherford, New Jersey Phone 973-240-7471 Email gordon@firstchoicemarketing Web firstchoicemarketing.us

August 7–8 Florida Association of Equine Practitioners 2nd Annual Promoting Excellence Foot/Farrier Symposium Orlando, Florida Web faep.net Compiled by Benjamin Hollis; send listings to bhollis@vetlearn.com.

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Compendium Equine | April 2009

Clinical Snapshot Particularly intriguing or difficult cases

Case Presentation #1 ❯❯ Amber L. Labelle, DVM ❯❯ Ralph E. Hamor, DVM, MS, DACVO* University of Illinois Urbana-Champaign A

We Don’t Just Build Hyperbaric Chambers...

A 12-year-old Quarter horse mare pre- rest. The direct pupillary light reflex sented to the Veterinary Teaching was slow/incomplete, and the consenHospital of the University of Illinois sual pupillary light reflex was normal Urbana-Champaign with a cataract in (from right eye to left eye). A hyperpigthe right eye. The owners reported mented iris was noted, as was pigment that the mare had intermittent epi- deposition on the anterior lens capsule. sodes of blepharospasm and epiphora Intraocular pressure in the right eye (over a period of 4 years) that usually was 12 mm Hg. No fluorescein uptake responded to oral administration of was noted in either eye. Tropicamide phenylbutazone. A cataract involving 1% ophthalmic solution was administhe right lens was diagnosed during a tered topically to both eyes for pharroutine examination 4 months before macologic mydriasis to facilitate further presentation. On ophthalmic examina- examination. Image A shows the right tion, the mare had a visual and com- eye after onset of mydriasis. fortable left eye with a normal direct and a slow/incomplete consensual pu- 1. What two lenticular abnormalities are present in image A? pillary light reflex (from left eye to right eye). The other results of the ocular 2. What is the most likely etiology? examination were within normal lim- 3. What options are available to improve the mare’s vision? its, with an intraocular pressure of 16 mm Hg. Examination of the right eye 4. What additional diagnostic procedure is indicated? revealed a nonvisual and comfortable SEE PAGE 108 FOR ANSWERS AND EXPLANATIONS. eye with a mildly mydriatic pupil at

*Dr. Hamor discloses that he has received financial benefits from Animal Eye Consultants, Chicago, Illinois.

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Clinical Snapshot Answers and Explanations Case Presentation #1 SEE PAGE 107 FOR CASE PRESENTATION.

A

1. A mature cataract with a temporal aphakic cres-

cent (A; arrow) is present. The presence of an aphakic crescent (the prominent space between the temporal lens equator and the temporal pupillary margin) is indicative of lens subluxation.

2. The most likely etiology is equine recurrent uveitis, the most common cause of cataracts in adult horses.1 Lens subluxation is often observed in the late stages of this disease. The lens is normally retained in the patellar fossa by zonular fibers that run from the ciliary processes of the ciliary body to the lens capsule. Chronic intraocular inflammation causes zonular degeneration with subsequent lens subluxation.2 Other ocular signs of equine recurrent uveitis in this patient included pigment deposition on the anterior lens capsule (likely a remnant of previous posterior synechiae or adhesions between the iris and the anterior lens capsule) and a hyperpigmented iris.

3. The only therapeutic option for improving vision when a mature cataract is present is removal of the cataractous lens. Phacoemulsification is the most frequently used technique for lens extraction in dogs and is being used more commonly for equine patients with visual impairment from cataracts.1 4. Before phacoemulsification, it is advisable to complete an ocular ultrasonographic examination to detect evidence of vitreoretinal lesions obscured by the cataract.2,3 Image B shows an ocular ultrasonographic image of this mare’s right eye (lens: small arrow). The ultrasonogram was obtained with a 12-MHz probe scanning transpalpebrally in the sagittal plane, revealing complete retinal detachment (large arrows). Retinal detachment is a common sequela of equine recurrent uveitis.1,2 Based on these ultrasonographic findings, removal of the cataract would not restore this patient’s vision.

B

References 1. Gelatt KN. Veterinary Ophthalmology. 4th ed. Ames: Blackwell Publishing; 2007:1165-1274.

2. Gilger BC. Equine Ophthalmology. St. Louis: Elsevier Saunders; 2005:269-322.

3. Ramirez S, Tucker RL. Ophthalmic imaging. Vet Clin North Am Equine Pract 2004; 20(2):441-457.

SHARE YOUR PICTUREPERFECT CASES IN CLINICAL SNAPSHOT

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Challenge your colleagues with a particularly intriguing or difficult case in Clinical Snapshot. Submit your photo(s) along with a brief case description, at least one test question, and detailed answers to each question posed. Each published submission entitles you to an honorarium of $100.

For more details, call 800-426-9119, extension 52434, or email editor@CompendiumEquine.com

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

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Clinical Forum

Clinical Forum openly discusses topics that might be a bit controversial or unusual.

❯❯ James N. Moore, DVM, PhD, Column Editor Department of Large Animal Medicine | College of Veterinary Medicine | The University of Georgia, Athens, GA 30602 ❯ phone 706-542-3325 ❯ fax 706-542-8833 ❯ email jmoore@uga.edu

Shock-Wave Therapy: How It Has Shocked or Bored Us ❯❯ Scott R. McClure, DVM,

PhD Iowa State University

S

hock-wave therapy was first used in horses to treat musculoskeletal injuries about 10 years ago. During the past decade, there have been proclamations of wonder and disgusted claims of quackery regarding this form of treatment. Fortunately, the reality lies somewhere in between. The development of this modality in human and veterinary medicine in the past 10 years has resulted in a fairly dynamic knowledge base.

A colleague and I described the physical generation of shock waves in Compendium 6 years ago.1 All true shock-wave generators use parabolic designs to focus the shock waves.

Some people have proposed generating “unfocused shock waves” (shock waves that simply do not converge to a focal point) to treat superficial and skin wounds.2

This column focuses on shock-wave therapy.

lying the response to this therapy remain somewhat of a mystery. One of the most commonly reported responses to shock-wave therapy is neovascularization, which has been demonstrated in tissues as diverse as bone and myocardium. Similarly, other studies have demonstrated that shock-wave therapy results in increased expression of cytokine genes in different tissues. It is hoped that the results of ongoing studies will identify the mechanisms that initiate the responses to pressure waves at a cellular level.

When the mechanisms underlying the responses to shock-wave therapy have been identified, it should be possible to “fine tune” the shock waves to maximize their beneficial effects and minimize unwanted effects. Because high-pressure waves are followed by the negative pressure component of the shock wave, they can cause cavitation, which is the production and collapse of bubbles within the fluid media or tissue. Collapse of the cavitation bubbles increases the pressure and temperature in the area. Although maximizing cavitation is beneficial during lithotripsy because it improves the effectiveness of stone fragmentation, it has been suggested that cavitation creates unwanted effects in soft tissues and may be responsible for initiating the pain associated with the treatment. If cavitation is not required for the desired effects in other applications, shock-wave generators can be made to minimize cavitation.

Additionally, identification of the mechanisms responsible for the effects of shock-wave therapy would permit the operator to control the energy levels, waveforms, and number of pulses needed to yield the desired outcome.

The Underlying Mechanisms

Suspensory Desmitis

Although positive results have been obtained in several studies on shockwave therapy, the mechanisms under-

It takes time to generate sufficient evidence to support or refute the effectiveness of any new modality. However, evidence for the use-

Shock Waves Versus Radial Pressure Waves There are striking differences between shock waves and radial pressure waves. Although these two waveforms are quite different, they continue to be confused and incorrectly grouped together.3 Some facts regarding shock waves and radi al pressure waves deserve a specific mention: These different waveforms have different energy levels and abilities to penetrate tissue.

It is inappropriate to assume that results obtained using one waveform will be similar to those obtained using the other.

According to the literature, both modalities have yielded positive and negative outcomes.

TO LEARN MORE

Visit CompendiumEquine.com for full-text articles, CE testing, and CE test answers.

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

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Clinical Forum fulness of shock-wave therapy has become available for horses with suspensory desmitis. The results of two controlled studies using a collagenase-induced desmitis model of this disease indicated that lesion size was decreased in limbs treated with shock-wave therapy compared with untreated controls and that there was histologic evidence of more new collagen fibrils and increased proteoglycan deposition in the treated limbs.4,5 These findings are similar to those in clinical practice, and the results of a prospective study of horses with naturally occurring suspensory desmitis in the forelimbs or hindlimbs indicated that a combination of shock-wave therapy and controlled exercise compared favorably with results obtained previously with other treatments.6

Damaged Tendons and Ligaments

CriticalPo nt The results of a prospective study of horses with naturally occurring suspensory desmitis in the forelimbs or hindlimbs indicated that a combination of shock-wave therapy and controlled exercise compared favorably with results obtained previously with other treatments.

The efficacy of shock-wave therapy in horses with damaged tendons and ligaments is much less clear, primarily because controlled exercise, NSAIDs, heat and cold therapy, and pressure wraps are all routinely used in conjunction with shock-wave therapy. There are even more difficult questions to address concerning the concurrent use of shock-wave therapy and biologics such as ACell Vet (ACell Inc., Jessup, MD) or stem cells in treating horses with tendon or ligament damage. The concept of providing a scaffold with ACell Vet or stem cells and then stimulating neovascularization with shock-wave therapy makes sense, and the efficacy of this approach appears to be borne out in a limited number of clinical cases. However, there is a concern that shockwave therapy administered shortly after injection of the cells may reduce their effectiveness. Thus, the protocol would be to administer the first of three shock-wave treatments, inject the biologic product, and then follow up with the last two shock-wave treatments at 3-week intervals.

Musculoskeletal Disorders The first application of shock-wave therapy for musculoskeletal disorders in humans and horses was to treat diseases that affect bone. Subsequent, large retrospective studies in humans have resulted in refinement of the treatment protocols to yield the expected response.7,8 New applications of shock-wave therapy, including treatment of osteonecrosis of the femoral neck, are showing promise.9 However, in horses, shock-wave therapy for bone disorders has not been pursued

112

as aggressively as it has in humans. This may be related to differences in case management: in equine patients, complete fractures are often inaccessible because of the application of casts.

The responses of incomplete fractures, such as dorsal cortical fractures, to shock-wave therapy are moderate at best. A better outcome would be expected based on two studies that demonstrated a positive stimulatory effect of shock-wave therapy on bone formation in the metacarpus. The first study was a pilot study involving two horses in which application of shock-wave therapy to the dorsal cortex of the metacarpus resulted in more new bone deposition than in the untreated control metacarpus.10 In the other study, application of shock-wave therapy to the proximal palmar aspect of the metacarpus resulted in a local increase in osteoblasts.11 Lower cellularity, thickness of the dorsal metacarpal cortex, and related distance to vasculature could be why some stress fractures of the metacarpus fail to respond as well as expected. The energy of the shock waves that are commonly used in practice may also be a factor. Stimulation of bone formation in the equine dorsal cortex may require a higher energy flux density than is routinely used (i.e., at or approaching the level [0.89 mJ/mm2] that was used in the pilot study).

Inflammation Veterinarians in clinical practice and in research have noticed a rapid decrease in the clinical signs of inflammation in some horses after shock-wave therapy. For example, shockwave therapy in horses with collagenaseinduced tendonitis resulted in a reduction in swelling on the palmar aspect of treated limbs.

Similarly, shock-wave therapy in horses with experimentally induced osteochondral fragments resulted in less severe lameness and a lower protein concentration in the synovial fluid on day 28 of the study, when lameness and synovial protein concentration were maximal in the control group.12 These findings are particularly interesting considering that many people would expect shock-wave therapy to result in increased inflammation. These findings also seem to dispel the opinion that shockwave therapy is simply an “internal blister.”

