The Practitioner Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 5 • 2011
In This Issue
| Pain Models and Scoring & Pain 6 Management in Horses 10 | 2011 Continuing Education – A Tremendous Success!
15 | 19 | 20 | 23 |
Arrhythmias in the Performance Horse FAEP Member Practice Highlight Endocrinopathic Laminitis The Genetic Basis for Muscle Disorders in Horses
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Letter from the President 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. EXECUTIVE COUNCIL Gregory D. BonenClark, DVM, Diplomate ACVS FAEP Council President
gbonenclark@fevaocala.com
Anne L. Moretta, VMD, MS FAEP Council Vice President
maroche1@aol.com Jacqueline S. Shellow, DVM, MS FAEP Council Past President
docshellow@bellsouth.net Mr. Philip J. Hinkle Executive Director
phinkle@fvma.org
COUNCIL REPRESENTATIVES J. Barry David, DVM, Diplomate ACVIM
bdavid@emcocala.com
Amanda M. House, DVM, Diplomate ACVIM
housea@ufl.edu
Suzan C. Oakley, DVM, Diplomate ABVP (Equine) FAEP Council
oakleyequine@gmail.com Liane D. Puccia, DVM
pucciavet@aol.com
Ruth-Anne Richter, BSc (Hon), DVM, MS
rrichter@surgi-carecenter.com Corey Miller, DVM, MS, Diplomate ACT FAEP Council Representative to the FVMA Executive Board
cmiller@emcocala.com
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 tremendous amount of time and effort this past year into helping our organization 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 enhancements 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 inception. 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 imaging 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 education 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
The Practitioner is an official publication of the Florida Association of Equine Practitioners an Equine-Exclusive Division of the Florida Veterinary Medical Association.
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The Practitioner • Issue 5
8th Annual Promoting Excellence Symposium in the Southeast World-class equine-exclusive continuing education in an oasis of serene elegance – Naples, the crown jewel of Florida’s Gulf Coast!
LECTURE TOPICS INCLUDE Lameness Imaging Neonatology Pre-purchase Exams Internal Medicine Regenerative Medicine Rehabilitation
LEISURE EVENTS FAEP’s Annual Golf Tournament
Mark Your Calendar . . .
OCTOBER 11 – 14, 2012 Naples Grande: A Waldorf Astoria Resort • Naples, FL MAGNIFICENT RESORT AMENITIES Cycling Canoeing and Kayaking Aqua Biking Windsurfing, snorkeling and sailing
FAEP’s Annual Fishing Tournament
Rees Jones Designed Golf Course
Picturesque Beach on the Gulf of Mexico
Golden Door Spa
World-Class Tennis
Pain Models and Scoring & Pain Management in Horses Overview Colic and lameness are two of the most clinically and economically important medical problems facing horses and their owners. Pain is a critical component of each disease process and its alleviation 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 stimulus, the stimulus is minimally invasive and ethically acceptable, the stimulus is controllable, reproducible, quantifiable, and the responses are reliable and quantifiable.1
Research Models of Visceral and Somatic Nociception Most 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 gastrointestinal tract. As such, information gained from these models can be applied only to clinical conditions that cause pain as a result of visceral distension, and these are typically models of acute pain. Because many naturally occurring conditions involve distension of one form or another, such models have provided 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 distension models is that both the stimulus (distension) and associated nociceptive behaviors (pawing, flank watching, etc.) mimic the clinical syndrome of colic. With the CRD, the associated behavior (expulsion 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 nociceptive 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 6
By Chris Sanchez, DVM, PhD, DACVIM
objective evaluation of somatic nociception, mostly associated with acute pain. With thresholdbased models, heat (thermal) and mechanical (pressure 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 agonists. Mechanical stimuli include the use of pneumatic devices to apply pressure to the coronary band or a pressure algometer at either the pastern or along the thoracolumbar musculature. The pneumatic 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 osteoarthritis, chiropractic therapy, phenylbutazone, massage therapy, sacroiliac dysfunction and distal forelimb irritants in Tennessee Walking Horses.9-12 The use of both mechanical and thermal stimuli to evaluate analgesic therapy is useful in that both types of stimuli are seen in clinical situations. Reversible models of lameness, such as a specialized shoe fitted with an adjustable screw to induce solar pressure, have been used to evaluate the analgesic effects of non-steroidal anti-inflammatory agents.13 These models offer the advantage of a naturally occurring stimulus and quantifiable nociceptive effects.
