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Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 4 • 2017



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The President's Line Ruth-Anne Richter, BSc (Hon), DVM, MS - FAEP President Dear Fellow Equine Practitioners, As 2017 comes to a close, we reflect upon the year that was. Full of challenges, it was a year to remember. The FAEP celebrated two conferences with outstanding speakers, and we enjoyed catching up with valued attendees. Hurricane Irma presented a particular challenge; closing the host hotel in Naples three weeks before the PES. Undaunted, and with great effort on the part of the FVMA staff, the conference was moved to Orlando. This turned out to be a banner event with record attendance, and a great host hotel whose staff pulled out all the stops to accommodate us. We look forward to 2018, and promise you will enjoy another season of prime continuing education. The Ocala Equine Conference is set to start off 2018, on January 19th – 21st, at the Ocala Hilton that has recently undergone extensive renovations. We are also excited to return to the Naples Grande in 2018. Their repairs were completed recently, and they are ready to host another exciting Promoting Excellence Symposium. We are honored to announce that Dr. Jean-Marie Denoix will speak and teach an informative wet lab on the biomechanical approach to lameness, as well as the ever-popular ultrasound component. Look for more exciting details as the date approaches. Best wishes for the holiday season. We hope to see you at our conferences in 2018, and it promises to be a great year, with innovative, passionate, and outstanding speakers who look forward to sharing their experiences and updating us all on current research. Many thanks and best wishes to our educational partners, and, of course, the FVMA staff for their support of the FAEP. Have a happy and safe holiday season; we look forward to seeing you in 2018!


Ruth-Anne Richter FAEP Council President

Corey Miller


Anne L. Moretta VMD, MS, CVSMT

Armon Blair DVM


Adam Cayot DVM


Amanda M. House DVM, DACVIM

Opinions and statements expressed in The Practitioner reflect the views of the contributors and do not represent the official policy of the Florida Association of Equine Practitioners or the Florida Veterinary Medical Association, unless so stated. Placement of an advertisement does not represent the FAEP’s or FVMA’s endorsement of the product or service. FAEP | 7207 MONETARY DRIVE, ORLANDO, FL 32809 | PH: (800) 992-3862 | FAX: (407) 240-3710 | EMAIL: INFO@FVMA.ORG | WEBSITE: WWW.FAEP.NET

OSPHOSÂŽ (clodronate injection)

The new FDA approved intramuscular bisphosphonate injection for navicular syndrome from Dechra Veterinary Products

Bisphosphonate For use in horses only. Brief Summary (For Full Prescribing Information, see package insert) CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. DESCRIPTION: Clodronate disodium is a non-amino, chloro-containing bisphosphonate. Chemically, clodronate disodium is (dichloromethylene) diphosphonic acid disodium salt and is manufactured from the tetrahydrate form. INDICATION: For the control of clinical signs associated with navicular syndrome in horses. CONTRAINDICATIONS: Horses with hypersensitivity to clodronate disodium should not receive OSPHOS. WARNINGS: Do not use in horses intended for human consumption. HUMAN WARNINGS: Not for human use. Keep this and all drugs out of the reach of children. Consult a physician in case of accidental human exposure. PRECAUTIONS: As a class, bisphosphonates may be associated with gastrointestinal and renal toxicity. Sensitivity to drug associated adverse reactions varies with the individual patient. Renal and gastrointestinal adverse reactions may be associated with plasma concentrations of the drug. Bisphosphonates are excreted by the kidney; therefore, conditions causing renal impairment may increase plasma bisphosphonate concentrations resulting in an increased risk for adverse reactions. Concurrent administration of other potentially nephrotoxic drugs should be approached with caution and renal function should be monitored. Use of bisphosphonates in patients with conditions or diseases affecting renal function is not recommended. Administration of bisphosphonates has been associated with abdominal pain (colic), discomfort, and agitation in horses. Clinical signs usually occur shortly after drug administration and may be associated with alterations in intestinal motility. In horses treated with OSPHOS these clinical signs usually began within 2 hours of treatment. Horses should be monitored for at least 2 hours following administration of OSPHOS. Bisphosphonates affect plasma concentrations of some minerals and electrolytes such as calcium, magnesium and potassium, immediately post-treatment, with effects lasting up to several hours. Caution should be used when administering bisphosphonates to horses with conditions affecting mineral or electrolyte homeostasis (e.g. hyperkalemic periodic paralysis, hypocalcemia, etc.). The safe use of OSPHOS has not been evaluated in horses less than 4 years of age. The effect of bisphosphonates on the skeleton of growing horses has not been studied; however, bisphosphonates inhibit osteoclast activity which impacts bone turnover and may affect bone growth. Bisphosphonates should not be used in pregnant or lactating mares, or mares intended for breeding. The safe use of OSPHOS has not been evaluated in breeding horses or pregnant or lactating mares. Bisphosphonates are incorporated into the bone matrix, from where they are gradually released over periods of months to years. The extent of bisphosphonate incorporation into adult bone, and hence, the amount available for release back into the systemic circulation, is directly related to the total dose and duration of bisphosphonate use. Bisphosphonates have been shown to cause fetal developmental abnormalities in laboratory animals. The uptake of bisphosphonates into fetal bone may be greater than into maternal bone creating a possible risk for skeletal or other abnormalities in the fetus. Many drugs, including bisphosphonates, may be excreted in milk and may be absorbed by nursing animals. Increased bone fragility has been observed in animals treated with bisphosphonates at high doses or for long periods of time. Bisphosphonates inhibit bone resorption and decrease bone turnover which may lead to an inability to repair micro damage within the bone. In humans, atypical femur fractures have been reported in patients on long term bisphosphonate therapy; however, a causal relationship has not been established. ADVERSE REACTIONS: The most common adverse reactions reported in the field study were clinical signs of discomfort or nervousness, colic and/or pawing. Other signs reported were lip licking, yawning, head shaking, injection site swelling, and hives/pruritus.

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Thank you to our

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Happy Holidays!



Muscular Causes of Poor Performance:

EVALUATION, REHABILITATION, AND PREVENTION ERICA MCKENZIE | BSC, BVMS, PHD, DACVIM, DACVSMR Muscular disorders are a common concern in exercising horses, however, they are frequently under-recognized due to nebulous clinical signs or concurrent disorders that are more evident on basic examination. Nonetheless, muscular disorders occur with considerable frequency, are often performance-limiting, and can result in frustration for owners and veterinarians alike.

(HYPP), glycogen branching enzyme deficiency (GBED), and polysaccharide storage myopathy (PSSM).

Muscle trauma and strain are common injuries of athletic horses in a variety of disciplines and probably go unrecognized much of the time. Excessive demands during exercise can result in damage to specific muscles or muscle groups, or occasionally more generalized damage. Activities associMuscle tissue is the largest and most demanding organ in ated with a high potential for acute muscle injury include the exercising horse, comprising as much as 55% of body polo, track racing, jumping, endurance racing, and Western weight, and attracting up to 80% of cardiac output. It is events. Factors that possibly predispose to muscular damage also a very responsive system which displays considerable during activity include early season competition, pre-existing adaptation to training stress over months to years, and also lameness, lack of warm-up exercise, and challenging and displays a strong response to dietary influences. Compared downhill terrain. Muscles of the hindlimbs and back are to other athletically capable species, horses have a consid- particularly at risk of injury. erably higher proportion of fast twitch muscle fibers. This is a key contributor to their capacity for speed and power, Mild or focal muscle damage can be hard to identify due but may also create vulnerability to injury during intense or to subtle clinical signs including poorly-localized lameness, prolonged exercise. Furthermore, since horses participate in reluctance to perform specific activities, and pain on palpation of specific regions. More serious injury is usually more readily recognized since it can result in overt lameness and/ or heat or swelling of the affected region. Over time, significant injury to muscle tissue, or altered use of an affected limb can also result in atrophy. Repeated injury to a specific muscle can eventually provoke fibrosis and even ossification of the tissue, which may result in unusual firmness on palpation and mechanical lameness. This is most likely in horses