Soft Tissue Disorders The use of shock-wave therapy for treating soft tissue disorders has increased in human medi-

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

Shock-Wave Therapy cine, primarily in response to increased interest in the results of studies reported more than 10 years ago. In one study, the use of shock-wave therapy to experimentally create skin wounds in pigs resulted in improved rates of epithelialization.13 In another study in rats, the use of shockwave therapy resulted in a significant decrease in necrosis of epigastric skin flaps.14 The results of initial clinical studies in humans with diabetic ulcers are promising,15 as are the results of a study involving skin wounds on the distal limbs of horses, in which several parameters associated with wound healing were evaluated.16

Analgesia A purported effect of shock-wave therapy is analgesia. In one study conducted on horses and sheep, there was evidence of local cutaneous analgesia for 72 hours after shock-wave therapy.17 In a study that evaluated the duration of analgesia associated with shock-wave therapy in horses with naturally occurring lameness, serial force-plate analyses were conducted before and after treatment.18 The results, which were based on decreased lameness demon-

strated by force-plate analysis, indicated that a significant analgesic effect was present from 8 hours through 48 hours after shock-wave therapy. After 48 hours, the lameness returned to the pretreatment level. As a result, racing jurisdictions in the United States as well as the Fédération Equestre Internationale require a 5to 7-day withdrawal period after shock-wave therapy before a horse is allowed to perform.

The Future Shock-wave equipment and applications have developed rapidly, and the evidence supporting the application of this technology in horses has continued to grow. While the exact mechanisms responsible for the effects of shock-wave therapy have not been identified, neovascularization is a consistent histologic outcome. At this time, the most common clinical application of shock-wave therapy in horses is in treating suspensory desmitis. Applications continue to expand, and the use of shock waves for stimulating wound healing is one current area of interest. Applications and equipment will likely continue to evolve at a rapid pace over the next few years.

CriticalPo nt While the exact mechanisms responsible for the effects of shockwave therapy have not been identified, neovascularization is a consistent histologic outcome.

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Clinical Forum

References 1. McClure SR, Merritt DK. Extracorporeal shock-wave therapy for equine musculoskeletal disorders. Compend Contin Educ Pract Vet 2003;25:68-70.

2. McClure SR. Extracorporeal shock wave therapy and radial pressure wave therapy: wave physics and equipment. In: Robinson, ed. Current Therapy in Equine Medicine. 6th ed. Philadelphia: WB Saunders; 2009:524-528.

3. Cleveland RO, Chitnis PV, McClure SR. Acoustic field of a ballistic shock wave therapy device. Ultrasound Med Biol 2007;33:1327-1335.

4. McClure SR, Van Sickle DV, Evans R, et al. The effects of extracorporeal shock wave therapy on the ultrasonographic and histologic appearance of collagenase induced equine forelimb suspensory ligament desmitis. Ultrasound Med Biol 2004;30:461-467.

5. Caminoto EH, Alves ALG, Amorim RL, et al. Ultrastructural and immunocytochemical evaluation of the effects of extracorporeal shock wave treatment in the hind limbs of horses with experimentally induced suspensory ligament desmitis. Am J Vet Res 2005;66:892-896.

6. Lischer CJ, Ringer SK, Schnewlin M, et al. Treatment of chronic proximal suspensory desmitis in horses using focused electrohydraulic shockwave therapy. Schweiz Arch Tierheilkd 2006;148(10): 561-568.

7. Schaden W, Fischer A, Sailler A. Extracorporeal shock wave therapy of nonunion or delayed osseous union. Clin Orthop Relat Res 2001;387:90-94.

8. Valentin A, Fischer A, Menschik A, et al. Extracorporeal shockwave therapy for non-unions and delayed healing fractures (abstract). Proc ISMST 11th Int Congr 2008:32-33.

9. Wang CJ, Wang FS, Huang CC, et al. Treatment for osteonecrosis of the femoral head: comparison of extracorporeal shock waves

PHARM

with core decompression and bone-grafting. J Bone Joint Surg 2006;87-A:2380-2388.

10. McClure SR, VanSickle DV, White MR. Effects of extracorporeal shock wave therapy on bone. Vet Surg 2004;33:40-48.

11. Bischofberger AS, Ring SK, Geyer H, et al. Histomorphologic evaluation of extracorporeal shock wave therapy on the fourth metatarsal bone and the origin of the suspensory ligament in horses without lameness. Am J Vet Res 2006;67:577-582.

12. Frisbie DD, Kawcak CE, McIlwraith CS. Evaluation of extracorporeal shock wave therapy for osteoarthritis. Proc 50th Annu Conv AAEP 2004:261-263.

13. Haupt G, Chavpil M. Effect of shock waves on the healing of partial thickness wounds in piglets. J Surg Res 1990;49:45-48.

14. Meirer R, Kamelger FS, Huemer GM, et al. Extracorporeal shock wave may enhance skin flap survival in an animal model. Br Assoc Plastic Surg 2005;58:53-57.

15. Saggini A, Figus A, Troccola V, et al. Extracorporeal shock wave therapy for management of chronic ulcers in the lower extremities.

Ultrasound Med Biol 2008;34:1261-1271.

16. McClure S, Morgan D. Extracorporeal shockwave therapy in the treatment of distal limb lacerations. Proc ISMST 10th Int Congr 2007:16-17.

17. McClure SR, Sonea IM, Evans RB, Yeager M. Evaluation of analgesia resulting from extracorporeal shockwave therapy and radial pressure wave therapy in the limbs of horses and sheep. Am J Vet Res 2005;66:1702-1708.

18. Dahlberg JA, McClure SR, Evans RB, Reinertson EL. Force platform evaluation of lameness severity following extracorporeal shock wave therapy in horses with unilateral forelimb lameness.

JAVMA 2006;229:100-103.

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EDUCATION THAT GOES INTO PRACTICE

c ec enter.c om

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

How Cell Membranes Work: Smoke on the Water Column Editors ❯❯ David J. Hurley, PhD The University of Georgia ❯ email djhurley@uga.edu ❯❯ James N. Moore, DVM, PhD The University of Georgia

ABSTR ACT * The scope of the present review focuses on the interfacial prop-

Illustrated by Kip Carter, MS, CMI,The University of Georgia

erties of cell membranes that may establish a link between the membrane and the cytosolic components. We present evidences that the current view of the membrane as a barrier of permeability that contains an aqueous solution of macromolecules may be replaced by one in which the membrane plays a structural and functional role. Although this idea has been previously suggested, the present is the first systematic work that puts into relevance the relation water–membrane in terms of thermodynamic and structural properties of the interphases that cannot be ignored in the understanding of cell function. To pursue this aim, we introduce a new definition of interphase, in which the water is organized in different levels on the surface with different binding energies. Altogether determines the surface free energy necessary for the structural response to changes in the surrounding media. The physical chemical properties of this region are interpreted in terms of hydration water and confined water, which explain the interaction with proteins and could affect the modulation of enzyme activity.

Information provided by several methodologies indicates that the organization of the hydration states is not restricted to the membrane plane albeit to a region extending into the cytoplasm, in which polar head groups play a relevant role. In addition, dynamic properties studied by cyclic voltammetry allow one to deduce the energetics of the conformational changes of the lipid head group in relation to the head–head interactions due to the presence of carbonyls and phosphates at the interphase. These groups are, apparently, surrounded by more than one layer of water molecules: a tightly bound shell, that mostly contributes to the dipole potential, and a second one that may be displaced by proteins and osmotic stress. Hydration water around carbonyl and phosphate groups may change by the presence of polyhydroxylated compounds or by changing the chemical groups esterified to the phosphates, mainly choline, ethanolamine or glycerol. Thus, surface membrane properA section of membrane is depicted with “sheets” of water molecules making up the associated liquid phase outside the ties, such as the dipole potential and the surface pressure, are cell, the hydration shell surrounding a transmembrane protein, modulated by the water at the interphase region by changing and small clusters of confined water molecules associated with the structure of the membrane components. An understandthe outer surface of the membrane. Because water molecules are quite small relative to the components of the membrane and very small relative to the size of proteins, this image is not drawn to scale. Its purpose is to provide a sense of the highly organized nature of water that interacts with cell membranes and affects cell function. (©UGA 2009)

116

*This abstract has been reprinted verbatim from Disalvo EA, Lairion F, Martini F, et al. Structural and functional properties of hydration and confined water in membrane interfaces. Biochimica et Biophysica Acta 2008;1778:2655-2670; with permission from Elsevier.

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

Abstract Thoughts ing of the properties of the structural water located at the hydration sites and the functional water confined around the polar head groups modulated by the hydrocarbon chains is helpful to interpret and analyze the consequences of water loss at the membranes of dehydrated cells. In this regard, a correlation between the effects of water activity on cell growth and the lipid composition is discussed in terms of the recovery of the cell volume and their viability.

Critical analyses of the properties of water at the interface of lipid membranes merging from these results and others from the literature suggest that the interface links the membrane with the aqueous soluble proteins in a functional unit in which the cell may be considered as a complex structure stabilized by water rather than a water solution of macromolecules surrounded by a semi permeable barrier.

COM MEN TA RY

Water is a critical factor in sustaining life. In fact, the horse’s body is about 70% water, and most of what we understand about the “chemistry of life” is in the context of chemical interactions and reactions that occur in a “water” environment.

As a first approximation, water is the universal vehicle of life.

Yet a paradox exists in the way we think about the fundamental units of life, namely the cells of the body. Our understanding of how cells work has been built around the concept that cells are bounded by a “water hating” (hydrophobic), double-layered, fatty membrane that does not easily allow passage of water. This membrane, usually called the lipid bilayer, is primarily composed of phospholipids that have two poles of opposite character. At one end is the “head group,” a molecule that is chemically polarized and carries a partial charge. Because water also has positive and negative ends, it interacts perfectly well with the head groups in phospholipids. The head group is bound to a glycerol molecule and is thereby linked to the other end of the phospholipid molecule—two fattyacid tails, which are nonpolar molecules that associate with each other to form the membrane core. Each membrane surface (inside and outside the cell) has head groups facing the water-loaded environment beyond the membrane. However, in the space between the head groups, the tails from regularly ori-

ented phospholipids “stack” and energetically stabilize the interior of the membrane.

This image of the membrane is a good representation of reality, particularly if our vantage point is at a distance. This model is also useful when contemplating the membrane as a barrier, as the membrane allows cells to be clearly and cleanly defined as separate units distinct from their outside environment.

However, this image of cells quickly starts to encounter problems on closer examination, especially when we contemplate how cells interact with each other, release their products into the environment, or take up materials from the outside. This is when the cell membrane and the wonderful properties of water become more critical.

First, let us examine the membrane. The fatty-acid chains that are part of the membrane are not homogeneous. If all the fattyacid chains were identical, membranes would not function very well. Fatty-acid chains would be packed so close, and there would be so many points of stabilization, that the membranes would essentially become crystallized.

Collectively, the enormous number of weak interactions among the very large number of fatty-acid chains in a membrane would stabilize the structure, making the bilayer rigid and essentially solid. This would not be good for cell function. However, in real cells, fatty-acid chains have various lengths (number of carbon atoms in the chain) and different numbers of single-, double-, and triple-unsaturated (double bonds within the chain) fatty acids. A double bond generates a “kink” (“bend”) in the fattyacid chain. This allows more “relaxed” packing of one fatty-acid chain over its neighbors, resulting in formation of gaps in the membrane and reduced stabilization energy. It also helps keep the membrane “fluid.” This fluid membrane structure allows components to move laterally, permitting proteins to interact with each other and with other nonlipid membrane components. Even with many double bonds in the fatty-acid chains of the membrane, the membrane has a very high degree of energetic stabilization, preventing most molecules from moving across the membrane bilayer.

Cell membranes also contain large numbers of proteins that interact with the inner and outer surfaces of the membrane, insert into lipid layers, or pass through the membrane. Proteins play

CriticalPo nt In biologic systems, water is more than a medium; it is an organizing medium.

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Abstract Thoughts

CriticalPo nt The cell may be considered as a complex structure stabilized by water rather than a water solution of macromolecules surrounded by a semipermeable barrier.

