Practitioner Issue 3, 2016 by FVMA

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 3 • 2016 FOOT LAMENESS IN THE SPORT HORSE -A CLINICAL APPROACH TO DIAGNOSIS

RICHARD D. MITCHELL | DVM, MRCVS, DACVSMR, CERT. ISELP

EQUINE RESCUE - MANAGING A DOWN HORSE AT AN EVENT - PARTS 1 & 2 NATHAN M. SLOVIS | DVM, DACVIM, CHT

Your Invitation to Attend

54thANNUAL OCALA

EQUINE CONFERENCE

EQUINE FOOT SYMPOSIUM

JANUARY 20–22, 2017 | OCALA, FLORIDA

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

Dear Fellow Equine Practitioners, I am very happy to report, as we’ve just concluded the 12th Annual Promoting Excellence Symposium, that the symposium was a great success and proved to be of tremendous value to all who attended. Despite the unforeseen challenge of a Zika epidemic taking hold in our host island paradise, veterinarians and vendors gathered in our exotic venue, San Juan, Puerto Rico, for five days of world-class CE and an excellent networking opportunity with fellow industry professionals from near and far. Now, we have turned our complete attention to our yearly CE offering in the “horse capital of the world,” Ocala, Marion County, Florida. We have combined the upcoming conference in January, with the FAEP Equine Foot Symposium, to offer a dynamic continuing education program on equine clinical practice and farriery. We last held our Foot Symposium, which focuses exclusively on the equine foot, in 2014, when a decision was taken to offer this unique program biennially. Its coupling with the 54th Annual Ocala Equine Conference from January 20-22, 2017, will bring members of the equine health care team together for the highest-quality educational exchange, while at the same time, focusing on fostering the veterinarian and farrier relationship. Save the date for the 54th Annual Ocala Equine Conference & Equine Foot Symposium. Be sure to register early to take advantage of discounted registration rates; and make accommodation reservations at the Hilton Ocala early to ensure you stay at our host hotel. We have included the Ocala conference program with its diverse offerings in dermatology, endocrinology, equine ultrasound and dentistry, and topics about farriery practice in this issue, as our center gatefold. It offers a glimpse of the renowned veterinary-farrier team, Dr. Jessica and Dallas Morgan CJF, and veterinarian-farrier Dr. Vern Dryden, who will headline an impressive lineup of world-class speakers and wet lab instructors which include Drs. Jack Easley, Toots Banner, Scott Marx, Jeremiah Easley, Martha Mallicote, Kent Allen, Tim Lynch, Pat McCue, Josie Traub-Dargatz, Suzi White, Ruth-Anne Richter and Aric Adams. We hope to see you in Ocala in January as we launch an exciting 2017 season, and invite you to get in touch if you have any questions about the FAEP and the services we provide, and about our conferences. We welcome your comments and suggestions, and encourage you to make contact with our council members or the FVMA/ FAEP staff, toll free, at 1(800) 992-3862.

EXECUTIVE COUNCIL

Ruth-Anne Richter FAEP Council President 2016

Corey Miller,

DVM, MS, DACT FAEP COUNCIL PAST PRESIDENT

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

cmiller@emcocala.com

Armon Blair, DVM abeqdoc@aol.com

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

Adam Cayot, DVM adamcayot@hotmail.com

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

Jacqueline S. Shellow, DVM, MS jackie@shellow.com

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

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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

Foot Lameness in the Sport Horse -A Clinical Approach to Diagnosis RICHARD D. MITCHELL | DVM, MRCVS, DACVSMR, CERT. ISELP Take Home Message

Diagnosis of lameness related to the distal limb requires a thorough clinical examination, including careful palpation, manipulative tests, hoof tester evaluation, examination of the horse in hand and under saddle, and regional anesthesia. Specific causative lesions may require technical imaging modalities to fully evaluate.

high-level sport result in more concussion, as well as greater extension and flexion, than casual exercise. Fatigue may not be as significant a factor in injuries of the sport horse compared to racing horses, but chronic, repetitive trauma most assuredly is a factor.

History and Clinical Signs

Introduction

Distal limb lameness may present in a peracute fashion, with extreme discomfort, such as with a P3 fracture or foot abscess, but more often, signs may be more subtle, with the horse having a subtle lameness that changes somewhat with work. “Gee doc, he feels tight in his shoulders,” is a frequent comment for more insidious forms of early front distal limb lameness. Distal hind limb issues may mimic more commonly thought-of conditions such as distal tarsitis or proximal suspensory desmopathy, in that the horse is “weak” behind and may “warm out” of the lameness. Some heat, swelling or increased digital pulse may be perceived in the distal limb, but often this is not the case. The current competitive environment in North America often allows for NSAID use in competing horses; horses with mild distal limb pain are able to compete comfortably. However, when Monday morning Anatomy and Risk Factors rolls around and the effects of the NSAIDS are gone, the horse For purposes of this discussion, the author will address the is suddenly more uncomfortable than prior to the event. This anatomical region distal to the fetlock. The bony structures presents a good opportunity to investigate the case. involve the proximal phalanx (P1, long pastern bone), the Horses may present with a unilateral lameness of varying middle phalanx (P2, short pastern bone), the distal phalanx degrees (0-5/5), or appear bilaterally lame, especially if circled (P3, coffin bone), and the distal sesamoid (navicular bone). or ridden, which will be discussed later. Some lameness may Each of the articulations is supported by collateral liga- be very subtle and will require special efforts to make it more mentous structures and fibrous joint capsules. The distal apparent for an objective diagnosis. Many horses vary in their sesamoidean ligaments (as the extension of the suspensory degree of lameness, improving profoundly with a few days off. apparatus) and the flexor tendons attach along the palmar aspect of the pastern and foot, and provide support and flexor Physical Examination functions respectively. The dorsal digital extensor courses This author is of the opinion that it is essential to have along the dorsal aspect, ultimately inserting on the extensor periodic veterinary inspections of the training sport horse, process of the distal phalanx. in order to catch subtle lameness and performance problems The distal limb plays a significant role in adaptation to before they become serious clinical issues. Although many footing and shock absorption in the working horse. Foot trainers and owners are very adept at catching subtle soundbalance, both medial/lateral and dorsal/palmar, can have ness and health-related issues, many things may be overa profound effect on the excursion of joints and the stress looked by the individual that sees the horse every day. Recent on soft tissues of the distal limb. Footing surfaces that are reviews suggest that lameness may exist in presumably sound very hard, excessively soft or unstable can result in aberrant horses, when examined with close scrutiny.1 Periodic veterimotion and stress that may result in injury. The demands of nary inspection should include a general health check and a Today’s high level sport horse represents a significant investment of time and money. High level show jumpers, dressage horses and western performance horses often take several years to train to their upper levels, and injuries or illness can substantially affect the time to produce a winning horse. Owners and trainers are concerned that these horses receive the best possible care without excess expenses and down time. The veterinary care of such horses should take a proactive approach to lameness diagnostics of the horse in training, not simply one of attending to lameness after it occurs. Recognition of potentially serious distal limb lameness early on may prevent significant loss of training and competition time, as well as extend the horse’s career.

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thorough lameness evaluation. The frequency of these exams will be somewhat dependent upon the age and activity of the horse, but two to four times yearly should be a minimum. Horses with successfully managed orthopedic disease may need to be checked more often. A typical lameness examination should first involve a thorough visual exam of the horse, taking notice of body symmetry and muscle structure. Observing the horse in its stall may give the examiner some clues regarding the horse’s level of comfort. Watching the horse step out of its stall may give big clues about chronic lameness issues. After the visual inspection, a palpation examination should be performed. The author uses a modification of an “acupuncture” examination that allows for complete palpation of the horse, while eliciting responses from potentially painful areas. Careful inspection of the feet for balance and symmetry should be performed. Flexion manipulations can then be performed in a “passive” sense (not asking the horse to walk or jog away), while noting any resistance or painful responses. It may be appropriate to use hoof testers at this point, before starting any exercise. Next, the horse can be moved in hand at a walk and trot, taking note of any obvious lameness or unusual foot flight or limb motion. It is useful to see the horse walk in circles, as well as on a straight line. Likewise, jogging the horse in circles, as well as in a straight line, may provide much more insight related to the horse’s level of comfort. For the fractious horse, jogging in hand on circles may be an acceptable alternative to lunging. The author frequently gives a small dose of sedative (detomidine hydrochloride, 1.5mg total dose)a to evaluate lameness if the horse is not well-behaved. Watching the horse move in straight lines and circles on both hard and soft footing can be immensely valuable in detecting lameness. The next step is to perform “active” flexion tests of all limbs. These may give clues to soreness that is not otherwise evident. It may be worth pursuing some positive flexion responses or readily apparent lameness at this point, while simply recording some others for future reference. Keep in mind that a positive distal limb flexion may indicate a problem in any number of places, from the distal interphalangeal joint (DIPJ) to even a suspensory ligament issue. It’s a tool for regionalization. “Wedge” tests are sometimes useful to aide in localization of the source of lameness. A reverse wedge that stretches the deep digital flexor tendon (DDFT) may increase a lameness related to that structure, while a wedge placed laterally under the foot, for example, may stretch the medial collateral ligament of the DIPJ and increase lameness if that structure is injured. Care should be taken to not over exert the very lame horse until a good sense of the nature of the problem is recognized.

