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Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 3 • 2015

Diagnosis and Management of Avulsion Injuries

o f th e Fo ot

Ted S. Stashak DVM, MS, DACVS, Professor Emeritus Surgery

The Variability in Response to Diagnostic Analgesia of the Digit W. Rich Redding


Equine Rectal Exam: What Am I Really Feeling? A Laparoscopic Perspective P.O. Eric Mueller


Join us at the

11th annual October 15-18, 2015

Promoting Excellence


Insights Into Optimizing Equine Athletic Performance


(clodronate injection) Bisphosphonate For use in horses only. Brief Summary (For Full Prescribing Information, see package insert) CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. DESCRIPTION: Clodronate disodium is a non-amino, chlorocontaining bisphosphonate. Chemically, clodronate disodium is (dichloromethylene) diphosphonic acid disodium salt and is manufactured from the tetrahydrate form.

A stride forward

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

for Navicular Syndrome

WARNINGS: Do not use in horses intended for human consumption. HUMAN WARNINGS: Not for human use. Keep this and all drugs out of the reach of children. Consult a physician in case of accidental human exposure.

Introducing OSPHOS, the new

PRECAUTIONS: As a class, bisphosphonates may be associated with gastrointestinal and renal toxicity. Sensitivity to drug associated adverse reactions varies with the individual patient. Renal and gastrointestinal adverse reactions may be associated with plasma concentrations of the drug. Bisphosphonates are excreted by the kidney; therefore, conditions causing renal impairment may increase plasma bisphosphonate concentrations resulting in an increased risk for adverse reactions. Concurrent administration of other potentially nephrotoxic drugs should be approached with caution and renal function should be monitored. Use of bisphosphonates in patients with conditions or diseases affecting renal function is not recommended. Administration of bisphosphonates has been associated with abdominal pain (colic), discomfort, and agitation in horses. Clinical signs usually occur shortly after drug administration and may be associated with alterations in intestinal motility. In horses treated with OSPHOS these clinical signs usually began within 2 hours of treatment. Horses should be monitored for at least 2 hours following administration of OSPHOS.

FDA approved intramuscular bisphosphonate injection from Dechra Veterinary Products

Easily administered via intramuscular injection

Well tolerated* in clinical trials

Proven efficacy* at 6 months post treatment

No Reconstitution required

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


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Bisphosphonates affect plasma concentrations of some minerals and electrolytes such as calcium, magnesium and potassium, immediately post-treatment, with effects lasting up to several hours. Caution should be used when administering bisphosphonates to horses with conditions affecting mineral or electrolyte homeostasis (e.g. hyperkalemic periodic paralysis, hypocalcemia, etc.). The safe use of OSPHOS has not been evaluated in horses less than 4 years of age. The effect of bisphosphonates on the skeleton of growing horses has not been studied; however, bisphosphonates inhibit osteoclast activity which impacts bone turnover and may affect bone growth. Bisphosphonates should not be used in pregnant or lactating mares, or mares intended for breeding. The safe use of OSPHOS has not been evaluated in breeding horses or pregnant or lactating mares. Bisphosphonates are incorporated into the bone matrix, from where they are gradually released over periods of months to years. The extent of bisphosphonate incorporation into adult bone, and hence, the amount available for release back into the systemic circulation, is directly related to the total dose and duration of bisphosphonate use. Bisphosphonates have been shown to cause fetal developmental abnormalities in laboratory animals. The uptake of bisphosphonates into fetal bone may be greater than into maternal bone creating a possible risk for skeletal or other abnormalities in the fetus. Many drugs, including bisphosphonates, may be excreted in milk and may be absorbed by nursing animals. Increased bone fragility has been observed in animals treated with bisphosphonates at high doses or for long periods of time. Bisphosphonates inhibit bone resorption and decrease bone turnover which may lead to an inability to repair micro damage within the bone. In humans, atypical femur fractures have been reported in patients on long term bisphosphonate therapy; however, a causal relationship has not been established. ADVERSE REACTIONS: The most common adverse reactions reported in the field study were clinical signs of discomfort or nervousness, colic and/or pawing. Other signs reported were lip licking, yawning, head shaking, injection site swelling, and hives/pruritus.

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

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

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KY97 EIV* strain contained in FLUVAC INNOVATOR®

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OH03 EIV strain contained in CALVENZA®-03 EIV/EHV

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

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

All trademarks are the property of Zoetis Inc., its affiliates and/or its licensors. All other trademarks are the property of their respective owners. ©2015 Zoetis Inc. All rights reserved. FLU-00076 

The Practitioner  3

The President's Line Corey Miller, DVM, MS, Diplomate ACT - FAEP President

With summer and Labor Day behind us, your FAEP is celebrating another successful Student Appreciation Day in Ocala. This collaboration between FAEP members, three private veterinary practices and numerous volunteers provides hands-on experience for UF veterinary students with an equine interest, and concentrates on five areas: joint injections, regional nerve blocks, digital radiography, stallion collection/semen evaluation and processing, and digital ultrasonographic imaging. We take pride in being able to offer this kind of experience to UF students and can only do this because of the financial support from our educational partners. I would like to give a heartfelt thanks to everyone who contributed to this event. We are making final preparations for the 11th Annual Promoting Excellence Symposium (PES), which is scheduled for October 15–17, 2015 in Naples, FL. I hope you are planning to join us for an exceptional program, themed “Insights into Optimizing Equine Athletic Performance.” With limited seats remaining and anticipated record attendance, I encourage you to register to secure your place in the Biomechanics Wet Lab, which will be instructed by the foremost equine musculoskeletal system anatomist, Professor Jean-Marie Denoix. This year PES provides 48 hours of CE and includes a rehabilitation track that is open to veterinarians and rehabilitation professionals, as well as sessions both in dispensing legend drugs and in laws and rules for Florida-licensed veterinarians, as required for Florida license renewal in 2016. Along with our exceptional CE schedule, we’ve programmed special events that will give you valuable opportunities to socialize and network with colleagues, friends and new acquaintances, as well as make your conference experience enjoyable and memorable. You may find the details of each lecture, as well as other aspects of the conference, at We are also well on our way to planning next year’s CE offerings. You will soon begin to hear more details about the Ocala Equine Conference in January 2016, our Equine Foot Symposium in Summer 2016, and PES 2016. Next year is also a license renewal year, and Florida licensed veterinarians need to secure their required CE by May 31, 2016. As always, please feel free to contact me, any member of the FAEP Council, or anyone in the FVMA office with your questions or suggestions. We are proud to serve in a leadership capacity on your behalf. See you in Naples!