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an important role in membrane function and the cell’s interaction with the outside world. Proteins that enter or cross the lipid layers contain “domains” that interact with fatty-acid chains and are stabilized by multiple nonpolar, hydrophobic interactions. However, the portions of proteins that interact with the cell’s cytoplasm or the fluid space outside the cell are stabilized by interaction with water in these environments. These proteins are produced by ribosomes located at the surface of a membrane stack within the cell.

They are guided to optimize their function with help from the leader sequence and from proteins that move newly formed peptide chains across membrane structures, organize their “folding,” and add nonprotein components such as sugars to them so that they become fully functional.

Water itself is also an important player in cell function and is the subject of the article we recommend in this column. What is so exciting about water? It is just two hydrogen atoms and an oxygen atom, right? Well, not exactly. First, the oxygen atom in the water molecule is very greedy and attempts to take strong control over the electron each hydrogen atom brings to the molecule. As a result, the oxygen molecule has a strong partial negative charge, leaving the hydrogen atoms with a partial positive charge.

This allows water to form multimolecular “networks,” both as two-dimensional sheets and three-dimensional lattices. Left to interact with itself as a liquid, water forms sheets of associated molecules that are stabilized by interactions between the negatively polarized oxygen in one molecule and the positively polarized hydrogen in another. These sheets are very long, giving water its high tensile strength.

In addition to interacting with itself, water interacts with hydrophilic (water-loving) parts of other molecules and structures, forming a hydration shell. Hydration shells link water to molecules and affect how they function.

Many proteins do not function as enzymes or as binding sites for hormones or drugs unless they are hydrated by a shell of water that allows them to assume a specific threedimensional structure. Furthermore, additional water molecules generally form a complex lattice structure by binding to the hydration water associated with proteins, further affecting their function.

The cell membrane surface is studded with proteins requiring a hydration shell to be func-

tional. The membrane also has molecules built out from the glycerol backbone, representing many types of phospholipids of different sizes and makeup that create “hills and valleys” on the cell’s surface (at least on the size scale of water molecules). Consequently, cell membranes appear more like the moon than smooth-surfaced soap bubbles. In the valleys, water may be confined to the surface, where it interacts with other water molecules to influence cell function.

Hydration water molecules that interact with polar chemical structures on and in the membrane as well as water confined in spaces at the membrane surface contribute to the energetics of membrane function. These molecules help regulate the activities of proteins, providing the barrier function of the membrane. The water shells around membrane structures, and the secondary “network” of water molecules interacting with these shells, mediate the effects of osmotic pressure when the availability of water changes.

How does this affect horses? Well, almost all medications delivered systemically are in a form requiring trafficking and delivery from the water-based environment between cells and in plasma contained in blood vessels. The chemistry that forms the basis of our understanding of the function of these drugs is based on reactions carried out in water. The physiologic regulation of body tissues and organs depends on the chemistry of enzymes and hormones functioning in a water environment. Thus, as the authors of this column’s recommended article so nicely put it … …the cell may be considered as a complex structure stabilized by water rather than a water solution of macromolecules surrounded by a semipermeable barrier.

This new perspective may help us better understand equine diseases and medicines.

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Understanding the intricacies and interpreting the findings of digital imaging

Imaging Is Believing ❯❯ Anthony Pease, DVM, MS, DACVR, Column Editor Michigan State University

Stifle Ultrasonography: A Case Study ❯❯ Elizabeth Charles, DVMa San Dieguito Equine Group San Marcos, California

❯❯ Natasha Werpy, DVM, DACVR Colorado State University

❯❯ Norman Rantanen, DVM, MS, DACVR Fallbrook, California

Digital imaging has revolutionized how veterinarians evaluate musculoskeletal problems in horses.

While it has become much easier to obtain images, veterinarians are still faced with the challenge of interpreting the findings properly.

Imaging Is Believing is designed to help equine practitioners meet this challenge and understand all the intricacies of digital imaging.

A

4-year-old racing Thoroughbred filly presented with a 1-month history of left hindlimb lameness. The filly was evaluated by the referring veterinarian at the initial onset of lameness, which developed acutely after exercise. The clinical examination revealed mild joint effusion of the left stifle and left hindlimb lameness (grade 2/5) that was not exacerbated by flexion. The lameness significantly improved with diagnostic anesthesia of the left medial femorotibial joint. Radiography revealed no osseous abnormalities. The joint was injected with corticosteroids, and a rest period was prescribed. The owners attempted to resume the filly’s race training; however, the lameness persisted, so they brought the filly to our clinic.

increase of fluid in the medial femorotibial joint with extensive debris throughout the joint compartment. There was extensive synovial proliferation at the joint capsule attachment, and the joint capsule was moderately thickened (FIGURE 1). A linear anechoic region was identified in the medial meniscus, beginning at the cranial margin of the medial collateral ligament, continuing through the cranial horn, and ending immediately adjacent to the transition into the medial cranial tibial menisFIGURE 1 Synovial proliferation (arrows) and severely increased fluid and debris within the medial femorotibial joint of the affected limb are readily identified with ultrasonography.

Physical Examination At presentation, approximately 45 days after the treatment and rest period, the filly’s vital signs were within normal limits. There was moderate effusion of the left femorotibial joint but no external evidence of trauma to the left hindlimb. The filly was evaluated at a walk and a trot in a straight line on hard ground.

At the walk, grade 1/5 left-hindlimb lameness was detected. When trotted, the filly exhibited grade 3/5 left-hindlimb lameness. The lameness was exacerbated by flexion. Diagnostic anesthesia was not performed at this time.

Synovial proliferation.

Diagnostic Imaging Because radiographic findings were within normal limits at the initial examination, the right and left stifles were evaluated via ultrasonography to visualize soft tissue and TO LEARN MORE bony structures.

Ultrasonographic examination of the left stif le revealed a marked Visit CompendiumEquine.com for full-text articles, CE testing, and CE test answers.

a

Dr. Charles discloses that she is a local equine expert on Dormosedan (Pfizer) and participates in roundtable discussions regarding the use of the drug.

Fluid Debris

Severely increased fluid and debris.

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Imaging Is Believing FIGURE 2 Images of the medial meniscus. The arrows outline the anechoic region, which represents a horizontal tear in the medial meniscus. In the non–weight-bearing position, the tear widens as outlined by the arrows, and the meniscus becomes further extruded.

Weight-bearing position.

CriticalPo nt Imaging of the medial meniscus with the limb in a non–weight-bearing position increased the length and width of the linear anechoic region at the axial tip of the meniscus. In addition, small defects were identified in the femoral and tibial surfaces of the meniscus.

cal ligament. The medial meniscus extended beyond the margins of the tibia and femur, indicating partial rupture. Imaging of the medial meniscus with the limb in a non– weight-bearing position increased the length and width of the linear anechoic region at the axial tip of the meniscus (FIGURE 2). In addition, small defects were identified in the femoral and tibial surfaces of the meniscus. The defects corresponded with the osteophytosis on the femur and tibia (FIGURE 3). Moderate periarticular osteophyte formation at the distal medial femur and proximal medial tibia was also noted.

These findings on ultrasonographic examination were consistent with a horizontal tear of the cranial horn of the medial meniscus.

The meniscal defects in the femoral and tibial surfaces indicated margin tears that were most likely associated with periarticular osteophyte formation on the femur and tibia and partial extrusion of the meniscus. There was evidence of moderate to severe chronic synovitis of the medial femorotibial joint.

Treatment Restricted exercise, systemic antiinflammatory therapy using an NSAID (phenylbutazone: 2 to 4 mg/kg PO q24h as needed), and further local treatment of the joint were recommended.

Surgical exploration was not pursued due to the poor prognosis for return to racing. The filly was retired and turned out in a small paddock and will become a broodmare. Because

FIGURE 3 Images of the medial meniscus. A small surface defect in the medial meniscus (arrow) likely caused by adjacent osteophytosis of the femur is identified in the non–weight-bearing position.

The defect is not seen in the weight-bearing image. Surface defects in the meniscus can be missed if non–weight-bearing images are not obtained.

Weight-bearing position.

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Non–weight-bearing position.

Non–weight-bearing position.

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Imaging Is Believing FIGURE 4 Images of the medial meniscus. Normal striations (arrows) are easily seen on gross examination and an ultrasonogram.

Photograph of a medial meniscus with striations.

the filly was comfortable at a walk, no further treatment was pursued.

Discussion In horses, the stifle is complex, the largest joint, and a common site of lesions that result in hindlimb lameness.1 Because of the intricate anatomy of the stifle, it can be challenging for equine practitioners to diagnose stifle injury.

Radiography has been the most commonly used imaging modality to evaluate the stifle.2 Although adequate for diagnosis of certain bony abnormalities, radiography of the stifle provides minimal information about the joint’s soft tissue structures, including the medial meniscus.3 A thorough diagnostic examination, including evaluation of bony and soft tissue structures via ultrasonography, can improve the likelihood of a correct diagnosis, especially if meniscal injury is suspected.4 The medial and lateral menisci of the stifle are fibrocartilaginous structures positioned between the tibia and femur. The menisci are not uniform in their anatomic structure; they are striated throughout. Thus, when imaging the menisci, it is important to obtain both weight-bearing and non–weight-bearing images to differentiate lesions from the normal anatomic appearance (FIGURE 4). The concave shape of the proximal surfaces of the menisci follows the contour of the femoral condyles,

Ultrasonogram of the medial meniscus showing the striations.

providing smooth articulation and shock absorption between the femur and tibia. Each meniscus is attached to the proximal aspect of the tibia by cranial and caudal ligaments.5 Injury to the soft tissues of the stifle, specifically the medial meniscus, should be considered in cases of hindlimb lameness. The degree of lameness associated with these injuries can initially be moderate to severe but may improve over time. Joint effusion and a positive response to flexion of the joint may be present. Diagnostic anesthesia of one or more of the joint pouches usually improves the lameness.1 Radiographic evidence of arthrosis affecting the medial aspect of the joint often accompanies medial meniscal injury and should lead to further evaluation of the soft tissue structures of the joint. However, absence of radiographic findings should not rule out meniscal injury because radiographic changes may not be present in acute or mild cases of meniscal injury.4 In this filly’s case, the clinical presentation and lack of bony abnormalities on radiographs were consistent with soft tissue injury of the stifle. However, a conclusive diagnosis was determined by ultrasonographic evaluation of the joint. Complete ultrasonographic examination of the stifle is readily accomplished with standard ultrasound equipment used by equine practitioners, such as a 10- to 12-MHz linear or an 8-MHz curvilinear ultrasound transducer6–8 (FIGURE 5).

CriticalPo nt It can be challenging for equine practitioners to diagnose stifle injury.

Radiography has been the most commonly used imaging modality to evaluate the stifle.

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Imaging Is Believing FIGURE 5

A multifrequency linear 7- to 14-MHz transducer is placed on the stifle to evaluate the medial meniscus.

CriticalPo nt A thorough diagnostic examination, including evaluation of bony and soft tissue structures via ultrasonography, can improve the likelihood of a correct diagnosis, especially if meniscal injury is suspected.

Without ultrasonography as a diagnostic option for evaluation of the stifle, exploratory arthroscopy is often the only way to evaluate the joint if radiographic findings are within normal limits. In this case, arthroscopy was not needed to confirm the diagnosis or provide additional prognostic information because horizontal tears of this nature carry a poor prognosis for return to soundness.9 In cases in which ultrasonography does not reveal evidence of meniscal injury or injury to other readily visible soft tissue structures, exploratory arthroscopy is indicated. Even in cases in which ultrasonographic examination reveals evidence of meniscal damage, arthroscopy may be indicated to further clarify the extent of the lesion, provide useful prognostic information, and allow surgical debridement, if possible.10 The major limitation of arthroscopy

is that exposure of the stifle is limited, thereby preventing complete evaluation of the joint.