8 The Practitioner

A detailed record of observations should be maintained for each examination. Following flexion tests, it is advisable to observe the horse work on a lunge line and under saddle. Some horses are difficult to lunge and may pose a hazard for injury to horse and handler. These horses should be lightly sedated or simply watched under tack. Many lameness conditions are not otherwise apparent until a rider is aboard and/ or the horse is asked to do more work.1 The riding examination may give the veterinarian a great deal of information not otherwise apparent, during the inhand exam. Rider weight may change the balance of the horse in such a way as to augment lameness. Weight on the back may be the source of discomfort and may be demonstrated by a change in the shape of the back, height of head carriage, shortening of stride, or disobedience. The horse should be asked to perform the various gaits while under saddle and carefully observed for changes in the level of lameness with each gait, transitions from one gait to another, and at directional changes. It is very important to consider more than just the “limbs” when searching for the answer to lameness and performance problems. Axial skeletal issues may arise that can produce serious limitation in function and may cause diminished function that mimics distal limb lameness. Conversely, chronic distal limb lameness may alter the function of the spine, resulting in pain and tension in the back. At this stage, the examiner should have a good sense of the state of the horse’s soundness and may proceed with more diagnostics such as nerve blocks, radiography, or ultrasound. When performing diagnostic blocks, the practitioner should be mindful of the seriousness of the lameness, and care should be taken regarding the activity level of the horse, following the administration of nerve blocks. The horse may further damage itself on an anesthetized limb, so activity should be carefully controlled. Diagnostic blocks are, nonetheless, esential in a good lameness workup, and should be employed as often as possible, to give more insight as to the locus of the lameness. Many lameness conditions look alike and flex alike, however, they are not of the same origin. If the lameness is of sufficient grade to produce a clear contrast and has not been reduced by exercise, i.e. warming up, the examiner would be wise to pursue the lameness with diagnostic nerve blocks. Once localized, further physical examination, radiographs, and diagnostic ultrasound may further elucidate the nature of the problem. In some cases, physical examination and diagnostic imaging may be sufficient to clearly define the diagnosis, and in such cases, nerve blocks may not be required, allowing the veterinarian to proceed with appropriate herapy. More complicated cases may require more advance imaging techniques, such as nuclear scintigraphy, magnetic resonance imaging (MRI), or computed tomography (CT).

Issue 3 • 2016

Diagnostic Anesthesia

Distal limb regional anesthetic techniques are reasonably simple, not terribly time-consuming to perform, and applicable for use except for the most fractious of horses. Mild sedation of the more difficult horse may aide the process and still permits a working examination as previously mentioned. The distal digital nerve block (posterior digital block) should be the initial block done just proximal to the level of the collateral cartilage.2 While much has been written in recent years about its lack of specificity, this block still provides a reliable indicator that the lameness is emanating from the foot. Using a smaller amount of anesthetic agent (mepivicaine 2%)b such as 1.5-2ml over each nerve will provide a reliable anesthetic effect at 5-8 minutes with less probable “drift.” Checking the foot with hoof testers prior to, and after the block, will ensure its efficacy. One may wish to block only one nerve at a time if hoof testers indicate significant asymmetrical pain, however, failure of this block does not eliminate the possibility of an asymmetrical cause, in this author’s experience. The sole region, podotrochlear apparatus, and DIPJ may be anesthetized with this block most commonly. Occasionally, some improvement of proximal interphalangeal joint (PIPJ) related lameness may be produced by this block, most likely due to the close proximity of the large palmar pouch of that joint. Lack of response to the distal digital nerve block does not rule out the foot as a source of lameness. There are multiple options for anesthetic techniques at this point. One may elect to simply move more proximally to the proximal digital nerve block or abaxial/basi-sesamoid block just distal to the fetlock joint. This block may effectively anesthetize the more dorsal structures of the digit that are sometimes missed

with the distal digital nerve block, however, more proximal regions, such as the fetlock joint and associated anatomy, may be affected.3 Intra-articular anesthesia of the DIPJ with 5 ml of anesthetic agent may render the horse sound when the distal digital block did not. This is certainly more confining to the foot, but not specific to the DIPJ, because the distal aspect of the deep digital flexor, navicular impar ligament, and navicular bone may be anesthetized as well. It has been reported that horses demonstrating MRI evidence of DDFT lesions do not reliably improve with palmar digital anesthesia, but 68% are improved with anesthesia of the distal interphalangeal joint.4 Also, deeper subchondral trauma may be slow or incomplete to block with the intra-articular approach. It has been proposed that lameness related to the distal DDFT may be diagnosed with an intrathecal block of the distal digital tendon sheath (3-5 ml), and certainly this may be true, but it must be kept in mind that this anesthetic technique can affect other structures on the palmar pastern.5 Potentially affected, would be the navicular bursa and various structures on the palmar aspect of the pastern, i.e., straight distal sesamoidean ligament (SDSL) and middle scutum, and other structures more proximally associated with the digital sheath. Anesthesia of the navicular bursa may be performed accurately using radiographic or ultrasound guidance in a compliant patient. Three ml of anesthetic agent is sufficient to establish a block. The author prefers to perform this block with the limb held up by an assistant using a previously described navicular position technique,6 and confirmed by imaging. This block is certainly specific to the foot and is a good indicator of problems in the podotrochlear apparatus.

Figure 1: Demonstrating sonographic transcuneal view and comparative anatomy

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FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 9

Figure 2: Radiograph of navicular bone and corresponding scintigraphy with IRU The PIPJ may be selectively anesthetized also with either dorsal or palmar approaches, the latter being the author’s preference. The large palmar pouch of the PIPJ reliably yields synovial fluid, and 5 ml of anesthetic will effectively block the joint in 5-8 minutes. The approach is oblique, avoiding the DDFT and SDSL. There is the potential to block other structures on the palmar pastern. Ring blocks of the proximal pastern are probably the most inaccurate and subject to the most “drift” proximally, and rarely used by this author for diagnostics distal to the fetlock; however, they can be an additional means of blocking the dorsal pastern.

block results, and more thorough physical examination may reveal information concerning conditions of the hoof capsule and sole, along with some issues more proximally in the digit; but it’s most likely that some form of technical imaging will need to be utilized to identify the origin of the lameness. The more common issues to consider are: 1. Solar bruising, abscesses, keratoma 2. Sheared heel syndrome 3. P3 trauma/inflammation or rotation (positive, negative and possible laminar tearing) 4. Desmopathy of the DIPJ collateral ligaments 5. Synovitis of the DIPJ 6. Navicular bone/bursal inflammation/navicular impar desmopathy Differential Diagnosis 7. DDFT tendinopathy (including dorsal fibrillation, core Having established that the site of the lameness is the distal lesions and enthesiopathy) limb, the next step is to consider the differential diagnosis for 8. Collateral sesamoidean and chondrocoronal desmopathe various issues in this region and the imaging techniques thy that can further establish a diagnosis. The most important 9. Desmopathy of the distal digital annular ligament imaging technique is simply thorough observation. Removal 10. Inflammation of the pastern joint (PIPJ) and associof the shoe certainly is the first of these techniques, and may ated collateral and palmar ligaments reveal a great deal. Foot symmetry, obvious deformity and 11. Trauma to the middle scutum readily-apparent pathology may establish a diagnosis without 12. Desmopathy of the various distal sesamoidean ligatechnical imaging. It’s probably not indicated to immediments ately move to radiographic imaging of an acute abscess or 13. Subchondral bone trauma/inflammation in any of heel bruise, but if these prove refractory to treatment, then the articulations imaging is indicated. A profoundly painful distal limb with 14. Consider the possibility that some fetlock region isno other apparent pathology is a candidate for immediate sues will occasionally improve with proximal digital radiographic imaging, at the very least. nerve blocks. The myriad of potential conditions and injuries that can Some of these conditions may be a straightforward visual/ affect the distal limb may easily escape the power of simple physical diagnosis, but most will require some degree of techobservation. Careful assessment of flexion responses, nerve

10 The Practitioner

Issue 3 • 2016

Figure 3: MR images demonstrating navicular bone lesions and DDFT core lesion nical imaging to elucidate. Most often, the above-mentioned conditions occur in various combinations related to function, foot balance and discipline.

best utilized. Areas of increased radioisotope uptake (IRU) are characteristic to some structures in working horses, and knowledge of this is required8, but this imaging modality can be extremely helpful in evaluating the findings of other modalities, such as radiography and ultrasound. A suspicious Imaging looking navicular bone that demonstrates dramatic IRU has Radiography still remains the gold standard for imaging of more clinical significance. the equine distal limb. Fractures, osteoarthritis, enthesiopaIn recent years, MRI has become more available to many thies, P3 rotation and malposition, advanced subchondral equine practitioners for lameness evaluation. It’s not a rebone changes, and dystrophic mineralization are frequently gionalization tool, but the sensitivity is excellent. Soft tissue detected in this manner. Many soft tissue abnormalities may issues not otherwise apparent, may be readily visible with escape detection with radiography, but some subtle signs of problems may be evident. Today’s digital radiography MRI. Bone inflammation, especially early, is often evident equipment can be very sensitive and the detail of images with MRI long before any appreciable radiographic changes are evident. The advantage in this, is that detection of bone can be very revealing. Ultrasound can be the next step in evaluating problems of trauma and inflammation at an earlier stage, may reduce the distal limb. Good knowledge of the anatomy is required the likelihood of further damage by virtue of misdirected 9 to properly evaluate the structures, but most of the tendinous treatment modalities and exercise management. The use of and ligamentous structures may be readily imaged. Collateral computed tomography (CT) and especially contrast CT, has ligament desmopathies and flexor tendon injuries are easily a similar application as MRI. evaluated with a 7.5-12 MgHz linear transducer. The palmar pastern, dorsal pastern and dorsal coronet may be examined. Conclusion Today’s sport horse represents a significant economic The palmar aspect of the foot, with some trimming and soakand emotional investment for the horse owner. Precise and ing preparation of the frog, may be examined by a transcuneal approach, to visualize the distal DDFT, the navicular bone accurate diagnosis that is done in an efficient and thorough and the insertion of the DDFT on P3.7 The proximal aspect fashion is essential and will be appreciated by the client. of the navicular bone, the bursa, and collateral sesamoidean The modern private practitioner has many basic skills that ligaments may be visualized with an 8-10 MgHz microconvex should be included in the basic work-up of a lameness case, before embarking upon advanced-level imaging. Advanced probe placed between the bulbs of the heel. imaging modalities can ultimately lead to a very accurate Nuclear scintigraphy is very useful in further regionalizing the source of the lameness. It can be very helpful in determin- and time-efficient diagnosis. ing what other diagnostics or imaging modalities might be Continued on Next Page

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OSPHOS® (clodronate injection)

References: 1. Dyson S, Greve L, Subjective gait assessment of 57 sports horses in normal work: a comparison of the response to flexion tests, movement in hand, on the lunge and ridden; JEVS 38 (2016) pp 1-7 2. Schumacher J, Taylor DR, Schramme MC, Schumacher J, Localization of pain in the equine foot emphasizing the physical examination and analgesic techniques. In: Proceedings. Am Assoc Equine Pract 2012; 58:138-156 3. Daniel AJ, Judy CE and Saveraid T, Magnetic resonance imaging of the metacarpo(tarso)phalangeal region in clinically lame horses responding to diagnostic analgesia of the palmar nerves at the base of the sesamoid bones: Five cases, EVE (May 2013) pp. 220-228 4. Dyson S, Murray R, Schramme M, and Branch M, Lameness in 46 horses associated with deep digital flexor tendinitis in the digit: diagnosis confirmed with magnetic resonance imaging, Equine Vet J (2003) 35 (7) 681-690 5. Schramme, MC, Deep digital flexor tendonopathy, Equine Vet Educ, August 2011, 403-415 6. Schramme, MC, An in vitro study to compare 5 different techniques for injection of the navicular bursa in the horse, Equine Vet. J (2000) 32, (3) 263-267 7. 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 8. Dyson SJ, Martinelli MJ, (2003) Image description and interpretation in musculoskeletal scintigraphy. In: Equine Scintigraphy, Eds: SJ Dyson, RC Pilsworth, AR Twardock, M Martinelli, EVJ, Newmarket, Suffolk, pp.89-91 9. Mitchell, RD, Edwards, R B, Makreel, LD, and Oliveira, TD, (2006) Standing MRI lesions identified in jumping and dressage horses with lameness isolated to the foot. In: Proceedings. Am. Ass. Equine Pract.52, 422-426 a Dormosedan®, Pfizer Animal Health, Exton, PA, USA 19341 b Carbocaine®-V, Pharmacia and Upjohn Company, Division of Pfizer Inc., NY, NY 10017

Richard "Rick" D. Mitchell, DVM, MRCVS, DACVSMR, Cert. ISELP

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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 has been 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.