Scoring Systems for Clinical Research In order to be useful, a pain scoring system should include clearly defined assessment criteria, be suitable 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 agreement 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 treatment, then re-assess pain score at various intervals). When critically assessing scoring systems, the investigator should control for signalment (age, breed, sex), observer (veterinarian, student, owner/ The Practitioner • Issue 5
Available Options for Systemic Analgesia in Horses
trainer), procedure, and other effects (food withdrawal, anesthesia, management, etc.). Continuous 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 performed on horses following arthroscopy.14 A numerical rating system was also used to assess the effect of a butorphanol constant rate infusion on physiologic and outcome variables in horses following colic surgery.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 alleviate the subjective nature of assessment. But, vital signs and cortisol are affected by a variety of factors in addition to pain, including hydration status, perfusion, 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 4
Gross pain behaviors a
None
Occasional
Continuous
Head position
Above withers
At withers
Below withers
Ear position
Forward, frequent movement
Slightly back, little movement
Location in stall
At door watching environment
Standing in middle, facing stall door
Spontaneous locomotion/ response to approach
Moves freely/ moves to observer
Occasional steps/looks at observer with ears forward
No movement/ ears back
Lifting feet
Freely lifts feet when asked
Lifts feet after mild encouragement
Extremely unwilling to lift feet
Standing in middle, facing sides of stall
Class NSAIDs
Standing in middle, facing back of stall
TOTAL SCORE
Gross pain behaviors include pawing, sweating, looking at the flank, flehmen (stretching neck and raising upper lip), and lying down/standing up repeatedly a
The Practitioner • Issue 5
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
Phenylbutazone
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 reduction from original dose
Xylazine
0.2-1.1
IV, IM
prn
Sedation outlasts analgesia
Detomidine
0.005-0.04
IV, IM
prn
Sedation outlasts analgesia
Romifidine
0.04-0.12
IV
prn
Analgesia may be insufficient for many procedures
Medetomidine
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.
Butorphanol
0.01-0.05
IV
3-4
0.04-0.1
IM
4-6
Can combine w/ α-2; good alone IM in foals
Butorphanol
18 µg/kg then 10-23 µg/ kg/hr
IV
CRI
Morphine
0.12-0.66
IV
4-6
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 palpation
Score α-2 Agonists
3
Opioids
2
Drug
Misc.
1
Dosages are summarized from the available literature and personal communication. These amounts must be titrated to the individual animal and situation.
Combine w/ α-2
7
Drugs/Combinations for Caudal Epidural Analgesia in Horses Drug
Dosage (mg/kg)
Duration
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
Lidocaine Xylazine
0.22 mg/kg 0.17 mg/kg
5-6 hours
Comments
qs to 30 ml w/ saline; may cause pruritis
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
Note that all drugs and/or combinations can cause ataxia. References 1. 2.
Gebhart GF, Ness TJ (1991), Central mechanisms of visceral pain, Can.J.Physiol Pharmacol. 69: 627-634 Kohn CW, Muir WW, III (1988), Selected aspects of the clinical pharmacology of visceral analgesics and gut motility 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 nociception 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 nociception in conscious horses, Equine Vet J 37: 122-127
5.
Merritt AM, Xie H, Lester GD, Burrow JA, LorenzoFigueras 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 electroacupuncture and butorphanol on respiratory and
8
cardiovascular effects and rectal pain threshold after controlled 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 mechanical 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 nociceptive 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
The Practitioner • Issue 5
Soar.
Sore.
Both depend on which therapy you choose. So choose the only FDA-approved I.V. joint therapy for equine non-infectious synovitis. 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
2011 Continuing Education – A Tremendous Success!
T
he first year out of the gate, the FAEP and the FVMA presented three tremendously successful 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 Symposium, was one of the most successful farrier and veterinarian 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 relevant and outstanding education for the equine practitioner. The end of October marked another successful educational event. The 49th Annual Ocala Equine Conference from Oct. 21-24 offered more cuttingedge equine-exclusive CE.
