P-Iss5_2011

The PractitionerPublished by the Florida Association of Equine Practitioners,

an Equine-Exclusive Division of the Florida Veterinary Medical AssociationIssue 5 • 2011

In This Issue 6 | Pain Models and Scoring & Pain

Management in Horses

10 | 2011 Continuing Education – A Tremendous Success!

15 | Arrhythmias in the Performance Horse

19 | FAEP Member Practice Highlight

20 | Endocrinopathic Laminitis

23 | The Genetic Basis for Muscle Disorders in Horses

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Letter from the President

EXECUTIVE COUNCILGregory D. BonenClark,

DVM, Diplomate ACVS FAEP Council President

[email protected] Anne L. Moretta, VMD, MS

FAEP Council Vice President [email protected]

Jacqueline S. Shellow, DVM, MS

FAEP Council Past President [email protected]

Mr. Philip J. Hinkle Executive Director [email protected]

COUNCIL REPRESENTATIVESJ. Barry David, DVM,

Diplomate ACVIM [email protected]

Amanda M. House, DVM, Diplomate ACVIM

[email protected] Suzan C. Oakley, DVM,

Diplomate ABVP (Equine) FAEP Council

[email protected] D. Puccia, DVM

[email protected] Richter, BSc

(Hon), DVM, MS [email protected] Miller, DVM, MS,

Diplomate ACT FAEP Council

Representative to the FVMA Executive Board [email protected]

The Practitioner is an official publication of the Florida Association of Equine Practitioners an Equine-Exclusive Division of the Florida Veterinary Medical Association.

Dear Fellow FAEP Members,

As the holidays rapidly approach, those of us who serve you as council members of the Florida Association of Equine Practitioners are proud of what we have accomplished in 2011.

Change is stressful even when change is necessary. We experienced a smooth transition with the FVMA/FAEP merger, thanks largely to the efforts of our 2011 Council President Dr. Jackie Shellow and FVMA Executive Director Philip Hinkle. Both Jackie and Phil invested a tremen-dous amount of time and effort this past year into helping our organiza-tion evolve and grow to better serve you. By combining forces, we are now in a stronger position to represent Florida veterinarians on the regulatory and legislative fronts in Tallahassee.

Another recent change, as a result of the merger, is with The Practitioner. The production of this publication is now handled by the FVMA staff. Changes have already taken place and additional enhance-ments will be implemented in the months ahead. The FAEP would like to thank former publisher Mr. Richard “Dick” Booth for his involvement in the production of the Practitioner for more than six years since its incep-tion. The Practitioner continues to be informative and well received among its recipients. The FAEP welcomes and encourages our members and practitioners to submit scientific-based articles to the FAEP Practitioner Publication Committee for consideration in future issues.

Our 2011 continuing education events were very well attended and received excellent reviews. The FVMA staff members were organized and handled all of our CE events with efficiency and professionalism. These included the 3rd Annual Foot Symposium in Orlando, the 7th Annual Promoting Excellence Symposium on Amelia Island (that included an im-aging wet lab), and the 49th Annual Ocala Equine Conference that featured both imaging and ophthalmology wet labs. The FAEP Council is hard at work planning our 2012 continuing education programs. I invite you to attend our 8th Annual Promoting Excellence Symposium in the Southeast being held on October 11-14, 2012 at the Naples Grande Beach Resort in Naples, Florida as well as our 50th Annual Ocala Equine Conference in the fall of 2012. These events would not be possible without the generous support of our Educational Partners who help to keep our registration fees affordable.

Our organization has evolved and the faces have changed. However, the primary mission that Dr. Rob Boswell challenged us with when he founded the FAEP in 2005 remains the same. We will continue to strive to provide you with the highest quality equine-exclusive continuing educa-tion opportunities available anywhere. I am honored to serve you as the 2012 FAEP Council President and take the responsibilities that come with this position very seriously. I encourage each of you to become more involved in the FAEP and the FVMA.

Wishing you all a very wonderful Thanksgiving holiday!

Sincerely, Greg BonenClark, DVM, DACVS FAEP 2012 Council President

4 The Practitioner • Issue 5

World-class equine-exclusive continuing education in an oasis of serene elegance – Naples, the crown jewel of Florida’s Gulf Coast!

8th Annual Promoting Excellence Symposium in the Southeast

LECTURE TOPICS INCLUDE

LEISURE EVENTS

MAGNIFICENT RESORT AMENITIES

Mark Your Calendar . . .OCTOBER 11 – 14, 2012Naples Grande: A Waldorf Astoria Resort • Naples, FL

CyclingCanoeing and KayakingAqua BikingWindsurfing, snorkeling and sailingRees Jones Designed Golf CourseWorld-Class Tennis Golden Door Spa

FAEP’s Annual Golf TournamentFAEP’s Annual Fishing TournamentPicturesque Beach on the Gulf of Mexico

LamenessImagingNeonatologyPre-purchase ExamsInternal MedicineRegenerative MedicineRehabilitation

OverviewColic and lameness are two of the most clini-

cally and economically important medical problems facing horses and their owners. Pain is a critical component of each disease process and its allevia-tion is often critical to a successful outcome. But, a limited number of analgesics are available for use in horses and many of these options are associated with significant untoward effects. Thus, one’s ability to objectively assess new pharmacologic options or new combinations of previously available options is critical to the advancement of equine medicine.

When assessing pain in animals or non-verbal humans, the assessment is always based upon the observer’s perception. For research models of pain in animals, Gebhart and Ness put forth the following necessary criteria: the subject is not anesthetized, the experimental stimulus mimics a natural stimu-lus, the stimulus is minimally invasive and ethically acceptable, the stimulus is controllable, reproduc-ible, quantifiable, and the responses are reliable and quantifiable.1

Research Models of Visceral and Somatic NociceptionMost models of visceral pain in horses and other

species (including humans) involve the use of some device resulting in distension of a portion of the gas-trointestinal tract. As such, information gained from these models can be applied only to clinical condi-tions that cause pain as a result of visceral distension, and these are typically models of acute pain. Because many naturally occurring conditions involve disten-sion of one form or another, such models have pro-vided clinically meaningful information regarding analgesic medications commonly used in the horse. Most equine models involve balloon distension of the cecum via a surgically implanted cecal cannula2, the duodenum via a surgically implanted gastric cannula3-5, or the distal small colon/rectum.3,4,6 The primary advantage of the cecal and duodenal dis-tension models is that both the stimulus (disten-sion) and associated nociceptive behaviors (pawing, flank watching, etc.) mimic the clinical syndrome of colic. With the CRD, the associated behavior (expul-sion of balloon) is not as clear and results may be more closely associated with the “urge to defecate” response in humans and therefore not truly nocicep-tive in nature. One potential disadvantage of these models is the potential effect of repeated distension on the nociceptive threshold.

A variety of models are currently in use for the

By Chris Sanchez, DVM, PhD, DACVIM

Pain Models and Scoring & Pain Management in Horses

objective evaluation of somatic nociception, mostly associated with acute pain. With threshold-based models, heat (thermal) and mechanical (pres-sure algometry) stimuli are most commonly used. Thermal threshold testing has been used in the horse to evaluate the effects of lidocaine, fentanyl, detomidine, acepromazine, and butorphanol.3,4 The main advantages of this method are ease of use and repeatability. Disadvantages include the potential for drug effect on skin temperature to affect results, such as occurs with the alpha-2 adrenoreceptor ago-nists. Mechanical stimuli include the use of pneu-matic devices to apply pressure to the coronary band or a pressure algometer at either the pastern or along the thoracolumbar musculature. The pneu-matic pressure models have been used to assess the somatic nociceptive effects of various drugs.7,8 The pressure algometer has been used to assess the effect of induced back pain, induced synovitis and osteoar-thritis, chiropractic therapy, phenylbutazone, mas-sage therapy, sacroiliac dysfunction and distal fore-limb irritants in Tennessee Walking Horses.9-12 The use of both mechanical and thermal stimuli to evalu-ate analgesic therapy is useful in that both types of stimuli are seen in clinical situations.

Reversible models of lameness, such as a special-ized shoe fitted with an adjustable screw to induce solar pressure, have been used to evaluate the anal-gesic effects of non-steroidal anti-inflammatory agents.13 These models offer the advantage of a natu-rally occurring stimulus and quantifiable nociceptive effects.

Scoring Systems for Clinical ResearchIn order to be useful, a pain scoring system should

include clearly defined assessment criteria, be suit-able for all observers, be simple and quick to use, be sensitive, have identified strengths and weaknesses, and be validated. Possible deficiencies include bias, inter- and intra-observer variability. A lack of agree-ment between observers is one of the flaws of simple scoring systems such as the visual analog scale (VAS), in which pain is scored on a numerical scale, when used in humans.

