P-Iss1_2012 by kevin white

The Practitioner Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 1 • 2012

In this Issue 6 |

Diagnosis and Management of Stifle Lameness

12 | 16 |

Hoof Wall Cracks

19 |

Florida Practitioner John Mitchell Leads AAEP membership in 2012

20 |

Treatment and Prognosis for Laryngeal Hemiplegia

Pituitary Pars Intermedia Dysfunction: Diagnosis and Treatment

http://www.vetxray.com/dyncat.cfm?catid=2236

Letter from the Executive Director Dear Members,

EXECUTIVE COUNCIL Gregory D. BonenClark, DVM, Diplomate ACVS FAEP Council President

gbonenclark@fevaocala.com

Anne L. Moretta, VMD, MS FAEP Council Vice President

maroche1@aol.com Jacqueline S. Shellow, DVM, MS FAEP Council Past President

docshellow@bellsouth.net Mr. Philip J. Hinkle Executive Director

phinkle@fvma.org

COUNCIL REPRESENTATIVES J. Barry David, DVM, Diplomate ACVIM

bdavid@emcocala.com

Amanda M. House, DVM, Diplomate ACVIM

housea@ufl.edu

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

oakleyequine@gmail.com Liane D. Puccia, DVM

pucciavet@aol.com

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

rrichter@surgi-carecenter.com Corey Miller, DVM, MS, Diplomate ACT FAEP Council Representative to the FVMA Executive Board

The FAEP just completed its first year of operation as the equine-exclusive division of the Florida Veterinary Medical Association. This past year, we have experienced tremendous growth in membership as well as an increase in attendance of more than 100 percent at both our Promoting Excellence Symposium (that was held in Amelia Island, Florida) as well as our Foot Symposium (held in Orlando). If you were unable to attend one of our meetings last year, I encourage you to make plans now to attend one or both of our meetings in 2012. The FAEP’s 8th Annual Promoting Excellence Symposium will be held October 11-14, 2012 at the Waldorf Astoria Naples Grande Beach Resort in Naples, Florida. Naples is the crown jewel of Florida’s Gulf Coast and the perfect escape for CE and relaxation. For more information on our 8th Annual Promoting Excellence Symposium, please see our ad on page five of this issue of The Practitioner. We are in the final planning stage of our 50th Annual Ocala Equine Conference being held November 16-19, 2012, in the Horse Capitol of the World. Complete details will be provided in the next issue of The Practitioner. Mark your calendars now and make plans to attend! I would like to personally thank the members of the FAEP Council for their unselfish dedication in support of the equine profession. They are driven with a passion to offer cutting-edge, world-class equine-exclusive continuing education to the equine practitioner striving for professional excellence. The FAEP’s 2011 continuing education programs and those being planned for 2012 are a testament to their professional acumen and commitment. I’m honored to be a part of such a dedicated group. In closing, I would like to thank our 2011 Educational Partners for their support which has enabled us to provide cutting-edge continuing education at an exceptional value. We appreciate their commitment to strengthen the equine discipline throughout the Southeast and thank them for their continued support in 2012.

cmiller@emcocala.com

I look forward to seeing you in Naples or Ocala this year! Sincerely,

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

Philip J. Hinkle, Executive Director

Special Thanks to our 2011 Educational Partners GOLD PARTNERS

4 The Practitioner

SILVER PARTNERS

Issue 1 • 2012

Mark Your Calendar . . .

OCTOBER 11–14, 2012 Naples Grande: A Waldorf Astoria Resort

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Veterinarians & Veterinary Staff Volunteers are Needed! How can you help animals when disaster strikes half way around the world or very close to home? You can help your community’s service animals and pets during times of crisis by becoming a volunteer with the Florida Medical Reserve Corps (MRC) Network Program. Volunteering is easy. We can provide you with the training that will prepare you to help local public health activities and emergency response teams. For more information visit www.servfl.com or contact the Florida Department of Health’s Bureau of Preparedness and Response at (850) 245-4040.

8th Annual Promoting Excellence Symposium in the Southeast

DISTINgUIShED SPEakERS

LECTURE TOPICS INCLUDE

Norm Ducharme, DVM, MSc, DACVS Lameness Lisa Fortier, DVM, DACVS Imaging Amanda House, DVM, DACVIM Neonatology Robert Hunt, DVM, DACVS Pre-purchase Exams Christopher Kawcak, DVM, MS, PhD, DACVS Internal Medicine Christiana Ober, DVM Regenerative Medicine Russell Peterson, DVM Rehabilitation Mike Ross, DVM, DACVS LEISURE EVENTS Sheila Schils, PhD Tracy Turner, DVM, MS, DACVS FAEP’s Annual Golf Tournament Natasha Werpy, DVM, DACVR FAEP’s Annual Fishing Tournament Pamela Wilkins, MS, DVM, PhD Picturesque Beach on the Gulf of Mexico

Diagnosis and Management of Stifle Lameness By Michael W. Ross, DVM, DACVS

he stifle is an important source of hock joint pain and pain arising from the hind limb pain causing lameness, MTPJ are more common. but lameness of the distal limb from the tarsus to the foot is much more Clinical Characteristics of common. Many clinicians will default to Horses with Stifle Pain thinking pain causing lameness is originatThere are no pathognomonic clinical ing from either the tarsus or the stifle and signs defining the way horses move with overlook other important regions such as stifle region pain. All horses are prone to the metatarsal region or metatarsophalan- develop stifle injuries, but horses negotigeal joint (MTPJ); importantly, diagnostic ating fences may be predisposed. Horses analgesia must be used whenever possible moving fast over fences, such as timber to sort out the authentic source of pain in horses and event horses, are prone to hit horses with hind limb lameness. In a year- the stifle region and can sustain fractures ling with hind limb lameness and severe of the patella and cranial tibial tuberosity. effusion of the femoropatellar joint (FPJ) Horses working on uneven or slippery surit is not necessary to perform diagnostic faces may be predisposed. In management analgesia. Radiography reveals the pres- of horses with stifle pain it is important to ence of osteochondritis dissecans (OCD) prevent slipping and quick sudden turns, and the diagnosis is confirmed. However, movements that accompany unlimited in a mature dressage horse with hind turn out; therefore, turn out exercise is limb lameness, a mildly positive response restricted. Palpation may reveal effusion to upper limb flexion, and mild effusion of one or more joint compartments. Mild of the FPJ, diagnostic analgesia must be effusion of the FPJ is common and there used to confirm pain is originating from are many false positives associated with the stifle since other sources of pain such this clinical sign. However, effusion of as proximal suspensory desmitis, distal the medial femorotibial joint (MFTJ) is