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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Patterson Veterinary’s Equine Division focuses solely on horses. Our equine specialists are dedicated industry professionals who know your business and provide an unmatched level of service.

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So when it comes to choosing a partner for your practice, make sure you put the emphasis on equine with Patterson Veterinary’s Equine Division.

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OUR DISTINGUISHED SPEAKERS WEPX-1 Wireless portable x-ray system

EPX-1

portable x-ray system

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MARTHA MALLICOTE DVM, DACVIM

SCOTT MARX DVM

PAT MCCUE DVM, PhD, DACT

SPONSORED BY:

JESSICA MORGAN DVM, Cert. ISELP

DALLAS MORGAN CJF

ADDITIONAL SPONSORS:

CECredits

RUTH-ANNE RICHTER BSc (Hon), DVM, MS

JOSIE TRAUB-DARGATZ DVM, MS, DACVIM

556 Morris Avenue • Summit, NJ 07901 • merck-animal-health-usa.com • 800-521-5767

SUZI WHITE DVM, DACVIM

COMPREHENSIVE EQUINE ULTRASOUND WET LAB

51358 Flu Avert HP Ad.indd 1

FRIDAY, JANUARY 20, 2017 | 8:15 AM - 4:30 PM STATION 1: Hind Suspensory Ligament - DR. KENT ALLEN STATION 2: Abdomen - DR. MARTHA MALLICOTE

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800.920.9525

info@vetray.com

www.vetray.com

SIMPLE. DEPENDABLE. SMART.

CALL 800.279.6452 OR VISIT US AT PATTERSONVET.COM TODAY.

ARIC ADAMS DVM, DACVS

EZ to Use

• Backed by research for behavioral problem management, without drowsiness or tranquilizing effects.

4747 Southwest 60th Avenue, Ocala, FL 34474 (352) 237-6151 | www.petersonsmith.com

equine care.

EQ U IN E D IVISIO N

CECredits

Adjustments - DR. TOOTS BANNER STATION 3: Diagnosis and Treatment - DR. JACK EASLEY

STATION 4: Dental Disease of the Incisor and Canine Teeth

Wet Lab Fees Include:

OURS IS, TOO.

EQUINE D IVISION

7/13/15 9:30 AM

ADDITIONAL SPONSORS:

TIMOTHY LYNCH DVM, DACVS, DACVSMR

- DR. SCOTT MARX

3146 Zylkene FAEP Ad.indd 1

SPONSORED BY:

JEREMIAH EASLEY DVM, DACVS

STATION 2: Oral Examination, Dental Charting and Occlusal

YOUR EMPHASIS IS ON

- Lunch

- Transportation to and from Hilton Ocala and Equine Medical Center of Ocala - Rotation through all four stations

Patterson Veterinary’s Equine Division focuses solely on horses. Our equine specialists are dedicated industry professionals who know your business and provide an unmatched level of service.

EQ U I N E DI V I S I O N

JACK EASLEY DVM, MS, DABVP, DAVDC (Equine)

- DR. JEREMIAH EASLEY

Relax, you’ve got

E DUCATIONAL PARTNE RS

VERN DRYDEN DVM, CJF

STATION 1: Sinuses

• Easy to give – administer one packet of appleflavored powder daily at meal time.

PETERSON & SMITH EQUINE HOSPITAL

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FRIDAY, JANUARY 20, 2017 | 8:30 AM - 5:30 PM

• Recommended for situational stress or behavior problems in horses and ponies.

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COMPREHENSIVE EQUINE DENTISTRY WET LAB

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CALL

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Large Animal Division

Give your patients the added advantage of Flu Avert® I.N.: • Just ONE dose required • Proven safe and effective in numerous challenge studies • Rapid onset of immunity

JANUARY 20–22, 2017 OCALA, FLORIDA

54 OCALA EQUINE th

So when it comes to choosing a partner for your practice, make sure you put the emphasis on equine with Patterson Veterinary’s Equine Division.

GOLD PARTNERS

EQUINE FOOT SYMPOSIUM

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ANNUAL OCALA EQUINE CONFERENCE & EQUINE FOOT SYMPOSIUM

GENERAL INFORMATION to make arrangements by contacting the FAEP office at (800) 992-3862 no later than December 30, 2016.

SCHEDULE AT-A-GLANCE

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 labs.)

Name badges are required and will be checked at all conference functions. You must be a registered conference attendee to receive a badge. An attendee traveling with a spouse/guest who does not want to attend the CE sessions, may purchase a spouse/guest badge that allows the spouse/ guest to attend all other conference food and social events for a cost of $125. That cost also covers lunch on Saturday, Sunday and dinner on Saturday.

Confirmation

On-Site Registration

One complimentary DVD copy with a link to the 54th Annual Ocala Equine Conference & Equine Foot Symposium proceedings will be provided to each registered attendee. Additional copies may be purchased at the FAEP registration desk. The proceedings will be available on the web to registered conference attendees one week prior to, and during the conference. The FAEP will send email notification to registered attendees when proceedings are available.

A confirmation of your registration will be mailed to your from the FAEP. Please contact us if any information in the confirmation is incorrect for timely correction of the error.

On-site registration will be available at the Hilton Ocala at the FAEP Registration Desk.

Exhibit Hall

Cancellation Policy Cancellation deadline for a full refund of registration fees minus a $50 administrative charge is December 30, 2016. Cancellations should be submitted to the FAEP in writing and acknowledged by the above date to be eligible for a refund. Cancellations after December 30, 2016, and no-shows are not refundable.

Americans With Disabilities Act Persons with disabilities who plan on attending the FAEP Conference and need auxiliary aids or services are requested

REGISTRATION HOURS Saturday, Jan. 21 Sunday, Jan. 22

7:00 a.m. – 6:00 p.m. 7:00 a.m. – 5:30 p.m.

Continuing Education Hours Offering 42 hours of cutting-edge equineexclusive continuing education presented by 15 distinguished speakers. Each 50-minute lecture is equal to one continuing education credit. Attendees may earn up to 26 credit hours.

EXHIBIT HALL HOURS Saturday, Jan. 21 Sunday, Jan. 22

9:40 a.m. – 6:55 p.m. 9:30 a.m. – 3:50 p.m.

For your convenience in recording your CE hours, one certificate will be included in your

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 are $119.00, Single and Double and $129.00, Triple and Quad; plus applicable taxes. Special extended stay reservations have been set up for the group rate from January 19-27 subject to availability. To reserve your room today, call the Group Reservations Department at Hilton Ocala at (877) 6024023. When making your reservations, be

sure to request the FAEP special room rates. The room block ends on December 30, 2016, so be sure to reserve your room to guarantee your stay at the Conference Host Hotel.

Air Transportation There are two nearby airport destinations for the FAEP’s 54th Annual Ocala Equine Conference & Equine Foot Symposium. One is the Gainesville Regional Airport (GNV) in Gainesville, Florida, located only 43 miles from the Hilton Ocala. The other is Orlando International Airport (MCO) in Orlando,

Florida, located 85 miles from the Hilton Ocala.

Airport/Ocala Shuttle Service A special FAEP group rate will be arranged with Shuttleliner of Ocala for those flying into the Orlando International Airport traveling to the Ocala Equine Conference. RESERVATIONS ARE REQUIRED FOR GUARANTEED SERVICE. Please call (352) 2379900 or visit www.shuttleliner.com to book your discounted conference transportation.

FOR MORE DETAILS - WWW.FAEP.NET

Churchill Ballrooms 4 & 5

Churchill Ballrooms 1&2

8:00 a.m. 8:50 a.m.

The Changing Face of Equine Dentistry Easley

Churchill Ballrooms 4 & 5

Time

Every Practitioner Can Take Good Dental Radiographs Easley

JANUARY 20-22, 2017 • OCALA, FLORIDA

PRE-REGISTRATION DEADLINE DECEMBER 30, 2016 CONFERENCE HOST HOTEL HILTON OCALA

General Assembly - 8:00 a.m. - 9:40 a.m.

"Forging" Your Way to Success

Morgan & Morgan

Venue: The Reserve - Pavilion Tent & Assembly Area 9:40 a.m. - 10:10 a.m. - Break - Visit the Exhibit Hall

9:40 a.m. - 10:10 a.m. Break - Visit the Exhibit Hall

10:10 a.m. 11:00 a.m.

11:00 a.m. 11:50 a.m.

Forelimb Lameness in the Athletic Horse: The Collateral Ligaments of the Coffin Joint Allen

2:30 p.m. 3:20 p.m.

Hindlimb Lameness in the Athletic Horse: The Proximal Suspensory Ligament

Managing Foot Infections

Allen

Dryden

Managing Critical and Complicated Laminitis Cases

Pruritus: Causes and Control Strategies White

Dryden

Treatment and Shoeing Strategies for Addressing Navicular Syndrome

Diagnostic Procedures in Dermatology White

Dryden

3:20 p.m. - 3:50 p.m. Break - Visit the Exhibit Hall

3:50 p.m. 4:40 p.m.