Image 1: Common activities can lead to muscular injuries

a variety of technically and physically demanding activities, there is great potential for traumatic muscle injury or damage from overexertion. In addition, specific breeds including Thoroughbreds, Quarter Horses, Standardbreds, Arabians and Warmbloods have a significant prevalence of heritable muscular disease as a result of selective breeding practices. A disturbing example of this issue comes from a recent study of hundreds of elite American Quarter Horses, which identified alleles for two or more hereditary disorders in nearly 20% of halter horses, including hyperkalemic periodic paralysis

Image 2: Bilateral gluteal muscle atrophy in a horse with chronic lumbosacral pain

6  The Practitioner  Issue 4 • 2017

working in disciplines that require sudden turns and sliding stops, which can provoke fibrosis of the semitendinosus and semimembranosus muscles. Diagnosing muscle injury can be challenging. Detailed physical examination is critical and must include visual assessment of symmetry of gait and musculature, as well as systematic palpation and comparison of muscle groups of the limbs and spine. Serum biochemistry can be invaluable to identify muscle injury, and to determine severity and chronicity. If acute injury has occurred, serum creatine kinase (CK) will peak typically within four to six hours after the muscular insult and should return to normal within 24 to 72 hours of injury depending on the amplitude of initial increase and if ongoing damage is occurring. However, severe, focal muscle damage, such as to an individual muscle, can provoke relatively modest increases in CK (< 5000 U/L), despite prominent signs such as profound lameness or even recumbency. Injuries to the gracilis and adductor muscles particularly can present in this fashion. Assessment of asparImage 3: Ultrasound image of a large adductor muscle tate transaminase (AST) activity should also be performed, tear that resulted in euthanasia of the affected horse since this enzyme peaks later, at 24 to 48 hours, and remains elevated for up to two weeks, it can be a good indicator of the It is possible to detect and assess edema, hematomas or fiber occurrence of and severity of muscle injury if biochemistry disruption, fibrosis, and ossification. Repeat examination was not performed in the first 24 hours to catch the eleva- over time can help monitor healing and direct rehabilitation tion of CK. Elevations of serum AST activity in horses with routines. Assessment of the contralateral musculature, or normal CK and gammaglutamyltransferase (GGT) activities sometimes other muscle groups can help interpretation of are strongly suggestive of muscle injury within the preced- findings in ultrasonography as well as thermography. In gening four to 10 days. Intense or prolonged exercise activities, eral, symmetry often rules out pathology, however, bilateral such as endurance riding, can provoke elevations in muscle disease is possible in some situations and interpretation of enzymes that reflect a physiologically appropriate response changes may be more challenging in these situations. rather than true pathology. Electromyography (EMG) has been recommended by some Muscle injury can also be identified through imaging experts to help determine the presence of and possible cause techniques. Although MRI is arguably the most sensitive of muscle injury. Needle EMG units are becoming cheaper, means of identifying muscle injury, it is not often clinically less complicated and portable, and can be a valuable addipracticable in horses. Furthermore, despite the high detail tion in the analysis of specific cases, particularly those with of this form of imaging, in human athletes, up to 50% of a component of atrophy or altered muscle use. Expertise and muscle injuries are found to be imaging negative, despite loss experience are also important in the practice and interpretaof functionality consistent with injury. It seems very likely tion of this modality. Surface EMG presents an intriguing that horses may encounter similar phenomena as human and non-invasive modality that was used to assess motion athletes, including imaging-negative muscle injuries and patterns in horses with Shivers, helping to determine the delayed onset muscle soreness (DOMS), however, there is etiology as central (cerebellar) versus peripheral in nature. Ficurrently no information regarding these issues in horses. nally, a recent case report describes a combination of acoustic myography, accelerometry, and bioimpedance to identify an Thermography is a very simple procedure that can be used upper limb muscle injury resulting in lameness in a horse. It to help localize damaged musculature in horses, whether is likely that these methods will become increasingly popular symmetric or asymmetric in nature. The equipment is rela- as technologic advances become more available. tively cheap and readily available, and the procedure simple and non-invasive. However, reliability is confounded by a Once identified as having a muscular injury, affected horses wide variety of factors (wind speed, bandaging, clipping etc.) must have their exercise routine modified as appropriate for and it is best performed by experienced operators, since mis- the level of injury and the area involved. Generally complete interpretation is common. Ultrasonography is useful for sig- cessation of exercise and stall rest is not ideal beyond the nificant lesions that create structural changes in the muscles. first three to five days, since it can result in behavioral issues WWW.FAEP.NET |



and potentially have detrimental effects on healing. Movement can help reduce pain and maintain range of motion, as well as providing low level appropriate stress to the healing muscle. If a focal area of muscle damage has been identified, application of ice may be the most appropriate method of providing analgesia and anti-inflammatory effects. If the affected muscle is relatively thin and superficial, it can be iced for 10 minutes several times per day. If it is a larger muscle mass, then more prolonged application of ice (20 mins) can be performed several times per day. Other treatment modalities have the potential to provide analgesia and facilitate return of function, including therapeutic ultrasound, cold laser, acupuncture, and massage. These can be used in combination for severe focal injuries, however, preliminary investigations indicate that laser and ultrasound are probably limited substantially by restricted penetration depth. In regard to pharmacologic management, although nonsteroidal anti-inflammatory medications are frequently used for suspected or confirmed muscular injuries, evidence in other species suggests that they can significantly delay healing due to disruption of muscle satellite cell function and other critical processes. Therefore they should be used judiciously, and only in cases where significant pain and inflammation necessitate their use. Muscular injuries that are associated with significant pain, rhabdomyolysis or impaired movement may also benefit from the use of muscle relaxants, including methocarbamol, phenytoin, diazepam or dantrolene sodium. These are often most beneficial in the acute stage when there is significant pain and/or loss of function, and potentially when large muscle groups are affected. The most well studied of these drugs in regard to muscular disorders is dantrolene sodium. The pharmacokinetics and clinical effects of this drug are published for horses. Dantrolene is a skeletal muscle calcium channel blocker which can be dosed orally in horses and which has utility in the treatment of severe or diffuse muscle injuries creating pain, lameness, and/or myoglobinuria. It prevents muscle necrosis and can speed healing and return of function. In horses it can be dosed at 4 mg/ kg per os two to three times daily (preferably accompanying recent feed intake) during initial treatment of significant muscle injury. However, it should probably be avoided in horses with uncertain or positive HYPP status, since it can induce hyperkalemia (only demonstrated after prolonged general anesthesia at this time).

Once control of pain and inflammation is achieved, horses can be exposed to escalating exercise routines that accommodate their limitations and encourage functional motion within the affected muscle group, applying appropriate limits to avoid re-injury. It is important to develop an individually appropriate warm-up routine to help with transition to more demanding exercise by preparing relevant muscle groups. Ideally, horses should have a regular (i.e. three to seven times per week) exercise routine since intermittent training has been shown to exacerbate episodes of rhabdomyolysis in horses with predisposing conditions, and higher post-exercise serum muscle enzyme activities have been demonstrated in healthy horses training two versus three times per week. Training volume should be incrementally increased over time, and a solid base of weeks to months accrued before any return to intensive or explosive exercise. Where possible, stall rest should be minimized and pasture turnout emphasized with appropriate companionship that does not encourage over-activity or traumatic interactions. Serial monitoring of muscle enzymes can be performed (e.g. pre- and post-competition) where underlying muscular disorders or repeat injury is possible. An example protocol for rehabilitating a horse with a significant hindlimb muscle injury might commence with seven to 14 days of directed treatment for pain and inflammation, encompassing ice, very light hand walking with stall restriction, and systemic or topical non-steroidal agents if required for severe pain or inflammation. Soft tissue mobilization above and below the area of concern can also provide pain relief and improve mobility and can continue over weeks if it appears to provide improvement. Direct massage of the injury site should be avoided initially, though crossfrictional massage followed by fiber direction massage has