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.
10
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.
Dr. Michelle LeBlanc, second from left, is congratulated on her Lifetime Achievement Award by Dr. Amanda House, left; Dr. Jackie Shellow, second from right, and Dr. Chris Sanchez.
The Practitioner • Issue 5
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.
Third Annual Equine Foot Symposium Dr. Gregory BonenClark, left center, assists Mitch Taylor, CJF, DWCF, instructor, 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.
This high caliber event promoted communication and teamwork between veterinarian and farrier attendees. hh 14 hours of cutting-edge continuing education hh Six speakers hh Some of the topics offered included: Fostering the veterinarian & farrier relationship, a Front and Hind Limb Anatomy Review, Hoof Cracks, Repair and Treatment, Hoof Balance, and Laminitis.
Practitioners and Farriers receive pointers during the Foot Symposium Wet Lab.
hh The Hands-On Anatomy Wet Lab offered instruction 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. Foot Symposium continuing education lecture.
The Practitioner • Issue 5
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Dr. Michael Ross, New Bolton Center, left, and Dr. Sue Dyson, Centre for Equine Studies, United Kingdom, 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.
7th Annual Promoting Excellence Symposium in the Southeast Keeping up with published scientific equine clinical advancements of the past year was presented 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, professor of surgery at the School of Veterinary Medicine, New Bolton Center, Kennett Square, PA. New to the FAEP program was a rehabilitation track featuring the very latest in rehabilitation protocols, modalities and techniques for the equine athlete. Rehabilitation expert Mike Torry, PhD, shared his insights on the correlation 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 University 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. hh 52 hours of continuing education available hh 22 nationally and internationally acclaimed speakers hh Lecture topics included Internal Medicine, Regenerative Medicine, Respiratory Disease, Reproduction, Acupuncture, Surgery, Pharmacy review, Lameness, Musculoskeletal Imaging, Endoscopy, Pain Management, Cardiology and Rehabilitation. hh Wet Lab – musculoskeletal ultrasound – was oriented towards veterinarians who
12
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.
perform diagnostic ultrasounds regularly and wanted to fine tune their imaging of more complex structures. “It was right up my alley, the musculoskeletal 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.” Virginia Loy, right, of MWI Veterinary Supply, chats with an attendee.
The Practitioner • Issue 5
LEFT: Dr. Nicholas 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.
49th Annual Ocala Equine Conference The FAEP concluded the 2011 season of continuing education events with the 49th Annual Ocala Equine Conference at the Hilton Ocala in the horse capital of the world. hh 40 hours of continuing education offered
Practitioners gained valuable information on ultrasound techniques which focused on musculoskeletal, respiratory and abdominal structures. An ophthamology wet lab offered views into eye trauma, treatment strategies and protocols.
hh 14 educator speakers in the equine industry hh Lecture topics included Colic Evaluations, Endocrinology, Ophthalmology, Orthopedics, Pharmacy, Respiratory Disease and Ultrasound. hh Wet labs were popular with conference attendees. The ultrasound wet lab featured Dr. Carol Gillis and focused on Musculoskeletal, 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 Metabolic 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.
The Practitioner • Issue 5
Each symposium offered a marketplace venue which showcased vendors and exhibitors who are well acquainted with the equine practitioners, 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 education and hands-on wet labs. Our exhibitors provide 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 attending the 7th Annual Promoting Excellence Symposium 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.”
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Special Thanks to our 2011 Educational 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!