In the medial aspect of the joint, the cranial tibial meniscal ligament and the cranial-most aspect of the cranial horn of the meniscus are often the only areas that can be seen via arthroscopy.11 Tears in the caudal aspect of the meniscus require ultrasonographic evaluation for diagnosis. Thus, arthroscopy and ultrasonography are often used in conjunction to evaluate the structures of the stifle.4 Radiography is often the initial diagnostic modality of choice to evaluate a horse’s stifle. Radiographs can be used to identify bony abnormalities and can lead to suspicion of soft tissue injury.1 However, bony changes may not be present in acute or mild injury.

Ultrasonography is a more sensitive method to detect bony changes and is the only modality readily available to evaluate the soft tissue structures of the stifle. Therefore, in cases of suspected meniscal injury or other soft tissue injury in the stifle, ultrasonography is a readily available noninvasive screening tool that can be used before arthroscopy to aid in diagnosis and prognosis.4

Acknowledgment: We thank Michael Manno, DVM, MS, at San Dieguito Equine Group, San Marcos, California, for referring this case to us.

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References 1. Walmsley JR, Phillips TJ, Townsend HG. Meniscal tears in horses: an evaluation of clinical signs and arthroscopic treatment of 80 cases. Equine Vet J 2003;35(4):402-406.

2. Hoegaerts M, Nicaise M, van Bree H, Saunders JH. Cross-sectional anatomy and comparative ultrasonography of the equine medial femorotibial joint and its related structures. Equine Vet J 2005;37(6):520-529.

3. Harrison LJ, Edwards GB. Radiographic investigation of the equine stifle. Equine Vet Educ 1995;7:161-168.

4. Flynn KA, Whitcomb MB. Equine meniscal injuries: a retrospective study of 14 horses. Proc AAEP 2002;48:249-254.

5. Sisson S, Grossman JD. Fasciae and muscles of the pelvic limb.

Anatomy of the Domestic Animals. 4th ed. Philadelphia: WB Saunders; 1953:234-241.

6. Denoix JM, Audigie F. Ultrasonographic examination of the sti-

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fle in horses. Proc ACVS 2003;38:122.

7. Hoegaerts M, Saunders JH. How to perform a standardized ultrasonographic examination of the equine stifle. Proc AAEP 2004; 50:212-218.

8. Penninck DG, Nyland TG, O’Brien TR, et al. Ultrasonography of the equine stifle. Vet Radiol Ultrasound 1990;31:293-298.

9. Schramme MC, Jones RM, May SA, et al. Comparison of radiographic, ultrasonographic and arthroscopic findings in 29 horses with meniscal tears. Proc 12th ESVOT Congress 2004:186.

10. Walmsley JR. Diagnosis and management of meniscal injuries in the horse. Proc 10th ESVOT Congress 2000:105.

11. Watts AE, Nixon AJ. Comparison of arthroscopic approaches and accessible anatomic structures during arthroscopy of the caudal pouches of equine femorotibial joints. Vet Surg 2006;35:219-226.

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3 CE CREDITS

CE Article 1 C NEW SERIES

Urolithiasis At a Glance Etiology Page 125

Diagnosis Page 126

Treatment Page 127

Postoperative Care and Recurrence Page 130

❯❯ Alicia Foley, BS, Kansas State University ❯❯ Sabrina H. Brounts, DVM, MS, DACVS, The University of Wisconsin, Madison ❯❯ Jan F. Hawkins, DVM, DACVS, Purdue University Abstract: This article reviews the diagnosis, treatment, and prognosis of urolithiasis in horses. The etiology of urolith formation is unknown, but with the use of rectal palpation, ultrasonography, and videoendoscopy, the diagnosis can easily be made. New technologic advancements, such as laser and shock-wave therapies, are less invasive and can be used to reduce patient morbidity and improve surgical outcomes. However, the traditional surgical techniques, such as laparocystotomy and perineal urethrotomy in males and urethral sphincterotomy and manual extraction in females, are still the preferred treatments for successfully resolving urolithiasis in horses. The overall prognosis for horses with urolithiasis is good to fair.

U

rolithiasis is an uncommon disease process in horses. At Purdue University’s Large Animal Hospital, only nine cases of equine urolithiasis were seen over a period of 10 years. Interestingly, urolithiasis is not more common in horses than other species despite the alkalinity of equine urine and the high amount of calcium excreted in equine urine. It would be expected that this would create an opportune environment for calculus formation. However, equine kidneys contain glands in the renal pelvis that produce large amounts of mucus that likely serve to protect against crystal formation.1 Equine urine also contains other components, such as pyrophosphate, citrate, magnesium, and glycosaminoglycans, that may inhibit urolith formation.2 Although cases of urolith formation in the kidneys, ureters, and urethra have been reported, the most common site for urolith formation in horses is the bladder.1,3–5 No obvious age, breed, or sex predisposition for urolithiasis has been observed in horses.1,6 However, urolithiasis more often becomes a clinical problem in males4,6,7 because their urethral anatomy predisposes them to obstructive urolithiasis. The male urethra is long and less dis-

tensible than the female urethra. Therefore, the male urethra impedes passage of calculi, but the short, distensible urethra of mares permits easier passage of small calculi; thus the incidence of urethral obstruction in males is higher than in mares.

Etiology The etiology of uroliths in horses is not completely understood. It is known that two steps must occur for a urolith to form: nucleation and crystal formation.1,5 Nucleation occurs when a nidus and the correct environment exist simultaneously.

The best environment for nidus formation is urine stasis and subsequent supersaturation of urine. Urine stasis increases the probability of contact between crystalloid material in the urine and the nidus, facilitating urolith formation.2 The nidus can consist of desquamated epithelial cells, leukocytes, necrotic debris, mucoproteins, and hyperhydrated calcium salts that precipitate to allow nucleation. Therefore, care must be taken during catheterization and endoscopy of the urinary tract to lessen trauma to the urethral and urinary bladder epithelium.2 Allowing a patient that is receiving

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FREE

CE Urolithiasis FIGURE 2

Courtesy of S. B. Adams, DVM, MS, DACVS

FIGURE 1

A type I urolith.

NSAIDs to become dehydrated can precipitate nidus formation due to subsequent sloughing of cells from the renal papilla.1 Intravesical foreign bodies and luminal penetration by absorbable or nonabsorbable sutures can also serve as a nidus for urolith formation in horses.8 Spontaneous nucleation alone does not cause calculus formation; for calculus formation to occur, urine stasis must also be present to increase the chance of contact between precipitating crystalloid material and the uroepithelium or damaged uroepithelial surfaces.2 Other contributing factors that facilitate urolith formation in horses include excretion of large amounts of calcium, increased uric acid concentration, increased oxalates, and inhibition of substances that inhibit crystal formation (i.e., pyrophosphate, citrate, magnesium, glycosaminoglycans, glycoproteins).2 Once a urolith forms, it enlarges by accumulating preexisting microscopic spherules on its surface.2 Two main types of uroliths have been described in horses.9 Type I uroliths are the most common and the easiest to break down for removal. These uroliths are yellow green, have a spiculated surface, and are normally composed of a variety of hydrated calcium carbonate salts (FIGURE 1). Type II uroliths are less common. They are white, have a smooth surface, and are harder than type I uroliths.

Type II uroliths are mainly composed of calcium carbonate salts but also contain magnesium and phosphorus. In an evaluation of the mineral composition of 32 equine uroliths by

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Cystoscopic examination of a bladder showing a type I urolith. Note the irritated cystic mucosa (traumatic cystitis) and the openings of both ureters (arrows).

Osborne et al,10 88% were completely composed of calcium carbonate, 6% were composed of mainly calcium carbonate salts, and 1% was composed of calcium oxalate monohydrate.

Diagnosis Urolithiasis is diagnosed based on history, clinical signs, and physical examination findings. A variety of clinical signs can be seen, depending on the specific location of the urolith and the degree of urinary tract obstruction.

The primary presenting clinical signs of urolithiasis in horses with cystic and urethral calculi include hematuria, tenesmus, pollakiuria, incontinence, stranguria, and dysuria. Horses with calculi of the kidneys and ureters often present with weight loss and signs of abdominal pain. In chronic cases of urolithiasis, urine scalding of the hindlimbs and perineum may be seen.1,4,6,9 Diagnostic procedures such as rectal palpation of the urinary tract, ultrasonography, and cystoscopy can help determine the site, size, and number of calculi. The diagnosis of cystic calculi can be confirmed during rectal palpation by direct palpation of the urolith.

However, it is imperative to examine the entire urinary tract when urolithiasis is diagnosed. In a report by Laverty et al,4 9% of the observed group had calculi in more than one location.

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Urolithiasis CE FIGURE 3

Treatment Conservative and surgical treatments of urolithiasis have been described in the literature.11–16 Surgical intervention is frequently required to resolve clinical signs of urolithiasis. Previously described surgical techniques include laparocystotomy, perineal urethrotomy, urethral sphincterotomy and manual extraction, laparoscopic cystotomy, and pararectal cystotomy (Gökel’s technique). Recent technologic innovations such as laser lithotripsy and shock-wave therapy have been used to disrupt calculi. Selection of the appropriate surgical technique depends on the site and size of the calculus, the sex of the animal, the availability of surgical facilities and instrumentation, the anesthetic risk, and economic constraints.

Because cystic calculi are the most common and treatment differs greatly between the sexes, this article discusses the surgical management of cystic calculi in female and male horses separately.

Surgical Treatment of Urolithiasis in Mares The mare urethra is wide and is easily distended using manual manipulation. Therefore, uroliths can be extracted manually in some instances.9,16 Following intravenous sedation and epidural anesthesia, the urethra is gently dilated with a well-lubricated, gloved hand.

The calculus is manipulated into the trigone of the bladder, usually by manual transrectal positioning. Once the calculus is forced into the trigone, a few fingers are inserted into the urethra; with the use of manual dilation, the calculus is extracted from the bladder.

This technique is particularly useful in mares with calculi less than 10 cm in diameter. If this technique is unsuccessful, the calculus

A lithotrite can help crush a urolith into smaller pieces.

Courtesy of S. B. Adams, DVM, MS, DACVS

Ultrasonography may help evaluate concurrent nephrolithiasis.1 Endoscopy is indicated to confirm urethral and cystic calculi5 (FIGURE 2).

Other laboratory tests that are frequently conducted when urolithiasis is diagnosed include complete white blood cell count to identify infectious processes, serum biochemistry to identify azotemia, and urinalysis to determine urine pH and the presence of crystals and bacteria.1,4–6 If bacteria are identified, a bacterial culture is also indicated.

can be fragmented with a lithotrite (FIGURE 3), divided with a mallet and osteotome, or physically disrupted with laser or shock-wave lithotripsy. The fragments are then manually removed or flushed from the bladder. The instillation of sterile lubricating jelly can help minimize trauma to the urinary bladder and urethral mucosa by lessening the adherence of calculi fragments to the urethral and urinary bladder epithelium. When using this method, urethral sphincterotomy may help access and remove larger stones.9,16 In addition, newer techniques have been developed to break calculi into smaller fragments. These techniques involve the holmium:yttrium–aluminum–garnet (holmium:YAG) laser, the pulsed dye laser, and electrohydraulic and ballistic shock-wave lithotripsy.16 Laparocystotomy is typically not used because the anatomic features of the mare’s urethra make standing surgical procedures technically more feasible.

CriticalPo nt No obvious age, breed, or sex predisposition for urolithiasis has been observed in horses.

However, urolithiasis more often becomes a clinical problem in males.

Surgical Treatment of Urolithiasis in Male Horses Many surgical techniques have been described for treating cystic calculi in male horses. Recumbent techniques with the horse under general

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CriticalPo nt Type I uroliths are the most common and the easiest to break down for removal. These uroliths are yellow green, have a spiculated surface, and are normally composed of a variety of hydrated calcium carbonate salts.

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anesthesia as well as standing procedures have been described. The recumbent techniques include laparocystotomy and laparoscopic cystotomy. The standing techniques include perineal urethrotomy and pararectal urethrotomy (Gökel’s technique). Either laser lithotripsy or shock-wave therapy can be used to facilitate removal of larger calculi.