6 The Practitioner

an important clinical sign; this joint is best palpated with the horse standing square or with the affected limb slightly cranial to the contralateral hind limb. In normal horses there is a depression between the medial patellar ligament and the medial collateral ligament, but in horses with effusion there is a “bulge” in this location. In horses with long-standing osteoarthritis (OA) of the MFTJ there is often marked thickening of the joint capsule, an important clinical sign. The LFT joint capsule is much more difficult to palpate, and while, uncommon-to-rare, effusion of this joint capsule, palpated between the lateral patellar and lateral collateral ligaments is as close to a pathognomonic sign as it gets. Sometimes effusion of this joint can be seen if the horse is carefully examined visually. Horses often resent palpation of the stifle and discomfort during palpation should not be mistaken for authentic stifle region pain. However, sometimes careful deep palpation with the limb in a flexed position may elicit pain not detected when compared to the Issue 6 • 2011

contralateral limb. Horses with fractures may have marked soft tissue pain and severe effusion. Horses get enormous swellings with stifle hematomas. Horses with substantial injuries such as fractures or disruption of the cruciate ligaments and medial collateral ligament will be severely, often non-weight-bearing lame and have instability of the stifle joint; instability can be hard to detect since horses are so painful. Careful palpation may reveal lateral dislocation/luxation of the patella. I often see coexistent MTPJ (fetlock) and stifle pain, particularly in racehorses. OA of the MFTJ and mal-adaptive bone remodelling of the distal aspect of the third metatarsal bone is quite common in TB and STB racehorses. There appears to be a relationship between these two regions, an example of intra-limb compensatory or coexistent lameness. Some horses, particularly young horses with stifle instability will knuckle, likely making them prone to development of MTPJ pain. Never forget the MTPJ in horses with stifle pain (Loren Evans, personal communication, 1983)! How do horses move with stifle region pain?1 Shortened cranial phase of the stride is a hallmark of stifle lameness, but this clinical sign is not pathognomonic and present in many horses with hind limb lameness. One of the best descriptions I have heard of how horses move while trotting with stifle pain, is “the limb just can’t quite keep up” (Dr. Kent Carter, Texas A&M University). In horses with severe OA, in young horses with OCD or other forms of osteochondrosis there can be marked shortening bilaterally, causing a gait described as “bunny hopping.” Only conditions of the tuber ischium or caudal thigh muscles cause more shortening of the cranial phase of the stride. Horses may appear to only partially load the affected hind limb and are quick to unload the limb while trotting. From the side it appears the stifle region is more prominent than normal with the limb appearing to be held in mild external rotation. From behind, the horse may swing, or abduct, the limb when pushing off during early protraction (the limb moves away from midline and then the foot is placed on the ground in the expected location, or just in front of the contralateral foot), or carry the affected limb straight; a “stabby” hind limb gait is seldom seen but differentiation from other sources of hind limb pain merely on the www.faep.net

basis of limb flight is fraught with error. There are variable degrees of pain from subtle nearly non-detectable to severe grade 4-5 ( on a scale of 0 being sound and 5 being non-weight-bearing). Lameness is more obvious while turning with the affected limb on the inside of a circle. There is often a positive response to upper limb flexion (the so-called spavin test) but horses with other sources of hindlimb pain respond positively as well. A stifle flexion test, hard flexion of the stifle without concomitant hard flexion of the hock, can be performed, but this test is somewhat dangerous and there are many false positive results. I use other forms of manipulation such as forcing the proximal aspect of the tibial caudally or forcing the patella proximally, both done with the horse standing bearing weight and followed by trotting. A horse may manifest a marked positive response to this test before moving or, the lameness grade may worsen considerably. Intra-articular analgesia is essential for diagnosis in mature horses, regardless of the presence of other clinical signs or imaging abnormalities. There is variable communication among the 3 joint compartments of the equine stifle joint and local anesthetic solution can either flow directly through communications or diffuse through synovial septae, but knowledge of the communications is essential to understanding results of diagnostic analgesia. Physical communication between the joint compartments was studied in cadaver specimens injected with latex; when the FPJ was injected there was communication with the MFTJ (60%) and with the LFTJ (3%).2 When the MFTJ was injected communication with the FPJ (80%) and LFTJ (3%) occurred.2 When the LFTJ was injected, communication with the FPJ occurred in only 1 (3%) specimen; in no specimens did the MFTJ and LFTJ communicate.2 Functional communication between the FPJ and femorotibial joints was found in 74% of horses, but authors recommended each compartment be blocked independently.3 Mepivacaine diffused between synovial compartments of the stifle joint in 85-100% of specimens, often in concentrations high enough to elicit analgesia. Authors concluded, that diffusion of local anesthetic solution occurred more frequently than did latex or dye, and separate compartment injections were not as specific as once thought.4 What can be learned from these studies?

To be safe, all 3 compartments of the stifle joint should be blocked independently. The specificity of intra-articular blocks must be questioned. The LFTJ, anatomically, is closest to being a solitary joint cavity, but could be blocked when the FPJ and MFTJ are blocked. In practice, I consider the LFTJ an independent synovial structure and have seen numerous horses in which analgesia of the other compartments failed to abolish pain originating from this joint; the LFTJ had to be blocked in order for horses to show improvement. So, to be safe, all 3 compartments should be blocked. This can be done all at once or sequentially, but if done sequentially, the results may lack specificity. I use 30 ml of mepivacaine and block independently all 3 compartments simultaneously in most horses. Importantly, the stifle joint is large and complex so horses should be given a minimum of 20-30 minutes before being re-evaluated after the block. If improvement is noted, an additional 20-30 minutes is given before any other diagnostic analgesia procedure is performed. The clinician should not expect 100% improvement unless the horse is lame in another limb; 70-80% improvement is conclusive that the primary source of pain causing lameness is the stifle joint.

Diagnostic Imaging Radiography is the first step in diagnostic imaging of horses with confirmed or suspected stifle region pain. Digital radiography has greatly improved image quality, but an occasional faint radiopacity in the intercondylar region, an artefact of digital imaging, should not be mistaken for fragmentation. Lateromedial, caudocranial, caudolateral-craniomedial oblique, and tangential (skyline) images should be obtained. Occasionally, craniolateral-caudomedial oblique images may be needed in horses with unusual fragmentation. Tangential images are not essential, but are quite useful in the diagnosis of patellar fragmentation and to assess patellar position. Well-positioned and well-exposed caudocranial images are essential for evaluating the femorotibial joint space. Narrowing of which, is the earliest sign of OA, but must be repeated if there is any overlap or horses are mal-positioned. In young-to-middle aged racehorses, other signs of OA such as osteophyte formation will be subtle, but authentic narrowing of the MFT joint space is indicative The Practitioner 7

of widespread cartilage damage. Ultrasonographic examination is quite useful in evaluating soft tissues of the stifle region and can be used to evaluate joint surface congruity. Examination of patellar ligaments, menisci and collateral ligaments, and observing effusion, synovial proliferation, osteophytes, and incongruity of the femoral condyle are all benefits of ultrasonography. There are false positive results, however, particularly when evaluating suspected meniscal injury. The cruciate ligaments cannot be examined completely, although disease of these ligaments is extremely rare. Magnetic resonance imaging and computed tomography, if available, can be hugely beneficial and will likely become more important in the near future. Scintigraphic examination is important, but has low sensitivity. In fact, I suspect 2 sources of pain in horses in which bone scan images are negative or equivocal, the stifle and proximal suspensory ligament. The caudal scintigraphic image is essential to evaluate the MFTJ for the presence of increased radiopharmaceutical uptake (IRU) in subchondral bone, which occurs in horses with OA and subchondral bone cysts. Even subtle areas of IRU of the distal, medial femoral condyle should be investigated radiologically. Arthroscopic examination gives direct information of the integrity of cartilage and soft tissues and I believe has been “undersold” in the past. In horses with obvious radiologically or ultrasonographically apparent lesions, arthroscopy can be therapeutic. The diagnostic value should not be underappreciated in horses in which pain-causing lameness can be abolished, but in which few, if any, imaging abnormalities are present. In these horses, often early and important cartilage damage involving the medial femoral condyle suggestive of OA is often found.