Suzan C. Oakley, DVM, MS, Diplomate ABVP(Equine), Cert. ISELP FAEP Council Past President

Adam Cayot, DVM

Anne L. Moretta, VMD, MS

Amanda M. House, DVM, Diplomate ACVIM Representative to FVMA Executive Board

Mr. Philip J. Hinkle Executive Director

Liane D. Puccia, DVM

Armon Blair, DVM

Ruth-Anne Richter, BSc (Hon), DVM, MS

Jacqueline S. Shellow, DVM, MS

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: | Website:

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

The link between FAST-ACTING and

LONG-LASTING relief 1, 2

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

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

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

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

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

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


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

Diagnosis and Management of Avulsion Injuries of the Foot Ted S. Stashak | DVM, MS, DACVS, Professor Emeritus Surgery Introduction Avulsion injury of the foot is relatively uncommon, but the injury may be serious enough to permanently limit function, and in some cases, euthanasia may be advised. The avulsion may be complete, where the tissue is totally removed, or incomplete, where a border remains intact. The injury may involve the hoof wall, the coronary band, and may extend to the pastern region or to the sole and to structures deep to the hoof capsule (e.g., distal phalanx, digital cushion, ungual [collateral] cartilage etc.). Generally, the deeper the avulsion and the more complete it is, the more serious the injury. However, even with significant loss of hoof, the foot has the capacity to heal, although slower than other tissues, with complete reforma­tion of hoof wall if the dermal coronary papilla and stratum germinativum of the epidermal laminae remain intact. The wound will need to be treated properly. Since a wound in the foot region does not heal by contraction, healing occurs primarily by epithelialization and reformation of the corium. These processes require a stable clean environment to reach an ideal conclusion. Although avulsion injuries of the coronary region, complete or incomplete, may result in deformities and/or permanent hoof wall defects, if treated properly initially, the majority heal without problems. If a horny spur develops as a result of incomplete avulsion or from partial avul­sion, it usually remains painful until surgical treatment is employed. Neither partial loss of the distal phalanx, or digital cushion, or collateral (ungual) cartilage of the distal phalanx appears to be a serious detriment to future soundness. Other complications that may arise from the injury include osteo­myelitis, septic arthritis of the coffin joint and tenosynovitis of the DDFT sheath (rare). Even if these complications are not present, the horse may remain permanently lame simply due to the volume of tissue loss.

Anatomy and Healing of the Hoof The hoof wall, or stratum corneum, is of epidermal origin and is usually divided into a stratum externum, which is a thin, superficial layer of horn that extends a variable distance from the periople, a stratum medium, which is thick and highly keratinized, and a softer stratum internum, which consists of the primary and secondary epidermal laminae (PEL and SEL, respectively). The stratum medium is composed of horn tubules that grow from the stratum germinativum of the coronary epidermis that surrounds the coronary papillae. The coronary corium and perioplic corium, both of dermal origin, and the coronary epidermis comprise the coronary band. The underlying modified subcutis, or coronary cushion, is often considered part of the coronary band. The lamellar corium, of dermal origin, overlies the periosteum of the distal phalanx and is tightly interlocked with the epidermal laminae of the hoof. In cases of avulsion, the stratum germinativum of the epidermal 

laminae usually remains adhered to the dermal laminae of the lamellar corium, thus sparing the cells which are responsible for the rapid epithelialization and keratinization often seen in the wound bed. The lamellar basement membrane, left intact, is used as a template for proliferating epidermal cells. Although the time required for healing of an avulsion injury depends on the size, location and extent of the avulsion injury and the method of treatment, the growth of the hoof wall distad in an adult is ~ 10 mm/month, which translates to ~ 9 months in the quarters and 12 months in the dorsal hoof wall for complete healing of an avulsion injury to proximal hoof wall. Hoof wall renewal time for foals is ~ 4-6 months, which is almost twice as fast as that of adults. Incomplete avulsions that are reconstructed surgically usually heal in 4-6 weeks. Even when healing appears complete, soundness may not be appreci­ated for many months, and in some cases, a year may be required.

Causes An incomplete avulsion of the hoof wall involving the heel/ quarter region, is usually initiated by a small vertical tear of the white line at the heel. If infection becomes established, it can result in progressive separation between the epidermal and dermal laminae. Vertical tears may occur following the horse kicking at or stepping on a sharp object or from improper shoe removal where nails are torn out of the heel and quarter regions. Avulsion of a portion of the hoof capsule is most often caused by kicking at or stepping on a sharp object but may occasionally occur when the foot becomes entrapped between two immovable objects. A portion of the hoof capsule may be totally avulsed, or partially avulsed, so that it remains attached to some degree, usually at the coronary band. Rarely, the hoof capsule is completely avulsed after the foot becomes entrapped momentarily between fixed objects during exercise. An avulsion may extend to the pastern region or sole, and may involve critical structures deep to the hoof capsule, such as the distal phalanx or distal interphalangeal joint.

Clinical Signs and Diagnosis The degree of lameness usually varies with the duration, extent, and location of the avulsion injury. Because of its close proximity to the ground, a wound in the hoof capsule quickly becomes contaminated with manure and dirt, and if the horse is not treated appropriately and promptly, contamination results in infection, which may cause separation of epidermal and dermal laminae (Fig. 1). In these, a hollow sound may be heard when the affected region of the hoof wall is struck with a solid object. The presence of a horny spur at the distal extent of the pastern region, typically growing at a right or oblique angle to the pastern and sometimes accompanied by abnormal growth of hoof wall distal to it, is an indication that the horse has suffered The Practitioner  7 

partial avulsion of a portion of the hoof capsule and coronary band (Fig. 2). Although the wound may be healed, the horse may traumatize the projecting spur, causing it to bleed at its attachment. Palpating the horny spur, and particularly pushing it proximally, is usually painful.

Figure 3:

Figure 1:

Left – An example of hoof wall separation as a result of undermining of the hoof capsule due to infection in the heel and quarter. Right – After the separated hoof wall was resected.

Figure 2: A horny spur that

developed in the pastern region following a partial avulsion injury to hoof wall and coronary band. Moderate lameness is usually seen with the acute superficial injury that does not involve deeper vital structures. However, palpation may cause considerable pain and render the animal nonweight-bearing. More extensive avulsion injuries usually result in a non-weight-bearing lameness. If the injury involves the digital vessels, hemorrhage may be excessive, resulting in shock. Gentle manipulation of the foot and phalanges can provide important information regarding the status of support struc­tures. Where laxity and instability of a joint indicate loss of collateral ligament support, a sucking noise may indicate an open joint. More discriminate palpation is performed after the region has been cleaned and antiseptically prepared. For the chronic avulsion injury, varying degrees of lameness will be seen. If the wound is healing without problems, lameness usually subsides with time. However, if lameness is persistent, look for the cause. This often requires radio­graphic examination, and in some cases, ultrasound examination may be helpful to assess soft tissue invol­vement. If a portion of the wound remains unhealed, and drainage is present, or his­torically drainage or pus is seen periodically, infection deep to the site is the likely problem. Although the diagnosis of avulsion injury is straightforward, the involvement of deeper structures should be identified. Prior to a more complete examination of the injury, the hair is clipped from the surrounding wound, after which, it is cleaned with an antiseptic scrub. The skin surrounding the wound and the wound are then irrigated with a dilute antiseptic solution (e.g., povidone 8  The Practitioner 

iodine [0.1%–0.2%] or chlorhexidine [0.5%]) delivered at least at 7 PSI. If the avulsion extends to the sole, the sole may be trimmed and cleaned in a similar fashion. Loose pieces of dead tissue and debris are removed during this cleaning process. Once complete, the wound is palpated with a gloved hand. Further manipulation of the foot and phalanges at this time may be helpful to identify an open synovial structure, torn support structure, or a potential fracture of the distal phalanx (Fig. 3). A sterile probe can be used for palpation of a small opening.

Left – Extensive incomplete avulsion injury that extends from the coronary band to the collateral sulci. Right – Palpation indicates instability of the avulsed hoof wall.

Radiographic Examination Since fracture of the distal and middle phalanx may accompany the injury, radiographic examination should be performed on all cases where deep avulsion is present (Fig. 4) or where a draining tract has developed during the healing process. Additionally, a contrast radiographic study of a draining tract may be helpful in iden­tifying any open synovial structures.

Figure 4: DP radiograph of the horse in Fig. 3 identifying a P3 fracture.

