Practitioner issue 4 2013 new

The Practitioner Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 4 • 2013

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The President's Starting Line OFF AND RUNNING WITH THE FAEP . . .

–

Anne L. Moretta, VMD, MS - FAEP President

It is an honor to serve as your 2013 FAEP President, and I am especially looking forward to the year ahead. Our council has been working diligently to create relevant and exciting programs for your continuing education with national and internationally recognized speakers. We will offer the most up-to-date, in-depth information in equine medicine, surgery, lameness and rehabilitation.

How often do we stay connected with our colleagues, learn new techniques and keep up with current research? Not often enough. Our continuing education venues are chosen to promote excellence in our profession by offering smaller, more cohesive, and interactive colleague-to-colleague experiences.

Over the past several years, since our merger with the FVMA, our association has experienced exponential growth.

There has been a significant increase in attendance at our meetings and a major increase in industry support. We are grateful to our educational partners for their continued support, for without their commitment our meetings would not be possible. Our conference attendees are a diverse group of veterinarians from all over the world, and they are an integral part of our efforts to provide quality veterinary education.

In these tougher economic times we need to reinvent our practices large and small. FAEP can help you diversify and grow your practice base, add a new revenue generating technique, find equipment ideas for greater productivity, network with colleagues, and get referrals. It is time to get creative.

It is with great pleasure that I officially invite you to come to beautiful, sunny Florida and connect with your veterinary colleagues from across the world. Experience one, or all three, of our world-class continuing education programs.

Our exciting 2013 Equine Foot Symposium will be held June 28 – 29, 2013, in Orlando,Florida. This meeting features a unique “hands-on” foot and distal limb dissection lab, led by Mitch Taylor, CJF. See further details about the Symposium in this issue.

Our flagship meeting, the 9th Annual Promoting Excellence Symposium in the Southeast, will be held October 17 – 20, 2013, at the Boca Raton Resort and Club in Boca Raton, Florida, a legendary destination in itself. Our symposium will incorporate a whole horse approach. There will be an in-depth Master Class on the Neck and Back and an in-depth Ophthalmology section. The symposium will also feature topics on the Biomechanics of Injury, Performance Horse Cardiology, Ultrasound, Surgery, Neurology, GI, and Rehabilitation. The popular Dyson and Ross News Hour will be back again this year.

In addition, do not miss our 51st Annual Ocala Equine Conference from November 15 – 18, 2013. Dr. Scott Palmer, Past President of AAEP will be our featured keynote speaker. We are offering an exciting Advanced Dentistry Wet Lab featuring dental extractions and periodontal disease, and a Field Procedures ‘How To’ Wet Lab. We are strengthening from our core with new office facilities and additional staff for our FVMA/FAEP offices. The participation and feedback from our membership is a crucial part of what makes our programs successful. The FAEP council would like to especially thank our 2012 President Dr. Greg Bonenclark and our outgoing council member Dr. Barry David for their dedication to the FAEP. I also need to extend my special thanks to all of the FAEP council members and FVMA staff whose commitment of time, energy, and ideas make our programs a tremendous success.

Resolve To Be Involved in 2013. Serve your FAEP by joining our council community, submitting scientific articles and promoting excellence in your practice.

Our entire FAEP council is looking forward to meeting you at one or all of our upcoming continuing education opportunities. Please make it a date!

• EXECUTIVE COUNCIL •

•

•

Suzan C. Oakley, DVM, Diplomate ABVP (Equine)

Gregory D. BonenClark, DVM, Diplomate ACVS

FAEP Council President-Elect FAEP Council Past President

oakleyequine@gmail.com

gbonenclark@fevaocala.com

Mr. Philip J. Hinkle

Executive Director phinkle@fvma.org

Amanda M. House, DVM, Diplomate ACVIM housea@ufl.edu

Liane D. Puccia, DVM pucciavet@aol.com

Corey Miller, Ruth-Anne Richter, Jacqueline S. Shellow, DVM, MS, Diplomate ACT BSc (Hon), DVM, MS DVM, MS Representative to the rrichter@surgi-carecenter.com cmiller@emcocala.com FVMA Executive Board

cmiller@emcocala.com

The Practitioner is an official publication of the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association.

4 The Practitioner

Issue 4 • 2013

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The Practitioner 5

Diagnosing the Horse with Recurrent Colic Amanda M. House, DVM, DACVIM Introduction

