Practitioner Issue 1, 2016 by FVMA

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 1 • 2016

MUSCULOSKELETAL ABNORMALITIES IN FOALS ARIC ADAMS | DVM, DACVS

ACVIM Consensus Statement on EIPH LAURENT COUETIL | DVM, PhD, DACVIM (LA)

Shivers and Other

Movement Disorders STEPHANIE J. VALBERG | DVM, PhD, DACVIM, DACVSMR

ULTRASOUND EXAMINATION OF THE EQUINE DIGIT

RICHARD D. MITCHELL | DVM, MRCVS, DACVSMR

OSPHOSÂŽ

(clodronate injection) 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, chlorocontaining bisphosphonate. Chemically, clodronate disodium is (dichloromethylene) diphosphonic acid disodium salt and is manufactured from the tetrahydrate form.

A stride forward

INDICATION: For the control of clinical signs associated with navicular syndrome in horses. CONTRAINDICATIONS: Horses with hypersensitivity to clodronate disodium should not receive OSPHOS.

for Navicular Syndrome

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.

Introducing OSPHOS, the new

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.

FDA approved intramuscular bisphosphonate injection from Dechra Veterinary Products

Easily administered via intramuscular injection

Well tolerated* in clinical trials

Proven efficacy* at 6 months post treatment

No Reconstitution required

OSPHOS contains clodronate disodium, a bisphosphonate indicated for the control of clinical signs associated with navicular syndrome in horses. OSPHOS is the only FDA-approved bisphosphonate for use in horses that is labeled for intramuscular injection. In a clinical trial evaluating OSPHOS in 86 horses, lameness improved in 74.7% of horses by at least one grade 56 days after treatment. Only 9% of horses displayed clinical signs of being uncomfortable, nervous, colicky and or pawing after receiving OSPHOS. Less than 1% of horses experienced colic requiring treatment.

WITH OSPHOS THE BENEFITS ARE CLEAR . . .

Learn more online

www.dechra-us.com www.equinelameness.com www.osphos.com

Call our 24 hour Tech Support

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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As with all drugs, side effects may occur. In field studies, the most common side effects reported were signs of discomfort or nervousness, colic, and/or pawing. OSPHOS should not be used in pregnant or lactating mares, or mares intended for breeding. Use of OSPHOS in patients with conditions affecting renal function or mineral or electrolyte homeostasis is not recommended. Refer to the prescribing information for complete details or visit www.dechra-us.com. CAUTION: Federal law restricts this drug to use by or on the order of licensed veterinarian. * Freedom of Information Summary, Original New Animal Drug Application, NADA 141-427, for OSPHOS. April 28, 2014.

Distributed by: Dechra Veterinary Products 7015 College Boulevard, Suite 525 Overland Park, KS 66211 866-933-2472 ÂŠ 2015 Dechra Ltd. OSPHOS is a registered trademark of Dechra Ltd. All rights reserved. NADA 141-427, Approved by FDA

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KY91 EIV strain contained in FLU AVERT® I.N.

Equine Influenza Virus West Nile-Innovator and Fluvac Innovator MDI Sales Data as of 12/31/14. Zoetis. Dec. 2014. Data on file, Study Report No. 671-02-001R, 671-08-004.R, 766-09-002.R, 10OREQBIO-01, 14OREQBIO-1 and 15EQRGBIO-02, Zoetis Inc. Calvenza vs. CO07 ACVIM 2011 abstract reference. Townsend HGG, Penner SJ, Watts TC, Cook A, Bogdan J, Haines DM, Griffin S, Chambers T, Holland RE, Whitaker-Dowling P, Youngner JS, and Sebring RW: Efficacy of cold-adapted, intranasal, equine influenza vaccine: challenge trials. Chambers TM, Holland RE, Tudor LR, Townsend HGG, Cook A, Bogdan J, Lunn DP, Hussey S, Whitaker-Dowling P, Youngner JS, Sebring RW, Penner SJ and Stiegler GL: A new modified-live equine influenza vaccine: phenotypic stability, restricted spread and efficacy against heterologous virus challenge.

The President's Line Ruth-Anne Richter, BSc (Hon), DVM, MS - FAEP President

Dear Fellow Equine Practitoners, I am excited to take over the reins as council president for 2016 from Dr Corey Miller; large shoes to fill, and I hope that I can continue the high standards. I have been fortunate to have been a member of the FVMA's Equine-Exclusive FAEP Council for a number of years, and have enjoyed being a part of the journey. As we move into the first quarter of this new year, I am excited to see how far we have progressed since our merger with the FVMA. This year, 2016, brings exciting changes, including the inception of updated bylaws. The FAEP council has worked hard to bring you, the equine practitioners quality continuing education. We are excited to announce that we will be traveling offshore once again, and will be holding, the Promoting Excellence Symposium in San Juan, Puerto Rico, October 20-23, 2016. Ocala Equine Conference 2016 was a huge success with record numbers of attendees and vendors alike. Another very well-received ultrasound wet lab was held this year at Equine Medical Center of Ocala, where participants honed their ultrasound skills of the thorax and abdomen, the hind suspensory ligament, the metacarpal region and the foot. Everyone that attended was enthusiastic and went away with helpful "pearls" from the instructors. We are currently working on the 2017 OEC, at which we are planning to include the unique veterinarian-farrier Foot Symposium. As always, the FAEP could not organize and hold these quality events without the efforts of the FVMA staff and our executive director, Phil Hinkle. The FVMA staff work diligently in the background to facilitate obtaining the beautiful venues where we hold our annual PES, and arranging the events associated with these conferences, making things appear seamless. We thank-you all for your support. Believe me, the staff may appear to be gliding across the still waters of the pond, but are paddling fiendishly to make it all work! The continued support of our educational partners is invaluable, without which we could not hold the quality CE events that we do. We hope that you will join us in Puerto Rico in October. Featured speakers include Dr. Robert MacKay, Dr. Anne Dwyer and Dr. Laurie Goodrich. Topics in internal medicine, sports medicine and ophthalmology are scheduled as well as the popular rehabilitation discussions. We look forward to seeing you there, and remember, as US citizens, no passport is required. Please feel free to contact any member of the FAEP or FVMA staff with any questions, comments or suggestions you may have.

EXECUTIVE COUNCIL

Ruth-Anne Richter FAEP Council President 2016

Corey Miller, DVM, MS, Diplomate ACT

FAEP COUNCIL PAST PRESIDENT cmiller@emcocala.com

Armon Blair, DVM abeqdoc@aol.com

Suzan C. Oakley, DVM, MS, Diplomate ABVP(Equine), Cert. ISELP oakleyequine@gmail.com

Anne L. Moretta, VMD, MS marochel@aol.com

Adam Cayot, DVM adamcayot@hotmail.com

Amanda M. House, DVM, Diplomate ACVIM REPRESENTATIVE TO FVMA EXECUTIVE BOARD housea@ufl.edu

Mr. Philip J. Hinkle EXECUTIVE DIRECTOR phinkle@fvma.org

Jacqueline S. Shellow, DVM, MS docshellow@bellsouth.net

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

A NEW dual ingredient injectable corticosteroid approved by the FDA exclusively for use in horses

The link between FAST-ACTING and

LONG-LASTING relief 1, 2

New BetaVet ® (betamethasone sodium phosphate & betamethasone acetate injectable suspension) is indicated for the control of pain and inflammation associated with osteoarthritis in horses. Learn more at www.betavetequine.com or call 1-800-458-0163.

Please see Brief Summary of Full Prescribing Information on the following page. From the manufacturer of Adequan® (polysulfated glycosaminoglycan)

INDICATION: BetaVet® is indicated for the control of pain and inflammation associated with osteoarthritis in horses.

IMPORTANT SAFETY INFORMATION For Intra-Articular (I.A.) Use in Horses.