GOLD PARTNERS
SILVER PARTNERS
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The Practitioner • Issue 5
Arrhythmias in the Performance Horse By Kim McGurrin, BSc, DVM, DVSc, DACVIM
N
Figure 1
ormal sinus rhythm requires the electrical impulse to be “smoothly” conducted from the sinoatrial node through the atrial tissue to the atrioventricular node on through inflammation, significant electrolyte the Purkinje network, terminating in the imbalances and cardiac glycoside toxicity. ventricular myocardium before the tissue It may be associated with pronounced repolarizes and the impulse starts again. bradycardia; such animals may be exerThe resultant rhythm is regular with the cise intolerant and prone to collapse. rhythm governed by the pacemaker at Mobitz type II may be associated with the sinoatrial node. atrial myocardial disease. With advanced Autonomic input in the normal horse block corticosteroids may be of benefit. can greatly influence the heart rate and rhythm. The horse is a parasympathetiSinus Arrhythmia cally driven animal and, if all autonomic Sinus arrhythmia is usually associated tone is removed, the intrinsic heart rate with sinus bradycardia when present at is 100 bpm. The resting rate is therefore rest. It is characterized by fluctuation in governed by vagal tone, and it is there- cardiac rhythm associated with respirafore not surprising that vagally mediated tion (respiratory sinus arrhythmia) from arrhythmias are common. These are, for changes in vagal tone and there is a rhyththe most part, benign, yet can remark- mical variation. The term also has been ably disrupt cardiac rhythm. The follow- used to describe fluctuations in cardiac ing notes describe the more common rhythm associated with exercise (exercise dysrhythmias that occur in the horse associated arrhythmia). This arrhythmia and some of the investigations into is commonly found in fit horses during the impact of dysrhythmia on equine cardiac deceleration following submaxiperformance. mal exercise and is likely associated with variation in autonomic feedback as the Second Degree Block sympathetic input decreases and the This is the most common dysrhythmia parasympathetic system regains control. in the horse. It is mediated by increased Respiratory sinus arrhythmia is not as vagal tone at the level of the atrioven- common or as obvious as in small anitricular node causing blocked conduction mals or humans. 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 irregular. However, the blocked interval is a multiple (i.e. usually twice) the basal interbeat interval. Because of the predictable length of the blocked interval this arrhythmia is usually identified as being regularly irregular. The arrhythmia should abate with increased heart rate Figure 2 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 The Practitioner • Issue 5
Sinus Arrest/Block Sinus 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 infrequently; in others, the frequency may be sufficient to confuse this rhythm disturbance with atrial fibrillation. Persistence at elevated heart rates may indicate a pathological basis. Prolonged (4 seconds or greater) blocked intervals or those associated with syncope are clinically 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 asymptomatic 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 Complexes These are depolarizations occurring within the atria, originating outside of the
15
sinoatrial node. By definition, this occurs before the sinus node depolarizes. Auscultatory 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 infrequent event, and would not be considered as abnormal in that instance. Persistent or high frequency may be caused by atrial myocardial disease or inflammation. Usually no treatment is required. Dexamethasone may be of benefit to control inflammation. Digoxin may be necessary to control rate if severe tachycardia is present.
Atrial Tachycardia This 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 presentation 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 possible. 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 myocardial inflammation or disease. Treatment is often successful through the identification and removal or treatment of underlying cause, such as electrolyte imbalance or inflammation. Antiarrhythmic medication may be indicated. Quinidine has been used with caution. Quinidine increases conduction through the AV node and conduction of previously blocked P waves will increase ventricular rate. Digoxin can be used to slow ventricular rate and to limit AV nodal conduction. Electrical cardioversion may be useful in stable cases; those
Figure 3
16
cases with second-degree block which will tolerate anaesthesia.