of the lesion or if comprehensive examination is required, the septae between the FPJ and each the MFTJ and LFTJ are removed easily using a synovial resector (can be done manually) creating a single joint compartment. This approach is more versatile and consistent than using individual compartment approaches. I struggle in evaluating the caudal compartments of the FTJs, approaches to which have been recently refined.5 A cranial intercondylar approach to the caudal pouch of the MFTJ6 was described and can be performed without a switching stick using the single cranial approach and septectomy. Loose fragments in the FPJ most often accumulate in the extensive suprapatellar pouch and removal sometimes requires a long lavage cannula, long Ferris-Smith rongeurs, or a separate more proximally positioned instrument portal. Intra-operative radiographs are used if size and number of fragments retrieved differs from pre-operative assessment. A synovial resector facilitates removal of embedded fragments at the insertions of the cranial meniscotibial ligaments and various intraarticular blades can be useful to remove meniscal tears. I use microfracture sparingly since aggressive debridement and puncture through calcified cartilage into the subchondral bone can cause a subchondral cyst to occur when one did not exist pre-operatively and the technique was not associated with success.7 Impressive results were reported using mosaic arthroplasty8 and autologous fibrin laded with growth factors and chondrocytes9. Specific lesions – OCD lesions in the FPJ are debrided and loose fragments removed; excessive debridement and abrasion arthroplasty are avoided, if possible. Prognosis is poor with extensive lesions of the lateral trochlear ridge of the femur (LTR), coexistent patellar chondromalacia and with intermittent patellar subManagement of Horses with luxation. Young horses with extensive Stifle Pain and Injuries – OCD lesions of the LTR should be given Emphasis on Surgery 3-6 months rest to allow potential reatThe FPJ and the cranial compartments tachment. Further debridement of the of the MFTJ and LFTJ can be evaluated LTR in these severely affected horses will separately, if desired. The horse is most make them more prone to patellar luxacommonly positioned in dorsal recum- tion and should be avoided. Some conbency. I routinely use fluid irrigation (gas sideration can be given to repair of these insufflation can be used) and a single lesions using polydioxanone pins.9 In portal approach for routine evaluation of general, prognosis is quite good in young the stifle joint with an initial arthroscopic horses with OCD of the FPJ. If lesions are portal between the middle and medial discovered in older horses, conservative patellar ligament. Depending on the site management, including injections into the

8 The Practitioner

FPJ, can be given. In some horses small lesions are found incidentally. Surgery is indicated given a willing owner since even small pieces, if they break off, can cause pronounced lameness and effusion, and the existence of lesions may complicate a future sale. Patellar fracture fragments, most common in horses negotiating fences (medial and proximal aspects) are removed. Occasionally additional instrument portals are needed. Distal patellar fragments occur after medial patellar desmotomy and are easily removed using standard FPJ portals. Occasionally, OA of the FPJ is seen in middle-aged and older horses and prognosis is poor. The relationship between the existence of OCD and the subsequent development of OA is compelling, but often not substantiated. For a long-term solution I still prefer to debride osseous cyst-like lesions of the medial femoral condyle. Reported success in horses 0-3 years-of-age (64%)10 was similar to that reported for injecting corticosteroids directly into the cyst lining (67%)11. In racehorses choice of technique is often directed by owner/trainer influence – if the horse must train and race soon after the procedure, I use arthroscopically-assisted injection of corticosteroids (methylprednisolone acetate). Caution is used in operating older horses with subchondral lucent defects since they usually have substantial OA and prognosis is poor (only 35% of horses > 3 years-of-age returned to soundness11). OA of the MFTJ (less commonly the LFTJ) is a common problem causing lameness in older nonracehorses and racehorses. Horses with subchondral bone cysts can be managed conservatively and given rest and intraarticular injections. However, prognosis appears better with surgical management. Arthroscopic evaluation in racehorses with severe OA is diagnostic but palliative and seldom curative. If racehorses have severe lameness, do not respond to intraarticular corticosteroids and have narrowing of the MFTJ space; I discourage arthroscopic examination. Non-racehorses most commonly develop OA with varying degrees of articular cartilage damage (early – soft, thin cartilage on the medial femoral condyle; later – full thickness cartilage loss and subchondral bone erosion, osteophyte formation). Coexistent meniscal fraying and tearing is seen in horses with OA, but I see very few horses with meniscal tears as the primary surgical lesion. I marvel Issue 6 • 2011