may include nasogastric intubation if the Diagnosis and treatment of horses with horse is actively displaying signs of colic. colic have certainly improved in the last Evaluation of a fecal sample for parasites 20 years. However, horses with recurrent and a thorough discussion about the horse’s colic continue to be a diagnostic and often, deworming program, diet, and pasture management challenge for both owners management is also recommended. Susand veterinarians. Recurrent colic is typi- pending manure in a plastic rectal sleeve cally defined as 3 or more episodes of tran- with water to test for sand can also be inforsient or prolonged colic over a period of mative, but does not definitively diagnose months or one year or more. The causes of the absence of sand or quantify of sand if recurrent colic are varied and can include it is present. parasites, gastric ulcers, sand accumulation, If the initial evaluation has not revealed impactions, ileal hypertrophy, intermittent a likely cause for the colic episodes, addigas colic, enteroliths, intra- or extra-lumi- tional diagnostic testing should be connal masses resulting in partial obstructions, sidered. Additional tests may include an inflammatory bowel disease (such as eosin- abdominocentesis, endoscopy of the stomophilic enteritis or enterocolitis), colonic ach and proximal duodenum, ultrasound displacements, and many others. Although examination of the abdomen, radiographs a definitive etiology cannot always be deter- of the abdomen, and small intestinal and/ mined without exploratory surgery, many or rectal biopsy. Abdominocentesis can diagnostics are currently available to assist be performed under light sedation with a in determining the most likely cause. local anesthetic (infiltration of 1-2 ml of subcutaneous lidocaine is recommended with a 25 gauge needle). A 2x2” area should Diagnostic Evaluation be clipped and sterilely prepped approxiA complete history and thorough physimately 3 cm caudal to the xyphoid and 1-2 cal examination with laboratory analysis is cm to the right of midline. Sterile gloves indicated for horses with recurrent colic. should be worn for the procedure. An 18 The physical exam should include an oral gauge 1.5 inch needle or sterile teat canula examination to evaluate the horse’s teeth. may be utilized. The author prefers a teat Horses in need of routine dental care may canula, as an 18 gauge needle may not be have difficulty chewing and can be predislong enough to allow for adequate sample posed to impactions. The physical examicollection. When a teat canula is utilized, nation should always include thorough a small stab incision should be made using thoracic and cardiac auscultation. Recura 15 blade scalpel prior to introduction of rent colic is typically considered abdomithe teat canula. As the teat canula advances, nal in origin; however, rare cases of other 2-3 “pops” will be felt as you advance disease within the thorax (pleuropneumothrough the muscle, abdominal wall, and nia, cardiac abnormalities, etc) may result peritoneum. Fluid should be collected in in flank watching and the perception of an EDTA tube for cytology, and red top for colic signs. A complete blood cell count culture if peritonitis is suspected. Inflamand biochemistry profile will evaluate red mation or infection within the abdomen blood cells, white blood cell count, electrocan result in changes in the peritoneal fluid. lytes, total protein, albumin, and liver and Normal values for abdominocentesis are: kidney values. The clinical sign of icterus total protein <2.5 g/dl, WBC < 5000-10,000 may be seen with prolonged anorexia, cells/uL. On cytology, neutrophils comhemolysis, and liver disease. If initial lab prise approximately 40% of cells, the rest work suggests liver disease, a serum bile being lymphocytes, macrophage and periacids concentration should be performed toneal cells. With intestinal strangulation, to assess liver function. Initial evaluation the protein will increase first (in the first should also include a rectal palpation, and 1-2 hours) such that the fluid will be clear 6 The Practitioner

but more yellow. After 3-4 hours of strangulation, RBC will also leak, and the fluid will take on an orange color. Typically, after about 6 hours, WBC will increase gradually, with the progression of intestinal necrosis.

Gastric ulcers are a common problem in performance horses, and have been reported in 66-93% of racehorses in training (Murray 1996, Hammond 1986, Vatistas 1999), 67% of endurance horses (Nieto 2004), and 58% of show horses (McClure 1999). Horses with equine gastric ulcer syndrome (EGUS) may exhibit poor performance, decreased appetite, weight loss, and recurrent mild to moderate signs of colic. Endoscopy of the esophagus, pylorus and stomach in a fasted horse enables a definitive diagnosis of EGUS. Endoscopy can also facilitate small intestinal biopsy of the duodenum if an infiltrative process is suspected. Prior to endoscopy, feed should be withheld for 12 hours. Water may also be withheld for several hours prior to the exam; however, for endoscopy units with suction capability, this is typically not necessary.

Ultrasound examination of the abdominal cavity enables evaluation of visible portions of the kidneys, liver, spleen, and intestinal tract (stomach, small intestine, colon, small colon, cecum). Thickening of the intestinal walls (≥0.5 cm) can be identified in conditions such as right dorsal colitis and other infiltrative and/or inflammatory intestinal diseases. Ultrasound may also identify abnormal masses in the abdomen such as an abscess or neoplasia. Sand can often be visualized on ultrasound exam as well; however, abdominal radiographs are ideal for documenting the presence and amount of intestinal sand. Radiographs will also be valuable in determining if enteroliths (intestinal stones/concretions) are present.

Rectal biopsy has been utilized for determination of infiltrative intestinal disease.

The procedure can be accomplished in the standing sedated horse, typically with a cervical biopsy forceps. Biopsy samples are typically obtained from the dorsolateral Issue 4 • 2013

rectal mucosa, at approximately 11 or 1 specific established diagnosis. o’clock. One gloved hand should identify and grasp the rectal mucosa, while References the other hand can manipulate the biopsy Bell RJ, Mogg TD, Kingston JK. Equine forceps. Samples are typically submitted gastric ulcer syndrome in adult horses: a in formalin for histopathology. However, review. NZ Vet Journal 2007 Feb; 55(1):p normal specimens do not rule out the pres- 1-12. ence of colonic lesions.

McClure SR, Carither DS, Gross SJ, and Despite all of the aforementioned Murray MJ. Gastric ulcer development in examinations, diagnosis can unfortunately horses in a simulated show or training still be elusive in some cases of recurrent environment. JAVMA 2005 Sep 1; 227(5): colic. With advances in diagnostic tech775-777. niques and surgical procedures, additional options include standing laparoscopic Merritt AM, Sanchez LC, Burrow JA, surgery and abdominal exploratory under Church M, and Ludzia S. Effect of Gastrogeneral anesthesia. In miniature horses, gard and three compounded oral omeprafoals, and some ponies, CT scan and MRI zole preparations on 24 h intragastric pH may be available at select referral centers. in gastrically cannulated mature horses.