Treatment The selection of restraint required for repair depends on the nature and extent of the injury. An acute laceration or avulsion injury to the coronary band, involving the hoof capsule, can usually be sutured with the horse sedated after the foot is desensitized by administering regional anesthesia. The horse should be anesthetized if the injury is extensive or involves the distal phalanx, a synovial cavity or a supporting structure, such as a collateral ligament or the deep digital flexor tendon sheath. To prepare the horse for surgery, the hoof capsule surrounding the wound should be rasped to remove contaminants, and the foot trimmed, if these procedures were not performed when the wound was initially evaluated. The wound and surrounding area should be cleaned as described previously, and the wound should be isolated with sterile drapes. Generally, systemic antibiotics are not required unless a question exists regarding the blood supply or the cleanliness of surgery, or a synovial structure was penetrated.

Incomplete Avulsion Injury of the Hoof Wall Incomplete avulsion of the hoof wall can be managed by Issue 3 • 2015

removing the avulsed wall. A sharp hoof knife and nippers can be used to excise the avulsed wall; however, care should be taken not to tear healthy dermal papillae and dermal laminar tissues. A motorized burr can be used to bevel the hoof wall at its attached edges to the dermal lamina, thus reducing the tendency for the edges to be snagged, resulting in further separation. All devitalized tissue and foreign material within the wound are debrided, including a fracture if present, until only healthy tissue remains (Fig. 5). If the dermal coronary papillae are intact, then horn tubules, which provide the structural strength to the layer, will form in the stratum medium during the healing process. If the papillae are lost, the structural strength of the stratum medium is lessened.

situation will be covered later under “Complete Avulsion.” An acute U-shaped incomplete avulsion injury of the coronary band and a small portion of the hoof wall may be treated by primary suture, if a good blood supply exists. The hoof wall adjacent to the defect, as well as the partially avulsed segment of hoof wall, can be thinned with a motorized burr to ease placement of sutures through the hoof wall, and the defect in the hoof wall is debrided to provide a clean, vascular bed into which the partially avulsed segment of hoof is replaced. The thinned horn of the partially avulsed segment is sutured to the thinned hoof wall adjacent to the defect using #0, or #1, nylon suture placed in a simple interrupted or vertical mattress pattern. If the blood supply is questionable or excessive contamination exists, delayed primary closure should be selected (Fig. 7). Usually, granulation tissue will have to be removed before the tissues are sutured. If left untreated, these incomplete avulsion injuries of the coronary band remain elevated, eventually producing a horny spur, while the remaining underlying tissue heals by scarring and epithelialization. Invariably, these partial avulsions protrude above the skin and hoof wall surface, making them susceptible to further trauma; and generally they are quite painful to palpation, and cause lameness.

Figure 7: Delayed closure was used to treat this incomplete Figure 5: Debridement of

avulsion injury at the cornet band. Granulation tissue was removed (upper right), and the avulsed horn was sutured.

hoof avulsion and fracture of P3 illustrated in Fig. 3. The dermal coronary papilla, just distal to the coronary band, are intact, below left. After debridement is complete, the wound should be irrigated with a mild antiseptic sterile salt solution delivered under pressure to achieve at least 7 PSI. Following this, an antiseptic dressing (e.g., betadine ointment or silver impregnated) should be applied to the wound, and held in place with a water impermeable bandage. Bandages are changed at two- to four-day intervals, at which time, the wound is cleaned, re-treated and protected in a similar fashion. Alternatively, a rubber or plastic boot can be used instead of a bandage, but a sterile dressing is still applied to the wound surface. Protection from contamination and the application of antiseptics are continued until exposed tissues become keratinized. After this, a full support shoe (eggbar, heart-bar shoe) can be ap­plied to eliminate the pressure on the healing hoof wall (Fig. 6). Doing this will optimize healing.

If the proximally displaced section of coronary band and horn tissue cannot be replaced into the hoof wall defect, or the injury is chronic and a prominent horn spur has formed, the horse is best treated by excising the germinal tissue that produces the horn spur (Fig. 2; 8, upper left & middle). This is especially the case if the horse is lame because of the spur, but becomes sound after the painful, horny spur is trimmed. Dermal papillae at

Figure 6: Example of a full support shoe. Note the nail placement on the right side.

Incomplete Avulsion Injury (coronary band involved and elevated) Incomplete avulsion injury to the coronary band is generally best managed by suture, although, in some cases, loss of blood supply will require excision of the separated tissue, thus converting it to a complete avulsion. The treatment for this latter 

Figure 8: Example of a chronic horn spur, resulting from an incomplete avulsion injury that was removed surgically. Note island grafts were used after a granulation tissue bed formed (below left). The Practitioner  9 

the coronary band should be spared as much as possible during excision of the more proximal germinal tissue. The resulting wound proximal to the coronary band is left to heal by second intention. If the wound is large, island grafts or a sheet graft can be used to shorten the healing time (Fig. 8). If the avulsion extends from the solar surface and extends proximad through the coronet, the majority of the hoof wall is removed to within 1 cm of the coronary region, and the coronary band and soft tissues are sutured. Accurate anatomic approximation of the coronary band is important (Fig. 9, left & center). The foot is then protected by application of a foot cast until the wound has healed. The cast is usually removed after 2-3 weeks, after which, bandages are maintained up to 6 weeks postopera­tively (Fig. 9, right). In cases where a portion of the hoof wall was excised, a full support shoe should be applied after the cast is removed to allow the healing region to rest. This is done shortly after the cast is removed.

of the wound, particularly if a dense scar has formed within the wound, can be helpful in restimulating the healing process.

Figure 10: Left – Complete avulsion injury involving the coronary band 3 weeks duration. Right – Complete healing, note the formation of imperfect hoof wall.

Conclusion Generally, incomplete avulsion injuries of the hoof wall alone and/or including the coronary band if they are sutured, will result in a functional, and in many cases, cosmetic end result. Prognosis for deeper avulsion injuries may have to be with­ held until complete healing has occurred. Complications such as fracture of the distal phalanx, osteomyelitis, septic arthritis and potential DJD of a damaged proximal interphalangeal joint and their implications in the prognosis should be discussed with the client at the onset of treatment.

Selected References:

Figure 9: Example of an incomplete avulsion injury where the

avulsed hoof wall was removed and the cornet band sutured. Right – A foot cast applied.

Complete Avulsion of the Hoof Wall and Coronary Band Second intention healing of a complete avulsion injury of the hoof wall and the coronary band, which includes the dermal papilla, will result in the formation of a hoof wall that lacks dermal papilla (Fig. 10, right). If the injury site is small and appears stable when the horse is walked, it may be managed by bandaging alone. If the wound is unstable and/or is large, a foot cast is recommended as soon as you are sure that infection will not be a problem (Fig. 10, right). The cast is usually left in place for 2-3 weeks. In some cases, several cast changes may be required before the wound is completely healed. The more stable the wound remains, the better the chance for reformation of the hoof wall to occur. If the injury is acute and involves deeper structures, the decision to apply a cast should be delayed until you are assured infection is not going to be a problem and a good blood supply exists. Debridement of necrotic tissue is important, including a lacerated ungual cartilage that ap­pears abnormal. All soft tissues and support structures should be assessed. If the injury has entered a synovial cavity, the cavity should be irrigated and adequate drainage should be afforded. Broad-spectrum antibiotics should be administered systemically. The injury should be protected in a sterile bandage until healthy tissue is formed. At this time, a foot cast can be applied. If the wound is chronic and already infected, cast application should be delayed until the infection is under control. Bandages are changed as often as necessary during this period. Addi­tionally, periodic debridement 10  The Practitioner 

Baxter GM, Stashak TS, Belknap J: Avulsion injuries of the foot. Adams & Stashak’s Lameness in horses, Baxter ed, 6th edition, Wiley Blackwell, 2011, pp 530-534. Honnas CM, et al: Surgical management of difficult foot problems in the horse: Current concepts. Proc AAEP, 1988, 34:249. Markel MD, Richardson GL, Peterson PR, Meagher DM: Surgical reconstruction of chronic coronary band avulsion in three horses. J Am Vet Med Assoc, 1987, 190:687. Pascoe JR: Difficult foot wounds. Proc, Bain Fallon Memorial Lecture, 1990, 12:33. Stashak TS: Management of lacerations and avulsion injuries of the foot and pastern region and hoof wall cracks. Vet Clin North Am: Equine Pract, 1989, 5:195. Young J: Hoof wall avulsion: Three case reports. J Equine Vet Sci, 1988, 8:420.