CONTRAINDICATIONS: BetaVet ® is contraindicated in horses with hypersensitivity to betamethasone. Intra-articular injection of corticosteroids for local effect is contraindicated in the presence of septic arthritis. WARNINGS: Do not use in horses intended for human consumption. Clinical and experimental data have demonstrated that corticosteroids administered orally or parenterally to animals may induce the first stage of parturition when administered during the last trimester of pregnancy and may precipitate premature parturition followed by dystocia, fetal death, retained placenta, and metritis. Additionally, corticosteroids administered to dogs, rabbits and rodents during pregnancy have resulted in cleft palate in offspring and in other congenital anomalies including deformed forelegs, phocomelia and anasarca. Therefore, before use of corticosteroids in pregnant animals, the possible benefits to the pregnant animal should be weighed against potential hazards to its developing embryo or fetus. Human Warnings: Not for use in humans. For use in animals only. Keep this and all medications out of the reach of children. Consult a physician in the case of accidental human exposure. PRECAUTIONS: Corticosteroids, including BetaVet , administered intra-articularly are systemically absorbed. Do not use in horses with acute infections. Acute moderate to severe exacerbation of pain, further loss of joint motion, fever, or malaise within several days following intra-articular injection may indicate a septic process. Because of the anti-inflammatory action of corticosteroids, signs of infection in the treated joint may be masked. Due to the potential for exacerbation ®

of clinical signs of laminitis, glucocorticoids should be used with caution in horses with a history of laminitis, or horses otherwise at a higher risk for laminitis. Use with caution in horses with chronic nephritis, equine pituitary pars intermedia dysfunction (PPID), and congestive heart failure. Concurrent use of other anti-inflammatory drugs, such as NSAIDs or other corticosteroids, should be approached with caution. Due to the potential for systemic exposure, concomitant use of NSAIDs and corticosteroids may increase the risk of gastrointestinal, renal, and other toxicity. Consider appropriate wash out times prior to administering additional NSAIDs or corticosteroids. ADVERSE REACTIONS: Adverse reactions reported during a field study of 239 horses of various breeds which had been administered either BetaVet ® (n=119) or a saline control (n=120) at five percent (5%) and above were: acute joint effusion and/or local injection site swelling (within 2 days of injection), 15% BetaVet ® and 13% saline control; increased lameness (within the first 5 days), 6.7% BetaVet ® and 8.3% saline control; loose stool, 5.9% BetaVet ® and 8.3% saline control; increased heat in joint, 2.5% BetaVet ® and 5% saline control; and depression, 5.9% BetaVet ® and 1.6% saline control. DOSAGE AND ADMINISTRATION: Shake well immediately before use. Use immediately after opening, then discard any remaining contents. RX ONLY References: 1.Houdeshell, JW. Field trials of a new long-acting corticosteroid on the treatment of equine arthropathies. Vet Med Small Anim Clin. Sept. 1969: 782-784. 2. Trotter GW. Intra-articular corticosteroids. In: McIlwraith CW, Trotter GW, eds. Joint Disease in the Horse. Philadelphia, PA: W.B. Saunders, 1996;237–256. BetaVet ® is a registered trademark of Luitpold Pharmaceuticals, Inc. © Luitpold Animal Health, division of Luitpold Pharmaceuticals, Inc. 2015. BVT003 Iss. 7/2015

LUITPOLD ANIMAL HEALTH

BRIEF SUMMARY OF PRESCRIBING INFORMATION (Betamethasone Sodium Phosphate and Betamethasone Acetate Injectable Suspension) 6 mg betamethasone per mL For Intra-Articular (I.A.) Use in Horses CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian. DESCRIPTION: BetaVet ® is a sterile aqueous suspension of betamethasone acetate in betamethasone sodium phosphate injection. The combined betamethasone content of the suspension is 6 mg/mL where each mL contains 3.15 mg betamethasone (as betamethasone sodium phosphate); 2.85 mg betamethasone (as betamethasone acetate); 7.1 mg dibasic sodium phosphate; 3.4 mg monobasic sodium phosphate; 0.1 mg edetate disodium; and 0.2 mg benzalkonium chloride, as a preservative in water for injection. The pH is adjusted to between 6.8 and 7.2. INDICATION: BetaVet ® is indicated for the control of pain and inflammation associated with osteoarthritis in horses. DOSAGE AND ADMINISTRATION: Shake well immediately before use. Using strict aseptic technique, administer 1.5 mL BetaVet ® (9 mg total betamethasone) per joint by intra-articular injection. BetaVet ® may be administered concurrently in up to 2 joints per horse. Use immediately after opening, then discard any remaining contents. CONTRAINDICATIONS: BetaVet ® is contraindicated in horses with hypersensitivity to betamethasone. Intra-articular injection of corticosteroids for local effect is contraindicated in the presence of septic arthritis. WARNINGS: Do not use in horses intended for human consumption. Clinical and experimental data have demonstrated that corticosteroids administered orally or parenterally to animals may induce the first stage of parturition when administered during the last trimester of pregnancy and may precipitate premature parturition followed by dystocia, fetal death, retained placenta, and metritis. Additionally, corticosteroids administered to dogs, rabbits and rodents during pregnancy have resulted in cleft palate in offspring. Corticosteroids administered to dogs during pregnancy have also resulted in other congenital anomalies including deformed forelegs, phocomelia and anasarca. Therefore, before use of corticosteroids in pregnant animals, the possible benefits to the pregnant animal should be weighed against potential hazards to its developing embryo or fetus. Human Warnings: Not for use in humans. For use in animals only. Keep this and all medications out of the reach of children. Consult a physician in the case of accidental human exposure. PRECAUTIONS: Corticosteroids, including BetaVet ®, administered intra-articularly are systemically absorbed. Do not use in horses with acute infections. Acute moderate to severe exacerbation of pain, further loss of joint motion, fever, or malaise within several days following intra-articular injection may indicate a septic process. Because of the anti-inflammatory action of corticosteroids, signs of infection in the treated joint may be masked. Appropriate examination of joint fluid is necessary to exclude a septic process. If a bacterial infection is present, appropriate antibacterial therapy should be instituted immediately. Additional doses of corticosteroids should not be administered until joint sepsis has been definitively ruled out. Due to the potential for exacerbation of clinical signs of laminitis, glucocorticoids should be used with caution in horses with a history of laminitis, or horses otherwise at a higher risk for laminitis. Use with caution in horses with chronic nephritis, equine pituitary pars intermedia dysfunction (PPID), and congestive heart failure. Concurrent use of other anti-inflammatory drugs, such as NSAIDs or other corticosteroids, should be approached with caution. Due to the potential for systemic exposure, concomitant use of NSAIDs and corticosteroids may increase the risk of gastrointestinal, renal, and other toxicity. Consider appropriate wash out times prior to administering additional NSAIDs or corticosteroids. ADVERSE REACTIONS: Adverse reactions reported during a field study of 239 horses of various breeds which had been administered either BetaVet ® (n=119) or a saline control (n=120) were: acute joint effusion and/or local injection site swelling (within 2 days of injection), 15% BetaVet ® and 13% saline control;

