Diagnosis and Management of Lameness in the Horse

SAUNDERS An Imprint of Elsevier Science 11830 Westline Industrial Drive St. Louis, Missouri 63146 Diagnosis and Management of Lameness in the Horse Copyright © 2003, Elsevier Science (USA). All rights reserved.

ISBN 0-7216-8342-8

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. NOTICE Veterinary medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the licensed prescriber, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the publisher nor the author assumes any liability for any injury and/or damage to persons or property arising from this publication.

Acquisitions Editor: Ray Kersey Developmental Editor: Denise LeMelledo Publishing Services Manager: Linda McKinley Project Manager: Judy Ahlers Designer: Julia Dummitt Cover Art: Fabio Torre EH/CW Printed in the United States of America 9

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Abbreviations AAEP ALARA ALDDFT ANA AST AVA BAP BID BSP CdCr CdL-CrMO Ci CK CNS COMP COX CrCd CRGP CS CSA CSF CT CTX CVM DDFT DFTS DIP joint DL-PaMO DL-PlMO DM-PaLO DM-PlLO DMSO DPa DPl DPr-PaDiO EDM EHVI EIPH EL EM EMG EPM ER EVA FAS FEI FFD GAG GBE GBq GRF GSH HDP H&E HU HyPP ICR IM IRU

American Association of Equine Practitioners As low as reasonably achievable Accessory ligament of the deep digital flexor tendon Antinuclear antibodies Aspartate aminotransferase Arteriovenous anastomosis Bone-specific alkaline phosphatase Twice daily Bone sialoprotein Caudocranial Caudolateral-craniomedial oblique Curie Creatine kinase Central nervous system Cartilage oligomeric matrix protein Cyclooxygenase Craniocaudal Calcitonin gene related peptide Chondroitin sulfate Cross-sectional area Cerebrospinal fluid Computed tomography Collagen C telopeptides Cervical vertebral malformation Deep digital flexor tendon Digital flexor tendon sheath Distal interphalangeal joint Dorsolateral-palmaromedial oblique Dorsolateral-plantaromedial oblique Dorsomedial-palmarolateral oblique Dorsomedial-plantarolateral oblique Dimethylsulfoxide Dorsopalmar Dorsoplantar Dorsoproximal-palmarodistal oblique Equine degenerative myeloencephalopathy Equine herpes virus I Exercise-induced pulmonary hemorrhage Exercise level Electron microscopy Electromyography Equine protozoal myelitis Exertional rhabdomyolysis Equine viral arteritis Fiber alignment score Federation Equestre Internationale Focus film distance Glycosaminoglycan Glycogen binding enzyme Giga becquerel Ground reaction force Glutathione peroxidase Hydroxymethane diphosphonate Hematoxylin and eosin Hounsfield unit Hyperkalemic periodic paralysis Instant center of rotation Intramuscularly Increased radiopharmaceutical uptake

IV KS LDH LF LH LH LM MAC MBq mCi McII McIII McIV MCP joint MDP MIC MMP MRI MSD MtII MtIII MtIV MTP joint NKA NPY NSAID OAAM OC PaPr-PaDiO PAS PASM PCR PET PHI PIP joint PMMA PSB PSGAG PSSM QH RER RF RH RVI SDFT SID SL SLE SP SPECT STB T1-T18 TB TENS TGF-β TNF TS VIP WBL

Intravenously Keratin sulfate Lactate dehydrogenase Left forelimb Left hindlimb Luteinizing hormone Lateromedial Minimum alveolar concentration Mega becquerel Millicurie Second metacarpal bone Third metacarpal bone Fourth metacarpal bone Metacarpophalangeal joint Methylene diphosphonate Minimum inhibitory concentration Metalloproteinase Magnetic resonance imaging Minimum sagittal diameter Second metatarsal bone Third metatarsal bone Fourth metatarsal bone Metatarsophalangeal joint Neurokinin A Neuropeptide Y Non-steroidal anti-inflammatory drug Occipitoatlantoaxial malformation Osteocalcin Palmaroproximal-palmarodistal oblique Periodic acid–Schiff Periodic acid–silver methanamine Polymerase chain reaction Photon emission tomography Peptide histidine isoleucine Proximal interphalangeal joint Polymethylmethacrylate Proximal sesamoid bone Polysulfated glycosaminoglycans Polysaccharide storage myopathy Quarter Horse Recurrent exertional rhabdomyolysis Right forelimb Right hindlimb Rubeola virus immunomodulator Superficial digital flexor tendon Once daily Suspensory ligament Systemic lupus erythematosus Substance P Single photon emission computed tomography Standardbred First to eighteenth thoracic vertebrae Thoroughbred Transcutaneous electrical stimulation Transforming growth factor β Tumor necrosis factor Type or echo score Vasoactive intestinal peptide Warmblood

CONTRIBUTORS EDITORS Mike W. Ross, DVM Professor of Surgery Department of Clinical Studies University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania Sue J. Dyson, MA, VetMB, PhD, DEO, FRCVS Head of Clinical Orthopaedics Centre for Equine Studies Animal Health Trust Newmarket Suffolk, United Kingdom

CONTRIBUTORS Rick M. Arthur, DVM Private Practice Sierra Madre, California Michael A. Ball, DVM Private Practice Early Winter Equine Medicine & Surgery Ithaca, New York Lance H. Bassage II, VMD, Dipl ACVS Assistant Professor of Equine Surgery Department of Veterinary Clinical Medicine College of Veterinary Medicine University of Illinois Urbana, Illinois Andrew P. Bathe, MA, VetMB, DEO, Dipl ECVS, MRCVS University Equine Surgeon The Queen’s Veterinary School Hospital University of Cambridge Cambridge, United Kingdom

Jerry B. Black, DVM Private Practice Oakdale, California James T. Blackford, DVM Professor of Large Animal Surgery Department of Large Animal Clinical Sciences College of Veterinary Medicine University of Tennessee Knoxville, Tennessee Joseph K. Boening, DMV Private Practice Tierklinik Munster-Tellgte Telgte, Germany Dr. Darryl Bonder, DVM Private Practice Toronto Equine Hospital Mississauga, Ontario, Canada Jane C. Boswell, MA, VetMB, Cert VA, Cert ES(Orth), Dipl ECVS, MRCVS Private Practice Liphook Equine Hospital Forest Mere Liphook Hampshire, United Kingdom Robert P. Boswell, DVM Private Practice Palm Beach Equine Clinic Wellington, Florida Robert M. Bowker, VMD Professor Department of Pathobiology and Diagnostic Investigation College of Veterinary Medicine Michigan State University East Lansing, Michigan

Jill Beech, VMD The Georgia and Philip Hofmann Chair in Medicine and Reproduction Professor of Surgery Department of Clinical Studies University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Thomas D. Brokken, DVM Private Practice Cooper City, Florida

Scott D. Bennett, DVM Private Practice Simpsonville, Kentucky

John P. Caron, DVM Department of Large Animal Clinical Sciences College of Veterinary Medicine Veterinary Medical Center Michigan State University East Lansing, Michigan

William V. Bernard, DVM Rood and Riddle Equine Hospital Lexington, Kentucky Alicia L. Bertone, DVM, PhD, Dipl ACVS Trueman Family Endowed Chair in Equine Clinical Studies Professor, Equine Orthopedic Surgery Department of Veterinary Clinical Sciences Daniel M. Galbreath Equine Center The Ohio State University Columbus, Ohio

Herbert J. Burns, VMD Private Practice Pine Bush Equine Pine Bush, New York

G. Kent Carter, DVM Department of Large Animal Medicine and Surgery Texas Veterinary Medical Center Texas A&M University College Station, Texas

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Contributors

Eddy Cauvin, DVM, MVM, PhD, Dipl ECVS Lecturer, Equine Surgery Departement Hippique Ecole Nationale Veterinaire de Lyon Marcy L’Etoile, France Mark W. Cheney, DVM Private Practice Lexington, Kentucky Chris Colles, BVetMed, PhD Hon FWCF, FRCVS Private Practice Avonvale Veterinary Group Oxfordshire, United Kingdom Robin M. Dabareiner, DVM, PhD, Dipl ACVS Assistant Professor Department of Large Animal Medicine Texas Veterinary Medical Center Texas A&M University College Station, Texas Jean-Marie Denoix, DVM, PhD, Agrégé Professor Head of Equine Clinic-CIRALE-IPC Ecole Veterinaire d’Alfort Maisons Alfort, France Stephen P. Dey III, VMD Private Practice Allentown, New Jersey Janet Douglas, MA, VetMB, PhD, MRCVS Four Elms East Leake, United Kingdom Matt Durham, DVM Private Practice Steinbeck Country Equine Clinic Salinas, California David R. Ellis, BVetMed, DEO, FRCVS Private Practice Greenwood Ellis and Partners Newmarket Suffolk, United Kingdom Kristiina Ertola, DVM Private Practice Tempereen Hevosklinikka Tampere Equine Clinic Tampere, Finland Loren H. Evans, DVM Professor Emeritus of Surgery University of Pennsylvania School of Veterinary Medicine Ronan, Montana Franco Ferrero, DVM Private Practice Cascina Lavignola Canonica D’Adda, Italy

David Frisbie, DVM, PhD, Dipl ACVS Assistant Professor of Equine Surgery Senior Scientist and Manager Equine Orthopaedic Research Laboratory Department of Clinical Sciences College of Veterinary Medicine and Biological Sciences Veterinary Teaching Hospital Colorado State University Ft. Collins, Colorado José M. García-López, VMD, Dipl ACVS Assistant Professor, Large Animal Surgery School of Veterinary Medicine Tufts University North Grafton, Massachusetts Richard Galley, DVM Private Practice Weatherford, Texas Ronald L. Genovese, VMD Private Practice Randall Veterinary Hospital, Inc. Warrensville Heights, Ohio Howard E. Gill, DVM Private Practice Pine Bush, New York Dallas O. Goble, DVM Associate Professor of Surgery College of Veterinary Medicine University of Tennessee Knoxville, Tennessee Barrie Grant, DVM Private Practice San Luis Rey Equine Hospital Bonsall, California Joyce C. Harman, DVM, MRCVS Private Practice Harmany Equine Clinic, LTD Washington, Virginia Kevin K. Haussler, DVM, DC, PhD Lecturer Department of Biomedical Sciences College of Veterinary Medicine Cornell University Ithaca, New York Dan L. Hawkins, DVM, MS, Dipl ACVS Private Practice Dubai Equine Hospital Dubai, United Arab Emirates Doug Herthel, DVM Alamo Pintada Equine Clinic Los Olivos, California Ted Hill, VMD The Jockey Club New York, New York

Contributors Jukka Houttu, DVM Private Practice Tempereen Hevosklinikka Tampere Equine Clinic Tampere, Finland Robert J. Hunt, DVM, MS, Dipl ACVS Private Practice Hagyard-Davidson-McGee Associates, PSC Lexington, Kentucky Kjerstin M. Jacobs, DVM Technical Services Veterinarian Pharmacia Animal Health Gladstone, New Jersey Joan S. Jorgensen, DVM, PhD, Dipl ACVIM, Large Animal Assistant Professor Department of Veterinary Biosciences College of Veterinary Medicine University of Illinois Urbana, Illinois Chris E. Kawcak, DVM, PhD Equine Orthopaedic Research Laboratory Department of Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Veterinary Teaching Hospital Colorado State University Ft. Collins, Colorado Kevin Keane, DVM Private Practice Delaware Equine Center Cochranville, Pennsylvania Kevin G. Keegan, DVM Associate Professor E. Paige Laurie Endowed Program in Equine Lameness College of Veterinary Medicine University of Missouri Columbia, Missouri

John Maas, DVM, MS, Dipl American College of Veterinary Nutrition, Dipl ACVIM Extension Veterinarian Veterinary Medicine Extension/Public Programs School of Veterinary Medicine University of California Davis, California John B. Madison, VMD Private Practice Ocala Equine Hospital Ocala, Florida Richard A. Mansmann, DVM, PhD Private Practice Central Carolina Equine Practice Chapel Hill, North Carolina Daniel Marks, VMD Private Practice Santa Fe, New Mexico Benson B. Martin, VMD Associate Professor of Sports Medicine Director, Jeffords High Speed Treadmill Facility University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania William H. McCormick, VMD Private Practice Middleburg Equine Clinic, Inc. Middleburg, Virginia Andrew McDiarmid, BVMBS, CertES (Orth), MRCVS Private Practice Peasebrook Equine Clinic Broadway Worchestershire, United Kingdom

John C. Kimmel, VMD John C. Kimmel Racing Stable Elmont, New York

Sue M. McDonnell, PhD Adjunct Associate Professor in Reproduction, Certified Animal Behaviorist University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Simon Knapp, BVetMed, MRCVS Private Practice Straight Mile Farm Billingbear Wokingham Berkshire, United Kingdom

P.J. McMahon, MVB, MRCVS Private Practice Kings Park Plaistow Billingshurst West Sussex, United Kingdom

Calvin N. Kobluk, DVM, DVSc, Dipl ACVS All Care Animal Referral Center Fountain Valley, California

Rose M. McMurphy, DVM Associate Professor and Head, Anesthesiology Department of Clinical Studies Veterinary Medical Teaching Hospital Kansas State University Manhattan, Kansas

Svend E. Kold, DMV, DrMedVet, MRCVS Private Practice Willesley Equine Clinic Gloucestershire, United Kingdom Robert D. Lewis, DVM Private Practice Elgin Veterinary Hospital, Inc. Elgin, Texas

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Martha M. Misheff, DVM Private Practice Dubai Equine Hospital Dubai, United Arab Emirates James B. Mitchell, DVM Private Practice Creamridge, New Jersey

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Contributors

John S. Mitchell, DVM Private Practice Boca Raton, Florida Richard D. Mitchell, DVM Private Practice Fairfield Equine Associates, PC Newtown, Connecticut Patrick J. Moloney, DVM Private Practice Stuart, Florida William A. Moyer, DVM Professor of Sports Medicine and Department Head Department of Large Animal Medicine and Surgery Texas Veterinary Medical Center Texas A&M University College Station, Texas Graham Munroe, BVSc, PhD, Dipl ECVS, Cert EO, DESM, FRCVS Private Practice Greenlow Duns Berwickshire, Scotland

Joe D. Pagan, MS, PhD President Kentucky Equine Research, Inc. Versailles, Kentucky Eric J. Parente, DVM, Dipl ACVS Assistant Professor of Surgery University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania Andrew H. Parks, MA, VetMB, MRCVS, Dipl ACVS Associate Professor of Large Animal Surgery Department of Large Animal Medicine College of Veterinary Medicine University of Georgia Athens, Georgia Robert C. Pilsworth, MA, VetMB, BSc, Cert VR, MRCVS Private Practice Beaufort Cottage Diagnostic Center Rossdale & Partners Beaufort Cottage Stables Newmarket Suffolk, United Kingdom

Rachel Murray, MA, VetMB, MS, PhD, Dipl ACVS, Dipl ECVS, MRCVS Head of Orthopaedic Research Centre for Equine Studies Animal Health Trust Newmarket Suffolk, United Kingdom

Christopher C. Pollitt, BVSc, PhD Reader in Equine Medicine Australian Equine Laminitis Research Unit Faculty of Natural Resources, Agriculture and Veterinary Science School of Veterinary Medicine The University of Queensland Queensland, Australia

Alastair Nelson, MA, VetMB, Cert VR, Cert ESM, MRCVS Private Practice Rainbow Farm Malton North Yorkshire, United Kingdom

Joanna Price, BSc, BVSc, MRCVS Senior Lecturer Department of Veterinary Basic Sciences Royal Veterinary College London, United Kingdom

Frank A. Nickels, DVM Department of Large Animal Clinical Sciences Veterinary Medical Center Michigan State University East Lansing, Michigan

Anthony G. Pusey, DO, MRO, FECert Registered Osteopath Private Practice A G Pusey & Associates West Sussex, England

Paul M. Nolan, DVM Private Practice Boca Raton, Florida

Norman W. Rantanen, DVM Private Practice Fullbrook, California

David M. Nunamaker, VMD Jacques Jenny Professor of Othopedic Surgery Professor of Surgery Chairman, Department of Clinical Studies School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Virginia B. Reef, DVM Professor of Medicine Widener Hospital Director Large Animal Cardiology and Diagnostic Ultrasonography Department of Clinical Studies Section of Sports Medicine and Imaging University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Thomas P.S. Oliver, DVM Private Practice Lahaska, Pennsylvania Gene Ovnicek, RFJ Private Shoeing Practice Chief Technician—Equine Digit Support System, Inc. Penrose, Colorado

Dean W. Richardson, DVM Charles W. Raker Professor of Equine Surgery Department of Clinical Studies University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania

Contributors Mark C. Rick, DVM Private Practice Alamo Pintada Equine Clinic Los Olivos, California Bradley S. Root, DVM Private Practice Albuquerque Equine Clinic Albuquerque, New Mexico Alan J. Ruggles, DVM, Dipl ACVS Private Practice Rood and Riddle Equine Hospital Lexington, Kentucky Bonnie R. Rush, DVM, MS, Dipl ACVIM Professor College of Veterinary Medicine Kansas State Veterinary and Medical Teaching Hospital Kansas State University Manhattan, Kansas Allen M. Schoen, MS, DVM Adjunct Professor School of Veterinary Medicine Tufts University Grafton, Massachusetts Affiliate Faculty College of Veterinary Medicine Colorado State University Ft. Collins, Colorado Director, Veterinary Institute for Therapeutic Alternatives Private Practice Sherman, Connecticut Michael C. Schramme, DrMedVet, CertEO, MRCVS, PhD, Dipl ECVS Senior Orthopaedic Research Clinician Center for Equine Studies Animal Health Trust Newmarket Suffolk, United Kingdom Robert Sigafoos University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania Roger K.W. Smith, MA, VetMB, PhD, DEO, Dipl ECVS, MRCVS Senior Lecturer in Equine Surgery Department of Veterinary Clinical Sciences Royal Veterinary College Hertfordshire, United Kingdom

Vivian S. Stacy, CNMT Senior Nuclear Medicine Technologist Section of Sports Medicine and Imaging Department of Clinical Studies University of Pennsylvania School of Veterinary Medicine New Bolton Center Kennett Square, Pennsylvania James C. Sternberg, DVM Private Practice Powell, Tennessee Anthony Stirk, BVSc, MRCVS Fountain Farms, Ripon North Yorkshire, United Kingdom Alain P. Théon, DVM, MS, Dipl ACVR-RO Professor, Oncology Service Chief Department of Surgery and Radiology School of Veterinary Medicine University of California Davis, California Fabio Torre, DVM, Dipl ECVS Private Practice Clinica Equina Bagnarola Budrio, Bologna, Italy Gayle W. Trotter, DVM Department of Clinical Sciences College of Veterinary Medicine and Biomedical Sciences Veterinary Teaching Hospital Colorado State University Ft. Collins, Colorado Tracy A. Turner, DVM College of Veterinary Medicine University of Minnesota St. Paul, Minnesota Stephanie J. Valberg, DVM, PhD, Dipl ACVIM Associate Professor Department of Clinical and Population Studies College of Veterinary Medicine University of Minnesota St. Paul, Minnesota Beth A. Valentine, DVM, PhD Assistant Professor Department of Biomedical Sciences College of Veterinary Medicine Oregon State University Corvallis, Oregon

Van E. Snow, DVM Private Practice Santa Ynez, California

Rob van Pelt, BVSc, BSc, Cert EP, MRCVS Private Practice Equine Veterinary Hospital, Tortington, Arundel West Sussex, United Kingdom

Sharon J. Spier, DVM, PhD, Dipl ACVIM Associate Professor Department of Medicine and Epidemiology School of Veterinary Medicine University of California Davis, California

John P. Walmsley, MA, VetMB, Cert EO, Dipl ECVS, MRCVS Private Practice The Liphook Equine Hospital Forest Mere, Liphook Hampshire, United Kingdom

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Contributors

Chris Whitton, BVSc, MRCVS, FACVSc, PhD Private Practice Newcastle Equine Centre Broadmeadow Racecourse Broadmeadow, New South Wales, Australia Jeffrey A. Williams, DVM, MS Private Practice Rhinebeck Equine, LLP Rhinebeck, New York

Paul Wollenman, DVM Private Practice Palm Beach Equine Clinic Wellington, Florida James Wood, BVetMed, MSc, MRCVS Head of Epidemiology Centre for Preventative Medicine Animal Health Trust Newmarket Suffolk, United Kingdom

FOREWORD t has been said that “no one drinks from the same water when dipping from a fast river.” Nothing is more true or better describes the fast flow of information that has come from veterinary medicine and surgery. I remember when I was a senior veterinary student watching a highly recognized equine specialist fire a horse with a large chip fracture of the distal, lateral radius. The horse was rested for sure and returned to training and did win. Yes, the old fracture became a large spur. Any swelling of the fetlock joint was considered an osselet and the horse was treated either by blister or firing and blister. This was done until Dr. Ed Churchill found it best to remove the apex fracture from the top of the proximal sesamoid bone. Dr. Churchill’s contribution inspired others such as Dr. Jacques Jenny and Dr. Charles Raker to perform surgery on horses with other fractures of the fetlock joint. Drs. Jenny and Raker were the first to remove a base fracture from the proximal sesamoid bone, to remove chip fractures from the carpus, and to reattach a slab fracture of the third carpal bone. These three men added a large clear stream to the veterinary river that many of us have used from the late ’50s to the present. Although Dr. Jenny was the first to use a lag screw to repair a stress fracture of the third metacarpal bone and many advocate this form of management, I still find that deep firing well above and below the fracture site is more satisfactory. In horses that are fired, there is no pain from the screw and the screw does not have to be removed. Dr. M.B. Teigland used this method, deep firing, to treat many good racehorses with stress fractures with excellent success. It is important to remember that methods that have worked well for many years are not necessarily worthless or antiquated. Many times a great river comes from many small but important tributaries. Other tributaries that helped swell the river were from the work of Dr. John Wheat on the subject of treating horses with tendonitis. He pointed out the necessity of preventing edema, which can lead to fibrosis of the injured tendon. Dr. James Rooney helped us better understand how lameness occurred, and Dr. Norman Rantanen and Dr. Ron Genovese were first to give us information on how to use ultrasound to better diagnose tendon and ligament injuries. Dr. Virginia Reef enlarged this tributary and made the use of the ultrasound more sophisticated in lameness diagnosis. Excellent radiologists such as Dr. Charles Reid at New Bolton Center and others have provided us with better knowledge when using our x-ray machines. The stream continued with better quality radio-

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graphs, xeroradiographs, scintigraphy, and recently, magnetic resonance imaging. These modalities have made us all better diagnosticians. When it comes to treating lame horses, we have to remember the flow that came from Dr. Larry Bramlage and Dr. David Nunamaker. When arthroscopic surgery was first done by Dr. Steve Selway in Florida and by Dr. Wayne McIlwraith in Colorado, many thought that it should never be used on the horse. Both men forged a very wide tributary, one that has helped us all become more effective surgeons. After arthroscopic surgery, horses suffer less and many return faster to competition. Fear of something new is only normal and being skeptical is expected, since most of us have tried something new that just did not work. With any fast-moving river there will always be something picked up that is superfluous, but it will soon settle out. The better one gets as a lameness diagnostician, the better he or she will be in selecting the best treatment. The many authors who have contributed to this book, Diagnosis and Management of Lameness in the Horse, have helped to clean false debris from the ever-increasing flow of veterinary knowledge and should be congratulated and thanked for sharing their knowledge and experiences with us. We will all be indebted to them after procuring and reading this book. Both Dr. Mike Ross and Dr. Sue Dyson were well acquainted with me early in their careers during internship (Sue) and surgical residency (Mike) programs at New Bolton Center, University of Pennsylvania, at which I taught for 32 years. They both know very well that one does not become skilled in lameness diagnosis and management overnight. They both became quickly aware that lameness diagnosis in the gaited American Saddler or the Dressage horse was considerably different than in the racing Standardbred or Thoroughbred. For these reasons I am especially pleased that they have added a new dimension by providing actual videos on the CD showing the abnormal gaits of lame horses. This will be great for everyone. I am confident that many will drink and benefit from the text, Diagnosis and Management of Lameness in the Horse, which should both widen and deepen the veterinary river. Loren H. Evans, DVM, MS Professor Emeritus of Surgery University of Pennsylvania, New Bolton Center August 2002 Ronan, Montana

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FOREWORD he history of veterinary lameness diagnosis and treatment has gone through three stages. TThe first stage could be termed the personal stage; there was principally anecdotal observation occasionally supported by post-mortem evidence. Much of this was limited to first- or second-hand accounts. The focus was on workhorses, with some information about cavalry mounts. Occasionally a gifted veterinarian was prescient and insightful. People like Horace Hayes and Dollar come to mind. They were very experienced horsemen and careful observers, with an intuitive insight into lameness. Unfortunately, intuition is not easily taught or passed on. The European veterinary literature was frequently dominated by pathologists, and the clinical findings were underemphasized. The second stage, beginning in the 1960s, was characterized by the organization of lameness and a more scientific approach to diagnosis. Included was the use of diagnostic nerve blocks, radiography, and later, ultrasonography and scintigraphy. By this time the focus had shifted from the workhorse to the light horse for pleasure and competition. This was typified by the work of J. Hickman in the United Kingdom and O.R. Adams in the United States. There was also good work and valuable observations by individuals or groups. This was reported in the veterinary literature and in various proceedings, some even as letters to the editor. Unfortunately, some of these are not easily discovered through literature searches. There was also the stimulating writing of J. Rooney to explain lameness from a biomechanical perspective. This has been followed by the work of Clayton, Denoix, Barrey, and others. Much of the work pertaining to conformation and its effect on performance has never found its way into the veterinary literature and remains in hippological sources. As so often happens in science, just when it appears that we are almost confident of our basic understanding, new observations question our assumptions. The past decade has seen a burst of new documented clinical investigation and anatomical knowledge. Some of the accepted and codified lameness beliefs are now in question. This includes nerve blocks. Unfortunately, rather than simplifying the subject, these careful observations have introduced complexities and uncertainties into what was previously regarded as a straightforward diagnostic procedure. As Dr. Sue Dyson was largely responsible for this, it is only apposite that she should make amends by way of contributing to this book. The same goes for Dr. Bowker. The third phase is one of synthesis. It combines the latest technology and science with an understanding that the lame horse must be viewed from an athletic perspective. This often depends on the demands of specific sports. This book, Diagnosis and Management of Lameness in the Horse by Ross and Dyson, is the prototype treatise for this phase. An important premise of this book considers “lameness” in its most sophisticated form, to subsume all of the musculoskeletal and neurological dysfunctions that have an impact on maximal athletic performance. This is much more than is obvious by just trotting the horse to evince gait asymmetry. There is an understanding that it is frequent to have two or more “lamenesses” in an individual and that their etiology, effects on specific movements, and prognosis are interrelated and require an understanding of the competitive implications to best manage the horse. Thus the chapters by veterinarians experienced with different types of horses are an integral part of this book. The adjunctive approaches of acupuncture, manipulative procedures, physical, and herbal medicine are

covered. It is hoped that the inclusion of these in a book with an impeccable scientific background will encourage practitioners to seek education in these modalities rather than be contemptuous prior to investigation. The Editors do not make the easy error of neglecting the clinical examination to focus principally on glamorous technology. All this culminates in maximum benefit to the veterinarian who must try to solve real-world problems. Hopefully the horse will also benefit. The incorporation of a CD-ROM with moving pictures is so obvious it is surprising it has not been done before. Verbal description of a visual (and to a much lesser extent, auditory) phenomenon is a poor substitute. This is especially so since there is not yet even a general agreement of how to describe the alterations of movement associated with lameness. Another vital but often perplexing area is communication with the horse’s connections. For example, many high-level dressage riders are acutely perceptive and analytical. Understanding is greatly facilitated by the veterinarian having a background in the field. One of the difficult problems is to decide whether a complaint about the horse’s performance results from a “lameness”; is a training or riding problem, a shoeing problem, or a tack (saddle, bitting, hobbles, boots) problem; results from the horse’s character and physiology; is an inherent biomechanical limitation for this individual; or even exists at all. There is a human tendency to discount what we cannot directly perceive. If the veterinarian cannot see any lameness or deficit in movement, then there is an inclination to assign the problem to being in the rider’s head,” or “the horse is just not good enough.” Now, the latter are real possibilities. How does one decide? There are many strategies: a course of non-steroidal anti-inflammatory analgesic drugs, treating suspected locations, blocking suspicious areas, incorporating acupuncture and chiropractic evaluation and treatment, or changing the training, the rider, the going, the shoeing, the tack, and so on. However, if the veterinarian is also an educated and a sensitive rider, who can get on the horse and interpret the feelings in biomechanical and diagnostic criteria, then you have someone like Sue Dyson. She is the rare combination of a high-level rider and horsewoman and a talented veterinarian. I can speak of Sue’s abilities because we have been friends and colleagues for over 20 years. I admire her for her veterinary and equestrian abilities, which include a rigorously honest intellectual approach with a tough dedication. Dr. Mike Ross I know through his many publications and lectures and the high standard of his academic work at a leading university and his pursuit of being in the forefront. His particular interest in Standardbred racehorses and methodical approach have provided a new perspective to lameness in these horses. This complementary combination of talent and experience make Mike and Sue ideal co-Editors. Notwithstanding Churchill’s comment about being divided by a common language, here is a successful collaboration between Editors on both sides of the pond. The incorporation of leading American, Australian, and European veterinarians as co-authors adds additional perspective. The nature of this book promises regular updates to include forthcoming knowledge. One hopes that the Editors’ schedules will permit this. Daniel Marks, VMD August 2002 Santa Fe, New Mexico