One of the most useful clinical applications of integrated pain scoring systems is the assessment of interventions (i.e. assess pain score, apply treat-ment, then re-assess pain score at various intervals). When critically assessing scoring systems, the inves-tigator should control for signalment (age, breed, sex), observer (veterinarian, student, owner/


Clas

s NS

AIDs

Drug Dosage (mg/kg unless noted)

Route Duration (h)

Comments

Flunixin 0.25-1.1 IV, PO 8-24 Avoid IM; avoid max. dose more than 2x/day

Ketoprofen 2.2 IV 24

Phenylbuta-zone

2.2-4.4 IV, PO 12-24

Carprofen 0.7 IV, PO 24

Firocoxib 0.1 PO, IV 24

Etodolac 2.3 IV, PO 12 10-fold reduc-tion from original dose

α-2 A

goni

sts

Xylazine 0.2-1.1 IV, IM prn Sedation out-lasts analgesia

Detomidine 0.005-0.04 IV, IM prn Sedation out-lasts analgesia

Romifidine 0.04-0.12 IV prn Analgesia may be insufficient for many pro-cedures

Medetomi-dine

0.004-0.01 IV prn

Detomidine Bolus 8.4 µg/kg then 7.5 µg/kg over 15 min then 4.5 µg/kg over 15 min then 0.15 µg/kg/min

IV CRI Do not continue longer than 4 hours.

Opio

ids

Butorphanol 0.01-0.05 IV 3-4 Can combine w/ α-2; good alone IM in foals

0.04-0.1 IM 4-6

Butorphanol 18 µg/kg then 10-23 µg/kg/hr

IV CRI

Morphine 0.12-0.66 IV 4-6 Combine w/ α-2

Misc

.

Ketamine 0.4-1.2 mg/kg/hr

IV CRI

Lidocaine 1.3 mg/kg bolus then 3 mg/kg/hr

IV CRI 75 ml/hr for 500kg horse (2%)

Buscopan 0.3 Slow IV Once Tachycardia; less for palpa-tion

Available Options for Systemic Analgesia in HorsesDosages are summarized from the available literature and

personal communication. These amounts must be titrated to the individual animal and situation.

trainer), procedure, and other effects (food with-drawal, anesthesia, management, etc.). Continu-ous video assessment allows for quantification of either time budgets (locations within the stall, ear position, head position, eating, lying down, etc.) or events (vocalizing, stomping feet, shifting weight, etc.). Time budget and event analyses has been per-formed on horses following arthroscopy.14 A numeri-cal rating system was also used to assess the effect of a butorphanol constant rate infusion on physiologic and outcome variables in horses following colic sur-gery.15 All horses received flunixin following surgery. Interestingly, horses receiving butorphanol had improved behavior scores in the 24 hours following surgery, decreased cortisol concentration, lost less weight, and were discharged from the hospital faster than horses receiving a placebo infusion.

Objective measures such as vital signs, plasma cortisol concentration, and force plate analyses alle-viate the subjective nature of assessment. But, vital signs and cortisol are affected by a variety of factors in addition to pain, including hydration status, per-fusion, sepsis and/or endotoxemia, fear and anxiety.

The practical application of these systems is to think about signs of pain that may otherwise go unnoticed. The following is a pain scoring system used at the University of Florida, which has been adapted from Sellon.15

1 2 3 4 Score

Gross pain behaviorsa

None Occasional Continuous

Head posi-tion

Above withers

At withers Below withers

Ear position Forward, frequent movement

Slightly back, little movement

Location in stall

At door watching environ-ment

Standing in middle, facing stall door

Standing in middle, facing sides of stall

Standing in middle, facing back of stall

Sponta-neous locomotion/response to approach

Moves freely/moves to observer

Occasional steps/looks at observer with ears forward

No move-ment/ears back

Lifting feet Freely lifts feet when asked

Lifts feet after mild encourage-ment

Extremely unwilling to lift feet

TOTAL SCORE

aGross pain behaviors include pawing, sweating, looking at the flank, flehmen (stretching neck and raising upper lip), and lying down/standing up repeatedly

The Practitioner • Issue 5 7

Soar.

Sore.

So choose the only FDA-approved I.V. joint therapy for equine non-infectious synovitis.

Both depend on which therapy you choose.

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

E11959n

Drug Dosage (mg/kg)

Duration Comments

Lidocaine 0.2 mg/kg 30-90 minutes

Xylazine 0.03-0.35 3-5 hours

Detomidine 0.06 2-3 hours

Morphine 0.1 8-16 hours qs to 30 ml w/ saline; may cause pruritis

LidocaineXylazine

0.22 mg/kg0.17 mg/kg

5-6 hours

Chris Sanchez, DVM, PhD, DACVIM + Associate professor, Large Animal Internal Medicine, University of Florida

+ DVM Degree University of Florida, 1995 + Internship at Equine Medical Associates in Edmond, OK.

+ Residency in Large Animal Internal Medicine, University of Florida

+ Diplomate status in the American College of Veterinary Internal Medicine in 1999.

+ PhD at the University of Florida in 2003

Drugs/Combinations for Caudal Epidural Analgesia in Horses

Note that all drugs and/or combinations can cause ataxia.

References1. Gebhart GF, Ness TJ (1991), Central mechanisms of visceral

pain, Can.J.Physiol Pharmacol. 69: 627-634

2. Kohn CW, Muir WW, III (1988), Selected aspects of the clinical pharmacology of visceral analgesics and gut motil-ity modifying drugs in the horse, J.Vet Intern.Med 2: 85-91

3. Sanchez LC, Robertson SA, Maxwell LK, Zientek K, Cole C (2007), Effect of fentanyl on visceral and somatic nocicep-tion in conscious horses, J Vet Intern.Med 21: 1067-1075

4. Robertson SA, Sanchez LC, Merritt AM, Doherty TJ (2005), Effect of systemic lidocaine on visceral and somatic noci-ception in conscious horses, Equine Vet J 37: 122-127

5. Merritt AM, Xie H, Lester GD, Burrow JA, Lorenzo-Figueras M, Mahfoud Z (2002), Evaluation of a method to experimentally induce colic in horses and the effects of acupuncture applied at the Guan-yuan-shu (similar to BL-21) acupoint, Am J.Vet Res 63: 1006-1011

6. Skarda RT, Muir WW, III (2003), Comparison of elec-troacupuncture and butorphanol on respiratory and

cardiovascular effects and rectal pain threshold after con-trolled rectal distention in mares, Am J.Vet Res 64: 137-144

7. Moens Y, Lanz F, Doherr MG, Schatzmann U (2003), A comparison of the antinociceptive effects of xylazine, detomidine and romifidine on experimental pain in horses, Veterinary Anaesthesia and Analgesia 30: 183-190

8. Schatzman U, Armbruster S, Stucki F, Busato A, Kohler I (2001), Analgesic effect of butorphanol and levomethadone in detomidine sedated horses, J Vet Med.A Physiol Pathol.Clin.Med. 48: 337-342

9. Sullivan KA, Hill AE, Haussler KK (2008), The effects of chiropractic, massage and phenylbutazone on spinal me-chanical nociceptive thresholds in horses without clinical signs, Equine Veterinary Journal 40: 14-20

10. Haussler KK, Erb HN (2006), Mechanical nociceptive thresholds in the axial skeleton of horses, Equine Veterinary Journal 38: 70-75

11. Haussler KK, Behre TH, Hill AE (2008), Mechanical noci-ceptive thresholds within the pastern region of Tennessee Walking Horses, Equine Veterinary Journal 40: 455-459

12. Varcoe-Cocks K, Sagar KN, Jeffcott LB, McGowan CM (2006), Pressure algometry to quantify muscle pain in racehorses with suspected sacroiliac dysfunction, Equine Veterinary Journal 38: 558-562

13. Foreman JH (2007), Phenylbutazone and flunixin meglumine used singly or in combination (“stacking”) in experimental lameness in horses, Journal of Veterinary Internal Medicine 21: 166

14. Price J, Catriona S, Welsh EM, Waran NK (2003), Preliminary evaluation of a behaviour-based system for assessment of post-operative pain in horses following arthroscopic surgery, Veterinary Anaesthesia and Analgesia 30: 124-137

15. Sellon DC, Roberts MC, Blikslager AT, Ulibarri C, Papich MG (2004), Effects of continuous rate intravenous infusion of butorphanol on physiologic and outcome variables in horses after celiotomy, J Vet Intern.Med. 18: 555-563


Soar.

Sore.

So choose the only FDA-approved I.V. joint therapy for equine non-infectious synovitis.

Both depend on which therapy you choose.

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

E11959n

Dr. Christopher N. Buchanan, center, was one of five winners of the Dr. Sue Dyson and Dr. Michael Ross book, “Lameness in the Horse” at the 7th Annual Promoting Excellence Symposium on Amelia Island Sept. 29 to Oct. 2. Dr. Dyson and Dr. Ross are pictured in the background.

T he first year out of the gate, the FAEP and the FVMA presented three tremendously success-ful continuing education events in 2011.