increased lameness (within the first 5 days), 6.7% BetaVet ® and 8.3% saline control; loose stool, 5.9% BetaVet ® and 8.3% saline control; increased heat in joint, 2.5% BetaVet ® and 5% saline control; depression, 5.9% BetaVet ® and 1.6% saline control; agitation/anxiety, 4.2% BetaVet ® and 2.5% saline control; delayed swelling of treated joint (5 or more days after injection), 2.5% BetaVet ® and 3.3% saline control; inappetance, 3.4% BetaVet ® and 2.5% saline control; dry stool, 1.7% BetaVet ® and 0% saline control; excessive sweating, 0.8% BetaVet ® and 0% saline control; acute non-weight bearing lameness, 0.8% BetaVet®and 0% saline control; and laminitis, 0.8% BetaVet® and 0% saline control. CLINICAL PHARMACOLOGY: Betamethasone is a potent glucocorticoid steroid with anti-inflammatory and immunosuppressive properties. Depending upon their physico-chemical properties, drugs administered intra-articularly may enter the general circulation because the synovial joint cavity is in direct equilibrium with the surrounding blood supply. After the intra-articular administration of 9 mg BetaVet ® in horses, there were quantifiable concentrations of betamethasone (above 1.0 ng/mL) in the plasma. EFFECTIVENESS: A negative control, randomized, masked field study provided data to evaluate the effectiveness of BetaVet ® administered at 1.5 mL (9 mg betamethasone) once intra-articularly for the control of pain and inflammation associated with osteoarthritis in horses. Clinical success was defined as improvement in one lameness grade according to the AAEP lameness scoring system on Day 5 following treatment. The success rate for horses in the BetaVet ® group was statistically significantly different (p=0.0061) than that in the saline group, with success rates of 75.73% and 52.52%, respectively (back-transformed from the logistic regression). ANIMAL SAFETY: A 3-week target animal safety (TAS) study was conducted to evaluate the safety of BetaVet ® in mature, healthy horses. Treatment groups included a control (isotonic saline at a volume equivalent to the 4x group); 1X (0.0225 mg betamethasone per pound bodyweight; BetaVet ®); 2X (0.045 mg betamethasone per pound bodyweight; BetaVet ®) and 4X (0.09 mg betamethasone per pound bodyweight; BetaVet ®). Treatments were administered by intra-articular injection into the left middle carpal joint once every 5-days for 3 treatments. Injection site reactions were the most common observations in all treatment groups. Injection site reactions were observed within 1 hour of dosing and included swelling at the injection site, lameness/stiffness of the left front limb, and flexing the left front knee at rest. The injection site reactions ranged from slight swelling (in many horses on multiple days in all treatment groups) to excessive fluid with swelling, pain, and lameness (4x group only). Injection site reactions were observed most commonly on treatment days, and generally decreased in number and severity over subsequent days. The incidence of injection site reactions increased after the second and third injection (number of abnormalities noted on day 10 > day 5 > day 0). In the BetaVet ® treated groups the number and severity of the injection site reactions were dose dependent. The 4X BetaVet ® group had the highest overall incidence of and severity of injection site reactions, which included heat, swelling, pain, bleeding, and holding the limb up at rest. The control group and 4X group (which received similar injection volumes) had a similar incidence of injection site reactions; however, the severity of reactions was greater in the 4X group. Absolute neutrophils were statistically significantly higher in the BetaVet ® treated groups as compared to the control group. Trends toward a decrease in lymphocytes and eosinophils, and an increase in monocytes were identified in the BetaVet ® treated groups after the initial dose of BetaVet ®. Individual animal values for white blood cells generally remained within the reference range. BetaVet ® treated horses also had a trend toward increased blood glucose after the initial dose. Some individual animals showed mild increases in blood glucose above the reference range. STORAGE CONDITIONS Store at 20° to 25°C (68° to 77°F) (See USP Controlled Room Temperature). Protect from light. Use carton to protect contents from light until used. HOW SUPPLIED BetaVet ®, One 5 mL vial containing 30 mg betamethasone; packaged in boxes of 1. SHAKE WELL BEFORE USING NADA 141-418, Approved by FDA

A Division of Luitpold Pharmaceuticals, Inc. One Luitpold Drive | P.O. Box 9001 | Shirley, NY 11967

Musculoskeletal Abnormalities in Foals ARIC ADAMS | DVM, DACVS

oals develop a variety of musculoskeletal problems, with some problems being unique to the young, growing animal, and others that are commonly seen in both young and mature animals. Many conditions seen in foals are rapidly progressive, so quick and accurate diagnosis of the disease process is essential in developing an appropriate treatment plan that will achieve the best outcome. We will discuss several musculoskeletal abnormalities commonly seen in foals, and try to differentiate factors in the history/signalment (H/S), physical exam and other diagnostics that may be useful in making a diagnosis. We will also look at current treatment options and prognosis associated with different treatments.

Septic Arthritis and Osteomyelitis in Foals

Types of Infections: 1. Synovial Infections (S-Type)1: involves synovial membrane and synovial fluid. • H/S: Often very young foals <1 week old. Acute lameness. Sometimes the history is “The foal was stepped on." • Clinical Signs: lameness, joint swelling and fever • Most Common Locations: Most often affects larger joints, such as tibiotarsal joints, femoropatellar joints and often, multiple joints. • Bloodwork: +/- Leukocytosis, +/- hyperfibrinogenemia • Synovial Fluid: 10,000 to 200,000+/µL, 90% neutrophils (degenerated), TP>2g/dL, elevated lactate • Radiographs: usually normal • Ultrasound: Synovial effusion, synovial proliferation • Treatment: Systemic antibiotics, joint lavage, intravenous regional limb perfusion (IVRLP), intra-articular antibiotics, arthroscopic synovial resection 2. Epiphyseal Infections (E-Type)1: involves articular epiphyseal complex. •

Epiphyseal infection WWW.FAEP.NET |

H/S: Foals usually weeks old and may have been previously ill (pneumonia, diarrhea, etc.) or had failure of passive transfer. May have mild intermittent lameness with acute onset of severe lameness or just severe lameness.

FLAEP |

• Clinical Signs: Lameness +/- joint effusion +/- fever • Most Common Locations: distal femur, talus, prox and distal radius, prox and distal tibia • Bloodwork: +/- Leukocytosis, Usually has hyperfibrinogenemia (often >900mg/dL). • Synovial Fluid: Varies from normal to similar values listed for S-Type infections. • Radiographs: May appear normal or may have a radiolucency in the affected epiphysis. • Ultrasound: +/- synovial effusion and may visualize an articular defect in the affected joint • Treatment: Systemic antibiotics, (IVRLP), +/- intra-articular antibiotics, +/- joint lavage, arthroscopic debridement 3. Physeal Infections (P-Type)1: involves the long bone physis +/- joint involvement. • H/S: Foals are older (weeks to months). May be healthy with no history of problems. Mild persistent lameness with development of acute severe lameness. • Clinical Signs: Lameness, periarticular edematous swelling that is sore to palpation. Fever • Most Common Locations: distal physis MC3/MT3, radius, tibia • Bloodwork: +/- Leukocytosis and Usually has hyperfibrinogenemia (often >900mg/dL). • Synovial Fluid: Often normal or may be similar values listed for S-Type infections. • Radiographs: May appear normal or may have a radiolucency in the effected physis. • Ultrasound: Irregularity of the affected physis, +/synovial effusion • Treatment: Systemic antibiotics, intravenous regional limb perfusion (IVRLP), intraphyseal injections, +/- intra-articular antibiotics, physeal debridement, antibiotic impregnated polymethylmethacrylate or plaster of paris Prognosis: 60-80% survival rate. Prognosis is negatively affected with multiple joint or bone involvement. Likelihood for long-term soundness is less clear. Multiple papers show a decreased chance of racing.

Angular Limb Deformities in Foals

Valgus deformities involve lateral deviation of the distal limb. Varus deformities involve medial deviation of the distal limb. Etiologies in the neonate include: incomplete ossification of the cuboidal bones, laxity of periarticular structures, abnormal intrauterine ossification. Etiologies in the older, developing foal include excessive grain intake, mineral imbalance in feed, excessive exercise or trauma. May be a type of developmental orthopedic disease (DOD).

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS

| The Practitioner 7

Severe Carpal Valgus

Epiphyseal wedging from severe carpal valgus

elevation (growth acceleration): If foal is young and has a lot of growth potential and if the ALD isn’t severe. The usefulness of this treatment has been questioned, because many foals ALDs correct with no treatment. Transphyseal bridging (growth retardation): Performed for ALDs, if the foal is young and the ALD is severe or in foals in which the rapid growth phase is over (after 8 weeks old for distal MC3/ MT3, 4 months old for distal tibia and 6 months old for distal radius). Distal MC/MT3 transphyseal screws for fetlock ALD foals. Screws and wires or transphyseal screws for carpal ALD foals. Transphyseal screws in the distal radius carry a higher risk of physitis and also premature physeal closure with overcorrection. Miniature horses: May have a complete ulna or fibula. Always radiograph to identify early and correct surgically. Prognosis: The prognosis for correction and soundness is good unless permanent bone deformation has occurred due to severe or prolonged angular limb deformities.