4:40 p.m. 5:30 p.m.

Morgan & Morgan

10:10 a.m. 11:00 a.m.

Venue: The Reserve - Pavilion Tent & Assembly Area

11:50 a.m. - 1:35 p.m. Lunch

1:35 p.m. 2:25 p.m.

Navigating Farriery in a Veterinary Treatment Protocol: Discussion and Q&A

Clinical Cases in Equine Reproduction - Problem Mares

Functional Farriery in Veterinary Treatment Protocols Part I

McCue

Morgan & Morgan

Clinical Cases in Equine Reproduction - Placentas, Stallions and Foals

Functional Farriery in Veterinary Treatment Protocols Part II

McCue

Morgan & Morgan

5:30 p.m. - 6:30 p.m. Cocktail Reception in the Exhibit Hall

DINNER - 6:30 P.M. -8:00 P.M. KEYNOTE PRESENTATION: 7:50 PM - 8:40 PM

Pathology Focused Conversations Between Veterinarians and Farriers: A Continuum of Interaction Morgan & Morgan

FloridaAEP

Equine Endocrinology: Diagnostic Review and Case Discussion

11:00 a.m. 11:50 a.m.

Mallicote 11:50 a.m. - 1:35 p.m. - Complimentary Lunch

Veterinary/Farrier Case Studies I Allen, Dryden, J. Morgan, Morgan

Anhidrosis: Review and Updates Mallicote

Veterinary/Farrier Case Studies II

Principles of Infection Control

Allen, Dryden, J. Morgan, D. Morgan

Traub-Dargatz

1:35 p.m. 2:25 p.m.

2:30 p.m. 3:20 p.m.

3:20 p.m. - 3:50 p.m. - Bingo Raffle & Drawing - Must Be Present to Win!

Veterinary/Farrier Case Studies III Allen, Dryden, J. Morgan, D. Morgan

Marketing Equine Infection Control Management

3:50 p.m. 4:40 p.m.

Traub-Dargatz

Veterinary/Farrier Case Studies IV Allen, Dryden, Morgan, D. Morgan

CONFERENCE EXHIBIT HALL

EXHIBIT HALL HOURS Saturday, Jan. 21 . . . 9:40 a.m. - 6:55 p.m. Sunday, Jan. 22 . . . . 9:30 a.m. - 3:50 p.m. The 54 Annual Ocala Equine Conference & Equine Foot Symposium Exhibit Hall will provide exhibitors and attendees with a valuable networking opportunity on Saturday and Sunday. Attendees are encouraged to take advantage of face-to-face contact with industry representatives. th

4:40 p.m. 5:30 p.m.

E asy W ays T o R egister

 Mail:

 Online:

FAEP/FVMA www.fvma.org 7207 Monetary Dr. info@fvma.org Orlando, FL 32809

 Phone:

(800) 992-3862 (407) 851-3862

Address

TO ENSURE YOUR ACCOMMODATIONS,

MEMBERSHIP

(407) 240-3710

$119 plus tax per night Single and Double Rooms $129 plus tax per night Triple and Quad Rooms ■ Special Room Rates End December 30, 2016 ■ Reserve Your Room Today! Call Group Reservations Department, (877) 602-4023

City

State

Phone

Fax

Zip

Email College Year of Graduation Business/Clinic/School

Save

$50 q My FAEP/FVMA Membership is current PR E R EG IS B q Yes, I would like to take advantage of the FAEP/FVMA joint membership special offer and register Y D EC T E R . 30 for the 54th Annual Ocala Equine Conference & Equine Foot Symposium as a member! I qualify for the following Membership Category (please check one) qRegular Member $255.00 qRecent Graduate (within last 2 years) $141.00 qState/Federal Employee $141.00 qPart-Time Employed $141.00 qNon-FL Resident $104.00

REGISTRATION

New FAEP/FVMA Member Fee

Your Registration Includes All of the Following

 CE Lectures  Friday Lunch Buffet

 All Breaks  Saturday Lunch Buffet

 Cocktail Reception  Saturday Dinner

FAEP/FVMA Member On or Before December 30 q $445.00 After December 30 q $495.00 To register at the discounted member rate, your FAEP/FVMA dues must be current!

Non-Member

On or Before December 30 q $645.00 After December 30 q $695.00

Farrier (Non-Veterinarian) On or Before December 30 q $325.00 After December 30 q $375.00 Student Registration – Currently enrolled in an AVMA-Accredited Veterinary College. q $195.00 School Attending ____________________________________________________________________________________

Spouse/Guest Registration – Spouse registration allows entrance to the Exhibit hall, social events, lunch on Friday and Saturday and Dinner on Saturday. Spouses who wish to attend C.E. sessions must pay full registration fees. Spouse/Guest Name _____________________________________________________________________ q $125.00

WET LABS

Conference Registration Fee

(Wet Lab Fees Include Lunch & Transportation to and from Wet Lab Venues)

Comprehensive Equine Dentistry Wet Lab

q Wet Lab with Conf. Reg. $895 q Wet Lab Only $1095

Comprehensive Equine Ultrasound Wet Lab q Wet Lab with Conf. Reg. $695

C Make checks payable to the FAEP/FVMA (U.S. Funds drawn on U.S. Banks)

This program is approved by:  PENDING AAVSB RACE APPROVAL  Sponsor of Continuing Education in New York State  Florida Board of Veterinary Medicine, DBPR FVMA Provider # 31  American Association of Professional Farriers (AAPF)

Name

q Wet Lab Only $895

Friday, January 20, Wet Lab Fee

PAYMENT INFORMATION

CONTINUING EDUCATION CREDITS

Total Registration Fee

$ $ $

q Check Enclosed Charge my credit card q VISA q MC q AMEX q DISCOVER Credit Card # Exp. Date Name on Card

This event has been approved for 15 American Association of Professional Farriers (AAPF) Continuing Education Credits. For more information visit their website - www.ProfessionalFarriers.com

Signature

A maximum of 26 credit hours may be earned at this conference. Offering a total of 42 hours of CE.

Florida-Association-of-Equine-Practitioners | Toll Free: (800) 992-3862

 Fax:

PERSONAL INFORMATION One registration per form. Please duplicate this form for additional registrants.

3600 SW 36th Ave. Ocala, FL 34474 www.hiltonocala.com Toll Free: (877) 602-4023 Telephone: (352) 854-1400 Fax: (352) 854-4010

■ Reserve Your Room Today! Request FAEP SPECIAL ROOM RATES

Be sure to stop by and visit more than 60 exhibitors displaying the very latest in equine-exclusive products and services.

REGISTRATION FORM A Proud Tradition of Quality Equine Practitioner Education

Navigating Farriery in a Veterinary Treatment Protocol 8:50 a.m. 9:40 a.m.

$119

Per night

All Lectures held at the Hilton Ocala

Packet Pick-up and Registration Desk Opens at 7:50 a.m.

Packet Pick-up and Registration Desk Opens at 7:00 a.m.

Proceedings

The Exhibit Hall at the 54 th Annual Ocala Equine Conference & Equine Foot Symposium will provide exhibitors and attendees with a dynamic networking showcase. It will be a hub of activity; providing a valuable opportunity to make contacts and to interact with industry representatives and other members of the equine veterinary medical care team.

Churchill Ballrooms 1 & 2

only

VISIT THE EXHIBIT HALL

S U N D AY - J A N U A R Y 2 2

The FAEP strongly recommends that you register in advance for the 54th Annual Ocala Equine Conference & Equine Foot Symposium. 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. Advanced registrations are taken at the FAEP office until December 30, 2016. After this date, a late registration fee of $50.00 will be added to all registrations, including on-site registrations.

Name Badges

Time

S A T U R D AY - J A N U A R Y 2 1

Advanced Registration

Starting at

FOR MORE DETAILS - WWW.FAEP.NET

ANNUAL OCALA EQUINE CONFERENCE & EQUINE FOOT SYMPOSIUM

GENERAL INFORMATION to make arrangements by contacting the FAEP office at (800) 992-3862 no later than December 30, 2016.

SCHEDULE AT-A-GLANCE

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 labs.)

Confirmation

On-Site Registration

A confirmation of your registration will be mailed to your from the FAEP. Please contact us if any information in the confirmation is incorrect for timely correction of the error.

On-site registration will be available at the Hilton Ocala at the FAEP Registration Desk.

Exhibit Hall

Americans With Disabilities Act Persons with disabilities who plan on attending the FAEP Conference and need auxiliary aids or services are requested

REGISTRATION HOURS Saturday, Jan. 21 Sunday, Jan. 22

7:00 a.m. – 6:00 p.m. 7:00 a.m. – 5:30 p.m.

EXHIBIT HALL HOURS Saturday, Jan. 21 Sunday, Jan. 22

9:40 a.m. – 6:55 p.m. 9:30 a.m. – 3:50 p.m.

For your convenience in recording your CE hours, one certificate will be included in your

sure to request the FAEP special room rates. The room block ends on December 30, 2016, so be sure to reserve your room to guarantee your stay at the Conference Host Hotel.

Florida, located 85 miles from the Hilton Ocala.

FOR MORE DETAILS - WWW.FAEP.NET

Churchill Ballrooms 4 & 5

Churchill Ballrooms 1&2

8:00 a.m. 8:50 a.m.

The Changing Face of Equine Dentistry Easley

Churchill Ballrooms 4 & 5

Time

Every Practitioner Can Take Good Dental Radiographs Easley

JANUARY 20-22, 2017 • OCALA, FLORIDA

PRE-REGISTRATION DEADLINE DECEMBER 30, 2016 CONFERENCE HOST HOTEL HILTON OCALA

General Assembly - 8:00 a.m. - 9:40 a.m.

"Forging" Your Way to Success

Morgan & Morgan

Venue: The Reserve - Pavilion Tent & Assembly Area 9:40 a.m. - 10:10 a.m. - Break - Visit the Exhibit Hall

9:40 a.m. - 10:10 a.m. Break - Visit the Exhibit Hall

10:10 a.m. 11:00 a.m.

11:00 a.m. 11:50 a.m.

Forelimb Lameness in the Athletic Horse: The Collateral Ligaments of the Coffin Joint Allen

2:30 p.m. 3:20 p.m.