2. Vacek JR, Ford TS, Honnas CM: Communication at the extensive experience of Walmsley with hand walking, then 4 weeks walking between the femoropatellar and medial and lateral et al.12 Meniscal injuries most commonly with a rider up (in a jog cart if a STB racefemorotibial joints in horses, Am J Vet Res 53:1431, occur in horses with other deterioration horse, or a mechanical walker) and then 4 1992. 3. Reeves MJ, Trotter GW, Rainer RA: Anatomical and of the MFTJ or LFTJ and seem to be asso- weeks walking and light trotting, if sound functional communications between the synovial ciated with rather than the cause of OA at this stage. I do not prescribe turn out sacs of the equine stifle joint, Equine Vet J 23:215, or lameness. There are rare exceptions, exercise in the first 6 months after injury 1991. 4. Gough MR, Munroe GA, Mayhew G: Diffusion of however. Prognosis in non-racehorses is or surgery. Uneven surfaces, slipping, mepivacaine between adjacent synovial structures adversely affected by age, severity of lame- quick turning and stopping all predispose in the horse. Part 2: tarsus and stifle, Equine Vet J ness, the presence of a large meniscal tear, horses to recurrent injury and may be the 34:85, 2002. 5. Watts AE, Nixon AJ: Comparison of arthroscopic and the severity of radiological changes.7 reason stifle pain developed initially. approaches and accessible anatomic structures Few horses have solely a soft tissue lesion How do you shoe a horse with stifle during arthroscopy of the caudal pouches of equine diagnosed at arthroscopy. Lameness is pain? There are no set rules, but some femorotibial joints, Vet Surg 35:219, 2006. 6. Muurlink T, Walmsley J, Young D, et al: A cranial usually caused by ongoing OA. Rarely, advocate raising the heels to allow easy intercondylar arthroscopic approach to the caudal cranial meniscal ligament tears can cause breakover, a practice that makes sense. medial femorotibial joint of the horse, Equine Vet substantial lameness. Since slipping is an important force preJ 41:5, 2009. 7. Cohen JM, Richardson DW, McKnight AL, et al: Fractures involving the stifle occur disposing to injury shoe additives (heel, Long-term outcome in 44 horses with stifle lamemost commonly in horses negotiating toe caulks, borium) make some sense to ness after arthroscopic exploration and debridefences and usually involve the patella help limit slipping. Various intra-articular ment, Vet Surg 38:453, 2009. 8. Bodó G, Hangody L, Modis L: Autologous osteo(see above) and cranial tibial tuberos- injections can be used and are commonly chondral grafting (mosaic arthroplasty) for treatity. Horses with non-displaced or mildly given to racehorses with OA. I avoid the ment of subchondral cystic lesions in the equine displaced tibial tuberosity fractures can, use of methylprednisolone acetate if posstifle and fetlock joints, Vet Surg 33:588, 2004. 9. Nixon AJ. Proceedings, 29th Annual Surgery Forum and should, be managed conservatively. sible, not because of a direct deleterious of the American College of Veterinary Surgeons, These fractures are usually non-articular. effect, but because the drug is quite effecChicago, October 2001. Two of 17 horses with this type of frac- tive at reducing inflammation and may 10. Smith MA, Walmsley JP, Phillips TJ, et al: Effect of age at presentation on outcome following ture were retired for reasons unrelated allow the horse with OA to overachieve, arthroscopic debridement of subchondral cystic to fracture and 12 of the remaining 15 risking further development of OA. Hyallesions of the medial femoral condyle: 85 horses (80%) returned to the previous level of uronan (double dose) and triamcinolone (1993—2003), Equine Vet J 35:175, 2005. 11. Wallis TW, Goodrich LR, McIlwraith CW, et al: competition.13 Horses with large, long acetonide are injected and are efficacious Arthroscopic injection of corticosteroids into the and articular fractures are likely surgical in the short-term, but additional injecfibrous tissue of subchondral cystic lesions of the candidates but tension band techniques, tions will be necessary and response in medial femoral condyle in horses: a retrospective study of 52 cases (2001-2006), Equine Vet J 40:461, such as application of a bone plate, should some horses is poor. Other injections such 2008. be used. Simple screw fixation can fail. as IRAP and PRP are currently being given, 12. Walmsley JP, Phillips TJ, Townsend HGG: Given the fact that implants are in the but efficacy is unknown. Meniscal tears in horses: an evaluation of clinical signs and arthroscopic treatment of 80 cases, Equine tibial diaphysis, special consideration for Vet J 35:402,2003. recovery from general anaesthesia should References 1. Ross MW: Movement, In: Ross MW, Dyson SJ, Eds, 13. A rnold C A, Schaer TP, Baird DL , et al: be given. The tibia can fail catastrophically. Diagnosis and management of lameness in the horse. St Conservative management of 17 horses with nonLouis: Elsevier, 2011. articular fractures of the tibial tuberosity, Equine Horses occasionally develop other unusual Vet J 35:202,2003. fractures or fragmentation, the origin of which can remain a mystery. Rarely a midMichael W. Ross, DVM, DACVS body fracture of the patella is diagnosed ++ Dr. Ross is a Professor of Surgery at New Bolton Center, University of Pennsylvania, and surgical management with screws and School of Veterinary Medicine. He developed and is Director of the Nuclear Medicine wires can be performed.

Conservative Management, Rest, Intra-Articular Injections Whether or not surgery is performed, horses with stifle pain need rest to allow healing of articular surfaces, subchondral bone, soft tissues; or in most horses, a combination of these tissues. Four to 6 months of rest is generally recommended particularly in older horses with substantial pain and in which surgery was performed. Many horses will require longer rest periods to become completely sound and are at risk for recurrent pain. Recurrence is a common problem in horses with stifle pain. I usually give a minimum of 4 weeks stall rest, then 4 weeks stall rest www.faep.net

Program at New Bolton Center. Dr. Ross has broad clinical interests including equine gastrointestinal, respiratory, and musculoskeletal surgery, but in recent years has concentrated efforts in the area of orthopedic surgery with a particular interest in arthroscopic surgical techniques. Equine lameness diagnosis and management has always been a clinical focus, with a special emphasis in the Standardbred and Thoroughbred racehorse. ++ Following graduation from Cornell University’s New York State College of Veterinary Medicine in 1981, he completed a large animal internship program there, completed a three-year large animal surgical residency program at New Bolton Center where he was appointed Lecturer in Surgery from 1985-1988, Assistant Professor of Surgery from 1988-1993, and Associate Professor of Surgery from 1993-1999. ++ Dr. Ross became a Diplomate of the American College of Veterinary Surgeons in 1986 and is an active member of the American Association of Equine Practitioners. ++ He is the author of more than 295 scientific papers, proceedings, abstracts and book chapters. Dr. Ross co-authored (with Dr. Sue Dyson) a new lameness textbook and companion CD, “Diagnosis and Management of Lameness in the Horse,” published December 2002 by WB Saunders (Elsevier Science), a culmination of more than 30 years of study and interest in clinical examination and management of the lame horse.

The Practitioner 9

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The Practitioner 11

Hoof Wall Cracks By Scott Morrison, DVM

Hoof Wall The hoof wall is a complex arrangement of epidermal tissue. It is designed to protect the sensitive inner structures, support and transfer the weight of the horse to the bone column and absorb vibrations generated during ground impact. The hoof wall is made up of three layers stratum externum, stratum medium and the stratum internum (lamellatum). The stratum externum and stratum medium are generated from the coronary corium and migrate distally. The stratum internum is generated from the germinal cells of the lamellar epidermis. The layers of the hoof wall merge together and migrate distally toward the ground surface. The stratum internum has very little proliferation in the normal horse. Its main function is to attach the epidermis to the underlying dermis or nonsensitive (epidermal) laminae to sensitive (dermal) laminae. It does play an important role in healing hoof-wall injuries or healing the bed of a full thickness crack. The stratum medium constitutes the majority of the hoof wall. It is also the pigmented layer and is made up of tubular and intertubular horn. The coronary papillae form the tubular horn and the tissue between the papillae generate the intertubular horn. The intertubular horn is therefore formed perpendicular to the tubular horn, thus creating a multidirectional, fiber reinforced composite.1,2 The coronary papillae, and thus, the horn tubule, are most dense toward the external surface and gradually decrease in density as they get closer to the internal layers. The moisture content of the hoof wall follows the tubular concentration and gradually increases toward the internal layers. The change in tubular horn and moisture content is a protective design to dissipate or dampen shock as you get closer to the sensitive layers and to limit the propagation of cracks to the external layers and prevent them from becoming full thickness or deep cracks. The keratinized cells of the tubular and intertubular horn are firmly adhered to each other creating an impermeable protective barrier. The inner hoof wall has no direct blood supply and therefore must receive its nutrients via diffusion from the dermis. Weak walls are a common problem. They are predisposed to cracking, deformation and are very vulnerable to moisture content changes. That is they are ineffective at establishing an impermeable barrier. In evaluating a case of weak, brittle walls with chronic superficial cracks there are two main categories that need to be considered – nutrition and mechanical causes. Walls require proper/balanced nutrition. Several nutrients are particularly important to hoof wall structure: biotin, calcium, zinc, iodine, vitamin A, Methionine. Cases of poor hoof quality may require a diet or 12 The Practitioner