Image 4: Horse warming up

8â&#x20AC;&#x201A; The Practitionerâ&#x20AC; Issue 4 â&#x20AC;˘ 2017

been described during rehabilitation of some horses with serious muscle injuries. Two to four weeks after the injury, if tolerated, passive range of motion exercises can begin with caution. Horses may exacerbate injury if they attempt sudden violent reclaiming of their limb. Example exercises may include lifting the limb several inches off the ground and making small circular motions with the foot, no larger than six inches diameter. Soft tissue mobilization and massage can be performed around and over the injury site. At three to four weeks, gentle stretching can commence, protracting the hindlimb, and can progress in degree and duration as tolerated without signs of discomfort. Hand walking can increase in duration at two to four weeks, and at three to four weeks, ground pole work can be introduced to better appreciate the horse’s stride length and hind limb flexion. These exercises can progress to cavaletti work to increase limb flexion after four to six weeks. Over time, as the horse improves, these exercises can move from in-hand to lunge line work. Sport specific exercise can be commenced if the injured area has comparable range of motion to the other side, and if there is no remaining lameness or discomfort evident. If tissue fibrosis is a concern, extracorporeal shockwave therapy could be considered four to six months after injury. Surgical release might be indicated if there are significant extension deficits resulting from scar tissue. Throughout the process, periodic re-evaluation with ultrasound can evaluate injury healing. At any point if exacerbation of injury is suspected, the protocol should be revised and contributing factors evaluated.

understanding of the pathophysiology of a disorder, which has proved challenging for most of the ER disorders of horses, despite extensive research efforts. Several different disorders have been identified that contribute to ER in horses, including malignant hyperthermia, polysaccharide storage myopathy, recurrent exertional rhabdomyolysis (RER), and most recently, myofibrillar myopathy (MFM). However, the full pathophysiology of all of these disorders has not yet been clarified, and relevant genetic mutations are not yet known for RER and MFM, which complicates definitive and convenient diagnosis. For diseases with known mutations (PSSM, MH), genetic testing at laboratories with scientifically-validated tests represent the most convenient and reliable means of diagnosis. For other disorders, diagnosis still relies on procedures such as exercise testing and muscle biopsy, which often fail to provide definitive results.

A growing body of evidence suggests that Thoroughbred and Standardbred horses have an analogous disorder causing ER, though the pathophysiology and genetic mutations have not been fully defined. Disease has been attributed to a heritable abnormality of skeletal muscle calcium kinetics, however, the genetic mutation(s) have remained elusive, suggesting complex inheritance, and there are no scientifically validated genetic tests available to confirm this disorder. In both breeds, young female horses with nervous temperaments are reportedly predisposed, with reports of comparable or superior performance in affected animals possibly promoting inadvertent selection of this trait. Probable The exertional rhabdomyolysis (ER) disorders represent trigger factors for episodes of clinical disease include high a group of diverse diseases that are prevalent within many starch rations and intermittent exercise regimens. Episodes equine breeds and athletic disciplines. A large amount of of clinical disease typically only occur in training, and not published information already exists and continues to accu- during racing. Since a genetic signature is currently lackmulate. Although the classic clinical signs of ER are usually ing in these cases, diagnosis relies on signalment, clinical readily recognized, including reluctance to continue exercise, signs, and measurement of elevated muscle enzyme activity; stiffness, inappropriate sweating, and high heart rates and skeletal muscle biopsy findings are non-specific. Affected respiratory rates, there is a range of clinical presentations horses can respond quickly to a regular exercise regimen which can be more challenging to identify. Some horses and reduction of starch in the ration (to ≤ 20% of daily present with signs mistaken for colic, including stretching digestible energy intake), however the impact of dietary out, pawing, rolling, and recumbency. Others will show changes on actual racing performance is not clearly known behavioral problems including bucking, rearing, and refusal which makes trainers often reluctant to transition to an apto commence exercise. Yet others will display poor technical propriate diet. Affected Thoroughbred horses also respond performance, such as in jumping and dressage activities, and well to treatment with dantrolene sodium with a reduction/ some have symmetric muscle atrophy along the topline and cessation in clinical signs and normalization of serum CK. in the gluteal muscles. Occasionally severe rhabdomyolysis However, dantrolene is not allowed in racing competition may be identified only by very high serum CK values (often and published withdrawal times are likely inappropriate since exceeding 50,000 U/L) with no overt signs of muscle damage they are based on low drug doses (≤ 1 mg/kg) administered beyond transient myoglobinuria, which can be easily missed. after prolonged fasting. Given the high prevalence of ER disorders in some groups (which exceeds 30% for specific breeds or athletic disciplines), PSSM (or Type 1 PSSM) is currently the best defined ER advances need to be made in the diagnosis and prevention disorder, and affects a wide variety of light and draft breeds. of all of the known ER disorders of horses at this time. Affected light breed horses often display typical signs of ER after a change in exercise or management regimes, although Advancing diagnosis and prevention requires thorough epaxial and gluteal atrophy without rhabdomyolysis is anWWW.FAEP.NET |



the daily digestible energy content of the ration, which may require forage analysis accompanied by removal or replacement of specific supplements. Fat supplementation may help further stabilize insulin/glucose dynamics of affected horses, and can also be used to replace starch in horses with high caloric demands. Warmblood horses have been previously identified as having a high prevalence of a disorder referred to as Type 2 PSSM. Affected horses typically present with subtle clinical signs including reduced enthusiasm for exercise and decreased technical performance, with normal muscle enzyme activities. These horses lack the GYS1 mutation associated with PSSM, and recent work has determined that they actually do Image 5: Severe gluteal and epaxial muscle atrophy in a not have a glycogen storage disorder at all, but rather they draft horse with PSSM might have a novel myofibrillar myopathy disorder that was recently identified in Arabian horses. A study of over 100 other fairly common indicator of this condition. Diagnosis Arabian endurance horses competing 50 mile distance identiis usually readily achieved through testing of hair or blood fied a 4% incidence of ER during racing, with another 12% for the known mutation in the skeletal muscle glycogen synof horses reported to have historical ER. Affected Arabian thase enzyme (GYS1). Most affected horses are heterozygotes, horses tend to show clinical signs of ER between five to 15 however, those that are homozygous for the GYS1 mutation, years of age, with stiffness, sweating, reduced speed, delayed or that are concurrently heterozygous for the RYR1 mutation heart rate recovery and myoglobinuria commonly occurassociated with equine malignant hyperthermia often are ring during the first five to 15 miles of competitive events, more severely clinically affected. Affected horses will often or in the first three to five miles of light exercise on return also show low-grade elevation of muscle enzymes at rest if to training after rest. Concerningly, some affected horses they are stall-confined. Even horses that are severely affected fail to display clinical signs beyond red urine during racing, with this disorder can usually be rehabilitated successfully to despite biochemical evidence of severe ER (CK > 100,000 prevent future episodes of disease, however owners need to U/L). Affected horses lack the GYS1 and RYR1 mutations be aware that this will be a time intensive commitment for associated with PSSM, but the disorder is considered likely the horse’s lifetime. Careful assessment of management is heritable based on biopsy study of related horses. Evalunecessary to identify trigger factors, including unaccustomed rest, dietary changes, or transport. Successful management of affected horses must combine dietary management with a regular exercise regime for optimal results. Horses should be turned out into a paddock or pasture at least 12 hours a day. They can be carefully returned to exercise, which may commence with as little as two to five minutes of forced light work for clinically severe horses, which can be increased in small increments each week. Starch must be reduced to less than 10% of Image 6: Arabian horse competing in an endurance race

10  The Practitioner  Issue 4 • 2017

ation of muscle tissue from affected horses has identified abnormal accumulations of specific cytoskeletal proteins, including desmin and αβ-crystallin, with degeneration of the Z-disc of the sarcomere. These findings are most evident on frozen sections and require submission to a lab that will perform frozen sections and desmin staining. There are no scientifically-validated genetic tests available to identify this disorder in Arabians or Warmbloods. It is currently not known how best to manage horses with MFM. Affected horses are frequently already consuming a low starch diet. Some endurance horse owners preemptively treat their horses with dantrolene prior to triggering activities such as exercise or trailering, and avoid rest days before competitive events. Some also report that aggressive warm up activities in which horses are rapidly brought into fast trot or canter are superior to longer, slower, warm up routines. Veterinarians assisting at endurance races should be aware that the clinical presentation of MFM can be very mild despite profound biochemical evidence of muscle damage, and they should encourage riders to consistently evaluate urine color and to pay attention to subtle gait abnormalities, delayed heart rate recovery, and other vague clinical signs that might indicate ER. Evaluation of pre- and post-competition serum CK is another method of determining how endurance horses are responding to training or competition. Ultimately, the muscle system is the primary driver of the athletic horse, and there are a myriad of ways to select horses for, and to maintain, a healthy muscle system. These include the use of scientifically-validated genetic tests to detect heritable disorders, appropriate training and warm up protocols, attention to nutrition, and rapid identification and response to injury or over-training. Acknowledgments The author would like to thank Dr. Kevin Haussler and Dr. Melissa King for providing information about rehabilitation utilized in this article. References

Flacco L, Colozzi A, Ripari P, et al. Dantrolene sodium in traumatic muscle contracture: double-blind clinical and pharmacological trial. Clin Ther 1989;161:623-32. Haussler KK. The role of manual therapies in equine pain management. Vet Clin North Am Equine Pract 2010;26(3):579-601.