Ted S. Stashak, DVM, MS, DACVS, Professor Emeritus Surgery Dr. Stashak received his DVM degree from the University of California at Davis in 1971, and completed an internship and a surgical residency at Colorado State University. Dr. Stashak received an MS degree from Colorado State University in 1974 and became a Diplomate of the American College of Veterinary Surgeons in 1977. He joined the surgical faculty at Colorado State University as an Assistant Professor in 1974, and in 1976 accepted a position in the School of Veterinary Medicine at the University of Florida. He became Chairman of the Department of Surgical Sciences in 1977. In 1979, he returned to Colorado State University and served as Head of Equine Services from 1987 to 1990, and from 1993 to 2002. Dr. Stashak retired from CSU in June, 2004 and is currently a Professor Emeritus, surgery at the School of Veterinary Medicine and Biomedical Sciences. Dr. Stashak has authored, edited or otherwise been involved in more than 120 equine and scientific publications and is a sought after equine speaker for state, national and international meetings. He served as a Regent for the American College of Veterinary Surgeons from 1996-1999 and served as President of the Veterinary Wound Management Society 2003-2006.

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The Practitioner  13

The Variability in Response to Diagnostic Analgesia of the Digit W. Rich Redding | DVM, MS, DACVS A thorough clinical examination is an essential part of any lameness examination of the horse. An accurate diagnosis is critical to direct the most effective treatment(s) and return the horse to soundness. However, a careful clinical examination does not always identify the cause of lameness, particularly if the source is within the foot. Diagnostic analgesia, commonly used by equine veterinarians, is utilized to confirm a region as a source of pain creating lameness and direct diagnostic imaging at that location. Diagnostic analgesia of the distal limb can be performed as a local (regional), intrasynovial or peri-neural infiltration technique. Peri-neural analgesia is the simplest approach, and most commonly used, but is the least specific. Proper technique requires careful placement of the needle over the nerve with injection of a minimal volume of anesthetic. However, confusing results often occur that are attributed to individual variations in nerve supply which influences the effectiveness of the local anesthetic; but also to the extent of the pathologic conditions creating with the lameness. This presentation discusses the limitations of diagnostic analgesia of the lower limb, the potential causes for misinterpretation, and options to provide more specific desensitization of the structures in the digit.

Diagnostic Analgesia of the Distal Limb The clinician should have a complete understanding of the anatomy of the limb and be familiar with the sites to perform perineural analgesia, and for intrasynovial injections. In the lower front limb, the clinician should be comfortable with performing the palmar digital, basi-sesamoid, low palmar (low four point) nerve blocks as well as the approaches to the distal interphalangeal (DIP), the navicular bursa, the digital flexor tendon sheath, proximal interphalangeal (PIP), and the metacarpophalangeal joints. Peri-neural diagnostic nerve blocks are less specific and should be performed in a distal to proximal sequence. Perineural nerve blocks carry the risk that structures proximal to the site of injection may be desensitized due to proximal diffusion. Intrasynovial (joints, sheaths, & bursae) blocks, being more specific, can be performed at any time in the lameness workup without regard to the sequence of peri-neural blocks. In an effort to minimize the number of blocks performed, intrasynovial blocks can be directed to the most likely site of pain that occurs in the discipline and level of training of the horse being examined. However, in the digit, this is not always appropriate. For example, local anesthetics injected in the DIP joint, given enough time and volume (10 minutes and more than 6 mLs), can diffuse out of the joint and desensitize the navicular bone and suspensory apparatus and palmar digital nerves. In contrast, some joints may not be effectively blocked by intra-synovial analgesia due to significant subchondral bone pain. Subchondral bone pain present in the distal phalanx associated with a subchondral bone cyst may occasionally be more effectively blocked by a palmar digital block than by intrasynovial analgesia. 14  The Practitionerâ€

Palmar Digital Nerve Block Recent studies have challenged the long-standing belief that a palmar digital nerve block eliminates pain from the palmar third of the foot. Studies by Sack (1975), Schumacher et al. (1999) and Easter et al. (2000) have determined that the entire DIP joint and sole of the foot can be effectively blocked by a PDN block. However, studies by Ross (1998) and Schumacher et al. (2003) have demonstrated the imprecision of the PDN block in localizing pain to the foot. Even properly performed nerve blocks can anesthetize structures proximal to the site of injection. The location of the PDN block should be at or distal to the level of the proximal margin of the ungular cartilages with a volume of no more than 1.5 mLs.

Abaxial Nerve Block (Basi-sesamoid) Analgesia of the palmar digital nerves and their dorsal branches at the level of the proximal sesamoid bones desensitizes the entire foot, the middle phalanx, the distopalmar aspect of the proximal phalanx, and the soft tissues of the pastern area (including the distal sesamoidean ligaments, the distal aspects of the deep and superficial flexor tendons and collateral ligaments of the DIP & PIP joints). The dorsal branches of the PDNs are thought to contribute little to the sensation of the foot other than the dorsal coronary band and dorsal laminae of the foot. A basi-sesamoid block should be performed to minimize the risk of desensitizing part of the metacarpophalangeal joint, whereby the needle is directed distally with no more than 2 mL anesthetic. Sesamoid problems such as fractures and axial sesamoid lesions, lameness originating within the fetlock, and suspensory branch desmitis have been desensitized by a properly applied abaxial sesamoid nerve block. If lameness is improved by an abaxial nerve block and an etiology for the lameness cannot be found distal to the fetlock, careful investigation of the fetlock area is indicated.

Analgesia of the DIP Joint Administration of 6 mL of mepivacaine into the DIP joint desensitizes the DIP joint, the navicular area and the toe region of the sole. Administration of 10 mL into the DIP joint causes the heel region of the sole to also be desensitized (Schumacher et al. 2001). Analgesia of the DIP joint has been reported to quickly (within 5 minutes) anesthetize amphotericin induced inflammation of the navicular bursa (Pleasant 1997). Analgesia of the DIP joint can be considered more specific than analgesia attained with a PDN block in localizing pain within the foot, because lameness caused by solar pain in the heel region is not resolved when 6 mL of local anesthetic solution is utilized. A positive response to analgesia of the DIP joint and a negative response to analgesia of the navicular bursa indicate within the DIP joint. However, failure to diminish lameness after analgesia of the DIP joint does not eliminate the navicular bone and its related structures as the source of pain. Issue 3 • 2015

Analgesia of the Navicular Bursa A positive response to analgesia of the navicular bursa indicates disease of the navicular bursa, navicular bone, the navicular suspensory ligaments, solar toe pain and the distal deep digital flexor tendon. Analgesia of the navicular bursa does not result in analgesia of the DIP joint or in anesthesia of the sole in the heel region of the foot. Analgesia of the navicular bursa, therefore, may help to differentiate pain associated with disease of the DIP joint from pain associated with disease of the navicular area or from pain associated with the sole in the heel region of the foot. Analgesia of the navicular bursa is more specific than analgesia of the DIP joint because lameness caused by pain either in the solar portion of the heel or within the DIP joint is not likely to be resolved by analgesia of the navicular bursa.