Hindlimb Lameness in the Athletic Horse: The Proximal Suspensory Ligament

Managing Foot Infections

Allen

Dryden

Managing Critical and Complicated Laminitis Cases

Pruritus: Causes and Control Strategies White

Dryden

Treatment and Shoeing Strategies for Addressing Navicular Syndrome

Diagnostic Procedures in Dermatology White

Dryden

3:20 p.m. - 3:50 p.m. Break - Visit the Exhibit Hall

3:50 p.m. 4:40 p.m.

4:40 p.m. 5:30 p.m.

Morgan & Morgan

10:10 a.m. 11:00 a.m.

Venue: The Reserve - Pavilion Tent & Assembly Area

11:50 a.m. - 1:35 p.m. Lunch

1:35 p.m. 2:25 p.m.

Navigating Farriery in a Veterinary Treatment Protocol: Discussion and Q&A

Clinical Cases in Equine Reproduction - Problem Mares

Functional Farriery in Veterinary Treatment Protocols Part I

McCue

Morgan & Morgan

Clinical Cases in Equine Reproduction - Placentas, Stallions and Foals

Functional Farriery in Veterinary Treatment Protocols Part II

McCue

Morgan & Morgan

5:30 p.m. - 6:30 p.m. Cocktail Reception in the Exhibit Hall

DINNER - 6:30 P.M. -8:00 P.M. KEYNOTE PRESENTATION: 7:50 PM - 8:40 PM

Pathology Focused Conversations Between Veterinarians and Farriers: A Continuum of Interaction Morgan & Morgan

FloridaAEP

Equine Endocrinology: Diagnostic Review and Case Discussion

11:00 a.m. 11:50 a.m.

Mallicote 11:50 a.m. - 1:35 p.m. - Complimentary Lunch

Veterinary/Farrier Case Studies I Allen, Dryden, J. Morgan, Morgan

Anhidrosis: Review and Updates Mallicote

Veterinary/Farrier Case Studies II

Principles of Infection Control

Allen, Dryden, J. Morgan, D. Morgan

Traub-Dargatz

1:35 p.m. 2:25 p.m.

2:30 p.m. 3:20 p.m.

3:20 p.m. - 3:50 p.m. - Bingo Raffle & Drawing - Must Be Present to Win!

Veterinary/Farrier Case Studies III Allen, Dryden, J. Morgan, D. Morgan

Marketing Equine Infection Control Management

3:50 p.m. 4:40 p.m.

Traub-Dargatz

Veterinary/Farrier Case Studies IV Allen, Dryden, Morgan, D. Morgan

CONFERENCE EXHIBIT HALL

4:40 p.m. 5:30 p.m.

E asy W ays T o R egister

 Mail:

 Online:

FAEP/FVMA www.fvma.org 7207 Monetary Dr. info@fvma.org Orlando, FL 32809

 Phone:

(800) 992-3862 (407) 851-3862

Address

TO ENSURE YOUR ACCOMMODATIONS,

MEMBERSHIP

(407) 240-3710

City

State

Phone

Fax

Zip

Email College Year of Graduation Business/Clinic/School

Save

REGISTRATION

New FAEP/FVMA Member Fee

Your Registration Includes All of the Following

 CE Lectures  Friday Lunch Buffet

 All Breaks  Saturday Lunch Buffet

 Cocktail Reception  Saturday Dinner

FAEP/FVMA Member On or Before December 30 q $445.00 After December 30 q $495.00 To register at the discounted member rate, your FAEP/FVMA dues must be current!

Non-Member

On or Before December 30 q $645.00 After December 30 q $695.00

WET LABS

Conference Registration Fee

(Wet Lab Fees Include Lunch & Transportation to and from Wet Lab Venues)

Comprehensive Equine Dentistry Wet Lab

q Wet Lab with Conf. Reg. $895 q Wet Lab Only $1095

Comprehensive Equine Ultrasound Wet Lab q Wet Lab with Conf. Reg. $695

C Make checks payable to the FAEP/FVMA (U.S. Funds drawn on U.S. Banks)

Name

q Wet Lab Only $895

Friday, January 20, Wet Lab Fee

PAYMENT INFORMATION

CONTINUING EDUCATION CREDITS

Total Registration Fee

$ $ $

q Check Enclosed Charge my credit card q VISA q MC q AMEX q DISCOVER Credit Card # Exp. Date Name on Card

This event has been approved for 15 American Association of Professional Farriers (AAPF) Continuing Education Credits. For more information visit their website - www.ProfessionalFarriers.com

Signature

A maximum of 26 credit hours may be earned at this conference. Offering a total of 42 hours of CE.

Florida-Association-of-Equine-Practitioners | Toll Free: (800) 992-3862

 Fax:

PERSONAL INFORMATION One registration per form. Please duplicate this form for additional registrants.

3600 SW 36th Ave. Ocala, FL 34474 www.hiltonocala.com Toll Free: (877) 602-4023 Telephone: (352) 854-1400 Fax: (352) 854-4010

■ Reserve Your Room Today! Request FAEP SPECIAL ROOM RATES

Be sure to stop by and visit more than 60 exhibitors displaying the very latest in equine-exclusive products and services.

REGISTRATION FORM A Proud Tradition of Quality Equine Practitioner Education

Navigating Farriery in a Veterinary Treatment Protocol 8:50 a.m. 9:40 a.m.

$119

Per night

All Lectures held at the Hilton Ocala

Packet Pick-up and Registration Desk Opens at 7:50 a.m.

Packet Pick-up and Registration Desk Opens at 7:00 a.m.

Proceedings

Churchill Ballrooms 1 & 2

only

VISIT THE EXHIBIT HALL

S U N D AY - J A N U A R Y 2 2

Name Badges

Time

S A T U R D AY - J A N U A R Y 2 1

Advanced Registration

Starting at

FOR MORE DETAILS - WWW.FAEP.NET

EQUINE RESCUE

- MANAGING A DOWN HORSE AT AN EVENT - PART 1 NATHAN M. SLOVIS | DVM, DACVIM, CHT

orses can become recumbent for a variety of reasons, therefore it is important to be able to determine what conditions are primary, preexisting, and what may be secondary to the animal being recumbent. As a veterinarian at an event, the goal is to triage, stabilize, and when appropriate, safely transport the horse to a referral hospital. Biosecurity standard operating procedures (SOP) should also be established for any down patient,where the cause of recumbency cannot be established. Examining, assessment and subsequent management of a recumbent horse are both difficult and challenging. Horse owners in our society currently have close and emotional relationships with their horses and with that come the increased expectations of the veterinary community to save their animals in what would have been an impossible scenario in the past. The art of technical equine rescue has grown due to these expectations. Veterinarians who will be supervising veterinary care at an event should understand the basic SOP of technical equine rescue. The demands of our clients have now required veterinarians to be able to properly assess and care for a recumbent horse. WWW.FAEP.NET |

FLAEP |

Safety of all involved should be considered when the cause of recumbency is unknown. Caution should be taken if there is a risk of infectious and/or zoonotic factors playing a role in the etiology of the disease, and appropriate measures should be taken such as personal protective equipment (PPE) and minimizing human exposure. Causes of recumbency can be divided into two main categories, Non-Neurologic and Neurologic. A number of the etiologies for each category will be discussed, however, for more detailed information of the diseases, other references should be reviewed.

CAUSES FOR RECUMBENCY

At an event, some of the common causes for non-neurologic recumbency would include fractures, hypotension and hypovolemia due to heat stroke, exhaustion, cardiac arrhythmias, extertional rhabdomyolysis, hyperkalemic periodic paralysis (HYPP), colic, hemorrhage, respiratory disease, and metabolic derangements that can lead to hypoglycemia, hyponatremia and hypocalcemia/hypomagnesemia. Neurological causes may include trauma to the nervous system (Brain, brain stem, spinal cord and peripheral nerves),

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitionerâ&#x20AC;&#x201A; 21

Rabies, Viral Encephalitis (Eastern, Western, Venezuelan and will not have altered behavior unless it becomes frantic in West Nile Virus), Equine Herpes Virus Myeloencephalopathy, its struggling, is dehydrated, exhausted or frightened. vestibular disease, and Equine protozoal myeloencephalitis. Close observation may be required to detect seizures. A seizure is a manifestation of cerebral cortex dysfunction EXAMINATION characterized by loss of consciousness or involuntary motor The initial assessment of function of all body systems activities. A seizure may be generalized, focal or focal with should be ascertained. Although many of these cases have secondary generalization. Generalized seizures are characterthe neurological system involved in the inability to rise, the ized by complete loss of consciousness and varying degrees of other body systems should not be ignored. Once a quick involuntary motor activity, including flailing of limbs, passage triage has been performed, one should not forget to obtain of urine and feces, nystagmus and vocalization. Focal seizures a good history (Vaccinations, travel, diet, signalment; and can take two forms; the first is characterized by localized question any person(s) that may have witnessed the horse involuntary movements and may not be accompanied by an right before it became recumbent). Safety and PPE (Gloves) obvious alteration of consciousness. The second may result are a necessity when examining a horse that has an unclear in momentary lapses of consciousness without collapse or history of why it became recumbent. significant motor activity. A focal seizure with secondary Neuroanatomical localization of the disease should be at- generalization has a focal onset, but subsequently, seizure tempted for all neurological causes of recumbency. Simply, activity spreads throughout the cerebral cortex, resulting is there brain involvement or does injury involve the spinal in generalized signs. These animals may show initial headcord or peripheral nerves? The aim of the neurological ex- turning or focal tremors, followed by a loss of consciousness amination is to determine if a neurologic disorder exists, and and generalized involuntary motor activity. if so, where the lesion or lesions are located. Lesion location Bizarre and inappropriate behavior such as head pressing, determines the differential diagnoses and allows the formula- licking objects, or compulsive wandering may be associated tion of a diagnostic plan. Several important components of with cerebral disease and is easy to recognize. Animals with the neurologic examination such as behavior, mental status, cerebral lesions that circle have a tendency to circle towards head posture, vision, pupillary light reflexes, and inspection the side of the lesion. for muscular symmetry can be noted in the general physical examination which should precede the detailed neurologic MENTAL STATUS examination. A thorough physical examination is important, Mental status is assessed based on the patient’s level of as disease of other systems or organs may account for the consciousness or awareness. The animal’s responsiveness neurological signs that are seen (e.g. hepatoencephalopa- to the internal and external environments is affected by the thy) or may take precedence for diagnosis or treatment (e.g. cerebral cortex and the ascending reticular activating system shock). The neurologic examination should be performed as (ARAS). These can be affected by stimuli from the sensory a systematic search for defects and asymmetries. The exact nervous system, and thus, responses to sensory stimuli should order of the examination is not important, but a common be considered; e.g. visual, tactile, auditory and painful stimuli. principle is to start at the head and progress caudally to Loss of awareness can be described as depression, lethargy, the tail to avoid omissions. The sequence of the neurologic somnolence, obtundation and stupor. The most profound loss examination is as follows: of awareness is described as coma. This is a state of complete 1. Head unresponsiveness to noxious stimuli. The deepest comas are Behavior usually related to brainstem, particularly midbrain, lesions. Mental status Head posture and coordination HEAD POSTURE AND COORDINATION Cranial nerves Normal animals maintain their heads in a certain posture 2. Gait and posture and are capable of quick and smooth head movement. The 3. Neck and forelimbs most obvious abnormality of head posture is head tilt or 4. Back and hind limbs turn. Unilateral, mild central and peripheral vestibular le5. Tail and anus sions frequently result in a head tilt that is characterized by BEHAVIOR a laterally deviated poll, with the caudal neck and muzzle The owner should be questioned about the patient’s behav- remaining on the midline. The head tilt, in this case, is deior and response patterns. In addition, the owner should be scribed by the direction of the poll deviation. A horse with questioned to determine if there has been a progression of a cerebral lesion that continually turns in circles, often has the syndrome over time. The patient’s age, breed or sex may the head and neck deviated to one side, but the head itself influence its behavior. A horse that is recumbent as a result is not tilted. A severe unilateral vestibular lesion can result of cervical spinal cord disease or musculoskeletal disease in a marked head tilt, in addition to a head and neck turn, 22 The Practitioner