Flexural Limb Deformities in Foals

Transphyseal screws and wire for carpal varus

• H/S: Angular limb deformity (ALD) present at birth or develops in the weeks or months after birth. If the foal is weeks-to-months old, there is often a history of feeding excessive grain and/or alfalfa. • Clinical Signs: No lameness is usually detected. The foal is seen to have an angular limb deformity when evaluated from in front, behind and at different angles. • Palpation: In neonates, evaluate the affected limb for laxity by joint manipulation and palpation. • Radiographs: If the foal is a neonate, always take radiographs to evaluate for incomplete ossification. Take radiographs if the angular limb deformity is severe, to evaluate for cuboidal bone wedging/crushing. • General Trends: Young foals: carpal valgus, fetlock varus. Older foals to yearlings: carpal varus • Treatment: Conservative Treatment: Stall rest for foals with incomplete ossification, severe angular limb deformities (>10 degrees), and laxity of periarticular structures. Splints for foals with incomplete ossification or laxity, but must use caution. Hoof manipulation with corrective trimming or glue-on extensions can be used in foals with mild ALDs. Valgus hoof extension medially. Varus hoof extension laterally. Repeated treatments with extracorporeal shockwave therapy on the convex side of the angular limb deformity has been shown to improve the disorder. Surgical Treatment: Periosteal transection and 8 The Practitioner

Can be congenital or acquired in origin. Congenital factors include intrauterine malpositioning, teratogens, and genetic predisposition. Acquired factors include nutrition (excessive intake), mineral imbalance, or prolonged lameness resulting in decreased weight bearing. May be a type of developmental orthopedic disease (DOD). • Diagnosis: Visual identification of a flexural deformity. Radiographs and ultrasound are not usually necessary, unless concurrent bone lesions or a tendinous injury is suspected.

Digital Hyperextension:

BEFORE

Foal with flexural laxity before and after heel extensions

AFTER

Seen in newborn foals due to muscle flaccidity. Mild cases usually correct with exercise. Severe cases respond to tape-on or glue-on heel extensions and protection of the skin over the fetlock with light bandages and exercise. Ruptured Common Digital Extensor Tendon (CDET): Seen in newborn foals and foals up to a few weeks old. Usually have effusion in the CDET sheath over the dorsolateral carpus. May be associated with other flexural deformities. Foals that buckle over at the carpus or fetlock may require splinting and analgesics. Issue 1 • 2016

1. Distal Interphalangeal Joint Flexural Deformity (DIPJ): Most commonly an acquired problem seen at 1-4 months of age, usually the forelimbs. Mild cases may respond to oxytetracycline treatment (especially if congenital), toe extension acrylic or shoes, analgesics, and dietary management if indicated. More severe cases may require inferior check desmotomy surgery, along with the previous treatments mentioned. Transection of the deep digital flexor tendon is usually considered a salvage procedure. 2. Metacarpophalangeal Joint (MCPJ) and Metatarsophalangeal (MTPJ) Joint Flexural Deformity:

general. The prognosis for surgical correction of the various flexural deformities has been evaluated in numerous papers and is favorable, depending on the severity of the deformity. Transection of the inferior check ligament for flexural deformity of the DIPJ carries a good prognosis for correction and soundness, although they are less likely to race than control horses in a retrospective study. Transection of the superior check ligament carries a good (80%) prognosis for soundness. Transection of the ulnaris lateralis and flexor carpi ulnaris for carpal flexural deformities corrected about 90% of horses with grade 1 or 2 carpal flexural deformities.

Osteochondrosis

Osteochondrosis (OC) is caused by abnormal endochondral ossification, with resulting irregularities in the thickness of epiphyseal cartilage. Type of developmental orthopedic disease (DOD). Occurs in developing foals, but is usually unrecognized until horses are placed in training. It is a dynamic process in which lesions may either worsen or improve with time. Proposed causative factors include local biomechanical damage to cartilage canals, rapid growth, lack of exercise, genetics, mineral imbalance, and trauma. Includes osteochondritis dissecans (OCD) and subchondral cystic lesions (SCLs). Is a type of DOD.

Flex Deform of the Fetlock MCPJ Can be either congenital or may be acquired (most commonly at 10-18 months old). Congenital cases may be treated with oxytetracycline, corrective podiatry, analgesics and splinting. Acquired cases should also incorporate dietary management. Palpation of the flexor tendons may identify if an inferior check desmotomy and/or a superior check desmotomy will be useful in treating the deformity.

Abnormal Endochondral Ossification for OCD

3. Carpal Flexural Deformity:

Foal with Carpal Flexural Deformity Usually congenital or seen in the first month of life. Treat with oxytetracyline, splinting or tube casts, and analgesics. Transection of the tendons of the ulnaris lateralis and flexor carpi ulnaris can benefit more severe cases that fail to respond to conservative treatments. Prognosis: The prognosis for correction is favorable in WWW.FAEP.NET |

FLAEP |

• H/S: If identified in foals, they are usually older foals. • Clinical Signs: Joint swelling +/- lameness • Most Common Locations in Foals: If foals show clinical signs related to OC, the lesion is usually large and is most often seen in the lateral trochlear ridge of the femur (LTRF) and distal intermediate ridge of the talus (DIRT). SCLs are not seen in foals as commonly, but large medial femoral condylar lesions may cause clinical signs in older foals. DIRT lesions most often develop after 1 month of age, and don’t change radiographically after 5 months of age. LTRF lesions most often develop after 3 months of age and don’t change after 8 months of age. • Radiographs: Show irregularity of the affected structure, or osteochondral fragmentation or a focal radiolucency. May appear normal with subtle lesions.

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| The Practitioner 9

• Ultrasound: Synovial effusion +/- articular cartilage irregularity • Treatment: Conservative: controlled exercise, antiinflammatories, intraarticular injections, and dietary management. Surgical: Arthroscopic debridement of OCD lesions and SCLs, intracystic injections of corticosteroids in SCLs, transosseous debridement of SCLs, treatment of medial femoral condylar SCLs with a transcondylar screw. Prognosis: The prognosis for surgical removal and debridement of OC/ OCD lesions is generally excellent to good depending on the joint and the size of the lesion. The exception Radiograph of would be that horses Distal Radial with OC lesions in the shoulder have a poor Physitis prognosis for soundness, with only 4 of 26 horses starting a Salter Harris Physeal Injuries race after arthroscopic While foals can sustain fractures to a variety of bones, just as debridement in one DIRT OCD Hock an adult horse can, they are also prone to fractures that involve study. About 50-65% the physis. There are six types of Salter Harris fractures. of horses with subchondral cystic lesions of the medial femoral 1. Type1: Fracture through the entire physis. Examples condyle that are treated conservatively return to soundness. Surinclude a femoral head fracture or type 1 olecranon fracture. gical treatment with debridement, arthroscopic guided intracystic 2. Type 2: Most common Salter Harris fracture in foals. injection of corticosteroid, and transcondylar screw placement Fracture extends along the physis and exits through the all improve the prognosis for soundness to about 75%, while the metaphysis. Seen commonly when foals are stepped on. transcondylar screw placement appears to be the only treatment Most common locations include distal third metacarpal/ that consistently decreases the size. metatarsal bone and proximal tibia. 3. Type 3: Uncommon; Fracture extends through the physis Physitis and exits through the epiphysis into the joint. Physitis is thought to be associated with Type V growth plate 4. Type 4: Uncommon; Fracture extends from the joint, injuries in foals, and is a type of developmental orthopedic through the physis and exits the metaphysis. disease (DOD). It may be seen at the periphery (usually medially) 5. Type 5: Physeal crushing at one region of the physis. or in the central part of the growth plate. Related to rapid growth, 6. Type 6: Periosteal bridge between the metaphysis and heredity, excessive grain intake, mineral imbalance which is epiphysis; Can result from periosteal trauma (from similar to other DOD disorders. Often seen in conjunction with surgery or external trauma), or infectious periostitis. angular limb deformities in which there is uneven loading on the physis and epiphysis. • H/S: History of limb swelling and lameness • Clinical Signs: Physeal swelling and lameness; Foals with a • H/S: If identified in foals during their rapid growth phases; fracture are usually non-weight bearing lame. May palpate History of limb swelling +/- lameness crepitus and instability. Foals with type 5 and 6 injuries • Clinical Signs: Physeal swelling +/- lameness may have localized to pain to palpation and may also be • Most Common Locations in Foals: Distal MC/MT3 of the developing an angular limb deformity. fetlock at 3-6 months, distal radius at 8-24 months, distal • Most Common Locations in Foals: Fractures usually occur tibia at 6-18 months at distal MC/MT3 of the fetlock from trauma. • Radiographs: Show radiolucency with irregularity of the • Radiographs: Demonstrate fracture through some portion affected portion of the physis. of the physis. Type 5 and 6 will show physeal remodeling • Treatment: Conservative: Rest with controlled exercise, and periosteal remodeling, respectively. anti-inflammatories, dietary restrictions and correction of mineral imbalance. Treatment/Prognosis: For Type 2 distal MC/MT3 fractures, apply a bandage and dorsal PVC splint from the tip of the toe Prognosis: Good with conservative treatment. to proximal MC3, or a plantar splint from the tip of the toe to 10 The Practitioner