Pastern Semi-ring Block To localize pain following lack of response to a PDNB, some clinicians perform the pastern semi-ring block to anesthetize the dorsal branches of the digital nerve as the next analgesic technique. To perform this block, 2 to 3 mL of local anesthetic solution is deposited subcutaneously through a 20 ga. 1 or 1.5 inch needle inserted at the site of the previously performed palmar digital nerve block and directed dorsolateral and dorsomedial parallel with the bearing surface of the foot. Because the dorsal branches of the digital nerve contribute little to sensation within the foot (Sack 1975), the pastern semi-ring block is unlikely to ameliorate a lameness that is not responsive to a PDNB.

Analgesia of the Digital Flexor Tendon Sheath Intrathecal analgesia of the digital flexor tendon sheath may be useful for localization of lameness that is unchanged after analgesia of the PDNs, but resolves after an abaxial sesamoid nerve block. It is thought that a portion of the deep digital flexor tendon within the foot receives its sensory supply from deep branches of the medial and lateral PDNs that enter the digital sheath more proximally. Resolution of lameness after intrathecal analgesia of the flexor tendon sheath justifies suspicion of a lesion of the digital portion of the deep digital flexor tendon (Schneider 2002). No specific research has evaluated which structures are desensitized by injecting local anesthetics into the digital sheath, but it is suspected that other than the DDF, it may also desensitize the SDF, SSL, OSL as the primary anular, and distal digital anular ligaments (Harper 2007). In humans, there appears to be quick diffusion out of the sheath with desensitization of local nerves. While this hasn’t been reported in the horse, it is recommended that the clinician should determine if skin sensation of the pastern is still present after a positive response to a sheath block to make sure there has not been diffusion of the anesthetic outside the sheath that might affect the PDNs.

Variations in the Results of Diagnostic Analgesia Inaccurate results occur and can be due to a variety of reasons. Lameness clinicians must always interpret the results of the diagnostic analgesia in the context of the clinical exam and imaging results. Clinician experience can lead to the recognition of significant physical findings that may or may not be associated with lameness. The availability of advanced imaging capabilities

can further enhance the clinician’s ability to recognize significant clinical findings. For example, the incorporation of MR imaging into the lameness workup of horses has often demonstrated obvious active lesions in locations thought not to be desensitized by a specific block (false positive). Some other common examples of incompatible diagnostic analgesia results are discussed. Improvement in lameness may be due to the horse “warming out” of the lameness and not due to the effects of a recently applied nerve block. Inadvertent (and unknowing) injection of the local analgesic into a blood vessel or underlying synovial structure, rather than perineurally, can lead to false negative results. Local anesthetics, being weak acids, require an alkaline environment typically found in normal subcutaneous tissue to dissociate and have an effect. Cellulitis or septic arthritis create a more acidic environment and diminishes dissociation of the anesthetic, therefore reducing effectiveness. An increase in lameness severity after a basi-sesamoid block has been reported (and in the author’s experience occurs rather often) in cases of proximal suspensory ligament desmitis of the front limb. Often, when the foot is desensitized (and is not at that time the primary source of pain), lameness may become worse. Desensitization of the foot reduces its proprioceptive function and the horse is less able to adapt its gait to decrease strain placed on the suspensory apparatus which can result in an increase in the degree of lameness. To confuse the issue even more, the foot may in fact be a co-existent source of lameness but only presents itself later after the treatment(s) and rehabilitation have reduced the pain associated with the desmitis. Severe foot pain in the form of subsolar abscesses, P3 fractures, navicular bone fractures, laminitis, or moderate to severe DDF tendinitis may be unaffected by PDN blocks, and often also, with blocks performed at the base of the proximal sesamoid bones (PSBs). Historically, it has been believed that an appropriately placed nerve block had minimal proximal diffusion from the site of injection. However, as mentioned earlier, structures proximal to the site of the nerve block have been effectively desensitized by a more distal block (creating a false positive response). This situation probably occurs more commonly than previously believed and is probably influenced by the volume of anesthetic used. A study looking at perineural injection of 2 mL of a radiodense contrast medium (iohexol) around the palmar nerves at the base of the PSB, demonstrated that there was immediate proximal spread of the contrast medium detected radiographically. Within 10 minutes, the mean proximal spread was 16.9 +/- 13.7 mm and further spread up to 30 minutes after injection (mean, 20.8 +/- 15.1 mm) (Nagy, Dyson 2009). In addition, distribution of contrast medium in a patch outside the neurovascular bundle occurred occasionally, as did proximal spread occurring in a lymphatic vessel. These observations may explain a delayed onset of desensitization or false-negative results. Diagnostic analgesia results of the horses that had MRI examination of the fetlock in 40 horses (Gonzalez 2010) was not reported but is discussed here. Lameness was completely resolved in 25 horses while 13 were significantly improved. As expected, intra-articular analgesia when done, improved lameness in 23 out of 26 horses in which it was performed and lameness was significantly improved, with a low 4- or 6-point nerve block in 12 horses. However, some very confusing results Continued on Page 18 

The Practitioner  15 

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did also occur. For example, palmar digital analgesia resulted in significant improvement of lameness in 7 horses and basisesamoid analgesia significantly improved lameness in 8 horses. Digital flexor tendon sheath analgesia was performed in 6 horses and lameness improved significantly in 5. Thirteen of 23 horses that improved to intra-articular analgesia had extra-articular soft tissue injuries confirmed with MR examination. Injury to the distal branches of the suspensory ligament (4/7 horses) or distal sesamoidean ligaments (6/9 horses) was abolished with intraarticular analgesia. MRI of the fetlock region has demonstrated that diagnostic analgesia is not as specific as had been previously believed.

References Sack, WO, Nerve distribution in the metacarpus and front digit of the horse. JAVMA. 1975 Aug 15,167, 298-335. Schumacher J, Schramme M, Schumacher J, DeGraves F, Steiger R, Smith R, Coker M:Abolition of lameness caused by experimentally induced solar pain in horses after analgesia of the distal interphalangeal joint; Proc. AAEP. 1999, Vol. 45, 193-194. Schumacher J, Schramme M, Schumacher J, DeGraves F, Steiger R, Smith R, Coker M: The effect of volume of local anesthetic administered into the coffin joint on solar toe or heel pain. Proc. AAEP. 2000, Vol. 46, 27-28.