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P R E FA C E e come from different equine, veterinary, and cultural backgrounds, but we share a passion for lameness diagnosis and have individually developed very similar diagnostic approaches, believing that there is both art and science to lameness diagnosis. In the past 20 years we have seen huge advances in our knowledge of conditions that cause lameness through careful clinical observation combined with the more stringent use of diagnostic analgesia. It was with consideration of a strong belief in the values of clinical examination and diagnostic analgesia that our list of contributors was formulated. We have experienced advances in diagnostic imaging with the development of ultrasonography, scintigraphy, diagnostic arthroscopy, and more recently, computed tomography and magnetic resonance imaging (MRI). Doubtless, while we continue to look, we will continue to find new causes of lameness and this text will rapidly become outdated. There have even been significant developments from the time of manuscript submission to completion of production of the book, especially in the field of MRI. It is nonetheless our aim to provide information as up to date as possible, based on our own experiences and those of other experienced veterinarians worldwide. When we embarked on this project, we felt strongly that the emphasis on different lameness conditions in other texts did not reflect our own personal experiences and it did not reflect the differences seen in horses used for a variety of sports disciplines. We set out to provide a comprehensive, thought-provoking text, viewed from a global perspective, sometimes challenging long-held dogma. We wanted to provide a balanced approach, reflecting as much as possible our own personal experiences based on careful observation while also including the opinions of other respected lameness diagnosticians in areas where we believed we did not have sufficient experience or expertise. We selected the term management of lameness carefully, recognizing that our treatment abilities are limited and currently fall behind our diagnostic capabilities. We have tried to be as broad minded as possible, including many aspects of alternative therapy. We recognize that many of these treatment modalities have not undergone scientific scrutiny, and they do not necessarily form part of our own therapeutic armamentarium. Although we are not implying endorsement, we felt that the experiences of others should be chronicled. We were fortunate to enlist a broad cross-section of coauthors, with widely ranging experiences, but regret that several notable veterinarians were unable to accept because of other commitments. We challenged all authors to provide practical information, reflecting not only the current literature but also their own experiences. However, when our experiences were strongly at variance with an author, we have added editorial comments accordingly. The book is divided into five major sections, first presenting an in-depth diagnostic approach, then dealing with lameness conditions based on anatomical location. Different disease entities are then considered in depth, followed by a broad review of different treatment modalities. The final section addresses different types of horses and the injuries to which they are particularly prone, providing a unique insight

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into different diagnostic and therapeutic approaches. It also provides a background to each sport, which is so important in understanding why particular problems occur and how they may be manifested. Inevitably, this approach creates some duplication of information, but often there are subtle and fascinating differences among authors based on the type of horse with which they deal and where in the world they practice. To encompass all this, of necessity we sacrificed didactic chapters on anatomy, and we have not included a comprehensive review of all standard radiographic views and surgical procedures. We believe that other dedicated texts are better suited to provide this information. We tried to be as generous as possible with page allocation to authors but found that we had hugely outstripped the total page allocation for the book. To try to reduce the text, we introduced many abbreviations, which some readers will find difficult. Therefore we have included a list of these abbreviations for easy reference. Space limitations made it necessary to limit the number of figures, which we regret. Ideally, we would have liked to provide examples of all conditions, but this was impractical. Good and useful examples have been chosen. Although the title of the book is Diagnosis and Management of Lameness in the Horse, we have tried to address all potential musculoskeletal and neurological causes of gait abnormalities or changes in performance of sport horses. We have addressed the common problem of what to do when a diagnosis cannot be made. We believe strongly that accurate diagnosis of lameness relies heavily on clinical experience and the development of an eye for the horse, both stationary and in movement. Lameness diagnosis cannot be taught in the classroom but must be learned from many hours of observation of normal and lame horses and tutelage. We have therefore included a CD-ROM, showing short video clips of a variety of lameness conditions, which we hope are representative examples and will assist an inexperienced clinician in developing an eye for lameness. When we embarked on this project, we were both keen to learn from other peoples’ experiences and to broaden our own horizons, and we have not been disappointed. We have learned a huge amount, both from each other and from contributing authors. We remain constantly excited by the challenges of lameness diagnosis and management, since many horses do not entirely fit the textbook picture. Nonetheless, we are also sometimes frustrated that a diagnosis eludes us. We hope that by continued careful observation and a logical, comprehensive diagnostic approach, in the future our knowledge will further expand to understand causes of lameness and altered performance better and to provide further information for the next edition of Diagnosis and Management of Lameness in the Horse. Sue J. Dyson Mike W. Ross Suffolk, United Kingdom, and Kennett Square, Pennsylvania 2002

xv

ACKNOWLEDGMENTS e owe a huge debt of gratitude to our co-authors, since the scope of this book far exceeds our combined knowledge and experience. Writing a book chapter brings no financial rewards and the time involved always far exceeds expectations. While it is invidious to single out specific authors, we are particularly grateful to Ron Genovese, who contributed large sections on ultrasonographic examination and soft tissue injuries and also gave constant encouragement through the long gestation period of the book. We were tremendously excited when our colleague, coauthor, and friend Fabio Torre agreed to help with our cover. His original paintings reflect the unique approach we have taken to review our beloved subject. Fabio’s illustrations, based on one of the earliest analytical assessments of gait ever to be made by Muybridge, encourage us to both look and see. We have received tremendous support from Karena Bean and Sally Whitefield, secretaries at the Animal Health Trust, who deciphered many editorial hieroglyphics and were responsible for cheerfully and tirelessly re-typing the majority of manuscripts. We thank Joyce Underwood, Vivian Stacy, and Karyn Van Norman from New Bolton Center for their help and support. We especially thank Jan Butler and John Wilkinson, who have produced a large number of the photographic illustrations, and Alex Baker for her excellent artwork. The book would not have been possible without key people from WB Saunders Company: Stephanie Donley, Ray Kersey, Arlene Chappelle, Denise LeMelledo, Judy Ahlers, Julia Dummitt, David Saracco, and Bruce Robison. We have both been influenced and tutored by notable people in our careers. Sue’s early teaching in equine orthopaedics came from John Hickman at the University of Cambridge, who was later a consultant at the Animal Health Trust. John Ayliffe, an equine practitioner and lameness enthusiast, encouraged Sue to go to the United States, where she spent a year at New Bolton Center and a year in practice. This was initially made possible through a Thouron Scholarship, one of the principal aims of which is to foster Anglo-American relationships. This book, with Sue and Mike as co-Editors, is a true fulfillment of that goal. Charlie Reid at the University of Pennsylvania stimulated an interest in diagnostic imaging, while Bill Moyer, Dan Marks, and Midge Leitch were all hugely influential in the development of an approach to lameness diagnosis. A little later Ron Genovese shared his knowledge, experience, and enthusiasm for ultrasonography. Colleagues, past and present at the Animal

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Health Trust, notably Svend Kold, Ian Wright, Chris Whitton, and Michael Schramme, have provided stimulus and support. The interns, by testing the hypothesis that by teaching you learn, have been a constant inspiration to improve diagnostic capabilities, to advance knowledge, and to distill clarity of thought. McGinty, Kinvarra, and Otterburn were internationally famous horses in their own right. As horses produced by Sue, they were great teachers in the art and science of equestrianism and in the diagnosis and management of lameness. For Mike, John “Jack” Lowe of Cornell University, whose support and encouragement were unequalled, instilled an early interest and passion for lameness. Jack allowed him the freedom of thought and provided a solid foundation of clinical investigation and experience on which to build. He had excellent instructors, colleagues, and friends at the New York State College of Veterinary Medicine, Cornell University as a student and intern, and from New Bolton Center, University of Pennsylvania as a surgery resident, lecturer, and faculty member, but special thanks go to Norm Ducharme, Dean Richardson, and David Freeman. Loren Evans, mentor, lameness diagnostician, horseman, surgeon, and friend, had a unique influence, instilling confidence and imparting knowledge but most importantly in showing him the value of careful clinical examination and observation. Mike owes tremendous gratitude to Howard “Gene” Gill, Ben Martin, Jim Palmer, Paul Nolan, and Ron Gurfein for their loyalty and guidance, and the Standardbred racehorse, which allowed him to “cut his teeth” and taught him so much. Mike has been motivated by the many dedicated interns and residents and referring veterinarians, whose ideas, energy, and enthusiasm for his work throughout the years have truly been inspirational. We must not forget the horse. Watching, palpating, listening to, and trying to understand the horse has taught us so much. Finally we owe an enormous thank you for the love, friendship and support of our partners, John and Debbie, themselves veterinarians. They have been extraordinarily patient and understanding throughout this huge project, have provided constructive criticism, have listened to our frustrations, and have shared our enthusiasm and passion for the book. Mike gives special thanks to Stone for his patience and love, and the inspiration only a son can endow, his daughter Kennedy, and his parents. Sue Dyson and Mike Ross

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ColorPlate 1 Thermal image of the sole of a horse's foot showing asymmetrical heat in the sole of the hoof (small arrows). The shoe on that side (bold arrow) is colder, indicating less friction on the shoe, probably as a result of avoiding the injured sole.

Color Plate 2 Thermal image of the left medial metacarpal region showing an active splint (A) that is causing secondary inflammation in the suspensory ligament distal to the injury (B).

Color Plate 3 Thermal image, front view, of a horse's chest showing increased heat over the lateral aspect of the right shoulder (black arrow) and decreased heat over the right bicipital tendon (white arrow). Ultrasonography showed increased fluid in the intertubercular (bicipital) bursa. The decreased heat over the muscle was presumed to be due to lack of use because of pain.

Color Plate 4 Thermal image of the lateral view of the right hip region showing increased heat over the third trochanter (A) and greater trochanter (B). In addition, the body of the gluteal muscle has increased heat (small arrows). This condition was diagnosed as a gluteal muscle strain.

Color Plate 5 Thermographs show the appearance of normal horses. The color scale represents 5.6 C, using 10 colors; that is, each color represents about a 0.5 C change in temperature. The color bar under the image shows the colors used; those to the right-hand side are the hottest and those to the left are the coldest. White is above the top of the scale and black below the scale. A, Lateral view of the head, neck, and shoulder. B, Lateral view of the thorax, abdomen, and hindquarters. C, Oblique dorsal view from behind the horse looking toward its head and neck. Temperature variation is 1 C over the neck, trunk, and hindquarters. A warm midline dorsal stripe along the back extends from the withers to the base of the tail, with symmetrical muscle temperature on either side. 0

0

0

Color Plate 6 Lateral view of the neck of horse with reduced mobility in the occipito-atlantal and atlanto-axial joints. A cool line runs obliquely from the region of the atlanto-axial joint caudally to the base of the neck and is 1.5° C cooler than the surrounding muscle, indicating an area of sympathetic dystonia.

Color Plate 7 Lateral view of the neck of horse with reduced mobility in the neck. Note the significant cooling from the occiput back to the level of the sixth and seventh cervical vertebrae, indicating a problem involving all joints in the neck.

Color Plate 8 Lateral views of the thoracolumbar area of two horses, both showing significant cooling in the musculature of the dorsal spine from the saddle region caudally. A, The vertical cranial boundary to the zone of cooling indicates that the injured area is in the region of the cervicothoracic junction, but the shoulder muscles overlying this area receive innervation from the lower neck, partly masking the muscles supplied by the upper thoracic area. B, The typical appearance of cooling in the muscle resulting from an injury to the region of the twelfth thoracic vertebra, with the cranial border of the region running obliquely down and back. This horse has been clipped, but long hair left on the hind limb shows as an area 5° C cooler than the surface temperature of the thorax of the horse.

Color Plate 9 Dorsal view of horse showing abnormal heat patterns of the thoracolumbar spine. Note the complete loss of the normal central stripe, with significant cooling indicating the presence of reduced mobility of the entire thoracolumbar spine and pelvis. The asymmetrical nature of the heat pattern indicates the horse is likely to move with an asymmetrical gait, resulting from increased muscle tone on the left-hand side of the body.

Color Plate 10 Examples of different thermographic foot patterns (solar views). A, This hoof has a medial corn, manifested as a focal hot spot (white) within an area of increased temperature. B, This hoof has subacute laminitis, with a pattern of increased heat in the region of the tip of the distal phalanx.

Color Plate 11 Palmar thermographic image and subsequent transverse (on the left) and longitudinal ultrasonographic images of an advanced event horse 10 days after successfully completing a Three Day Event. The horse was having a routine examination, and no clinical localizing signs were evident in the tendon. The thermogram demonstrates a focal hot spot over the left distal superficial digital flexor tendon (arrow), and the ultrasonographic images reveal a hypoechoic core lesion in the same region.

Color Plate 12 Computerized saddle pressure analysis images. Cranial is to the left, and left is to the bottom. A, This image shows a poorly fitting saddle, with a focal pressure point in the left wither region. B, This image demonstrates failure of a gel pad to alleviate the pressure point and the development of an additional pressure point caudally.

SECTION • 1 The Lameness Examination CHAPTER •

1

Lameness Examination: Historical Perspective Mike W. Ross If your horse is lame in his shoulder, take off his shoes…Young and inexperienced practitioners are quite too apt to commit the error of overlooking the examination of the foot, looking upon it as a matter of secondary importance, and attending to it as a routine and formal affair only. A. Liautard, 18881 s the twenty-first century begins, the extent of change in the diagnosis of lameness in the horse depends on the individual’s clinical and ideological perspective. A veritable explosion of new imaging capabilities has advanced the current understanding of many musculoskeletal abnormalities. Yet, to accurately assess clinical relevance, the clinician must possess a feel for the horse, developed only by careful clinical examination, a procedure that has changed little in hundreds of years. Successful detection of equine lameness does not so much require knowledge of science as it does art. Inasmuch as art is defined as “skilled workmanship, craft, or studied action,”2 the lameness examination demands artistic experience acquired by years of clinical practice and working and learning from experienced practitioners. From Liautard’s advice more than 100 years ago to that of modern lameness diagnosticians, the change in the basic skills of lameness diagnosis may be small. Development of the artistic skills needed to become a true lameness diagnostician requires a thorough, somewhat methodical approach, much like that of a crime scene detective. I often refer to the lameness diagnostician as a lameness detective, and although this statement may lack sophistication, in reality, how boring the task would be if the horse could talk. To make a horse talk to you through careful palpation and observation is the essence of the lameness examination yet the most difficult to teach. Great lameness diagnosticians likely possess this ability to read or feel the horse and skilled, workmanship-like qualities to appreciate the art in lameness diagnosis. Some, with the added ability to share this knowledge effectively, have influenced clinicians more than others simply by writing about those experiences. In the mid- to late 1900s, Adams had the most profound influence by his teachings and writings. His former students and friends acknowledge his artistic talent, gained primarily from a ground-up approach to the lame horse, and his profound interest in corrective shoeing. More important, Adams’ original lameness notes became his classic textbook.3 For most clinicians, Lameness in Horses represented the “lameness Bible,” an excellent resource of information on equine lameness. Adams himself revised the textbook several times; most recently, his respected colleague, Ted S. Stashak, has continued in Adams’ footsteps. This important work served as the foundation for the fundamentals of equine lameness. Adams was influenced greatly by the work of Dollar and Lacroix. Adams’ original notes contain many drawings similar to those originally published in Dollar’s A Handbook of Horseshoeing,4 a wonderful collection of drawings and excellent descriptions of shoeing, conformation, and lameness of the equine foot. Adams references the work of Lacroix5 in the late 1800s. In fact, until Adams’ treatise on lameness, scant informa-

A

tion existed about equine lameness. The information available in the American literature during most of the 1900s consisted of only sporadic case reports or case series in the Journal of the American Veterinary Medical Association. A potential explanation may lie in the importance of the World Wars or other important social events in the early to mid-1900s. Experience in the cavalry also may have influenced later writings in the 1900s. Peters’6 work detailing lameness in the Thoroughbred racehorse emphasized the importance of lameness in the racetrack practice and the most common cause of poor performance. Many problems he observed in 1939 still exist, although treatment options have expanded considerably. Early important writings included manuscripts by Churchill7 and Wheat and Rhode8 on surgical removal of proximal sesamoid bone fractures (the Churchill approach), Forsell9 on surgical management of navicular bursitis and tendonitis, and Lundvall10 and later Delahanty11 debating the subject of the existence or nonexistence of fibular fractures. An early reference of note was the surgical textbook by Frank.12 Originally written in 1939, with several subsequent editions, this influential and often quoted textbook contained information about numerous musculoskeletal problems and often sensational examples of common and rare abnormalities. In the late 1800s, several informative, interesting, and entertaining textbooks about equine lameness were written, primarily by European authors. Most publications contained wonderful descriptions of lame horses, and many emphasized shoeing techniques, a mainstay in management of the lame horse both then and now. The writings of Percivall13 and Gamgee14 are particularly informative. Although a definitive reason was not provided, Gamgee observed that 42% of horses in the United Kingdom were lame, whereas only 9% of horses in Paris were lame. Disorders of the foot, many of which increased in frequency with age, were most common, and marked remodeling of the distal phalanx was seen in horses undergoing postmortem examination.14 In addition to the time-honored management technique of shoeing the lame horse, conformation and its relationship to lameness also were emphasized. In How to Judge a Horse, Bach15 emphasized balance, body part length and angulation, and distal extremity conformational faults. In a chapter entitled “Horse-Docturing in the Nineteenth Century,” Dunlop and Williams16 emphasized the contribution of Mayhew, described as artist, activist, and veterinary surgeon. Mayhew described and illustrated many common abnormalities of the locomotor system recognized at that time, including splints, spavin, curb, tendon sprains, and thoroughpin, most of which are still recognized today.16 Of interest, Mayhew was credited for trying “experimental” injections into inflamed areas, an obviously important

CHAPTER 1

• Lameness Examination: Historical Perspective

treatment modality practiced today.16 Detailed descriptions of laminitis, navicular disease, and other common conditions of the equine foot were provided.16 Dunlop and Williams,17 in their treatise on the history of veterinary medicine, also detailed the transition from farriery to veterinary medicine that occurred in the 1700s, although the close association and harmonious working relationships between blacksmiths and equine diagnosticians remain integral parts of a successful lameness management team today. In fact, “the term veterinarian came into use when colleges were established in different parts of Europe for improving, or rather for creating the art of treating disease in the lower animals.”17 The first veterinary school was founded in France in 1761, and soon veterinary schools were formed in the United Kingdom.17 Although an exhaustive historical review might be interesting, this brief review highlights critical issues central to modern lameness diagnosis. First, the basics have not changed for hundreds of years and will likely not change in the foreseeable future. Second, with the exception of Adams’ work, few comprehensive reports on lameness diagnosis were written in the 1900s. The modern lameness detective likely has learned most from experience working with accomplished lameness diagnosticians and by word of mouth. Third, many of the most knowledgeable colleagues have not published writings but have made their contributions in day-to-day teachings in academic settings, private practice, and small gatherings at national meetings. Since 1955 the annual convention of the American Association of Equine Practitioners has played a special role in the dissemination of information and ideas about lameness. Early meetings included a handful of practitioners, gathering and discussing equine medicine and surgery, sometimes late into the night. Much current lameness experience can be traced to these early meetings and practitioners such as Adams, Peters, Frank, Farquharson, Churchill, Goddall, Gabel, and Delahanty. Loren Evans and Howard “Gene” Gill influenced the molding of many modern lameness detectives, including me. Emphasizing the value of acquiring horse sense and spending time palpating and “learning” the horse, Gill often quotes Will Rogers, “…the outside of a horse is good for the inside of a man.” In the United Kingdom the British Equine Veterinary Association was established in 1961, providing a similar formula for dissemination of information through its annual congress and regular day meetings. The establishment of the Equine Veterinary Journal in 1968 provided a high-quality, refereed journal. The standard for the journal was set by the first editor, John Hickman, an astute observer of lame horses and an influence on many practitioners.

CHAPTER •

3

No substitute exists for careful clinical examination and observation, experience gained over many years of treating and developing a feel for the lame horse. This textbook on lameness is a collection of the best and most knowledgeable lameness diagnosticians worldwide. Some are “household lameness names,” whereas others are less renowned. All have one thing in common: they practice the art of lameness diagnosis in the horse.

REFERENCES 1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins Press. 2. Barnhart CL, editor: The American college dictionary, New York, 1970, Random House. 3. Adams OR: Veterinary notes on lameness and shoeing of horses, Denver, Colo, 1957, Colorado State University. 4. Dollar JAW: A handbook of horseshoeing, New York, 1898, William R Jenkins. 5. Lacroix JV: Lameness in the horse, Am J Vet Med, 1916. 6. Peters JE: Lameness incident to training and racing of the thoroughbred, J Am Vet Med Assoc Feb:200, 1940. 7. Churchill EA: Surgical removal of fracture fragments of the proximal sesamoid bone, J Am Vet Med Assoc 128:581, 1956. 8. Wheat JD, Rhode EA: The surgical treatment of fractures of the proximal sesamoid bones in the horse, J Am Vet Med Assoc 132:378, 1958. 9. Forsell G: The operative treatment of traumatic inflammation of the navicular bursae with preservation of the deep flexor tendon, North Am Vet 11, 1930. 10. Lundvall RL: Fracture of the fibula in the horse, J Am Vet Med Assoc 129:16, 1956. 11. Delahanty DD: Defects—not fracture of the fibula in the horse, J Am Vet Med Assoc 133:258, 1958. 12. Frank ER: Veterinary surgery, ed 7, Minneapolis, 1964, Burgess. 13. Percivall W: Lameness in the horse, London, 1852, Longmans, Brown, Green and Longmans. 14. Gamgee J: A treatise on horse-shoeing and lameness, London, 1871, Longmans, Green. 15. Bach FW: How to judge a horse, New York, 1893, William R Jenkins. 16. Dunlop RH, Williams DJ: Veterinary medicine: an illustrated history, St Louis, 1996, Mosby. 17. Stewart J: The stable book—a treatise on the management of horses, New York, 1858, AO Moore.

2

Lameness in Horses: Basic Facts before Starting Mike W. Ross

DEFINITION Lameness is therefore not so much an original evil, a disease per se, as it is a symptom and manifestation of some antecedent vital physical lesion, either isolated or complicated, affecting one or several parts of the locomotive apparatus.—A. Liautard, 18881

The clinical manifestations of lameness in the horse are well known, but an exact definition is difficult. The word lame is an adjective, meaning “crippled or physically disabled, as a person or animal,…in the foot or leg so as to limp or walk with difficulty.”2 A medical dictionary defines lameness as “incapable of normal locomotion, deviation from the normal

CHAPTER 1

• Lameness Examination: Historical Perspective

treatment modality practiced today.16 Detailed descriptions of laminitis, navicular disease, and other common conditions of the equine foot were provided.16 Dunlop and Williams,17 in their treatise on the history of veterinary medicine, also detailed the transition from farriery to veterinary medicine that occurred in the 1700s, although the close association and harmonious working relationships between blacksmiths and equine diagnosticians remain integral parts of a successful lameness management team today. In fact, “the term veterinarian came into use when colleges were established in different parts of Europe for improving, or rather for creating the art of treating disease in the lower animals.”17 The first veterinary school was founded in France in 1761, and soon veterinary schools were formed in the United Kingdom.17 Although an exhaustive historical review might be interesting, this brief review highlights critical issues central to modern lameness diagnosis. First, the basics have not changed for hundreds of years and will likely not change in the foreseeable future. Second, with the exception of Adams’ work, few comprehensive reports on lameness diagnosis were written in the 1900s. The modern lameness detective likely has learned most from experience working with accomplished lameness diagnosticians and by word of mouth. Third, many of the most knowledgeable colleagues have not published writings but have made their contributions in day-to-day teachings in academic settings, private practice, and small gatherings at national meetings. Since 1955 the annual convention of the American Association of Equine Practitioners has played a special role in the dissemination of information and ideas about lameness. Early meetings included a handful of practitioners, gathering and discussing equine medicine and surgery, sometimes late into the night. Much current lameness experience can be traced to these early meetings and practitioners such as Adams, Peters, Frank, Farquharson, Churchill, Goddall, Gabel, and Delahanty. Loren Evans and Howard “Gene” Gill influenced the molding of many modern lameness detectives, including me. Emphasizing the value of acquiring horse sense and spending time palpating and “learning” the horse, Gill often quotes Will Rogers, “…the outside of a horse is good for the inside of a man.” In the United Kingdom the British Equine Veterinary Association was established in 1961, providing a similar formula for dissemination of information through its annual congress and regular day meetings. The establishment of the Equine Veterinary Journal in 1968 provided a high-quality, refereed journal. The standard for the journal was set by the first editor, John Hickman, an astute observer of lame horses and an influence on many practitioners.

CHAPTER •

3

No substitute exists for careful clinical examination and observation, experience gained over many years of treating and developing a feel for the lame horse. This textbook on lameness is a collection of the best and most knowledgeable lameness diagnosticians worldwide. Some are “household lameness names,” whereas others are less renowned. All have one thing in common: they practice the art of lameness diagnosis in the horse.

REFERENCES 1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins Press. 2. Barnhart CL, editor: The American college dictionary, New York, 1970, Random House. 3. Adams OR: Veterinary notes on lameness and shoeing of horses, Denver, Colo, 1957, Colorado State University. 4. Dollar JAW: A handbook of horseshoeing, New York, 1898, William R Jenkins. 5. Lacroix JV: Lameness in the horse, Am J Vet Med, 1916. 6. Peters JE: Lameness incident to training and racing of the thoroughbred, J Am Vet Med Assoc Feb:200, 1940. 7. Churchill EA: Surgical removal of fracture fragments of the proximal sesamoid bone, J Am Vet Med Assoc 128:581, 1956. 8. Wheat JD, Rhode EA: The surgical treatment of fractures of the proximal sesamoid bones in the horse, J Am Vet Med Assoc 132:378, 1958. 9. Forsell G: The operative treatment of traumatic inflammation of the navicular bursae with preservation of the deep flexor tendon, North Am Vet 11, 1930. 10. Lundvall RL: Fracture of the fibula in the horse, J Am Vet Med Assoc 129:16, 1956. 11. Delahanty DD: Defects—not fracture of the fibula in the horse, J Am Vet Med Assoc 133:258, 1958. 12. Frank ER: Veterinary surgery, ed 7, Minneapolis, 1964, Burgess. 13. Percivall W: Lameness in the horse, London, 1852, Longmans, Brown, Green and Longmans. 14. Gamgee J: A treatise on horse-shoeing and lameness, London, 1871, Longmans, Green. 15. Bach FW: How to judge a horse, New York, 1893, William R Jenkins. 16. Dunlop RH, Williams DJ: Veterinary medicine: an illustrated history, St Louis, 1996, Mosby. 17. Stewart J: The stable book—a treatise on the management of horses, New York, 1858, AO Moore.

2

Lameness in Horses: Basic Facts before Starting Mike W. Ross

DEFINITION Lameness is therefore not so much an original evil, a disease per se, as it is a symptom and manifestation of some antecedent vital physical lesion, either isolated or complicated, affecting one or several parts of the locomotive apparatus.—A. Liautard, 18881

The clinical manifestations of lameness in the horse are well known, but an exact definition is difficult. The word lame is an adjective, meaning “crippled or physically disabled, as a person or animal,…in the foot or leg so as to limp or walk with difficulty.”2 A medical dictionary defines lameness as “incapable of normal locomotion, deviation from the normal

4

PART I

•

Diagnosis of Lameness

gait.”3 The noun lameness can be but infrequently is used interchangeably with claudication, described as “limping or lameness.”3 Lameness is simply a clinical sign, a manifestation of the signs of inflammation, including pain, or a mechanical defect, that results in a gait abnormality characterized by limping. The definition is simple, but recognition, localization, characterization, and management are complex.

LOCALIZATION OF PAIN In certain conditions, characteristic gait abnormalities allow immediate and straightforward recognition and localization of the problem. Sweeny, fibrotic myopathy, upward fixation of the patella, stringhalt, shivers, and radial nerve paresis are examples. However, similar gait deficits exist for a variety of lameness problems, complicating recognition and localization. A fundamental concept in lameness diagnosis is the application of diagnostic analgesic techniques to localize the source of pain causing lameness. The sequence of properly determining the lame leg (recognition) and then abolishing the clinical sign of lameness by use of diagnostic analgesia (localization), only to have lameness return when the local anesthetic effects abate, is essential for accurate diagnosis. With experience and under certain circumstances, this step in lameness diagnosis can be omitted. The degree of lameness, certain gait characteristics, and palpation findings allow the clinician to strongly suspect a certain diagnosis. The next step may be diagnostic imaging. Trial and error also occasionally work and in some instances may be the preferred approach. However, because pathognomonic signs are rare, proficiency in diagnostic analgesic techniques is mandatory for the lameness diagnostician.