Our first educational program as the newly formed FAEP Council, an equine exclusive division of the FVMA, was held in July. This joint venture, the Third Annual Promoting Excellence Equine Foot Sympo-sium, was one of the most successful farrier and vet-erinarian educational programs in Florida. This event was followed by the 7th Annual Promoting Excellence Symposium staged on Amelia Island from Sept. 29 to Oct. 2. This meeting, attracting a record attendance, proved the FAEP’s mission of providing currently rel-evant and outstanding education for the equine prac-titioner. The end of October marked another success-ful educational event. The 49th Annual Ocala Equine Conference from Oct. 21-24 offered more cutting-edge equine-exclusive CE.

2011 Continuing Education – A Tremendous Success!

Dr. Michelle LeBlanc, second from left, is con-gratulated on her Lifetime Achievement Award by Dr. Amanda House, left; Dr. Jackie Shellow, second from right, and Dr. Chris Sanchez.

The FAEP Council members are (from the left): Dr. Amanda M. House, Dr. Suzan C. Oakley, Dr. Anne L. Moretta, Vice President; Dr. Ruth-Anne M. Richter, Dr. J. Barry David, Dr. Liane D. Puccia, Dr. Corey Miller, Dr. Gregory D. BonenClark, President; and Dr. Jacqueline S. Shellow, Immediate Past President.


Third Annual Equine Foot SymposiumThis high caliber event promoted communica-

tion and teamwork between veterinarian and farrier attendees.

h 14 hours of cutting-edge continuing education

h Six speakers

h Some of the topics offered included: Foster-ing the veterinarian & farrier relationship, a Front and Hind Limb Anatomy Review, Hoof Cracks, Repair and Treatment, Hoof Balance, and Laminitis.

h The Hands-On Anatomy Wet Lab offered instruc-tion by Mitch Taylor, CJF, DWCF, assisted by Dr. Ruth-Ann Richter and Dr. Scott Morrison. The functional anatomy and biomechanics of the distal limb were covered in depth. The wet lab was a great opportunity for veterinarians and farriers to have a hands on exchange of ideas.

Dr. Gregory BonenClark, left center, assists Mitch Taylor, CJF, DWCF, instruc-tor, during the Front and Hind Limb Anatomy Wet Lab at the Third Annual Promoting Excellence Equine Foot Symposium, July 22-23 in Orlando. Far left are Dr. Liane Puccia and Eric Nygaard.

Practitioners and Farriers receive pointers during the Foot Symposium Wet Lab.

Above: Instructor Mitch Taylor, CJF, DWCF, and practitioners attend the Front and Hind Limb Anatomy Wet Lab at held at the Third Annual Promoting Excellence Equine Foot Symposium, July 22-23 in Orlando.

Left: Dr Ruth-Anne Richter, right, aided attendees in their anatomy review.

Foot Symposium continuing education lecture.


Virginia Loy, right, of MWI Veterinary Supply, chats with an attendee.

perform diagnostic ultrasounds regu-larly and wanted to fine tune their imaging of more complex structures.

“It was right up my alley, the musculoskel-etal ultrasound techniques,” said Dr. Nancy Brennan of Kentucky. “It was extremely informative. I loved the venue. I was on cloud nine and will make it a point to participate in the next conference no matter what.”

7th Annual Promoting Excellence Symposium in the Southeast

Keeping up with published scientific equine clinical advancements of the past year was pre-sented through brief, yet specific reviews of selected papers presented by world-renowned experts in the equine industry, Dr. Sue Dyson, senior orthopaedic clinician at the Center for Equine Studies at the Animal Health Trust, United Kingdom, and Dr. Michael Ross, profes-sor of surgery at the School of Veterinary Medi-cine, New Bolton Center, Kennett Square, PA.

New to the FAEP program was a rehabilita-tion track featuring the very latest in rehabili-tation protocols, modalities and techniques for the equine athlete. Rehabilitation expert Mike Torry, PhD, shared his insights on the correla-tion between human and equine rehabilitation, exploring the biomechanics of horse injuries.

Dr. Willem Back, DVM, Cert. Pract. KNMvD equine practice, PhD, Spec. KNMvD (equine surgery) and DECVS and professor of the Uni-versity of Gent, and Dr. Carol Gillis, DVM, PhD, DACVSMR, reviewed current research in equine rehabilitation and shared ways to measure its effectiveness through outcome assessment and monitoring.

h 52 hours of continuing education available

h 22 nationally and internationally acclaimed speakers

h Lecture topics included Internal Medicine, Regenerative Medicine, Respiratory Dis-ease, Reproduction, Acupuncture, Surgery, Pharmacy review, Lameness, Musculoskel-etal Imaging, Endoscopy, Pain Management, Cardiology and Rehabilitation.

h Wet Lab – musculoskeletal ultrasound – was oriented towards veterinarians who

Dr. Michael Ross, New Bolton Center, left, and Dr. Sue Dyson, Centre for Equine Studies, United King-dom, briefed attendees on published scientific equine clinical advancements of the past year in their presentation at the 7th Annual Promoting Excellence Symposium held on Amelia Island, Sept. 29-Oct. 2.

The Musculoskeletal Ultrasound Wet Lab was presented at the Promoting Excellence Symposium. Shown are attendees with the instructors. Clockwise from top right are Dr. Tim Lynch, Dr. Suzan Oakley, Dr. Alison J. Morton and Dr. Carol Gillis.


Practitioners gained valuable information on ultrasound techniques which focused on musculoskeletal, respiratory and abdominal structures. An ophthamology wet lab offered views into eye trauma, treat-ment strategies and protocols.

49th Annual Ocala Equine ConferenceThe FAEP concluded the 2011 season of con-

tinuing education events with the 49th Annual Ocala Equine Conference at the Hilton Ocala in the horse capital of the world.

h 40 hours of continuing education offered

h 14 educator speakers in the equine industry

h Lecture topics included Colic Evaluations, Endocrinology, Ophthalmology, Orthope-dics, Pharmacy, Respiratory Disease and Ultrasound.

h Wet labs were popular with conference attendees. The ultrasound wet lab featured Dr. Carol Gillis and focused on Musculoskel-etal, Respiratory, and Abdominal Ultrasound. Dr. Dennis Brooks led the Ophthamology wet lab which offered insight into eye trauma, treatment strategies and protocols.

“Fat, Founder and Frustration: Equine Meta-bolic Syndrome and Endocrinopathic Laminitis” was presented by Nicholas Frank, DVM, PhD, DACVIM, Professor and Chair, Department of Clinical Sciences, Tufts Cummings School of Veterinary Medicine as the keynote address on Saturday evening of the event.

Each symposium offered a marketplace venue which showcased vendors and exhibitors who are well acquainted with the equine practitio-ners, their equipment needs and requirements.

The FAEP strives to satisfy the needs of each practitioner at every conference. Our mission is to provide the highest quality continuing educa-tion and hands-on wet labs. Our exhibitors pro-vide the latest in equipment and products in the marketplace.

“There are three things you do when you are a veterinarian going to a conference,” said Dr. Khris Crowe of Gainesville, Texas attend-ing the 7th Annual Promoting Excellence Sym-posium on Amelia Island, “attend continuing education to help you in your practice, make purchases in the exhibit area, and to be able to have a little social activity. You people knocked that out of the ball park.”

LEFT: Dr. Nicho-las Frank gave a keynote address on Fat, Founder and Frustration: Equine Metabolic Syndrome and Endocrinopathic Laminitis on Oct. 22 at the 49th Annual Ocala Equine Conference. RIGHT: Practitioners attend the Frank keynote address.


SILVER PARTNERS

GOLD PARTNERS

Their support of this program keeps your registration fees affordable.Please visit the “Market Place” at each event and thank them for their support!

Special Thanks to our 2011 Educational Partners


Normal sinus rhythm requires the electrical impulse to be

“smoothly” conducted from the sinoatrial node through the atrial tissue to the atrioventricular node on through the Purkinje network, terminating in the ventricular myocardium before the tissue repolarizes and the impulse starts again. The resultant rhythm is regular with the rhythm governed by the pacemaker at the sinoatrial node.

Autonomic input in the normal horse can greatly influence the heart rate and rhythm. The horse is a parasympatheti-cally driven animal and, if all autonomic tone is removed, the intrinsic heart rate is 100 bpm. The resting rate is therefore governed by vagal tone, and it is there-fore not surprising that vagally mediated arrhythmias are common. These are, for the most part, benign, yet can remark-ably disrupt cardiac rhythm. The follow-ing notes describe the more common dysrhythmias that occur in the horse and some of the investigations into the impact of dysrhythmia on equine performance.

Second Degree BlockThis is the most common dysrhythmia

in the horse. It is mediated by increased vagal tone at the level of the atrioven-tricular node causing blocked conduction at that level. For the most part, this is a normal finding and is more prevalent in horses with a history of fitness. On auscultation the heart rhythm is irregu-lar. However, the blocked interval is a multiple (i.e. usually twice) the basal interbeat interval. Because of the pre-dictable length of the blocked interval this arrhythmia is usually identified as being regularly irregular. The arrhythmia should abate with increased heart rate or with decreased vagal tone. Therefore, it should resolve with light exercise or excitation.