W. Rich Redding, DVM, MS, DACVS Dr. W. Rich Redding was a 1983 graduate of the University of Florida School of Veterinary Medicine. After graduation he moved to Lexington, KY and worked at a large Standardbred farm, and followed with a rotating internship at Virginia-Maryland Regional College of Veterinary Medicine at equine hospitals in Blacksburg and Leesburg. After spending two years in private practice in Middleburg, VA specializing in lameness of the performance horse, Dr. Redding took up large animal residency training in surgery in 1987 at Iowa State University which he completed in 1990. He developed a lameness/ ultrasound/surgery consultation practice at 3 racetracks in the Midwest then passed his ACVS examination in 1995. Since then he’s been a member of faculty of North Carolina State College of Veterinary Medicine where he is a Clinical Associate Professor in lameness and orthopedics. Dr. Redding’s mixed background has allowed him to develop an expertise in lameness, diagnostic imaging and orthopedic surgery specific to the performance horse.

Easter LE, Watkins JP, Stephens S, Carter GK, Hague BA, Dutton DW, Honnas CM, Effects of regional anesthesia on experimentally induced coffin joint synovitis. Proc. AAEP. 46 / 2000, 214-216. Ross MW. Observations in horses with lameness abolished by palmar digital analgesia,. Proc. AAEP, 1998, Vol. 44; 230–232.

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Schumacher J, Livesey L, Schramme MC, et al. Effect of anesthesia of the palmar digital nerves on lameness caused by pain in the proximal interphalangeal joint, Proc AAEP,Vol. 49, 2003; 287–290. Pleasant RS, Moll HD, Ley WB, et al. Intra-articular analgesia of the DIP joint alleviates lameness associated with the navicular bursa in horses. Vet Surg 1997;26:137–140. Carter K, Diagnostic analgesia in the lameness exam; potential areas of confusion. Proceedings. Proc AAEP, 2005, Vol. 51,1-5. Gonzalez L, Schramme MC, Robertson ID, Thrall DE, Redding W R, MRI Features of Metacarpo(tarso)phalangeal Region Lameness in 40 Horses, Vet Rad & Ultrasound, 51, 4, July/August 2010, 404-14. Harper J, Schumacher J, DeGraves F, Schramme M, Schumacher J, Effects of analgesia of the digital flexor tendon sheath on pain originating in the sole, distal interphalangeal joint o rnavicular bursa of horse. EVJ (2007), 39, (6), 356-359. Nagy A, Bodo G, Dyson S, et al. Diffusion of contrast medium after perineural injection of the palmar nerves: an in vivo and in vitro study. Equine Vet J 2009;41:379–383.

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Issue 3 • 2015



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The Practitioner  19 

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The Practitioner  21 

Equine Rectal Exam:

What Am I Really Feeling? A Laparoscopic Perspective P.O. Eric Mueller | DVM, PhD, DACVS Introduction

fingers and thumb of the hand should be kept together in an A complete and thorough rectal examination is an essential extended position throughout the entire examination. Once the component of a diagnostic evaluation when examining horses hand is through the anal sphincter, the feces within the rectum with abdominal pain. Rectal examination findings should are evacuated. The amount and consistency of fecal material in always be considered in conjunction with the results of physical the rectum should be noted. Absence of fecal material, or the examination, nasogastric intubation, abdominocentesis, and presence of dry, fibrin and mucous covered feces is abnormal and laboratory evaluation. A rectal examination should always be is consistent with delayed intestinal transit. Fetid, watery, fecal performed before abdominocentesis in order to recognize an material is often present in horses with colitis. Large amounts extremely gas-distended or ingesta-filled cecum or large intestine. of sand within the feces may be indicative of a sand impaction or If these abnormalities are identified, extreme care must be taken sand-induced colitis. After evacuation of feces from the rectum, when performing an abdominocentesis to avoid accidental intra-rectal administration of 50-60 mL of 2% lidocaine via a 60 enterocentesis. cc catheter tip syringe may help promote further rectal relaxation Occasionally, rectal examination findings clearly indicate the and reduce straining. The syringe may also be used to administer specific disease, such as a renosplenic entrapment, early ileal additional lubrication into the rectum at this time. impaction, or herniation of small intestine through the inguinal The examiner’s arm is then re-introduced into the rectum ring in a stallion. Most often, however, rectal examination does and advanced slowly and steadily as far as comfortably possible. not yield a specific diagnosis, but yields information regarding The arm is left in this position without excessive movement for the severity of the problem and the need for surgical intervention. 20 to 30 seconds. In most cases, this initial delay in internal Abnormal rectal examination findings include abnormal palpation will allow the rectum to relax around the examiner's positioning of the intestine, distention of the intestine with gas arm, facilitating a more thorough palpation of the more cranial or ingesta, abnormally thickened intestinal wall, and the presence aspects of the abdomen. Initial examination of the caudal aspects of intra- or extra-luminal masses. of the abdomen with a half-inserted arm is not recommended The size and depth of the peritoneal cavity in the horse limit because it usually results in straining and excessive peristaltic the examiner to palpation of the caudal 25-30% of the peritoneal contraction of the rectum. cavity. Because of the inability to examine the entire peritoneal The most severe complication associated with rectal palpation cavity, subtle abnormalities identified on examination are often is an iatrogenic rectal tear. Although rare, tears usually occur used to make inferences concerning the more cranial regions of dorsally between the 10 and 12 o'clock positions. Most rectal the peritoneal cavity. Consequently, the lack of abnormal rectal tears can be avoided by proper restraint, adequate lubrication, examination findings does not completely rule out an intestinal and steady and careful palpation technique. If a peristaltic abnormality. contraction or increased resistance is felt during examination, the hand should immediately be withdrawn from the rectum to Technique avoid potential rectal injury. When performing a rectal examination, proper restraint is of The examination should be performed in a consistent, the utmost importance to assure the safety of the horse and the systematic manner to assure a complete and thorough examiner. Inadequate restraint may result in iatrogenic rectal examination and minimize the chance of missing a lesion. I prefer tear, a potentially fatal complication of rectal examination, or a clockwise approach, starting with the spleen in the left dorsal serious injury to the examiner. A nose twitch should always be abdominal quadrant. This is followed by examination of the right used to control the patient. Horses that resist rectal examination, dorsal, right ventral, and left ventral quadrants. The pelvic canal or those with signs of unrelenting abdominal pain should be and more caudal structures are examined just before removal of sedated with xylazine (0.3-0.5 mg/kg, IV) or detomidine (.01-.05 the hand from the rectum. mg/kg, IV). The anticholinergic drug, N-butylscopolammonium In general, palpable characteristics of the abdominal contents bromidea may also be administered (0.3 mg/kg, IV or 7-ml/450-kg and viscera are often helpful in identifying the particular segment horse) to promote rectal relaxation. It should be noted that the of the intestine involved and the severity of the condition. The anticholinergic actions of the drug cause a marked increase in small intestine has a characteristically smooth serosal surface, heart rate that may last for up to 30 minutes after administration. with distention usually involving multiple loops of small intestine. Adequate lubrication of the examiner's hand and arm is The serosal surface of cecum, and ventral ascending colon contains necessary to minimize irritation to the rectal mucosa. Hydrated multiple sacculations (haustra) and fibrous bands (taenia), while methylcellulose (Obstetric lube) is the most commonly used the dorsal colons and pelvic flexure have relatively smooth lubricant. Initial introduction of the examiner's hand through surfaces with no palpable bands. Severe gas or ingesta-distended the anal sphincter is often met with great resistance. Therefore, intestine, tight mesentery or taenia (bands), or thickened this should be performed with a slow and steady motion. The or turgid intestine are indicative of intestinal obstruction or 22  The Practitioner 

Issue 3 • 2015

strangulation. Free peritoneal gas or crepitus within the intestinal wall is usually indicative of intestinal rupture. A gritty or granular texture of the peritoneal cavity is indicative of intestinal rupture with contamination of the serosal and peritoneal surfaces with ingesta. It should be emphasized that rectal examination findings should always be interpreted in conjunction with the physical examination and laboratory findings.