Compared with standing surgical removal, surgical removal with the patient under general anesthesia allows more control and access by the surgeon, who can ensure that all uroliths and fragments are removed. However, standing surgical techniques require fewer personnel and less equipment and do not carry the risks associated with general anesthesia and recovery. In addition, standing surgery is more economical for clients with financial restraints. However, large uroliths may not be removable with standing procedures without the help of additional techniques, such as laser lithotripsy or shock-wave therapy to fragment the urolith. If all uroliths are not removed, remaining fragments can act as a new nidus for stone formation and can result in subsequent obstruction of the urinary tract in male horses.

Recumbent Surgical Techniques Laparocystotomy has been recommended as the preferred treatment for cystic calculi in male horses. Described approaches include paramedian, ventral midline, and parainguinal laparocystotomy.9,12,17–19 The parainguinal approach has some advantages over the other approaches. The parainguinal approach avoids the major pudendal and superficial epigastric blood vessels and minimizes dead space created by reflection of the prepuce, which is encountered in the other approaches. In general, horses are positioned in dorsal recumbency under general anesthesia. An incision is made in the abdominal wall as described elsewhere or according to the surgeon’s preference. Once the abdominal cavity is entered, the bladder is palpated. The urinary bladder is often located just over the pelvic brim.

Typically, the bladder is thickened secondary to the chronicity of the cystic calculus. The bladder is exteriorized by grasping the calcu-

lus and slowly pulling the bladder to the level of the abdominal incision. Exteriorization of the bladder can be greatly aided by preoperative administration of diuretics such as furosemide (1.1 mg/kg IV) and dimethyl sulfoxide 90% (500 mL per 5 L of balanced polyionic fluid to make a 10% solution) as well as crystalloid intravenous fluids (a 10-L bolus before surgery). Preoperative administration of intravenous fluids and diuretics should distend the urinary bladder, making exteriorization of the bladder easier during surgery.

Once the bladder is exteriorized, stay sutures made of absorbable material are placed into the bladder. One surgeon has also recommended placement of a laparotomy sponge around the bladder neck to maintain bladder retraction following cystotomy.12 A cystotomy incision is made on the ventral aspect of the bladder, just large enough to facilitate easy removal of the calculus. It is important to remove all calculi to lessen the chance of recurrence. After calculi removal, the bladder is lavaged and the mucosa evaluated. The cystotomy and abdominal wall are closed routinely as described elsewhere.

Complications of laparocystotomy include septic peritonitis, bladder leakage resulting in uroperitoneum, and abdominal incision infection and dehiscence.1,9,14,19 Fortunately, complications are unusual if proper surgical and aseptic principles are employed. The benefits of laparocystotomy include complete visualization of the bladder and calculi, removal of all calculi, and reduced trauma to the urethra and bladder. This method does not require specialized equipment beyond readily available surgical instrumentation.

Laparoscopic or laparoscopic-assisted surgery has been performed by some surgeons within the past 10 years to treat urolithiasis. The positioning of the laparoscopic portals and the surgical techniques have been described elsewhere.18–21 Laparoscopic removal of cystic calculi is performed with the horse under general anesthesia and positioned in dorsal recumbency in Trendelenburg’s position.

Laparoscopic-assisted urolith removal involves a combination of laparoscopic visu-

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Urolithiasis CE alization and parainguinal laparocystotomy. A portal is created at the umbilicus for the laparoscope, and an instrument portal is created 2 to 3 cm medial to the external inguinal ring.

The cranial aspect of the bladder is grasped with laparoscopic grasping forceps and elevated to the ventral abdominal wall in the parainguinal region. The instrument portal is then longitudinally extended to facilitate exteriorization of the apex of the bladder, open cystotomy, and extraction of the urolith. After cystotomy closure, the bladder is repositioned and the incisions are closed.21 Closed laparoscopic urolith removal involves a similar initial approach for the laparoscopic and instrument portals; however, the cystotomy, urolith removal, and cystotomy closure are performed completely within the abdominal cavity using intracorporeal techniques.19 Once removed from the bladder, the uroliths are placed in a specialized sterile plastic bag.

The bladder is then lavaged and closed using intracorporeal suture techniques. After cystotomy closure, one of the laparoscopic portals is enlarged to facilitate removal of the plastic bag containing the calculi.

The primary advantages of laparoscopic techniques are that they negate the need for large abdominal incisions and minimize the postoperative recovery time. Laparoscopic techniques also allow enhanced visualization of the bladder and tension-free bladder closure. Disadvantages of laparoscopic removal of cystic calculi include prolonged surgical times and the need for specialized surgical instrumentation and advanced surgical training in laparoscopic techniques. An additional complication associated with the ventral laparoscopic technique is iatrogenic damage to the caudal epigastric artery and vein during portal placement.20

Standing Surgical Techniques Perineal urethrotomy can be performed in a standing male horse under epidural anesthesia.1,15,22 Small calculi (<5 cm in diameter) and fragments of calculi can be removed from the bladder by lavage or with sponge forceps, canine whelping forceps, or lithotrites, all of which are inserted through the perineal ure-

thral incision. Larger calculi (>10 cm in diameter) require crushing with lithotrites or with a mallet and osteotome. Likewise, techniques such as laser lithotripsy or shock-wave therapy can be used to fragment the calculus.1,23–27 Perioperative endoscopic visualization is re quired to ensure complete removal of calculi.

Small fragments should not be left within the bladder because they can result in urethral obstruction following healing of the urethrostomy incision or serve as a nidus for future urolith formation.6 These small fragments can be removed through lavage of the bladder with fluids. Iatrogenic trauma to the urethra and bladder mucosa is not unusual when this technique is used. The perineal urethrostomy incision is left open to heal by second intention. Urethral trauma during this procedure may result in postoperative urethra stricture or fistula formation. Fortunately, stricture of the urethra in equine patients is unusual following perineal urethrostomy. A greater incidence for calculi recurrence has been reported secondary to debris remaining in the bladder following surgical removal because of poor visualization and chronic cystitis.1,4 Pararectal cystotomy (Gökel’s technique) has been described as an alternative to perineal urethrostomy in horses with cystic calculus.

However, this procedure is not widely used because of complications such as an increased risk of entrance into the abdominal cavity and damage to the genitourinary tract, poor visualization of the bladder, and the need for deep dissection.1,12,13 Pararectal cystotomy is performed following standing chemical restraint and epidural anesthesia. An incision is made between the rectum and the semimembranosus muscle, and blunt dissection is used to expose the neck of the urinary bladder. The bladder is retracted to the level of the incision, the bladder neck is incised dorsolaterally, and the uroliths are removed with assistance per rectum. The wound is packed with gauze, and all incisions are allowed to heal by second intention. In one case report, this method was used successfully when other methods were not practical. However, the horse did develop unilateral orchitis secondary to the surgical procedure.13

CriticalPo nt Selection of the appropriate surgical technique depends on the site and size of the calculus, the patient’s sex, the availability of surgical facilities and instrumentation, the anesthetic risk, and economic constraints.

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CE Urolithiasis Additional Treatment Options for Urolithiasis Laser lithotripsy has been described for fragmentation of uroliths in male and female horses.23–25 Lithotripsy is usually performed in combination with perineal urethrostomy in males and via direct insertion into the urethra in females. Two surgical lasers have been used: the holmium:YAG laser and the pulsed dye laser.

Holmium:YAG lasers use a photothermal mode of action, which requires the calculus to be surrounded by water to absorb laser energy.

This photothermal effect allows precise placement of the energy on a region of the calculus for fragmentation.25 The photothermal effect does not appear to predispose horses to a greater risk for soft tissue damage. In addition to being used to fragment a calculus, this laser has been successfully used to make grooves in uroliths to place a lithotrite before removal. Successful use of the holmium:YAG laser to fragment small, less dense uroliths has been reported.25 However, failure of the holmium:YAG laser to fragment very large, dense uroliths for removal has also been reported.24 Pulsed dye lasers use a mechanical photoacoustic effect to fragment uroliths. They form a cavitation bubble, which is created by heated water around the calculus. When the bubble collapses, it emits an acoustic shock wave, resulting in fragmentation of the urolith.24 The pulsed dye laser has been associated with minimal trauma to the soft tissue and has been used successfully in treating not only cystic calculi but also urethral calculi in horses.23 With both lasers, an endoscope is used to directly visualize the whole procedure and to prevent soft tissue damage. The pulsed dye and holmium:YAG lasers are delivered to the calculus transendoscopically.23,25 Disadvantages associated with these lasers are the costs of use or purchase and prolonged operative times. The use of lasers can be expensive, ranging from $550 (for holmium:YAG lasers) to $1500 (for pulsed dye lasers) to rent them per treatment. The cost of purchasing a laser could range from $20,000 to $100,000.

According to the literature, the mean operative time for laser lithotripsy is approximately 2 hours; the time for actual use ranges from 12 to 30 minutes.23,25

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Shock-wave lithotripsy has also been used for urolith removal. Shock-wave lithotripsy is used in combination with an endoscope and either perineal urethrotomy in males or urethral sphincterotomy in females. 26,27 Electrohydraulic and ballistic shock-wave lithotripsy have been described for fragmentation of urinary calculi.3,16,26–30 Electrohydraulic shock-wave lithotripsy works by the generation of a spark across two electrodes. The formation and dispersion of the spark generate the shock waves that act on a large focus area in the urolith. Shearing forces generated by the absorption of the electrohydraulic shock waves disrupt the urolith’s crystalline structure, causing urolith fragmentation.28 The electrohydraulic lithotriptor must be kept in close contact with the urolith because if it contacts the epithelium, it can cause burns and eventual scar tissue formation.3 Rodger et al,3 MacHarg et al,16 and Eustace and Hunt29 all had success in using electrohydraulic lithotripsy to treat cystic calculi in a colt, a mare, and two geldings, respectively.

Ballistic shock-wave lithotripsy is less frequently described than electrohydraulic shockwave lithotripsy. The mechanism of action for the ballistic shock-wave lithotriptor is the acceleration of a long, thin lithoclast probe by a gas-driven lithoclast handle. The extension length of the lithoclast probe is limited to 2 mm, thereby preventing serious injury to the uroepithelium of the bladder wall as a result of its elasticity.27 The described procedure was actually performed successfully by Koening et al 27 with the use of perineal urethrotomy and with the patient in dorsal recumbency.

However, they also theorize that this modality could also be used in a standing animal.27 The specialized equipment and training and the long operative time might prevent widespread use of shock-wave lithotripsy.

Postoperative Care and Recurrence Postoperative management should include adequate water intake for proper hydration, antimicrobial therapy to control bacterial cystitis, and NSAID administration to reduce abdominal discomfort. When bacterial cystitis is present, antimicrobial selection should

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Urolithiasis CE be based on culture and sensitivity results.

Antimicrobial choice and duration of administration should be based on the degree of cystitis and the amount of urine spillage in the abdomen during the procedure.30 Trimethoprim–sulfamethoxazole, ampicillin, penicillin, aminoglycosides, and ceftiofur are possible choices in the postoperative treatment of cystic calculi in horses.30,31 In horses without concurrent bacterial cystitis, duration of treatment is normally 48 to 72 hours after surgery.30 NSAIDs such as flunixin meglumine are recommended for pain management following surgery.30 In addition, the horse should be checked regularly for proper urination.