BASELINE AND INDUCED LAMENESS Baseline, or primary, lameness is the gait abnormality recognized when the animal is examined at a walk or trot in hand, before flexion or manipulative tests are used. The clinician usually recognizes this abnormality by watching the horse on a firm or hard surface, while it is being trotted in a straight line. Diagnostic analgesia is used to abolish this lameness. Changing the surface or nature of the exercise by lunging, or circling the horse at a trot in hand, potentially changes the baseline lameness. The surface and exercise (gait and speed) must be consistent. In some horses, no observable lameness is present at a walk or trot in hand. Lameness may be evident when the horse is ridden, and this lameness becomes the baseline lameness. Flexion tests and other forms of manipulation are used to exacerbate baseline lameness or to induce lameness. An induced lameness is one that is observed after flexion or manipulative tests, but induced lameness may not be the same as the baseline lameness. Manipulative tests are expected to, and often do, exacerbate the primary lameness. However, flexion and manipulative tests can cause development of additional lameness, unrelated to the primary or baseline lameness, and test results must be interpreted carefully.

COEXISTENT LAMENESS Horses often have several sites of pain, although one usually is most obvious and the cause of baseline lameness. In many horses, secondary or compensatory (sometimes referred to as complimentary) lameness develops in predictable sites or limbs. Concomitant bilateral forelimb or hindlimb lameness is common, but horses often demonstrate more prominent clinical signs in one limb or the other. In horses with palmar heel

pain, initially pronounced single forelimb lameness that is abolished by palmar digital analgesia may be present, with subsequent recognition of contralateral forelimb lameness. In racehorses, bilateral lameness, such as in the carpi or metacarpophalangeal or metatarsophalangeal joints, is common. The clinician should carefully examine the contralateral limb. Predictable compensatory or secondary lameness often exists in the ipsilateral or contralateral forelimb, when primary lameness is present in the hindlimb, or vice versa. In a Thoroughbred (TB) racehorse with left forelimb lameness, compensatory problems in the right forelimb and left hindlimb are not uncommon, because these limbs presumably are succumbing to excessive loads, while protecting the primary source of pain. In a trotter, diagonal lameness often occurs (primary lameness in the left hindlimb and compensatory lameness in the right forelimb), whereas in pacers, ipsilateral lameness is most common (primary right forelimb and compensatory right hindlimb). When several limbs are involved, identification of the primary or major source of pain is important. If forelimb and hindlimb lameness exist simultaneously, diagnostic analgesic techniques should begin in the hindlimb (see Chapter 10). A common secondary lameness abnormality, proximal suspensory desmitis, can develop in the compensating forelimb or hindlimb.

LAMENESS DISTRIBUTION Among all types of horses, forelimb lameness is more common than hindlimb lameness. A horse’s center of gravity or balance, while dictated to a certain extent by conformation (see Chapter 4), is not located in the center of the horse but is closer to the forelimbs than the hindlimbs. Thus the forelimb/hindlimb (F/H) weight (load) distribution ratio is approximately 60%:40% (Fig. 2-1). Higher loads are expected on the individual forelimbs (30% each), predisposing the horse to greater injury. At certain times during the stride cycle of gaits such as the canter (three-beat gait) and gallop (four-beat gait), a single forelimb is weight bearing, which predisposes the limb to injury. The weight of a rider may shift F/H load distribution to 70%:30% (Fig. 2-2). Two-beat gaits, such as the pace and trot, allow more equal load sharing between forelimbs and hindlimbs because a forelimb and hindlimb (ideally, if the gait is balanced perfectly) hit the ground simultaneously. In pacers and trotters the proportion of forelimb lameness is less. The added load of pulling a sulky, cart, or any heavy load increases the likelihood of hindlimb lameness in Standardbreds (STBs), other harness breeds, and draft horses (Fig. 2-3). The F/H distribution of lameness in STB racehorses is 55%:45%. Sporting activities such as dressage and jumping also may shift lameness distribution to the hindlimbs because collection (working off the hindlimbs) and propulsion needed by horses to perform these activities may predispose to hindlimb lameness. In the forelimb, up to 95% of lameness problems occur at the level of or distal to the carpus.4 The distal parts of the limb always should be excluded as a potential source of lameness before the upper limb is addressed, although many owners believe otherwise, and may try to mislead an inexperienced practitioner. The foot should be suspected first. Pain in the foot is one of the most common causes of forelimb lameness in all types of horses, except draft breed horses, in which the foot is the most common site of pain in the hindlimb.

Hindlimb Lameness Hindlimb lameness should not be underplayed, although its recognition is more difficult. In the forelimb lameness–prone TB racehorse, many hindlimb lameness problems are overlooked. However, a rider or jockey often may suspect a hindlimb problem when the lameness actually exists in the forelimb.

Center of balance

Fig. 2-1 The center of balance (gravity) of the horse is located closer to the forelimbs, which accounts for the load distribution difference between the forelimbs and hindlimbs. Conformation, namely the angles of the shoulder and rump, and weight of the head and neck and gait can change this load distribution. WEIGHT

Cranial shift in center of balance

Gaits such as the canter and gallop (depicted) and the added weight of a rider, as shown here in a Thoroughbred racehorse, increase load on the forelimbs by shifting the center of balance, thus increasing the likelihood of forelimb lameness.

Fig. 2-2

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Diagnosis of Lameness

WEIGHT

Caudal Caudal shift shiftin in center center ofofbalance balance

Fig. 2-3 In a Standardbred racehorse (pacer depicted), the hindlimbs share added load compared with a Thoroughbred racehorse because of a caudal shift in the center of balance. The type of harness with the overcheck bit, the added weight of the sulky and driver, and the necessity of pulling a load increase the likelihood of hindlimb lameness in this breed.

A practitioner should consider carefully the distribution of sites of hindlimb lameness. Historically, the hock has been regarded as the major source of problems, and although it is an important source of hindlimb lameness, other sites also are important. For instance, in the STB racehorse the metatarsophalangeal joint is a major source of lameness that historically has been overlooked.5,6 Stress or nonadaptive bone remodeling of the distal third metatarsal bone (MtIII) cannot be seen radiographically in early stages and requires careful diagnostic analgesic techniques to achieve localization. Scintigraphic examination is mandatory for definitive diagnosis.7 Lameness of the metatarsophalangeal joint in STBs is almost as common as that of the hock, but without careful examination and the use of diagnostic analgesia, hock lameness is suspected in many such horses and they are treated for it. The combined use of diagnostic analgesia, ultrasonography, and scintigraphy has increased clinical knowledge of the broad spectrum of lameness conditions in the hindlimbs. In the draft horse, lameness in the hindlimb most commonly develops in the foot. Lameness in this area reflects the work performed by these horses, and innate characteristics of the draft horse foot, which predispose the foot to conditions such as laminitis. In jumping and dressage horses, problems in the fetlock region such as osteoarthritis and tenosynovitis are common and reflect the stress imposed by these disciplines. Although owners, trainers, and veterinarians often suspect an upper hindlimb lameness, gait characteristics of lower limb lameness problems often are similar. Only use of diagnostic analgesia allows an accurate diagnosis.

RELATIONSHIP OF LAMENESS AND CONFORMATION Conformation of the distal extremities, and to a lesser extent the overall body, plays a major role in the development of forelimb and hindlimb lameness (see Chapter 4). When a practitioner examines a weanling or yearling with poor conformation, predicting the time and the exact way the lameness will occur may be difficult, but many well-recognized conformational faults can lead directly to lameness problems. Conformation faults of the carpus, such as carpus varus or valgus, back-at-the-knee, and offset knees, can be important factors in carpal and lower forelimb lameness. In the hindlimbs, excessively straight hindlimbs (“straight behind”), sickle hocked, and in-at-the-hock conformation can lead directly to predictable lameness conditions. Although exceptions do exist, in the case of poor conformation, predictable lameness conditions consistently develop in poorly conformed horses. Evaluation of conformation is therefore an essential part of a lameness examination.

POOR PERFORMANCE Convincing trainers and owners may be difficult, but the leading cause of poor performance in racehorses is lameness, and lameness is the most prevalent health problem among all horses.8-11 In a recent study, 50% of U.S. operations with three or more horses had one or more lame horses, and 5% of the

CHAPTER 2

• Lameness in Horses: Basic Facts before Starting

horses could be expected to be lame.10 In another study, 74% of racehorses evaluated for poor racing performance had substantial musculoskeletal abnormalities contributing to poor performance. Lameness examination was emphasized as a most important aspect of comprehensive performance evaluation.12,13 Others have emphasized the importance of lameness in epidemiological studies evaluating wastage in TB racehorses.14,15 The same is likely true among all sport horses, particularly those competing at upper levels, although comprehensive studies have not been performed. Obvious lameness need not be demonstrated for performance to be compromised in horses, especially those competing at high speeds or upper levels. The possibility of achieving maximal performance in horses with substantial lameness is a common misconception. Notwithstanding the ignorance of many in the horse industry, the ability of many horses with obvious lameness to compete is a tribute to the mental and physical toughness. For example, bilateral forelimb or hindlimb lameness is common in STBs, but in some instances goes unrecognized if the condition is of similar severity. Unilateral lameness of this magnitude would be recognized easily, but because the lameness is bilateral, horses still race, albeit at a lower level. Bilateral third carpal slab fractures and sagittal fractures of the proximal phalanx have been diagnosed in horses examined for poor racing performance but, if seen unilaterally, would have caused pronounced lameness.

GAIT DEFICITS NOT CAUSED BY LAMENESS Gait abnormalities can exist with or without the presence of clinically apparent lameness. Deficits such as stringhalt, mild intermittent upward fixation of the patella, and shivers (see Chapter 49) can be present without obvious lameness and may complicate diagnosis of a completely different primary source of lameness. Horses with neurological disease may have gait deficits that are considered the result of painful lameness conditions (see Chapter 11). Horses with lower motor neuron diseases, such as equine protozoal myelitis, may have lameness associated with muscle atrophy or unexplained low-grade lameness associated with the disease. Concomitant lameness conditions can and do occur in these horses. Recurrent exertional rhabdomyolysis can cause stiffness and in some instances lameness, or it can cause poor racing performance, all of which can be misinterpreted as lameness (see Chapter 84).

UNEXPLAINED LAMENESS A diagnosis is made for most, but not, all lame horses through careful clinical examination and ancillary imaging modalities. Even with advanced imaging techniques a solution is not always found (see Chapter 12), but hopefully future innovations in clinical examination and imaging will result in the continued expansion of the science of lameness diagnosis.

COMPONENTS OF THE LAMENESS EXAMINATION AND LAMENESS STRATEGY Lameness Examination Lameness examinations should be performed in an orderly, step-by-step way, but many factors may change or abbreviate the examination (Box 2-1). Owner financial constraints may not allow performance of certain diagnostic tests and may curtail the time necessary to complete the entire examination. Drug testing of competing racehorses or show horses may limit a practitioner’s ability to perform diagnostic analgesic tech-

7

Box • 2-1 Components of the Lameness Examination History—anamnesis Examination from a distance—conformation, symmetry, posture Palpation Hoof tester examination Physical examination—other ancillary testing Movement Baseline Additional movement Selected examinations–manipulation, flexion, direct pressure, wedge Diagnostic analgesia Imaging Diagnosis Certain, presumptive, open Management Follow-up examination

niques and restrict management options. Clients do not always understand the need for diagnostic analgesia. Education about the value of this technique, and the difficulties of interpretation of the results of diagnostic imaging without it, is vital. Abbreviated lameness examinations often are performed in horses that exhibit severe lameness compatible with a fracture. Typical or obvious clinical signs may accompany severe lameness, and in many instances, prolonged or extensive lameness examination is contraindicated. If incomplete fractures are suspected, diagnostic analgesic techniques may be dangerous and should be performed only in certain situations. A clinician may proceed directly to conventional or advanced imaging techniques before completing the initial steps of the conventional lameness examination. Many other factors affect the ability to complete a comprehensive evaluation. Time constraints (usually of the veterinarian) often are cited, although shortcuts, if taken, usually create future problems. Omission of a diagnostic block or failure to perform detailed palpation often leads to misdiagnosis. Omission of a brief physical examination, including assessment of the horse’s temperature, can lead to embarrassing situations. The footing available on which to complete the lameness examination can be problematic. A dry, flat, hard surface or space for lunging or riding may be unavailable. The horse’s temperament may preclude adequate movement and often limits the practitioner’s ability to perform diagnostic analgesia. Many ill-tempered horses are referred for advanced imaging techniques, such as scintigraphic examination, because diagnostic analgesic techniques are dangerous to the veterinarian and handler.

Lameness Etiquette Owners frequently request an opinion from more than one veterinarian. Therefore professional, ethical conduct is important, with practitioner acknowledgment that horses can appear very different every day and response to diagnostic analgesia is not always consistent. For example, differences of opinion concerning radiographic interpretation can exist. A good working relationship with the client or agent is essential but should extend also to the farrier and any paraprofessionals involved in the management of the horse, even when opinions differ.

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Diagnosis of Lameness

Prognosis Assessment

REFERENCES

Assessment of prognosis for performance is important, but because few published data relating to many sports disciplines are available, clinicians often must rely on personal experience based on an understanding of the sport. Owners and trainers should consider prognosis carefully when making decisions to pursue therapeutic options, particularly when a long layoff period is required. I prefer to define prognosis as the “chance the horse will return to its previous level of competition.” However, this may not be a fair or reasonable definition. Retrospective studies can be used to evaluate prognosis after surgical or conservative management for various conditions in racehorses. Objective data such as numbers of race starts, race times, earnings per start, and time from treatment to first race start can be assessed. The criterion, earnings per start, is important because it establishes racing class or level of competition. However, in most retrospective studies, earnings per start decrease after treatment. The question is whether practitioners can accurately state that the horse will drop in class after treatment and whether this drop in class is the result of the injury, treatment, or aging of the horse an additional year before returning to racing. Use of this information is not easy. Most owners and trainers have a different view of prognosis than the veterinarian. In considering the prognosis for a horse undergoing arthroscopic surgical removal of a small osteochondral fracture of the carpus, most owners emphasize the surgery rather than the original injury. Clinicians must explain thoroughly the magnitude of the injury and related damage and discuss prognosis, using terminology that clearly indicates that the extent of injury is the factor that determines prognosis. Expecting a racehorse to return to its previous racing class may be an unrealistic expectation or at least a very strict definition for success. In a recent retrospective study of postoperative racing performance of STBs treated for carpal chip fractures, 74% of horses made at least one race start after surgery.16 Median earnings per start significantly decreased, but the median race mark (best winning time) also significantly decreased, indicating horses made less money but ran faster after surgery.16 These results must be compared with a normal population of STBs as the horses age, without considering injury, because STB racing performance is not standard over time.17 Average earnings per start is highest in 2-year-old horses and decreases exponentially until retirement.17 A population of horses undergoing any long-term layoff that requires recommencement of racing the following year can be expected naturally (unrelated to the original injury) to have lower earnings per start, regardless of whether the injury occurred or treatment was given. Therefore retrospective studies may underestimate prognosis associated with injuries and management choices. Success criteria and outcome assessment must be standardized to compare treatment results and define prognosis. The current standard for racehorses is comparison of performance for five starts before and after injury and treatment. This criterion is strict; a practitioner first may prefer to predict the chance of the horse returning to racing and then assess the chance that the horse will perform at or near its previous level. Other statistical methods have been used to evaluate racing performance in TBs using a regression model accounting for variables such as track surface, race distance, and age.18-20 To date, this performance analysis has been restricted to evaluation of horses after upper respiratory tract surgery but probably will be applied to horses with musculoskeletal injuries.

1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins Press. 2. Barnhart CL, editor: The American college dictionary, New York, 1970, Random House. 3. Dorland’s medical dictionary, Philadelphia, 1974, WB Saunders. 4. Adams OR: Veterinary notes on lameness and shoeing of horses, dissertation, Fort Collins, Colo, 1957, Colorado State University. 5. Ross MW, Nolan PM, Palmer JA, et al: The importance of the metatarsophalangeal joint in standardbred lameness, Proc Am Assoc Equine Pract 37:155, 1992. 6. Ross MW, Nolan PM, Palmer JA, et al: The importance of the metatarsophalangeal joint in standardbred lameness, Vet Surg 21:404, 1992. 7. Ross MW: Scintigraphic and clinical findings in the standardbred metatarsophalangeal joint: 114 cases (19931995), Equine Vet J 30:131, 1998. 8. Kaneene JB, Ross WA, Miller R: The Michigan equine monitoring system. II. Frequencies and impact of selected health problems, Prev Vet Med 29:277, 1997. 9. United States Department of Agriculture: Equine ’98 needs assessment survey results. USDA:APHIS:VS, CEAH, National Animal Health Monitoring System Pub No N236.597, Fort Collins, Colo, USDA, 1997. 10. Kane AJ, Traub-Dargatz J, Losinger WC, et al: The occurrence and causes of lameness and laminitis in the US horse population, Proc Am Assoc Equine Pract 46:277, 2000. 11. Ross WA, Kaneene JB, Gardiner JC: Survival analysis of risk factors associated with the occurrence of lameness in a Michigan horse population, Am J Vet Res 59:23, 1998. 12. Seeherman HJ, Morris E, O’Callahan MW: Comprehensive clinical evaluation of performance. In Auer JA, editor: Equine surgery, Philadelphia, 1992, WB Saunders. 13. Morris E, Seeherman HJ: Clinical evaluation of poor racing performance in the racehorse: the results of 275 evaluations, Equine Vet J 23:169, 1991. 14. Kobluk CN, Robinson RA, Clayton CJ, et al: A comparison of the exercise level and problem rate of 95 thoroughbred horses in a cohort study, Proc Am Assoc Equine Pract 36:47, 1990. 15. Jeffcott LB, Rossdale PD, Freestone J, et al: An assessment of wastage in thoroughbred racing from conception to 4 years of age, Equine Vet J 14:185, 1982. 16. Lucas JM, Ross MW, Richardson DW: Postoperative performance of racing standardbreds treated arthroscopically for carpal chip fractures: 176 cases (1986-1993), Equine Vet J 31:48, 1999. 17. Martinelli MJ, Freeman DE, Reid SWJ: Analysis of performance parameters in the population of standardbred racehorses in the US (1984-1993), Proc Am Assoc Equine Pract 42:174, 1996. 18. Martin GS, Strand E, Kearney MT: Use of statistical models to evaluate racing performance in thoroughbreds, J Am Vet Med Assoc 209:1900, 1996. 19. Martin GS, Strand E, Kearney MT: Validation of a regression model for standardizing lifetime racing performances of thoroughbreds, J Am Vet Med Assoc 210:1641, 1997. 20. Strand E, Martin GS, Haynes PF, et al: Career racing performance in thoroughbreds treated with prosthetic laryngoplasty for laryngeal neuropathy: 52 cases (1981-1989), J Am Vet Med Assoc 217:1689, 2000.

CHAPTER 3

CHAPTER •

• Anamnesis (History)

9

3

Anamnesis (History) Mike W. Ross

he importance of a detailed clinical history, the anamnesis, cannot be overemphasized. Information is divided into two categories, basic facts necessary for every patient and additional information from questions tailored to the specific patient. The veterinarian must understand the breed, use, and level of competition of each horse, because prognosis varies greatly among different types of sport horses. Firsthand experience of the particular type of sport horse being examined is useful but is not essential. Clinicians must understand the language associated with the particular sporting event, and this may be a challenge. For some sporting events, understanding the clinical history and the ability to ask the right questions is like speaking a different language. A veterinarian unfamiliar with the sporting activity should briefly review the type of activities performed and the array of potential lameness problems encountered with them. In some instances the veterinarian may lose credibility when talking to trainers or riders, particularly those involved in upper-level competition, if they perceive unfamiliarity. The veterinarian must understand the difference between subjective and objective information in the clinical history. Objective information is gained from the horse, and subjective information is perceived by the rider or owner. Information about a horse’s performance such as “the horse is bearing out,” “the horse is on the right line,” “the horse is lugging in,” “the horse has just started to refuse fences,” or “the horse no longer takes the right lead” is valuable objective information. Common examples of information perceived by the owner or rider include “the horse feels off behind,” “the horse is stiff behind,” or “the horse is lame behind” and it “feels up high.” Such information generally is useful and indicates a change in the horse’s gait, but only an experienced rider or trainer can discriminate accurately between forelimb and hindlimb lameness at any gait. Erroneous information obtained from the rider can complicate communication during lameness examination, particularly if the individual is strong willed and seemingly authoritative; this situation occurs if riders or trainers insist they are correct and the veterinarian disagrees. In my experience, many horses considered to have hindlimb lameness by a rider actually are lame in front, but convincing a disbelieving trainer is difficult. Similarly, lameness perceived as “up high” in most horses originates from the lower part of the limb. The veterinarian must understand that everyone is trying resolve the problem, but sometimes diplomacy is needed for successful communication. The veterinarian must be forthright and objective to determine the current source of lameness, even if the determination contradicts well-intentioned but strong-willed trainers. Clinical history is important but should not override clinical findings. In racehorses that perform at high speed, physical examination generally supports the finding that a horse bears away from the source of pain. During counterclockwise racing or training and with left forelimb lameness, a Thoroughbred (TB) will lug out (away from the inside of the track) and a Standardbred (STB) will be on the “left line” (bearing out; the driver must pull harder on the left line).

T

Some horses, however, especially STBs with medial right forelimb pain, bear out particularly in the turns, presumably because the source of pain is medial or on the compression side of the limb. The veterinarian must seek out as much information as possible, particularly if the problem is complex or not readily apparent. Videotapes are useful, particularly if the gait deficit, behavioral problem, or any other circumstances necessary to elicit the suspected lameness cannot be duplicated during the examination. Paraprofessionals working with the horse provide useful information, but not everyone may agree about the source of the problem, and in some instances diplomacy is key to negotiating among concerned individuals.

CLINICAL HISTORY: BASIC INFORMATION Signalment Age The age, sex, breed, and use of the horse are basic vital facts (Box 3-1). Flexural deformities, physitis, other manifestations of osteochondrosis, and angular limb deformities are agerelated problems. Infectious arthritis (hematological origin), lateral luxation of the patella, and rupture of the common digital extensor tendon are conditions usually unique to foals. Emphasis on training skeletally immature, 2- and 3-year-old racehorses causes predictable soft tissue and bone changes, often resulting in stress-related injury. Liautard observed more than 100 years ago: “When an undeveloped colt, whose stamina is not yet established and constitution not yet confirmed, with tendons and ligaments relatively tender and weak, and bones scarcely out of the gristle, is unwisely condemned to hard labor, it is irrational to expect any other results than lesions of one or another portion of the abused apparatus of locomotion. They will be fortunate if they escape a fate still worse, and become sufferers from nothing worse than mere lameness.”1 This statement aptly summarizes the situation then and now. The high value of races for 2- and 3-year-olds results in high-intensity training as an early 2-year-old, which may result in injury such as nonadaptive remodeling of the third carpal bone (C3), precluding racing at a young age. Some problems are unique to older horses (Box 3-2). Overall, osteoarthritis and other degenerative conditions such as navicular disease are most common but certainly not unique to the geriatric patient. These problems worsen with advancing age, particularly if several limbs are involved. In former racehorses, progressive osteoarthritis is of particular concern; this condition most commonly affects the carpal and metacarpophalangeal joints (Fig. 3-1). Occasionally in older horses, severe, progressive osteoarthritis of the carpometacarpal joint occurs without any history of carpal lameness (Fig. 3-2). In some horses, angular deformities develop at the carpometacarpal joint. Primary osteoarthritis of this joint is rare in young horses, even in racehorses with middle carpal joint abnormalities, unless C3 slab fracture or infectious arthritis occurs. Osteoarthritis of the coxofemoral joint is rare

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Diagnosis of Lameness

Box • 3-1 Anamnesis: Basic and Specific Information Basic Information Signalment: age, sex, breed, use Current lameness: what is the problem? History of trauma Duration of lameness Deterioration or improvement of lameness Circumstances when lameness worsens or improves Effects of exercise: worsening or improvement in lameness Management changes Changes in shoeing and related issues Changes in training or performance intensity Changes in surface Changes in diet and health Changes in housing Current medication and response; response to rest Past lameness problems

Specific Information Type of sporting activity Level of competition: current and future Additional sources Videotapes Images Records Discussions with others

Box • 3-2 Summary of Lameness Conditions of the Geriatric Horse Chronic, progressive osteoarthritis Proximal, distal interphalangeal joints Metacarpophalangeal joint Carpometacarpal joint* Coxofemoral joint* Femorotibial joints Tarsus Progressive osteoarthritis—previous injury (usually retired racehorses) Navicular disease Unexplained, severe soft tissue injuries* Superficial digital flexor tendonitis Flexural deformity Suspensory desmitis Fractures during anesthetic recovery *Some of these conditions are unique to the older horse and often are unexplainable.

in horses with the exception of young horses with osteochondrosis, but it does occur in older horses. An unusual group of soft tissue injuries of unknown origin occurs in older horses. Superficial digital flexor tendonitis and suspensory desmitis generally are considered

Fig. 3-1 An aged Thoroughbred broodmare with severe forelimb deformity caused by primary severe osteoarthritis of the right metacarpophalangeal joint and secondary or compensatory (chronic overload) carpus varus in the left forelimb.

overuse injuries and usually occur in upper-level performance horses or racehorses. However, severe tendonitis and desmitis do occur, often suddenly and without provocation, in older (teenage) horses. Horses usually are turned out at pasture when initial lameness is observed. In some patients, superficial digital flexor tendonitis is severe and progressive, leading to later flexural deformity because of adhesions. Suspensory desmitis may be unilateral or bilateral, may involve the forelimbs or hindlimbs, and is most common in the older broodmares. Older horses, particularly older broodmares, are at greater risk than younger horses to fracture long bones during recovery from general anesthesia.2 Between 1988 and 1994, 9 of 14 horses with catastrophic fractures or dislocations that developed during recovery from general anesthesia were older than 10 years of age. Age prominently affects prognosis. A common premise in considering lameness in foals is that young horses have time to outgrow the problem. Maturation will aid in angular limb deformities, some forms of osteochondrosis, and distal phalanx and diaphyseal fractures. However, fractures of important physes such as the proximal tibia may result in progressive angular deformities or disparity in limb length, limiting future prognosis. Early surgical management of flexural deformity of the distal interphalangeal (DIP) joint before 6 to 8 months of age optimizes future soundness and the possibil-

CHAPTER 3

• Anamnesis (History)

11

Owners are more likely to refrain from racing females and elect treatment for geldings and, in some instances, stallions. Future stallion prospects usually must prove race or performance success, thereby putting pressure on trainers to continue horses in training or racing. Behavioral abnormalities associated with the estrous cycle in fillies or mares are well recognized and may cause performance problems confused or misinterpreted as lameness (refusing fences, going off stride, striking) (see Chapter 50). An ill-defined behavioral problem in middle-aged nonracehorse mares could explain sudden performance problems often associated with or misinterpreted as lameness.5 Recurrent exertional rhabdomyolysis (RER) is more common in female TB racehorses6 and event horses.7 An association between sex and RER in STBs may exist and be more common in fillies administered anabolic steroids. Obscure or unexplained hindlimb lameness has been attributed, rightly or wrongly, to retained testicles. The origin of lameness in these horses is difficult to prove without removing the retained testicle, and anecdotal reports suggest that hindlimb lameness has resolved after castration in some horses. The origin of pain in an abdominal cryptorchid is difficult to explain and questionable. The source of pain may be easier to understand in a horse with a testicle located within the inguinal canal. Activity of the external and internal abdominal oblique muscles and tension on the spermatic cord are possible explanations.

Breed and Use Most lameness conditions affect all breeds of horses. Although breed has considerable influence on sporting activity, sporting activity or use primarily has the greatest impact on lameness distribution (see Chapters 116 through 130).

Current Lameness Determination of the Problem

Dorsolateral-palmaromedial oblique radiograph of the carpus of an aged horse showing unusual, severe osteoarthritis of the carpometacarpal joint.

Fig. 3-2

ities for normal hoof conformation. In one study the reported success rate was 80%.3 If surgical management is done later in life or when deformity is severe, the prognosis decreases substantially. The prognosis for survival of foals treated for infectious arthritis is reasonable, but only 31% of TB foals and 36% of STB foals started one or more races, indicating the prognosis for future racing performance is poor, because articular healing even in young foals is not possible.4 In middle-aged (12 to 18 years of age), upper-level performance horses, prognosis is difficult to assess, particularly in horses with several problems. Level of competition, rather than age, may be the most important factor, and often performance level declines.