hair/hoof analysis as part of the diagnostic evaluation. Although very few horses I see are being deprived of nutrients, it is far more common to see over feeding and unbalanced nutrition programs. Over feeding some nutrients can cause toxicities or can interfere with the absorption of other nutrients. Mechanical causes can be as simple as poor trimming, superficial and low nailing that splits the wall, excessive bathing with detergents and excessive finishing of the outer hoof wall. Superficial cracks can begin on the distal or ground surface of the foot and propagate proximally; these are commonly referred to as sand cracks or can begin in the proximal regions of the hoof. Deeper/full thickness cracks are generally associated with imbalance and abnormal stresses on the hoof. It is fairly rare for a normal well-balanced foot (free of hoof capsule distortion) to suffer a toe or quarter crack. The normal/healthy hoof is very capable of withstanding normal loading forces. During normal locomotion the stratum medium experiences only one-tenth of the compressive forces required to cause structural failure.3 Therefore the hoof must be weakened or distorted first before structural failure of cracking occurs. Hoof cracks are usually classified according to their location and/or origin (i.e. toe crack, quarter crack, heel crack.) A true quarter crack begins at the coronary band, is full thickness, and propagates distally. However, a sand crack in the quarter begins distally and is superficial. Generally, quarter cracks are the result of an imbalance in the frontal and sagital planes. This imbalance places more stress on the quarter then it is designed to accommodate resulting in vertical, proximal displacement of the coronary band. The displaced coronary band interferes with the abduction of the collateral cartilage resulting in a quarter crack. These cracks usually start in the stratum internum and propagate externally. Occasionally, a quarter will crack internally and have a delayed propagation to the external surface (blind quarter crack). These are usually sensitive as serum and hemorrhaging can build up slight pressure under the wall. Mending a quarter crack begins with trimming and shoeing first. The foot should be trimmed and shod to restore balance or more even weight distribution. Often the use of a heartbar or arch support aids in taking some weight off the overloaded quarter. Ideally, the coronary band should be allowed to drop from its vertical displacement before patching, but this is not always possible. Methods to help the coronary band to settle are grooving, flotation, overnight poulticing or just re-establishing balance and time (going barefoot during this time, if possible, is helpful). Once the foot is properly trimmed and shod, the bed of the crack should be packed off with antiseptic powder, calcium carbonate barrier (Dycal) or a drain. The crack can then be stabilized by various methods: 1) Wire suture/lacing, acrylic and epoxy 2) Composite cloth, acrylic and epoxy 3) Metal plate and screws Issue 1 • 2012

Stabilization of a quarter crack should address both non-weight bearing, and close excessively or have overtensile and shearing forces. A metal-band alone stabi- lapping margins, during weight bearing. These cracks lizes tensile forces, but does little for shear forces. Usu- should be stabilized in the non-weight bearing posially, sufficient stabilization requires a composite mesh tion as this best opposes the margins of the wall. Care cloth and resin or acrylic. Some cases require metal wire should be taken not to cover any crack with equilox or adhesive as this makes the perfect environment for a stitching and lacing as well. Toe cracks generally occur secondary to excessive ten- submural abscess. Crack beds should be packed off with sion on the anterior hoof wall. This tension is from the antiseptic powder, cotton saturated with antiseptic, or a DDFT pulling on the coffin bone causing excessive rota- drain. It is important to realize that even the best crack tional pull on the coffin bone and tensile strain on the repair patch or stitching technique is useless without anterior laminae and hoof wall. The dorsal hoof wall usu- first addressing the trimming and/or shoeing. ally becomes concave or dished prior to the crack forming. References Toe cracks are seen in flat feet with excessively long toes 1- Pollitt CC, The Anatomy and Physiology of the Suspensory and breakover too far forward, or in club feet. Both hoof Apparatus of the Distal Phalanx. Vet Clin North Am Equine Pract 2010;26(1):29-49 conformations have increased strain on the dorsal wall. 2- Bertram JEA, Gosline JM. Functional Design of Horse Hoof Keratin: the modulation of mechanical properties through hydration effects. J Exp Biol 1987;130:121-136. 3- Thomason JJ, B iewener AA, Bertram JEA. Surface Strain on the Equine Hoof Wall in Vivo; implications fof material design and functional morphology of the wall. J Exp Biol 1992;166:145-165

Treatment of Toe Cracks Trimming and shoeing to re-balance the hoof and ease breakover is the first step. Generally, the breakover point should be set directly beneath the proximal aspect of the crack or directly beneath where the dish starts. I am generally more aggressive and gently roll the toe forward from a plum line dropped from the anterior coronary band. This alone heals the majority of toe cracks. If the horse is lame from the crack or if the crack is unstable (opens and closes with weight bearing) then it needs to be stabilized. Usually addressing tensile forces with a metal plate (aluminum plate glued across the crack) is sufficient. Toe cracks open, when

Scott E. Morrison, DVM, Farrier ++ Veterinarian at Rood and Riddle Equine Hospital Podiatry Center, Lexington, KY, since 1999. Currently performing 100 percent podiatry work ++ DVM , VA-MD Regional College of Veterinary Medicine ++ U.S. and international consulting, lecturing, clinics working on various foot conditions ++ Farrier, Danny Ward’s Eastern School of Farriery

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The Practitioner 13

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The Practitioner 15

Pituitary Pars Intermedia Dysfunction: Diagnosis and Treatment By Nicholas Frank, DVM, PhD, DACVIM

DIAGNOSIS Pituitary pars intermedia dysfunction (PPID, also called equine Cushing’s disease) is associated with laminitis, muscle atrophy, immunosuppression, and regional fat redistribution.1 It is particularly important to diagnose PPID before laminitis develops in order to prevent this devastating disease. Unfortunately, PPID is more difficult to recognize in its earlier stages and diagnostic tests have lower accuracy at this point. This discussion will focus on early PPID. Age – Since PPID is more common in older horses, this diagnosis should generally be considered in any horse > 15 years-of-age. However, horses with Equine Metabolic Syndrome can develop PPID at a younger age (> 10 years). Haircoat abnormalities – Hypertrichosis (commonly called hirsutism) is an easily recognized clinical sign of advanced PPID, but haircoat abnormalities associated with early PPID are less specific and harder to detect. Affected horses exhibit delayed shedding of the winter haircoat, increased hair length, and dullness of the haircoat. If this problem is suspected, owners should record the time that their horse sheds its winter haircoat and compare it with other horses in the same barn. A horse with early PPID may retain its winter haircoat for a several weeks longer than other horses. Examination of control horses from the same barn is recommended because the timing of haircoat shedding depends upon day length and therefore geographical location. Retention of winter hairs in certain regions of the body – Some horses with early PPID shed most of their winter haircoat, but retain hairs along the palmar or plantar aspects of the legs, behind the elbow, or beneath the mandibles. A thorough physical examination is required to detect this problem and the client must be questioned about the horse’s normal haircoat. For example, clients must be asked whether longer hairs along the palmar/ plantar aspects of the legs are normal for their animal. 16 The Practitioner