Issue 3 • 2016

both usually toward the side of the lesion. Bilateral peripheral vestibular disease can result in wide swinging movements of the head and neck. The cerebellum acts to modulate movements of the head and limbs. Fine control of head positioning and movements is often lost, with cerebellar disease resulting in awkward, jerky movements and head tremor that is seen at rest. Increasing voluntary effort exaggerates the abnormality, and the resulting fine jerky movements of the head are called an intention tremor. Such animals frequently have difficulty with head positioning to perform acts such as prehension and commonly “overshoot.” CRANIAL NERVES Cranial nerve (CN) examination assists in localizing a lesion near or within the brainstem. The examination should start with the most rostral nerve and proceed caudally. Generally, the more distal a cranial nerve lesion, the fewer clinical signs are seen, and when more than one cranial nerve is involved, a more central lesion is likely. The anatomic relationship of cranial nerve nuclei and their peripheral pathways should be considered when interpreting findings. The cell bodies of cranial nerves III (oculomotor), IV (trochlear), V (trigeminal), and VI (abducens) are closely related in the brain and at their points of exit from the cranial vault. Cranial nerves VII (facial) and VIII (vestibulocochlear) are closely related at their point of exit from the cranium and are frequently damaged by disorders of the petrous temporal bone, with which they are closely related. Cranial nerves IX (glossopharyngeal), X (vagus), XI (accessory), and XII (hypoglossal) are found in close association adjacent to the dorsal wall of the medial compartment of the guttural pouch.

is 80-90% crossing of optic fibers at the optic chiasm. Some animals may not respond to a menace response test and a true visual deficiency may be detected by placing objects in front of the animal and observing its behavior, or ideally, by performing a maze test. Menace deficit can also be the result of facial nerve paralysis, in which case, the animal is unable to blink, but usually will show avoidance movements of the head. Such animals will also have other signs of facial nerve involvement; e.g. facial drooping on the same side. Animals with cerebellar disease may also display a menace deficit, yet possess normal vision. The precise mechanism by which the cerebellum affects this pathway is not known, but is thought to involve upper motor neuron control of the facial nerve. These animals retain visual acuity and will be able to perform a maze test. The motor component is mediated through the facial nerve and its nucleus is in the medulla. The afferent side of the response is extensive and involves a cerebral pathway, which implicates a learned response. It is usually present by 5-7 days in foals. Therefore, testing the menace response in a neonatal foal will be unrewarding. Unilateral blindness (hemianopia) can be difficult to assess and it may take repeated efforts, such as blindfolding each eye in turn, to detect it. An ophthalmologic examination should be included in the neurological examination. Lesions of the eye and optic nerve result in ipsilateral blindness. Lesions of the optic tracts and lateral geniculate nucleus cause contralateral blindness. Space occupying lesions of the brain frequently produce blindness by either direct involvement of the visual pathways or pressure of the mass and cerebral edema forcing the occipital lobes caudally. The resultant blindness is contralateral to the lesion but often bilateral, because of associated diffuse brain swelling.

Olfactory Nerve (I) Clinical deficit of smell (anosmia) is difficult to assess and Oculomotor Nerve (III) is more frequently caused by disease within the nasal passages, The diameter of the pupillary aperture is controlled by two rather than a cranial nerve lesion. A crude estimation is the muscle groups; the constrictor muscles of the pupil, which are patient’s ability to smell and track feed. Irritating substances, innervated by the parasympathetic fibers in the oculomotor such as ammonia, should not be used to determine sense nerve, and dilator muscles of the pupil, which are innervated of smell, as these stimulate nociceptors in the nasal mucosa, by the sympathetic fibers from the cranial cervical ganglion. which are the dendrites of the maxillary nerve (CN V). These autonomic innervations originate in the brainstem and change pupil diameter in response to light (oculomotor) and fear, or excitement (sympathetic). The response of the pupils Optic Nerve (II) Vision is the function of CN II. A good initial assessment to light directed into the eye should be noted. The normal is the animal’s response to its environment, e.g. walking into response to light directed into one eye is constriction of both objects. Depressed patients or those with vestibular disease pupils; this is as a result of a direct response in the ipsilateral (loss of balance) may be incorrectly reported as blind by or illuminated eye and indirect response in the contralateral their owners because they may stumble over objects. The or non-illuminated eye. Response to this test should take visual pathway is tested by the menace response. The hand is into account the ambient light and emotional status of the moved rapidly toward the eye in a threatening gesture. This animal. It may be necessary to decrease the ambient light results in eyelid closure and the head may be jerked away. to allow for pupillary dilation before this test is performed. The pupillary light reflex occurs within the brainstem and For practical purposes, the vision in one eye is perceived by the visual cortex of the contralateral cerebral cortex, as there thus is not affected by lesions in the visual cortex. Thus, a WWW.FAEP.NET |

FLAEP |

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

widely dilated (mydriatic) pupil that is unresponsive to direct light in an eye with normal vision suggests an oculomotor lesion. If the contralateral eye has normal oculomotor function, it will respond to both ipsilateral (direct) and contralateral (indirect) illumination. A retrobulbar lesion involving the optic and oculomotor nerves will appear as a mydriatic pupil unresponsive to light shone in either eye, in addition to a menace deficit. The oculomotor nerves are subject to damage by edema and space occupying lesions in the forebrain, resulting in pressure ventrally on the brainstem. Asymmetric swelling of cerebral tissue may exert greater pressure to one oculomotor nerve, causing unequal pupil size (anisocoria). Severe brainstem lesions can produce pupillary abnormalities, in association with changes in mental status such as coma. Progressive, bilateral pupillary dilation in a recumbent warrants a grave prognosis. Oculomotor (III), Trochlear (IV), Abducens (VI) In addition to innervation of pupillary constrictor muscles, the oculomotor nerve also innervates extraocular muscles with the trochlear and abducens nerves. These cranial nerves thus control the position of the globe and dysfunction of these nerves results in deviation of the globe that is constant in all head positions. Oculomotor dysfunction results in a ventrolateral strabismus. Trochlear nerve dysfunction results in a dorsomedial strabismus. It should be noted that trochlear nerve lesions can result in ipsilateral or contralateral strabismus, depending on the location of the lesion in the brainstem, as the trochlear nerve crosses the midline twice in the area of the midbrain before exiting the cranial vault. Abducens nerve dysfunction results in medial strabismus and an inability to retract the globe, which is best assessed by applying a tactile stimulus to the cornea. When determining the function of these nerves, consideration should also be given to normal responses of the eyes to head posture and movement. When the head is elevated, the eyes tend to maintain a horizontal position and thus move ventrally in the orbits. When the head is moved from side to side, the eyes do not remain fixed, but move rhythmically, with a slow phase movement in the direction opposite to the direction in which the head is moved followed by a fast phase in the direction that the head is moved. When the head ceases to move, the eyes return to the center of the orbits. These eye movements are regarded as normal vestibular nystagmus and result from the connection between the vestibular nuclei and the nuclei of the cranial nerves controlling eye movement (III, IV, VI). It can thus be deduced that normal vestibular nystagmus requires an intact vestibular system; intact cranial nerves III, IV, VI; and an intact connection between them. Thus, lesions of the vestibular system can result in abnormal eye position (strabismus) or movement (nystagmus). However, vestibular lesions result in a strabis24â&#x20AC;&#x201A; The Practitionerâ&#x20AC;

mus that changes when the head and neck are moved rather than the constant deviation that is seen with direct lesions to the cranial nerves III, IV and VI. In addition, vestibular dysfunction also results in spontaneous nystagmus. Other points to note are that congenitally blind horses may have abnormal globe position and movement; and periorbital lesions often cause mechanical globe deviations. Trigeminal Nerve (V) The trigeminal nerve provides sensation to the face through all three branches (mandibular, maxillary and ophthalmic) and motor stimulus to the muscles of mastication via the mandibular branch. Sensory functions are assessed by lightly stimulating the skin of the face using a closed hemostat or fingers. It is important to remember that some areas such as the periorbital region, nasal planum and lips are more sensitive. Lightly brushing the ears, eyelids, external nares and lips results in movement that is mediated through the sensory branches of the trigeminal nerve and motor branches of the facial nerve. These reflexes thus require an intact brainstem and trigeminal and facial nuclei, but do not require the animal to be consciously aware of the stimulus. Unilateral loss of facial sensation most commonly results from damage to the peripheral portion of the trigeminal nerve, the trigeminal ganglion in the petrosal bone of the skull or the contralateral cerebral cortex. Lesions affecting the spinal tract of the trigeminal nerve in the medulla and midbrain would most likely be fatal, as they would also most likely affect the adjacent cardiovascular and respiratory centers in the brainstem. Patients with bilateral facial hypoesthesia most likely have bilateral cerebral cortex disease. Loss of motor function of the mandibular nerve bilaterally, results in a dropped jaw and inability to chew. The tongue may appear to protrude as it moves rostrally in the mouth, but it can be retracted normally when stimulated. Animals with dropped jaws also exhibit sialosis as a result of a lack of jaw movement. Unilateral lesions of the trigeminal nerve produce asymmetric jaw closure, with a slight gap between the occlusal surfaces of the teeth on the affected side; however, it is the accompanying muscle atrophy that is usually most apparent. Facial Nerve (VII) The facial nerve provides motor innervation to the muscles of facial expression. The facial nerve is the motor pathway for many of the reflexes that have already been tested in the neurologic examination. General inspection for facial symmetry is useful, but some animals may have a subtle deviation of the nostrils or muzzle to one side. Comparison of tone in the ears, lips and eyelids on each side may aid in detecting subtle weakness. Facial paralysis is generally seen as a drooping of the ear and lips with retraction of the nose toward the unaffected side. There may also be tongue protruIssue 3 â&#x20AC;˘ 2016