Sex Most lameness conditions affect stallions, geldings, and mares with similar frequency. Sex-specific conditions are unusual but do exist. The most important consideration, however, regarding the sex of the patient is future breeding potential or lack thereof in the case of geldings. In many types of horses, and specifically in racehorses, decisions about future performance or racing potential often are important when considering management options and financial aspects. This factor is particularly important when life-or-death decisions must be made after catastrophic injury (see Chapter 13). Frank discussions about the prognosis for return to the current sporting activity or level of performance often are necessary, and the clinician should consider reproductive capability of the horse.

Accurate information is necessary to determine precisely the horse’s current problem. Obtaining reliable information may be difficult if the horse has been purchased recently. Additional objective information may be necessary to assess the effect of lameness on the horse’s performance. Evaluation of the horse’s race record may indicate when the problem began and if it is ongoing or new. The groom, rider (if not the owner), assistant trainer, blacksmith, and other paraprofessionals may have other pertinent information. Horses with poor performance usually are lame, although respiratory problems, rhabdomyolysis, shoeing, tack or equipment, and other medical problems can contribute. The horse’s past history is important in determining the cause of the current problem, particularly in racehorses training or racing with existing low-grade osteoarthritis that develop new overload injury to supporting limbs (secondary or compensatory lameness). Existing problems such as osteoarthritis worsen insidiously but may reach critical levels, causing sudden, severe unexpected lameness. Osteoarthritis of the metacarpophalangeal joint may exist for months in racehorses without causing obvious lameness, although in many horses joint effusion ultimately leads to treatment (“maintenance injections”). The horse suddenly may be much lamer after racing or training, and the trainer may assume the cause is different. Because intra-articular analgesia may only partially relieve lameness, persuading the trainer that the problem is still the fetlock may be difficult. Horses can endure extensive cartilage damage in any joint for many months, but at some point they reach a threshold level beyond which they cannot tolerate the pain.

History of Trauma Many lameness problems develop during or shortly after a traumatic incident, but unfortunately many owners presume trauma played a role, even though no one witnessed the

12

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Diagnosis of Lameness

alleged incident. A common but often erroneous assumption when examining a lame foal is that the dam stepped on it, but usually infection is the cause. Conditions such as osteochondrosis dissecans of the shoulder or stifle often are expressed after a traumatic incident, and yet most lame weanlings or yearlings are assumed to be lame because of trauma, not a developmental problem.

Duration The veterinarian must understand the duration of the current lameness problem and determine whether a preexisting chronic, low-grade lameness exists and if now sudden exacerbation of this problem has occurred, or a completely unrelated new problem has developed.

Worsening of Condition The veterinarian must establish if the horse’s current problem is worsening or improving, under which conditions or circumstances the lameness deteriorates or improves, and if the horse responds to treatment such as shoeing or management changes. Most lameness problems worsen with time, particularly if training or performance continues despite owner or trainer recognition. Racehorses with stress-related bone injury often are noticeably lame after work but become sound relatively quickly, within 1 to 3 days. A minimal number of other clinical signs are present, particularly because the most common bones (tibia, humerus) are difficult to palpate and buried by soft tissue. This cycle of lame-sound-work-lame is an important part of the history. Improvement of lameness with rest is important from historical and therapeutic perspectives. Lameness in most horses with severe articular damage, usually from severe osteoarthritis, does not improve substantially with rest. Severe osteoarthritis most commonly appears in the fetlock, femorotibial, and tarsocrural joints. Horses with fractures or mild to moderate soft tissue injuries generally improve with rest.

Warming into Lameness Warming into lameness means the horse’s lameness worsens during the exercise period. Warming out of lameness means the lameness improves. This concept is important. Lameness associated with stress or incomplete fractures, soft tissue injuries (tendonitis and suspensory desmitis), splints, curb, and foot soreness worsens with exercise. In racehorses a worsening lameness appears as progressive bearing in or out during training or racing. In riding horses, this may be progressive stumbling, problems taking leads, progressive asymmetry in diagonals, or refusing to jump later fences. Horses with osteoarthritis may be stiff and obviously lame at a walk, but lameness may improve with work. In western performance horses, osteoarthritis of the proximal and distal interphalangeal joints, and in some horses navicular syndrome, cause lameness with this characteristic. The most dramatic example is distal hock joint pain, particularly in racehorses. Horses may be noticeably lame at a walk and trot, warm out of the lameness to the point of racing successfully, and then show pronounced lameness after the race. One frequent statement at the racetrack is that the horse throws the lameness away at speed. This decrease occurs with some lameness conditions, such as distal hock joint pain, but two other factors are important. A horse may be able to race with lameness but not be able to perform at peak, particularly if lameness is bilateral. Horses often can race with bilateral conditions and show minimal signs of lameness, but performance is reduced. Lameness at the gallop may be impossible to perceive, and even at the fast trot or pace, most persons have difficulty seeing lameness. The same limitation occurs in observing a dressage or jumping horse at the canter. The veterinarian may gain some information by observing that a horse is reluctant to take either the left or right lead, but lameness is difficult if not impossible to detect at the canter. Unless slow-motion video analysis is available, the horse appears to

be able to “throw lameness away,” but lameness is present but difficult to see. In this situation, horses do not warm out of lameness but simply cope with the pain while racing. Horses in this situation are at risk of developing compensatory problems. Older horses with osteoarthritis may have difficulty in getting up and later may warm out of the lameness. Horses of any age with pelvic fractures or severe lameness may have difficulty in rising.

Recent Management Changes Many lameness conditions start after a change in management. Changes in shoeing, training or performance intensity, surface, housing, and diet or other medical issues can have a profound effect on the musculoskeletal system. Changes in ownership often dictate changes in exercise intensity and certainly in owner expectations. The veterinarian must be careful in questioning and responding to questions if a horse has been purchased recently, especially if a colleague performed a prepurchase examination. Clinicians should avoid implying that a condition may have been preexisting or missed. Shoeing. The veterinarian should determine when the horse was last shod and whether the shoeing strategy was changed. Nail bind often causes acute progressive lameness related temporally to shoe application. Abscesses that result from a “close nail” may take several days to cause lameness. Foot balance is critical and, in some horses, changing foot angles results in lameness. A substantial increase or decrease in heel angle in a horse with chronic laminitis may exacerbate lameness. In horses with palmar heel pain, raising the heel angle may produce an obvious improvement in clinical signs briefly, whereas in horses with subchondral pain of the distal phalanx, raising the heel may worsen clinical signs. In racehorses with “sore feet” resulting from soft tissue and bone pain, changing shoes may result in improvement, related in part to temporary reduction in weight bearing in the painful area of the foot. Temporary lameness often occurs in horses with recently trimmed but unshod hooves, particularly if the horses’ hooves are trimmed aggressively or the ground is unusually hard for that time of year. The veterinarian must remember that a horse with recently trimmed hooves often shows bilateral forelimb lameness when trotted on flat or uneven hard surfaces, regardless of the primary cause of the current lameness. The horse should be reassessed on a soft surface. Attempts to make both front feet symmetrical may create substantial lameness immediately after trimming. Horses may cope well with different size and shaped front feet, but when radical trimming is performed, they may develop severe lameness. The veterinarian must determine whether any recent or past changes in shoeing either improved or worsened lameness. Lameness in a STB trotter with foot pain may improve by changing from conventional shoes, such as half-round or flat steel shoes in the front, to the “flip-flop” shoe. The farrier often first notices the common problem that a horse is reluctance to pick up the hindlimbs. In some horses, this problem is purely behavioral, whereas in others it is a real sign of pain. This history most often is associated with conditions such as osteoarthritis of one or more joints but also may be a sign of pelvic or sacroiliac pain. In Warmbloods, draft breeds, and draft-cross horses, reluctance to pick up a hindlimb may be an early sign of shivers. Training or performance intensity. Lameness that worsens in response to recent increase in training intensity may be related to stress-related subchondral or cortical bone injury. Stress fractures, bucked shins, or nonadaptive stressrelated injuries of subchondral bone occur typically during defined periods of training and often after brief periods of rest. When horses in active race training are given time off, even

CHAPTER 3 brief periods such as 7 to 21 days, bone undergoes detraining, leaving it subject to stress-related injury. If training resumes at the pre-rest level or is accelerated, stress fractures or bucked shins often develop. In 3-year-old TBs, stress fractures of the humerus often occur within 4 to 8 weeks after returning to training. Bucked shins often develop in 2-year-old horses after a brief rest period for an unrelated medical condition. Surface. Most lameness conditions worsen if the horse performs on a harder surface. In show horses such as the Arabian or half-Arabian breeds, foot lameness often results when horses are warmed up or shown on harder surfaces. An association exists between fracture development and hard racing surfaces. A dramatic change in any racing surface may lead to unexpected episodic lameness in racehorses. On breeding farms, anecdotal evidence suggests drought conditions causing harder than normal pastures lead to a higher prevalence of osteochondrosis or distal phalanx fractures. Lameness that is most pronounced on hard surfaces is often seen with conditions of the foot. Lameness that worsens on softer surfaces, however, may be associated with soft tissue injuries such as proximal suspensory desmitis. Uneven surfaces may exacerbate lameness and other gait abnormalities. Horses prone to stumbling on uneven surfaces may have palmar heel pain, proximal suspensory desmitis, or neurological disease. Horses with bilateral lameness may be lame in one leg going in a particular direction on a banked surface (such as a racetrack) and lame in the opposite leg going the other way. Bilateral lameness may be confused with other causes of poor performance because of inconsistencies in gait. Lameness may worsen or improve when a horse goes uphill or downhill. Diet and health. Changes in diet or dietary factors may lead to or exacerbate existing lameness conditions. Dietary factors, especially dietary excesses or deficiencies, are important in the many manifestations of developmental orthopedic disease (see Chapter 57). Sudden changes in diet, such as those associated with turning horses out on lush pastures or consumption of large quantities of grain (grain overload), may cause laminitis or exacerbate existing chronic laminitis. Overweight horses normally consuming a high-grain diet may be prone to laminitis or gastrointestinal tract disturbances that lead to laminitis. Lameness may be associated with, or result from, other medical conditions. Obvious associations exist in foals between conditions such as infectious arthritis and physitis with umbilical, gastrointestinal, or respiratory tract infections. Immune-mediated synovitis also occurs in older foals with chronic infections (see Chapter 67). In adult horses, infectious arthritis generally develops after intra-articular injections or penetrating wounds but may result from hematological spread of bacteria. Occasionally, horses develop distal extremity edema and lameness after vaccination, presumably caused by vasculitis or other immune-related mechanisms. Similar signs appear in horses with purpura hemorrhagica or viral illnesses such as equine viral arteritis. Housing. Many lameness conditions develop while a horse is turned out, or as the result of turnout, often as the result of trauma such as kick wounds or fence-related injuries. Sudden changes in weather may excite horses, particularly those turned out at pasture. During thunderstorms horses may run into fences or buildings and suffer unexpected injuries. One such problem is suprascapular nerve injury. Minimizing problems with turnout requires the use of wellgroomed and well-maintained pastures or paddocks with individual paddocks to reduce horse to horse interactions. Dramatic housing changes have a substantial impact on the development of lameness. Shipping to and from sales, foaling, and weaning are associated with soft tissue injuries, puncture or kick wounds, and other injuries.

• Anamnesis (History)

13

Current Medication Changes and Response The veterinarian must establish if the horse currently is receiving medication or was administered medication recently and the response to treatment. Response to medication or a management change is important information in formulating a treatment plan. For example, recent improvement with rest and the administration of nonsteroidal anti-inflammatory drugs indicates more of the same treatment may be reasonable. The veterinarian must establish dosages of medication because a horse may not respond to phenylbutazone because of under-dosage. Many owners and trainers do not understand that although intra-articular analgesia relieves lameness, intra-articular medication may not, thus causing doubt about the diagnosis. This characteristic commonly appears in horses with subchondral bone pain and is useful in diagnosis. Horses with early osteoarthritis and negative or equivocal radiographic signs, or those with short, incomplete fractures, often do not respond to intra-articular medication. Negative radiographic findings are a good sign because dramatic radiographic evidence of subchondral lucency or fracture reduces the prognosis considerably. However, convincing the trainer of the validity of the diagnosis may be difficult. The amount and quality of rest are important. Many acquired conditions, such as osteoarthritis, or degenerative conditions, such as navicular syndrome, take many months and usually years to develop. Therefore expectation that a horse will show marked improvement with a brief rest period is unreasonable. Lameness in many horses with severe osteoarthritis may not improve substantially, even with prolonged rest. In horses with early osteoarthritis in which pain occurs primarily in subchondral bone and for which radiographic findings are negative or equivocal, rest or controlled exercise for 3 to 6 months may be necessary. The same regimen applies for horses with navicular syndrome, fractures, and many soft tissue injuries. Quality of rest is equally important. Did the horse receive absolute box stall rest with handwalking, or was it lunged or turned out in a paddock or field with other horses? Was a brief rest period followed by an attempt to ride or train the horse? Those associated with the horse often consider this type of intermittent rest complete rest, but many conditions remain chronically active. Without adequate rest, re-injury follows temporary improvement and early healing.

Past Lameness History Obtaining the horse’s entire lameness history may not be necessary or possible, but the veterinarian should gather as much information as is practically available. Prognosis for many injuries is affected adversely by recurrence, and often management options differ in these situations. Recurrence may prompt more aggressive therapy, considerations for referral, or perhaps surgical evaluation if the problem involves a joint. If a reliable diagnosis was made previously, retreatment for the past problem may be a reasonable or preferred management approach, particularly between races or competitions. If a horse has responded previously to intraarticular medication, re-injection may be reasonable. However, in many horses with progressive osteoarthritis, results of additional therapy often are diminished. The veterinarian should not assume that the failed response to intraarticular medication means the problem lies elsewhere because medication does not affect subchondral bone pain in early or late osteoarthritis. Recent history is important. Small, innocuous-looking wounds over the third metacarpal bone or third metatarsal bone, radius, tibia may be associated with bone trauma with delayed-onset severe lameness. Incomplete or spiral fractures may develop from small cortical defects (Fig. 3-3).

14

PART I

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Diagnosis of Lameness

A

B

Craniocaudal radiograph of the left antebrachium of a 5-year-old Thoroughbred mare showing a displaced, long oblique fracture of the radius. This filly had sustained a small puncture wound to the lateral aspect of the antebrachium 5 days earlier but was sound. The mare was turned out and developed acute, severe lameness and was later euthanized.

Fig. 3-3 Dorsopalmar radiographs of left third metacarpal bone in an 18-year-old Thoroughbred gelding showing initial (A) and 2-week follow-up (B) views. The initial view was taken after the horse was found to have a small skin wound in the region but was sound. Acute, severe lameness developed 9 days after initial injury, and the follow-up radiograph shows a long oblique fracture of the third metacarpal bone.

Fig. 3-4

Catastrophic failure of long bones occurs even when initial radiographs show no or minimal cortical trauma. The radius appears to be at greatest risk (Fig. 3-4). New problems may and often do arise despite a long history of recurrent lameness. Comprehensive reevaluation is the best and safest approach to avoid delays in proper diagnosis and treatment.

REFERENCES

FURTHER INFORMATION Full understanding of the horse’s use, type and level of sporting activity, and value, all of which help the veterinarian assess prognosis, requires specific information. If the horse previously was under the veterinary care of another individual in the same or different practice, it is important to obtain accurate case records and view previous radiographs and other images.

1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins Press. 2. Olsen K, Nann L: Unpublished data. Kennett Square, Pa, 1995, University of Pennsylvania. 3. Wagner PC, Grant BD, Kaneps AJ, et al: Long-term results of desmotomy of the accessory ligament of the deep digital flexor tendon (distal check ligament) in horses, J Am Vet Med Assoc 187:1351, 1985. 4. Steel CM, Hunt AR, Adams PL, et al: Factors associated with prognosis for survival and athletic use in foals with septic arthritis: 93 cases (1987-1994), J Am Vet Med Assoc 215:973, 1999. 5. Bousum P: Personal communication, 1995. 6. MacLeay JM, Sorum SA, Valberg SJ, et al: Epidemiologic analysis of factors influencing exertional rhabdomyolysis in thoroughbreds, Am J Vet Res 60:1562, 1999. 7. Dyson S: Personal communication, 2000

CHAPTER 4

CHAPTER •

• Conformation and Lameness

15

4

Conformation and Lameness Mike W. Ross The idea of a good horse with poor legs is a misnomer, the legs are the essence of the horse, and every other part of the equine machine is of only subservient and tributary importance. A. Liautard1 hat the way a horse is conformed determines the way it moves is well accepted. The relationship of conformation, especially of the distal extremities, and lameness also is well recognized. “Conformation determines the shape, wear, flight of the foot, and distribution of weight.”2 Veterinarians often are asked to comment on conformation during lameness and prepurchase examinations, especially with regard to the suitability of the horse to perform the intended task. In some instances, as in the case of presale yearling evaluations, the veterinarian’s opinion is paramount, and purchase is contingent on judgment of the yearling’s potential to perform as a racehorse, given its conformation, or in some instances its conformational faults (see Chapter 102). “It is by a study of conformation that we assign to a horse the particular place and purpose to which he is best adapted as a living machine and estimate his capacity for work, and the highest success in this connection will be best attained by the judicious blending of practice with science.”3 Evaluation of conformation and its influence on lameness is based largely on observation, experience, and pattern recognition. Recognizing desirable conformational traits in horses suited for a particular sporting activity and learning when to overlook a minor fault that has little clinical relevance is important.

T

RELEVANCE OF CONFORMATION EVALUATION Conformation is one piece of the complex puzzle of a lame horse, although poor conformation does not necessarily condemn a horse to lameness: “faulty conformation is not an unsoundness…it is a warning sign.”2 All lameness diagnosticians should evaluate conformation briefly at the beginning of each examination. The association of lameness and faulty conformation will be obvious. The clinician must evaluate the horse from afar, assessing the whole horse for balance, angles and lengths, and posture and symmetry. The clinician must remember that horses come in all shapes, sizes, and types, and therefore conformation varies accordingly, but certain conformational faults produce predictable lameness conditions and are undesirable. However, good conformation is not synonymous with success, and although horses of certain body types tend to have longer strides and are more athletic than others, intelligence, aggression, “will to win,” and other intangible factors are important. I am convinced that a well-bred horse from a successful family can endure faulty conformation much better than a poor- or mediocre-bred horse.

HEREDITARY ASPECTS OF CONFORMATION Certain conformational faults appear to be highly heritable traits. Evaluation of broodmares and foals often reveals that the early conformational defects seen in a foal are present in the dam. The dam seems to contribute more to faulty con-

formation than does the sire, although the stallion also is important. This difference may be explained in part by the fact that fillies with faulty conformation may develop problems or be retired early and subsequently bred, whereas most stallions usually are proven performers with exceptional conformation. Conformational faults such as toeing in and toeing out commonly are passed down from generation to generation. Back-at-the-knee (calf-knee), offset (bench) knee, tiedin below the knee, sickle-hock, and straight behind conditions are also highly heritable. Certain lameness conditions are common in horses with faulty conformation, but similar lameness conditions develop inexplicably in some breeding lines year after year in offspring with apparently acceptable conformation. Lameness of the carpus or tarsus appears to be most important. For example, in Standardbreds (STBs), siblings commonly develop similar lameness conditions, such as proximal suspensory avulsion injury, carpal osteochondral fragments, distal hock joint pain, or curb.

OBJECTIVE EVALUATION OF CONFORMATION: IS IT POSSIBLE? A recent attempt to quantify conformation used a linear assessment trait evaluation system that allows the observer to assess where, given a particular trait, a single animal falls within a population of animals.4 A population of 101 Irish Thoroughbred (TB) flat racehorses and 19 top stallions was used and 27 common conformational traits were evaluated, including various heights, lengths, angles, and distal extremity conformation (Figs. 4-1 to 4-3). Of the 27 traits, 6 were significantly linked to age, and 5 were linked to sex (head and neck shape; neck size at poll and larynx and at withers, and manubrium of the sternum; and forelimb hoof pastern axis). Most traits exhibited large phenotypic variation within the population, but 21 of 27 non–age-linked traits were judged suitable for possible inclusion in a linear assessment protocol.4 Researchers judged a high percentage of horses to be toed out, suggesting this trait may even be desirable. More recent studies have used video-image analysis, but direct physical measurements may be more accurate than those obtained by analyzing videotapes or photographs.5 Potential errors in image analysis occur because of movement of skin markers over selected bony protuberances, a phenomenon more common in the upper limb and in motion studies.5,6 Skin marker location is critical for evaluation of joint angulation and movement during locomotion or conformation analysis. Instant center or axis of rotation (ICR) is defined as the point with zero velocity during movement of that joint; accurate measurements of joint angulation require positioning markers at the ICR.7 Conventional positions of skin markers and ICR in most joints agree well, but use of traditional marker sites on the scapulohumeral and femorotibial

16

PART I

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Diagnosis of Lameness

Head Size a- Parotid salivary gland to tip of nose b- Parotid salivary gland to groove made by facial artery c- Groove made by facial artery to tip of lip

Stature/Height * From highest point of withers, standing square on level ground

Intramandibular width

Back Length *

b a c

Croup Length Highest point of croup to root of tail

Highest point of withers to highest point of croup

Head Shape 1 - Light and small 4 - Intermediate 7 - Heavy and big 4

1

Neck Size * Circumference a - At poll and larynx b - At withers and manubrium of sternum

7

b

a

Neck Shape 1 - Long and thin 4 - Intermediate 7 - Short and thick

Withers * 1 - Low and mutton 4 - Intermediate 7 - High and bony

Back Shape 1 - Sunken 4 - Intermediate 7 - Roach

1

4

7

Croup Shape

1

1 - Short and level 4 - Intermediate 7 - Long and sloping

4

7

Fig. 4-1 Conformation traits used for linear assessment of conformation in a population of Irish Thoroughbreds. Asterisks indicate traits significantly linked to age. (Modified from Mawdsley A, Kelly AP, Smith FH, et al: Linear assessment of the Thoroughbred horse: an approach to conformation evaluation, Equine Vet J 28:461, 1996.) joints results in overestimation and underestimation, respectively, of caudal joint angles.8 Although video-image analysis may be fraught with potential or in some instances real error, objectivity is a major advantage. Other advantages include the ability to replay images, reduction of observer fatigue, elimination of observations and measurements in real time, and permanent recording of the observation. Ideally, objective measurements would withstand statistical evaluation, distinguish between desirable and undesirable traits, and account for differences among different types of horses.5 A combination of direct measurement and photography has been used to to evaluate conformation of Swedish Warmblood and elite sport horses.9,10 Whereas most of the conformational defects were mild or moderate, 80% of Warmblood (WBL) horses were toed out behind, suggesting this may be a normal finding in this breed as in the STB trotter. More than 50% of horses had bench knees and 5% were toed out in front, contrary to findings in STB trotters.9,11 Many of the elite horses were bucked kneed, whereas the riding school horses tended to have calf knees. It was speculated that this occurred because elite horses were evaluated after competition and muscle fatigue may have contributed to the tendency to be over at the knee. Sex had significant influence on conformation; females were smaller and had longer bodies and smaller forearms and metacarpi. There were interesting findings regarding hock

angle. A sickle hock is defined as a hock angle of 53° or less; a large hock angle is referred to as straight behind. Sickle-hocked conformation was nearly absent in elite horses, and it was hypothesized that sickle-hocked conformation either predisposed a horse to lameness or impaired a horse’s ability to achieve upper levels of competition.9 A positive relationship between larger hock angles and soundness in STB trotters also exists.12 In forelimbs of WBL show jumpers and the forelimbs and hindlimbs of STB trotters, smaller fetlock joint angles (less upright) were desirable.9,12 Radiography was used to assess the degree of hyperextension of the carpus to study the potential effect of backat-the-knee (calf-knee) conformation on the subsequent development of carpal chip fractures.13 Lateromedial radiographic views of 21 horses with carpal chip fractures and of 10 normal horses were obtained, with and without the contralateral limb raised. No relationship between measured carpal angle and carpal chip fracture formation existed, suggesting that this group of TB racehorses did not develop carpal chip fractures as a result of calf-knee conformation. The sample size was small, however, and a larger study may produce different results. Horses with severe calf-kneed conformation may develop other problems and not advance enough in training to develop carpal chip fractures. They may be judged poor surgical candidates, are not referred, or are slow.

• Conformation and Lameness

CHAPTER 4

FORELIMBS Shoulder to ground

FORELIMBS Knees 1

1 - Camped–under 4 - Intermediate 7 - Camped–out

1 - Bucked knees 4 - Intermediate 7 - Calf knees

4

1

7

FORELIMBS * Knees 2

FORELIMBS Upstandingness

1 - Tied–in knees 4 - Straight knees 7 - Chopped at knees

1 - Base–wide 4 - Intermediate 7 - Base–narrow

4

1

7 4

1

FORELIMBS Cannon angle

1 - Offset cannon 4 - Straight 7 - Inset cannon

FORELIMBS Hoof–pastern axis

FORELIMBS Pastern angle

7

FORELIMBS Knees relative to cannon or forearm

1 - Bow–legged 4 - Straight 7 - Knock–kneed

1 - Broken and upright 4 - Straight 7 - Sloping

17

FORELIMBS Foot slope 1 - Straight 4 - Intermediate 7 - Sloping 1

1

4

4

1

7

4

7

7

1 - Toe out 4 - Straight 7 - Toe in

Conformation traits used for linear assessment of conformation in a population of Irish Thoroughbreds. Asterisk indicates traits significantly linked to age. (From Mawdsley A, Kelly AP, Smith FH, et al: Linear assessment of the Thoroughbred horse: an approach to conformation evaluation, Equine Vet J 28:461, 1996.)

Fig. 4-2

Two recent studies evaluated TBs and Quarter Horses (QHs) using skin markers, photography (three views: front, side, back), and computer-image analysis. The TB study evaluated the change in conformation with age; as expected, most body parts increased in length from birth to 2 years. Horses became more bench kneed from birth to 3 years, and the dorsal hoof angle decreased as horses grew (hoof wall became less upright). A strong relationship existed between long bone length and withers height, including the radius (taller horses have longer bones).14 In the TBs, clinical observations (lameness) associated with conformational variables included effusion of the fetlock and carpal joints, carpal fractures, and other traumatic conditions of the fetlock joint. Risk of effusion of the fetlock joint increased with increased dorsal hoof angle, and the odds of carpal fracture decreased with scapular length. Carpus valgus decreased risk for carpal fracture, but fetlock lameness increased in horses with offset knees.14 In the second study, odds ratios were created for increase in bone length of 2.54 cm (1 inch) or joint angle of 1° and development of lameness. For every 1-inch increase in

humeral length, odds for fracture of the proximal phalanx or carpal synovitis or capsulitis increased. Increased length from elbow to ground and increased toe length increased chances for carpal fracture, and in horses with offset knees greater than 10% the potential for carpal or fetlock synovitis or capsulitis increased. The potential for fracture of the proximal phalanx increased with an increase in shoulder angle.14 The relationship of many lower limb lameness conditions with limb length is interesting and somewhat unexpected because longer limb length generally is considered desirable. Although a relationship between longer toes and carpal fracture is not unexpected, the increased chance for fetlock lameness with more upright hooves is surprising. The relationship between offset knees and lower limb lameness was expected, but unexpected were fewer carpal fractures in TBs with this conformational fault. Because development of lameness, termed clinical outcomes in these studies, is complex, confounding variables such as track conditions, training regimen, breeding, individual horse ability, and experimental error could have contributed to outcome.

18

PART I

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Diagnosis of Lameness

Hindlimbs Hip to ground

Hindlimbs Hock set

1 - Stands under 4 - Intermediate 7 - Camped-out

1 - Straight and posty 4 - Intermediate 7 - Sickled

4

1

Hindlimbs Hoof–pastern axis

7

Hindlimbs * Foot slope

1 - Broken and upright 4 - Straight 7 - Broken forward axis, sloping 1 pastern

1 - Straight 4 - Intermediate 7 - Sloping

4

7

1

Hindlimbs Upstandingness

Hindlimbs Hock set

1 - Base-wide 4 - Intermediate 7 - Base-narrow

1 - Bow-hocked 4 - Straight 7 - Cow-hocked

1

Hindlimbs Pastern angle

4

1

7

1

4 4

1

7

4

4

7

7

7

1 - Toe out 4 - Straight 7 - Toe in

Conformation traits used for linear assessment of conformation in a population of Irish Thoroughbreds. Asterisk indicates traits significantly linked to age. (From Mawdsley A, Kelly AP, Smith FH, et al: Linear assessment of the Thoroughbred horse: an approach to conformation evaluation, Equine Vet J 28:461, 1996.)

Fig. 4-3

Little doubt exists that acquiring objective information is useful, not only to determine what is abnormal but also to define what is normal in a population. In both WBLs and STB trotters in Europe, toed-out conformation in the hindlimbs should likely be considered normal because a majority of both breeds have this conformational trait.9,11 These populations differed, however, in forelimb conformation. Few STB trotters had bench-kneed conformation, a finding supported by my clinical observations that this conformational fault is highly undesirable in this breed (see Chapter 109).