Issue 1 • 2016

proximal MT3. Stabilization with a cast or with internal fixation and a cast usually provides a good prognosis. Fractures of the femoral and humeral head typically have a poor prognosis. Salter Harris type 2 fractures of the proximal tibia are difficult to splint. A bandage and lateral splint from distal MT3 up past the stifle onto the lateral thigh may provide some stability. Internal fixation provides a good prognosis.

References:

Anderson TM, et al. Longitudinal development of the equine conformation from weanling to age 3 years in the Thoroughbred. Equine Vet J. 2004;36:563 Anderson TM, et al. The role of conformation in musculoskeletal problems in the racing Thoroughbred. Equine Vet J. 2004;36:571 Auer JA: Angular Limb Deformities. p 1201. In Auer JA, Stick JA (eds): Equine Surgery. 4th Ed. Elsevier, St Louis, 2012 Baker WT, et al. Improvement in bilateral carpal valgus deviation in 9 foals after unilateral distolateral radial periosteal transection and elevation. Vet Surg. 2015;44:547-50 Bathe AP, et al. Treatment of angular limb deformities using radial extracorporeal shock wave therapy: A prospective clinical trial. Proc World Vet Assoc. 2006;9:167 Baxter GM, Turner AS. Diseases of Bone and Related Structures. P 401. In Stashak TS (ed): Adams’ Lameness In Horses. 5th Ed. Lippincott, Philadelphia, 2002 Bramlage LR. Identification, examination and treatment of physitis in the foal. Proc Am Assoc Equine Pract. 1993;39:57 Charman RE, Vasey JR. Surgical treatment of carpal flexural deformity in 72 horses. Aust Vet J. 2008;86:195-9.

of the deep digital flexor tendon (distal check ligament) in horses. J Am Med Assoc. 1985;187:1351-3 Wamsley EA, et al. Retrospective study of outcome following desmotomy of the accessory ligament of the deep digital flexor tendon for type 1 flexural deformity in the Thoroughbreds. Aust Vet J. 2011;89:265-8 Ytrehus B: Osteochondrosis, A morphological study of etiology and pathogenesis. Thesis. Oslo, Norwegian School of Veterinary Science. 2004

Aric Adams, DVM, DACVS Dr. Adams was a farrier for 8 years while obtaining his undergraduate and veterinary degrees. After graduation from veterinary college, he completed an internship at an equine hospital in Colorado. Dr. Adams then practiced for one year at an equine hospital in Utah, before moving to Florida to begin his surgical training. He completed his surgical residency at the University of Florida in 2005, and after working in Tallahassee and Brandon, Florida as an associate equine surgeon, Dr. Adams joined Equine Medical Center of Ocala in 2006. Dr. Adams’ practice focus includes lameness and podiatry, laparoscopy, and colic surgery.

Dik KJ, Enzerink EE, van Weeren PR: Radiographic development of osteochondral abnormalities in the hock and stifle of Dutch Warmblood foals, from age 1 to 11 months. Equine Vet J Suppl 31:9,1999 Ellis DR. Physitis. p 638. In Ross MW, Dyson SJ (eds): Diagnosis and Management of Lameness in the Horse. 2nd Ed. Elsevier, St Louis, 2011 Hall MS, et al. Surgical treatment of septic physitis in 17 foals. Aust Vet J 2012; 90:479-84 Hepworth-Warren KL, et al. Bacterial isolates, antimicrobial susceptibility patterns, and factors associated with infection and outcome in foals with septic arthritis: 83 cases (1998-2013). J Am Vet Med Assoc 2015; 246:785-93. Jenner F, et al. Scapulohumeral Osteochondrosis. A retrospective study of 32 horses. Vet Comp Orthop Traumatol. 2008;21:406-412 Kidd JA: Flexural Limb Deformities. p 1221. In Auer JA, Stick JA (eds): Equine Surgery. 4th Ed. Elsevier, St Louis, 2012 Neil KM, et al. Retrospective study of 108 foals with septic osteomyelitis. Aust Vet J. 2010; 88:4-12 Richardson DW, Ahern BJ: Synovial and Osseous Infections. p. 1189. In Auer JA, Stick JA (eds): Equine Surgery. 4th Ed. Elsevier, St Louis, 2012

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Richardson DW: Diagnosis and Management of Osteochondrosis and Osseous Cystlike Lesions. p 631. In Ross MW, Dyson SJ (eds): Diagnosis and Management of Lameness in the Horse. 2nd Ed. Elsevier, St Louis, 2011 Santschi EM, et al. Preliminary investigation of the treatment of equine medial femoral condylar subchondral cystic lesions with a transcondylar screw. Vet Surg. 2015; 44:281-8 Steel CM, et al. Factors associated with prognosis for survival and athletic use in foals with septic arthritis: 93 cases (1987-1994). J Am Med Assoc. 1999; 215:973-77. Stewart B, Reed CF. Osseous cyst-like lesions of the medial femoral condyle in the horse. J Am Vet Med Assoc. 1982; 180:254 Van Weeren PR: Osteochondrosis. p 1239. In Auer JA, Stick JA (eds): Equine Surgery. 4th Ed. Elsevier, St Louis, 2012

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ACVIM CONSENSUS STATEMENT ON EIPH LAURENT COUETIL | DVM, PhD, DACVIM (LA)

SUDDEN DEATH in racehorses occurs in 0.08-0.29 horses per 1000 starts

panel of 7 experts wrote a consensus statement on exercise-induced pulmonary hemorrhage (EIPH) in horses for the American College of Veterinary Internal Medicine (ACVIM). The work was presented in June 2014 at the ACVIM Forum in Nashville, TN and the draft paper was posted on the ACVIM listserv to solicit comments from the membership as well as the members of the European College of Equine Internal Medicine (ECEIM). Subsequently, the manuscript was submitted to the Journal of Veterinary Internal Medicine for peer-review and was published in May 2015.1

findings and recommendations regarding EIPH as it relates to 4 broad areas: 1) health and welfare of horses; 2) the effect of EIPH on performance; 3) prophylaxis for EIPH; 4) the effect of furosemide on performance.

The definition of EIPH is the evidence of bleeding that originates from the lungs during exercise. This is typically detected as presence of blood grossly visible during endoscopy of the airways after exercise or by cytologic examination of respiratory secretions. The objectives of the consensus statement were to evaluate the peer-reviewed literature and summarize

Effects of EIPH on Health and Welfare of Horses:

12 The Practitioner

A systematic review of the scientific literature was conducted. The quality of evidence from published articles was evaluated and recommendations were made based on the GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology.2 Clinical signs associated with EIPH are blood in the airways (e.g. epistaxis, endoscopy, cytology of respiratory secretions), poor performance, coughing, increased respiratory rate, respiratory distress or abnormal behavior, and abnormal imaging of the thorax (radiography, ultrasonography). The detection of Issue 1 • 2016

blood by endoscopy of the airways is the gold standard for the diagnosis of EIPH and grading its severity. Epistaxis following exercise is strongly suggestive of EIPH (moderate quality evidence). However, the other clinical signs are not reliable signs of EIPH and the evidence of their association with EIPH is of very low quality. Treadmill studies have shown impaired blood-gas exchanges and higher blood lactate in horses with EIPH during exercise but the quality of evidence is very low.

bleeding by counting red blood cells in bronchoalveolar lavage fluid collected 1 hour after exercise but the strength of evidence is small because of the small sample size (3 studies; n = 46) and potential bias. Many other drugs have been investigated as prophylaxis for EIPH but all studies provide very low-quality evidence because of small sample size, exercise conducted on treadmill, or EIPH severity was not assessed. Furthermore, none of those studies demonstrated mitigating effects on EIPH.