Shift in metabolism – Owners sometimes report that their horse has undergone a “shift in metabolism” (from easy keeper to a hard keeper) and is now losing weight and body condition. This problem is difficult to confirm unless a complete dietary history has been recorded, but clinicians should suspect PPID when a middle-aged horse begins to lose muscle mass and requires more calories than it did in the past. Owners may attribute this to aging, but the clinician should judge whether the decrease in muscle mass is appropriate or accelerated in an individual horse. In many cases, loss of muscle mass has occurred over a few months, instead of the gradual process associated with aging. Regional adiposity – This clinical sign is associated with both Equine Metabolic Syndrome (EMS) and PPID. In the case of EMS, regional adiposity first develops at an earlier age (< 15 years) and then persists. In contrast, detection of regional adiposity for the first time in an older (> 15 years) horse indicates the development of PPID. As discussed below, horses can develop EMS at an earlier age and then concurrent PPID as they get older. These patients have fat deposits that were previously associated with EMS and now become a component of PPID. Regional adiposity refers to enlarged adipose tissues within the neck region (“cresty neck”) and fat pads cranial to the tailhead. Poor performance, change in attitude, and declining general appearance – These vague presenting complaints sometimes lead to the diagnosis of early PPID. Poor performance has not been documented in horses with PPID, but this problem prompts assessment of the horse’s appearance and body condition, which leads to consultation with a veterinarian. Lameness – This problem is a presenting complaint for PPID in early and advanced cases. Pituitary pars intermedia dysfunction has been associated with laminitis1 and is a predisposing factor for this condition. Infertility – Pituitary pars intermedia dysfunction should be considered when aged mares develop fertility problems.

More research is required to determine the effects of PPID on the reproductive cycle and uterine environment. At present, only anecdotal evidence is available to suggest that reproductive performance improves in mares with PPID that are treated.

TREATMENT

Pergolide mesylate – This ergot alkaloid dopamine receptor agonist is administered to horses with PPID to restore dopaminergic inhibition of melanotropes. Interaction with D2 receptors inhibits hormone secretion and is therefore associated with improvement in clinical signs. It has not been determined whether pergolide treatment also inhibits the development of pituitary hyperplasia or reduces the size of pituitary adenomas, but these beneficial effects are plausible considering the mechanism of action of this drug. Pergolide was previously marketed as Permax® (previously manufactured by Eli Lilly Co.) and used for the treatment of Parkinson’s disease. However, this product was voluntarily withdrawn from the market in March 2007 after the Federal Drug Administration (FDA) issued a warning that pergolide was associated with increased incidence of valvular regurgitation in people.3,4 Since that time, pergolide has only been available through compounding pharmacies. This has lowered the price of the drug, but also raised concerns about the stability and efficacy of compounded pergolide. At present, the recommended approach is to purchase pergolide in granule form and assume a 60-day shelf life or as an aqueous suspension and assume a 30-day shelf life. In a recent study, Davis et al.5 demonstrated that pergolide lacked stability over a 35-day period when prepared as an aqueous suspension. This group also showed that higher temperatures and exposure to light enhanced degradation, so aqueous preparations should be stored in dark containers and refrigerated. Even under these conditions, a maximum 30-day shelf life should be assumed for aqueous preparations. Pergolide is prescribed on a total dose basis using a starting dose of 1.0 mg/ Issue 6 • 2011

day or 0.5 mg/day for horses and ponies, respectively. If the horse owner is willing to administer half the dose twice daily, this may be preferable on the basis of recent pharmacokinetic data.6 Some owners report loss of appetite when pergolide is first started. If anorexia develops, treatment should be halted for 2 days or until appetite improves, and then restarted at 0.25 mg/day for 2 days, 0.5 mg/day for 2 days, and 0.75 mg/kg for 2 days. Another side effect of pergolide treatment is temporary dullness after initiating therapy and this can be addressed using the same strategy. Pergolide was purchased from compounding pharmacies as a 1.0 mg per 2 mL suspension and costs approximately $1.60/day for a horse receiving 1 mg/day. However, a pergolide product was under review by the FDA.It is now available. Cyproheptadine – Both pergolide and cyproheptadine lower plasma ACTH concentrations in PPID horses,7 but pergolide is more effective.8 Donaldson et al.8 reported that 17 of 20 horses (85%) with PPID improved with pergolide treatment, compared with only 2/7 horses treated with cyproheptadine. Cyproheptadine antagonizes serotonin which is thought to be a stimulatory neurotransmitter for pars intermedia melanotropes. Treated horses occasionally exhibit sedation when treatment is initiated. A dosage of 0.25 mg/kg PO q12h is recommended and the drug is available as 4 mg tablets in labeled (Periactin®, Merck & Company, Inc.) and generic forms. At present, tablets cost approximately $0.50 each ($14/day for a 450-kg horse), so most practitioners order the drug from compounding pharmacies. Cyproheptadine is compounded into an aqueous suspension at 50, 100, or 150 mg/mL concentrations and costs approximately $1.30/day for a horse weighing 450 to 525 kg. REFERENCES

1. Donaldson MT, Jorgensen AJ, Beech J. Evaluation of suspected pituitary pars intermedia dysfunction in horses with laminitis. J Am Vet Med Assoc 2004;224:1123-1127. 2. Johnson PJ, Slight SH, Ganjam VK, et al. Glucocorticoids and laminitis in the horse. Vet Clin North Am Equine Pract 2002;18:219-236. 3. Beec h J, Boston R , L i ndborg S, et a l. Adrenocorticotropin concentration following administration of thyrotropin-releasing hormone in healthy horses and those with pituitary pars intermedia dysfunction and pituitary gland hyperplasia. J Am Vet Med Assoc 2007;231:417-426. 4. Miller MA, Pardo ID, Jackson LP, et al. Correlation of pituitary histomorphometry with adrenocorticotrophic hormone response to domperidone

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Recommended Diagnostic Tests For Pituitary Pars Intermedia Dysfunction PPID: Resting ACTH Concentration

PPID: Dexamethasone Suppression Test

Considerations

• Higher concentrations are detected in healthy horses in the late summer and autumn • Pain and stress raise ACTH concentrations

• False positives are detected in healthy horses in the late summer and autumn • Owner concerns about inducing laminitis

Procedure

• Collect blood in a tube containing EDTA • Keep the blood sample cool at all times • Centrifuge the same morning or afternoon • Mail to the laboratory with a cool pack

• Collect a pre-injection blood sample (optional) • Inject 0.04 mg/kg (20 mg) dexamethasone intravenously or intramuscularly • Collect a blood sample 19 or 24 hours later

Interpretation

• Positive if ACTH > 35 pg/mL (> 50 pg/mL in August to October) • Results may fall within reference range for horses with early/mild PPID. • Use the fall as a natural stimulation test