In a study by Laverty et al,4 12 of 29 horses available for follow-up had clinical recurrence of urolithiasis. Postoperative acidification of urine is recommended by some authors to prevent recurrence of uroliths.1,6,27 Urine acidifiers decrease the urine pH enough that a urolith nidus cannot form. Calcium carbonate crystals, the main components of equine uroliths, form in an alkaline environment and dissolve in an acidic environment. It has been reported that calcium carbonate crystals are not found in urinary sediment at a pH lower than 6.0.32 Several urine acidifiers (e.g., ammonium chloride, ammonium sulfate, ascorbic acid) have reportedly been used in horses.1,6,11,27,32 Ammonium chloride does not consistently maintain a low urinary pH.33 Remillard et al32 found ammonium chloride to be unpalatable to horses and instead administered ammonium sulfate at a dosage of 175 mg/kg/PO bid to achieve a urinary pH of 5.0 for 7 months. Sertich et al11 used ascorbic acid as a urine acidifier at a dosage of 4000 mg PO q12h to reduce a stallion’s urine pH from 8.5 to 7.5. A dose of 1 kg/ horse PO q24h of ascorbic acid has also been described to achieve more adequate acidification of urine.1 A definitive timeline for the course of treatment with urinary acidifiers has not been tested or described. However, in a case report

by Remillard et al,32 after a 7-month course of ammonium sulfate, a horse with a history of chronic, recurrent urolithiasis was successfully managed by diet alone for 2 years without recurrence of the condition. Urinary acidifiers

were used intermittently in the cases that were reviewed for this article. Acidifier use varied by type, dose, and duration of treatment. However, no prospective research has been conducted to determine the efficacy of acidifiers or a standardized method of treatment. Lack of efficacy data, a standard method of use, and the success that we and others have had without using urine acidifiers suggest that caution should be exercised when using urine acidifiers. More research is needed to determine their value and develop definitive regimens for treating equine urolithiasis.

Dietary change in addition to the use of urinary acidifiers has also been described for reducing the recurrence of urolith formation.11,33 Horses absorb a large amount of calcium through their gastrointestinal tract and subsequently excrete large amounts through their kidneys.32 Reducing the amount of calcium in their diet might help prevent urolith formation. Another method of dietary management is to control the dietary cation–anion balance (DCAB) to influence systemic pH and mineral excretion. A DCAB of less than 100 mEq/kg of dry feed matter makes the rations acidogenic. This decreases venous and urine pH and enhances the excretion of minerals, especially calcium.3,32,33 Increasing the amount of grain in the diet or feeding lower-quality hay usually lowers the DCAB. However, this method needs to be investigated further to determine its efficacy in preventing urolith formation and its safety for an extended period of time.

CriticalPo nt New modalities of laser and shockwave therapy offer equine practitioners less traumatic and less invasive methods of treating urolithiasis, but they are not yet being used routinely.

Conclusion Scientific and technologic advancements have opened new avenues for treating urolithiasis in horses. Currently, we believe that laparocystotomy, perhaps combined with laparoscopy, will remain the preferred treatment for urolithiasis in male horses. However, the increased use of lithotripsy with radial shock waves may result in outcomes similar to those associated with laparocystotomy. The use of laser lithotripsy is currently limited to referral centers, mainly because of the higher costs associated with purchasing or renting this equipment. In female horses, urolithiasis can generally be

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CE Urolithiasis managed with manual extraction or lithotripsy techniques performed via the urethra. New modalities of laser and shock-wave therapies offer equine practitioners less traumatic and less invasive methods of treating urolithiasis, but they are not yet being used routinely.

These modalities need to be refined to reduce surgical time and offer a greater probability of success before they can be recommended as replacements for more conventional treatments. Postoperative management of horses with urolithiasis should include broad-spectrum antimicrobial therapy for at least 48 to 72 hours. In addition, NSAIDs should be used for postoperative pain management. Although

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it is important to ensure adequate water consumption, the use of postoperative urinary acidifiers is questionable because of the lack of evidence of their efficacy and the absence of a definitive treatment regimen.

References 1. Mair T, Holt P. The aetiology and treatment of equine urolithiasis.

Equine Vet Educ 1994;6:189-192.

2. Schott II HC. Obstructive disease of the urinary tract. In: Reed SM, Bayly WM, eds. Equine Internal Medicine. Philadelphia: WB Saunders; 1998:880-890.

3. Rodger L, Carlson G, Moran M, et al. Resolution of a left ureteral stone using electrohydraulic lithotripsy in a thoroughbred colt.

J Vet Intern Med 1995;9:280-282.

4. Laverty S, Pascoe J, Ling G, et al. Urolithiasis in 68 horses. Vet Surg 1992;21:56-62.

5. Saam D. Urethrolithiasis and nephrolithiasis in a horse. Can Vet J 2001;42:880-883.

6. De Jaeger E, De Keersmaecker S, Hannes C. Cystic urolithiasis in horses. Equine Vet Educ 2000;Feb:30-35.

7. Johnson PJ, Crenshaw KL. The treatment of cystic and urethral calculi in a gelding. Vet Med 1990;85:891-900.

8. Textor J, Slone D, Clark C. Cystolithiasis secondary to intravesical foreign body in a horse. Vet Rec 2005;156:24-26.

9. Lillich JD, Fischer Jr AT, Debowes RM. Bladder. In: Auer JA, Stick JA, ed. Equine Surgery. St Louis: Saunders Elsevier; 2006:877-887.

10. Osborne C, Sanna J, Unger L, et al. Analyzing the mineral composition of uroliths from dogs, cats, horses, cattle, sheep, goats, and pigs. Vet Med 1989;Aug:750-764.

11. Sertich P, Pozor M, Meyers S, et al. Medical management of urinary calculi in a stallion with breeding dysfunction. JAVMA 1998;213:843-846.

12. Beard W. Parainguinal laparocystotomy for urolith removal in geldings. Vet Surg 2004;33:386-390.

13. van Dongen P, Plenderleith R. Equine urolithiasis: surgical treatment

by Gökels pararectal cystotomy. Equine Vet Educ 1994;6:186-188.

14. Holt PE, Pearson H. Urolithiasis in the horse: a review of 13 cases. Equine Vet J 1984;16:31-34.

15. DeBowes RM. Surgical management of urolithiasis. Vet Clin North Am Equine Pract 1988;4:461-471.

16. MacHarg M, Foerner J, Phillips T. Electrohydraulic lithotripsy for treatment of a cystic calculus in a mare. Vet Surg 1985;14:325-327.

17. Reed D. Suprapubic cystotomy in a stallion. Can J Comp Med Vet Sci 1964:28.

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18. Lowe J. Surgical removal of equine uroliths via the laparocystotomy approach. JAVMA 1961;139:345-348.

19. Ragle CA. Laparoscopic removal of cystic calculi. In: Fischer Jr AT, ed. Equine Diagnostic & Surgical Laparoscopy. Philadelphia: WB Saunders; 2002:229-234.

20. Ragle CA. Dorsally recumbent urinary endoscopic surgery.

Vet Clin North Am Equine Pract 2000;16:343-350.

21. Röcken M, Stehle C, Mosel G, et al. Laparoscopic-assisted cystotomy for urolith removal in geldings. Vet Surg 2006;35(4):394-397.

22. Hanson RR, Poland HM. Perineal urethrotomy for removal of cystic calculi in a gelding. JAVMA 1995;207:418-420.

23. Howard R, Plesant R, May K. Pulsed dye laser lithotripsy for treatment of urolithiasis in two geldings. JAVMA 1998;212:1600-1603.

24. May K, Pleasant S, Howard R, et al. Failure of holmium:yttriumaluminum-garnet laser lithotripsy in two horses with calculi in the urinary bladder. JAVMA 2001;219:957-961.

25. Judy C, Galuppo L. Endoscopic-assisted disruption of urinary calculi using a holmium:YAG laser in standing horses. Vet Surg 2002;31:245-250.

26. Foerner JJ, Santschi EM. How to use radial shock waves to remove bladder uroliths through a perineal urethrotomy. Proc AAEP 2005.

27. Koening J, Hurtig M, Pearce S, et al. Ballistic shock wave lithotripsy in an 18-year-old gelding. Can Vet J 1999;40:185-186.

28. Adams L, Senior D. Electrohydraulic and extracorporeal shock-wave lithotripsy. Vet Clin North Am Small Anim Pract 1999;29:293-301.

29. Eustace R, Hunt J. Electrohydraulic lithotripsy for the treatment of cystic calculus in two geldings. Equine Vet J 1988;20:221-223.

30. McIlwraith CW, Robertson JT. McIlwraith and Turner’s Equine Surgery, Advanced Techniques. Baltimore: Williams & Wilkins; 1998:401-404.

31. Schott II HC. Urinary tract infections. In: Reed SM, Bayly WM, eds. Equine Internal Medicine. Philadelphia: WB Saunders; 1998:875-879.

32. Remillard R, Modransky P, Welker F, et al. Dietary management of cystic calculi in a horse. J Equine Vet Sci 1992;12:359-363.

33. Wall DL, Topplier DR, Freeman DW. Effects of dietary cation–anion balance on urinary mineral excretion in exercised horses. Proc Equine Nutr Physiol Symp 1991:121-126.

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Urolithiasis CE

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 conditions must be present for urolith formation to occur? a. presence of a nidus and urine acidity b. calcium carbonate crystals and increased urine volume c. urine stasis and material to act as a nidus d. urine alkalinity and high-fraction excretion of calcium 2. Uroliths clinically present most frequently in the a. penile urethra of stallions. b. ureters of geldings. c. kidneys of mares. d. bladder of male horses.

3. The holmium:YAG laser may fail to fragment cystic calculi when a. large, very dense calculi are present. b. smaller, denser calculi are present. c. the calculi are in the ureters. d. calculi are composed of calcium carbonate crystals.

4. A complication associated with laparoscopic cystotomy is a. poor anesthetic recovery associated with prolonged recumbency in Trendelenburg’s position. b. injury to the caudal epigastric artery vein. c. longer surgical times for instrument portal placement. d. the inability to adequately visualize the bladder.

5. Which of the following regarding electrohydraulic shock-wave lithotripsy should be avoided? a. use in the kidneys b. the pressure generated when the cavitation bubble collapses c. contact between the epithelium and electrode, which may cause burning and scarring d. use on a large, dense urolith 6. When urolithiasis is suspected in a horse, it is a. not important to check the whole urinary tract if the clinician has already palpated a calculus in the bladder. b. important to check the whole urinary tract because nephroliths are the most common calculi.

c. not important to check the whole urinary tract in mares because of their lower incidence of urolithiasis. d. important to check the whole urinary tract because multiple calculi can be present in several locations.

7. Which statement regarding NSAID administration and patient hydration in horses with urolithiasis is correct? a. It is important to ensure adequate hydration in affected patients because cells that slough from the renal papilla can serve as a nidus for calculus formation. b. Patient hydration is not important when NSAIDs are administered. c. Only male horses need to be adequately hydrated because they cannot excrete calculi as easily as females. d. It is important to ensure adequate patient hydration because NSAIDs must be excreted through the urine to be effective.

8. The most common urolith found in horses is a. type I, which is smooth and white. b. type II, which is smooth and white. c. type I, which is yellow green and spiculated. d. type II, which is yellow green and spiculated.

9. The most commonly used method of urolith removal in mares is a. laparocystotomy. b. Gökel’s pararectal cystotomy. c. manual removal through the urethra with or without sphincterotomy. d. pararectal cystotomy.

10. In electrohydraulic shock-wave lithotripsy, calculus fragmentation is achieved through a. a photothermal mode of action. b. crystalline structure disruption by shearing forces that are created by shock waves. c. cavitation bubble formation, which emits an acoustic shock wave. d. a mechanical photoacoustic effect.

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Perinatal Asphyxia Syndrome in Foals *

❯❯ Wendy E. Vaala, VMD, DACVIMa Equine Technical Services | Intervet, Inc. | Millsboro, Delaware

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he most common effects of perinatal asphyxia are: Neurologic deficits ranging from hypotonia to grand mal seizures Gastrointestinal (GI) disturbances ranging from mild ileus and delayed gastric emptying to severe, bloody diarrhea and necrotizing enterocolitis Renal compromise accompanied by varying degrees of oliguria

*Updated by the author and reprinted with permission from Standards of Care: Equine Diagnosis and Treatment 2002;2.1:1-7. a Dr. Vaala discloses that she is employed by Intervet/Schering-Plough Animal Health.