Sudden death in racehorses occurs in 0.08-0.29 horses per 1000 starts. In a case series of Thoroughbreds that died suddenly within 1 hour of racing or training, 35% of deaths with a known cause were attributed to pulmonary hemorrhage (low-quality evidence). However, pulmonary hemorrhage may have been the primary cause of death or resulted from another cause of death (e.g. cardiac failure). In addition, there is no evidence that EIPH increases the risk of sudden death.

Four treadmill studies have shown that nasal strips resulted in a reduction of red blood cells in bronchoalveolar lavage fluid collected 1 hour after exercise, however, the strength of evidence is low.

Severe EIPH (grade 4 or epistaxis) is associated with shorter racing career but mild to moderate EIPH is not (moderate quality evidence). Studies have suggested that EIPH is a progressive condition related to career duration rather than age of the horse.

Effects of EIPH on Performance: Performance is difficult to measure in racehorses because there are many horse-related factors (e.g. gender, age, fitness level, horse quality) and external factors (e.g. jockey, track conditions, distance, environmental conditions, horse field) that may influence the outcome of the race. Therefore, it is important that studies attempt to control those factors in the analysis of data in order to compare performance between horses. Studies of higher quality conducted during normal racing have shown that EIPH is associated with worse-finishing (inferior position and farther-behind winner) and lower race earnings (moderate-quality evidence). Lower-quality studies failed to demonstrate an effect of EIPH on performance. There, lowquality evidence of a dose-response relationship between EIPH and performance, that is to say more severe EIPH, is associated with worse performance.

Prophylaxis for EIPH: There are no published studies on the effects of treatments aimed at decreasing severity of EIPH or progression of lung lesions in subsequent races. Similarly, no studies have examined if treatments or interventions during training may alleviate EIPH during subsequent racing. Therefore, we reviewed publications describing drugs or interventions administered prior to exercise in order to prevent EIPH. The outcome of interest (EIPH) was measured either by endoscopic visualization of blood in airways (yes/no or grading scale) or by quantifying red blood cells in bronchoalveolar lavage fluid following strenuous exercise. There is preponderance of evidence that administration of furosemide (0.5-1 mg/kg IV) 4 hours prior to exercise decreases the severity and the incidence of EIPH (high-quality evidence). The strongest evidence is coming from studies that quantified EIPH by grading bleeding in the trachea during endoscopy 1 hour following racing (2 studies; 422 horses). Some studies quantified WWW.FAEP.NET |

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Effects of Furosemide on Performance: Most studies conducted on racetracks have evaluated performance by measuring adjusted race time to cover a given distance. Treadmill studies have used distance covered or time to fatigue. The preponderance of evidence is that furosemide administered IV 4 hours prior to racing improves performance (moderate-quality evidence) and the magnitude of the effect varies from 0.12 to 1.1 s faster time per mile compared to horses not treated with furosemide.

References: 1. Hinchcliff KW, Couetil LL, Knight PK, Morley PS, Robinson NE, Sweeney CR, et al. Exercise induced pulmonary hemorrhage in horses: American College of Veterinary Internal Medicine consensus statement. J Vet Intern Med 2015 May;29(3):743–58. 2. Guyatt G, Oxman AD, Akl EA, Kunz R, Vist G, Brozek J, et al. GRADE guidelines: 1. Introduction-GRADE evidence profiles and summary of findings tables. J Clin Epidemiol. 2011 Apr;64(4):383–94.

Laurent Couetil, DVM, PhD, DACVIM (LA) Dr. Couetil is a professor of large animal medicine at Purdue University. He obtained his veterinary degree from the French National Veterinary School of Alfort and then worked for 6 years in equine private practice in Chantilly, France. Dr. Couetil completed a large animal medicine residency at Tufts University and a PhD in respiratory physiology at the University of Liege, Belgium. Dr. Couetil has been a faculty member at Purdue University College of Veterinary Medicine since 1995, where he is Director of the Equine Research Program and of the Equine Sports Medicine Center. Dr. Couetil is the current President of the Large Animal Internal Medicine specialty of the American College of Veterinary Internal Medicine (ACVIM). His research interest is investigating the causes and treatment of poor performance in athletic horses, in particular chronic respiratory diseases.

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Shivers and Other Movement Disorders STEPHANIE J. VALBERG | DVM, PhD, DACVIM, DACVSMR

Locomotion is a mechanically complex task that involves the precise activation and inhibition of many muscles, the pattern of which varies between gaits. The key features of simple forward gaits are rhythm, ipsilateral coordination of flexors and extensors across the same or different joints in a limb, as well as left/ right and fore/hind coordination. Pain can disrupt this pattern, causing classic signs of lameness, however, neural pathways can also be disrupted, resulting in a gait abnormality or movement disorder not associated with pain. At a spinal level, central pattern generators (CPGs) located in the thoracic and lumbar spinal cord afford the spinal cord nearly autonomous rapid control of basic locomotor rhythms. More complex locomotion requires adaptability from the simple and fast-acting, to the complex and long-lasting. Higher neural structures, including the brainstem, cerebellum, and motor cortex are required for more complex movement. Disruption in the function of one of these regions in the nervous system can produce movement disorders. Because movement disorders fall into a grey area between lameness and neurology, they remain poorly understood. The purpose of our research is to develop a clinical characterization of locomotor-induced movement disorders in horses and to identify pathophysiologic bases for these conditions.

Clinical Characterization of Movement Disorders The Neuromuscular Diagnostic Laboratory at the University of Minnesota solicited owners of horses with movement disorders, loosely termed Shivers, to fill in an on-line questionnaire and submit videos of their horses walking, turning, backing and lifting their limbs. Over 200 owners described their horses’ movement and many provided videos of their horses. Based on examination of this material, several distinct categories of movement disorders were apparent.[1] 1. Dystonia of the head and neck • Resistance to manual flexion of either forelimb • Trembling of the forelimb once flexed • Patterned extension and twisting of the neck to one side with movement of the lips and eyelids when forelimb is manually flexed • Normal backwards and forwards walking 2. Hyperflexion of a hindlimb • Occurs when manually picking up the limb • Normal backwards and forwards walking 3. Hitch • Hyperflexion of the hindlimb, a pause and then placement at a normal speedback to the ground • Occurs intermittently for a few strides when walking forward • Backwards walking occurs normally and willingly

18 The Practitioner

Fig. 1: Shivers Side View 4. Stringhalt • Rapid hyperflexion of the limb forward and under the belly while walking forward followed by a return of the limb to the ground • Abnormal movement occurs for most strides when walking forward and occurs walking backward • Horses often resemble a Shivers horse when walking backward • Hyperflexion usually persists at a trot • May be bilateral or unilateral The above movement disorders were not classified as "Shivers” as there could be many different neural or pain pathways that contributed to the abnormal movement. For the purposes of our research, Shivers was defined as a disorder that always affected the ability to walk backwards. 5. Shivers • Occurs with backwards walking especially if horse has been standing still,transported or stressed • Forward walking and trotting are normal in early stages • Difficulty with farrier work due to inability to hold limb flexed when standing • Backwards walking occurs with resistance and reluctance • Hyperflexion: Hyperflexion and abduction of the hindlimb, muscle trembling of the flexed hindlimb, a pause and then placement at a normal or slightly increased speed back to the ground when walking backwards • Hyperextension: in this alternative form, hyperextension of the hindlimb occurred causing extreme difficulty flexing to move backwards and a shuffling backward gait of only a few strides. 6. Advanced Shivers • Hyperflexion and abduction of the hindlimb, muscle Issue 1 • 2016

trembling of the flexed hindlimb, a pause and then placement at a rapid speed back to the ground when walking backwards • Alternatively, hyperextension of hindlimbs and inability to flex the limb or to walk backwards • Occurs consistently with backwards walking, when pushed sideways, when turned sharply or for a few strides walking forward • Backwards walking occurs with resistance and reluctance • Trotting is unaffected • Inability to trim hind feet because horse cannot hold the limb flexed and will slam the foot to the ground • Occasional tremor of upper lip