Järvinen, Mackey AL, Mikkelsen UR, et al. Rehabilitation of muscle after injury - the role of anti-inflammatory drugs. Scand J Med Sci Sports 2012;22(4):e8-14. Järvinen TA, Järvinen M, Kalimo H. Regeneration of injured skeletal muscle after the injury. Muscles Ligaments Tendons J 2014;3(4):337-45. Järvinen TA, Järvinen TL, Kääriäinen M, et al. Muscle injuries: biology and treatment. Am J Sports Med 2005;33(5):745-64.



McKenzie EC, Valberg SJ, Godden SM, et al. The effect of oral dantrolene sodium on recurrent exertional rhabdomyolysis in treadmill exercised Thoroughbred horses. Am J Vet Res 2004;65:74-79. McKenzie EC, Firshman AM. Optimal diet of horses with chronic exertional myopathies. Veterinary Clinics of North America: Equine Practice: Nutrition and Dietary Management 2009;25:121-135, vii. McKenzie EC, Garrett RL, Payton ME, et al. Effect of feed restriction on plasma dantrolene concentrations in horses. Equine Vet J Suppl 2010;38:613-617. McKenzie EC. Biochemical abnormalities of athletic horses. In: Hinchcliff, KW, Kaneps AJ, Geor RJ, eds. Equine Sports Medicine and Surgery, 2nd ed. Saunders Elsevier, 2014; 931-938. McKenzie EC, Di Concetto S, Payton ME, et al. Effect of dantrolene premedication on various cardiac and biochemical variables and the recovery of healthy isoflurane-anesthetized horses Am J Vet Res 2015;76:293-301. Montgomery L, Elliott SB, Adair HS. Muscle and tendon heating rates with therapeutic ultrasound in horses. Vet Surg. 2013;42(3):243-9. Piercy RJ, Rivero J. Muscle disorders of equine athletes. In: Hinchcliff, KW, Kaneps AJ, Geor RJ, eds. Equine Sports Medicine and Surgery, 2nd ed. Saunders Elsevier, 2014; 109-143. Riis KH, Harrison AP, Riis-Olesen K. Non-invasive assessment of equine muscular function: A case study. Open Vet J 2013;3(2):80-4. Tryon RC, Penedo MC, McCue ME, et al. Evaluation of allele frequencies of inherited disease genes in subgroups of American Quarter Horses. J Am Vet Med Assoc 2009;234:120-125. Valberg SJ, McKenzie EC, Eyrich LV, et al. Suspected myofibrillar myopathy in Arabian horses with a history of exertional rhabdomyolysis. Equine Vet J. 2016;48(5):548-56. Walmsley E.A, Steel C.M, Richardson J.L, Hesse K.L, Whitton R.C. Muscle strain injuries of the hindlimb in eight horses: diagnostic imaging, management and outcomes. Aust Vet J 2010;88(8):313–321. Wilberger MS, McKenzie EC, Payton ME, et al. Prevalence of exertional rhabdomyolysis in endurance horses in the Pacific Northwestern United States. Equine Vet J 2015;47:165-170.

Dr. Erica McKenzie Dr. McKenzie graduated from Murdoch University, Western Australia in 1996 before completing a combined large animal medicine residency/PhD program with Dr. Stephanie Valberg at the University of Minnesota in 2003, investigating nutritional and pharmacologic methods of controlling ‘tying-up’ in Thoroughbred horses. This was followed by a two-year, post-doctoral fellowship at Oklahoma State University Performance Laboratory performing research investigations in exercising horses and racing sled dogs. Dr. McKenzie has been a faculty member at Oregon State University since 2005. She is a charter diplomate and member of the board of directors for the American College of Veterinary Sports Medicine and Rehabilitation; the author of over 30 research manuscripts relevant to exercising horses and dogs, and a member of the editorial consultant board for the Equine Veterinary Journal. Special interests include characterization and prevention of myopathies in horses, the factors relevant to successful athletic performance, and features of nutrition and disease relevant to long distance exercise in horses, dogs and humans.




Horses often develop neurologic problems that are alarming to owners and veterinarians alike. Many veterinarians dislike neurologic emergencies due to physical and safety challenges, as well as inherent difficulties in establishing definitive diagnoses in living horses. Familiarity with the most common types of neurologic problems and the most likely causes will allow the practitioner to formulate easily- applicable diagnostic and treatment plans in advance, thus improving management of emergency situations.

Common emergencies and what to do



The most common type of ataxia is general proprioceptive (also known as “spinal”) ataxia, resulting from damage to the spinal cord. Horses display a combination of proprioceptive deficits and paresis (weakness). The majority of horses in the author’s practice that suddenly develop ataxia have either equine protozoal myeloencephalitis (EPM), or cervical vertebral stenotic myelopathy (CVSM). Neck trauma is also relatively common. Less common causes include West Nile virus, and equine herpesvirus-1 myeloencephalopathy (EHM).

Picture 1: This survey radiograph shows abnormal angulation and malarticulation between C6 and C7.

Ataxia is generally easy to recognize clinically, but it is often difficult to differentiate EPM from a focal compressive or traumatic lesion based on neurologic evaluation. Signs that are more often observed with EPM include severely asymmetric ataxia, asymmetric muscle atrophy, dull or obtunded mental status, and cranial nerve deficits. Specific diagnostic tests for ataxia most commonly include imaging the affected area of the vertebral column, such as by obtaining cervical radiographs, and performing cerebrospinal fluid (CSF) analysis, as well as immunological testing on blood, CSF, or (preferably) both for EPM or other causes. Radiographs obtained in the field can be diagnostic but, due to equipment limitations, are generally of lower quality than those obtained at a referral center with an overhead system. One (preferably two) no-additive or serum separator tubes of blood should be collected for serologic testing. If EHM is considered possible, blood (placed in EDTA tubes) and nasal swabs (placed in no-additive red-top tubes) should also be collected for PCR testing. If the veterinarian is comfortable collecting spinal fluid, samples should be obtained for cytology and immunologic testing. Emergency treatment for ataxia generally includes stall confinement, anti-inflammatory medication (corticosteroids or non-steroidal anti-inflammatory drugs), and antiprotozoal treatment. The author’s preference, when treating horses without a definitive diagnosis on an emergency basis, is to begin treatment with a loading dose of ponazuril (15 - 35 mg/kg) and a moderate dose of dexamethasone (0.1 mg/kg), followed by continued EPM treatment and a short tapering steroid course until specific test results are available. Prognosis depends on the underlying cause. Approximately 60% of horses with EPM improve.1 In the author’s experience, horses with EPM that show an acute onset of more severe signs are actually more likely to show significant improvement than those horses with an insidious onset of less severe signs. Horses with CVSM usually show at least transient improvement with rest and anti-inflammatory treatment, but signs might worsen when treatment is withdrawn or the horse’s activity level increases. Note on spinal trauma: There is a long-standing debate about steroids for treatment of spinal trauma in people. The most recent meta-analysis2 did not show a significant long-term benefit for steroid use in patients with acute traumatic spinal cord injury, and findings did not support routine use of methylprednisolone.The relevance of this analysis to equine medicine is unclear.