Advanced block (multiple cycles at a time) may be due to myocardial

Arrhythmias in the Performance HorseBy Kim McGurrin, BSc, DVM, DVSc, DACVIM

inflammation, significant electrolyte imbalances and cardiac glycoside toxicity. It may be associated with pronounced bradycardia; such animals may be exer-cise intolerant and prone to collapse. Mobitz type II may be associated with atrial myocardial disease. With advanced block corticosteroids may be of benefit.

Sinus ArrhythmiaSinus arrhythmia is usually associated

with sinus bradycardia when present at rest. It is characterized by fluctuation in cardiac rhythm associated with respira-tion (respiratory sinus arrhythmia) from changes in vagal tone and there is a rhyth-mical variation. The term also has been used to describe fluctuations in cardiac rhythm associated with exercise (exercise associated arrhythmia). This arrhythmia is commonly found in fit horses during cardiac deceleration following submaxi-mal exercise and is likely associated with variation in autonomic feedback as the sympathetic input decreases and the parasympathetic system regains control. Respiratory sinus arrhythmia is not as common or as obvious as in small ani-mals or humans.

Sinus Arrest/BlockSinus arrest/block is a normal, albeit

infrequent, variation in resting fit horses. It is likely associated with variations in vagal tone. Auscultatory findings are of intermittent pauses of variable lengths. In some animals, blocks may occur infre-quently; in others, the frequency may be sufficient to confuse this rhythm disturbance with atrial fibrillation. Per-sistence at elevated heart rates may indi-cate a pathological basis. Prolonged (4 seconds or greater) blocked intervals or those associated with syncope are clini-cally relevant. Evaluation of horses with advanced block is indicated through the use of exercise ECGs. Resolution of the rhythm disturbance with excitation or exercise would indicate that it was likely benign, providing the horse was asymp-tomatic at rest. No treatment is required for the benign form. Anti-inflammatory therapy could be considered. Pacemaker implantation would be only option for advanced block/arrest.

Atrial Premature ComplexesThese are depolarizations occurring

within the atria, originating outside of the

Figure 2

Figure 1


sinoatrial node. By definition, this occurs before the sinus node depolarizes. Aus-cultatory findings would be of early beats usually without complete compensatory pause due to resetting of the sinus node. This usually occurs as a single or infre-quent event, and would not be considered as abnormal in that instance. Persistent or high frequency may be caused by atrial myocardial disease or inflammation. Usu-ally no treatment is required. Dexametha-sone may be of benefit to control inflam-mation. Digoxin may be necessary to con-trol rate if severe tachycardia is present.

Atrial TachycardiaThis is an uncommon condition and

is considered clinically relevant. It occurs when there are runs of 4 or more atrial ectopics. In some instances the atrial tachycardia is sustained. The clinical pre-sentation may vary from a horse with a normal ventricular rate, due to high degree second degree block, to one with severe tachycardia. In the latter animal, severe exercise intolerance and syncope are pos-sible. In the former group, the animal may present with limited clinical signs or may alternate into tachycardia only when vagal tone is reduced. It may be due to myocar-dial inflammation or disease. Treatment is often successful through the identifica-tion and removal or treatment of under-lying cause, such as electrolyte imbalance or inflammation. Antiarrhythmic medica-tion may be indicated. Quinidine has been used with caution. Quinidine increases conduction through the AV node and con-duction of previously blocked P waves will increase ventricular rate. Digoxin can be used to slow ventricular rate and to limit AV nodal conduction. Electrical cardiover-sion may be useful in stable cases; those

cases with second-degree block which will tolerate anaesthesia.

Atrial FibrillationAtrial fibrillation (AF) is the most

common clinically relevant dysrhythmia in the horse with an estimated incidence ranging from 0.3-2.5% of the equine pop-ulation. The initiating event is not known in the horse. Horses may be predisposed to AF because of high vagal tone and large atrial dimension. Vagal tone leads to variability in action potential duration across the atrial tissue. The large atrial dimension in horses allows conduction through multiple pathways within the atria. In cases of lone AF, restoration of sinus rhythm should result in complete resolution of clinical signs. If underly-ing cardiac disease is present, the prog-nosis for restoration and maintenance of sinus rhythm is poor and treatment may be contraindicated. Quinidine salts have long been the modality of choice. Flecainide has had some success orally, and has proven difficult to use intrave-nously. Amiodarone is moderately suc-cessful when titrated over a no more than 48-hour course. Transvenous electrical cardioversion has proven highly success-ful, but is technically challenging and requires specialized equipment.

Third-Degree BlockThis is a rare condition in the horse.

In general, it has been associated with damage to the atrioventricular node; i.e. myocarditis, pericarditis and aortic aneu-risms. Clinically, this condition is usually associated with profound exercise intoler-ance and potentially syncope. Bradycardia with usually regular ventricular rate of 10-20 bpm is characteristic. Auscultatory

findings are of regularly spaced S1and S2 with a more rapid S4. With prolonged auscultation S4 will be heard to be inde-pendent and may summate onto the other heart sounds causing loud ‘bruit de cannon’ sounds. Pacemaker implantation is possi-ble. Pharmacological therapy is of limited value. Atropine/glycopyrrolate (vagolytic) administration is usually unsuccessful. The use of sympathomimetics, such as iso-proterenol, has been reported; however, caution should be used due to the risk of ventricular tachyarrhythmias (have lido-caine ready). Corticosteroids may be of benefit to treat inflammation.

Ventricular Premature ComplexesThese are depolarizations that origi-

nate in the ventricle, outside of the Pur-kinje fibres/conduction system. Auscul-tatory findings would be of early beats usually with complete compensatory pause. Usually occurring as a single or infrequent event, it would not be consid-ered as abnormal in that instance. Persis-tent or high frequency may be caused by ventricular myocardial disease or inflam-mation. Usually no treatment is required. Dexamethasone may be of benefit to con-trol inflammation.

Ventricular TachycardiaVentricular tachycardia exists when

there are runs of VPCs of four or more in succession. It may be monoform, (originating from one site), or polyform (originating from multiple sites). It may be sustained or may alternate with the sinus rhythm. If the heart rate is close to normal (<50 bpm), the rhythm is better termed as accelerated idioventricular rhythm. With regards to correcting the rhythm, first correct underlying con-ditions such as electrolyte imbalances. Consider treatment if the heart rate is above 120 bpm, if clinical signs are noted or if the VTAC is polymorphic. Lidocaine is the safest option and should be consid-ered as the first line. This author has had success with careful titration of intrave-nous potassium levels to the high range of normal, while administering lidocaine. Magnesium sulphate has been of some use, but more so in cases of torsades de points. Other antiarrhythmics such as phenytoin, propranolol and amiodarone have also been reported to be successful in some cases.

Figure 3


Exercise ECGIn some cases, heart rhythm abnor-

malities may only appear at exercise. Horses that present for poor perfor-mance, and in which there are no other abnormalities, are candidates for exer-cise ECGs. It is this author’s opinion that this should be part of a comprehensive poor performance examination as there may be more than one abnormality; or, if no abnormality is detected on ECG, then time and resources are not wasted.

Continuous electrocardiography during treadmill or trackside testing is integral rather than attempting to col-lect recordings intermittently or once the horse has pulled up. Variations in cardiac rhythm on the exercising and immedi-ate post exercise electrocardiogram have been noted in several studies.

During one retrospective evaluation of comprehensive poor performance evaluation, definitive diagnosis was reached in 73.5% of horses. (JAVMA 2000; 216:554). Of these animals, 21% (74/256) were considered to have cardiac abnormalities with most of these having dysrhythmias (55/74). It is important to note that some of these horses also had other abnormalities.

In another study, 88 poor perform-ing Thoroughbred racehorses were evaluated on the treadmill. (EVJ Suppl. 2006; 36:163) It was found that 62.5% of horses had at least one ectopic beat during or immediately after exercise (predominantly after). Most of the horses in this study (69.3%) had con-current upper respiratory abnormalities. The clinical relevance of the ECG findings is not known. A single ectopic is unlikely to have much hemodynamic effect.

The predominant reasoning is that if greater than 2 single ectopics are pres-ent during actual exercise, if more than 5 ectopics are present or if there are pairs or runs of ectopy in the immedi-ate post exercise period, then the horse is abnormal. Whether this guideline is realistic has recently been open to debate with findings in exercising “normal” race-horses being reported.

Another study was conducted on Thor-oughbred racehorses considered by their trainers to have no evidence of poor per-formance. (EVJ; 2005: 37:265) Of 105 horses, 15% had ventricular and 19% had supraventricular ectopics during

the immediate recovery period. 13 and 11% of these animals, respectively, had ventricular or supraventricular ectopics in the warm-up period and 3% had ven-tricular ectopics during peak exercise.