Most CT and MRI units are not capable of Equine Vet J 2003 Nov; 35(7): p 691-695. abdominal scans on animals larger than Mair TS and Hilllyer MH. Chronic colic 300 pounds. If an abnormality is identiin the mature horse: A retrospective review fied with CT or MRI, surgery may still be of 106 cases. Equine Vet J 1997 Nov; 29(6): required to correct the underlying problem.

415-420.

Fortunately, complications from abdominal surgery have diminished and success rates have improved considerably for horses that require surgical intervention. The exact prognosis will depend on the underlying cause.

Prognosis In one study (Mair and Hillyer, EVJ 1997), causes of chronic colic included colonic impaction (31%), peritonitis (16%), no diagnosis (8%), enteritis/colitis (7%), colonic displacement/torsion (6%), lymphosarcoma (4%), and to lesser extent, intestinal adhesions, ileal obstructions, liver disease, cecal impactions, thromboembolic disease, and intussusceptions. Exploratory celiotomy is necessary in many cases to make a definitive diagnosis, but owners should be aware that some cases are not amenable to treatment. The prognosis for successful resolution is determined by the lesion, as for any type of colic, but is probably comparable to the prognosis for acute forms of colic. In some horses in which a specific cause is not found at surgery, clinical signs can persist after surgery, and usually dietary and management changes are recommended for these horses. Thorough evaluation and understanding of possible causes of the problem can assist the owner and veterinarian in determining the most likely etiology of the colic. Treatment and management of affected horses are most effective when they can be targeted at a www.faep.net

Amanda M. House DVM, DACVIM Dr. Amanda House is a Clinical Associate Professor in the department of large animal clinical sciences at the University of Florida’s College of Veterinary Medicine. She is a large animal medicine clinician in the equine hospital and coordinates equine continuing education and outreach programs at the College of Veterinary Medicine.

Dr. House is the Director of the Practice-Based Equine Clerkship program and the Equine Research Program. She completed her BS in Animal Science from Cornell University. After graduating from Tufts University School of Veterinary Medicine in 2001, Dr. House completed an internship and large animal internal medicine residency at the University of Georgia’s Veterinary Teaching Hospital. Dr. House became board certified in large animal internal medicine in 2005. Her professional interests include neonatology, infectious disease, and preventative health care.

The Practitioner 7

8 The Practitioner

Issue 4 • 2013

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The Practitioner 9

surgery Dennis E. Brooks

Surgeries Of The Eye Of The Horse Dennis E. Brooks, DVM, PhD Eyelid lacerations:

to migrate and adhere to the ulcer surface.

conjunctival graft.

Very common especially when horses are irritated by insects and seek objects to rub their eyes on. THE MOST COMMON CAUSE IS ENTRAPMENT OF THE LID IN A BUCKET HANDLE!!! Counsel owners to tape up bucket handles BEFORE injuries occur. Intralesional anesthetics will make the horses positive for drug testing.

Great care should be taken with the repair including: minimal debridement, careful apposition of the torn pedicle, use of small (3-0, 4-0) suture, closure of the eyelid margin using a figure of eight suture pattern that keeps suture tags from abrading the cornea. I find standing surgery is helped by resting the chin of the sedated horse on bales or a large trash can, and using a very short (5 1/2”) Olsen Hegar needle holder and forceps. Be careful if you decide to use a two-layer closure—the inner layer MUST not abrade the cornea. In the field, single layer closures with meticulous deep bites are often the safest repairs. Temporary tarsorrhaphies may stabilize the tarsal plate in severe tears. Check the globe carefully for concurrent injury or uveitis. Use NSAIDs and topical and/or systemic antibiotics for several days.

Formation of a third-eyelid flap with attachment to the upper eyelid is perConjunctival Flaps formed by placing 2-4 horizontal mattress Conjunctival grafts or flaps are used sutures. Initially, pass the cutting needle frequently in equine ophthalmology for through the upper eyelid through the the clinical management of deep, melting, fornix at the desired location. Direct the and large corneal ulcers, descemetoceles, needle (3-0 suture) through the anterior and for perforated corneal ulcers with and face of the TE approximately 3 mm from without iris prolapse. the leading edge, and then again in the skin To augment lost corneal thickness and through the fornix adjacent to the first bite. strength, deep corneal ulcers threatening These sutures should not be full-thickness perforation may require conjunctival flap in the TE. One to three additional sutures placement. Conjunctival flaps are associ- are placed and then tied. ated with some scarring of the ulcer site.

Coverage with a 360º, hood, island, pedicle, or bridge flap should be maintained for 4 Temporary tarsorrhaphy to 12 weeks. Reoccurrence of the inflamHorizontal mattress sutures enter the mation may occur following flap removal. eyelid two to three millimeters from the eyelid margin with the cutting needle A conjunctival pedicle flap is made by emerging from the central aspect (Meiboincising conjunctiva (excluding Tenon's mian gland line) of the eyelid margin, and capsule) 1-2 mm posterior to and parallel then reentering the apposing lid margin to to the limbus with Steven's tenotomy scisexit in the skin. 4-0 silk or nylon is comsors. The flap is undermined posteriorly monly used for this procedure. toward the fornix as needed. A perpendicular incision is made at the distal end of the flap, and an incision parallel to the first Enucleation incision and limbus is made several milPanophthalmitis following perforation limeters posterior to the first incision. The of an infected corneal stromal ulcer has flap is rotated over the defect and sutured a poor prognosis. Phthisis bulbi is likely in place with absorbable 5-0 to 7-0 suture.