EVALUATION OF CONFORMATION Conformation determines the way a horse moves, and I am convinced that a relationship exists between faulty conformation and the development of lameness. Therefore assessment of conformation should be an integral part of lameness examination. Conformation evaluation has four basic components: (1) balance, (2) assessment of lengths, angles and heights, (3) muscling, and (4) conformation of the limbs. All are intertwined but should be evaluated separately, considering the whole horse not just the limbs, and then consolidated. The clinician should evaluate the horse on firm, level ground, preferably a smooth, nonslip surface that does not obscure the view of the feet. The horse should stand squarely with equal weight on all four limbs. Dynamic assessment of limb conformation while the horse is walking also is essential.

Balance Balance is the way all parts of the horse fit together and is linked directly with assessment of lengths, angles, and heights. The horse should be proportional and thus well balanced. A horse may be visualized in thirds—the forehand, the midbody, and the hindquarters—by drawing three circles incorporating these areas (Fig. 4-4). The circles should overlap but not excessively. Horses in good balance are likely to be superior athletes. Horses with a short, thick (throatlatch and shoulder regions) neck are often heavy and straight in the shoulders (Fig. 4-5). A horse with a short back has naturally closer dorsal spinous processes and may be predisposed to impingement or over-riding, whereas a horse with a long back (Fig. 4-6) may have difficulty engaging the hindlimbs properly. The clinician must assess the relative heights of the withers and hindquarters. A horse that is taller behind than in front (rump height is greater than height at the withers) is predisposed to forelimb lameness. A horse that also is underdeveloped in the shoulders and upper forelimbs (weak up front) and heavy behind is more at risk. Limb lengths should be proportional to body size and height. In general, the body length (point of shoulder to point of rump) should be equal or slightly longer than withers height (see Fig. 4-4). Head conformation is not relevant to lameness, but the size of the head relative to the body and the angulation between the head and neck influence the ease with which the horse can work “on the bit” (see Chapters 100 and 117). A horse’s ability to see is important. A horse with ocular abnormalities may exhibit bizarre behavioral abnormalities or unusual head and neck

CHAPTER 4

• Conformation and Lameness

19

X

Y

Z

Fig. 4-4 Diagrammatic depiction of assessing balance during conformation evaluation. Three circles (from left to right: forehand, midbody, hind quarters) are visualized and should overlap by approximately one third. Excessive overlapping of circles (short coupled) or barely overlapping of circles (long, weak in back) are common conformational abnormalities. Body length (X) should be equal to or slightly longer than withers height (Y), and withers height and rump height (Z) should be the same.

Horse with short, heavy neck; heavy, short, and straight shoulder; and withers set forward. This horse is prone to forelimb lameness and likely to have a short stride.

Fig. 4-5

Fig. 4-6 Unbalanced Appaloosa gelding that is long and weak in the barrel (back). The rump height is slightly higher than withers height.

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PART I

•

Diagnosis of Lameness undesirable. In STB pacers a good chest width is desirable, but in trotters a narrow chest is preferred (see Chapter 109). Rump length also is important in determining stride length, and a longer length of the rump is desirable. Many horses with long rumps have larger rump angles (flat croup) and those with short rumps have smaller rump angle (steep croup). Long, flat croup regions are desirable. The ideal horse should have a long gaskin (crus) and a short, strong metatarsal region (hocks close to the ground) to maximize stride length. The angles of the shoulder and rump are important factors in determining stride length and balance. Undesirable shoulder and rump angles often accompany other conformational faults and may predispose to lameness. The ideal angle of the shoulder (relative to the ground) has classically been determined as 45° (see Fig. 4-7). Horses with steep shoulder angles (>50° to 55°) usually have short shoulders and short, upright pasterns, which predispose to lower limb lameness. The forelimb pastern angle should be equal to the shoulder angle. Steep shoulder angle shifts the center of gravity forward, predisposing to forelimb lameness. Horses with a flat rump or croup generally have longer rump lengths and longer strides (Fig. 4-8). Horses with short, steep rumps (goose rump), often have short, choppy gaits, and many have hindlimb lameness (Fig. 4-9). A steep rump angle shifts the center of gravity caudally, predisposing to hindlimb lameness.

carriages, possibly misinterpreted as the result of pain. A rare cause of “being on a line” occurs in driving horses, such as a STB with unilateral blindness. The horse turns the head away from the blind side to see and thus is on the contralateral line (to straighten the head, the driver must pull on the contralateral line). This mimics a contralateral (to the blind eye) lameness.

Assessment of Lengths, Angles, and Heights Body length is important in determining stride length (see Fig. 4-4). Short coupled conformation predisposes horses to short strides and problems with interference, especially in racehorses. If horses are too long, they can be weak in the back. The length of the neck is important in assessing balance and should be proportional to the overall body length. Some horses have long, weak necks. The neck may be “set on low” relative to the shoulder with a depression (ventral deviation) of the dorsal topline cranial to the withers (ewe necked), giving the appearance of prominent withers laid too far caudally. Horses should have adequate depth in the girth region (depth of girth). Shoulder length (top of withers to the point of the shoulder) may be related directly to stride length, and horses with longer shoulders usually have longer strides (Fig. 4-7). Those with short shoulders usually have shorter strides (see Fig. 4-6). Shoulder length and shoulder angle often are related; long shoulders often are more sloping (smaller shoulder angle) and short shoulders often are straight. Good shoulder length appears to be important and desirable, but recent objective data from TB racehorses suggest that horses with long limbs may be at increased risk of lower limb lameness.14 In TBs particularly a long radius (forearm) and short, strong third metacarpal bone (McIII) are desirable for adequate strength and maximum stride length. Chest width should be commensurate with overall body size. A wide chest with a basenarrow (front feet close when evaluating the horse from the front) limb stance or a narrow chest with a base-wide stance are

Limbs It is critical to evaluate limb conformation with the horse standing squarely on a firm, flat surface and with an experienced handler who can make the horse cooperate. If the clinician observes a fault that may result from how the horse is standing, he or she should reevaluate the horse after repositioning. Horses often stand camped out, both behind and in front, simply as the result of improper positioning. The plumb line concept allows evaluation of each limb from the front or back and the side (Fig. 4-10). For example,

Rump length

Shoulder length

A

B

D Shoulder angle

Rump angle

C

Pastern angle

Stride length

E

Measurement of shoulder length (A), rump length (B), shoulder angle (C), and rump angle (D). The pastern angle (E) should be equal to the shoulder angle. Shoulder angle and length are important in determining stride length.

Fig. 4-7

CHAPTER 4 a vertical line from the point of the shoulder should bisect the limb. The clinician also should evaluate the horse while it is walking because some defects are dynamic. Horses that toe in or toe out, or those with fetlock or carpus varus deformities, may stand reasonably well, particularly with corrective trimming and shoeing, but the defect may be readily apparent while the horse is walking.

• Conformation and Lameness

21

the forelimbs lateral to the plumb line and generally are narrow in the chest, resulting in overload of the medial aspect of the lower limb, predisposing to lameness. Horses that are base wide, toed in tend to wing out or paddle during protraction (Figs. 4-11, B and 4-12, A). Winging out predisposes trotters to interference with the ipsilateral hindlimb. Base-wide, toed-out

FORELIMB CONFORMATION Front Perspective Several forelimb conformational abnormalities are apparent when evaluating a horse from the front. Base-wide conformation may occur alone or in combination with toed-in or toedout conditions (Fig. 4-11). Horses that are base wide stand with

Desirable hindlimb conformation. The flat rump angle and good rump length would likely increase stride length and allow good support and strength of the hindlimbs.

Fig. 4-8

A

B

Undesirable hindlimb conformation characterized by short, steep rump (goose rump), predisposing to hindlimb lameness.

Fig. 4-9

C

D

Fig. 4-10 Diagram demonstrating use of plumb lines to evaluate limb conformation from three perspectives. Vertical lines are visualized from the front (A) forelimb (line runs from point of the shoulder, bisecting the limb), side (B) forelimb (line bisects elbow joint, carpus, and fetlock joint and intersects the ground approximately 5 cm behind the solar surface of the heel), and side (C) hindlimb (line runs from point of rump to the ground, touching the point of the hock and plantar metatarsus and intersecting the ground approximately 7.5 to 10 cm behind the heel) and from the back (D) hindlimb (line drawn from point of rump, bisecting the hindlimb).

22

PART I

•

Diagnosis of Lameness

B

A

C

Three variations of base-wide forelimb conformation, including (A) simple base wide, (B) base wide, toed in, and (C) base wide, toed out.

Fig. 4-11

RF

LF

RF

LF

B

A

MIDLINE

MIDLINE

A, Toed-in conformation often causes horses to wing out or paddle during advancement of the forelimb. B, Toed-out conformation causes horses to wing in, predisposing to interference with the contralateral forelimb.

Fig. 4-12

conformation appears most often in horses with uncorrected carpus valgus deformities (Figs. 4-11, C and 4-12, B) and results in excessive loading on the medial aspect of the foot and misshapen feet. Interference with the contralateral forelimb may occur in severely affected horses. Base-narrow conformation may occur alone or in combination with toed-in or toed-out conformation (Fig. 4-13). Horses that are base narrow stand with the forelimbs inside the plumb line and overload the outside of the lower limb and foot. Horses that are base narrow, toed in tend to wing out, and those that are base narrow, toed out tend to wing in during protraction (see Figs. 4-12 and 4-13).

With in-at-the-knee, knock-kneed, or carpus valgus conformation (Fig. 4-14) the carpi are medial to the plumb line, creating an angular deformity and concentrating the weight of the horse on the medial aspect of the carpus and proximal metacarpal region. This condition, if severe, may predispose the horse to carpal lameness and splints. In some horses, particularly foals, carpus valgus may be accompanied by external rotation of the entire limb or just the distal aspect (toed out). Severely affected horses wear the inside aspect of the hoof or shoe abnormally. Out-at-the-knee (bow-legged, bandy-legged) conformation usually is a consequence of early carpus varus and often is career

CHAPTER 4

A

B

• Conformation and Lameness

23

C

Fig. 4-13 Three variations of base-narrow forelimb conformation including (A) simple base narrow, (B) base narrow, toed in, and (C) base narrow, toed out.

Fig. 4-14 A horse with in-at-the-knee conformation that is worse in the right forelimb. limiting, particularly if the fault is pronounced (Fig. 4-15). The carpus is bowed outward, lateral to the plumb line. Many horses are also toed in, accentuating abnormal forces on the lateral aspect of the entire distal forelimb, predisposing to osteoarthritis of the carpus or fetlock or lateral suspensory branch desmitis and sesamoiditis. In most foals with this deformity, lateral deviation of the elbow usually is present. Correction is difficult. Offset or bench-knee conformation is classically defined as lateral positioning of the metacarpal region relative to the central axis of the radius (Fig. 4-16). However, radiographs demonstrate that the actual displacement usually is at the antebrachiocarpal joint. Displacement may be unilateral or

Two-year-old Thoroughbred filly with moderate to severe carpus varus (out-at-the-knee) conformation in the left forelimb and mild deformity in the right forelimb. The filly also is toed in, a common finding in horses with this type of conformation. Another common finding is lateral deviation or bowing of the elbow, prompting clinical suspicion that a deformity also exists at this joint.

Fig. 4-15

bilateral with differing degrees of severity on each side. This conformation often is associated with carpal or metacarpal lameness (Fig. 4-17). Many 2-year-old STBs with offset knees are precocious during early training but often develop carpal lameness at 3 or 4 years of age. TBs with offset knees are believed to perform better on the soft turf tracks in Europe, as opposed to the firm turf or dirt tracks in the United States.

24

PART I

•

Diagnosis of Lameness

Fig. 4-16 Standard Thoroughbred with a prominently offset (bench) knee in the left forelimb. An apparent lateral deviation or shifting (offset) of the cannon bone and distal extremity occurs relative to the plumb line dropped through the left radius.

Fig. 4-17

Toed-in conformation, or internal rotation of the distal extremity, exists alone or in combination with abnormalities of stance (base-narrow or base-wide), other conformational faults such as carpus varus, and being wide in the chest (see Fig. 4-15). Horses that are toed in usually wing out (paddle) (see Fig. 4-12). Toed-in conformation is particularly undesirable in a trotter because of potential interference at speed. Toed-in conformation predisposes horses to lateral splints, lameness of the lateral aspect of the fetlock joint region (e.g., lateral branch suspensory desmitis), and osteoarthritis of the interphalangeal joints. Horses that are toed in wear the outside aspect of the foot. Toed-out conformation, or external rotation of the distal extremity, is common and if mild may be considered normal or inconsequential (Fig. 4-18). Mild toed-out conformation appears in 50% of STBs and is common behind in STBs and WBLs.9,11 It first develops in foals and, if pronounced, persists in the mature horse. In foals, toed-out conformation often accompanies carpus valgus deformities but may result from external rotation primarily from the fetlock down but, in more severe deformities, from further proximally (Fig. 4-19). Mild toed-out conformation usually resolves as a foal matures and with corrective trimming. Toed-out conformation results in abnormal wear on the inside aspect of the foot. Horses tend to wing in; if winging in is severe, particularly if accompanied by base-narrow conformation, it may interfere with the opposite forelimb (see Fig. 4-12). Exostoses (splints) on the second metacarpal bone (McII) or McIII may develop, requiring protective boots to be worn during exercise. In STBs, interference injury occurs as high as the distal radius.

Lateral Perspective

Dorsopalmar xeroradiograph of 3-year-old STB colt with longitudinal fracture of the third metacarpal bone (small arrow). Medial is to the right. The lateral displacement (“step”) at the antebrachiocarpal joint (large arrow) gives the clinical appearance of an offset (bench) knee.

Horses camped out in front stand consistently with the entire forelimb ahead of the plumb line, but this conformation usually is a temporary problem with the horse’s stance and can be corrected by repositioning the horse, or it reflects pain caused by laminitis, for example. Camped under in front is unusual and usually also results from temporary malpositioning of the horse (Fig. 4-20). If a horse prefers to stand camped under and is otherwise sound, however, this trait may be a sign of “extreme speed.” Back-at-the-knee or calf-knee (sheep-knee) conformation describes a concave dorsal aspect of the limb, with the carpus behind the plumb line (Figs. 4-21 to 4-23). On radiographs of a normal carpus the proximal and distal rows of carpal bones are aligned in a proximal to distal direction, and the dorsal faces of these bones are parallel to the radius and McIII (Fig. 4-22, A). With back-at-the-knee conformation the proximal row of carpal bones is set back (Fig. 4-22, B). Horses that stand back at the knee are considered predisposed to carpal injuries because of the natural tendency of the carpus to hyperextend (larger carpal angle) during fatigue. In my experience, TB racehorses are particularly at risk, despite limited contrary evidence (see page 16).13 In the STB, mild calf-knee conformation is common in pacers and acceptable, whereas in the trotter this defect is undesirable. In other breeds, mild calf-knee conformation may not directly lead to lameness. In young horses with lameness from unrelated sources such as osteochondrosis or fracture of the distal phalanx, back-at-the-knee conformation and clubfoot (small, upright foot) may accompany flexural deformity

CHAPTER 4

A

• Conformation and Lameness

25

B

Fig. 4-18

Trotter showing inconsequential mild toed-out conformation. Toe weights often are used in trotters to balance gait and correct interference.

Fig. 4-20

Fig. 4-19 Thoroughbred foal with pronounced external rotation or toed-out left forelimb limb conformation. The deformity involves the entire limb, beginning well above the carpus.

Fig. 4-21

of the limb (see Fig. 4-23). This deformity is a combination of contraction (clubfoot) and laxity (calf knee) caused by chronic lameness and partial weight bearing and warrants a guarded prognosis. Over-at-the-knee, bucked-knee (knee-sprung), or hangingknee conformation describes a convex dorsal surface of the carpus, with the carpus in front of the plumb line (Fig. 4-24). In young, untrained horses, bucked-knee conformation may be a predictor of lameness, but in mature horses it appears to be an acquired characteristic and occurs primarily in horses that jump. Older cross-country horses, steeplechasers, jumpers, or

field hunters are prone to buck knee and often stand over at the knee with no obvious lameness. These horses may exhibit a tendency to buck forward to such an extent that they appear on the verge of collapse or prone to stumbling yet show good stability. Tied in below the knee (Fig. 4-25) describes a distinct notch just distal to the accessory carpal bone on the palmar aspect of the limb. Normally, McIII and the flexor tendons are in parallel alignment from the accessory carpal bone to the proximal sesamoid bones. With tied-in conformation the flexor tendons appear to enter the carpus in a dorsoproximal direction. If the horse also is bucked kneed, the tied-in appearance

Diagram showing (A) camped-out in front and (B) camped-under in front conformation, both in relation to plumb lines.

Thoroughbred yearling with back-at-the-knee (calfknee) conformation most noticeable in the left forelimb. This conformational fault is undesirable, particularly in racing breeds.

26

PART I

•

Diagnosis of Lameness

A

B

Fig. 4-22 Lateromedial radiographs of two different horses with carpal lameness. A, In a horse with nondisplaced slab fracture of the third carpal bone, normal carpal conformation is present: the proximal and distal rows of carpal bones are aligned and parallel to the radius and third metacarpal bone. B, In a horse with distal, lateral radius chip fracture, there is palmar deviation of the proximal row of carpal bones. This radiographic appearance is typical of back-at-the-knee conformation. is accentuated. Young horses are prone to superficial flexor tendonitis. In STBs this defect is worse for a pacer than a trotter. The junction of the carpus and McIII should be flat. Cut out under knee describes a notch under the dorsal surface of the carpus (see Fig. 4-25). In horses with this defect, McIII appears thin (dorsopalmar direction) and weak. Horses with this conformational abnormality also are often back at the knee, predisposing them to carpal and metacarpal problems. Some young racehorses, typically late yearlings or early 2-year-olds in training, appear to have distention of the middle carpal joint capsule or an unusually prominent distal radial epiphysis. These findings give the impression of an unusually large gap between these structures, described as open at the knee. I have not seen a correlation between this clinical observation and obvious radiographic changes, although in young horses with this conformation the distal radial physis remains visible. Whether this conformation is relevant to lameness in young racehorses is debatable. Over-at-the-fetlock usually is seen in young horses with flexor deformity of this joint (see Chapter 61). This conformational fault may persist in a mature horse, causing upright pasterns or knuckling of the fetlock joint. In some horses this condition causes a progressive, permanent deformity and severe lameness, whereas in others a dynamic, intermittent

knuckling occurs and some of these horses remain surprisingly sound. Knuckling also may be a sequel to desmitis of the accessory ligament of the deep digital flexor tendon.

HINDLIMB CONFORMATION Lateral Perspective Hindlimb conformational faults generally are less numerous and problematic than those in the forelimb because of differences in weight distribution and center of gravity. Plumb lines also are useful in evaluating conformation of the hindlimb with the horse standing squarely, loading all limbs (see Fig. 4-10). Camped-out conformation is unusual and generally results from faulty positioning of the horse during the examination. Horses that are truly camped out usually have short strides and poor athletic ability. Camped under behind often is associated with sickle-hocked conformation but also appears in horses that are straight behind (Fig. 4-26). Horses with this type of conformation often have short, choppy strides (Fig. 4-27). A particularly severe conformational fault that leads directly to lameness is straight behind, otherwise called straight hocks or post (posty) leg. Horses that are straight behind have larger stifle and hock angles but smaller fetlock joint angles compared

CHAPTER 4

• Conformation and Lameness

27

Fig. 4-24 Older horse without obvious lameness with over-atthe-knee (bucked-knee) conformation.

Clydesdale yearling with calf-knee conformation and clubfoot secondary to osteochondrosis of the shoulder joint. This conformation is primarily the result of chronic lameness, decreased weight bearing, and the development of a flexural deformity.

Fig. 4-23

with ideal hindlimb conformation (see Fig. 4-26; Fig. 4-28). Straight behind, sickle-hocked, and in-at-the-hock conformation are the three most important hindlimb conformational faults and all may lead directly to lameness. Horses that are straight behind often develop upward fixation of the patella, a condition seen most often in WBLs. Suspensory desmitis and fetlock osteoarthritis also occur frequently. Horses with normal initial hindlimb conformation may become straight behind if they develop severe suspensory desmitis and lose support of the fetlock joint. Sickle-hocked conformation is one of the most common conformational faults, and it leads directly to lameness of the tarsus and plantar soft tissues. Horses that are sickle-hocked stand with the lower hindlimb well ahead of the plumb line, with an exaggerated concave dorsal surface of the hindlimb (resembling a sickle), creating a smaller than normal hock angle (see Fig. 4-26; Fig. 4-29). This type of conformation is often called curby conformation because horses frequently develop curbs (see Chapter 79). Sickle-hocked conformation concentrates load in the distal, plantar aspect of the hock, predisposing to curb and to distal hock joint pain. In foals with incomplete or delayed ossification of the tarsal bones, marked sickle-hocked conformation may occur (see Chapter 45). Sickle-hocked conformation is undesirable, particularly in racing breeds, but if mild is not detrimental. In STB pacers, some prefer a mild degree of sickle-hocked conformation because horses can extend the hindlimbs farther forward without risk of interference. In STB trotters the condition

a A

B

b

A, Diagrammatic representation of tied in below the knee. The dorsal-palmar length of a is less than b, giving the appearance that the flexor tendons run obliquely, proximally to enter the distal carpal region more dorsal than expected. B, A horse that is cut out under the knee has a concave appearance of the dorsal aspect of the distal carpus and proximal metacarpal region.

Fig. 4-25

28

PART I

•

A

Diagnosis of Lameness

B

C

D

Diagrammatic representation of conformational faults of the hindlimb from the lateral perspective. Compared with ideal conformation, horses with sickle-hocked conformation (A) have a concave dorsal surface of the limb with the distal extremity dorsal to the plumb line, but those that are straight behind (B) have large stifle and hock joint angles but smaller fetlock joint angles. Horses that are camped under (C) often are sickle-hocked as well. Camped-out conformation (D) is unusual and most often results from faulty positioning of the horse.

Fig. 4-26

Horse with camped-under and mild sickle-hocked conformation, a combination leading to a short, choppy gait.

Fig. 4-27

Standardbred filly with straight hindlimb conformation and suspensory desmitis.

Fig. 4-28

CHAPTER 4

• Conformation and Lameness

29

often predisposes to distal hock joint pain and curb, but these horses tend to be fast, although unsound. In Western reining horses, sickle-hocked horses may be able to slide better.

Rear Perspective A majority of STB and WBL horses toe out behind, which should be considered normal. Horses with mild external rotation of the distal extremity are called toed out and usually also have external rotation of hocks, causing the points of the hocks to be closer than normal. This fault is called cow-hocked conformation and is a rotational change of the hindlimb (Fig. 4-30). Cow-hocked conformation occurs in combination with basewide or base-narrow deformities or independently. Cow-hocked and base-narrow conformation is most common. Base-wide and base-narrow conformation may occur without cow-hocked conformation. These conformational faults seldom lead to lameness but have a substantial effect on gait in some horses. Horses that are base narrow travel close behind, particularly at a walk. Some travel close at a trot, pace, or gallop, whereas others seem to widen out when going faster, thus avoiding interference. Those that travel close at speed often interfere, causing injury to the medial aspect of the contralateral hindlimb. Bow-legged hindlimb conformation, in which the point of both hocks is truly outside the plumb line, is uncommon (see Fig. 4-30). Occasionally horses that are base-narrow appear to be bow-legged. Unilateral bow-legged conformation occurs in foals born with windswept deformity or in those with tarsus varus deformity. Bilateral tarsus varus deformity is unusual. In-at-the-hock or tarsus valgus is an angular deformity (Fig. 4-31). The deformity can be corrected in foals. If it persists in a mature horse, particularly a racehorse with other conformational abnormalities, such as sickle-hocks, abnormal forces or load occur in the tarsal region, predisposing the horse to distal hock joint pain, curb, and proximal metatarsal lameness. Horses can be toed in or toed out behind, but in general the conformational abnormality starts above the fetlock joint, causing the lower limb abnormality to be linked with the upper limb. Thus a horse that is toed in generally is bow-legged, and one that is toed out is cow hocked. In some foals, however,

Fig. 4-29 This 4-year-old Standardbred has sickle-hocked conformation and has developed curb, which has been treated by freeze-firing, resulting in white marks on the plantar aspect of the hock.

A

B

C

D

Fig. 4-30 Hindlimb conformational abnormalities viewed from the rear. A, Cow-hocked conformation is a common fault characterized by external rotation of the limb, usually without angular deformity, causing the hocks to be too close together. Mild external rotation of the hindlimbs is common and does not appear to cause lameness. B, Cow-hock, base-narrow conformation. C, Base-narrow conformation. D, Base-wide conformation is uncommon. E, Bow-legged conformation is uncommon and undesirable.

E

30

•

PART I

Diagnosis of Lameness fetlock varus occurs independent of upper limb conformational abnormalities. This abnormality usually appears in windswept foals in which upper limb deformities have resolved, leaving a fetlock varus. This is an angular deformity, but with abnormal hoof wear, toed-in conformation can develop. Fetlock varus and the resulting toed-in conformational defect may cause osteoarthritis of the fetlock and interphalangeal joints and can be career limiting.

CONFORMATION OF THE DIGIT

Mature Standardbred racehorse with in-at-the-hock (tarsus valgus) conformation. This conformational abnormality is characterized by an angular deformity as opposed to the rotational deformity seen in cow-hocked conformation. The characteristic white marks were produced by cryotherapy for treatment of bilateral curb.

Fig. 4-31

A

B

More detailed aspects of conformation of the foot and limb flight characteristics are discussed in Chapters 5 and 7. Many of the changes in hoof growth or conformational changes in the hoof are the result of wear, shoeing, and exercise demands of training and performance and often are not present in a young horse. The pastern angle is usually similar to the angle of the shoulder (see Fig. 4-7). The pastern foot axis should be straight. The pastern should be neither excessively sloped (low angle) nor upright (high angle). The angle of the pastern is important in determining the amount of load on the lower limb structures. In general, the more upright the pastern (steeper pastern angle), the shorter the stride and vice versa. Horses with upright pasterns appear to be prone to foot lameness and perhaps superficial digital flexor tendonitis. Those with long, sloping pasterns may be at risk to develop osteoarthritis of the fetlock joint and proximal phalangeal fractures. Horses with short, upright pasterns but relatively normal hoof angles have a broken foot-pastern axis—the foot axis is lower than the pastern axis— and are at risk of developing foot lameness (Fig. 4-32). If the pastern axis is lower than the foot axis, called coon footed, it causes undue strain on the soft tissue structures supporting the fetlock joint. This type of conformation may result from severe suspensory desmitis and loss of support of the fetlock joint. Pastern length is important and usually is related to pastern angle. Horses with long pasterns commonly have more slope or lower pastern angles. The plumb line should drop approximately 5 cm behind the heel in a well-conformed horse. In horses with long, sloping, and weak pasterns, the line drops more than 5 cm behind the heel. Those with short pasterns usually have more upright pasterns, and the plumb line drops

C

Diagrammatic representation of ideal pastern and foot conformation and the concept of a broken pastern-foot axis. Ideally the foot and pastern angles (A) should be identical to allow full and even weight bearing on all aspects of the foot. A broken foot axis (B) occurs when pastern angle is more upright than that of the foot or vice versa (C). In both latter situations, uneven load distribution on the foot or soft tissue structures may cause lameness.

Fig. 4-32

• Observation: Symmetry and Posture

CHAPTER 5 through the foot. A variety of pastern lengths and angles occur, but the pastern length should be in proportion to the overall length of the limb. Viewed from the front, the plumb line may divide the pastern and foot asymmetrically with more pastern and foot laterally, which often is associated with some degree of distortion of the hoof capsule, with a steeper medial wall and some flaring laterally. This results in asymmetrical loading of the distal limb joints and may predispose to lameness. Buttress foot is an acquired firm bulge or swelling at and proximal to the dorsal aspect of the coronary band and usually reflects osteoarthritis of the distal interphalangeal joint.

7. 8. 9.

10.

REFERENCES 1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins Press. 2. Adams OR: Veterinary notes on lameness and shoeing of horses, Ft. Collins, Colo, 1957, Colorado State University. 3. Belloy E, Bathe AP: The importance of standardising the evaluation of conformation in the horse, Equine Vet J 28:429, 1996. 4. Mawdsley A, Kelly EP, Smith FH, et al: Linear assessment of the Thoroughbred horse: an approach to conformation evaluation, Equine Vet J 28:461, 1996. 5. Delahunty D, Webb S, Kelly EP, et al: Intermandibular width and cannon bone length in “winners” versus “others,” J Equine Vet Sci 11:258, 1991. 6. Hunt WF, Thomas VG, Stiefel W: Analysis of videorecorded images to determine linear and angular

CHAPTER •

11.