Rectal Palpation of the Normal Horse In the normal horse, moist, soft fecal balls should be present in the rectal ampulla. The descending colon is easily identifiable in the caudal abdomen. It contains multiple, distinct fecal balls and is freely movable within the abdomen. Other intra-abdominal structures palpable in the normal horse starting in the left dorsal abdominal quadrant, and progressing in a clock-wise direction include: caudal border of the spleen, renosplenic ligament, caudal pole of the left kidney, portions of the mesentery ventral cecal taenia (no tension), cecal base (empty), and the pelvic flexure (Fig. 1). Normally, the duodenum and remaining small intestine are too soft and relaxed to be identified unless an underlying abnormality exists.

taenia with the tips of the examiner’s forefingers. These bands usually course in a dorsocaudal to ventrocranial direction, just to the right of the midline. Because the majority of the body and apex of the cecum are beyond the examiner’s reach, the tautness of the ventral and medial cecal taenia is used as an indicator of the amount of ingesta within the cecum. Normally, the cecal taenia should be loose and easily movable. With increased amounts of ingesta in the cecum, the taenia becomes more taut. In addition to cecal disease, pain elicited upon palpation of the ventral or medial cecal taenia may be associated with tension of the ileum or its mesentery. This has been associated with pain originating from the ileum and its vasculature, such as occurs with entrapment of the ileum in the epiploic foramen. Moving caudally and to the left side, the pelvic flexure may or may not be palpable in the caudal left abdomen, depending on the amount of ingesta within the large colon. If the pelvic flexure and associated left dorsal large colon are palpable, they may be identified by soft ingesta, and the absence of the taenia and haustra (sacculations). The adjacent left ventral colon contains similar contents and has two free palpable taenia and haustra. The taenia should course in a cranial to caudal direction, from the left caudal abdomen to the left cranial abdomen. Additional structures in the caudal abdomen included in a complete rectal examination are: bladder, uterus and ovaries in the mare, and internal inguinal rings in the stallion. The inguinal rings are identified just cranial, lateral, and slightly ventral to the iliopectineal eminence of the anterior brim of the pelvis. In stallions, the inguinal rings are large enough for insertion of a finger. If the testis or epididymis has descended, the ductus deference is palpable in the caudomedial aspect of the ring. In geldings, the inguinal ring is palpable as only a slight depression and decreases in size with age.

Recognition of Intestinal Abnormalities Small Intestine

Figure 1: Caudal view depicting palpable intra-abdominal structures in a normal horse.

The spleen is located in the left dorsal abdomen. The caudal edge of the spleen is palpable against the body wall. The renosplenic ligament can be palpated coursing from the medial aspect of the head of the spleen, toward midline to the caudal pole of the left kidney. Immediately dorsal to the ligament is the renosplenic space. Three to four fingers may be placed in the renosplenic space. Moving the arm to the right and cranially along the dorsal midline, the aorta and portions of the mesentery may be palpated. The pulse in the aorta is easily palpable; however, the mesentery may be difficult to feel unless it is under tension secondary to intestinal distention or volvulus. Continuing to move in a clockwise direction, the base of the cecum is palpable in the right dorsal-lateral abdominal quadrant. The ventral and sometimes medial cecal taenia are usually palpable by sweeping the hand medial to lateral and caudally, hooking the 

Palpable small intestinal distention (Fig. 2) is always an indication of small intestinal obstruction. The obstruction may be a physical obstruction, such as an ileal impaction or small intestinal strangulation, or it may be a functional obstruction such as ileus, secondary to enteritis or non-strangulation intestinal infarction. The small intestine is of a similar diameter to the descending colon. The small colon is distinguished from the small intestine by the presence of both a mesenteric and antimesenteric band and fecal balls. Obstruction of the small intestine causes rapid dehydration of the ingesta in the ascending colon due to lack of fluid entering from the small intestine and ongoing absorption of fluid from the ascending colon. The colon becomes hard and indurated and feels as if it were vacuum-sealed. In a horse with an early small intestinal obstruction and little or no palpable small intestinal distention, the inexperienced examiner may interpret this finding as a primary large colon impaction. The taenia and haustra of an ascending colon that is secondarily dehydrated contour to the ingesta within the intestinal lumen and are easily palpable. This is in contrast to a primary large colon impaction, where the taenia and haustra become less distinct with increasing colonic distention. Non-specific small intestinal distention is the most common The Practitioner  23 

finding in horses with small intestinal lesions. However, occasionally specific findings identified on rectal examination will lead to a diagnosis. An ileal impaction, detected early in the disease process, may be palpable as a firm, tubular structure in the center of the abdomen, coursing toward the cecum. Herniation of small intestine through the inguinal ring in a stallion is palpable as small intestinal distention with a segment of small intestine or mesentery coursing into one of the inguinal rings. In these cases, the inguinal rings often feel asymmetric, and gentle traction on the mesentery associated with the affected ring elicits a painful response. Jejunojejunal intussusception causes generalized small intestinal distention, but the intussusceptum is occasionally palpable as an extremely thickened, edematous, tubular structure in the caudal aspect of the abdomen. Ileocecal intussusceptions are difficult to identify per rectum, but early in the disease process are occasionally identified as a turgid mass in the right dorsal abdomen. Rectal examination findings in horses with proximal enteritis may mimic those of a physical obstruction. With enteritis, however, the small intestinal distention is often less severe and easily compressible. With nasogastric decompression and intravenous fluid therapy, the intestinal distention often decreases.

just within the reach of the examiner. As the cecum becomes further distended, the weight of ingesta in the apex pulls the cecal base cranially within the abdomen, and the ventral taenia, which normally courses from the right dorsal to right ventral quadrant, crosses diagonally across the caudal abdomen, from the right dorsal to left cranioventral quadrant. As the cecum fills above the cecocolic orifice, complete obstruction occurs and the cecal base fills with fluid and gas. In cases of severe cecal tympany the cecal base feels like a tightly distended balloon in the right dorsal quadrant. The presence of severe cecal mural edema or emphysema is an indicator of intestinal compromise and possible cecal rupture, and is associated with a poor prognosis. The distinction between cecal impaction and right dorsal displacement of the large colon may be difficult during rectal examination. The cecum has a dorsalateral mesenteric attachment to the right abdominal wall. This attachment prevents the examiner from passing the hand lateral to the cecum. With right dorsal displacement of the large colon, the cecal base and taenia are cranial to the displaced large intestine, and therefore, are not palpable and the examiner's hand can be passed between the displaced colon and right lateral abdominal wall. Additionally, primary cecal impactions are palpable more cranially in the abdomen, while large colon distention will often extend caudally into the pelvic inlet.