• Positive if cortisol concentration > 10 ng/mL (27 nmol/L) at 19 or 24 h • Results may be normal in horses with early/mild PPID • Only the negative result is significant when testing in the late summer or autumn

administration in the diagnosis of equine pituitary pars intermedia dysfunction. Vet Pathol 2008;45:26-38. 5. Donaldson MT, McDonnell SM, Schanbacher BJ, et al. Variation in plasma adrenocorticotropic hormone concentration and dexamethasone suppression test results with season, age, and sex in healthy ponies and horses. J Vet Intern Med 2005;19:217-222. 6. Treiber KH, Kronfeld DS, Hess TM, et al. Evaluation of genetic and metabolic predispositions and nutritional risk factors for pasture-associated laminitis in ponies. J Am Vet Med Assoc 2006;228:1538-1545. 7. Carter RA, Treiber KH, Geor RJ, et al. Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies. Equine Vet J 2009;41:171-178. 8. Vick MM, Sessions DR, Murphy BA, et al. Obesity is associated with altered metabolic and reproductive activity in the mare: effects of metformin on insulin sensitivity and reproductive cyclicity. Reprod Fertil Dev 2006;18:609-617. 9. Eiler H, Frank N, Andrews FM, et al. Physiologic assessment of blood glucose homeostasis via combined intravenous glucose and insulin testing in horses. Am J Vet Res 2005;66:1598-1604. 10. Frank N. Equine Metabolic Syndrome. J Equine Vet Sci 2009;29:259-265. 11. Vick MM, Adams A A, Murphy BA, et al. Relationships among inflammatory cytokines, obesity, and insulin sensitivity in the horse. J Anim Sci 2007;85:1144-1155. 12. Xu H, Barnes GT, Yang Q, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest 2003;112:1821-1830. 13. Vincent HK, Innes KE, Vincent KR. Oxidative stress and potential interventions to reduce oxidative stress in overweight and obesity. Diabetes Obes Metab 2007;9:813-839. 14. McFarlane D, Cribb AE. Systemic and pituitary pars intermedia antioxidant capacity associated

with pars intermedia oxidative stress and dysfunction in horses. Am J Vet Res 2005;66:2065-2072. 15. Garcia MC, Beech J. Equine intravenous glucose tolerance test: glucose and insulin responses of healthy horses fed grain or hay and of horses with pituitary adenoma. Am J Vet Res 1986;47:570-572.

Nicholas Frank, DVM, PhD, DACVIM ++ Dr. Frank is Professor and Chair of the Department of Clinical Sciences Tufts Cummings School of Veterinary Medicine, North Grafton, MA. He continues to consult on equine internal medicine cases and coordinate clinical research. ++ Growing up in the United Kingdom, he trained in the United States and received his BSc degree in biology from the University of North Carolina in 1989 and his DVM degree from Purdue University in 1993. After working for two years in private equine practice in Illinois, he returned to Purdue University and completed his large animal medicine residency training and PhD degree. ++ In 2002, Dr. Frank joined the faculty of the University of Tennessee as a clinician and developed research programs in the areas of equine endocrinology, metabolism, gastrointestinal disease, and laminitis.

The Practitioner 17

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18 The Practitioner

Issue 1 • 2012

Florida Practitioner John Mitchell Leads AAEP membership in 2012

acetrack practitioner Dr. John Mitchell began his service as the president of the American Association of Equine Practitioners during the association’s 57th Annual Convention in San Antonio. Dr. Mitchell was sworn in as president during the Nov. 21, 2011 President’s Luncheon. Dr. Mitchell has provided the AAEP with insight into racehorse welfare, veterinary ethics and practice management. Since 1975, Dr. Mitchell has worked as a racetrack and pleasure horse practitioner in Boca Raton. His focus has been the care of Standardbred racehorses at Pompano Park Racetrack. Dr. Mitchell attended The Ohio State University where he received his veterinary degree in 1972. He completed an equine internship at Auburn University in Alabama in 1973. In 1975, Dr. Mitchell established a racetrack and pleasure horse

practice, Equine Associates, in Boca Raton. After 10 years of operating the practice, Dr. Mitchell decided to downsize and concentrate predominantly on Standardbred care at the racetrack. He retired from practice in 1994 to spend time with his wife, Lynne, who passed away in 2004. He returned to practice part-time at Pompano Park in 2004. Throughout his career, Dr. Mitchell has worked with clients to weigh the economic value of veterinary treatment options. He is passionate about personal finance, and has written articles and presented on the topic of financial planning for veterinarians at national meetings. An active AAEP member since 1972, Dr. Mitchell has served on the Educational Programs, Racing, Practice Management and Foundation Advisory committees. He held the office of AAEP treasurer from 2002-2005, and has been instrumental

in the development of programs for the annual AAEP Practice Management Seminar, a meeting he chaired in 2002. During his term as president, Dr. Mitchell hopes to make more members aware of the value their AAEP membership can add to their professional and personal lives. The American Association of Equine Practitioners, headquartered in Lexington, Ky., was founded in 1954 as a nonprofit organization dedicated to the health and welfare of the horse. Currently, the AAEP reaches more than 5 million horse owners through its nearly 10,000 members worldwide and is actively involved in ethics issues, practice management, research and continuing education in the equine veterinary profession and horse industry.

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The Practitioner 19

Treatment and Prognosis for Laryngeal Hemiplegia

aryngeal hemiplegia (recurrent laryngeal neuropathy) has been recognized for many years and is one of the most common problems of the upper respiratory tract, but is still challenging to effectively treat. There are multiple methods of treatment, and the tieback (laryngoplasty) procedure is still the most common method of treatment. Performing a tieback to abduct and lock the left arytenoid in an open position is a simple concept, but much more complex than it appears. Part of the complexity is taking what should be a dynamic functional larynx and making it into a somewhat static structure without complications. Furthermore, we are working with tissues (cartilage) that have significant variability to their shape and stiffness and thus, the ability to construct and maintain a rigid structure is difficult. This leads to significant variability of success and success that is greatly dependent upon the primary complaint and the expected level of performance for the individual horse. The success rate for treatment of nonracehorses is generally very high (>80%), while the success for a racehorse is reported to be from 25-70% depending on the criteria and methodology used to determine success. The primary reason for the limited success is the inability to maintain an adequate airway during exercise. Other reasons involve complications as a result of the surgery. Aspiration or coughing is a significant concern, but anecdotally, appears to be a function of the surgeon’s experience and not directly associated with the degree of abduction. The occurrence of seroma formation is <10%, and infection at the surgical site even lower. The first step to success is obtaining an accurate diagnosis. The diagnosis is most often made with resting endoscopy. Several different laryngeal grading systems have been developed for horses examined while standing loosely restrained in a box stall or in stocks, with a twitch applied and without tranquilization or sedation. The majority of grading systems are similar to what is described here with minor variations. Grade I (synchronous and symmetrical abduction) and grade II (symmetrical but asynchronous abduction) are considered normal, in that the horse is capable of obtaining and maintaining complete abduction of the arytenoid cartilages during sustained exercise. Laryngeal grades III and IV are abnormal. Any horse with grade IV laryngeal movements clearly demonstrates progressive and severe axial collapse of the paralyzed arytenoid cartilage during