Epidemiology of Shivers In our epidemiologic study of Shivers, we found that clinical signs often began at < 7 yrs and progressed in 74% of cases.[2] Owner-reported additional clinical signs included muscle twitching (85%), muscle atrophy (44%), reduced strength (33%) and exercise intolerance (33%). Shivering horses were significantly taller (>16.3 hands high) with more geldings affected than mares. No potential triggering factors or effective treatments were reported. We concluded that Shivers is a chronic, often gradually progressive movement disorder that usually begins before 7 years of age with a greater prevalence in tall male horses.

common pathologic abnormality in many regions of the central nervous system of both control and Shivers horses. Using special immunohistochemical stains (calbindin stain), 80-fold more degenerative axonal swellings (spheroids) were found in Purkinje cell axons within the deep cerebellar nuclei of horses with Shivers when compared to controls. The immunohistochemical and ultrastructural characteristics of the lesion combined with their functional neuroanatomical distribution indicate, for the first time, that Shivers is characterized by end terminal neuroaxonal degeneration in the deep cerebellar nuclei, which results in context-specific hypermetria and myoclonus.[3]

References:

1.Draper A.C., Trumble T.N., Firshman A.M., Baird J.D., Reed S., Mayhew I.G., MacKay R.,and Valberg S.J. (2015). Posture and movement characteristics of forward and backwardwalking in horses with shivering and acquired bilateral stringhalt. Equine Vet. J. 47: 175-181. 2. Draper ACE, Bender JB, Firshman AM, Baird JD, Reed S, Mayhew IJ and Valberg SJ. Epidemiology of Characterisation of Shivers in Horses Equine Vet J 2015 Mar;47(2):182-7. 3. Valberg S.J., Lewis S.S., Shivers J.L., Barnes N.E., Konczak J., Draper A.C., and ArmienA.G. (2015). The Equine Movement Disorder "Shivers" Is Associated With SelectiveCerebellar Purkinje Cell Axonal Degeneration. Vet. Pathol. 2016 Jan;53(1):77-86.

Pathophysiologic Basis for Shivers Given that neither the neurophysiological nor the pathological mechanisms of Shivers were known and no neuroanatomical locus of the disease had been identified, we undertook a detailed analysis of the central nervous system and skeletal muscles of horses with Shivers and clinically normal control horses. No abnormalities were identified in the examined hindlimb and forelimb skeletal muscles or the associated peripheral nerves. There was no evidence of polysaccharide storage myopathy in any Shivers case. Axonal swellings were a

Stephanie J. Valberg DVM, PhD, DACVIM, DACVSMR Stephanie Valberg is Mary Anne McPhail Dressage Chair in Equine Sports Medicine, McPhail Equine Performance Center, Michigan State University. She received her DVM from the Ontario Veterinary College and completed a PhD in equine exercise physiology at the Swedish University of Animal Science. She is a board certified internal medicine and sports medicine clinician. Dr. Valberg’s research centers on neuromuscular diseases in horses with a special focus on genetic diseases of skeletal muscle and their nutritional management. She was inducted into the Equine Research Hall of Fame in 2012, and has received several awards including British Equine Veterinary Association Clinical Award 2014, University of Minnesota’s Postdoctoral Mentor 2013, MVMA outstanding faculty award 2013, The 2012 Milne lecture at AAEP, the 2001 and 2010 Pfizer Award for Research Excellence, and the 1999 EquiSci International Award. Dr. Valberg has over 136 scientific publications and is a frequent speaker at national and international veterinary, nutrition and genetic conferences. She is an avid 3-day eventer with her 5- yearold Warmblood, Cajun.

Fig. 2: Shivers Rear View WWW.FAEP.NET |

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Ultrasound Examination of the Equine Digit RICHARD D. MITCHELL | DVM, MRCVS, DACVSMR

Introduction Ultrasound examination of the distal limb of the horse can contribute greatly to a correct and efficient lameness diagnosis. Once it has been reasonably established that the “digit” is the source of lameness, examination of soft tissue structures and bony surfaces can often be the ultimate means of diagnosing the issue(s) at hand. Ultrasound may be used as a stand-alone technique or in a complimentary fashion to radiography, scintigraphy or even magnetic resonance imaging.1 The bony structures of the digit involve the proximal phalanx (P1, long pastern bone), the middle phalanx (P2, short pastern bone), the distal phalanx (P3, coffin bone), and the distal sesamoid (navicular bone). Each of the articulations is supported by collateral ligamentous structures and fibrous joint capsules. The distal sesamoidean ligaments (as the extension of the suspensory apparatus) and the flexor tendons attach along the palmar aspect of the pastern and foot and provide support and flexor functions respectively. The dorsal digital extensor courses along the dorsal aspect, ultimately inserting on the extensor process of the distal phalanx.

axis with the SDFT becoming thinner distally and the DDFT becoming more superficial.3 Moving down the palmar aspect of the pastern along P1, the SDFT develops tear-drop-shaped medial and lateral branches which course abaxially to ultimately insert on the middle scutum which is attached to distal P1 and proximal P2. The more superficial PDAL can be difficult to see unless it is thickened in this region. The DDFT develops two distinct lobes and becomes somewhat thinner as it courses distally. The converging oblique distal sesamoidean ligaments (ODSL), which originated on the base of each proximal sesamoid, become evident on the medial and lateral aspects of the SDSL. These ligaments become thinner distally as they insert on the middle third of the palmar aspect of P1 deep to the SDSL. The synovial fluid (synovial plica) within the DFTS is visible between the DDFT and SDSL. Approaching the region of the proximal interphalangeal joint,

Examination Technique

Good knowledge of the anatomy is required to properly evaluate specific structures, but most of the tendinous and ligamentous structures may be readily imaged.2 Distal sesamoidean ligaments, collateral ligaments, and flexor tendons are easily evaluated with a 7.5-12 MgHz linear transducer. Clipping and washing the skin will greatly enhance the ability to view structures. Because structures are fairly superficial, a silicone stand-off pad is often best employed to get a superior view, but it really depends on the depth of the structure of interest. The palmar, medial, lateral and dorsal pastern as well as the dorsal coronet may be examined. The hoof wall limits access to structures within the hoof capsule. The proximal aspect of the navicular bone, the bursa and collateral sesamoidean ligaments may be visualized with an 8-10 MgHz microconvex probe placed between the bulbs of the heel in either a transverse or longitudinal (sagittal) orientation. The palmar aspect of the hoof, with some trimming and soaking preparation of the frog, may be examined by a transcuneal approach. It is possible to visualize the distal deep digital flexor tendon (DDFT), the navicular bone and the insertion of the DDFT on P3 using a linear or curved array ultrasound probe. Beginning with the proximal palmar pastern (P1) in the transverse plane, the superficial digital flexor tendon (SDFT) may be viewed as a crescent shaped homogenously echogenic structure bordered exteriorly by a thin (0.3-0.6 mm) proximal digital annular ligament (PDAL). The SDFT partially surrounds the DDFT which has an oval shape. The DDFT is separated from a deeper straight distal sesamoidean ligament (SDSL) by an anechoic zone that is the fluid in the digital flexor tendon sheath (DFTS). The structures may also be visualized in the longitudinal 22 The Practitioner