sion from the unaffected side. In chronic paralysis, the face may be deviated toward the affected side because of atrophy and contracture of the denervated musculature. Ptosis of the upper eyelid occurs as a result of paralysis of one of the muscles that raises the upper lid. Lesions of the middle and inner ear, causing vestibular signs often have accompanying facial paralysis. This is because the facial nerve lies in the petrous temporal bone and is separated from the tympanic cavity of the middle ear by only a thin membrane. Some cerebral and focal thalamic lesions may result in hypertonia and hyperreflexia of facial muscles, resulting in “grimacing.” This can occur spontaneously or may be reflexinitiated. This is because of involvement of the higher motor centers of upper motor neurons controlling facial movement that normally have an inhibitory effect on the facial muscles. Grimacing can also be caused by irritative lesions, such as peracute encephalitides. Vestibulocochlear Nerve (VIII) The auditory or cochlear division of the nerve is responsible for the sense of hearing. Bilateral middle ear disease can cause deafness, but unilateral hearing loss is difficult to detect. Vestibular system: The vestibular system comprises the sensory structures in the inner ear (semicircular canals, utricles and saccules), the vestibular portion of CN VIII, and the central components of the vestibular system in the medulla oblongata and cerebellum. The vestibular system controls orientation of the head, body, limbs and eyes in space, with respect to gravity and motion. Dysfunction of the vestibular system results in signs such as a staggering gait, circling, falling, head tilt and spontaneous nystagmus. Signs of vestibular disease can be classified as peripheral, central or paradoxical. Peripheral lesions are those that affect the inner ear or CN VIII. Central lesions are those that affect vestibular structures in the medulla oblongata. Paradoxical lesions are those that affect the vestibular structures in the cerebellum. The direction of nystagmus may help in determining the site of the lesion and is always described by referring to the fast phase. In peripheral vestibular disorders, the nystagmus (fast phase) is always directed away from the side of the lesion and thus the side of the head tilt, and is usually horizontal. Central vestibular disorders result in spontaneous and positional nystagmus, which can be horizontal, vertical or rotary, and may change direction with changes in head posture. Central lesions can affect adjacent structures such as the reticular formation and pathways for voluntary limb movement, resulting in concomitant depression and ataxia. Blindfolding affected animals result in a worsening of clinical signs due to the removal of compensatory mechanisms from the optic centers. Recumbent animals with vestibular lesions tend to lie with the side of the lesion down and may resist attempts to turn them. When turned, many of these animals spontaneously rotate back to the lesion-down position. Such WWW.FAEP.NET |

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animals may experience great difficulty in rising. Signs of peripheral vestibular disease often improve markedly within several days as the patient accommodates. Glossopharyngeal Nerve (IX), Vagus Nerve (X), Accessory Nerve (XI) The major function of these nerves is the innervation of the pharynx and larynx with sensory and motor fibers. The most important clinical sign associated with lesions of these nerves is paralysis of the pharynx and larynx, with the severity of signs depending on whether lesions are unilateral or bilateral. The function of these nerves can be tested by listening for normal laryngeal sounds (unilateral laryngeal paralysis results in “roaring”); observing normal swallowing, and inspection of the pharynx and larynx with an endoscope if necessary. The “slap test” is a test of the function of vagal innervation of the larynx. It is performed by slapping the skin in the area of the withers (caudal to the dorsal scapula), while the larynx is observed with an endoscope or the dorsolateral larynx is palpated. The normal response is for the contralateral arytenoid cartilage to adduct briefly, resulting in a palpable twitch at the laryngeal musculature. The afferent pathway is via segmental thoracic nerves, cranially via the contralateral cervical spinal cord white matter, and finally to the contralateral vagal nucleus in the medulla oblongata. The efferent pathway is via the vagus nerve to the cranial thorax, then back up the neck via the recurrent laryngeal nerve to the larynx. This reflex can be interrupted at any of these sites. Many severe, diffuse brain diseases may cause dysphagia with an absence of lesions in the medulla oblongata. This is a result of disruption of higher motor control of swallowing. Dysphagia can also be seen with diffuse lower motor neuron and neuromuscular paralysis, e.g. botulism. The accessory nerve provides the motor supply to at least part of the trapezius, cranial part of the sternocephalicus, and brachiocephalicus muscles. Signs of dysfunction are rare. Hypoglossal (XII) The hypoglossal nerve provides motor innervation to the muscles of the tongue and the geniohyoideus muscle. The function of this nerve is tested by examining the tongue for symmetry and normal movement. A normal horse will resist its tongue being withdrawn from the mouth. A unilateral lesion usually results in unilateral atrophy and weak retraction; however, the tongue does not usually protrude from the mouth. Bilateral involvement interferes with prehension and swallowing, with protrusion of the tongue and an inability to draw it back into the mouth. Severe cerebral lesions may result in tongue protrusion and slow retraction as a result of interference with voluntary control pathways. An example of this is the impaired tongue, jaw and lip movement seen with cerebral edema secondary to hyponatremia upper motor neuron (basal nuclei) lesion in nigropallidal encephalomalacia (yellow-star thistle poisoning).

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 25

Recumbent animals that can attain a dog-sitting posture or use their thoracic limbs well in attempts to rise most likely have a lesion caudal to T2. If the thoracic limbs cannot be used, the lesion is likely to be located in the cervical spinal cord. If the head, but not the neck can be lifted off the ground, the lesion is in the cranial cervical area. If the head and neck can be lifted off the ground, but thoracic limb function is decreased, such that the animal cannot maintain sternal recumbency or attain a dog-sitting posture, there is likely to be a severe caudal cervical lesion. Muscle tone can be assessed by manipulating each limb. Lower motor lesions result in a flaccid limb with no motor activity. Caution should be used in interpreting tone in heavy animals or limbs that have been lain upon. Increased muscle tone with decreased or absent voluntary effort, may occur with a severe upper motor neuron lesion to the thoracic limbs (cranial to C6). This is the result of the loss of the calming influences of the descending upper motor neuron pathways. This spastic paralysis can also be seen with lesions from C6-T2, if little or no gray matter is affected. Spinal reflexes should be tested in the thoracic limbs, but it is important to note that a spinal reflex can be intact without the animal perceiving the stimulus and demonstrating a related behavioral response, as perception involves intact ascending sensory pathways to the forebrain. Pinching the skin of the distal forelimb results in flexion of the fetlock, knee, elbow and shoulder. If the reflex is absent and cannot be accounted for by decubital changes, the lesion likely involves C6-T2 gray matter, peripheral nerves or flexor muscles of the forelimb. Lesions cranial to C7 may result in an exaggerated response. The biceps reflex is performed by placing two to three fingers firmly on the biceps and brachialis muscles on the cranial aspect of the elbow joint, and feeling for contraction of the those muscles and observing for flexion of the elbow, while balloting the muscles with a plexor. This reflex, which has its afferent and efferent pathways in the musculocutaneous nerve, and involves spinal cord segments C7 and C8, is difficult to evoke, except in small foals. The triceps reflex is tested by holding the relaxed limb slightly flexed and balloting the distal portion of the long head of the triceps and then insertion of the tendon. Contraction of the triceps muscle, which causes extension of the elbow, should be observed and palpated. This reflex has afferent and efferent pathways in the radial nerve and involves spinal cord segments C7 to T1. This reflex is normally difficult to demonstrate in adult horses and is often most useful when easily elicited, indicating an upper motor neuron lesion cranial to the spinal cord segments. Voluntary effort and muscle tone is assessed by observing the animal’s attempts to rise or its response to stimuli while in lateral recumbency. Asymmetry in voluntary effort may also help to localize a lesion. The pelvic limb spinal reflexes 26 The Practitioner

should be assessed in recumbent animals and in animals that can be safely restrained in lateral recumbency (usually only foals). The patellar reflex is assessed by supporting the limb in a partly flexed position, tapping the intermediate patellar ligament, and observing for reflex contraction of the quadriceps muscle and extension of the stifle. This reflex involves sensory and motor fibers in the femoral nerve and spinal cord segments at L4 and L5. The flexor reflex is assessed by pinching the skin of the distal limb and observing for flexion. This may be difficult to assess in larger horses, especially those that have been recumbent for some time. This reflex involves sensory and motor fibers in the sciatic nerve and spinal cord segments L5-S2. At this point in the examination, the presence and location of lesions in the brain, spinal cord cranial to T3 and peripheral nerves, or muscles of the thoracic limbs should have been identified. Part 2 - Continued on Page 28

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FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 27