20 The Practitioner

By Eric J. Parente, DVM, DACVS

exercise. Its clinical significance will depend on the level of exercise and how the horse is judged (performance or noise). Most racehorses with grade III (asynchronous and asymmetrical movement) dysfunction will also experience dynamic arytenoid collapse, but many show horses will not. Since laryngeal dysfunction is almost always left sided, any right sided observations should cause the clinician to pause and reevaluate the horse. Right sided dysfunction is most commonly secondary to 4th branchial arch disease. This should be confirmed prior to considering surgery since structural abnormalities may prohibit the chance of a successful laryngoplasty procedure. It can be confidently diagnosed with ultrasound or MRI. The first challenge of laryngoplasty surgery is attaining the exact position of the arytenoid desired at the time of surgery. Intraoperative videoendoscopy is essential to more precisely position the arytenoid. Despite videoendoscopy, less than two thirds of the horses had the ideal position of abduction on the morning following surgery in one retrospective study. Futhermore, the most common complication postoperatively is loss of abduction. One study reported a loss of abduction of one grade or more in almost half of the horses over a 6-week period. There are likely multiple causes for loss of abduction, and many different causes have been proposed, but none have been clearly defined. There is no evidence that the prosthesis material, the horse’s age, or the preoperative degree of dysfunction impacts laryngoplasty failure. Thus, there is no benefit of waiting until a horse is completely paralyzed before pursuing surgery. There is actually more recent data to show that horses undergoing laryngoplasty that were not completely paralyzed returned to a higher level of performance than horses that were completely paralyzed. Several years ago, we developed a different approach to minimize abduction loss and improve stability with a modified laryngoplasty approach. There are two significant modifications from the standard laryngoplasty. The first is approaching the muscular process caudal to the cricopharyngeus muscle rather than between the crico and thyropharyngeus. The second is transecting the insertion of the cricoarytenoideus dorsalis muscle from the muscular process and entering the cricoarytenoid (CA) joint to debride part of the articular cartilage and facilitate ankylosis of the CA joint. An experimental study demonstrated the effectiveness of this technique. We are completing a Issue 1 • 2012

retrospective analysis of racehorses treated by a modified laryngoplasty relative to cohorts. Since performance outcome is measured differently in many studies, the reader should be cautious in making direct comparisons amongst studies. One common deficit in many studies is the short term performance analysis. We evaluated horses over several years and looked at quarterly earnings. Our data indicate that the horses treated by modified laryngoplasty earn as much over time, and compete as long or longer than their cohorts. While laryngoplasty may never be the perfect procedure, if the goal is to create a stable partially abducted arytenoid, methods as described above to improve the probability of achieving this goal could be employed. The only potential disadvantage of this technique is if the appropriate degree of abduction is not achieved, there will be a limited time of opportunity to change the position of the arytenoid before a joint ankylosis ensues. If several months after surgery the horse exhibits significant aspiration, or on the other extreme a lack of adequate abduction, repeat laryngoplasty is unlikely to be an effective option for surgical correction. An arytenoidectomy would be recommended. Other potential reasons for limited improvement in performance after laryngoplasty do not just revolve around structural stability, but involve dynamic function. There is evidence that the horse with limited resting abduction after laryngoplasty can often undergo further dynamic collapse of the affected arytenoid, or have other soft tissue structures obstructing the airway during strenuous exercise. If there is not adequate abduction of the left arytenoid it is common that the left aryepiglottic fold and/or the right vocal cord will deviate axially during inspiration and result in partial obstruction and noise. If the arytenoid is poorly abducted it is likely that the left arytenoid will undergo further dynamic collapse during exercise. Resting evaluation of the arytenoid cannot predict stability under exercising conditions accurately. There is also experimental evidence that horses, after laryngoplasty, may not have gross evidence of aspiration, but can have microscopic contamination of their lower airway. The impact of this lower airway contamination on performance is unknown, but it is easy to speculate that it could initiate a complex of lower airway inflammation that does impact gas exchange. Given the challenge of obtaining a positive outcome with laryngoplasty, other alternative treatments of cordectomy, ventriculectomy, arytenoidectomy, or reinnervation have been considered as viable treatment options. These different surgical options are tailored more to the use of the horse and the degree of laryngeal dysfunction. Arytenoidectomy is generally reserved for chondropathies and reinnervation has limited success, but www.faep.netâ&#x20AC;

vocal cordectomies can still be successful in select cases of laryngeal dysfunction. The vocal cordectomy (sometimes in conjunction with the ventriculectomy) is reserved for horses that maintain some abduction capability and that are not racehorses. The goal is to minimize noise production for show horses. It is rarely recommended as a sole treatment for a racehorse. Vocal cordectomy can be performed in the standing horse with transendoscopic laser resection or via laryngotomy (standing or anesthetized). While bilateral ventriculocordectomy is advocated by some clinicians to decrease abnormal noise, and can be performed successfully with traditional surgery, it should not be attempted with transendoscopic laser surgery at one time because it will likely lead to ventral scar/webbing formation in the larynx. The value of a ventriculectomy is arguable. If the vocal cord is completely resected, the ventriculectomy likely has little benefit.

Pre operative photo of laryngeal hemiplegia.

Selected References:

Post operative photo after

modified laryngoplasty. Ahern B, Parente E: Mechanical evaluation of the equine laryngoplasty. Vet Surg 315 39:661-666, 2010. Brown J A, Derksen F J, Stick J A, et al 2003 Ventriculocordectomy reduces respiratory noise in horses with laryngeal hemiplegia. Equine Veterinary Journal 35(6):570-574 Dahlberg JA, Valdes-Martineez A, Boston RC, Parente EJ. Analysis of conformational variations of the cricoid cartilages in Thoroughbred horses using computed tomography. Equine Veterinary Journal in press 2010. Dixon P M, McGorum B C, Railton D I, et al 2003A. Long-term survey of laryngoplasty and ventriculocordectomy in an older, mixed-breed population of 200 horses. Part 1: Maintenance of surgical arytenoid abduction and complications of surgery. Equine Veterinary Journal 35:389-396 Parente EJ, Birks E. Habecker P. A modified laryngoplasty approach promoting ankylosis of the cricoarytenoid joint. Veterinary Surgery 40:204-210, 2011. Radcliffe C, Woodie J, Hackett R, et al: A comparison of laryngoplasty and 300 modified partial arytenoidectomy as treatments for laryngeal hemiplegia in 301 exercising horses. Vet Surg 35:643-652, 2006. Witte T, Mohammed H, Radcliffe C, et al: Racing performance after combined 262 prosthetic laryngoplasty and ipsilateral ventriculocordectomy or partial 263 arytenoidectomy: 135 Thoroughbred racehorses competing at less than 2400 m 264 (1997-2007). Equine Vet J 41:70-75, 2009.

Eric J. Parente, DVM, DACVS ++ Dr. Parente is an Associate Professor of Surgery at New Bolton Center, University of Pennsylvania, School of Veterinary Medicine. He has specialized in performance evaluations and upper respiratory surgery. ++ He earned his veterinary degree from Cornell University, completed his internship at Rood and Riddle Equine Clinic, and then his surgical residency at New Bolton Center. ++ Dr. Parente received his board certification from the American College of Veterinary Surgeons in 1994 and continues to be an active member on various committees, as well as a presenter at its annual symposium. ++ He is internationally recognized as a respiratory surgeon and is well published in both texts and journals.

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