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Perinatal Asphyxia Syndrome in Foals

Based on the neurologic deficits (including loss of affinity for the dam, seizures, impaired sucking and swallowing reflexes, and abnormal vocalization), affected foals have been called dummies, convulsives, barkers, and wanderers. Neonatal encephalopathy, neonatal maladjustment syndrome, and hypoxicischemic encephalopathy are commonly used to describe this condition. Central nervous system (CNS) disturbances associated with this condition ultimately result from necrosis and occasional hemorrhage.

During severe in utero compromise, there is sequential loss of fetal reflexes, with the most oxygen-demanding fetal activities disappearing first. Fetal reflexes are lost in the following order: 1. Fetal heart rate reactivity (the ability to increase heart rate in response to fetal activity) 2. Fetal breathing 3. Generalized fetal movements 4. Fetal tone These biophysical events, in addition to amniotic fluid volume estimation and placental integrity, can be evaluated in late pregnancy using transabdominal ultrasonography.

Diagnostic Criteria Historical Information

Thiamine Thiamine (1–20 mg/kg q12h) can be added to IV fluids to help preserve aerobic brain metabolism. Thiamine deficiency has been associated with intracellular and extracellular edema and neuronal cell death due to glutamate-induced, NMDA receptor– mediated excitotoxicity and compromised mitochondrial function. placentitis, hydrops allantois, hydrops amnii, prepubic tendon rupture) are more likely to deliver affected foals. Severe maternal illness accompanied by anemia, hypoproteinemia, or endotoxemia can alter uteroplacental blood flow, resulting in fetal asphyxia. Postterm pregnancies have been associated with varying degrees of placental insufficiency and the birth of small, underweight, maladapted foals.

Foals may appear normal at birth and then develop a host of behavioral abnormalities, including the loss of coordinated swallowing and sucking reflexes, the inability to locate the udder, the tendency to wander from the mare and walk into walls, generalized hypotonia, and seizures.

Physical Examination Findings

No sex or breed predilection.

Signs of peripartum asphyxia during the first 24 to 72 hours of life.

Delivery may be outwardly normal in cases in which prepartum asphyxia is due to some form of unrecognized placental insufficiency and in utero hypoxia. Events during delivery that are associated with hypoxia include the following: Dystocia Premature placental separation (“redbag” delivery) Twinning Meconium staining of fetal fluids, placenta, and/or foal Evidence of diffuse placental pathology, including an unusually heavy or edematous placenta (e.g., placental weight >10% to 11% of the foal’s birth weight).

Mares with reproductive tract disease (e.g.,

Mildly affected foals exhibit jitteriness and hyperexcitability.

Moderately affected foals exhibit stupor, somnolence, lethargy, and hypotonia, which may be accompanied by epileptiform seizures and extensor rigidity. Additional clinical signs include dysphagia, decreased tongue tone, odontoprisis, central blindness, mydriasis, anisocoria, nystagmus, head tilting, and loss of the suckle reflex.

Premature foals are more likely to experience “subtle seizures” characterized by paroxysmal events, including eye blinking, eye deviation, nystagmus, pedaling movements, a variety of oral–buccal–lingual movements (e.g., intermittent tongue protrusion, sucking behavior), whole body thrashing, and other vasomotor changes (e.g., apnea, abnormal breathing patterns, changes in heart rate). Tonic posturing is another subtle seizure activity characterized

CriticalPo nt Foals may appear normal at birth and then develop a host of behavioral abnormalities, including the loss of coordinated swallowing and sucking reflexes, the inability to locate the udder, the tendency to wander from the mare and walk into walls, generalized hypotonia, and seizures.

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Perinatal Asphyxia Syndrome in Foals

CriticalPo nt Severely affected foals exhibit marked CNS depression, coma, and loss of central regulation of respiration, blood pressure, and temperature, ultimately leading to death.

by symmetric limb hyperextension or flexion and is often accompanied by abnormal eye movements and apnea.

Severely affected foals exhibit marked CNS depression, coma, and loss of central regulation of respiration, blood pressure, and temperature, ultimately leading to death.

Limb deficits and generalized spasticity are less common.

Signs of renal compromise include decreased urine production with subsequent peripheral edema formation.

The GI tract is often affected. Mild cases may involve transient ileus, constipation, and mild colic. The most severe form of intestinal dysfunction is necrotizing enterocolitis. During GI ischemia, mucosal cell metabolism diminishes and production of the protective mucous layer ceases, allowing proteolytic enzymes to begin autodigestion of the mucosal barrier. Bacteria within the lumen can then colonize, multiply, and invade the bowel wall. Intramural gas is produced by certain species of bacteria, and pneumatosis intestinalis develops. Possible complications include intestinal rupture, pneumoperitoneum, severe bacterial peritonitis, and septicemia.

Laboratory Findings TABLE 1 lists clinical signs associated with specific organ system dysfunction and the laboratory abnormalities to anticipate.

Metabolic acidosis: pH <7.3; bicarbonate concentration <20 mEq/L. Prepartum placental insufficiency may be associated with neonatal azotemia: creatinine concentration >3.5 mg/dL. Foals experiencing respiratory depression may develop hypoxemia and respiratory acidosis: Po2 <60 mm Hg; Pco2 >65 mm Hg.

Other Significant Diagnostic Findings Transabdominal ultrasonography of the pregnant mare should be used to evaluate fetal well-being and placental integrity: The mare’s ventral midline must be cleaned and clipped from the level of the umbilicus caudally to the mammary gland, and a viscous coupling gel should be applied.

Minimal maternal restraint is usually

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required. Chemical sedation should be avoided because drugs such as xylazine and detomidine induce fetal bradycardia and decrease fetal movement.

A 2.5- to 3.5-MHz transducer is used.

Signs suggestive of fetal or placental compromise during the last month of gestation include the following: Persistent fetal bradycardia: fetal heart rate <50 to 60 bpm; loss of fetal heart rate variability Reduced or absent fetal movement for prolonged periods (>30 min) Decreased volume of fetal fluids: maximum ventral fetal fluid pocket depths average 8 cm for amniotic fluid and 13 cm for allantoic fluid Large areas of placental separation Generalized placental thickening: combined uteroplacental thickness >15 mm Transrectal measurements of uteroplacental thickness around the cervical star should not exceed 12 mm after day 330 of gestation.

Foals with necrotizing enterocolitis have generalized ileus and thickening of the bowel wall with or without intramural gas accumulation visible on transabdominal ultrasonography when a 5- to 7.5-MHz transducer is used.

Summary of Diagnostic Criteria History of abnormal periparturient events, including fetal compromise on ultrasonography, gross placental abnormalities, or delivery complicated by dystocia; premature placental separation; or meconium staining.

Development of neurologic deficits in the newborn foal within the first 24 to 72 hours of life; the most common CNS disturbances include hypotonia, loss of suckle reflex, loss of affinity for the dam, and focal or grand mal seizures.

No other obvious cause of CNS disease, including septic meningitis, electrolyte disturbances, and trauma.

Hemogram and serum chemistries are often normal, except for azotemia associated with placental compromise and metabolic acidosis.

Foals experiencing severe dystocia often

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Perinatal Asphyxia Syndrome in Foals have elevated serum concentrations of the muscle-specific enzyme creatine kinase.

The neonatal pancreas and liver can also sustain injury.

Foals with pancreatic damage may demonstrate insulin-responsive hyperglycemia.

Neonates sustaining hepatic injury may have elevated concentrations of the hepatocellular enzyme sorbitol dehydrogenase.

Computed tomography and magnetic resonance imaging are newer modalities being used to evaluate CNS lesions.

Differential Diagnosis Seizures during the first few days of life can be congenital or acquired. Causes of acquired seizures include the following: Metabolic disorders: Hypocalcemia, hypomagnesemia, hyponatremia, hypernatremia, hypoglycemia Hyperosmolality: Hyperlipemia, hyperglycemia TABLE 1

Severe azotemia Hepatoencephalopathy: Elevated liver enzyme (aspartate aminotransferase, γ-glutamyltransferase, sorbitol dehydrogenase), serum ammonia, and bilirubin levels concurrent with low blood glucose and blood urea nitrogen levels Infectious conditions: Bacterial meningitis Spinal fluid analysis: leukocytes >5 to 10 cells/μL; total protein >150 mg/dL Positive blood culture result Abnormal hemogram results: leukopenia, neutropenia, toxic granules in neutrophils Viral meningitis associated with equine herpesvirus 1 infection Positive presuckle viral titers Virus isolation from buffy coat Polymerase chain reaction testing using nasal swabs and buffy coat samples Cranial trauma

Checkpoint Some experts disagree on the use of mannitol and DMSO for treating cerebral edema.

Clinicopathologic Conditions Associated with Perinatal Asphyxia Syndrome

Organ System

Clinical Signs

Laboratory Findings

Pathology/Lesions

CNS

Hypotonia, hypertonia, seizures, coma, loss of suckle reflex, proprioceptive deficits, apnea

Increased intracranial pressure, blood–brain barrier permeability, and albumin quotient

CNS hemorrhage, intracellular edema, ischemic necrosis

Renal

Oliguria, anuria, generalized edema

Azotemia, hyponatremia, hypochloremia, abnormal urinalysis results

Tubular necrosis, glomerular damage

Gastrointestinal

Colic, ileus, abdominal distention, bloody diarrhea, gastric reflux

Occult blood in the feces and reflux, pneumatosis intestinalis

Ischemic mucosal necrosis, enterocolitis, ulceration

Respiratory

Respiratory distress, tachypnea, dyspnea, rib retractions

Hypoxemia, hypercapnia, respiratory acidosis

Hyaline membrane disease, atelectasis, meconium aspiration, rib fractures, pulmonary hypertension

Cardiac

Arrhythmia, weak pulses, tachycardia, edema, hypotension

Hypoxemia, elevated myocardial enzymes

Myocardial infarct, valvular insufficiency, persistent fetal circulation

Hepatic

Icterus, abnormal mentation

Hyperbilirubinemia, elevated liver enzymes

Hepatocellular necrosis, biliary stasis

Endocrine (adrenal and parathyroid glands)

Weakness, apnea, seizures

Hypocortisolemia, hypocalcemia

Necrosis, hemorrhage

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

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Perinatal Asphyxia Syndrome in Foals

CriticalPo nt CSF analysis is indicated if septic meningitis is a possible differential. Septic meningitis produces an increased nucleated cell count, protein concentration, and IgG index in the CSF. Brain damage may result in an increased albumin quotient in the CSF compatible with increased blood–brain barrier permeability.

Congenital causes of seizures include CNS malformations, including hydrocephalus, corpus callosum agenesis, cerebellar abiotrophy (most common in Arabians), hydranencephaly, and lavender foal syndrome (observed in Arabian foals of Egyptian lineage that have diluted coat color).

Normal serum chemistry results help rule out metabolic disturbances.

A normal leukogram or the absence of severe leukopenia, neutropenia, and toxic neutrophil changes may help rule out septic conditions.

Cerebrospinal fluid (CSF) analysis is indicated if septic meningitis is a possible differential. Septic meningitis produces an increased nucleated cell count, protein concentration, and IgG index in the CSF. Brain damage may result in an increased albumin quotient in the CSF compatible with increased blood–brain barrier permeability.

Treatment Recommendations (TABLE 2) Initial Treatment Seizure Control Diazepam (0.11 to 0.44 mg/kg IV) Can repeat dose in 30 minutes Rapid onset of action, but short duration of effect Inactivated by plastic and sunlight Avoid repetitive doses to reduce risk of respiratory depression Phenobarbital (2 to 10 mg/kg slowly IV q8–12h) High doses and rapid rate of administration are associated with respiratory depression.

Infuse slowly over 15 to 20 minutes.

Expect peak effect within 45 minutes.

Possible Treatments for CNS Cellular Damage Mannitol (0.25 to 1.0 g/kg IV given as a 20% solution over 20 to 30 min q4–12h).

May exacerbate severe intracranial hemorrhage.