Large Colon Abnormalities of the large colon have a variety of intestinal positions and degrees of intestinal distention, and include large colon impaction, left and right dorsal colon displacement, and colon volvulus. Impaction of the large colon usually occurs at the pelvic flexure and may be felt in the left or right caudal abdominal quadrants. The colon is enlarged, and easily identifiable upon palpation. The two free taenia of the ventral colon course in a cranial to caudal direction, from the left cranial abdomen to the left caudal abdomen. As the impaction enlarges, the taenia may continue to the right caudal abdomen, with the pelvic flexure lying in the right caudal abdomen, just cranial to the pelvic rim, with the taenia coursing right to left just cranial to the pelvic canal. The consistency of the ingesta forming the impaction may vary from soft and indentable to firm and indurated. With severe impaction, the colon may fill the entire caudal abdomen, and the haustra of the ventral colon become indistinct. It is imFigure 2: Caudal view of the abdomen depicting small intestinal perative that the examiner rule out a large colon displacement distention and a secondarily dehydrated large colon. before initiating aggressive medical therapy. Primary large colon impactions are usually treated medically; whereas horses with Cecum Cecal distention may be a primary problem, such as impaction colon displacements and secondary impaction require surgery of the cecum with ingesta or fluid, or more commonly, for resolution of the impaction. Horses with impactions or obstructions (enteroliths) of the secondary to obstruction of the large or small colon. Early in the development of a cecal impaction, the apex of the cecum right dorsal colon and transverse colon most often present with becomes distended with ingesta, but is beyond the reach of the generalized cecal and large colon tympany. Occasionally, however, examiner. Therefore, palpation of the ventral cecal taenia is used the lesion may be identified on rectal examination, particularly if as an indirect indicator of cecal filling. Normally, the cecal taenia a concurrent right dorsal colon displacement exists (see below). should be loose and easily movable. With increased filling of the In these cases, the impaction or enterolith may be balloted with cecum with ingesta, the taenia become more taut, and the cecum the examiner's fingertips, but cannot be palpated in its entirety. Right dorsal displacement of the large colon may assume a displaces cranial and toward the midline. If a cecal impaction is suspected, it is important to pay particular attention to the more variety of anatomic configurations, but the common finding for all cranial aspects of the right caudal abdomen, because the weight right dorsal displacements is displacement of the left ventral and of the ingesta in the cecum will cause it to displace cranially, often dorsal colon lateral to the cecum. The colon retroflexes on itself 24  The Practitionerâ€

Issue 3 • 2015

and passes between the cecum and right body wall. The colon and associated taenia are felt immediately cranial to the pelvic canal, coursing from the right caudal abdomen, transversely across the abdomen, and then continuing toward the left cranial abdomen (Fig. 3). While this orientation of the colon and taenia may be similar to that of a severe large colon impaction, with a primary displacement, the colon is distended primarily with gas, as opposed to ingesta, and the pelvic flexure usually comes to lie in the left cranial abdomen, beyond the reach of the examiner. The colon displaces the cecum medially, and cranially, making it difficult to palpate. With increased duration, the cecum often becomes secondarily distended with gas. The degree of intestinal distention is variable and severe gas distention of the colon will preclude complete examination of the abdomen.

Figure 4: Caudal view of the abdomen depicting left dorsal displacement of the large colon with colonic bands coursing over the renosplenic space.


Figure 3: Caudal view of the abdomen depicting right dorsal displacement of the large colon with colonic bands coursing horizontally across the abdomen.

Left dorsal displacement of the large colon (renosplenic entrapment) can be diagnosed by rectal examination if the colon is not markedly distended. The left dorsal and ventral colon become entrapped within the renosplenic space, between the spleen and left kidney (Fig. 4). The majority of the colon is palpable on the left side of the abdomen with the taenia coursing from the left craniodorsal abdomen to the left or right caudoventral abdomen. Following the taenia cranially and dorsally, the examiner can feel the taenia enter the renosplenic space. When moving the hand from left dorsal abdomen to the dorsal midline, the examiner should feel the head of the spleen, compressed large colon and associated taenia as it hangs over the renosplenic ligament, and left kidney to confirm the diagnosis of left dorsal colon displacement. With increased duration, the cecum often becomes secondarily distended with gas. If the colon is severely distended, the colon may fill the left caudal abdomen and preclude examination of the renosplenic region. In this case, left dorsal displacement may be suspected but should be further evaluated with transcutaneous ultrasonography of the renosplenic region. Displacement of the spleen medially and ventrally may be associated with left dorsal displacement, but these findings alone do not confirm the diagnosis of left dorsal 

Torsion or volvulus of the large colon is easy to diagnose in the later stages of the disease. The horse's abdomen is visibly distended and the large colon fills the entire abdomen. In extremely advanced cases, the examiner cannot introduce the hand beyond the pelvic rim. The marked colonic distention causes the colon to fan-fold (pretzel) within the limited space of the abdominal cavity. This is often evident as colonic taenia courses transversely across the caudal abdomen, and may be difficult to distinguish from that of a right dorsal displacement. In the early stages of colon volvulus, colonic distention may not be severe. Often the pelvic flexure and left colon will be evident in the left abdominal quadrant. The pelvic flexure may be moderately distended with gas, displaced cranially, and appear to be suspended within the middle left abdomen. The haustra and taenia of the ventral colon may be palpated dorsal to the smooth dorsal colon, indicating malpositioning of the colon. The remainders of the colon and entire cecum are displaced cranially and beyond the reach of the examiner. In these cases, persistent abdominal pain and progressive colonic distention are often evident on sequential examinations.

Small Colon and Rectum Rectal examination of the horse with obstruction of the proximal small colon (fecalith or enterolith) is usually characterized by generalized cecal and colonic tympany. Impaction of the middle to distal small colon has additional findings of continuous, solid ingesta within the descending colon and marked rectal mucosal edema. This forms a uniform, smooth tube of variable length in the central caudal abdomen. Individual fecal balls and haustra of the descending colon are not usually prominent in horses with small colon impaction. However, the pencil diameter, “rope-like” mesenteric band is unique to the small colon and a helpful identifying characteristic of the small The Practitioner  25 

colon. The ingesta is most often soft and easily indentable, in contrast to large colon impactions. In severe cases, the entire small colon becomes impacted with ingesta and the weight of the impaction pulls the rectal ampulla and associated mesentery ventrally and to the left of midline. This makes complete examination of the rest of the abdomen difficult if not impossible.

References and Footnote: Roe RL and White NA. Diagnosis of Gastrointestinal Disease. In White NA, Moore JN, Mair TS ed. The Equine Acute Abdomen. Jackson, WY: Teton New Media, 2008;252-264. Mueller, POE. Rectal examination. In Divers, TJ and Ducharme, NG ed. Manual of Equine Gastroenterology. Philadelphia:W.B. Saunders Co, 2002:6-9. Mueller POE, Moore JN. Rectal examination of horses with acute abdominal pain. Compend Contin Educ Pract Vet 2000, 22(6):606-615. a. Buscopan®, Boehringer, St. Joseph, MO.

P.O. Eric Mueller, DVM, PhD, DACVS P.O. Eric Mueller is a professor of surgery, director of equine programs, chief medical officer-large animal hospital, and equine surgeon in the department of large animal medicine and surgery at the University of Georgia College of Veterinary Medicine in Athens, Georgia. Dr. Mueller received his undergraduate degree from the University of Vermont and DVM from Michigan State University. He completed a residency in large animal surgery and PhD in gastrointestinal physiology at the University of Georgia. He is a Diplomate of the American College of Veterinary Surgeons. He served as chief of staff of the veterinary medical teaching hospital at the University of Georgia from 2002-2008. His clinical interests are gastrointestinal surgery, minimally invasive surgical techniques, and the evaluation and treatment of equine lameness. His research interests have focused on the pathophysiology and prevention of postoperative intra-abdominal adhesion formation. Dr. Mueller has authored over 60 scientific publications and 20 veterinary book chapters. He is a frequent speaker at national and international scientific and continuing education meetings.

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Practitioner Issue 3, 2015  

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association

Practitioner Issue 3, 2015  

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association