Debridement, Keratectomy and to result after a chronically painful course.

Keratotomy Affected horses can be febrile and manifest Removing necrotic tissue, SCC and Amniotic Membrane Flaps signs of septicemia. To spare the unfortumicrobial debris by keratectomy speeds nate animal this discomfort, enucleation is Amniotic membrane transplantation healing, minimizes scarring, and decreases the humane alternative. Histopathologic may provide decreased fibrosis, reduced the stimulus for iridocyclitis. examination of the globe is recommended. vascularization of corneal ulcers, and faster Persistent superficial ulcers may need reepithelialization in horses with superficial surgical debridement and keratotomy to and/or deep corneal ulcers. They may be Penetrating Keratoplasty in the remove the hyaline membrane slowing epi- used alone or with conjunctival flaps.

Horse: thelial healing.

Surgical Procedures Debridement to remove abnormal epi- Third-Eyelid (TE) Flaps Three basic corneal transplantation surthelium of refractory superficial erosions gical procedures have been described for Nictitating membrane flaps are used can be accomplished with topical anesthethe horse: penetrating keratoplasty (PK) for for superficial corneal diseases including sia and a cotton-tipped applicator. full thickness stromal abscesses or ulcers/ corneal erosions, neuroparalytic and neuiris prolapses, and two split thickness forms Superficial punctate or grid keratotomy rotropic keratitis, temporary exposure keraof PK, the posterior lamellar keratoplasty of superficial ulcers with a 20-gauge needle titis, superficial corneal ulcers, superficial (PLK) for deep stromal abscesses (DSA) can increase the ability of the epithelial cells stromal abscesses, and to reinforce a bulbar

10 The Practitioner

Issue 4 • 2013

with a clear overlying anterior stroma in the axial cornea and the deep lamellar endothelial keratoplasty (DLEK) for limbal DSA where the superficial cornea may be vascularized but is otherwise normal. A third lamellar keratoplasty, the deep anterior lamellar keratoplasty (DALK) has also recently been used in horses with severe melting ulcers.

closure of the wound, blood and fibrin clots in the anterior chamber are carefully removed by gentle anterior chamber irrigation with lactated Ringer’s solution, or more appropriately digested with tissue plasminogen activator (TPA) (50-150 micrograms in 0.1 ml via intracameral injection). TPA can successfully digest blood clots in the anterior chamber that have been present for 2 weeks in horses. Wound closure is Lamellar keratoplasty is utilized for completed and the anterior chamber is tectonic reasons to replace damaged reformed with hyaluronic acid, lactated stroma in melting corneal ulcers as it proRinger's solution (LRS), or an air bubble. vides enhanced donor graft survival, and improved visual outcomes compared to PK. Deep lamellar endothelial keratoplasty Endothelial detachment fol(DLEK) and posterior lamellar keratoplasty lowing blunt trauma (PLK) are split thickness lamellar keratoProfound and persistent corneal edema plasties (LK) utilized to replace diseased may be present following blunt trauma to endothelium from Fuch’s endothelial dysthe globe of the horse. Detachment of the trophy and bullous keratopathy in humans, endothelium is a proposed mechanism of and deep stromal abscesses in horses. The this syndrome. The prognosis for a return remaining healthy anterior corneal layers to normal is poor. Hypertonic solutions are preserved in DLEK and PLK, and the (5% sodium chloride) may be beneficial in healthy posterior cornea preserved in the early stages. Thermatokeratoplasty may DALK. be necessary to reduce the edema in severe cases. Endothelial cell reattachment and cellular hypertrophy can occur to resolve Corneal foreign bodies the condition in some horses.

Penetrating and perforating corneal foreign bodies cause varying degrees of keratitis and uveitis, and are common in Immune Mediated Keratitis horses. Superficial foreign bodies can be Several forms of NIK are found in removed under topical anesthesia and the Europe. Some are associated with a “hissubsequent ulcer treated medically. Deep tory of ocular trauma.” The etiology is precorneal and penetrating foreign bodies may sumed to be altered corneal immune privicause severe uveitis/endophthalmitis and lege from abnormal exposure or expression require more aggressive care. of corneal antigens inducing autoimmune dysregulation. Nonulcerative superficial and nonulcerative recurrent forms of stroCorneal lacerations mal keratitis are two types of NIK noted in Full thickness lacerations need to be European warmbloods. Stromal pigmentasutured with 7-0 suture in a simple intertion may occur in some eyes. An endotherupted pattern. The anterior chamber is liitis with slight corneal edema is another refilled with LRS. Postoperative medicaform of NIK. These eyes may partially tions are used to eliminate infection and respond to topically administered corticoreduce uveitis. steroids, NSAIDs, tacrolimus or cyclosporine A, and may require parenteral antibiotics, corticosteroids, or NSAIDs. EndotheSurgical Repair of Iris Prolapse liitis may be found with lens subluxations.