Fig. 1 - Paired images of the LF and RF palmar pasterns of a horse with RF lameness. The SDSL demonstrates a significant hypoechoic region; medial is to the left. the branches of the SDFT are no longer visible on the palmar aspect of the pastern and the bi-lobed DDFT is very superficial just under the skin. A small amount of fluid may be evident superficial to the DDFT. The SDSL becomes thicker and more hypoechoic as it attaches to the middle scutum. The branches of the SDFT may be followed along the palmarolateral and palmaromedial aspects of the pastern to their insertions on the middle scutum. The axial and abaxial palmar ligaments of the pastern joint may be seen deep and abaxially to the SDSL, coursing from the palmar aspect of P1 to the middle scutum. These ligaments may be difficult to discern. The DDFT courses distally over the palmar surface of the middle scutum still with a bi-lobed appearance and continues to the palmar aspect of P3. Structures just proximal of the middle scutum may be clearly visible with a linear array probe in both transverse Issue 1 • 2016

and longitudinal planes, however further examination of the pastern at the level of the middle scutum and beyond may only be accomplished with the longitudinal view of the linear probe (level of the middle scutum) or with a micro-convex array probe (distal to the middle scutum). Distal to the proximal interphalangeal joint the DDFT continues within the digital sheath surrounded superficially by the distal digital annular ligament (DDAL) that is quite thin (0.5mm) and difficult to discern. On transverse view, the bi-lobed structure of the DDFT can easily be seen, and it may be possible to identify the fibrocartilaginous part of the DDFT as it slides over the proximal aspect of P2. Moving down the pastern the view will be through a portion of the digital cushion looking at the DDFT, the navicular bursa, the collateral sesamoidean ligaments and the proximal recess of the distal interphalangeal joint (DIPJ/coffin joint). Coursing further distally, the view will be through the digital cushion looking at the DDFT and the surface of the navicular bone. Depending upon fluid content, the navicular bursa may be evident. Turning the probe 90 degrees will allow for an excellent view, in the sagittal plane, of the DDFT, distal extent of the DFTS, the DDAL, the DDFT, the proximal recess of the navicular bursa, the collateral sesamoidean ligaments, the proximal margin of the navicular bone, and the proximal recess of the DIPJ.4 Remaining structures of the palmar foot will be examined via the transcuneal view and will be discussed later in this paper. The “palmarocollateral” (palmar medial and lateral) aspects of the pastern may be examined to view proximal aspects of the

Fig. 3 - Medial and lateral branches of the SDFT of the left fore. The image on the right demonstrates a significant hypoechoic lesion in the lateral branch. dorsal. The course is slightly cranial to caudal as well as proximal to distal. Structures of importance on the dorsal aspect of the pastern include the dorsal digital extensor tendon, the PIPJ, and the DIPJ with the extensor process. A fibrous pad is seen associated with

Fig. 3 - Transverse views of the collateral ligaments of the PIPJ; the image labeled left lateral demonstrates enlargement and a hypoechoic core lesion within the ligament (ligament is outlined).

Fig. 2 - Parasagittal distal palmar pastern view with microconvex probe. Heavy white arrow denotes the proximal border of the navicular bone, yellow arrow, the collateral sesamoidean ligament, light white arrow, DDFT; dorsal is to the left. ODSLs as they course distally from the base of each proximal sesamoid and also the extensor branches of the suspensory ligament as they course distally and dorsally. As previously mentioned, the branches of the SDFT can be seen to develop as tear-drop-shaped structures on transverse view coursing distally to blend into the middle scutum. The examiner needs to keep in mind to look more laterally and medially to avoid missing lesions of the branches of the SDFT. The collateral view (medial and lateral) allows for visualization of the collateral ligaments of the pastern joint. These ligaments may seem somewhat more distal than expected and perhaps less WWW.FAEP.NET |

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the dorsal recess of the DIPJ. Ultrasound is quite sensitive in detecting early bone changes of osteoarthritis in either joint or extensor process fragments in the DIPJ. While over the DIPJ, the collateral ligaments of the joint may be examined. The window for viewing the ligaments is fairly small on the coronet band right at the periopal, dorsomedially and dorsolaterally. If viewing the foot from above, picture the coronet as a clock and the extensor process as twelve o’clock. The proper points of view are at ten o’clock and two o’clock. In viewing the ligaments in cross-section, the ultrasound probe is held slightly above parallel to the bearing surface. In viewing the longitudinal fiber pattern, the probe is held perpendicular to the bearing surface (not parallel to the long axis of the pastern). Suspected lesions in each ligament should be compared to the opposite ligament and the same ligament on the opposite foot for best confirmation. The entire course of the collateral ligaments cannot be visualized as the insertion is deep within the hoof wall on P3 but a good indication of their structure can be determined. The palmar aspect of the foot may be examined by a transcuneal approach to visualize the distal DDFT, the navicular bone and the insertion of the DDFT on P3.5 This will normally require some preparation and can be a frustrating exercise on a hard, dry foot

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 23

Fig. 4 - Collateral ligaments of the DIPJ in transverse and longitudinal views. The white arrows demonstrate fiber pattern disruption.

Fig. 5 - Transcuneal view and anatomical specimen demonstrating fibrocartilaginous (right side arrows in each image) and fibrous portions of distal DDFT at semilunar crest (left arrows).

structure. Trimming and soaking the foot in advance is advised. This author most frequently uses a wet clay poultice with plastic wrap overnight or all day and then washes and trims the foot to soft moist tissue before attempting to examine it. A broad flat frog is the best window, while a narrow frog with a deep central sulcus makes visualization difficult. A 7-8 MgHz linear probe, or a similar curved array probe, can provide an excellent view of the corium of the frog, the DDFT, the flexor surface of the navicular bone, the distal sesamoidean impar ligament and P3. View orientation can be in longitudinal (sagittal) or transverse planes. The fibrocartilaginous portion of the DDFT at the flexor surface of the navicular bone will be anechoic normally while the fibrous portion at the insertion on P3 should be more echoic. Distal navicular border fragmentation and DDFT insertional tendinopathies may be detectable.

Conclusion

Once lameness is localized to the region, ultrasonographic examination of the equine digit, either as a stand-alone technique or in combination with other modalities, can be a very effective means of elucidating probable causes. The sonographic techniques mentioned in this article can greatly enhance the accuracy and sophistication of possible field diagnoses for the veterinary practitioner.

Reference

1. Mitchell, RD, Distal limb lameness in the sport horse-a clinical approach to diagnosis, Proceedings, AAEP, Dec 7-11, 2013, pp 244-249

24 The Practitioner

2.Denoix, J-M, Lecture notes from “The foot and pastern,” International Society of Equine Locomotor Pathology, July 11-13, 2014, Newtown, CT, USA 3. Coudry, V, Denoix, J-M, Ultrasonographic examination of the palmar aspect of the pastern of the horse: Digital flexor tendons and digital sheath, Equine Vet Educ, April, 2013, pp 196-202 4. Bolen, G, Busconi, V, Jacqmot, O, Snaps, F, Sonographic anatomy of the palmarodistal aspect of the equine digit, Vet. Radiology and Ultrasound, Vol. 48, No.3, 2007, pp 270-275 5. Jacquet, S and Denoix, JM, Ultrasonographic examination of the distal podotrochlear apparatus of the horse: A transcuneal approach, Equine Vet Educ, Feb 2012, pp. 90-96

Richard D. Mitchell, DVM, MRCVS, DACVSMR Dr. Rick Mitchell graduated from the Oklahoma State University College of Veterinary Medicine in 1974. He served on active duty in the USAF Veterinary Corps for two years following graduation and then began private practice in Connecticut with his mentor, Dr. Howard Raven in 1976. Dr. Mitchell is currently a part owner of Fairfield Equine Associates in Newtown, CT and practices equine medicine and surgery with an emphasis on lameness and imaging. He is internationally certified in veterinary acupuncture and equine locomotor pathology and completed requirements for Diplomate status in the American College of Veterinary Sports Medicine and Rehabilitation (ACVSMR) in 2015. Dr. Mitchell has been involved in national and international equine competitions as both a rider and veterinarian, has won two national championships and one world championship in various disciplines, and has authored multiple nationally- and internationally-published articles and textbook chapters on equine health care.

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