12  The Practitioner  Issue 4 • 2017

- Continued from page 13



In the author’s practice, the two most common neurologic causes of dysphagia are botulism and EPM, with a less common cause being guttural pouch disease (particularly mycosis). Although neurologic Lyme disease (neuroborreliosis) is quite rare, the majority of cases seen by the author were dysphagic. Initial signs of botulism often mimic an episode of colic or esophageal obstruction. Affected horses might act lethargic, not finish their feedings, lie down frequently or for prolonged periods, have feed or water discharge from the nostrils, or have muscle tremors. Early recognition of botulism is imperative for treatment and survival, so practitioners in endemic areas should maintain a high degree of suspicion for this disease. Always consider botulism if a suspected choke case ‘resolves’ easily when nasogastric intubation is initially performed or if a “colic” case appears to want to eat or relaxes when recumbent. Two clinical tests Picture 3: The photo is an endoscopic image of the right guttural should be performed immediately: the tongue stress test, pouch demonstrating an enlarged stylohyoid bone, typical for during which the tongue is gently withdrawn from the temporohyoid osteoarthropathy. Note the clubby appearance of the proximal stylohyoid. mouth with the jaw closed and observed for appropriate retraction, and the grain test, during which the horse is fed eight ounces of grain in a feed pan and timed (normal are intimately associated with the guttural pouch; these horses finish the grain in less than two minutes).8 Addi- include the glossopharyngeal, vagus, and hypoglossal tional signs that might be present include mydriasis and nerves. Guttural pouch disease should be considered if slow pupillary light reflexes, weak eyelid tone, weak tail there is any history of purulent nasal discharge or epistaxis. tone, and weak anal tone. Endoscopy provides quick diagnosis of guttural pouch disBotulism diagnosis is primarily clinical. Confirmatory ease, allowing referral for definitive treatment such as laboratory tests include the mouse bioassay or PCR on sus- coil embolization for guttural pouch mycosis. Prognosis pect feed, gastrointestinal contents, or fecal samples. These depends on the amount of inflammation and subsequent samples can be collected and frozen for submission to a scarring around the cranial nerves, but can be favorable. In reference laboratory if desired. However, treatment should one retrospective study of transarterial coil embolization be initiated immediately without waiting for laboratory for treatment of guttural pouch mycosis, overall survival test results. was 84% (26/31), and 82% (9/11) horses with dysphagia Treatment of botulism is focused on specific anti-toxin recovered.10 However, another study showed only a 50% administration and general supportive care. Botulism anti- survival rate, with significant correlation between dysphatoxin can be obtained from Lake Immunogenics (Ontario, gia and non-survival.11 NY) or Plasvacc (Templeton, CA), and should be administered as soon as possible. Supportive care consists largely of maintaining adequate hydration and nutrition, generally via nasogastric intubation. Assuming appropriate treatVestibular signs include head tilt, nystagmus, and ment, prognosis is very good for horses that retain the abilloss of balance with a tendency to lean, drift, or fall to one ity to stand (95% survival), but poor (<20% survival) for side. Vestibular disease is categorized as peripheral or centhose that become totally recumbent.9 tral based on lesion location. Horses with peripheral vesDysphagia is the most common ‘brainstem’ sign seen by tibular disease generally have a head tilt towards the side the author in horses with EPM. Generally, the horse will of the lesion, horizontal or rotary nystagmus with the fast also be dull or obtunded and show proprioceptive (spinal) phase away from the side of the lesion, and normal mental ataxia. These clues should point the practitioner away from status. Although the vestibular ataxia can be so severe as botulism, as horses with botulism are generally alert and to cause recumbency, there is no evidence of proprioceprelatively coordinated, though they can show profound tive ataxia with peripheral disease. The peripheral course weakness. Treatment is as described in the “EPM” section, of the facial nerve is very close to that of the vestibular although clearly nasogastric administration of medication nerve, so facial paralysis might be seen in conjunction with is often required. Similar to EPM cases with altered behavperipheral vestibular disease. Horses with central vestibular ior, EPM cases with dysphagia have a reduced prognosis disease might have a head tilt towards or away from the and higher likelihood of relapse than EPM cases with just side of the lesion, any type of nystagmus, an altered mental spinal ataxia.5 status, proprioceptive deficits, and multiple cranial nerve Several cranial nerves that control eating and swallowing


Vestibular disease

20  The Practitioner  Issue 4 • 2017


Abnormal behavior

Horses with abnormal behavior often act obtunded or maniacal, with compulsive movements and seeming disPicture 2: This photo demonregard to their safety or the welfare of others. Abnormal strates early signs behavior generally implies dysfunction of the forebrain, of botulism, includthough brainstem disease can also cause obtundation to ing weak tongue tone and failure to stupor. Common causes of abnormal behavior include retract tongue into metabolic encephalopathies, EPM, and head trauma. Viral the mouth. encephalitides are common causes in certain regions, Image Credit: although less so for horses with appropriate vaccination Dr. Robert H. histories. Whitlock The two most common metabolic encephalopathies in horses are “intestinal encephalopathy,” or hyperammonemia associated with intestinal dysfunction, and hepatic encephalopathy. Signs of metabolic encephalopathy include central blindness, bizarre behavior, compulsive walking, obtunded or stuporous mental status, seizures, and mild ataxia. Forebrain (prosencephalic) signs generally predominate. Additionally, horses with intestinal encephalopathy often show signs of colic or diarrhea prior to developing neurologic signs. Diagnosis of intestinal encephalopathy and supportive evidence for hepatic encephalopathy requires accurate measurement of ammonia in blood or CSF, which is often difficult in field settings. Identification of a laboratory that can perform blood ammonia testing (as well as clarification Horses with altered behavior due to EPM are treated of ideal sample storage and handling) in advance of needing this service is advantageous. Clinically affected horses similarly to horses with spinal ataxia due to EPM, but often have levels over 200 µmol/L, although neurologic the overall prognosis is worse,5 and relapses seem to be signs have been observed with levels as low as 60 µmol/L.3 If more common. Note on head trauma: There is a limited amount of inforhepatic dysfunction is present, liver enzyme activities (AST, SDH, GGT, ALP), as well as indicators of hepatic function mation on equine traumatic brain injury, but one retrospec(bilirubin, bile acids), are likely to be increased. Metabolic tive study6 suggests that the most common clinical signs are ataxia, nystagmus, abnormal mental status, abnormal (lactic) acidosis and hyperglycemia are common findings. Emergency treatment for hyperammonemia or hepatic pupils (size, symmetry, or PLRs), and head tilt. Poll injury encephalopathy should focus on minimizing trauma sec- from falling over backwards was more common than frontal ondary to bizarre behavior, restoring adequate hydration injury. In this study of 34 horses, the survival rate was 62%. and acid-base status, and neuroprotection.4 Most horses Prolonged recumbency (> 4 four hrs after admission) and require sedation to be handled safely and to prevent basilar skull bone fractures were risk factors for nonsurpatient-induced trauma. Intermittent doses of detomidine vival. The most important principles for managing head (10-20 µg/kg IV) or a CRI of detomidine (5-20 µg/kg/hr) trauma include maintenance of adequate brain oxygenare recommended. If available and not cost-prohibitive, ation and perfusion, which requires careful attention to phenobarbital (5-10 mg/kg IV) can be used to prolong respiratory and circulatory status. Hypotension is a wellsedation or reduce seizure activity. Intravenous fluids with established predictor of death in people with traumatic supplemental KCl (20-40 mEq/L) are invariably required. brain injury, so intravenous fluids should be administered Hypertonic saline (2-4 mL/kg) or mannitol (0.5 – 1 g/kg) to restore circulating volume. Reduction of cerebral edema can be administered to reduce cerebral edema, which might (if present) will improve brain perfusion and overall neuor might not be part of the pathogenesis. Either lactulose rologic function. In a field setting, hypertonic saline (2-4 (0.2 – 0.3 mL/kg q 6-12h) or neomycin (20 mg/kg q 12-24) mL/kg), followed by isotonic crystalloid fluid administracan be administered orally or via nasogastric intubation to tion is the easiest way to accomplish both of these goals. If there are open wounds or fractures, broad-spectrum reduce ammonia absorption or production. Prognosis is guarded to fair for intestinal encephalopa- antimicrobial treatment should be initiated. Anti-fungal thy; reported survival in one retrospective study was 39%.3 treatment should be considered based on region and locaIn the author’s experience, horses that recover usually do tion of wounds. Whether steroid treatment is beneficial for so quickly, with significant improvement in six to 24 hours, affected horses remains unclear; steroid treatment is no and horses that do not recover often die or require euthana- longer recommended for people with traumatic brain injury, sia in the same time period. Prognosis is guarded for hepatic as the most recent meta-analysis7 showed an increase in encephalopathy as the inciting hepatic problem is often mortality with steroid use. - Continued on page 20 irreversible. WWW.FAEP.NET |



| The Practitioner  13








Professor of Veterinary Anatomy and Equine Lameness at the École Nationale Vétérinaire ďAlfort, France


In the demonstration section of the wet lab, both groups will observe Dr. Jean-Marie Denoix while he performs both physical and biomechanical examinations, plus ultrasound on live horses.