Excessive administration may induce significant alterations in plasma osmolality. Monitor hydration status.

Dimethyl sulfoxide (DMSO; 0.5 to 1.0 g/kg IV given as a 20% solution slowly over 1 hr q12–24h).

Use cautiously in hypotensive neonates.

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Alternative route of administration is via nasogastric intubation but is not usually recommended in critically ill neonatal foals.

Therapy for Central Respiratory Center Depression and Periodic Apnea Caffeine (10 mg/kg PO or per rectum as initial loading dose, followed by maintenance dose of 2.5 to 3.0 mg/kg PO q24h).

Helps increase carbon dioxide sensitivity of central respiratory center, leading to an increased respiratory rate Most effective when hypercapnia has produced significant acidosis In certain cases of persistent hypercapnia, positive pressure ventilation may be necessary.

Broad-Spectrum, Bactericidal Antimicrobials to Treat and Prevent Secondary Sepsis Amikacin (20 to 28 mg/kg IV q24h) and potassium penicillin (22,000 to 40,000 IU/kg IV q6h) or ampicillin sodium (20 to 50 mg/ kg IV q6h); if amikacin is used, peak and trough monitoring is recommended.

Ceftiofur (5 to 10 mg/kg IV q6–12h)

Alternative/Optional Treatments Seizure control: Pentobarbital (2 to 10 mg/kg IV q4–8h or to effect) is an alternative to phenobarbital. Long-term use is not recommended.

Midazolam (2 to 5 mg IM for a 110-lb [50kg] foal) can be given IV, but hypotension and apnea may occur following rapid IV administration. Use lowest effective dose.

Naloxone (0.01 to 0.02 mg/kg IV), an opiate antagonist, has been used to diminish CNS depression.

Low doses of magnesium sulfate (50 mg/ kg/hr diluted to 1% solution and given slowly IV as a constant-rate infusion for 1 hr, then decreased to 25 mg/kg/hr as a constant-rate infusion for up to 24 hr) may be considered.

Magnesium acts as an NMDA-receptor antagonist and may reduce the hypoxia-induced increase in oxygen free radical generation.

Ascorbic acid (vitamin C) has been advocated as an antioxidant. It is believed to act as a neuromodulator that inhibits neurotransmitter binding to NMDA receptors. The optimal dose for neuroprotection has not been determined. Oral doses vary from 50 to 100 mg/kg/day.

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

Perinatal Asphyxia Syndrome in Foals -Tocopherol (vitamin E) has also been advocated for its antioxidant effect. Peroxyl radicals liberated during hypoxia-induced lipid peroxidation react with α-tocopherol instead of a free fatty acid, thereby terminating a potentially destructive process. The optimal dose of vitamin E has not been established. I have used 500 to 1000 U/day PO.

Supportive Treatment Protect the foal from self-trauma during seizures.

Provide a padded environment and soft, absorbent bedding.

Wrap limbs.

TABLE 2

Apply artificial tears to the eyes to prevent secondary corneal ulceration.

Ensure adequate passive transfer of colostral antibodies.

The foal’s serum IgG should be >800 mg/dL by 18 to 24 hours of age. If IgG is <800 mg/dL: Give a minimum of 10 mL/kg of hyperimmune plasma IV if the foal is >18 to 24 hours of age or gut function is compromised.

Give a minimum of 40 g/kg IgG PO by bottle or nasogastric tube using good-quality colostrum or an artificial IgG supplement if the foal is <12 to 18 hours of age and has a functional gut

Drugs Commonly Used to Treat Foals

Organ System

Clinical Signs

Drug Therapy

CNS

Seizures

Diazepam: 0.11–0.44 mg/kg IV Phenobarbital: 2–10 mg/kg IV q12h (give slowly, monitor serum level) or 2–10 mg/kg IV to effect DMSO: 0.5–1.0 g/kg IV as 20% solution over 1 hr; can be repeated q12h Mannitol: 0.25–1.0 g/kg IV as 20% solution over 15–20 min q12–24h

Renal

Oliguria, anuria

Dobutamine infusion: 2–15 μg/kg/min; consider use if cardiac dysfunction is contributing to hypotension and poor renal perfusion

Gastrointestinal

Ileus, GI distention

Erythromycin: 1–2 mg/kg PO q6h or 1–2 mg/kg/hr IV infusion q6h Cisapride: 10 mg PO q6–8h Metoclopramide: 0.25–0.5 mg/kg/hr CRI q6–8h or 0.6 mg/kg PO q4–6h Bethanechol: 0.03 mg/kg SC q8h or 0.16–0.2 mg/kg PO q8h

Ulcers

Sucralfate: 20–40 mg/kg PO q6h Ranitidine: 5–10 mg/kg PO q6–8h or 1–2 mg/kg IV q8h Cimetidine: 15 mg/kg PO q6h or 6.6 mg/kg IV q6h Omeprazole: 4.0 mg/kg PO q24h (not labelled for use in foals < 4 weeks of age)

Cardiac

Hypotension

Vasopressin infusion: 0.25–1.0 mU/kg/min Dobutamine infusion: 2–15 μg/kg/min Digoxin: 0.02–0.035 mg/kg PO q24h if cardiac failure is suspected

Respiratory

Hypoxemia

Intranasal humidified oxygen insufflation: 2–10 L/min

Apnea

Caffeine: Loading dose: 10 mg/kg PO Maintenance dose: 2.5–3.0 mg/kg PO q24h (Some experts prefer doxapram HCl instead of caffeine in neonatal foals.a,b)

Endocrine

Hypocortisolemia

Adrenocorticotropic hormone (depot): 0.26 mg IM q8–12h

Immune

Failure of passive transfer, leukopenia

Hyperimmune plasma: 10–20 mL/kg IV; monitor serum IgG level and leukocyte count

a

Giguère S, Sanchez LC, Shih A, et al. Comparison of the effects of caffeine and doxapram on respiratory and cardiovascular function in foals with induced respiratory acidosis. Am J Vet Res 2007;68(12):1407-1416. b Giguère S, Slade JK, Sanchez LC. Retrospective comparison of caffeine and doxapram for the treatment of hypercapnia in foals with hypoxic-ischemic encephalopathy. J Vet Intern Med 2008;22(2):401-405.

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

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Perinatal Asphyxia Syndrome in Foals

Recommended d Reading Paradis MR. Neurologic dysfunction. In: Paradis MR, ed. Equine Neonatal Medicine—A Case-Based Approach.

Philadelphia: Elsevier Saunders; 2006:179190.

Vaala WE. Peripartum asphyxia. Vet Clin North Am Equine Pract 1994;10(1):187-218.

Vaala WE. Peripartum asphyxia syndrome in foals. Proc AAEP 1999;45:247-253.

Vaala WE, House JK. Perinatal adaptation, asphyxia, resuscitation.

In: Smith BC, ed. Large Animal Internal Medicine, ed 3. Philadelphia: Mosby; 2002:266-276.

Wilkins PA. Magnesium infusion in hypoxic-ischemic encephalopathy. Proc 19th ACVIM Forum 2001:242-244.

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(e.g., no signs of colic or reflux).

Provide adequate nutrition and monitor glucose level until the foal can nurse normally from the mare.

Minimal nutritional requirement = 10% of the foal’s body weight per day as milk fed as small meals every 1 to 2 hours (e.g., a 110-lb [50-kg] foal would require a minimum of 5 L or 11 pints of milk per day divided into 10 to 12 feedings per day).

Offer milk by bottle if the foal has a strong suckle reflex and a coordinated swallow reflex.

Tube feed by nasogastric intubation if the suckle or swallow reflexes are ineffective.

Consider IV fluids supplemented with dextrose if the foal is inappetent; however, use parenteral nutrition if the foal is critically ill or has severe necrotizing enterocolitis.

Continue to milk the mare every 2 to 3 hours until the foal can nurse normally.

Maintain cerebral perfusion, tissue perfusion, and blood pressure by administration of IV crystalloid fluids.

Patient Monitoring Perform serial neurologic evaluations to assess the response to treatment.

Monitor vital signs (including blood pressure), manure and urine production, and peripheral pulses. If respiratory depression is present, check the arterial blood gases to assess pulmonary function and the need for oxygen therapy.

Frequently monitor the blood glucose level.

Caution Use caution and monitor renal parameters (creatinine and blood urea nitrogen levels, urinalysis) when administering potentially nephrotoxic medications (amikacin, flunixin meglumine) to critically ill neonatal foals.

Prognosis With proper support, 70% to 80% of foals with this condition recover. Most foals recover completely, and many “survivors” perform successfully as racehorses and other athletes.

Foals with the poorest prognosis develop sepsis, fail to show any signs of neurologic improvement within the first 5 days of life, remain comatose and difficult to arouse, and experience severe, recurrent seizures.

Dysmature and premature foals with prolonged in utero insult are more likely to have refractory hypotension and persistent subtle seizure activity than are full-term foals. Rare, long-term CNS sequelae include unusual docility as an adult, vision impairment, residual gait spasticity, and recurrent seizures.

Favorable Criteria A full-term foal experiencing a brief in utero or peripartum insult Minimal or mild GI and renal involvement A foal that is normal at birth, with CNS deficits developing within 12 to 24 hours of delivery

Unfavorable Criteria Milestones/Recovery Time Frames Expect to see stabilization of CNS signs within the first 48 to 72 hours following delivery.

Expect to observe gradual improvement in neurologic signs within the first 3 to 5 days.

Some foals may not regain the ability to nurse from the mare for 7 to 10 days.

Treatment Contraindications Avoid acepromazine because it lowers the seizure threshold.

Avoid xylazine because it causes transient hypertension that can exacerbate CNS hemorrhage.

Advanced prematurity in addition to an in utero or peripartum insult Concurrent septicemia Severe necrotizing enterocolitis Nonresponsive hypotension and oliguria Persistent seizures that continue past 5 days of age despite anticonvulsive therapy A foal that is abnormal immediately following delivery and remains comatose and nonresponsive Signs of severe brainstem damage: loss of thermoregulatory control, profound apnea, marked increase in intraocular pressure suggestive of increased intracranial pressure.

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

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142

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

You Might Be a Mixed Animal Practitioner If …

S

ome practitioners say that the time of the “James Herriot” veterinarian is long gone and that the future of mixed animal practice is bleak because of the perception of long hours, lower pay, and difficult work or working conditions. I believe that mixed animal practice is a lifestyle choice. Some practitioners find it unacceptable to live 10 miles from a grocery store or gas station or to drive an hour to go to a movie or a nice restaurant. After more than 33 years as a mixed animal practitioner, I still find that it’s what I’ve always wanted to do.

Here are some other lifestyle markers for my profession. You might be a mixed animal practitioner if …

… a client has found you at a school Christmas program to tell you he has a cow problem. … you can discuss gross pathology at the dinner table. … you’ve gotten into your truck and found that the farmer’s wife has left you a sack of zucchini, tomatoes, or sweet corn. … a farmer has invited you into his kitchen for fresh-baked cookies and coffee. … you’ve attended your child’s school events—academic, musical, or athletic— in your work clothes, and your work odors followed you. … a client has found you at a school Christmas program to tell you he has a cow problem. … you’ve attended your child’s wedding with tattoo ink on your fingers. … you can identify the muscle you’re

144

eating for dinner when asked by your children. … you find satisfaction in solving a difficult case of dystocia. … you have looked at the clock in your truck and were still on schedule at 5:00 PM, which made you smile. … you’ll go to the office to look at a sick puppy while dressed in your Sunday best. … you’ve smiled at the successful outcome of a milk fever case. … you’ve enlisted the aid of an owner when performing a cesarean section. … you’ve performed cesarean sections on all major holidays and at all times of the day and night. … you can make a diagnosis and prescribe treatment using only your thermometer, stethoscope, eyes, ears, and hands. … you can make a diagnosis and prescribe treatment without conducting a complete blood count, chemistry profile, or urinalysis. … your clients are your friends and call you Doc.

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

CompendiumEquine.com

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

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