This author was involved in a recent study conducted on Standardbred race-horses. (JVIM; 2010: 24: 1158) Holter monitors were placed prior to warm-up and remained through actual racing. In this study, 27.8% of recordings showed dysrhythmia in the immediate post-race period (less than two minutes post-race). 11.6% showed ventricular ectopics, and 15.9% showed complex ventricular dys-rhythmias. Few horses showed dysrhyth-mia during the race, all of which were lim-ited to single ectopics. There was no obvi-ous correlation with performance, other than horses that showed these rhythms were more likely to have a “stretch condi-tion” (broken gait, been distanced at the wire) prior to developing the post-race dysrhythmia. This might suggest that the hard drive that these horses endured increased the likelihood. The presence of increased post-race vagal tone also increased the risk of arrhythmia.

During the immediate “recovery period” there is a complex interplay of sympathetic and parasympathetic tone. Sympathetic tone is decreasing while parasympathetic tone increases. Addi-tionally, post-maximal effort, electrolyte and metabolic abnormalities are common. Fluctuations in cardiac rhythm at this time might therefore be anticipated and variations in sinus rhythm, occasional second-degree block at high rate and infrequent ectopics, are easy to dismiss.

However, the significance of multiple ectopics, multiform ectopics and runs of ectopy remains elusive. To err on the side of safety, especially in the face of histori-cal poor performance, would be prudent.

References Martin, BB. et al. J Am Vet Med Ass 2000;216: 554. Ohmura

H et al.J Vet Med Sci. 2000;62(7):711. Frye MA et al J Am Vet Med Assoc. 2002;22:(7):1039. van Loon G et al Vet Rec. 2002;151:541. Young LE Et al Eq Vet J suppl;2002 34: 467. Durando MM Clin Tech Eq Pract; 2003: 2 (3):266. Poole, DC, Eq Comp Ex Phys 2004:1(1);5-22. van Loon G et al Equine Vet J. 2004; 36(7):609. LeLeu C et al Vet Rec; 2005: 156: 339. McGurrin MK et al J Vet Intern Med. 2005;19(5):695. Rezakhani A et al Pakistan Vet J. 2005;25(1): 40. Schwarzwald CC et al; J Vet Intern Med. 2005;19(5):703. McGurrin MK et al J Vet Cardiol. 2005 Nov;7(2):109-19. Ryan N et al Eq Vet J; 2005: 37: 265. Risberg AI et al J Vet Intern Med. 2006 ;20(1):207. Schwarzwald CC et al J Vet Intern Med. 2007;21(1):166. De Clercq D, et al Equine Vet J. 2007;39(4):344. De Clercq D et al Vet J. 2008;177(2):198-204. McGurrin MK, et al J Vet Intern Med 2008;22(3):609. Nostel K Et al J Vet Cardiol 2008: 10:105. De Clercq D et al Am J Vet Res. 2009;70(2):223. Mullen KR et al J Am Vet Med Assoc. 2009; 235 (10):1156. Buhl R et al Eq Vet J Suppl; 2010 ; 38:196. Linder AE. J Anim Sci 2010 88:950. Physick-Sheard PW Et al. J Vet Intern Med; 2010: 24: 1158. Schefer KD et al JVIM 2010; 24: 918.

Kim McGurrin, BSc, DVM, DVSc, DACVIM

+ Staff at Ontario Veterinary College in the areas of Large Animal Medicine and Cardiology since 2003

+ Graduated from the Ontario Veterinary College in 1998

+ One-year rotating internship in Large Animal Medicine and Surgery

+ Three-year internal medicine resi-dency, Ontario Veterinary College

+ DVSc studies investigating Equine Atrial Fibrillation and developing skills in Large Animal Cardiology


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Equine Medical Center of Ocala

FAEP Member Practice Highlight

The Equine Medical Center of Ocala is the only equine referral hospital in Marion County with board-certified specialists in surgery, reproduction and internal medi-

cine. The hospital provides a wide variety of services including colic surgery, orthopedic and soft-tissue surgeries, advanced reproductive technologies, internal medicine diagnostics, 24-7 intensive care for critically ill foals and adults, a standing MRI, digital radiography, a full-service diagnostic laboratory and after-hours emergency services.

New Services in 2011• Lameness Locator dramatically increasing the abil-

ity to detect and quantify lameness in horses. Visit www.equinosis.com to learn more.

• Eklin Mark V 14 x 17 Digital Radiography• Laparoscopic Surgery

The Equine Medical Center of Ocala incorporates new tech-nologies with specialized staff and team-oriented client ser-vices to achieve goals of satisfied clients and healthy patients.

Board-Certified Specialists• Surgery specializing in equine orthopedic and soft-tis-

sue surgeries and diagnostic evaluations: John G. Peloso, DVM, MS, Diplomate ACVS, and Aric R. Adams, DVM, Diplomate ACVS.

• Reproduction specializing in stallion and mare repro-duction with emphasis on infertility and frozen semen; Corey D. Miller, DVM, MS, Diplomate ACT, and Devon W. Strickland, DVM, Diplomate ACT.

• Internal Medicine specializing in neurology, cardiol-ogy, neonatology and intensive care with J. Barry David, DVM, Diplomate ACVIM.

Generalists• Dr. Patrick C. Worden specializes in the Thoroughbred

racehorse and sale horse.• Dr. Rafael J. Borges concentrates on lameness with a

focus on the needs of the Paso Fino.• Dr. Fred W. Benker concentrates on equine reproduction.• Dr. Liane D. Puccia focuses on the needs of the Thor-

oughbred racehorse.• Dr. Carolin A. Von Rosenberg has exclusive focus on

equine reproduction and the neonate.• Dr. Janine A. Weller concentrates on pre-purchase

exams, lameness, evaluations, acupuncture, dentistry, general medical issues and preventative medicine.

• Dr. Lauren A. Danskin, Dr. James Fukuda, Dr. Amanda M. Ramseyer, Dr. Sarah Shaw and Dr. Marshall Stevens.

The Equine Medical Center of Ocala is located at 7107 West Highway 326, Ocala, FL 34482; (352) 873-7830; Fax, (352) 873-7700. Visit the website at www.emcOcala.com for more infor-mation on staff, equine services and free workshops.

Dr. John Peloso doing an arthroscopic surgery. Dr. Peloso is a board certified surgeon and the senior partner in the practice.

Dr. John Peloso (EMCO) and Dr. Barrie Grant (Equine Wobblers) doing a basket surgery at EMCO. Both doctors are board certified surgeons.

Dr. Barry David, EMCO board certified internal medicine, doing a myelogram.

Dr. Corey Miller, EMCO board certified Theriogenologist, doing a stallion collection.


HyperadrenocorticismHistological alterations in the integument associated with

hyperadrenocorticism in other species include protein deple-tion, inhibition of fibroblast growth, and reduced collagen syn-thesis.1,2 Johnson et al.1 described lengthening and attenuation of primary and secondary dermal lamellae in horses with glu-cocorticoid excess and suggested that this represents pulling apart of lamellae as structures weaken. Vascular changes may also accompany hyperadrenocorticism. Flow-mediated vasodila-tion of the brachial artery is reduced in humans with Cushing’s disease3 and hypertrophic remodeling of small resistance arter-ies occurs within subcutaneous tissues.4 Hooves of horses with PPID may therefore be more susceptible to lamellar failure and less capable of repair after laminitis has occurred. These assump-tions are based on theory rather than scientific evidence at this point, so further studies are required to examine hooves from horses with PPID.

Glucocorticoids inhibit the actions of insulin by disrupting post-receptor signaling pathways,5,6 and administration of dexa-methasone has been shown to induce insulin resistance (IR) in horses.7-9 Interestingly, hyperinsulinemia is detected in some horses with PPID,10,11 whereas others have normal insulin con-centrations. One explanation for this observation is that IR only occurs with PPID when the horse is predisposed to this prob-lem. An alternative explanation is that horses with PPID differ in the types and amounts of POMC-derived hormones secreted from the pars intermedia, so those with IR have higher ACTH-stimulated cortisol secretion. It is important to assess insulin sensitivity in horses with PPID because insulin-resistant horses respond differently to their diet and are predisposed to lamini-tis. In a recent study, horses with PPID had higher overall insu-lin concentrations across a 12-month period while grazing on pasture when compared to unaffected aged horses.12 Insulin concentrations above 188.6 µU/mL have also been identified as a poor prognostic indicator for 1- to 2-year survival in horses with PPID.13 It should also be noted that insulin concentrations can increase for other reasons, including systemic inflammation, stress and pain.14,15 One final point is that some horses with PPID suffer from laminitis, whereas others do not. Horses with PPID and concurrent IR are more likely to suffer from laminitis than those with normal insulin sensitivity, which suggests that IR is a key determinant or marker of laminitis susceptibility.

Endocrinopathic Laminitis By NICHOLAS FRANK, DVM, PhD, DACVIM

ObesityObesity, IR, hyperinsulinemia, and laminitis are associated

in equids (they are key components of Equine Metabolic Syn-dome), but it should be noted that some obese animals exhibit normal insulin sensitivity when tested.16-18 These animals may be more tolerant of obesity or require more time for IR to develop. One theory linking obesity with IR is the release of inflammatory cytokines from adipose tissues. More tumor necrosis factor alpha (TNFα) is secreted from adipose tissues as body mass index increases in humans and this inflammatory cytokine inhibits insulin receptor signaling, which lowers insu-lin sensitivity.19 Vick et al18 detected higher blood TNFα mRNA expression in obese horses, which suggests that the same mech-anism contributes to obesity-associated IR in equids. Increased inflammatory cytokine production by adipose tissues may also contribute to laminitis susceptibility.