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The FAEP strongly recommends that you register in advance for the 55th Annual Ocala Equine Conference. Registration is required for all aspects of the meeting. Your registration covers all CE sessions, access to the Exhibit Hall, lunch on Saturday and Sunday, dinner on Saturday, all breaks, social events, and conference proceedings. Advance registrations are taken at the FAEP office until December 22, 2017. After this date, a late registration fee of $50.00 will be added to all registrations, including on-site registrations.

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HOST HOTEL & TRANSPORTATION Hotel Reservations A block of rooms has been reserved at the Hilton Ocala located at 3600 SW 36th Ave., Ocala, FL 34474. The special room rates begin at $139.00, plus applicable taxes. Special extended stay reservations have been set up for the group rates from January 17-22nd, subject to availability. To reserve your room today, call the Group Reservations Department at Hilton Ocala at (352) 8541400. When making your reservations, be sure to request the FAEP special room rate. The room block ends on December 22, 2017,

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Each 50-minute lecture is equal to one continuing education credit. Attendees may earn up to 25 credit hours. For your convenience in recording your CE hours, one certificate will be included in your registration packet. It is your responsibility to document the sessions you attend and the number of hours you receive. (Separate certificates will be issued at the wet lab, Dispensing Legend Drugs and Florida Laws & Rules Governing Veterinary Medicine).

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Conference Exhibit Hall The Exhibit Hall at the 55th Annual Ocala Equine Conference will provide attendees with a dynamic networking opportunity to make contacts and to interact with industry representatives and other members of the equine veterinary medical care team. CONFERENCE EXHIBIT HALL HOURS Saturday, Jan. 20 9:40 a.m. – 6:30 p.m. Sunday, Jan. 21 9:40 a.m. – 1:40 p.m.

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Selecting Diagnostics in Equine Reproduction, a Clinical Approach

Sport Horse Lameness

Current Understanding of Biofilm and Latent Endometritis Ferris

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deficits with or without facial paralysis. The most common cause of peripheral vestibular disease is temporohyoid osteoarthropathy (THO), in which the stylohyoid bone becomes pathologically fused to the petrous temporal bone, which can subsequently fracture and disrupt the vestibular nerve, the facial nerve, or both. THO is occasionally accompanied by otitis media-interna, and horses rarely have otitis media-interna as the cause of vestibular disease in the absence of THO. Signs of THO include difficulty eating or painful eating, facial paralysis, and vestibular disease. Although the condition is chronic, neurologic signs generally develop acutely when the petrous temporal bone fractures. Guttural pouch endoscopy is more reliable than radiography for diagnosis.12 Conservative (medical) treatment generally entails antiinflammatory medication (NSAID or corticosteroid), as well as antimicrobial treatment (often trimethoprim sulfamethoxazole, sometimes chloramphenicol or enrofloxacin). Surgical treatment generally consists of a ceratohyoidectomy13,14,15 and leads to immediate pain relief and significantly decreased risk of future fractures, but not necessarily improved neurologic status. One retrospective study12 documented a survival rate of 67%, with 70% of surviving horses returning to prior athletic use. A larger, more recent retrospective study15 showed an overall survival rate of 81%, with improved survival in horses undergoing surgery compared to horses treated with medical therapy alone. The most common cause of central vestibular disease in the author’s practice is EPM, which should always be a primary rule-out for THO. If obvious cranial nerve signs other than facial and vestibular nerve deficits are present, or if obvious general proprioceptive (spinal) ataxia is observed, EPM becomes the more likely diagnosis. References

1. Furr M, Kennedy T, MacKay R, et al. Efficacy of ponazuril 15% oral paste as a treatment for equine protozoal myeloencephalitis. Vet Ther 2001;2:215-222. 2. Evaniew N, Belley-Cote EP, Fallah N. Methylprednisolone for the treatment of patients with acute spinal cord injuries: a systematic review and meta-analysis. J Neurotrauma 2016;33:468-481. 3. Dunkel B, Chaney KP, Dallap-Schaer BL, et al. Putative intestinal hyperammonemia in horses: 36 cases. Equine Vet J 2011;43:133-140. 4. Divers TJ. Metabolic causes of encephalopathy in horses. Vet Clin North Am Equine Pract 2011;27:589-596. 5. Johnson AL, Burton AJ, Sweeney RW. Utility of 2 immunological tests for antemortem diagnosis of equine protozoal myeloencephalitis (Sarcocystis neurona infection) in naturally occurring cases. J Vet Intern Med 2010;24:1184-1189. 6. Feary DJ, Magdesian KG, Aleman MA, et al. Traumatic brain injury in horses: 34 cases (1994-2004). J Am Vet Med Assoc 2007;231:259-266. 7. Alderson P, Roberts I. Corticosteroids for acute traumatic brain injury. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD000196. 8. Whitlock RH, McAdams S. Equine Botulism. Clinical Techniques in Equine Practice 2006;5:37-42. 9. Johnson AL, McAdams-Gallagher SC, Aceto H. Outcome of adult horses with botulism treated at a veterinary hospital: 92 cases (1989-2013). J Vet Intern Med 2015 Jan;29(1):311- 9. 10. Lepage OM, Piccot-Crézollet C. Transarterial coil embolisation in 31 horses (1999-2002) with guttural pouch mycosis: a 2-year follow-up. Equine Vet J 2005;37:430-434.



Picture 4: This dorsoventral skull radiograph shows a normal left stylohyoid bone and a markedly thickened right stylohyoid bone with increased opacity in the region of the temporohyoid articulation representing fracture and callous formation.

11. Dobesova O, Schwarz B, Velde K, et al. Guttural pouch mycosis in horses: a retrospective study of 28 cases. Vet Rec 2012;171:561. 12. Walker AM, Sellon DC, Cornelisse CJ, et al. Temporohyoid osteoarthropathy in 33 horses (1993-2000). J Vet Intern Med 2002;16:697-703. 13. Pease AP, van Biervliet J, Dykes NL, et al. Complication of partial stylohyoidectomy for treatment of temporohyoid osteoarthropathy and an alternative surgical technique in three cases. Equine Vet J 2004;36:546-550. 14. Oliver ST, Hardy J. Ceratohyoidectomy for treatment of equine temporohyoid osteoarthropathy (15 cases). Can Vet J 2015;56:382-386. 15. Espinosa P, Nieto JE, Estell KE, et al. Outcomes after medical and surgical interventions in horses with temporohyoid osteoarthropathy. Equine Vet J 2017 May 18. doi: 10.1111/evj.12701. [Epub ahead of print]

Amy L. Johnson, DVM, DACVIM -LAIM & Neurology Dr. Johnson received her DVM from Cornell University in 2003. Following an internship at B.W. Furlong and Associates, Dr. Johnson went back to Cornell for a residency in large animal internal medicine. In 2007 she began working as a clinician at New Bolton Center while concurrently completing a residency in neurology at the University of Pennsylvania. In 2011 Dr. Johnson became the 3rd veterinarian in the world to obtain board-certification in neurology as well as large animal internal medicine. She currently works at New Bolton Center as Assistant Professor of Large Animal Medicine and Neurology. Her research efforts focus on improving diagnosis of neurologic disease in the living horse, and she has special interests in equine protozoal myeloencephalitis (EPM), Lyme neuroborreliosis, and botulism.