findings are of regularly spaced S1and S2 with a more rapid S4. With prolonged auscultation S4 will be heard to be indeAtrial Fibrillation pendent and may summate onto the other Atrial fibrillation (AF) is the most heart sounds causing loud ‘bruit de cannon’ common clinically relevant dysrhythmia sounds. Pacemaker implantation is possiin the horse with an estimated incidence ble. Pharmacological therapy is of limited ranging from 0.3-2.5% of the equine pop- value. Atropine/glycopyrrolate (vagolytic) ulation. The initiating event is not known administration is usually unsuccessful. in the horse. Horses may be predisposed The use of sympathomimetics, such as isoto AF because of high vagal tone and proterenol, has been reported; however, large atrial dimension. Vagal tone leads caution should be used due to the risk of to variability in action potential duration ventricular tachyarrhythmias (have lidoacross the atrial tissue. The large atrial caine ready). Corticosteroids may be of dimension in horses allows conduction benefit to treat inflammation. through multiple pathways within the atria. In cases of lone AF, restoration of Ventricular Premature Complexes sinus rhythm should result in complete These are depolarizations that origiresolution of clinical signs. If underly- nate in the ventricle, outside of the Puring cardiac disease is present, the prog- kinje fibres/conduction system. Ausculnosis for restoration and maintenance tatory findings would be of early beats of sinus rhythm is poor and treatment usually with complete compensatory may be contraindicated. Quinidine salts pause. Usually occurring as a single or have long been the modality of choice. infrequent event, it would not be considFlecainide has had some success orally, ered as abnormal in that instance. Persisand has proven difficult to use intrave- tent or high frequency may be caused by nously. Amiodarone is moderately suc- ventricular myocardial disease or inflamcessful when titrated over a no more than mation. Usually no treatment is required. 48-hour course. Transvenous electrical Dexamethasone may be of benefit to concardioversion has proven highly success- trol inflammation. ful, but is technically challenging and requires specialized equipment. Ventricular Tachycardia Ventricular tachycardia exists when Third-Degree Block there are runs of VPCs of four or more This is a rare condition in the horse. in succession. It may be monoform, In general, it has been associated with (originating from one site), or polyform damage to the atrioventricular node; i.e. (originating from multiple sites). It may myocarditis, pericarditis and aortic aneu- be sustained or may alternate with the risms. Clinically, this condition is usually sinus rhythm. If the heart rate is close to associated with profound exercise intoler- normal (<50 bpm), the rhythm is better ance and potentially syncope. Bradycardia termed as accelerated idioventricular with usually regular ventricular rate of rhythm. With regards to correcting the 10-20 bpm is characteristic. Auscultatory rhythm, first correct underlying conditions 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 considered as the first line. This author has had success with careful titration of intravenous 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. The Practitioner • Issue 5
Exercise ECG In some cases, heart rhythm abnormalities may only appear at exercise. Horses that present for poor performance, and in which there are no other abnormalities, are candidates for exercise 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 collect recordings intermittently or once the horse has pulled up. Variations in cardiac rhythm on the exercising and immediate 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 performing 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 concurrent 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 present during actual exercise, if more than 5 ectopics are present or if there are pairs or runs of ectopy in the immediate post exercise period, then the horse is abnormal. Whether this guideline is realistic has recently been open to debate with findings in exercising “normal” racehorses being reported. Another study was conducted on Thoroughbred racehorses considered by their trainers to have no evidence of poor performance. (EVJ; 2005: 37:265) Of 105 horses, 15% had ventricular and 19% had supraventricular ectopics during The Practitioner • Issue 5
the immediate recovery period. 13 and However, the significance of multiple 11% of these animals, respectively, had ectopics, multiform ectopics and runs of ventricular or supraventricular ectopics ectopy remains elusive. To err on the side in the warm-up period and 3% had ven- of safety, especially in the face of historitricular ectopics during peak exercise. cal poor performance, would be prudent. This author was involved in a recent study conducted on Standardbred race- References Martin, BB. et al. J Am Vet Med Ass 2000;216: 554. Ohmura horses. (JVIM; 2010: 24: 1158) Holter 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. monitors were placed prior to warm-up 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, and remained through actual racing. In Eq Comp Ex Phys 2004:1(1);5-22. van Loon G et al Equine this study, 27.8% of recordings showed 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. dysrhythmia in the immediate post-race Rezakhani A et al Pakistan Vet J. 2005;25(1): 40. Schwarzwald CC et al; J Vet Intern Med. 2005;19(5):703. period (less than two minutes post-race). 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 11.6% showed ventricular ectopics, and Intern Med. 2006 ;20(1):207. Schwarzwald CC et al J Vet 15.9% showed complex ventricular dysIntern 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):198rhythmias. Few horses showed dysrhyth204. 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 mia during the race, all of which were limal Am J Vet Res. 2009;70(2):223. Mullen KR et al J Am ited to single ectopics. There was no obviVet 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. ous correlation with performance, other Physick-Sheard PW Et al. J Vet Intern Med; 2010: 24: 1158. Schefer KD et al JVIM 2010; 24: 918. than horses that showed these rhythms were more likely to have a “stretch condition” (broken gait, been distanced at the wire) prior to developing the post-race Kim McGurrin, BSc, DVM, DVSc, dysrhythmia. This might suggest that DACVIM the hard drive that these horses endured ++ Staff at Ontario Veterinary College in increased the likelihood. The presence the areas of Large Animal Medicine of increased post-race vagal tone also and Cardiology since 2003 ++ Graduated from the Ontario increased the risk of arrhythmia. Veterinary College in 1998 During the immediate “recovery ++ One-year rotating internship in Large period” there is a complex interplay of Animal Medicine and Surgery sympathetic and parasympathetic tone. ++ Three-year internal medicine resiSympathetic tone is decreasing while dency, Ontario parasympathetic tone increases. AddiVeterinary College tionally, post-maximal effort, electrolyte ++ DVSc studies and metabolic abnormalities are common. investigating Equine Fluctuations in cardiac rhythm at this Atrial Fibrillation time might therefore be anticipated and and developing variations in sinus rhythm, occasional skills in Large Animal Cardiology second-degree block at high rate and infrequent ectopics, are easy to dismiss.