12.

13. 14.

31

dimensions in the growing horse, Equine Vet J 31:402, 1999. Clayton HM: Advances in motion analysis, Vet Clin North Am 7:365, 1991. Leach DH, Dyson S: Instant centres of rotation of equine limb joints and their relationship to standard skin marker locations, Equine Vet J Suppl 6:113, 1988. Holmström M, Magnusson L-E, Philipsson J: Variation in conformation of Swedish Warmblood horses and conformational characteristics of élite sport horses, Equine Vet J 22:186, 1990. Magnusson L-E: Studies on the conformation and related traits of Standardbred trotters in Sweden. I. An objective method for measuring the equine conformation, master’s thesis, Skara, Sweden, 1985, Sveriges Lantbruks Universitet. Magnusson L-E, Thafvelin B: Studies on the conformation and related traits of Standardbred trotters in Sweden. II. The variation in conformation of the Standardbred trotter, master’s thesis, Skara, Sweden, 1985, Sveriges Lantbruks Universitet. Magnusson L-E, Thafvelin B: Studies on the conformation and related traits of Standardbred trotters in Sweden. IV. Relationship between the conformation and soundness of four-year-old Standardbred trotter, master’s thesis, Skara, Sweden, 1985, Sveriges Lantbruks Universitet. Barr ARS: Carpal conformation in relation to carpal chip fracture, Vet Rec 134:646, 1994. Anderson TM, McIlwraith CW: Conformation and lameness. In Proceedings. 27th Ann Surg Forum Am Coll Vet Surg 181, 1999.

5

Observation: Symmetry and Posture Mike W. Ross

ssessments of symmetry and posture are important aspects of a lameness examination. Comparison between the normal and abnormal sides facilitates identification of abnormalities, unless the condition is bilateral so that no recognizable differences exist between the left and right limbs. The horse should be standing squarely on a flat surface in a quiet, insect-free environment. Horses with severe lameness often are reluctant to stand correctly, but information gained about symmetry and posture of severely lame horses is valuable. The veterinarian should look carefully at size, shape, contour, heights, and widths, and compare with the opposite side.

A

FORELIMB SYMMETRY Muscle Atrophy The symmetry of skeletal muscle in the forearm, pectoral, and cervical areas should be assessed. Muscle atrophy that occurs in horses with chronic lameness conditions is called disuse atrophy and in those with neurological disease is called

neurogenic atrophy. Horses with muscle atrophy and lower motor neuron disease (see Chapter 11) may be lame, sometimes the result of muscle pain or nerve root pain, complicating differentiation between these causes of muscle atrophy. In most but not all horses with neurogenic atrophy, other clinical signs suggestive of neurological disease may be present. Horses with disuse atrophy resulting from chronic lameness usually have generalized atrophy of the ipsilateral forelimb. Muscle loss usually is not pronounced but involves the forearm (extensors are most commonly affected), triceps, and shoulder muscles. Shoulder muscle atrophy involving the infraspinatus and supraspinatus muscles generally is not pronounced, and lateral subluxation of the shoulder joint during weight bearing is not present (see Chapter 41). Development of disuse atrophy resulting from chronic lameness generally takes weeks to months unless severe lameness exists. In horses with severe or non–weight-bearing lameness, atrophy may develop within 10 to 14 days. In horses with severe forelimb lameness, carpal contraction (flexor deformity of the carpus) may occur simultaneously with muscle atrophy. The most common cause of carpal contraction because of

• Observation: Symmetry and Posture

CHAPTER 5 through the foot. A variety of pastern lengths and angles occur, but the pastern length should be in proportion to the overall length of the limb. Viewed from the front, the plumb line may divide the pastern and foot asymmetrically with more pastern and foot laterally, which often is associated with some degree of distortion of the hoof capsule, with a steeper medial wall and some flaring laterally. This results in asymmetrical loading of the distal limb joints and may predispose to lameness. Buttress foot is an acquired firm bulge or swelling at and proximal to the dorsal aspect of the coronary band and usually reflects osteoarthritis of the distal interphalangeal joint.

7. 8. 9.

10.

REFERENCES 1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins Press. 2. Adams OR: Veterinary notes on lameness and shoeing of horses, Ft. Collins, Colo, 1957, Colorado State University. 3. Belloy E, Bathe AP: The importance of standardising the evaluation of conformation in the horse, Equine Vet J 28:429, 1996. 4. Mawdsley A, Kelly EP, Smith FH, et al: Linear assessment of the Thoroughbred horse: an approach to conformation evaluation, Equine Vet J 28:461, 1996. 5. Delahunty D, Webb S, Kelly EP, et al: Intermandibular width and cannon bone length in “winners” versus “others,” J Equine Vet Sci 11:258, 1991. 6. Hunt WF, Thomas VG, Stiefel W: Analysis of videorecorded images to determine linear and angular

CHAPTER •

11.

12.

13. 14.

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dimensions in the growing horse, Equine Vet J 31:402, 1999. Clayton HM: Advances in motion analysis, Vet Clin North Am 7:365, 1991. Leach DH, Dyson S: Instant centres of rotation of equine limb joints and their relationship to standard skin marker locations, Equine Vet J Suppl 6:113, 1988. Holmström M, Magnusson L-E, Philipsson J: Variation in conformation of Swedish Warmblood horses and conformational characteristics of élite sport horses, Equine Vet J 22:186, 1990. Magnusson L-E: Studies on the conformation and related traits of Standardbred trotters in Sweden. I. An objective method for measuring the equine conformation, master’s thesis, Skara, Sweden, 1985, Sveriges Lantbruks Universitet. Magnusson L-E, Thafvelin B: Studies on the conformation and related traits of Standardbred trotters in Sweden. II. The variation in conformation of the Standardbred trotter, master’s thesis, Skara, Sweden, 1985, Sveriges Lantbruks Universitet. Magnusson L-E, Thafvelin B: Studies on the conformation and related traits of Standardbred trotters in Sweden. IV. Relationship between the conformation and soundness of four-year-old Standardbred trotter, master’s thesis, Skara, Sweden, 1985, Sveriges Lantbruks Universitet. Barr ARS: Carpal conformation in relation to carpal chip fracture, Vet Rec 134:646, 1994. Anderson TM, McIlwraith CW: Conformation and lameness. In Proceedings. 27th Ann Surg Forum Am Coll Vet Surg 181, 1999.

5

Observation: Symmetry and Posture Mike W. Ross

ssessments of symmetry and posture are important aspects of a lameness examination. Comparison between the normal and abnormal sides facilitates identification of abnormalities, unless the condition is bilateral so that no recognizable differences exist between the left and right limbs. The horse should be standing squarely on a flat surface in a quiet, insect-free environment. Horses with severe lameness often are reluctant to stand correctly, but information gained about symmetry and posture of severely lame horses is valuable. The veterinarian should look carefully at size, shape, contour, heights, and widths, and compare with the opposite side.

A

FORELIMB SYMMETRY Muscle Atrophy The symmetry of skeletal muscle in the forearm, pectoral, and cervical areas should be assessed. Muscle atrophy that occurs in horses with chronic lameness conditions is called disuse atrophy and in those with neurological disease is called

neurogenic atrophy. Horses with muscle atrophy and lower motor neuron disease (see Chapter 11) may be lame, sometimes the result of muscle pain or nerve root pain, complicating differentiation between these causes of muscle atrophy. In most but not all horses with neurogenic atrophy, other clinical signs suggestive of neurological disease may be present. Horses with disuse atrophy resulting from chronic lameness usually have generalized atrophy of the ipsilateral forelimb. Muscle loss usually is not pronounced but involves the forearm (extensors are most commonly affected), triceps, and shoulder muscles. Shoulder muscle atrophy involving the infraspinatus and supraspinatus muscles generally is not pronounced, and lateral subluxation of the shoulder joint during weight bearing is not present (see Chapter 41). Development of disuse atrophy resulting from chronic lameness generally takes weeks to months unless severe lameness exists. In horses with severe or non–weight-bearing lameness, atrophy may develop within 10 to 14 days. In horses with severe forelimb lameness, carpal contraction (flexor deformity of the carpus) may occur simultaneously with muscle atrophy. The most common cause of carpal contraction because of

32

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Diagnosis of Lameness

ipsilateral forelimb lameness is olecranon process fracture or other elbow lameness, but carpal contraction may occur in horses with severe shoulder or even lower limb lameness. Atrophy of the triceps muscles usually is recognized before other muscle atrophy in severely lame horses. Horses with neurogenic atrophy may have profound atrophy of one or more muscles in the forearm, pectoral, or cervical regions. Atrophy often is much more pronounced than expected based on the degree of lameness, prompting suspicion of neurological disease. Pronounced, unilateral pectoral or triceps atrophy with mild atrophy of the forearm muscles suggests neurological disease. Severe atrophy localized to the infraspinatus or supraspinatus muscles without subluxation of the shoulder joint usually results from injury of the suprascapular nerve caused by external trauma. Atrophy and subluxation of the shoulder joint is associated with injury of the brachial plexus or nerve roots. Other muscles may also show atrophy. Localized muscle atrophy or fibrosis occurs in horses with previous injury and subsequent scar tissue formation within muscle bellies. This condition is more common in the hindlimb, but occasionally occurs in the forelimb.

formation and accompanies a myriad of problems in the distal extremities. Bony changes may be active, causing the current lameness problem, or old and inactive, causing few or no clinical signs. For example, old inactive bony swelling of the shin or osselets (bony and fibrous swelling of the fetlock joint) may be prominent in ex-racehorses but have little to no relevance to current lameness.

Foot Size Ideally both front feet should be identical in size and shape, or nearly so, and any asymmetry should be noted. Horses with chronic lameness may have disparity in foot size, usually with the smaller foot being ipsilateral to lameness. The small foot often is contracted and more upright (Fig. 5-1). Chronic reduction in weight bearing results in foot size disparity in some, but not all, horses. Mild disparity in foot size is a normal finding in some horses. Mild clubfoot conformation, acquired from previous flexor deformity, may be present incidentally in adult horses. Previous lameness may have caused contraction of the foot but has since resolved, resulting in disparity in foot

Swelling Swelling, a common sign of inflammation, often causes asymmetry. Swelling within a joint capsule caused by excess joint fluid, effusion, is a general reaction of the joint to several traumatic or degenerative processes. Edema, cellulitis (lymphangitis), bleeding, fibrosis, and bony enlargement can cause soft tissue swelling. Edema usually signals acute inflammation and pits (a distinct impression is visible) when compressed by digital palpation (pitting edema). Horses develop edema around and often distal to the site of inflammation. In some horses, especially racehorses left unbandaged when accustomed to being bandaged, benign mild to moderate edema of the distal extremities develops. This process is called “stocking-up” and should not be misinterpreted as a pathological process. In these horses the edematous area is not painful and usually does not pit, and the horse is not lame. Cellulitis describes infection within the tissue planes of the distal extremities (see Chapter 14) and is sometimes called lymphangitis. Lymphangitis, by definition, is inflammation of the lymphatic circulation of the limb, but the conditions are similar and the terms are used interchangeably. Swelling is firm, warm, and painful, and lameness is often pronounced. “Stove-pipe” swelling describes this condition (“the horse is all stoved-up”). Horses generally show systemic signs such as fever and elevated white blood cell count. This condition usually results from small puncture wounds that may be difficult to discover or occurs after articular, periarticular, or subcutaneous injections. Infection develops in subcutaneous tissues or deeper in the dense fascial planes and can be difficult to eradicate. Blunt trauma or fractures may cause bleeding within tissue planes. Severe lameness and swelling accompany fractures of the scapula and humerus, because large vessels are nearby. Bleeding may be severe and cause a decrease in plasma protein and packed blood cell volume values. In horses with fractures located more distal in the limb, swelling is less pronounced but still prominent. The most likely location of injury is the swollen area, but swelling may occur distal to the site of injury because of venous and lymphatic congestion. Fibrosis or scar tissue formation as the result of previous cellulitis or trauma causes asymmetry of the distal extremities but may not be the source of the current lameness. The veterinarian should avoid overinterpreting areas of scar tissue formation unless evidence of recrudescent inflammation exists. Horses may have scars caused by previous application of counterirritants or from healed wounds, leaving large, painless, and thus benign blemishes. Bony swelling is a common cause of asymmetry. Proliferative change results in periosteal or periarticular new bone

A

B

A horse with disparity in front foot size caused by chronic lameness. The right forelimb foot is smaller compared with the normal left forelimb foot when viewed from the front (A) and more upright when viewed from the side (B).

Fig. 5-1

CHAPTER 5 size and shape but no residual lameness. Clubfoot conformation appears to be better tolerated in Thoroughbred (TB) than in Standardbred (STB) racehorses.

Fetlock Height Fetlock position should be assessed in the standing horse and during movement. In a standing horse, fetlock height should be symmetrical, assuming the horse is loading the limbs equally. Horses with severe lameness commonly “point” or hold the limb in front of the opposite forelimb, thus taking weight off the limb. This standing posture obviously causes disparity in fetlock height but should be carefully interpreted. Loss of support of a fetlock in the standing horse causes the affected fetlock to drop and occurs most commonly with acute, traumatic disruption of the suspensory apparatus in racehorses but also appears with chronic, active desmitis (Fig. 5-2). Severe superficial digital flexor (SDF) tendonitis or lacerations resulting in fiber damage of the deep or superficial digital flexor tendons can cause similar clinical signs. In horses with mild flexor deformity of the metacarpophalangeal joint, dynamic knuckling (buckling forward, flexion) of the fetlock joint may occur in the standing position (Fig. 5-3). Joint position usually returns to normal during movement. In horses with severe flexor deformity, normal fetlock position is never achieved. Knuckling of the fetlock also may result from desmitis of the accessory ligament of the deep digital flexor tendon.

Scapular Height Disparity in scapular height is a rare clinical sign in a lame horse. The veterinarian must stand behind and above the horse to observe scapular height. The horse’s mane may obscure

A Standardbred racehorse with severe suspensory desmitis and a “dropped fetlock.” The level of the right forelimb fetlock joint is lower than the left forelimb, caused by chronic, severe desmitis. Similar clinical signs and severe lameness appear in horses with acute traumatic disruption of the suspensory apparatus.

Fig. 5-2

• Observation: Symmetry and Posture

33

observation from a distance, requiring closer examination by palpation. Traumatic or neurological conditions affect scapular height, causing either injury or dysfunction of the serratus ventralis muscle, respectively. With both conditions the dorsal aspect of the scapula is higher on the affected side. The veterinarian may place pieces of white tape or other suitable markers on both sides of the horse and stand back to compare height or may use two assistants to point to the locations.

HINDLIMB SYMMETRY Muscle Atrophy Asymmetry of bone and muscle mass in the hindlimbs and pelvis is a common clinical sign but must be differentiated carefully. The horse should stand squarely on a flat, even surface. The clinician must determine whether asymmetry exists, and if so, if the problem involves muscle, bone, or a combination of the tissues. Muscle atrophy is most common and, if unilateral muscle atrophy exists, easily can be confused with bony asymmetry caused by pelvic fractures or sacroiliac asymmetry. Disuse and neurogenic muscle atrophy occur in the hindlimb. Horses with chronic hindlimb lameness develop ipsilateral gluteal muscle atrophy, but asymmetry may be subtle. Mild muscle atrophy usually first appears just lateral to the tuber sacrale. The veterinarian should differentiate muscle atrophy from disparity in height of the tubera sacrale (Fig. 5-4). Recognition of muscle atrophy helps determine the lame leg and provides some information about the duration of the problem. Severe muscle atrophy develops in horses with long-standing, severe lameness or in those with neurological disease (Fig. 5-5). In horses with neurogenic atrophy of the gluteal muscles the degree of muscle loss is inappropriately severe compared

Fig. 5-3 Knuckling forward of the right front fetlock joint occurs in a standing position in this horse with mild flexor deformity of the metacarpophalangeal joint. This dynamic instability abates somewhat when the horse moves, but the left front fetlock also is straight, indicating the presence of bilateral flexor deformity.

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Diagnosis of Lameness

Three-year-old Thoroughbred filly with subtle disparity in tuber sacrale height. The left tuber sacrale is slightly lower (arrow) than the right, caused by a fracture at the base of the tuber sacrale. This clinical finding can easily be missed or confused with mild muscle atrophy.

Fig. 5-4

Fig. 5-6 A Thoroughbred broodmare with severe lameness and swelling of the left thigh caused by a comminuted femoral fracture. Selective atrophy of individual muscles or muscle groups occurs in horses with neurological disease or injuries causing focal muscle loss and scarring. Horses with trauma involving fracture of the tubera ischii may develop focal muscle loss of the semitendinosus or semimembranosus muscles. A depression resulting from localized muscle atrophy replaces initial swelling of the point of the rump. Horses with fibrotic myopathy, which in most horses is believed to result from injury and scarring of the semitendinosus muscle, usually have palpable scars or defects of the caudal thigh muscles. Degenerative neuropathy of the nerves supplying the distal aspect of the semitendinosus muscle also may cause fibrotic myopathy1 (see Chapter 49).

Swelling

A 4-year-old Standardbred with severe left gluteal atrophy caused by neurological disease. The presumptive clinical diagnosis was equine protozoal myelitis.

Fig. 5-5

with observed lameness. Neurological signs such as weakness and proprioceptive deficits usually appear in horses with neurogenic atrophy, but early in the course of diseases such as equine protozoal myelitis (EPM) the only observable signs may be muscle atrophy and mild lameness.

Swelling is especially important in horses with acute, severe lameness when the clinician must differentiate between catastrophic injury, such as pelvic or long bone fracture, and more common conditions, such as cellulitis. Horses with pelvic fractures may develop mild swelling in the thigh, but swelling is not prominent in most horses. In horses with fracture of the tuber coxae or ilial wing or shaft, mild swelling may develop distally but usually is not prominent. Inappropriate lameness and lack of swelling should prompt the clinician to perform a rectal examination, checking for internal asymmetry or crepitus. Horses with femoral fractures develop acute, severe swelling of the thigh, accompanied by severe lameness, instability, and often crepitus (Fig. 5-6). Horses may develop severe swelling of the stifle and thigh resulting from trauma and secondary bleeding. Large stifle hematomas resemble the

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• Observation: Symmetry and Posture

35

Moderate, fluctuant soft tissue swelling over the stifle caused by subcutaneous bleeding (hematoma). In this situation, swelling is much more pronounced than expected for the observed degree of lameness.

Fig. 5-7

swelling in horses with femoral fractures, and in some horses hematomas can be confused with severe femoropatellar effusion (Fig. 5-7). Excessive bleeding from subcutaneous vessels also may involve the ventral, lateral abdominal region. In horses with stifle hematoma, lameness is not as prominent as expected, and swelling fluctuates, which is useful in differentiating this cause of lameness from femoral fractures. Generalized, diffuse soft tissue swelling appears in horses with cellulitis or lymphangitis in the hindlimb (Fig. 5-8).

Bony Asymmetry Comparison of the height of the tubera coxae is important to determine the nature and extent of pelvic bony injury (Fig. 5-9). Two assistants, one on each side of the horse, may point to the dorsal aspect of the tubera coxae, or the veterinarian may use temporary markers to compare the height. Determining the height of the tubera sacrale may be difficult and requires careful palpation to differentiate bone, ligament, and muscle asymmetry. Accurate determination may be possible only by ultrasonography. Estimating the midline-to-lateral pelvic width also aids in diagnosing acute or chronic pelvic fractures.

Tubera Coxae Asymmetry in height of the tubera coxae accompanies many different pelvic fractures. The most common fracture involves the tuber coxae itself, often called knocked-down hip. Marked ventral and medial displacement of the fracture fragment occurs because of muscle attachment to the bony prominence. The veterinarian also must palpate the actual shape of the tuber coxae, because ventral displacement occurs with other pelvic injuries. Displacement and rotation occurs in horses with fracture of the wing of the ilium caudal to the tuber coxae without an obvious change in size or shape of the tuber coxae. However, with a partial fracture of the ventral aspect of the tuber coxae, there is a change in its shape, without displacement of the dorsal aspect of the bone.

Soft tissue swelling caused by cellulitis. Firm, painful swelling appears in the entire limb.

Fig. 5-8

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PART I

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Diagnosis of Lameness

Fig. 5-10 Asymmetry of the tubera sacrale. The left tuber sacrale (arrow) is higher than the right. This horse has chronic left sacroiliac subluxation.

Fig. 5-9 A well-positioned horse to determine tubera coxae height and the midline-to-lateral pelvic width (X, Y). In a normal horse, X = Y.

Tubera Sacrale The term hunter’s bump describes the prominence of the tubera sacrale. This finding may reflect the horse’s conformation, poorly developed surrounding musculature, or a change in position of one or both tubera sacrale. Increase or decrease in size of the overlying dorsal sacroiliac ligament also results in apparent asymmetry. Many clinically normal horses have slight apparent asymmetry of the tubera sacrale. Asymmetry in height of the tubera sacrale occurs in horses with acute or chronic sacroiliac joint disruption (Fig. 5-10). In horses with acute fractures of the base of the tubera sacrale, the affected side is lower2 (see Chapter 51). Ultrasonography and nuclear scintigraphy may help identify the cause of asymmetry.

Midline-to-Lateral Pelvic Width A change in the relative width of each hemipelvis is a subtle but important clinical sign of pelvic injury. In most horses with pelvic fractures, the injured side is narrower than the normal side. Over-riding and displacement of fracture fragments results in compression on the injured side.

Swelling over the Greater Trochanter Mild swelling over the lateral aspect of the coxofemoral joint may be a subtle clinical sign of acetabular or proximal femoral fractures. When standing behind the horse, the veterinarian should carefully observe for enlargement over the affected hip joint. This clinical sign usually is not noticeable initially, but soft tissue enlargement is visible within 2 to 3 weeks after intra-articular fracture. The groove between the greater trochanter and the biceps femoris muscle should be compared carefully; usually a slight bulge or subtle enlargement on the affected side is visible.

Crepitus Bone-on-bone grating is a valuable clinical sign, particularly in horses with pelvic injury. Crepitus can be heard (with or

Fig. 5-11 A horse with partial disruption of the left gastrocnemius. An injury to the origin of the lateral head of the gastrocnemius muscle in this horse caused an unusual gait deficit, lameness, and mild distal displacement (drop) of the hock and fetlock. without a stethoscope) or felt (external or rectal palpation) and most often is caused by movement of bone fragments in horses with displaced fractures (see Chapter 6). In horses with pelvic fractures, crepitus usually is not observed for several days to weeks after injury because muscle tone and fracture hematoma apparently stabilize fracture fragments and delay onset. Crepitus also can be felt or heard in horses with end-stage osteoarthritis.

Calcaneus The points of the hock should be of equal height when observed from the side or from behind. There is dramatic lowering of the point of the hock with complete disruption of the

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37

Warmblood gelding with chronic, severe, bilateral hindlimb suspensory desmitis causing noticeable fetlock drop in the left hindlimb.

Fig. 5-13

Fig. 5-12 A horse with a comminuted fracture of the left femur. The point of the left hock is higher than the right as a result of over-riding of fracture fragments and muscle contraction, effectively shortening the limb.

common calcaneal tendon or gastrocnemius tendon alone. Partial injury of the gastrocnemius muscle origin, the musculotendonous junction, or the tendon itself causes varying degrees of asymmetry in height of the point of the hock, both in a standing horse and during movement.3 Other gait abnormalities such as unusual rotation or instability of the limb usually are present (Fig. 5-11). The point of the hock is elevated in horses with severe pelvic fractures involving the acetabulum, luxation of the coxofemoral joint, and some femoral fractures (Fig. 5-12). Evaluating elevation is difficult because horses with severe lameness usually cannot bear weight, causing a dramatic alteration in limb position. However, in horses with true elevation in the point of the hock, the hock is extended, whereas with most non–weight-bearing conditions, the hock is flexed.

Fetlock Height Assessment of fetlock position is as important in the hindlimb as in the forelimb. Horses with excessively straight hindlimb conformation (straight hocks) may have more obvious excursion of the fetlock (fetlock drop) while moving or shifting position during standing. Pathological fetlock drop generally accompanies suspensory desmitis (Fig. 5-13) but also occurs with partial disruption of the gastrocnemius and other ligamentous and tendonous injuries.

POSTURE Body posture provides important clues to the source of lameness, but some abnormalities may be missed unless the horse is observed over long periods. Normal horses tend to rest one hindlimb and may alternate between limbs. Resting a forelimb is uncommon but does occur. Distractions in the environment may make a horse stand normally despite pain. However, abnormal posture because of mechanical or neurological dysfunction usually is evident. The horse has a well-developed stay apparatus in both the forelimbs and hindlimbs.4 It is assumed that the main purpose of the stay apparatus is to allow the horse to remain standing for long periods. The stay apparatus in the hindlimbs is better developed than in the forelimbs and includes ligamentous and tendonous structures dictating predictable movement of joints in the limb. If intact, the hindlimb stay apparatus demands reciprocal movement of the hock and stifle and often is called the reciprocal apparatus. A change in posture usually means a part of the reciprocal apparatus is broken.

FORELIMB POSTURE Pointing Horses that are severely lame often point or hold the affected forelimb ahead of the unaffected forelimb. These horses usually are severely lame at a walk. Horses with severe, bilateral forelimb lameness caused by laminitis may stand camped out in front, attempting to point with both forelimbs simultaneously. However, pointing is not synonymous with the presence

38

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Diagnosis of Lameness

Forelimb posture in a foal with infectious osteomyelitis (scapula) and arthritis (shoulder joint). With severe lameness of the shoulder or bicipital bursa, horses are reluctant to stand or move normally and often hold the limb caudally. This posture may be difficult to differentiate from that seen with loss of the triceps apparatus (see Fig. 5-14).

Fig. 5-15

Classic forelimb posture most often called radial nerve paresis or paralysis. The horse cannot extend or fix the elbow, causing the appearance of dropped elbow. The inability to fix the elbow (loss of triceps apparatus) commonly occurs in horses with olecranon fractures.

Fig. 5-14

of pain or lameness or its degree. Some horses prefer to point one forelimb or another and walk and trot normally. In general, pointing is unusual and often signals resting pain or subtle pain relieved by adopting this posture. Some horses stack bedding under the heels to stand in a toe-down position, indicating a degree of unilateral or bilateral foot pain. These horses often are not as lame as expected based on the degree of postural change seen at rest.

of buckling forward at the knee, both at rest and during movement. Specific injury of the distal aspect of the radial nerve causes similar clinical signs. In foals, rupture of the common digital extensor tendon or other extensor tendons may cause this posture (see Chapter 78).

Dropped Elbow A dropped elbow results from failure of the triceps apparatus to maintain elbow extension (Fig. 5-14) and usually results from fracture of the olecranon process. It also may result from injury to the radial nerve or brachial plexus. Similar clinical signs appear in horses with lesions of the nerve roots (neuritis, radiculopathy) or nerve cell bodies in the cervical intumescence, usually the result of lower motor neuron disease. A most unusual cause of this posture appears in horses with “root signature” (see “Neck Pain”).

Severe Lameness of the Shoulder Region Treading Constant shifting of weight from one forelimb to the other may indicate bilateral forelimb lameness. Laminitis, severe soft tissue injuries such as tendonitis or suspensory desmitis, or severe osteoarthritis may cause treading. Horses with chronic, severe unilateral forelimb lameness often stand with little weight on the affected limb, overload the unaffected limb, and seldom tread. The development of treading in such circumstances is an ominous sign because the horse now is trying to shift weight from the previously unaffected limb, probably because of laminitis.

Buckling Forward at the Knee Horses with bucked-knee or over-at-the-knee conformation may buckle forward at the knee while standing. In clinically normal older field hunters or other heavily used riding horses with bilateral over-at-the-knee conformation, this may be particularly obvious. The carpus is locked in extension primarily by the action of the extensor muscles. Neurological disease (e.g., EPM) affecting forelimb extensor muscles is a rare cause

Horses with severe shoulder pain may stand with the affected limb more caudal than usual (Fig. 5-15) and often drag the limb even with the slightest movement. This posture is similar to dropped-elbow posture, but in horses with a dropped elbow the limb is held at, or even slightly cranial to, the expected position.

Neck Pain Horses with neck pain often hold the head and neck lower than expected at a level equal to or slightly lower than the withers (Fig. 5-16). In horses with severe pain muscle tremors or spasms are visible, especially when approaching the horse or causing the horse to move, and the horse stands in a guarded position. The horse may be reluctant to turn or move and may be unable or unwilling to eat food from the ground or an elevated position. An unusual but characteristic sign of neck pain is posturing of a single forelimb, usually on the side of the lesion. The limb is held extended or pointed in front of the other forelimb; rarely the limb is held in slight flexion (see Fig. 55-10, A). This sign appears in dogs with cervical pain, most commonly from intervertebral disk disease, and is

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39

Fig. 5-16 Yearling Standardbred with neck pain on the left side showing typical stance and head and neck posture. termed root signature.5,6 Pain associated with the nerve roots supplying the brachial plexus may be the cause. Some horses with cervical pain also have unilateral forelimb lameness.7

A 2-year-old Belgian gelding with a fracture of the right femoral head and neck exhibits external rotation of the right hindlimb. Varus deformity of the left hindlimb also is visible.