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Forelimb Lameness in the Athletic Horse: The Collateral Ligaments of the Coffin Joint KENT ALLEN | DVM, CERT. ISELP

Figure 1: Location of the collateral ligaments of the coffin joint marked by blue. Images courtesy of Dr. Kurt Selberg.

Collateral ligament injuries of the coffin joint are an increasingly diagnosed injury thanks to the increased use of advanced imaging, namely MRI (1). The paired collateral ligaments (CL) of the coffin joint originate on the dorsolateral and dorsomedial aspects of the second phalanx and course distally to insert on the lateral and medial aspects of the third phalanx, respectively (Figure 1). Roughly twothirds of the ligament lies within the hoof capsule with the proximal third above the coronary band at the “10 and 2” positions.

Figure 2: Injury to the MCL of the right front foot showing increased signal and size of the ligament compared to the LCL.



Horses with CL injuries can present with an acute or chronic lameness. Those with chronic injuries often have not responded to intra-articular injection of the coffin or pastern joints in the past. With unilateral injury, the horse may be more lame circling one direction than the other, as the injured ligament will be more painful when stretched (1). For example, a right front lateral CL injury may present as a horse that is lame when circling to the left, and sound when circling to the right. Lameness present on the straight line is variable, and horses are often worse on a circle, and may be worse at the walk than the trot due to greater extension of the coffin joint at the walk (1). Palpation findings are not sensitive enough to rule in or out CL injury because severe injury is required to cause a palpable or visible swelling above the coronary band. Roughly 60-70 percent of horses with a CL injury will block to a palmar digital nerve block, with the remainder typically blocking to an abaxial sesamoid (1). With unilateral injury, the horse may successfully block with only the injured side anesthetized, which is a blocking pattern that is supportive of a CL injury. However, failure to improve with a unilateral block on the affected side does not rule out a CL injury. MRI is the most sensitive diagnostic option. Depending on the population of horses, 15- 31 percent of horses undergoing MR for lameness in the foot were diagnosed with a CL injury, with 15 percent considered the primary cause of the lameness of the total population (2). MR findings consistent with CL injury include increased signal in the ligament and enlargement compared to the unaffected foot or contralateral ligament (Figure 2) (1,2, 2). Chronic and/ or severe injuries may have radiographic changes present


Figure 3: Position of the CLs on D65PO and navicular skyline radiographs showing lysis and bony remodeling at the insertion, marked by red. Images courtesy of Dr. Kurt Selberg.

at the insertion of the CLs on P3 characterized by lysis and bony remodeling (Figure 3). Of interest, horses with entheseous new bone at the insertion were found to be sounder after injury than horses without it in one study (1). Ultrasound is useful to identify injury to the proximal third of the ligament, but is unable to penetrate the hoof capsule obscuring the distal portion. The CL is best imaged by locating the extensor process of P3, then rotating laterally (or medially) to identify the ligament at the “10 and 2” positions. Normally, it is round to oval shaped (3). The ligament has a spiral structure so it should be imaged in multiple planes to avoid off-incidence artifact that can mimic injury. Injury to the CLs result in enlargement and disruption of the fiber pattern that should be visible in both transverse and longitudinal views (Figure 4) (4). Treatments for CL injuries are limited due to the surrounding anatomy. A CL shoe should be placed with the wide branch on the affected side throughout the rehabilitation period (5). Shockwave therapy may be beneficial if the injury is in the proximal third of the ligament. The hoof wall prevents adequate penetration of shockwave to injuries below this level. Severe injuries may be treated with

Platelet Rich Plasma (PRP), or other regenerative therapies like stem cells. These treatments should be done with ultrasound and radiographic guidance to ensure proper placement (6,7, 7). The coffin joint is in close proximity and inadvertent injection into this joint is not uncommon (Figure 5). The rehabilitation protocol typically includes a period of ride-walking or handwalking for two to three months, but depends on the extent of the injury, with gradual increases in work over the following six months to year. Initially, horses should begin rehab on a smooth, firm surface in straight lines, with minimal bending lines to reduce torque on the injured ligament (1). Horses with CL injuries have a fair prognosis, with 50-60 percent of CL injuries returning to their previous level of work (1,8,9). References/Suggested Reading 1.


Dyson, S. Equine lameness: Clinical judgement meets advanced diagnostic imaging. Proc 59th Am Assoc Equine Pract (2013) 59, 92-122 Dyson S, et al. Lameness associated with foot pain: Results of magnetic resonance imaging in 199 Horses (January

Figure 4: Ultrasound of coffin joint CL desmitis. The MCL is enlarged with hypoechoic change, the LCL is more normal in appearance.

24  The Practitioner  Issue 4 • 2017

Kent Allen , DVM, Cert. ISELP Dr. A. Kent Allen received his veterinary degree from the University of Missouri in 1979. His practice, Virginia Equine Imaging in Middleburg, Va., focuses on top-level sports medicine, lameness and diagnostic imaging. Allen is Certified by the International Society of Equine Locomotor Pathology (ISELP) and serves as its Vice President and Executive Director. He serves as the volunteer Chairman of the United States Equestrian Federation (USEF) Veterinary and Drug and Medications Committees. He has served as USEF Team Veterinarian in multiple roles in multiple disciplines. He has served on the Board of Directors for USEF and United States Eventing Association (USEA). Allen is the National Head Veterinarian for the Federation Equestrian Internationale (FEI) for the United States and serves on the FEI Veterinary and List Committees. He has been the Foreign Veterinary Delegate (Veterinary Judge and Technical Delegate) in two Olympic Games, two Pan American Games and served as the Veterinary Services Manager at an Olympic and World Equestrian Games.

Figure 5: Radiograph guided injection of regenerative therapy into the MCL.

2001--December 2003) and response to treatment. Equine vet. J. (2005) 37 (2) 113-121 3.



6. 7.



Denoix J, Bertoni L, Heitzmann A, Werpy NM, Audigie F. Ultrasonographic examination of the collateral ligaments of the distal interphalangeal joint in horses: Part A: Technique and normal images. Equine Vet Educ (2011) 23, 574-580. Denoix J, Dupays A, Bertoni L. Ultrasonographic examination of the collateral ligaments of the distal interphalangeal joint in horses. Part B: Abnormal findings and lesions. Equine Vet Educ (2011) 32, 612-625 Denoix JM, Chateau H, Crevier-Denoix N. Corrective shoeing of equine foot injuries. In: Proceedings of the 10th Geneva Congress of Equine Medicine and Surgery, December, 2007: 136-143 Lewis D, et al. Feasibility for ultrasound-guided injection of the collateral ligaments of the distal interphalangeal joint in horses. Vet Radiol Ultrasound. (2016) 57(3) 299-305 Werpy NM, Farrington L, Frisbie D. How to perform radiographic-guided needle placement into the collateral ligaments of the distal interphalangeal joint. Proc 57th Am Assoc Equine Pract 2011;57:451â&#x20AC;&#x201C;455. Gutierrez-Nibeyro S, White N, et al. Magnetic Resonance Imaging Findings of Desmopathy of the Collateral Ligaments of the Equine Distal Interphalangeal Joint. Vet Radiol Ultrasound (2009) 50(1) 21-31 Dakin SG, et al. Osseous abnormalities associated with collateral desmopathy of the distal interphalangeal joint: Part 2: Treatment and outcome. Equine vet. J. (2009) 41 (8) 794-799

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Hindlimb Lameness in the Athletic Horse: The Proximal Suspensory Ligament KENT ALLEN | DVM, CERT. ISELP


roximal Suspensory Ligament Desmitis is a common yet underdiagnosed cause of hindlimb lameness and poor performance in athletic horses (1,2). The proximal suspensory ligament(PSL) primarily originates from the plantaroproximal aspect of the cannon bone just below the hock, then travels distally where it branches into medial and lateral branches that insert on the apices of the proximal sesamoid bones. These branches then extend to insert on the front of the pastern as the extensor branches of the suspensory ligament. The ligament is encased by the medial and lateral splint bones and thick fascia at its origin. When the ligament is injured and swells, a compartment syndrome type injury develops because of the surrounding bones and thick fascia. These horses often present for hindlimb lameness or poor performance that has been unresponsive to other therapies like hock or stifle injections, or only improved the condition for a short time (days to weeks). They will often have a shortened cranial phase of the stride on the