Several concepts are important in the microsurgery of iris prolapse repair. If an iris prolapse is fresh, an attempt is made to Iris and ciliary body cysts replace the protruding iris. If the iris tissue Uveal cysts are a hallmark of the herediis damaged or necrotic, the protruding iris tary anterior segment abnormalities of the is excised with electrocautery. The cornea Rocky Mountain Horse, the Connemara is sutured with a simple interrupted patpony and the miniature horse. Iris cysts tern (1 mm apart) using 5-0 to 7-0 Vicryl may be found sporadically in other breeds. or nylon suture. A Seidel's test is used to The cysts contain a thick vitreous gel-like test for suture line integrity. After partial www.faep.net

material. Cysts at the ventral pupil margin appear to cause more vision problems.

Cysts that interfere with vision may be ablated with laser therapy.

EQUINE RECURRENT UVEITIS Equine recurrent uveitis (ERU) is a common cause of blindness in horses. It is a group of immune-mediated diseases of multiple origins.

Recurrence of anterior uveitis is the hallmark of ERU. The disease is bilateral in approximately 20% of the cases.

While the pathogenesis is clearly immune-mediated, the specific causes of ERU are unknown. Hypersensitivity to infectious agents such as Leptospira interrogans serovars is commonly implicated as a possible cause. Autoimmune activity against retinal proteins and antigens is also an etiologic component of this disease.

ERU Therapy The major goals of treatment of ERU are to preserve vision, decrease pain, and prevent or minimize the recurrence of attacks of uveitis. Specific prevention and therapy is often difficult, as the etiology is not identified in each case.

Surgical considerations for ERU In addition to medical treatment, pars plana vitrectomy in horses with ERU has been used successfully to remove fibrin, inflammatory cells and debris trapped in the vitreous in order to improve vision and delay the progression of the clinical signs.

Vitrectomy appears more beneficial in European warmbloods with ERU than in Appaloosas with ERU in the USA. The reasons for this are not known. Cataracts occur in a high percentage of cases postvitrectomy in both regions. Retinal detachment can also occur postoperatively.

Sustained release intravitreal cyclosporine A implants may also be beneficial to treating ERU. Equine Cataract Surgery Most veterinary ophthalmologists recommend surgical removal of cataracts in foals less than 6 months of age if the foal The Practitioner 11

is healthy, no uveitis or other ocular problems are present, and the foal's personality will tolerate aggressive topical medical therapy. Horses considered for lens extraction should be in good physical condition.

Complete ophthalmic and general physical examinations should be performed.

Examine foals for subclinical Rhodococcus pneumonia and treat it prior to surgery if present. Adult horses with visual impairment due to cataracts are also candidates for cataract surgery. Slow or absent pupillary light reflexes (PLRs) may indicate active iridocyclitis with or without posterior synechiation, retinal disease, optic nerve disease, or iris sphincter muscle atrophy.

Afferent pupillary defects in a cataractous eye cannot be attributed to the cataract alone, as well as the fact that normal PLRs do not exclude some degree of retinal or optic nerve disease. Any signs of inflammatory eyelid, conjunctival, or corneal disease, and anterior uveitis should delay cataract surgery until the inflammation has been successfully treated. B-scan ultrasound and electroretinography (ERG) are beneficial in assessing the anatomic and functional status of the retina if a cataract is present.

General anesthesia with its attendant risks is required for cataract surgery.

Phacoemulsification cataract surgery is the most useful technique for the horse.

This extracapsular procedure through a 3.2mm corneal incision utilizes a piezoelectric handpiece with an ultrasonic titanium needle in a silicone sleeve to fragment and emulsify the lens nucleus and cortex following removal of the anterior capsule. The emulsified lens is then aspirated from the eye while intraocular pressure is maintained. The thin posterior capsule is left intact. There is little inflammation postoperatively in most horses following phacoemulsification cataract surgery and a quicker return to normal activity with phacoemulsification than other surgical techniques.

pain from ciliary muscle spasm, and causes pupillary dilatation. Atropine may used as often as q6h, with the frequency of administration reduced as soon as the pupil dilates.

Topically applied corticosteroids, such as prednisolone acetate (1%), are essential to suppress pre- and postoperative inflammation. Systemically administered NSAIDs can be used orally or parenterally, and are effective in reducing anterior uveitis in horses with cataracts. Topically administered NSAIDs such as diclofenac, flurbiprofen and suprofen must also be used to suppress signs of anterior uveitis. The results of cataract surgery in foals by experienced veterinary ophthalmologists are generally very good, but the cataract surgical results in adult horses with cataracts caused by ERU are often poor. The problem is that new blood vessels form on the iris and anterior lens capsule in the eyes with ERU and they can bleed during the surgeries. The surgeon often cannot stop the hemorrhage and severe hyphema results.

Horses with previous or concurrent uveitis, aged horses, and Appaloosas are at increased risk for the development of glaucoma.

Laser destruction of the ciliary body (cyclophotocoagulation) works the best at controlling IOP and preserving vision in horses.

Reference

Gelatt KN: Veterinary Ophthalmology 5 th Ed, Lippincott, Williams and Wilkins, Philadelphia, 2013.

Brooks DE: Ophtha lmolog y for the Equine Practitioner. Teton NewMedia, Jackson, WY, 2008.

Gilger BC (ed): Equine Ophthalmology, Ed 2. Elsevier, Maryland Heights, MO, 2010.

Clinical Techniques in Equine Practice: Equine Ophthalmology, 4(1); 2005.

Postoperative complications include persistent iridocyclitis and plasmoid aqueous, fibropupillary membranes, synechiae, corneal ulceration, corneal edema, posterior capsular opacification, retained lens cortex, wound leakage, vitreous presentation into anterior chamber, retinal detachment and infectious endophthalmitis.