Fig. 5-17

HINDLIMB POSTURE Resting a Hindlimb Normally a horse rests one hindlimb or another, but immediately resting a hindlimb after work, or a combination of resting the hindlimb and trembling in the flank or stifle region, may indicate lameness.

Abnormal Tail Position Horses may carry the tail in an abnormal position during movement, often alerting an observer to possible hindlimb pain. The tail usually is carried away from the lame limb, but this finding is inconsistent. Horses seldom have an abnormal tail posture at rest unless the tail has been traumatized or set, or there is severe hindlimb lameness.

External Rotation of the Hindlimb Cow-hocked conformation is common, but unilateral external rotation may reflect pelvic injury (Fig. 5-17). The veterinarian should verify this change in posture by moving and reevaluating the horse. Horses with pronounced unilateral external rotation usually have fractures of the acetabulum or proximal femur but may have non-articular ilial shaft or wing fractures.

Hindlimb Varus Posture Horses with chronic, severe unilateral hindlimb lameness may develop varus conformation of the contralateral limb (see Fig. 5-17). This posture most often appears in foals and may develop 7 to 10 days after onset of lameness.

Treading Constant shifting of weight between the hindlimbs, or treading, is an unusual clinical sign and usually indicates pronounced bilateral lameness. Horses with bilateral hindlimb laminitis or severe osteoarthritis of any joint may tread. Horses with chronic, severe unilateral hindlimb lameness can endure 4 to 6 weeks or more of weight bearing on the contralateral limb, but treading may be the earliest sign of traumatic laminitis in the supporting limb.

Camped Under Camped under appears only in horses with bilateral hindlimb laminitis and is rare. Horses often tread and exhibit an unusual hindlimb gait (shortened caudal phase of the stride) when moved.

Soft Tissue Injuries Altering Hindlimb Posture Upward fixation of the patella causes rigid extension of all hindlimb joints in the standing horse (Fig. 5-18). Patellar dysfunction resulting in fixed extension of the stifle also causes extension of the tarsus and lower limb joints because of the hindlimb reciprocal apparatus. The horse may maintain this posture during movement, or the posture may be intermittent and resolve when the horse is moved. Occasionally a horse with severe hindlimb lameness assumes a similar posture, apparently hanging the limb, but the limb is not locked

40

PART I

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Diagnosis of Lameness

A horse with the classic posture seen with upward fixation of the patella. All joints are held in rigid extension, and the horse is forced to rest or bear weight on the dorsal aspect of the hoof wall.

Fig. 5-18

in extension (Fig. 5-19). Normal horses simply resting a hindlimb, or those with severe lameness, usually keep the sole facing the ground. Foals with unilateral or bilateral lateral patellar luxation have an unusual crouched hindlimb posture similar to femoral nerve paresis. The foal may have difficulty in rising if the condition is bilateral and severe or long-standing. Disruption of fibularis (peroneus) tertius allows the hock to extend abnormally during weight bearing. Foals occasionally stand excessively straight in the hock (extended) in the affected hindlimb. In foals the injury usually causes tearing at the origin of fibularis tertius from the distal femur, but in adults injury may occur in the crus or at the distal aspect of the ligament as it courses over the hock. Swelling and excessive hock extension may occur with the latter injury (Fig. 5-20). The diagnosis is confirmed by manipulation: the hock can be extended while the stifle is flexed. Rupture of the gastrocnemius tendon, or severe injury at any level of the muscle-tendon unit, causes mild or severe hindlimb postural change. During weight bearing, the hock flexes excessively as the stifle is held in extension, so the point of the hock drops. This injury is called disruption of the caudal component of the reciprocal apparatus.8,9

Peripheral Nerve Deficits Sciatic nerve damage is rare. It occurs in foals as a result of injections into the thigh or rump or may occur transiently after injection of local anesthetic solution caudal to the coxofemoral joint. Horses with sciatic nerve damage support weight but appear to be crouched behind, because innervation to the gastrocnemius, flexor, and extensor muscles causes the hock to drop and fetlock to knuckle forward. Careful

Fig. 5-19 Belgian gelding shown in Fig. 5-17. This horse occasionally rested the left hindlimb in this extended position, similar to that of upward fixation of the patella. Most normal horses, or those with severe lameness, prefer to rest the limb with the sole facing the ground. observation of stifle action and the ability to support weight are useful when attempting to differentiate this deficit from femoral nerve paresis. Horses with femoral nerve paresis also assume a crouched hindlimb posture but are unable to bear weight, and the stifle drops substantially (Fig. 5-21). Because the reciprocal apparatus is intact, the inability to fix the stifle leads to hock flexion and knuckling (flexion) of the fetlock joint. If the condition is bilateral, the horse is unable to rise for more than a few seconds. Femoral nerve paresis may occur unilaterally or bilaterally after general anesthesia or may result from lower motor neuron disease or injury. Solitary tibial nerve injury is rare. Fibular (peroneal) nerve injury usually is recognized after general anesthesia and causes characteristic knuckling of the fetlock joint. Tibial nerve injury is differentiated from sciatic injury by lack of involvement of the tibial nerve, and thus normal positioning of the hock, and from femoral nerve injury, because horses are able to support weight and fix the stifle.

Other Unusual Leg Positions Horses with severe lameness occasionally rest a hindlimb back, forward, or abducted. Often these positions also are maintained during movement. Horses with caudal thigh or pelvic pain prefer to keep the affected hindlimb back, behind the unaffected limb. Horses with shivers may stand with the limb slightly abducted and more caudal than expected, with elevation of the tail head (see Chapter 49). Horses with pelvic fractures, in particular those involving the acetabulum, may stand with the limb slightly forward

CHAPTER 5

• Observation: Symmetry and Posture

41

Fig. 5-20 This Thoroughbred racehorse with fibularis tertius injury has swelling over the dorsal aspect of the hock (arrow) and straight-in-the-hock conformation.

and often are reluctant to place the limb behind the unaffected limb, thus reducing the caudal phase of the stride at the walk. Horses with pain in the medial thigh and groin area stand with the limb abducted and may travel in this manner. Adductor muscle damage, medial thigh abscessation, and scirrhous cord or other inguinal problems also cause this posture.

REFERENCES 1. Valentine BA, Rousselle SD, Sams AE, et al: Denervation atrophy in three horses with fibrotic myopathy, J Am Vet Med Assoc 205:332, 1994. 2. Pilsworth RC, Sheperd MC, Herinckx BMB, et al: A review of 10 cases of fracture of the wing of the ilium, Equine Vet J 26:94, 1994. 3. Swor TM, Schneider RK, Ross MW, et al: Injury of the gastrocnemius muscle as a cause of lameness in 4 horses, J Am Vet Med Assoc 219:215, 2001. 4. Sack WO, Habel RE: Rooney’s guide to the dissection of the horse, Ithaca, NY, 1977, Veterinary Textbooks.

Fig. 5-21 Thoroughbred with transient, post-anesthesia, unilateral (left hindlimb) femoral nerve paresis. The crouched posture of the left hindlimb includes flexion (knuckling) of the fetlock joint.

5. Taylor SM: Disorders of the spinal cord. In Nelson RW, Couto CG, editors: Small animal internal medicine, St Louis, 1998, Mosby. 6. Seim HB, Prata RG: Ventral decompression for the treatment of cervical disc disease in the dog: a review of 54 cases, J Am Anim Hosp Assoc 18:233, 1982. 7. Ricardi G, Dyson SJ: Forelimb lameness associated with radiographic abnormalities of the cervical vertebrae, Equine Vet J 25:422, 1993. 8. Shoemaker RS, Martin GS, Hillmann DJ, et al: Disruption of the caudal component of the reciprocal apparatus in two horses, J Am Vet Med Assoc 198:120, 1991. 9. Reeves MJ, Trotter GW: Reciprocal apparatus dysfunction as a cause of severe hindlimb lameness in a horse, J Am Vet Med Assoc 199:1047, 1991.

42

PART I

•

Diagnosis of Lameness

CHAPTER •

6

Palpation Mike W. Ross alpation is an important part of a lameness examination. In some sport horses, it becomes more important because, for example, suspensory desmitis often is not associated with overt lameness but may compromise performance. The veterinarian must develop a system to evaluate comprehensively all parts of the musculoskeletal system. I palpate in order each forelimb, the neck, back, pelvic regions, and then the hindlimbs. Each limb should be assessed when bearing weight and then again with the limb elevated from the ground. Deep palpation is used to describe direct, digital palpation, with the limb in an elevated position. If time permits, palpation should be completed before the horse is moved, because if the lame limb is identified first, the other limbs may be overlooked and compensatory problems may be missed. For example, in a Thoroughbred (TB) racehorse, superficial digital flexor (SDF) tendonitis is a common compensatory problem caused by contralateral limb lameness resulting in overload. If a lame horse with left forelimb (LF) lameness is first examined while the horse is moving, and subsequent palpation of the limb reveals signs of possible fetlock osteoarthritis, mild swelling of the right forelimb (RF) SDF tendon may be missed. Comprehensive palpation may allow the clinician to make predictions about lameness, to “read” the horse. Palpation before exercise also facilitates identification of localized heat or swelling, because limb temperature increases with exercise and swelling often decreases.

P

THE ART OF PALPATION The veterinarian should palpate and manipulate every possible anatomical structure, using the fingers and hands to push, prod, and feel. Interpretation of an abnormal response requires appreciation of the normal response. There are nerves beneath or adjacent to many structures, and direct pressure may elicit an apparently positive response. Such false-positive responses often occur during palpation of the origin of the suspensory ligament (SL) or the proximal sesamoid bones (PSBs). Care should be taken to apply pressure only in the desired location. During palpation of the PSBs, distal aspect of the SL, and flexor tendons, it is easy to apply pressure over the dorsal aspect of the third metacarpal bone (McIII), and a painful response may actually reflect sore shins. The clinician should look for signs of inflammation: heat, pain, redness, swelling, and loss of function. One side of the horse should be compared with the other, but it should be remembered that both sides may be abnormal. Heat is one of the earliest clinical signs to develop with articular or nonarticular problems and may be the only sign. Subchondral remodeling and sclerosis of the third carpal bone often cause lameness in young racehorses, but effusion of the middle carpal joint and a positive response to flexion are found inconsistently. Usually prominent heat is detectable on the dorsal aspect of the carpus. It is important to recognize normality. A normal horse may have disparity in foot temperature. Horses often have two or three cold feet, but the other feet feel warm. A few hours later, feet that previously were cool may feel warm. Foot temperature often reflects

variations in ambient temperature, and care must be taken not to over-interpret this normal finding. In general, palpation is done with the palm side of the hand, although the back of the hand may be more sensitive to detection of warmth. The veterinarian should assess the quality or strength of the digital pulse. In a normal horse, reliable detection of a digital pulse may be difficult, especially in cold weather or in horses with a thick hair coat. Increased or elevated digital pulse refers to the detection of increased strength or the bounding nature of the digital pulse. Inflammatory conditions in the foot or pastern region, such as abscesses, laminitis, hoof avulsions, or cracks, are the most common causes of increased digital pulse. Complete absence of hindlimb digital pulse may occur with aortoiliac thromboembolism or other vascular problems, but care should be taken when interpreting weak or near absent hindlimb digital pulses, because hindlimb digital pulses can be difficult to feel in normal horses. Redness is difficult to perceive in the horse because of skin pigmentation, but in the foot, solar bruising or redness at the coronary band can be observed, especially in horses with nonpigmented feet. Swelling is often detected by observation, but subtle enlargement of structures such as the SL, or presence of effusion may be determined only by careful palpation. Loss of function of tissues and regions can be assessed during palpation. Manipulation, flexion, and extension of the joints or soft tissues provide a better idea of function or loss of function. Static flexion and extension determines the range of motion of a joint and the horse’s response to the procedure. Chronic osteoarthritis of the fetlock or carpal joints often results in reduced range of flexion. However, many horses in work but without lameness resent hard flexion of the lower limbs. Good correlation between a reduction in fetlock flexion range, lameness and severity of osteoarthritis was found in TB racehorses.1 A reduction in fetlock flexibility in young Warmbloods may be a predictor of future lameness.2 The response to rotation of joints also should be assessed. Crepitus, the grating or crackling sound made by bone rubbing on bone, is an unusual and ominous clinical sign usually determined by palpation, although in horses with prominent osteoarthritis or fractures, a grating sound may be heard. A stethoscope may be useful for detection of subtle crepitus. Other factors may confound the results of palpation. Clipped areas usually are warmer than an adjacent area with normal hair length. Blistering or freeze firing can cause localized pain for weeks after application, even if lameness has resolved. Any type of skin lesion, such as those found in horses with scratches or boot rubs, can cause extreme soreness to palpation but no signs of lameness. Some individual horses are more sensitive to palpation than others, and interpretation of apparent pain can be frustrating.

PALPATION OF THE FORELIMB Foot The importance of the foot cannot be overemphasized, and it is for this reason that palpation of the forelimb begins here. The feet are included in evaluation of conformation, symme-

CHAPTER 6

• Palpation

43

Fig. 6-1 Instruments needed to examine the hoof, remove a shoe without tearing the hoof wall, and prepare the hoof for radiographic examination. Shown are apron, rasp, shoe pullers, nail pullers, clinch tool, hoof knife, hammer and hoof pick, and wire brush.

Elevated foot viewed from the palmar aspects shows that the hairline at the medial bulb of heel (on the right) is displaced proximally compared with the lateral heel bulb. The medial wall is longer. Note also the prominent cleft between the heel bulbs. These features are typical of sheared heels.

Fig. 6-3

Fig. 6-2 The coronary band is uneven compared with the ground in this trotter’s unbalanced hoof. The medial wall (right) appears to be shorter than the lateral wall. try, and posture. Detailed static examination (examination at rest) of the foot must always be supplemented with, and correlated to, dynamic observations of foot flight and foot striking patterns. Some horses continually attempt to pick up the limb as the clinician tries to evaluate it with the horse in the

standing position; it may be necessary to stroke the contralateral limb to divert attention. A hoof pick, wire brush, hoof knife, shoe-removing equipment, and hoof testers are required (Fig. 6-1). The sole and frog and wall of the foot should be cleaned thoroughly. Removal of the shoe at this stage in the examination usually is indicated only if a sub-solar abscess is suspected. The veterinarian should take care to preserve the hoof wall, and if cracked, protect it with tape. Foot and hoof balance are assessed by evaluating toe and heel length, hoof capsule conformation, condition and integrity, type of shoe and shoe position relative to the hoof capsule, hoof and pastern angle (axis), medial to lateral hoof balance, coronary band conformation, and distal interphalangeal (coffin) joint capsule distention and response to hoof testers. The coronary band should normally be parallel to the ground surface. Deviation from parallel often indicates mediolateral foot imbalance (Fig. 6-2). Medial and lateral wall lengths should be assessed while the horse is standing and again with the limb off the ground, viewing the foot from palmar to dorsal along the solar aspect. The limb is lifted and held in neutral position so the solar surface is perpendicular to the ground. Sheared and underrun heels are commonly associated with lameness (Fig. 6-3). Deformation of the hoof capsule is not necessarily a cause of lameness. Many horses with proximal displacement of the medial heel bulb have level foot strikes and otherwise balanced feet. Toe and heel length should be assessed, and the hoof-pastern axis should be determined. The angle of the hoof and pastern should be equal to allow equal loading of all portions of the foot. Forelimb hoof-pastern angles normally range from 48° to 55°, but the absolute angle should not be overemphasized. A straight pastern-foot axis is more important. A long-toe, underrun heel foot conformation causes a broken foot axis and predisposes to palmar heel pain (Fig. 6-4). The conformation, condition, and integrity of the hoof capsule should be assessed. It is easy to miss hoof wall defects on the medial aspect. Small quarter or heel cracks and defects at the

44

PART I

•

Diagnosis of Lameness

Palpation of the coronary band should include assessing the dorsal joint pouch of the distal interphalangeal joint. In this horse, distal interphalangeal effusion and fibrosis appear as a bulge just proximal to the coronary band, dorsally.

Fig. 6-5

the cartilage of the foot to the distal phalanx is an occasional cause of lameness, and compression of the heel with hoof testers may elicit pain in some horses. Fig. 6-4 This trotter has long toe, under-run heel hoof conformation, and broken hoof-pastern axis. coronary band should not be overlooked. The clinician should evaluate the solar surface, bars, and frog. Thrush, although a reflection of poor management, rarely causes lameness. The shoe type, shoe wear patterns, and the shoe size relative to the foot need to be assessed. The clinician should note the presence of pads or additions to the shoe, such as toe grabs, borium, and heel caulks. There is an association between toe grabs and suspensory apparatus failure in TB racehorses.3 Low heel angle also has been associated with injury.4 Shoe wear is important, because it reflects how the horse has been moving over the last several weeks. The clinician should note the breakover point and whether one branch of the shoe is worn more than the other. Shoe size should be assessed relative to foot size and the fit of the shoe. A shoe that is too small or set too close to the frog may predispose to lameness. Careful palpation of the coronary band in the standing and non–weight-bearing position is critical in detecting foot soreness (Fig. 6-5). In horses with sore feet, heat and pain often are detected on the sore side of the foot, and a prominent digital pulse usually is present. Effusion of the distal interphalangeal joint capsule accompanies many abnormalities of the foot, from early synovitis to chronic osteoarthritis of the distal interphalangeal joint, and those with non-specific foot soreness. The clinician places one finger lateral to, and another medial to, the common digital extensor tendon and gently pushes in on the joint capsule, first laterally and then medially. Ballottement is a useful technique to detect effusion in many synovial structures: with effusion, pushing in on the capsule on one side of the tendon causes elevation of the capsule on the other side. The clinician should palpate the cartilages of the foot, either with the horse standing or with the limb elevated. Sidebone, mineralization of the cartilages of the foot, rarely causes lameness. The cartilages of the foot normally are pliable and readily compressed axially. Fracture at the attachment of

Hoof Tester Examination “…I feel naked going into a stall without my hoof testers!”5 Hoof testers are essential for evaluation of the foot and are a basic requirement for all lameness examinations. Many types of hoof testers are available (Fig. 6-6), but I favor one that is adjustable and can be applied with one hand. A proper evaluation of the foot with hoof testers cannot be done with a pad in place, although useful information can be acquired. The instrument can be applied with or without a shoe in place. The amount of force to apply varies from horse to horse and by region of the hoof, and both false-positive and false-negative responses occur. More force is required when the instrument is used across the heels than when used from sole to quarter. The foot should be held between the clinician’s legs in a relaxed manner. The clinician must be able to feel the horse react to subtle pressure, and if the leg is held too tightly or the horse is not calm during the examination, it is difficult to feel a response. The veterinarian should be careful not to place the outside jaw of the instrument too close to the coronary band, because this may cause a false-positive result. Sole sensitivity is assessed by applying the instrument to three to five sites from heel to toe, on both the medial and lateral aspects of the foot, starting from the angle of the sole (seat of the corn) and proceeding dorsally (Fig. 6-7). The responses should be compared. If the sole is readily compressible, pain from bruising, a sub-solar abscess, laminitis, fracture of the distal phalanx, and other injuries may be elicited, but in horses with hard horn the response may be negative. To evaluate sensitivity of the frog and underlying deeper structures, the hoof testers should be applied from the lateral aspect of the frog to the medial wall, and from the medial aspect of the frog to the lateral wall, each in the palmar, mid-portion, and dorsal aspects of the frog (Fig. 6-8). Pain over the middle third of the frog has been attributed to navicular disease or navicular syndrome, but the specificity of this association is questionable and there are many false-negative responses. Horses with generalized foot soreness or any other cause of palmar

CHAPTER 6

A variety of hoof testers are available for lameness examinations. I prefer hoof testers that are easily adjusted and used in one hand (two pairs on the right). Large hoof testers (left) can be applied only with two hands, and small hoof testers (bottom) are inappropriate for medium to large hooves.

• Palpation

45

Fig. 6-6

Hoof testers applied from the middle of the frog to the contralateral hoof wall put pressure on the navicular region. Horses with many abnormal conditions of the hoof may manifest a positive response.

Fig. 6-8

Fig. 6-7 Hoof testers should be applied from the sole to the wall, from the heel to toe, and to both sides of the hoof. heel pain may respond positively or not at all. Only 19 of 42 horses with navicular region pain responded positively to hoof tester examination in the middle third of the frog, with 50% specificity, 50% positive predictive value, and 48% accuracy.6 Horses with palmar heel pain caused by other conditions were as likely to respond to the test, a finding that obviously prompts questioning of the value of hoof tester examination.6 It is difficult if not impossible to create adequate pressure to cause pain in large breed horses or if the horn is hard. Application of a poultice or soaking the foot may be necessary to soften a hard foot, and re-examination after several days may be rewarding. Hoof tester application to the small feet of foals or ponies may elicit a false-positive response, and hoof tester size or amount of compression may require adjustment. Application of hoof testers across the heels may cause pain in horses with palmar heel pain but is not specific (Fig. 6-9). Application of the hoof tester to the area of the sole adjacent to each nail, nail hole, or defect in the sole or white line, is useful

Fig. 6-9 Adjustable hoof testers are easily placed across the heels. I prefer to apply hoof testers in this manner to assess horses for palmar heel pain during static examination and as a provocative test for lameness.

46

PART I

•

Diagnosis of Lameness

Acute, severe lameness causing increase in digital pulse and profound hoof tester sensitivity in the toe region resulted from this hoof abscess. Exudate drains from the pared region at the toe. (Courtesy Greg Staller, Pottersville, New Jersey.)

Fig. 6-10

to detect a sub-solar abscess or a close nail (Fig. 6-10). Areas of pain can be gently explored with a hoof knife, but unless clearly indicated, the veterinarian should refrain from digging too deep. The hoof tester can then be used as a hammer to percuss each nail in the shoe and the frog and toe regions. After completing the hoof tester examination, the clinician should re-assess the digital pulses. In horses with foot pain the digital pulse may now be bounding. Horses that have recently been shod or trimmed, or have raced or performed recently, especially on hard surfaces, may have mild elevations in digital pulse and may show hoof tester sensitivity normally. Pain causing lameness may not be in the foot.

Fig. 6-11

Palpation of oblique distal sesamoidean ligaments.

Pastern The proximal interphalangeal (pastern) joint capsule is assessed by ballottement, although severe effusion must be present to perceive fluid distention. Bony swelling associated with this joint, proximal or high ringbone, is a classic cause of lameness yet an unusual clinical finding. Osteoarthritis of the proximal interphalangeal joint is a common diagnosis, but one made by a combination of clinical findings, diagnostic analgesia, radiography, and sometimes scintigraphy. The distal extent of the digital flexor tendon sheath (DFTS), deep digital flexor tendon (DDFT), and distal sesamoidean ligaments are palpated. Deep pain associated with the origin and insertion of these structures is assessed by palpation with the limb in flexion (Fig. 6-11). The oblique sesamoidean ligaments are difficult to differentiate from the branches of the SDFT, but injury of the SDFT is more common. Distal sesamoidean desmitis or chronic suspensory desmitis may result in subluxation of the proximal interphalangeal joint (Fig. 6-12). The proximal interphalangeal joint is manipulated in a medial to lateral direction to assess pain and collateral ligament integrity and is flexed independently of the fetlock joint. The proximal, dorsal aspect of the proximal phalanx is palpated (Fig. 6-13). Horses with short, mid-sagittal fractures of the proximal phalanx may show pain. Occasionally enthesophyte formation at the common digital extensor tendon attachment, seen most commonly in older, ex-racehorses with chronic osteoarthritis of the fetlock joint, results in prominent bony and soft tissue swelling and pain on palpation.

Fetlock The clinician palpates the joint capsule of the metacarpophalangeal (fetlock) joint with the limb bearing weight, bearing in mind that pain associated with the joint can be present

Subluxation and osteoarthritis of the left front proximal interphalangeal joint resulted from primary suspensory desmitis.

Fig. 6-12

without localizing clinical signs. The dorsal aspect is palpated using ballottement on either side of the common digital extensor tendon. The clinician should determine whether localized heat is present. Osselets is a North American term used to describe early osteoarthritis of the metacarpophalangeal joint in young racehorses, with firm bony and soft tissue swelling on

CHAPTER 6

Proliferative changes at the common digital extensor attachment or pain from mid-sagittal fracture of the proximal phalanx should be palpated along the dorsal, proximal aspect of the proximal phalanx.

• Palpation

47

Fig. 6-13

the dorsal, medial aspect of the proximal phalanx, and the distal aspect of McIII, caused by traumatic capsulitis and early enthesophyte formation. Occasionally in horses with prominent effusion of the metacarpophalangeal joint, a soft tissue swelling can be palpated in the proximal, dorsal aspect of the joint from excessive proliferation of the dorsal synovial pads, called proliferative or villonodular synovitis. The palmar pouch of the metacarpophalangeal joint is palpated dorsal to the SL branches, both medially and laterally. Mild effusion may be present without associated lameness, especially in older performance horses. The PSBs are palpated and assessed for mild swelling and heat, clinical signs of sesamoiditis, or SL avulsion injury. The digital pulse is re-assessed by placing fingers both medially and laterally, abaxial to both PSBs (Fig. 6-14). The DFTS extends from the distal metacarpal region to the distal palmar pastern. Usually no palpable fluid is found. Effusion of the DFTS (tenosynovitis) causes swelling in the palmar fetlock region that must be differentiated from effusion of the metacarpophalangeal joint. Tenosynovitis causes swelling palmar to the branches of the SL medially and laterally. Fluid can be compressed from medial to lateral. With severe effusion, distention is found in the palmar pastern, but there may be distention proximal to the palmar annular ligament without obvious distention distally. Wind puffs or wind galls describe incidental fluid distention of the DFTS, commonly seen in older performance horses unassociated with lameness. Tenosynovitis can cause lameness, but additional diagnostic techniques are required to confirm the diagnosis. The limb is elevated to assess range of joint motion and the horse’s response to flexion. Normally the fetlock can be flexed to 90° (the angle between the proximal phalanx and McIII) or slightly more. A reduction in fetlock flexion range is indicative of chronic fibrosis but is not necessarily a cause for concern. A pronounced response to static flexion is noteworthy, but many horses resent static flexion but do not show a positive response to dynamic flexion (lower limb or fetlock flexion tests; see Chapter 8). Horses with clinically relevant tenosynovitis usually strongly resent fetlock flexion. With the limb in flexion, the clinician palpates the PSBs and the branches of the SL, avoiding compression of the palmar digital nerves.

Digital pulse quality can be assessed easily at the level of the proximal sesamoid bones.

Fig. 6-14

Metacarpal Region The clinician should assess the dorsal aspect of McIII for heat and swelling. This is a common area for traumatic injury (barked shins) or stress-related bone injury (bucked shin syndrome). Many ex-racehorses have incidental, prominent, chronic, and non-painful swelling of McIII caused by extensive modeling and remodeling of the dorsal cortex while in race training. Racehorses currently in training may have heat and pain on deep palpation (performed with the limb elevated), but prominent swelling may be lacking. Any combination of palpation findings is possible in horses with stress-related bone injury of McIII. It is difficult to apply deep pressure to the dorsal aspect of McIII without concomitant pressure to the palmar soft tissue structures or PSBs, so the responses should be assessed carefully. The entire length (abaxial surface) of the second and fourth metacarpal bones (McII/IV) should be palpated with the horse in the standing position to detect exostoses, callus, or fractures. Swelling of the SL branches or body may make this difficult. Palpation of McII/IV should be repeated with the limb elevated, because the axial aspect of these bones is impossible to assess in the weight-bearing position. Splint exostoses are common, particularly in young horses. Therefore the presence of even large bony swellings is not unusual. Exostoses detected axially, possibly impinging on the SL (or so-called blind splints) should be carefully noted. Pain from even small exostoses of McII/IV usually is more accurately assessed immediately after training or racing, because pain and lameness resulting from these swellings can be subtle and transient. The clinician should carefully palpate the SL branches. Differentiation of branch or SL body injuries is important: the latter injuries usually are more serious and have a worse prognosis. The medial and lateral palmar digital vein, artery, and nerve, in dorsal to palmar orientation, respectively, are located between the SL and DDFT. The accessory ligament (distal or inferior check ligament) of the DDFT (ALDDFT) normally is difficult to palpate and even when enlarged cannot easily be differentiated from the DDFT, but injuries of the ALDDFT are more common. All soft tissue structures should be palpated

48

PART I

•

Diagnosis of Lameness

Fig. 6-15 The soft tissue structures in the palmar metacarpal region should be carefully palpated with the horse in standing and flexed (shown) positions for heat, pain on compression, and swelling. Most ridden horses have mild pain, but in racehorses a painful response is an early sign of tendonitis or desmitis. carefully, using digital compression, with the limb elevated (Fig. 6-15). Acute or chronic swelling should be assessed, as should the horse’s response to deep palpation. Obvious swelling and pain indicate the presence of tendonitis or desmitis. In some horses with acute severe tendonitis or desmitis the structure feels “mushy” or soft in the area of fiber damage. This finding, especially in horses with fetlock drop, indicates near rupture of the structure. There are many false-positive and even false-negative responses to palpation of the flexor tendons and SL. In most ridden performance horses a mild painful response (false-positive) to deep palpation of the SL is normal. However, in racehorses, false-positive responses are less common, and a painful response to deep palpation may indicate the presence of early desmitis or tendonitis. In many horses with foot lameness, secondary, mild suspensory desmitis is common. There is a painful response to palpation of the body and origin of the SL. It may be difficult to decide whether this is a true or false-positive response, a determination that often is made in hindsight after the lameness examination is finished. False-positive and false-negative responses to palpation of the proximal palmar metacarpal region also occur. This is a common site of lameness and should be examined carefully. Palpation must be done with the limb in flexion, and the presence of swelling and pain must be carefully interpreted (Fig. 6-16). Horses with acute injuries, such as proximal suspensory desmitis (PSD), avulsion or longitudinal fracture of McIII, and stress reaction of McIII at the origin of the SL, may have swelling and pain. Deep palpation may create pressure on the palmar metacarpal nerves resulting in a false-positive pain response, and many horses with PSD have no localizing signs. The proximal dorsal aspect of McIII should be palpated in a flexed position (Fig. 6-17). Occasionally, dorsomedial articular fracture of McIII results in a subtle painful swelling. Swelling (effusion) of the carpal sheath may be detected in the proximal medial metacarpal region, but large veins (medial palmar, accessory cephalic, and cephalic veins), may interfere with accurate palpation. With mild tenosynovitis, effusion may be difficult to discern.