Obesity also affects adipokine production by adipose tis-sues. Adipokines are hormones produced by adipocytes that have local (paracrine) and remote (endocrine) effects on tissues. Leptin and adiponectin are the most well-known adipokines, and obesity has been associated with elevated plasma leptin concentrations and lower plasma adiponectin concentrations in horses.20 Adiponectin enhances insulin sensitivity, so lower plasma concentrations are associated with IR.20 Low adiponec-tin concentrations are also associated with impaired endothe-lium-dependent vasodilation in obese humans.21 Resistin is another adipokine that affects insulin sensitivity. This hormone has been examined in mice and humans, and hyperresistinemia is associated with IR and type 2 diabetes mellitus.22

It should be noted that some insulin-resistant horses exhibit a leaner overall body condition. Abnormal fat deposition is pres-ent regionally in some lean animals, and may be responsible for the production of inflammatory mediators and adipokines that lower insulin sensitivity. Other horses appear normal, and the mechanisms underlying IR in these animals require further study.

Finally, laminitis may occur more readily in obese horses because they carry more weight on their hooves, which increases forces exerted upon dermo-epidermal attachments.

Insulin Resistance and Vascular DynamicsInsulin possesses vasoregulatory properties and this might

explain why IR predisposes horses to laminitis. Slow vasodila-tion occurs in response to insulin through increased synthesis of nitric oxide (NO) by endothelial cells.23 However, insulin also promotes vasoconstriction by stimulating endothelin-1 (ET-1) synthesis and activating the sympathetic nervous system. Under normal conditions, the opposing actions of NO (vasodilation) and ET-1 (vasoconstriction) are in balance because both arms of the insulin signaling cascade are active; activation of the insulin receptor therefore, stimulates two different signaling pathways within the vascular endothelial cell (Figure 1). Nitric oxide is secreted when the phosphatidylinositol 3-kinase (PI3K) path-way is activated, whereas activation of the mitogen-activated

The exact mechanisms involved in endocrinopathic laminitis have not been elucidated, but potential patho-physiological mechanisms include:


protein kinase (MAPK) pathway leads to release of ET-1.24 Both the vasodilatory effects of insulin and insulin-dependent stim-ulation of glucose uptake are mediated by PI3K, and this path-way becomes disrupted when IR develops. Consequently, vaso-constriction is promoted in insulin-resistant animals because only the MAPK pathway remains fully functional. Development of compensatory hyperinsulinemia in response to IR can fur-ther stimulate MAPK signaling and increase ET-1 synthesis.25 Eades et al.26 detected an increase in plasma ET-1 concentration within blood collected from digital veins 12 hours after carbo-hydrate was administered to induce laminitis in healthy horses. This finding suggests that digital vessels undergo vasoconstric-tion as a result of carbohydrate overload in horses, which may contribute to the development of laminitis. Horses with chronic IR may be more likely to develop laminitis since vasoconstric-tion is already promoted.

Hyperinsulinemia and Vascular DynamicsLaminitis has been experimentally induced in healthy ponies

and Standardbred horses by inducing hyperinsulinemia.27,28 In both studies, glucose and insulin were infused intravenously according to the euglycemic-hyperinsulinemic clamp proce-dure, with mean serum insulin concentrations exceeding 1,000 µU/mL. Mean time to onset of Obel grade 2 laminitis was 46 hours in horses compared with 55 hours in ponies and hoof wall surface temperature increased in response to insulin infusion, indicating that vasodilation occurred within the foot. These results suggest that hyperinsulinemia itself induces laminitis through a mechanism involving vasodilation. If this is the case, then hyperinsulinemia-induced vasodilation would overcome vasoconstriction promoted by IR. It has also been proposed that hyperinsulinemia-induced vasodilation increases glucose delivery to hoof tissues, leading to local glucotoxicity.28 This may lead to the formation of advanced glycation end-products that damage tissues. Advanced glycation end-products develop as glucose reacts with amino acids within tissues and these products play an important role in the development of diabetic angiopathy in humans.29

Figure 1 – Theoretical relationships between insulin sensitivity and vascular tone in horses. Alterations in insulin sensitivity may determine which path-way predominates after activation by circulating insulin.

References1. Johnson PJ, Slight SH, Ganjam VK, et al. Glucocorticoids and laminitis in the horse. Vet

Clin North Am Equine Pract 2002;18:219-236.

2. Kahan V, Andersen ML, Tomimori J, et al. Stress, immunity and skin collagen integrity: evidence from animal models and clinical conditions. Brain Behav Immun 2009;23:1089-1095.

3. Baykan M, Erem C, Gedikli O, et al. Impairment of flow-mediated vasodilatation of brachial artery in patients with Cushing’s Syndrome. Endocrine 2007;31:300-304.

4. Rizzoni D, Porteri E, De Ciuceis C, et al. Hypertrophic remodeling of subcutaneous small resistance arteries in patients with Cushing’s syndrome. J Clin Endocrinol Metab 2009;94:5010-5018.

5. Ruzzin J, Wagman AS, Jensen J. Glucocorticoid-induced insulin resistance in skeletal muscles: defects in insulin signalling and the effects of a selective glycogen synthase kinase-3 inhibitor. Diabetologia 2005;48:2119-2130.

6. Buren J, Liu HX, Jensen J, et al. Dexamethasone impairs insulin signalling and glucose transport by depletion of insulin receptor substrate-1, phosphatidylinositol 3-kinase and protein kinase B in primary cultured rat adipocytes. Eur J Endocrinol 2002;146:419-429.

7. Tiley HA, Geor RJ, McCutcheon LJ. Effects of dexamethasone on glucose dynamics and insulin sensitivity in healthy horses. Am J Vet Res 2007;68:753-759.

8. Tiley HA, Geor RJ, McCutcheon LJ. Effects of dexamethasone administration on insulin resistance and components of insulin signaling and glucose metabolism in equine skeletal muscle. Am J Vet Res 2008;69:51-58.

9. Tóth F, Frank N, Geor RJ, et al. Effects of pretreatment with dexamethasone or levo-thyroxine sodium on endotoxin-induced alterations in glucose and insulin dynamics in horses. Am J Vet Res 2010;71:60-68.

10. Reeves HJ, Lees R, McGowan CM. Measurement of basal serum insulin concentration in the diagnosis of Cushing’s disease in ponies. Vet Rec 2001;149:449-452.

11. Schott HC, 2nd. Pituitary pars intermedia dysfunction: equine Cushing’s disease. Vet Clin North Am Equine Pract 2002;18:237-270.

12. Frank N, Elliott SB, Chameroy KA, et al. Association of Season and Pasture Grazing with Blood Hormone and Metabolite Concentrations in Horses with Presumed Pituitary Pars Intermedia Dysfunction. J Vet Intern Med 2010;24:1167-1175.

13. McGowan CM, Frost R, Pfeiffer DU, et al. Serum insulin concentrations in horses with equine Cushing’s syndrome: response to a cortisol inhibitor and prognostic value. Equine Vet J 2004;36:295-298.

14. Frank N. Equine Metabolic Syndrome. J Equine Vet Sci 2009;29:259-265.15. Marik PE, Raghavan M. Stress-hyperglycemia, insulin and immunomodulation in sepsis.

Intensive Care Med 2004;30:748-756.

16. Treiber KH, Kronfeld DS, Hess TM, et al. Evaluation of genetic and metabolic predisposi-tions and nutritional risk factors for pasture-associated laminitis in ponies. J Am Vet Med Assoc 2006;228:1538-1545.

17. Carter RA, Treiber KH, Geor RJ, et al. Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies. Equine Vet J 2009;41:171-178.

18. Vick MM, Adams AA, Murphy BA, et al. Relationships among inflammatory cytokines, obesity, and insulin sensitivity in the horse. J Anim Sci 2007;85:1144-1155.

19. Hartge MM, Unger T, Kintscher U. The endothelium and vascular inflammation in diabe-tes. Diab Vasc Dis Res 2007;4:84-88.

20. Kearns CF, McKeever KH, Roegner V, et al. Adiponectin and leptin are related to fat mass in horses. Vet J 2006;172:460-465.

21. Ritchie SA, Ewart MA, Perry CG, et al. The role of insulin and the adipocytokines in regula-tion of vascular endothelial function. Clin Sci (Lond) 2004;107:519-532.

22. Radin MJ, Sharkey LC, Holycross BJ. Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses. Vet Clin Pathol 2009;38:136-156.

23. Muniyappa R, Montagnani M, Koh KK, et al. Cardiovascular actions of insulin. Endocr Rev 2007;28:463-491.

24. Muniyappa R, Iantorno M, Quon MJ. An integrated view of insulin resistance and endo-thelial dysfunction. Endocrinol Metab Clin North Am 2008;37:685-711, ix-x.