Aphakic Vision in Horses Most reliable reports of vision in successful cataract surgery in horses indicate vision is functional postoperatively. From an optical standpoint, the aphakic eye should be quite far-sighted or hyperopic postoperatively, and was +9.94D in one study. Images close to the eye would be blurry and appear magnified. The loss of accommodation could be severely debilitating to some horses. Theoretically, intraocular lenses (IOL) should improve postoperative visual outcome in horses. IOL refractive power of 25D resulted in +8D hyperopia by retinoscopy in one study of pseudophakic horses.

Postoperative cataract surgery therapy and results EQUINE GLAUCOMA A broad-spectrum topically applied antiThe glaucomas are a group of diseases biotic solution should be utilized pre- and resulting from alterations of aqueous postoperatively. Frequency of medication humor dynamics that cause an intraocular varies from q4h to q8h. Topically applied pressure (IOP) increase above that which 1 percent atropine is effective in stabilizis compatible with normal function of the ing the blood-aqueous barrier, minimizing retinal ganglion cells and optic nerve.

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Issue 4 • 2013

The Value of Ridden Exercise in Lameness Investigation Sue Dyson, Centre for Equine Studies

Fig.1 Croup high in canter left bilateral foot pain Ridden exercise may be crucial for detection of lameness which is the cause of a performance problem. Mild hindlimb lameness may not be detectable in hand and on the lunge and assessment of the horse ridden may be critical. It is important to recognise the influence of the weight of a rider on hindlimb gait, especially when in rising trot. The lameness is usually accentuated when the rider sits on the diagonal of the lame hindlimb and the horse feels more uncomfortable to the rider on this diagonal. The horse may adjust its rhythm to try to shift the rider back to the opposite diagonal.

A heavier weight rider is more likely to accentuate lameness than a lighter weight rider. A subtle lameness may still be unapparent and riding consecutive 8 – 10 metre diameter circles to the left and to the right may induce irregularities of rhythm reflecting lameness and a change in the speed, with the horse slowing down when uncomfortable. Likewise, performing so–called lateral movements such as shoulder-in, travers, and half pass may induce gait irregularities that are otherwise not apparent. In some horses the only manifestation of a hindlimb gait abnormality may be a tendency to change limbs behind in canter, to become disunited.

Alternatively, the horse may have difficulties in performing canter pirouettes in one direction, or flying changes either from left to right, or from right to left. It is important to be aware of the influence of a rider; an unskilled rider who lacks balance may induce lameness, whereas a highly skilled rider may conceal lameness.

A rider who is constantly moving his hands may cause irregular movement of the horse’s head, which may mimic forelimb lameness. A rider who restricts the horse with his hands may cause a loss of hindlimb propulsion and/ or irregular steps. Unless the rider is sufficiently skilled, lameness that is only apparent when www.faep.net

a horse is working in maximum collection may not be apparent.

Evaluation of the horse working to a contact, ‘on the bit’, compared with ‘on a long rein’ may reveal that lameness is apparent under one circumstance, but not the other.

The way in which a multilimb lameness may influence a horse’s performance when ridden must also be understood. There may be no overt lameness, therefore grading the degree of lameness may be impossible, although the gait of the horse is altered and performance compromised. For example there may be no detectable lameness, but on the lunge a horse may lean the body inwards and look to the outside, while the inside hindlimb crosses in under the body towards the contralateral forelimb during protraction. This may well be a manifestation of lameness, but is not quantifiable and can only be described. It is also not specific for lameness, because a young unbalanced horse, lacking musculoskeletal strength and coordination, may show a similar gait. When ridden, the same horse with poor performance may lack hindlimb engagement and impulsion and tend to be croup high in downward transitions.

Superficially, to an inexperienced eye the horse may appear normal and the appearance may markedly underplay the discomfort experienced by the horse. Leaning on the bit, taking an uneven contact, tilting the head, opening the mouth, raising the head, becoming over bent, stiffness in the neck or back, crookedness, difficulties to turn in one direction, reluctance to go forwards or undue hurrying, evasiveness and spookiness can all be manifestations of lameness.

The complete transformation of balance, impulsion, engagement, quality of contact with the bit and willingness to work following appropriate local analgesia to abolish subclinical lameness will The Practitioner 17

is often refractory to any diagnostic analgesic technique, is nonresponsive to non-steroidal anti-inflammatory drugs (NSAIDs) and comprehensive investigation using diagnostic imaging usually fails to identify a cause.

Fig. 2 Overbent & on forehand bilateral foot pain

Unilateral primary strain of a braciocephalicus muscle may manifest as lameness only discernible when the horse is ridden at walk. It is characterised by lifting of the head and neck as the limb is protracted and a shortened cranial phase of the stride. Some horses with injuries of the tendon of biceps brachii have also shown lameness only when ridden, which was markedly more severe at the walk than at the trot. Low-grade shoulder-slip may be more obvious at a walk than at faster gaits, and when ridden compared with in-hand.