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The Practitioner • Issue 5
FAEP Member Practice Highlight
T
he Equine Medical Center of Ocala is the only equine referral hospital in Marion County with board-certified specialists in surgery, reproduction and internal medicine. 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.
Equine Medical Center of Ocala
New Services in 2011 • • •
Lameness Locator dramatically increasing the ability 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 technologies with specialized staff and team-oriented client services to achieve goals of satisfied clients and healthy patients.
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.
Board-Certified Specialists •
•
•
Surgery specializing in equine orthopedic and soft-tissue surgeries and diagnostic evaluations: John G. Peloso, DVM, MS, Diplomate ACVS, and Aric R. Adams, DVM, Diplomate ACVS. Reproduction specializing in stallion and mare reproduction 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, cardiology, 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 Thoroughbred 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.
Dr. Barry David, EMCO board certified internal medicine, doing a myelogram.
Dr. Corey Miller, EMCO board certified Theriogenologist, doing a stallion collection.
The Equine Medical Center of Ocala is located at 7107 West Highway 326, Ocala, FL 34482; (352) 873-7830; Fax, (352) 8737700. Visit the website at www.emcOcala.com for more information on staff, equine services and free workshops.
The Practitioner • Issue 5
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Endocrinopathic Laminitis The exact mechanisms involved in endocrinopathic laminitis have not been elucidated, but potential pathophysiological mechanisms include: Hyperadrenocorticism Histological alterations in the integument associated with hyperadrenocorticism in other species include protein depletion, inhibition of fibroblast growth, and reduced collagen synthesis.1,2 Johnson et al.1 described lengthening and attenuation of primary and secondary dermal lamellae in horses with glucocorticoid excess and suggested that this represents pulling apart of lamellae as structures weaken. Vascular changes may also accompany hyperadrenocorticism. Flow-mediated vasodilation of the brachial artery is reduced in humans with Cushing’s disease3 and hypertrophic remodeling of small resistance arteries 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 assumptions 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 dexamethasone 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 concentrations. One explanation for this observation is that IR only occurs with PPID when the horse is predisposed to this problem. 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 ACTHstimulated 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 laminitis. In a recent study, horses with PPID had higher overall insulin 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. 20
By NICHOLAS FRANK, DVM, PhD, DACVIM
Obesity Obesity, IR, hyperinsulinemia, and laminitis are associated in equids (they are key components of Equine Metabolic Syndome), 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 insulin sensitivity.19 Vick et al18 detected higher blood TNFα mRNA expression in obese horses, which suggests that the same mechanism 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 tissues. 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 adiponectin concentrations are also associated with impaired endothelium-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 present 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 Dynamics Insulin possesses vasoregulatory properties and this might explain why IR predisposes horses to laminitis. Slow vasodilation 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) pathway is activated, whereas activation of the mitogen-activated The Practitioner • Issue 5
References 1. 2.
3. 4.