25. Kim JA, Montagnani M, Koh KK, et al. Reciprocal relationships between insulin resistance and endothelial dysfunction: molecular and pathophysiological mechanisms. Circulation 2006;113:1888-1904.

26. Eades SC, Stokes AM, Johnson PJ, et al. Serial alterations in digital hemodynamics and endothelin-1 immunoreactivity, platelet-neutrophil aggregation, and concentrations of nitric oxide, insulin, and glucose in blood obtained from horses following carbohydrate overload. Am J Vet Res 2007;68:87-94.

27. Asplin KE, Sillence MN, Pollitt CC, et al. Induction of laminitis by prolonged hyperinsu-linaemia in clinically normal ponies. Vet J 2007;174:530-535.

28. de Laat MA, McGowan CM, Sillence MN, et al. Equine laminitis: Induced by 48 h hyperin-sulinaemia in Standardbred horses. Equine Vet J 2010;42:129-135.

29. Yamagishi S. Advanced glycation end products and receptor-oxidative stress system in diabetic vascular complications. Ther Apher Dial 2009;13:534-539.

Nicholas Frank, DVM, PhD, DACVIM + Professor and Chair, Dept. of Clinical Sciences, Tufts Cum-mings School of Veterinary Medicine, North Grafton, Mass.

+ DVM Degree Purdue University, 1993 + Large Animal Residency and PhD Purdue University, 2002 on the faculty of the University of Tennessee as clinician, developed research programs in the areas of Equine endocrinology, metabolism, gastrointestinal disease and laminitis.


New frontiers in equine genetics have opened up with the development of new technologies. Gnome map-ping techniques provide new opportunities to identify

single gene traits, as well as genetic risk factors for diseases that have a polygenic basis. This paper will briefly review the currently known genetic disorders of equine skeletal muscle that are caused by a single gene or a gene of major effect. This includes recessive conditions of glycogen branching enzyme deficiency, as well as dominant conditions such as Hyperka-lemic periodic paralysis (HyPP), type 1 and type 2 polysac-charide storage myopathy (PSSM), malignant hyperthermia (MH) and recurrent exertional rhabdomyolysis (RER).

Hyperkalemic Periodic ParalysisHyperkalemic periodic paralysis (HyPP) is an autosomal

dominant trait affecting Quarter Horses, American Paint Horses, Appaloosas and crossbred Quarter Horses. It was the first equine disease attributed to a specific genetic mutation. A single base pair substitution in the SCN4A gene caused a phenylalanine/leucine substitution in a key part of the volt-age-dependent skeletal muscle sodium channel alpha subunit. Impressive, a prolific Quarter Horse sire born in 1969 appears to have been the origin of the HyPP mutation. Impressive and his 355,000 registered descendants are usually heavily mus-cles and have therefore dominated the halter horse industry. Approximately 4% of the Quarter Horse breed may be affected, most of which are heterozygous for the mutation; however, some horses are homozygous for this dominant trait. It is highly advisable to perform genetic testing on horses related to Impressive during a pre-purchase examination or prior to heavy sedation and anesthesia. Owners should be fully aware that breeding an affected horse to a normal horse results in a 50% chance of perpetuating the disorder in future generations.Clinical Signs: Intermittent clinical signs are usually evident by 3 years-of-age, but the severity of clinical signs is highly variable ranging from no signs to infrequent muscle fascicula-tions to marked tremors that progress to weakness and paraly-sis. Some horses may develop severe muscle cramping. Persis-tent depolarization of the muscle cells can progress to cause weakness characterized by staggering, dog sitting and recum-bency. Episodes often last 15 to 60 minutes during which time horses remain anxious, but alert. Respiratory stridor, distress and dysphagia, may occur, particularly in homozygous horses, as a result of pharyngeal collapse and edema, laryngopalatal dislocation and laryngeal paralysis. Several horses have died during acute episodes.

Expression of HyPP is influenced by dietary potassium con-centrations, fasting, heavy sedation, anaesthesia, trailer rides and stress; however, often there is no apparent inciting cause. Exercise per se does not appear to stimulate clinical signs, and

usually serum CK is within normal limits or only modestly increased during episodes.

Diagnosis: Blood samples obtained during episodes show hyperkalemia (6–9 mEq/L), hemoconcentration and mild hyponatremia. Serum potassium concentration return to normal soon after an episode. A DNA test is available for the mutation in the gene encoding for the alpha subunit of the sodium channel (www.vgl.ucdavis.edu).Treatment: Many horses spontaneously recover from epi-sodes of HyPP and appear normal by the time a veterinarian arrives. Some owners find mild exercise or administration of corn syrup may abort a mild episode. In severe cases, intra-venous administration of calcium gluconate (0.2 to 0.4 ml/kg of a 23% solution diluted in 1 litre of 5% dextrose or saline) will often provide immediate improvement. Other treatment options, include intravenous dextrose (6 ml/kg of a 5% solu-tion) alone or combined with sodium bicarbonate (1 to 2 mEq/kg) or intramuscular administration of epinephrine (3 ml of 1:1000/500 kg).Control: Ideally, horses suffering from HyPP should be fed a balanced diet containing between 0.6% and 1.1% total potas-sium concentration by weight. Each meal should contain less than 33 g of potassium. High potassium feeds such as alfalfa hay, orchard grass hay, brome hay, soybean meal, and sugar molasses and beet molasses should be avoided. Optimally, later cuts of Timothy or Bermuda grass hay and grains such as oats, corn, wheat and barley, and beet pulp should be fed in small meals several times a day. The potassium concentra-tion of forages can vary widely so it may be prudent to per-form a forage analysis to determine potassium concentrations. Regular exercise and/or frequent access to a large paddock or yard are also beneficial. Although potassium concentrations may be high in grasses, the high water content in this forage appears to dilute the potassium load making them safe for pastured horses. Commercially available complete feeds with a guaranteed K+ content may be more convenient for some HyPP horses.

Acetazolamide (2-3 mg/kg orally, every 8 to 12 hours) or hydrochlorothiazide (0.5-1 mg/kg orally, every 12 hours) may be indicated for horses whose episodes are not controlled by adjusting the diet. These diuretics increase renal potassium excretion and acetazolamide also stimulates insulin secretion which drives blood glucose and potassium into cells.

Glycogen Branching Enzyme DeficiencyGlycogen branching enzyme deficiency (GBED) is an auto-

somal recessive glycogen storage disorder that affects neo-natal Quarter Horse or Paint Horse foals or aborted feti. The disease is due to a mutation in the GBE1 gene which mark-edly reduces the function of the glycogen branching enzyme.

The Genetic Basis for Muscle Disorders in Horses By STEPHANIE VALBERG,

DVM, PhD, DACVIM, DACVSMR


As a result, tissues such as cardiac and skeletal muscle, liver and the brain cannot store and mobilize glycogen to maintain normal glucose homeostasis. Carriers of GBED trace back to the sire King P234 in most cases, however, King’s sire Zan-tanon may also have carried GBED. The majority of Quarter Horses, however, are descendants of these two stallions so pedigree analysis is not very helpful. GBED has likely been in the Quarter Horse breed at least since its inception in 1940. Approximately 8% of both Quarter and Paint Horses are car-riers of GBED.1 Homozygous GBED feti was detected in 2–4% of 2nd and 3rd trimester abortions submitted to two diagnostic laboratories. Many GBED cases likely are undiagnosed due to the similarity of clinical signs with many neonatal diseases and the current lack of genetic testing of stillborn foals and aborted feti.Clinical Signs: The most common presentation of GBED is likely stillbirth or 2nd or 3rd trimester abortion. Foals that survive to parturition are often hypothermic and weak, but gain strength when given milk by bottle feeding or through assistance to stand and nurse. Correctable flexural deformi-ties of all 4 limbs are common in GBED foals. Progression of signs can be highly variable. Some foals have early onset ven-tilatory failure and die even with mechanical ventilation.15 Other foals show intermittent collapse due to hypoglycemia, particularly if access to suckling is restricted. Sudden death is reported in some foals whereas others are euthanized due to muscle weakness and inability to rise. Most GBED-affected foals die or are euthanized by 8 weeks of age, however, one foal survived with nursing care to 18 weeks of age. Common hematological findings include a low white blood cell count (<4500 cells/ul), and mild to moderate elevations in serum creatine kinase (CK), aspartate transaminase (AST) and gama glutamyl transferase (GGT).Diagnosis: Muscle biopsy specimens or samples of cardiac tissue obtained at necropsy from foals with GBED often, but do not always, contain basophilic globules and eosinophilic crystalline material in routine hematoxylin and eosin stains. Aborted feti or foals of Quarter Horse-related breeds that die at less than 8 weeks of age should have cardiac and muscle sections obtained for period acid Schiff’s staining. GBED foal tissues contain PAS positive globular inclusions with, in some cases, smaller crystalline inclusions. Abnormal polysaccharide can be identified in neural tissue and is inconsistently found in the liver. The most accurate diagnosis of GBED can be obtained through genetic testing by licensed laboratories such as the University of California, Davis (www.vgl.ucdavis.edu) or Vet Gen (www.vetgen.com). Mane or tail hairs with roots intact can be submitted to identify foals homozygous for GBED.