There is a lameness typified by a shortened cranial phase of the stride of one hindlimb at the walk, when ridden ‘on the bit’ (or emphasize the degree of pain that the horse was experiencing. driven), but not when ridden (or driven) on a loose rein, nor when Problems that are only evident ridden have frequently been lunged, even with side reins adjusted to simulate the position of attributed to pathology in the thoracolumbar-sacral spine. Primary the horse’s head and neck when working ‘on the bit’. No lameness back pain may induce back stiffness and limited hindlimb impul- is detectable at other gaits. This lameness is also refractory to any sion, or a restricted gait all round. However, lameness can induce diagnostic analgesic technique, is non-responsive to NSAIDs and similar symptoms. Likewise neck stiffness is often attributed to comprehensive investigation using diagnostic imaging usually neck pain, but can also be a manifestation of lameness. Comparison fails to identify a cause. Prolonged rest does not alter the problem, of a horse ridden in rising and sitting trot can help to identify a nor does physiotherapy, acupuncture, chiropractic or osteopathic component of primary back pain. In sitting trot, a horse with back treatment. pain is more likely to alter its rhythm and /or speed, and alter the There remains a small but important group of horses in which position of the head and neck, becoming slightly above the bit, even a highly skilled and experienced lameness clinician cannot see compared with a lame horse. lameness, but a skilful rider can feel lameness and/or compromise Some lameness may only be apparent under specific circum- in performance. I never cease to be amazed by the large degree of stances. For example, with forelimb lameness the horse may be apparent asymmetry of movement I can feel when riding a horse unwilling to land with the left forelimb leading in canter. The which I cannot detect by visual appraisal. However, it must also ground reaction force is greater in the trailing (non-lead) fore- be recognised that some highly successful competition riders are limb on landing,8 so unwillingness to land with the left forelimb apparently unable to feel even quite obvious lameness, whereas leading is protecting the right forelimb from concussion. However some far less talented riders do have the ability to feel even lowthere is greater stress on the suspensory apparatus of the leading grade lameness. forelimb, so unwillingness to land with the left forelimb leading Ridden exercise is not, however, a substitute for assessment in could reflect suspensory injury in the left forelimb. Pushing off the hand and on the lunge, because there are some lamenesses, espehindlimbs unevenly can cause a horse to jump crookedly across cially forelimb lameness, that may only be apparent in hand and / a fence, with the hindlimbs drifting towards the lame limb. With or on the lunge. It is curious that even when ridden on a long rein low-grade hindlimb problems, lameness may manifest as unwillunder identical circumstances such lameness may be concealed. It ingness to perform flying changes from left to right in canter (or should also be borne in mind that a horse which shows lameness vice versa), or inability to maintain a regular rhythm in piaffe, which is evident when trotted in hand that can be abolished using passage or pirouettes. The hindlimbs may be unable to support diagnostic analgesia, may also demonstrate another lameness due weight normally, so there may be a tendency to place them more to an unrelated cause when ridden. closely together in canter. Particularly when the lame limb is on the inside of a circle, it will not be protracted as far as normal and will therefore be placed closer than normal to the outside hindlimb.

A stiff, stilted canter or poor hindlimb propulsion in canter, with the hindlimbs trailing, may be the most obvious manifestations of a bilateral hindlimb lameness.

There are also some specific lamenesses that are generally only evident when a horse is ridden. There is a hopping-type forelimb lameness, characterised by a shortened cranial phase of the stride and a marked lift of the head and neck as the lame forelimb is protracted. It can vary in degree within a work period and may disappear if the horse is ridden on a long rein. It is often, but not invariably, worst with the affected limb on the outside of a circle. It may be sensitive to the diagonal on which the rider sits. Such lameness 18 The Practitioner

Fig. 3 Ridden exercise difficulty in turning to right PSD

Issue 4 • 2013

Proximal Injuries of the Accessory Ligament of the Deep Digital Flexor Tendon in Hindlimbs Sue Dyson, Centre for Equine Studies

Anatomy The ALDDFT in hindlimbs is smaller than in forelimbs (Dyce 1987), and based on a cadaver study of 165 limbs, is sometimes absent (6%) and is occasionally bifid or trifid (Muylle et al. 2010).

The proximal aspect of the hindlimb ALDDFT has not been well described, but based on MRI, it appears to originate from both the plantar aspect of the ligament that runs between the calcaneus and the central and third tarsal bones and from the fused first and second tarsal bones (Dyson and Murray 2011).

The proximal aspect of the ALDDFT was assessed ultrasonographically bilaterally in 10 normal horses. In hindlimbs, the origin of the ALDDFT was not easy to identify. In the proximal metatarsal region, the ALDDFT varied considerably in thickness among horses, but was usually bilaterally symmetrical. It was usually more echogenic than the suspensory ligament or the deep digital flexor

Fig. 1 tendon. In 1 of 10 horses, the distal two-thirds of the ALDDFT was bifid bilaterally.

Injuries of the ALDDFT in hindlimbs Proximal lesions of the ALDDFT have been recognised most commonly in Warmblood and Thoroughbred sports horses (Dyson 2010a,b), whereas lesions in the mid metatarsal region are recognised most commonly in cob-types, British native pony breeds and Quarterhorses, and are usually older horses (Boswell and Schramme 2000; Eliashar et al. 2005; Dyson 2010a, b). These lesions are probably associated with degenerative changes of the ALDDFT, characterized by chondroid metaplasia.

a postural abnormality characterised by inability to load the heel of the affected limb, or knuckling over at the fetlock. This posture should prompt ultrasonographic examination of the metatarsal

Fig. 2 Normal 4 cm HL

region even if no palpable abnormalities can be identified. The condition may be unilateral or bilateral. The thick skin and dense hair coat may make it extremely difficult to perform accurate palpation, but invariably the ALDDFT is enlarged and there may be associated heat and pain on palpation. In horses with lameness, plantar and plantar metatarsal nerve blocks at subtarsal level may be required to completely abolish lameness.