EQUINE RESCUE

- MANAGING A DOWN HORSE AT AN EVENT - PART 2 NATHAN M. SLOVIS | DVM, DACVIM, CHT TECHNICAL EQUINE RESCUE

You never know where the recumbent horse may be located, for example, in the stall or out on the cross country field; so therefore you should have the basic equipment (listed below) in order to be prepared in handling/moving the recumbent horse safely. This manuscript will describe the protocols that I utilize to perform a forward and backward assist, as well as a sideways assist. The use of the equine rescue glide will also be discussed for the transportation of the horse to a referral facility. The most important safety advice is that all people must stay clear of the horse’s legs at all times. The use of sedatives or short acting anesthesia is often required during technical equine rescue. The decision between sedation and shortterm anesthesia is based on the patient’s level of cooperation and physical status. The administration of ∞2-adrenergic agonist such as xylazine (0.5 to 1.1 mg/kg IV) or Detomidine (0.01 to 0.015 mg/kg IV) in combination with an opioid such as butorphanol (0.01 to 0.03 mg/kg IV), provides excellent sedation. Neither of the ∞2-adrenergic agonist nor butorphanol induce a direct increase in intracranial pressure and are safe to use in patients with suspected head trauma. For horses with seizures, sedation in a combination of diazepam (0.033 to 0.066 mg/kg IV) and xylazine may be helpful in controlling the seizures. Patients that are cardiovascularly stable and not suspected of head trauma can have general anesthesia using a combination of xylazine (1.1mg/kg IV) followed by Ketamine (2.2 mg/kg IV). This will usually provide approximately 10 minutes of anesthesia and 15 to 20 minutes of recumbency. Horses that may need prolonged recumbency for travel can be administered 1L of 5% or 500ml of 10% guaifenesin, with Xylazine (1.1 mg/ kg) and Ketamine (2.2mg/kg) added. This solution may be administered at a slow drip, and when necessary, rapidly to effect, and then slowed down to a slow drip. In certain circumstances, a horse may be unable to support itself on an extremity to walk or stand in a trailer for transport

Figure 1 Forward Assist (Figure 1)  Use 3 to 4 inch webbing (15 to 20 ft long)  “Floss” under the neck  Center mark is placed over the withers  Both loops are passed between the front legs to a referral hospital. Alternatively, it may have a neurological disease, viremia, shock or traumatic injuries that prevent normal transportation of the animal. A safe way would be to transport the animal in lateral recumbency in the trailer. Because of the weight of the animal, it is difficult to move safely, which can often cause damage to the legs, neck, head and eyes, as well as safety concerns to the horse and handler (injuries from struggling, etc.). The utilization of the rescue glide should only be attempted with trained individuals. The plastic rescue glide is very resilient and can be folded easily to fit into any car. The tough resilient plastic is flexible; that is, it can move over almost any type of terrain. This plastic glide helps prevent iatrogenic injury to the face, skin and eyes, because the animal is positioned totally on the glide.

EQUIPMENT NEEDED INCLUDE:  Equine Rescue Glide (www.rescueglides.com)  3 inch ratchet straps  OR large rubber mat, plywood attached to  2 inch webbing with industrial strength a gate or tarp/horse blanket Velcro that is 6 ft long  (2) 20ft section of 4 in width nylon webbing  Hobble rope, 15 ft long with a simple pully (Fire hose or tow strap) and carabiner 28 The Practitioner

 Hobbles with prusick loops and carabiners  Fleece pads (a minimum of 5)  Head protection (Towels, shirt saddle pad)  Sedatives (Xylazine, Detomidine, Romifidine)  IV catheters/fluid lines and extension sets Issue 3 • 2016

 Repeat this procedure for the hind

Figure 2 Backwards Assist (Figure 2)  Use 3 to 4 inch webbing (15 to 20 ft long)  “Floss” under the back end  Lift the rear end off the ground with the tail  Center mark is placed over the middle of the back  Both loops are passed between the hind legs  BE CAREFUL OF THE PENIS, SCROTUM OR UDDER Placing and transporting the horse on the glide (Figure 3)  Place protection over the head  Slide a 15-20 ft section of nylon webbing under the horse and behind the front legs to help move the horse onto the glide.  Use the nylon web, mane and tail to properly perform a sideways assist and position the horse properly on the rescue glide  Always have someone on the head to prevent further injury  ALTERNATIVELY, the horse can be rolled onto the glide with control of any injured extremities and the head. MAKE SURE FRONT LEGS DO NOT INTERFERE with the anchor openings on the glide.

end by placing the strap over the flank region in front of the hind legs.  TENSION SHOULD BE ASSESSED SEVERAL TIMES during packaging and transport to ensure that it is tight enough to hold the animal down but not so tight as to interfere with breathing  Attach the four hobbles to the pas tern area of the legs. It is safest to attach hobbles by keeping your body near the back to work on the legs.  Using the carabiner, connect the front leg and back leg hob bles from the same side to each other. If here is an INJURED EXTREMITY then do not connect to the hobbles. Instead, a rope may be tied to the prusik loop on the hobble for control of the extremity during movement  Tie one end of the hobble rope (the one with the pulley and carabiner) to the same opening where the front ratchet is attached to the glide  Slide the free end of the rope through the same anchor opening where the other end is tied to the glide. Place a fleece pad under the rope over the horse’s chest.  Pull the free end of the rope through the pulley, and flex all four legs as close as possible to the body.  Now tie the free end of the rope to the glide to maintain the legs in proper position  Pull the Velcro head strap from underneath the Glide through the front slit openings. Secure the head to the glide with the Velcro strap  The horse is ready to be moved. Straps should be checked for tension regularly and after movement across terrain or once in the trailer. (Figure 3) Always monitor for signs of shock and hyperthermia. A horse is less capable of thermoregulating when combining

 One person must keep control of the

horse’s head at all times even when sedated. A knee over the neck and tipping of the nose upwards decreases the chance of the horse getting up during the procedure. This person can monitor the vital signs  Place one of the ratchet straps over the rib cage at the point of the withers and behind the shoulder of the front legs. Secure both ends of the strap to the glide and fit into the opening underneath to prevent loss of the anchor. Put tension on the strap until the edges of the glide start to lift. USE FLEECE PADS TO PROTECT the skin from the strap and ratchet. WWW.FAEP.NET |

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Figure 3 FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 29

sedation with lateral recumbency for several hours. The use of the following SOP provides an option for successful movement and transport of the recumbent horse during an emergency. REMEMBER, use of this equipment requires significant personnel training.

Treatment

Treatment must be tailored to the primary disease and conditions associated with the recumbent animal. If an animal is exhausted and hyperthermic, then cold water or ice packs may be placed on some of the great vessels in order to properly thermoregulate the horse. The author has occasionally had to give ice water enemas to help reverse life-threatening hyperthermia. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay drugs in equine medicine for their antiinflammatory and analgesic properties. These are ideal medication for the management of the recumbent horse. Adequate hydration is vital when using NSAIDS as acute renal tubular necrosis can occur. Phenylbutazone (1.1 mg/ kg bwt IV or PO q 12 hours), Flunixin Meglumine (1.1 mg/ kg IV or PO q 12 hours) and ketoprofen (2.2 mg/kg IV Q 24 hours) are commonly used in horses. Corticosteroids (CS) are still considered a drug of choice for acute neurological disease, but it is not without some controversy. Doses and CS commonly used by the author include dexamethasone 0.1 mg/kg IV Q 12 to 24 hours for 24-72 hours. A favorable response can be noted as early as 4-8 hours post CS administration. The use of methylprednisolone sodium succinate is also used at a rate of 1-2 mg/kg IV Q 6-24 hours depending on the cause for the recumbency. The neuroprotectve effects of CS have been shown to be mediated by free-radical scavenging and decrease apoptosisrelated cell death in rats subjected to traumatic spinal cord injury. Other potential effects of CS include reduction in the spread of morphological damage, prevention of the loss of axonal conduction and reflex activity, preservation of vascular membrane integrity, and stabilization of white matter neuronal cell membranes in the presence of central hemorrhagic lesions. In conclusion, there is data illustrating the beneficial effects of CS for neurotrauma and therefore the author believes CS should be considered a drug of choice for acute neurological disease. Dimethylsulphoxide (DMSO) 1g/kg IV SID to BID as a 10-20% solution for 3 consecutive days followed by 3 more treatments every other day, has been found to be of benefit in acute neurological disease. Reported benefits include increased brain and spinal cord blood flow, decreased brain and spinal cord edema, increased vasodilating PGE1, decreased platelet aggregation, decreased PGE2, and PGF2, protection of cell membranes and trapping of hydroxyl radicals. The exact mechanisms of DMSO are unknown and the use remains controversial. Osmotic diuretics such as 20% mannitol (0.5 to 1mg/kg IV over 20 minutes Q 6-24 hours) are effective for reducing 30 The Practitioner

cerebral edema and increased cerebral intracranial pressure. These medications have a very rapid onset of action (10-20 minutes) and work because of their hyperosmolar nature. Hypertonic saline administered early in the treatment of shock with head trauma, may enhance return of cerebral blood flow and cell membrane function. Effects of hypertonic saline are due to its ability to move water out of cells, and to decrease tissue pressure and cell size by osmotic plasma expansion. Hypertonic saline has been given in the author's practice for head trauma patients as a 5% of 7% sodium chloride solution in a 4 ml/kg to as high as 6ml/kg bolus IV over 15-20 minutes.

Antimicrobial medications

Antimicrobial medications may be required for secondary complications associated with a recumbent horse; for example, decubital ulcers, laceration and pneumonia. The author has diagnosed bacterial meningitis in patients that appeared to have sustained traumatic head injury 5-7 days before presentation. Therefore, the use of antimicrobials may be warranted as a prophylactic measure against bacterial meningitis in these patients.

Summary

Managing recumbent horses is now common practice at equine events, and although demanding and time consuming, can be a rewarding endeavor as many of these horses regain normal function. A complete exam should be performed in order to make an accurate diagnosis. This may include ancillary diagnostics such as radiology, clinical pathology and /or spinal fluid evaluations.

Nathan Marc Slovis, DVM, DACVIM, CHT Dr. Nathan Slovis is the Director of the McGee Medical and Critical Care Center at the Hagyard Equine Medical Institute located in Lexington, Kentucky. He is a native of Annapolis, Maryland. He received his Bachelor of Science from Radford University, Doctor of Veterinary Medicine from Purdue University, interned at Arizona Equine Center and completed his residency in Internal Medicine at the University of California, Davis. Dr. Slovis has published over 40 manuscripts in both national and international peer reviewed veterinary journals. He is the Editor of both the Atlas of Equine Endoscopy and The Atlas of Diseases/Disorders of the Foal, both distributed by Elsevier. He implemented the current Infectious Disease and Equine Emergency Response Programs at Hagyard Equine Medical Institute. Dr. Slovis is also a Certified Hyperbaric Technologist and a Member of the Veterinary Infectious Disease Society. He maintains strong interests in infectious diseases, neonatology, neurology, cardiology, dermatology, critical care medicine and hyperbaric medicine.

Issue 3 • 2016

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