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. 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.
protein kinase (MAPK) pathway leads to release of ET-1.24 Both the vasodilatory effects of insulin and insulin-dependent stimulation of glucose uptake are mediated by PI3K, and this pathway becomes disrupted when IR develops. Consequently, vasoconstriction is promoted in insulin-resistant animals because only the MAPK pathway remains fully functional. Development of compensatory hyperinsulinemia in response to IR can further 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 carbohydrate was administered to induce laminitis in healthy horses. This finding suggests that digital vessels undergo vasoconstriction 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 vasoconstriction is already promoted.
Hyperinsulinemia and Vascular Dynamics Laminitis 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 procedure, 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 The Practitioner • Issue 5
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. 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.
8.
Figure 1 – Theoretical relationships between insulin sensitivity and vascular tone in horses. Alterations in insulin sensitivity may determine which pathway predominates after activation by circulating insulin.
Johnson PJ, Slight SH, Ganjam VK, et al. Glucocorticoids and laminitis in the horse. Vet Clin North Am Equine Pract 2002;18:219-236. 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.
Tóth F, Frank N, Geor RJ, et al. Effects of pretreatment with dexamethasone or levothyroxine 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 predispositions 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 diabetes. 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 regulation 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 endothelial 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 hyperinsulinaemia 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 hyperinsulinaemia 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 Cummings 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.
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The Practitioner • Issue 5
The Genetic Basis for Muscle Disorders in Horses
N
ew frontiers in equine genetics have opened up with the development of new technologies. Gnome mapping 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 Hyperkalemic periodic paralysis (HyPP), type 1 and type 2 polysaccharide storage myopathy (PSSM), malignant hyperthermia (MH) and recurrent exertional rhabdomyolysis (RER).
Hyperkalemic Periodic Paralysis Hyperkalemic 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 voltage-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 muscles 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 fasciculations to marked tremors that progress to weakness and paralysis. Some horses may develop severe muscle cramping. Persistent depolarization of the muscle cells can progress to cause weakness characterized by staggering, dog sitting and recumbency. 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 concentrations, 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
The Practitioner • Issue 5
By STEPHANIE VALBERG, DVM, PhD, DACVIM, DACVSMR
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 episodes 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, intravenous 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% solution) 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 potassium 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 concentration of forages can vary widely so it may be prudent to perform 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 Deficiency Glycogen branching enzyme deficiency (GBED) is an autosomal recessive glycogen storage disorder that affects neonatal Quarter Horse or Paint Horse foals or aborted feti. The disease is due to a mutation in the GBE1 gene which markedly reduces the function of the glycogen branching enzyme.
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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 Zantanon 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 carriers 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 deformities of all 4 limbs are common in GBED foals. Progression of signs can be highly variable. Some foals have early onset ventilatory 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 offspring. 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 neonate 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. 24
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 western 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 characterized by persistently abnormal CK are common. Clinical signs in Draft horses may include loss of muscle mass, progressive 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 identification 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, Morgans, 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 exercise intolerance without necessarily a concomitant rise in serum CK activity. Diagnosis: A diagnosis is made by identifying excessive glycogen storage in muscle biopsies in a horse with a negative GYS1 genetic test. Dietary Management: Horses with type 1 PSSM have a constantly 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 proportion 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 prevent horses becoming obese on a high-fat diet. Improvement in signs of exertional rhabdomyolysis for horses with PSSM
The Practitioner • Issue 5
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 following 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 malignant 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 anesthesia. There is no cost effective means to deliver dantrolene to horses intravenously once an episode has begun. Unfortunately, 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 ryanodine 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 following 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 malignant 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 anesthesia. There is no cost effective means to deliver dantrolene to horses intravenously once an episode has begun. Unfortunately, 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
The Practitioner • Issue 5
breeds are affected. The heritable basis for RER is believed to be polygenic, but has been reported to be passed on in a dominant 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 rhabdomyolysis is aimed at decreasing the triggering factors for excitement and pharmacologic alteration of intracellular calcium 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, lowstarch diet is beneficial, possibly by decreasing excitement. In contrast to PSSM, horses that have recurrent exertional rhabdomyolysis 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 nonstructural 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. Phenytoin (1.4-2.7 mg/kg, PO, bid), also has been advocated as a treatment for horses with recurrent exertional rhabdomyolysis. 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 valbe001@umn.edu
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 internal medicine at University of California, Davis
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