Ultrasonographic examination can be challenging because of the thick skin. It may be necessary to reduce the transducer frequency and increase the gain controls to obtain images of satisfactory quality. Lesions are usually characterised by enlargement of the ALDDFT and a mild diffuse decreased echogenicity with decreased fibre pattern in longitudinal images.

Horses with lameness may respond favourably to rest, but horses with postural abnormalities have a very guarded prognosis.

Injuries of the AL-DDFT in the proximal third of the metatarsus

With acute injuries, there may be mild oedematous swelling in the proximal metatarsal region, usually most obvious medially and localised heat. Occasionally, swelling is also seen laterally. Generally, it has not been possible to elicit pain on palpation. Lameness has varied from no to mild lameness detectable at the walk; at the Horses with lesions in the mid-metatarsal region are pre- trot, the lameness in straight lines has varied from grade 2 (out of sented for investigation either because of lameness, or because of 8), to grade 5, with a median of 4.

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by marked enlargement of the ALDDFT and extensive hypoechogenic to anechogenic areas, extending from just distal to the TMT joint up to 9 cm distally. One horse had enlargement of the ALDDFT and patchy hypoechogenic areas which extended as far proximally as the ligament could be followed in the plantar tarsal region. This horse had increased radiopharmaceutical uptake in the plantar aspect of the distal row of tarsal bones. Magnetic resonance imaging revealed increased signal intensity in the proximal aspect of the ALDDFT in T1- and T2- weighted images and fat suppressed images. There was an irregular plantar contour of the third tarsal bone and decreased signal intensity in T1- and T2- weighted images in the endosteal bone consistent with mineralisation.

Fig. 3a Gold Thatch RH 7 cm TMT

Diagnosis has generally been based on the clinical signs and ultrasonography. However, one horse had mild generalised soft tissue thickening in the proximal metatarsal region. In this horse plantar (at the junction of the proximal ¾ and distal ¼ of the metatarsal region) and plantar metatarsal, nerve blocks did not

Four of six horses (67%) for which long-term follow-up (minimum of two years after resumption of full work) returned to work, but one owner elected not to compete again. In all six horses the ALDDFT remained enlarged, but relatively normal echogenicity was restored. Two horses resumed work, but subsequently experienced recurrent injury of the ALDDFT after three and five months respectively. Horses in which the injury occurred subsequent to previous PSD were retired.

In an ongoing post mortem study of horses with chronic PSD, in three of 18 limbs, there have been tough fibrous adhesions between the proximal aspect of the ALDDFT and the suspensory ligament. Such adhesions may predispose to subsequent injury of the ALDDFT. These adhesions have not been detected during prospective ultrasonographic examination or using high-field MRI post mortem.

References

Fig. 3b Gold Thatch RH LS 1a

alter the lameness, but perineural analgesia of the deep branch of the lateral plantar nerve (3 ml mepivacaine) improved lameness by approximately 80%. Intra-articular analgesia of the tarsometatarsal (TMT) joint did not alter the lameness. No significant radiological abnormality of the tarsus and proximal metatarsal region was detected in any horse.

Three horses have had previous proximal suspensory desmopathy (PSD) which was treated by neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy. Two of these horses returned to full athletic function and experienced recurrent lameness due to an injury of the ALDDFT. The third horse suffered recurrent lameness when only in light work.

Boswell, J. and Schramme, M, (2000) Desmitis of the accessory ligament of the deep digital flexor tendon in the hindlimb in a horse. Equine vet. Educ. 12, 129-132.

Dyce, K. (1987) The hindlimb of the horse. In: Textbook of Veterinary Anatomy, Eds: Dyce K., Sack, W. and Wensing, C., Saunders, Philadelphia, USA. pp. 576-595.

Dyson, S. (1991) Desmitis of the accessory ligament of the deep digital flexor tendon: 27 cases (1986-1990). Equine Vet J. 23, 438-444.

Dyson, S. (2010a) Desmitis of the accessory ligament of the deep digital flexor tendon.

In: Diagnosis and Management of Lameness in the Horse. Eds: Ross, M. and Dyson, S. 2nd ed. Elsevier, St. Louis. pp. 734 - 738 Dyson, S. (2010b) Injuries of the accessory ligament of the accessory ligament of the deep digital flexor tendon in the equine hindlimb: a problem of middle-age.

The Vet. J. 184, 255 – 256.

Dyson, S., Murray, R. (2011) The tarsus. In: Equine MRI Ed. Murray, R. 1st ed. WileyBlackwell, Oxford. pp 221 – 235.

Eliashar, E., Dyson, S., Archer, A., Singer, E., Smith, R. (2005) Two clinical manifestations of desmopathy of the accessory ligament of the deep digital flexor tendon in the hindlimb of 23 horses. Equine vet. J. 37, 495 – 500.

Jorgensen, A., Seco Diaz, O., Reef, V. (2007) Ultrasonographic diagnosis – desmitis of the accessory ligament of the deep digital flexor tendon in a hindlimb in a horse.

Vet. Radiol. Ultrasound 49, 303 – 306.

Muylle, S., Vanderperren, K., Saunders, J., Simoens, P. (2010) Morphometric data on the accessory ligament of the deep digital flexor tendon in the hindlimb of normal horses. The Vet. J. 184, 298-302.

Ultrasonographic abnormalities were only identified in the lame limb and those horses with oedematous swelling were characterised 20 The Practitioner

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