Many stallion owners offer a free repeat breeding to owners that lose foals; and if a diagnosis is not established, the owner will have a 25% chance of having another GBED-affected off-spring. Testing mane hairs for heterozygosity for GBED is strongly recommended for Quarter Horse-related mares that experience abortion, still birth or unexplained death of a neo-nate less than 8 weeks of age.Treatment: There is no treatment for GBED. Early recognition and euthanasia can save considerable expense for owners of foals in neonatal intensive care units.

Polysaccharide Storage Myopathy (PSSM)Type 1 PSSM is caused by a dominantly inherited mutation

in the glycogen synthase 1 (GYS1) gene. It is seen frequently in Quarter Horse-related breeds (especially halter and west-ern pleasure horses) Morgans and Draft horses, but is also present in at least 20 other horse breeds (Table 1).Clinical Signs: Quarter Horse-related breeds and other cross bred or light-breeds of horses with type 1 PSSM often develop episodes of rhabdomyolysis at a young age with little exercise. Rest for a few days prior to exercise is a common triggering factor. Episodes are characterized by a tucked-up abdomen, a camped-out stance, muscle fasciculations, sweating, gait asymmetry, hind limb stiffness, and reluctance to move. Some horses paw or roll resembling colic. Serum CK and AST are increased during an episode (usually >1,000 U/L) and, unlike in other forms of rhabdomyolysis, subclinical episodes char-acterized by persistently abnormal CK are common. Clinical signs in Draft horses may include loss of muscle mass, pro-gressive weakness, and recumbency. CK and AST may be normal in draft horses with this syndrome. On the occasion that draft horses develop rhabdomyolysis CK and AST may be markedly elevated and horses can become myoglobinuric, weak and reluctant to rise.Diagnosis: A diagnosis of type 1 PSSM is based on identifica-tion of the GYS1 mutation (www.vdl.umn.edu/vdl/ourservices/neuromuscular.html) and/or the presence of muscle fibers with subsarcolemmal vacuoles, dark periodic acid-Schiff (PAS) staining for glycogen, and most notably, amylase-resistant abnormal complex polysaccharide accumulation.

Type 2 PSSM occurs in light breeds such as Arabians, Mor-gans, Thoroughbreds, a variety of Warmblood breeds and some Quarter Horses. In appears to be inherited although the genetic basis for this is not yet known.Clinical Signs: In Quarter Horses, less than one year of age, it may cause difficulty rising from a recumbent position. Chronic episodes of muscle stiffness, soreness, and muscle atrophy with modest elevations in serum CK activity are common in horses with type 2 PSSM. The most common presentation of this disorder in Warmbloods, is a gait abnormality and exer-cise intolerance without necessarily a concomitant rise in serum CK activity.Diagnosis: A diagnosis is made by identifying excessive glyco-gen storage in muscle biopsies in a horse with a negative GYS1 genetic test.Dietary Management: Horses with type 1 PSSM have a con-stantly active glycogen synthase enzyme further stimulated by insulin resulting in high muscle glycogen concentrations. When fed a starch meal, these horses take up a higher propor-tion of the absorbed glucose in their muscles compared with healthy horses. Horses with type 2 PSSM also have excessive glycogen storage. Thus, the ideal diet for PSSM is based on feeding forage at a rate of 1.5-2% of body weight, providing

<15% of digestible energy as fat and limiting starch to <10% of daily digestible energy by limiting grain or replacing it with a fat supplement. Caloric needs should be assessed first to pre-vent horses becoming obese on a high-fat diet. Improvement in signs of exertional rhabdomyolysis for horses with PSSM


Stephanie Valberg, DVM, PhD, DACVIM, DACVSMR + Professor and director University of Minnesota Equine Center, St. Paul

+ DVM degree from Ontario Veterinary College

+ PhD in equine exercise physiology, Swedish University of Agriculture Science in Uppsala, Sweden

+ Post doctoral work University of California, Davis, in muscle disorder

+ Residency in large animal in-ternal medicine at University of California, Davis

requires both dietary changes and gradual increases in the amount of daily exercise and turn-out.Clinical Signs: Classic episodes of MH include lactic acidosis and hyperthermia > 40 C under halothane anesthesia or fol-lowing succinyl choline injection. Horses with MH also may intermittently develop clinical signs of tying up. MH can occur together with type 1 PSSM and when this occurs, the clinical signs of tying up are more severe and sudden death may occur during an episode.Diagnosis: A genetic test is available (www.vgl.ucdavis.edu, (www.vdl.umn.edu/vdl/ourservices/neuromuscular.html) to identify this mutation in Quarter Horses and Paint Horses. This mutation is not present in all horses that develop malig-nant hyperthermia and in other breeds there may be other yet unidentified mutations that cause signs of hyperthermia and metabolic acidosis during anesthesia.Treatment: The most successful outcome for a horse with suspected malignant hyperthermia would be pretreatment with oral dantrolene (4 mg/kg) 30-60 minutes prior to anes-thesia. There is no cost effective means to deliver dantrolene to horses intravenously once an episode has begun. Unfortu-nately, once a fulminant episode is underway, it is difficult to prevent cardiac arrest.

Malignant Hyperthermia (MH)MH occurs in Paint and Quarter Horses and is due to an

autosomal dominant mutation in the skeletal muscle ryano-dine receptor gene (RYR1). It affects less than 1% of these breeds, but may be concentrated in some pleasure and halter horse families.Clinical Signs: Classic episodes of MH include lactic acidosis and hyperthermia > 40 C under halothane anesthesia or fol-lowing succinyl choline injection. Horses with MH also may intermittently develop clinical signs of tying up. MH can occur together with type 1 PSSM and when this occurs, the clinical signs of tying up are more severe and sudden death may occur during an episode.Diagnosis: A genetic test is available (www.vgl.ucdavis.edu, (www.vdl.umn.edu/vdl/ourservices/neuromuscular.html) to identify this mutation in Quarter Horses and Paint Horses. This mutation is not present in all horses that develop malig-nant hyperthermia and in other breeds there may be other yet unidentified mutations that cause signs of hyperthermia and metabolic acidosis during anesthesia.Treatment: The most successful outcome for a horse with suspected malignant hyperthermia would be pretreatment with oral dantrolene (4 mg/kg) 30-60 minutes prior to anes-thesia. There is no cost effective means to deliver dantrolene to horses intravenously once an episode has begun. Unfortu-nately, once a fulminant episode is under way, it is difficult to prevent cardiac arrest.

Recurrent Exertional Rhabdomyolysis (RER)RER is seen frequently in Thoroughbreds, Standardbreds

and Arabian horses. It is likely due to abnormal regulation of skeletal muscle contraction possibly involving intracellular calcium regulation. Approximately 5-10% of horses of these

breeds are affected. The heritable basis for RER is believed to be polygenic, but has been reported to be passed on in a domi-nant fashion in some thoroughbred families.Clinical Signs: Episodes of exertional rhabdomyolysis are intermittent and particularly occur when horses susceptible to the condition are fit and have a nervous temperament.Diagnosis: A diagnosis of RER is usually based on history, clinical signs, and elevations in serum CK and AST activity. If muscle biopsy is performed when horses have active episodes, centrally located nuclei in mature myofibers and an absence of abnormal polysaccharide are characteristic features.Management: Management of recurrent exertional rhab-domyolysis is aimed at decreasing the triggering factors for excitement and pharmacologic alteration of intracellular cal-cium flux with contraction. Management changes that may decrease excitement include minimizing stall confinement by using turn-out or a hot walker, exercising and feeding horses with recurrent exertional rhabdomyolysis before other horses, providing compatible equine company, and the judicious use of low-dose tranquilizers during training. A high-fat, low-starch diet is beneficial, possibly by decreasing excitement. In contrast to PSSM, horses that have recurrent exertional rhab-domyolysis often require higher caloric intakes (>24 MCal/day). At these high caloric intakes, specialized feeds designed for exertional rhabdomyolysis are necessary, as additional vegetable oil or rice bran cannot supply enough calories for athletes in intense training. Hay should be fed at 1.5-2% of body weight and high-fat, low-starch concentrates should be selected that provide <20% of daily digestible energy as non-structural carbohydrate and 20-25% of digestible energy as fat.

Dantrolene (4 mg/kg, PO) given 1 hour before exercise to horses that are not fed prior to exercise, may decrease the release of calcium from the calcium release channel. Phe-nytoin (1.4-2.7 mg/kg, PO, bid), also has been advocated as a treatment for horses with recurrent exertional rhabdomy-olysis. Therapeutic levels vary, so oral dosages are adjusted by monitoring serum levels to achieve between 8 µg/mL and 12 µg/mL. Long-term treatment with dantrolene or phenytoin is expensive, however.

References Available upon request [email protected]


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