Figure 2: Area to be clipped for ultrasound of the hind suspensory ligament outlined by white. WWW.FAEP.NET |


Figure 1: Needle placement site (red dot) 2 cm below head of lateral splint bone (white line), and limb positioning with fetlock flexed and tendons distracted medially.

affected limb. In most horses, and unlike the forelimbs, the disease affects both legs. They will often have a moderate to severe response to full limb flexions. Horses working in deep footing or with a straight hind limb conformation are more prone to PSL injury (1,2). The blocks most commonly used for regional analgesia of the proximal suspensory ligament (PSL) are the deep branch of the lateral plantar nerve block or direct infiltration at the origin of the ligament (3). The deep branch of the lateral plantar nerve is reached by inserting a small gauge, 1â&#x20AC;? needle 1-2cm below the head of the lateral splint along its axial border perpendicular to the back of the cannon bone (Figure 1). Direct infiltration of the ligament is done at the same level, but local anesthetic is fanned out through the ligament. Due to the proximity to the hock joints, sterile preparation of the site is recommended. Both of these approaches are best done with the limb held back and the fetlock flexed to relieve tension on the flexor tendons and allow them to be pulled medially away from the needle. If direct infiltration of the ligament is utilized, the limb should be ultrasounded first due to artifact that is introduced with the injection. Like with all nerve blocks, other structures, including the distal hock joints, may be anesthetized as well, so thorough evaluation of the hocks and surrounding structures is vital for proper diagnosis (4). When preparing to ultrasound the PSL, the limb should be clipped in an inverted triangular shape extending from the medial aspect at the hock joints around the back of the leg and extending down about 1/3 of the distance of the cannon bone (Figure 2). Any surface dirt or debris should




Figures 3A and 3B: Ultrasound images of enlarged PSLs. The PSL should be roughly wedge or triangle shaped and lie within a line drawn between the splint bones (white arrows). These are rounded and enlarged with hypoechoic change. a. The PSL imaged with the limb weight-bearing. b. The PSL imaged with the limb non-weight-bearing. This is performed with the limb flexed and the flexor tendons relaxed. The foot can be placed in a stand or held by an assistant.

be removed with alcohol or water soaked gauze and ultrasound gel applied. The ligament should be ultrasounded in transverse, longitudinal and non-weight-bearing positions as described in previous literature (Figures 3 and 4) (5, 6, 7). Damage is indicated by enlargement of the ligament beyond the borders of the medial and lateral splint bones and increased hypoechogenicity (Figure 3a and 3b). At least two views (lateromedial, and dorsoplantar) should be taken of each hock on a limb with suspected suspensory ligament desmitis. The proximal third of the cannon bone should ideally be included in each view to evaluate for bony changes that can occur with proximal suspensory ligament desmitis, including sclerosis or avulsion of the underlying bone (Figure 5a). The hock joints should be evaluated for evidence of arthritis as well, as the plantar pouches of the distal hock joints are in close proximity to the areas being blocked, as discussed above. For horses evaluated with nuclear scintigraphy or bone scan, increased IRU is often seen at the proximoplantar aspect of the cannon bone, commonly focused on the head of the lateral splint bone, on horses with proximal suspensory ligament desmitis (Figure 5b). Surgery, extracorporeal shockwave therapy (ESWT), and regenerative therapy are a few of the many treatment modalities that have been reported for PSL desmitis. Only 14% of horses return to full work following rest alone, therefore rest is not considered a sufficient option (1). Different surgical options for hind limb PSL desmitis, such as desmoplasty/fasciotomy, and neurectomy/fasciotomy have been reported (1). A recent retrospective study compared shockwave therapy to neurectomy of the deep branch of the lateral plantar nerve and fasciotomy and found similar success rates approaching 70 percent for each. The initial rehabilitation protocols are different for horses undergoing shockwave and surgery. Horses that undergo surgery are

Figure 4: Normal PSL in transverse and longitudinal weight bearing views. Vessel edge artifact is marked by white arrows.

28  The Practitioner  Issue 4 • 2017



Figures 5: A. Radiographs of a normal cannon bone on the left and abnormal on the right. B. Bone scan images of PSL desmitis with bony inflammation (black arrows).

under strict stall rest for two to four weeks and then transitioned into hand walking, ride walking and small paddock turn out over the following four to six weeks at the discretion of the surgeon. Horses receiving ESWT are confined to small paddock turn out with hand or ride walking for 10 weeks with three shockwave sessions three weeks apart at the beginning. Walking should be limited to 20-30 minutes, five to seven times per week. After the initial rehabilitation is complete, a complete lameness exam and ultrasound exam should be performed. Horses showing significant improvement can be transitioned into work. A detailed program of daily exercise is outlined for the rider, adding in an additional two minutes of trot work per week split up with walk breaks. Monthly rechecks should be performed to ensure the soundness of the horse. Horses failing to response to initial therapy can be treated with additional shockwave sessions, or sent for surgery if not previously elected. Adequate imaging and diagnostic blocks are required to properly diagnose PSL desmitis in the hind limb. Properly diagnosed and treated horses have a good prognosis for return to athletic performance. References/Suggested Reading 1.




Dyson S, Murray R. Management of hindlimb proximal suspensory desmopathy by neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy: 155 horses (2003-2008). Equine Vet J (2011) 44,361-367. Murray R, Dyson S, Tranquille C, Adams V. Association of type of sport and performance level with anatomical site of orthopaedic injury and injury diagnosis. Equine Vet J Suppl (2006) 36, 411-416. Hughes T, Eliashar E, Smith R. In vitro evaluation of a single injection technique for diagnostic analgesia of the proximal suspensory ligament of the equine pelvic limb. Vet Surg (2007) 36, 760-764. Contino E, King M, Valdés-Martínez A, McIlwraith C. In vivo diffusion characteristics following perineural injection of the



deep branch of the lateral plantar nerve with mepivicaine or iohexol in horses. Equine Vet J; (2014) epub ahead of print. 5. Hewes C, White N. Outcome of desmoplasty and fasciotomy for desmitis involving the origin of the suspensory ligament in horses: 27 cases (1995-2004). J Am Vet Med Assoc (2006) 229, 407-412. 6. Dyson S. Diagnosis and management of common suspensory lesions in the forelimbs and hindlimbs of sport horses. Clin Tech Equine Pract (2007) 6, 179-188. 7. Denoix JM, Farres D. Ultrasonographic imaging of the proximal third interosseous muscle in the pelvic limb using a plantaromedial approach. J of Eq Vet S (1995) 15, 246-350 8. Norvall A, et al. Diagnosis, treatment, and outcome of hindlimb proximal suspensory desmopathy in sport horses: 75 Cases (2008 –2014). Proc 61th Am Assoc Equine Pract (2015) 61, 358

Kent Allen , DVM, Cert. ISELP Dr. A. Kent Allen received his veterinary degree from the University of Missouri in 1979. His practice, Virginia Equine Imaging in Middleburg, Va., focuses on toplevel sports medicine, lameness and diagnostic imaging. Allen is Certified by the International Society of Equine Locomotor Pathology (ISELP) and serves as its Vice President and Executive Director. He serves as the volunteer Chairman of the United States Equestrian Federation (USEF) Veterinary and Drug and Medications Committees. He has served as USEF Team Veterinarian in multiple roles in multiple disciplines. He has served on the Board of Directors for USEF and United States Eventing Association (USEA). Allen is the National Head Veterinarian for the Federation Equestrian Internationale (FEI) for the United States and serves on the FEI Veterinary and List Committees. He has been the Foreign Veterinary Delegate (Veterinary Judge and Technical Delegate) in two Olympic Games, two Pan American Games and served as the Veterinary Services Manager at an Olympic and World Equestrian Games.



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Practitioner Issue 4, 2017  

A publication by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Your Invitation to Attend the Oc...

Practitioner Issue 4, 2017  

A publication by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Your Invitation to Attend the Oc...

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