Carpus Detection of warmth on the dorsal aspect of the carpus is a reliable indicator of underlying inflammation. Obviously, one side should be compared with the other, but bilateral condi-

Palpation of the proximopalmar metacarpal region is essential in diagnosing proximal suspensory desmitis and other conditions of the suspensory origin and differentiating lameness in the region from carpal lameness. (Courtesy Ross Rich, Cave Creek, Arizona.)

Fig. 6-16

Careful palpation of the proximal, dorsal metacarpal region identifies pain associated with dorsomedial articular fracture or other fractures of the proximal aspect of the third metacarpal bone. (Courtesy Ross Rich, Cave Creek, Arizona.)

Fig. 6-17

tions exist commonly. Previous application of counterirritants interferes with the reliable detection of warmth. Carpal joint lameness without obvious signs of synovitis is common, but if present, effusion is easily palpated using ballottement. With the horse in the standing position, a finger is placed dorsolaterally between the extensor carpi radialis and common digital

CHAPTER 6

• Palpation

49

A

Fig. 6-18 Carpal tenosynovitis must be differentiated from effusion of the antebrachiocarpal joint. This horse with severe superficial digital flexor tendonitis has moderate distention of the carpal sheath (arrow) in the caudal, distal aspect of the antebrachium and medially in the proximal metacarpal region (not shown).

extensor tendons, and another finger is placed just medial to the extensor carpi radialis tendon. These openings are used for palpation and arthrocentesis of both the middle carpal and antebrachiocarpal joints. The middle carpal and carpometacarpal joints always communicate, but a small synovial compartment and dense overlying soft tissue structures limit palpation of the carpometacarpal joint. Both the middle carpal and antebrachiocarpal joints have a palmarolateral pouch that may be distended if effusion is severe. If swelling is detected just caudal to the radius, it is necessary to differentiate distention of the palmarolateral pouch of the antebrachiocarpal joint from the carpal sheath (Fig. 6-18). In horses with antebrachiocarpal joint effusion the dorsal outpouchings also should be prominent, whereas in those with carpal sheath effusion, fluid distention is restricted to the palmar aspect and also detected medially, both proximal and distal to the accessory carpal bone. Tenosynovitis of the extensor carpi radialis, common digital extensor, or lateral digital extensor sheaths results in vertically oriented swellings that traverse the carpal joints, may extend proximal or distal to the carpus, and usually are multi-lobed, being divided by bands of extensor retinaculum located dorsally and laterally. Normally the carpus can easily be flexed completely, so that the palmar metacarpal region and bulbs of the heel touch the caudal antebrachium. Reduced flexion may be caused by pain with or without chronic fibrosis associated with osteoarthritis. Pain during carpal flexion is a reliable indicator of carpal region lameness but does not indicate the cause. The carpal sheath is compressed and the extensor tendons are stretched during this maneuver, and conditions involving these structures and the accessory carpal bone can cause pain during

B

Careful palpation of the dorsal aspect of each carpal bone can be done with one hand (A) or by placing the distal limb between the clinician’s legs and using both hands (B). A painful response indicates an osteochondral fragment or an osteophyte. Occasionally a loose osteochondral fragment can be palpated.

Fig. 6-19

flexion. The elbow joint is flexed simultaneously; therefore a positive response to carpal flexion can rarely result from elbow pain. The examiner should palpate the dorsal surfaces of the carpal bones with the limb in partial flexion (Fig. 6-19). Many pathological conditions associated with the carpus are manifested dorsally, and pain associated with osteochondral fragmentation, slab fractures or other severe injuries, or

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osteoarthritis can be assessed with the limb in this position. Focal pain can be identified, and occasionally loose fragments associated with the third carpal bone or distal lateral radius can be identified.

Antebrachium (Forearm) Digital palpation of the forearm usually is performed with the limb bearing weight. The examiner should look primarily for muscle atrophy, wounds, or mild swelling associated with the radius. Small wounds in the antebrachium may look innocuous, but inappropriately severe lameness and pain on palpation may reflect a spiral radial fracture. The examiner should pay particular attention to the medial aspect of the limb; this area is easily overlooked when palpating from the lateral side. Distally, fluid distention of the carpal sheath or acute swelling associated with injury of the accessory (proximal or superior check ligament) ligament of the SDFT, or the flexor muscles and tendons can occur. The amount of muscle in the extensors and flexors should be compared with the contralateral limb, because subtle atrophy may be missed during observation.

Elbow Frank swelling and prominent lameness accompanies many injuries of the elbow region, but other problems of the elbow joint are discovered only after diagnostic analgesia has localized pain to this area or by use of advanced imaging modalities. It is nearly impossible to use diagnostic analgesic techniques to abolish pain in the distal humerus and proximal radius and ulna; therefore advanced imaging techniques are often required to identify problems in these structures. The clinician should palpate the olecranon process and the lateral and medial collateral ligaments with the limb bearing weight. Effusion is difficult to detect, but excess fluid occasionally can be found using ballottement, by placing fingers both cranial and caudal to the lateral collateral ligament. The elbow is flexed by pulling the distal limb in a cranial and proximal direction, and then extended, by pulling the lower limb in a caudal direction. The shoulder joint is undergoing the opposite reaction during this manipulation, and pain associated with that joint or the bicipital bursa can cause a positive response during elbow manipulation.

Brachium (Arm) and Shoulder The shoulder and intertubercular (bicipital) bursa are regularly blamed as the cause of lameness yet are seldom involved. Normal horses may resent palpation of this area. Pain in the muscles surrounding the shoulder joint may develop secondary to primary lower limb lameness. In Standardbred (STB) racehorses with carpal lameness, secondary pain often is detected when palpating the bicipital bursa. Palpation of the arm is limited because overlying muscles obscure much of the humerus. Horses with displaced humeral fractures usually are unwilling to bear weight and have severe soft tissue swelling. Those with humeral stress fractures usually have no localizing signs except a positive response to upper limb manipulation. A normal intertubercular (bicipital) bursa is not palpable. Horses with bicipital bursitis usually resent direct compression of the greater tubercle of the humerus and fluid distention may be palpable, but ballottement is usually limited. Effusion of the scapulohumeral (shoulder) joint is palpable only if severe and even then is easily overlooked. Upper limb manipulation, including static flexion and extension to assess the range of motion of the shoulder and elbow joints and the presence of a painful response, should always be performed. This can be done during palpation of the elbow or later when the clinician finishes the shoulder region. Most horses with shoulder joint lameness or bicipital bursitis show a painful response when the limb is pulled back (shoulder flexion, elbow extension), whereas those with

This horse shows atrophy of the supraspinatus and infraspinatus muscles with concomitant lateral subluxation of the left shoulder joint.

Fig. 6-20

elbow lameness may show a painful response when the limb is pulled forward (shoulder extension, elbow flexion). The examiner should palpate the scapular area and move the mane if necessary. Atrophy of the infraspinatus and supraspinatus muscles may indicate suprascapular nerve or brachial plexus injury (Fig. 6-20). Muscle atrophy of these and other forelimb muscles can be caused by other neurogenic causes or by disuse. Upper limb palpation often is used to confirm those findings recognized during observation of the horse. Scapular height is compared manually. Although rare, damage to the innervation of the serratus ventralis muscle allows abnormal elevation of the injured side when the horse is standing or during movement. Pectoral muscle atrophy can easily be missed during observation, and the pectoral region should be palpated to assess pectoral muscle mass and identify swellings or wounds that may cause lameness.

PALPATION OF THE CERVICAL AND THORACOLUMBAR SPINE Cervical Spine (Neck) Palpation of the neck is limited. I usually palpate the brachiocephalicus muscle after shoulder palpation and manipulation, a procedure thought to have predictive, but non-specific value in horses with forelimb lameness.8 The muscle is squeezed just cranial to the shoulder joint; most horses flinch, but some

CHAPTER 6 horses with ipsilateral forelimb lameness show a marked painful response. The examiner should palpate both sides of the neck, noting any swelling or muscle atrophy. Cervical abscessation can cause signs of neck pain and forelimb lameness. Muscle atrophy may indicate long-standing cervical pain or ipsilateral forelimb lameness. Muscle development of the neck may be asymmetrical especially if viewed from above (the perspective of a rider).2 Palpation of the poll region is important because undue soreness cranial to the wings of the atlas may be associated with poor performance.2 The head should be moved from side to side to evaluate the horse’s willingness to move the neck. One hand is place on the mid-cervical region to use as a fulcrum, and the other hand is used to bend the head and neck toward the examiner. Food also can be used to entice the horse to move the head and neck from side to side. Normally a horse can reach around to the girth region on either side to ingest food, and reluctance to do so may indicate neck pain. This procedure may more closely mimic the horse’s natural head and neck movement than using a hand in the mid-cervical area as a fulcrum. A more comprehensive examination, including neurological or chiropractic evaluations, may be necessary after completion of the lameness examination. Up and down movement of the head also should be assessed. Although usually not a part of a routine lameness examination, evaluation of the temporomandibular joints and the mouth may be necessary in horses with poor performance.2

Thoracolumbar Spine (Back) Additional detailed palpation of the back and pelvis may be necessary once the lameness examination is completed. Chiropractic manipulation and assessment of acupuncture points may be useful, but it usually is reserved for specific horses or when history and clinical signs warrant such an examination and if the clinician is qualified to complete it. The cranial thoracic spine has already been briefly evaluated during examination of the shoulder for scapular symmetry. The withers should be examined closely for conformational abnormalities, such as those seen with fracture of the dorsal spinous processes or fistulous withers. The presence of sores may indicate an ill-fitting saddle and can cause performance-related problems. Using a hand on each side of the spine the examiner should apply digital pressure to assess vertebral height, presence of pain, muscle atrophy, and to confirm symmetry (Fig. 6-21). Many horses resent deep and aggressive palpation of the epaxial muscles, and the response of normal horses should be learned before a pathological response is presumed. Most horses readily become mildly lordotic (“scootch”) during deep digital palpation or by using a blunt object such as a pen. Some clinicians prefer to use the ends of the fingers to “run” (apply digital pressure while moving the fingers caudally) the muscles from cranial to caudal, parallel to the spinal column. When this is continued along the gluteal muscles and rump. most normal horses become somewhat kyphotic and move forward slightly. Aggressive use of blunt or sharp objects to assess pain should be avoided. Some horses are stoic during palpation, and it may be impossible to stimulate them to extend and flex the thoracolumbar region without the use of a blunt instrument.2 In these horses, firmly stroking the ventral abdomen may stimulate movement.2 With one hand on the horse’s back during movement of the thoracolumbar spine, the clinician may be able to feel muscle “cracking” during the release of tension in the epaxial muscles.2 The observation of muscle fasciculations during or after palpation usually indicates a degree of muscle pain. Failure to exhibit the normal lordotic or kyphotic responses, assuming a guarded posture, or vocalizing during the examination are further signs of back pain. In many horses, back pain, and more specifically, muscle pain, is secondary to hindlimb lameness, resulting from altered gait and posture. Any site of pain in the hindlimb may alter

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Palpation of the thoracolumbar region should be performed in a quiet, careful manner. Many horses object to sudden or sharp stimuli applied to this region. Direct, even pressure is applied to the epaxial muscles (shown) and the summits of the dorsal spinous processes.

Fig. 6-21

the gait to cause secondary upper limb or back muscle pain. The use of diagnostic analgesia to confirm the primary source of pain (in the hindlimb or locally in the back) may be required to make the true diagnosis. Back pain often is complex and may be caused by many factors including illfitting saddles, poor riding, and other primary problems, such as overriding of dorsal spinous processes or other bony causes. The clinician should palpate carefully to detect localized swelling in the area of the saddle. Even small areas of hair loss without swelling may indicate a loose or ill-fitting saddle, abnormal movement of the saddle associated with hindlimb lameness, or a rider sitting crookedly.2 It is doubtful that muscular pain alone can cause unilateral hindlimb lameness. Back pain was induced in STB horses by injection of lactic acid into the left longissimus dorsi muscle and subsequently exercised and observed with high-speed cinematography.8 Frank lameness was not observed, but there was slight modification of left hindlimb stride and reduced performance. This supports the clinical observation that back pain usually is the result, not the cause, of obvious hindlimb lameness, although it may result in slight alterations in gait. Severe vertebral abnormalities or an abscess in the epaxial muscles may result in lameness or neurological dysfunction.

PALPATION OF THE LATERAL AND VENTRAL THORAX AND ABDOMEN History or observation of lameness, performance, or behavioral abnormalities seen only when a horse is ridden or wearing tack should prompt examination of the thoracic region. Irritation from an ill-fitting girth or other sores or wounds can contribute to poor performance, and injury of the sternum or ribs can cause pain associated with saddling or being ridden. Traumatically induced hernias of the ventral abdomen can cause gait deficits or guarding of the abdomen.

PALPATION OF THE EXTERNAL GENITALIA Testicular or inguinal pain should be considered as a cause of gait modification. Swelling, infection from previous castration, scirrhous cord, and mastitis can cause a change in gait. The veterinarian should determine the sex of the horse and the presence of one or both testicles.

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PALPATION OF THE PELVIS Palpation of the pelvis is performed to confirm previous observations. The horse should stand as squarely as possible. The clinician should palpate all bony protuberances, including the tubera coxae, tubera sacrale, and tubera ischii. The examiner stands behind the horse and palpates these paired protuberances simultaneously if it is safe to do so (Fig. 6-22). Fracture of a tuber coxae or ilial shaft may result in asymmetry, but if the ventral aspect of the tuber coxae is fractured, the height of the dorsal aspect may be equal to the contralateral side, but the anatomy of the ventral aspect is distorted. Small muscle defects may be associated with fracture or enthesopathy of the tubera ischii, but even with a displaced fracture, palpation of this area may be unrewarding (Fig. 6-23). If a pelvic injury or fracture is suspected, the clinician should gently rock (move) the horse from side to side. Subtle crepitus may be detected, but with many pelvic fractures this is not apparent until days to weeks after injury and only during the initial portions of the examination before muscle guarding supervenes. The veterinarian should grasp the tail and elevate it. Many horses resist this, but in those with fractures of the base of the tail (most commonly from sitting in the starting gate or trailer), a true painful response is elicited. Subtle swelling also may be present. Lack of tail tone may indicate neurological disease.

Fig. 6-22 Although the veterinarian must take care when standing behind any horse, this perspective is crucial in determining pelvic heights and widths. The height of each tuber coxae is compared in this photograph. Alternatively, an assistant on each side can be asked to point to a comparable location, or tape can be applied.

Muscle pain and muscle atrophy should be assessed. The clinician carefully examines the gluteal musculature, the origin of the caudal thigh muscles, and the tensor fascia lata (see Chapter 46 for further discussion of muscle assessment and palpation of the greater trochanter of the femur). Pain or soreness noted during palpation of the semimembranosus and semitendinosus muscles may be associated with injury of the ipsilateral tuber ischium.2

PALPATION OF THE PELVIS PER RECTUM Rectal examination is not part of the routine lameness examination and should be reserved as a special examination procedure if pelvic fracture or aortoiliac thrombosis is suspected. With the wrist just inside the anus the veterinarian should palpate the medial and dorsal aspects of the acetabulum, comparing sides. In young horses, there is a membranous junction between pelvic bones in the center of the acetabulum; a defect and a small amount of motion normally can be felt. Just cranial to the acetabulum is the cranial aspect of the pubis (brim of the pelvis). With the arm at elbow depth the examiner should sweep the arm dorsally on each side to palpate the medial aspect of each ilium. The ventral aspect of the sacrum and sacroiliac region are compared. The clinician should compare the pulse quality between the right and left external iliac arteries and evaluate conformation and pulse quality of the terminal aorta and branches. Horses with aortoiliac thromboembolism have abnormal conformation and altered pulse quality. Crepitus may be felt more easily by gently rocking the horse from side to side, picking up one hindlimb, or walking the horse a short distance with the veterinarian’s arm still within the rectum. Asymmetry, swelling, actual fracture lines, fragments or callus, and crepitus are assessed. In horses with acute pelvic fractures, crepitus, fracture fragments or lines, and callus usually are not detectable, but hematoma and soft tissue swelling usually can be felt. In horses with ilial wing or shaft

The tubera ischii (shown) and third trochanters are palpated carefully. Enthesopathy or fracture causes lameness that is difficult to locate without careful palpation or scintigraphic examination. Occasionally, horses with small muscle defects located distal to the tubera ischii have chronic lameness from previous fracture. (Courtesy Carolyn Arnold, Kennett Square, Pennsylvania.)

Fig. 6-23

CHAPTER 6 fractures, large fracture hematomas often are present, but the absence of swelling does not preclude presence of ilial fractures. These horses are at risk to develop fatal hemorrhage. Edges of fracture fragments may be evident with comminuted or grossly displaced fractures. With chronic pelvic fractures, crepitus and callus may be more obvious.

PALPATION OF THE HINDLIMB For safety reasons, I prefer to start proximally and work distally in a hindlimb, allowing the horse to become accustomed to palpation. Horses often object to palpation of the flank and stifle regions, and this should not be misinterpreted as a sign of pain. The clinician should grasp the tail and pull it gently toward himself or herself to keep the ipsilateral hindlimb bearing weight and reduce the chance of the horse kicking. It may be useful to pick up the ipsilateral forelimb. In the large majority of horses the entire limb can be safely examined while bearing weight, but pain in the lame limb or contralateral limb or the horse’s behavior may make it difficult or impossible to pick up the limb. Reluctance to pick up the hindlimbs has been attributed to unilateral or bilateral sacroiliac pain.2 Horses with shivers often are reluctant or anxious to pick up one or both hindlimbs. It may be necessary to spend a small amount of time coaxing the horse to elevate the hindlimb, at first just high enough to examine or pick out the hind foot and then progressing to full flexion. Although historically the hock and stifle joints have been regarded as the principal sources of pain causing hindlimb lameness, there are many other potential sites, and the metatarsal and fetlock regions in particular should be examined with care.

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However, normal young horses (weanlings to early 2-yearolds) often have prominent bilateral fluid distention of the femoropatellar joint capsules. The clinician should find the medial patellar ligament and follow it proximally and distally. At the proximal extent, the medial fibrocartilage of the patella can be felt medial to the medial trochlear ridge of the femur. It is this normal arrangement of the medial aspect of the patella and the medial trochlear ridge that allows the veterinarian to determine whether a horse has patellar luxation. The position of the patella is difficult to confirm if the horse is standing with the stifle flexed. True patellar luxation is rare. The examiner should determine if the medial patellar ligament is enlarged, which usually reflects previous desmotomy. Usually a distinct depression is present between the medial patellar ligament and the medial collateral ligament, but effusion of the medial femorotibial (MFT) joint may result in a substantial “bulge” (Fig. 6-24). This may be the only clinical sign indicative of MFT joint injury. The lateral patellar ligament is palpated from its origin to insertion. Patellar desmitis is unusual, but does occur; it usually involves the middle patellar ligament and may cause mild swelling. Previous injection with counterirritants causes firm, fibrous areas over the patellar ligaments, a common finding in racehorses. Gently rocking the horse from side to side to assess motion of the patella may give some indication of the potential for intermittent upward fixation of the patella (IUFP). In horses prone to IUFP, jerky rather than the normal smooth motion of the patella sometimes is detected.2 The

Thigh The clinician should assess the thigh for swelling, muscle atrophy, or scarring. Horses with femoral fractures usually have obvious severe swelling, crepitus, and instability of the limb. The third trochanter of the femur is difficult to feel, and clinical abnormalities associated with enthesopathy of the insertion of the superficial gluteal muscle or a fracture usually are impossible to detect. Scarring associated with the semitendinosus, semimembranosus, and rarely, the biceps femoris can lead to mechanical gait deficits, known as fibrotic myopathy. The gastrocnemius muscle arises from the distal caudal femur, and acute tearing of this muscle may cause swelling in the caudal stifle area. This is difficult to perceive, but severe muscle injury results in a marked postural change, which should provoke more careful assessment of this region.

Stifle Palpation of the stifle is limited to the cranial, lateral, and medial aspects; unfortunately, the caudal and proximal aspects of the joint are inaccessible. Many horses, especially fillies, object to palpation of the stifle, a normal response often misinterpreted as a painful reaction. The veterinarian should palpate the stifle with the limb bearing weight. The foot should be flat on the ground. This may be impossible if the horse has severe pain prohibiting complete assessment of the stifle. The limb should be in a neutral and not in an abducted position, and should be perpendicular to the spine or slightly ahead of the other hindlimb. If the limb is retracted, it is more difficult to palpate the patellar ligaments and joint outpouchings. The middle patellar ligament is identified and followed proximally to the distal aspect of the patella. The clinician should feel the femoropatellar joint capsule between either the middle and medial or the middle and lateral patellar ligaments and should determine the presence of effusion. In horses with osteochondrosis dissecans (OCD), fluid distention can be pronounced.

The medial femorotibial joint (right stifle, cranial view) is the most common location for osteoarthritis of the stifle joint and is palpated medially (needle in joint) between the medial patellar ligament and the medial collateral ligament. Normally a depression is present at this location, but a bulge from effusion can be palpated.

Fig. 6-24

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lateral femorotibial joint capsule is accessed between the lateral patellar and lateral collateral ligaments, but even with severe effusion it is difficult to palpate. Overlying and adjacent soft tissue structures obscure palpation. Deep palpation of the medial collateral ligament and the medial patellar ligament with the limb in flexion may elicit a painful response in horses with stifle lameness, but it probably is not specific for the source of pain in the stifle. The medial collateral stress test is perhaps the most reliable manipulative test of the stifle, although horses with lower limb lameness also may respond. With the leg in partial flexion, the shoulder or one hand is used as a fulcrum on the lateral aspect of the stifle, and the distal extremity is pulled laterally, thus placing valgus stress on the stifle (Fig. 6-25). Care should be taken because horses may resent this manipulative test. If possible, the valgus motion should be applied by using the shoulder as a fulcrum and both hands on the crus, thus eliminating possible false-positive results from the lower limb. Patellar manipulation may cause a painful response, particularly in horses with femorotibial joint disease. During this procedure, caudal movement of the femur also may exacerbate cruciate injuries. With the limb on the ground in a weight-bearing position, the clinician’s hand is placed on the distal aspect of the patella, and the patella is forced upward (Fig. 6-26). Theoretically during this test, multiple movements of the stifle are induced. The patellar ligaments are stretched, the patella is forced proximally, and on release the patella rapidly moves distally against the trochlear ridges, and the femur is forced caudally. Tests to assess cruciate ligament damage have been described but are dangerous to perform, and I have not found them particularly useful.9 Complete tearing of the cruciate or collateral ligaments is rare, and partial tearing does not cause clinically detectable instability. In horses with severe lameness and gross stifle instability, it is obvious that the stifle is the source of lameness and pain usually prohibits manipulation.

Fig. 6-25 The valgus stress test of the stifle is difficult to perform and is accomplished by using a hand (shown) or shoulder as a fulcrum. This test can be done during static examination or a provocative test followed by trotting (see Chapter 8).

Crus The examiner should palpate the crus using both hands with the limb bearing weight. Subtle swelling of the medial aspect of the tibia can be palpated, but palpation of the caudolateral aspect of the tibia, the area in which stress fractures are diagnosed most frequently, is limited. Often no palpable abnormality is associated with a stress fracture. Any small wound or any form of swelling should be thoroughly investigated for the possibility of underlying bone damage, such as an occult tibial fracture. The veterinarian should palpate the caudal soft tissues. Proximally, the musculotendonous junction of the gastrocnemius muscle is a rare site of pain. The common calcaneal tendon is assessed. Swelling may indicate damage to any one of the contributing tendons. Effusion of the tarsal sheath causes swelling just proximal to the tarsus, at the caudal aspect of the crus, and should be differentiated from bog spavin. Deep palpation of the medial and caudal aspects of the crus is performed with the limb elevated (Fig. 6-27). Horses with tibial stress fractures or those with spiral fracture or other tibial trauma may show a painful response, but falsepositive responses are frequent. Tibial percussion, performed medially by using a clenched fist (knuckles) as a hammer, may elicit a painful response in horses with stress fractures, but many normal horses resent this test.

Tarsus Five common swellings of the hock are important to differentiate, but hock swelling is not synonymous with hock pain. Capped hock is swelling located at the point of the hock (the proximal aspect of the calcaneus) and usually is an incidental finding, but in some horses the condition does cause lameness (Fig. 6-28). The most common form involves the development of firm, fibrous subcutaneous tissue in the false bursa that lies over the point of the hock. This is a common area for

Used as a static or provocative test, patellar manipulation is performed by placing the palm of the hand over the cranial aspect of the patella and manually forcing the patella proximally several times in succession. This maneuver can exacerbate pain from conditions of the patella and femoropatellar joint and forces the distal femur in a caudal direction. Pain from soft tissue injuries such as patellar, cruciate or collateral ligament tears, and osteoarthritis of the femorotibial joints can be exacerbated, but false-negative and false-positive results are common. (Courtesy Carolyn Arnold, Kennett Square, Pennsylvania.)

Fig. 6-26

abrasions and excoriation, and fibrous tissue formation results in a blemish but usually no lameness. Horses may be sensitive to palpation if the area has been traumatized recently. Infection or trauma leading to osteitis of the calcaneus can cause a clinically important capped hock and severe lameness. In these horses the problem involves the calcaneal bursa, located between the common calcaneal tendon and the calca-

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A

55

B

Fig. 6-27 A, Palpation of the medial aspect of the tibia in a flexed position or B, tibial percussion in the standing position sometimes elicits pain in horses with tibial stress fractures, but falsepositive results are common.

neus. If surrounding soft tissue swelling is minimal, fluid distention of the calcaneal bursa may be felt by ballottement. The bursa can be felt both medially and laterally at the proximal aspect of the calcaneus. Lateral, or less commonly, medial dislocation (luxation) of the SDFT results in similar swelling, but in the acute situation, lameness is present. Careful palpation may reveal the SDFT coursing laterally (Fig. 6-29), unless excessive soft tissue swelling is present. Effusion of the tarsal sheath, thoroughpin, must be differentiated from bog spavin (see following text). Tarsal tenosynovitis causes swelling both medially and laterally in the depression between the calcaneal tendon and caudal tibia (Fig. 6-30). With severe effusion of the tarsal sheath, fluid distention can be palpated distal to the hock on the medial aspect. Thoroughpin usually is an incidental finding, seen most commonly in Western performance horses, but acute lameness accompanied by tarsal tenosynovitis can indicate strain or injury of the sheath, often associated with adjacent bony injury. Unusually, swelling in the distal, caudal crus identical to that seen with classic thoroughpin is seen, but communication with and concomitant swelling of the tarsal sheath is absent. The term spavin refers to “any disease of the hock joint of horses in which enlargements occur, often causing lameness…the enlargement may be due to collection of fluids or to bony growth.”10 Bog spavin is fluid distention of the tarsocrural joint capsule. The tarsocrural joint has four outpouchings: dorsolateral, dorsomedial, plantarolateral, and plantaromedial. All joint pouches may be distended, although the dorsomedial and plantarolateral pouches are large and most prominent (Fig. 6-31). Using ballottement, fluid can be pushed between pouches on the dorsal or plantar aspects, thus differentiating this condition from thoroughpin. Bone spavin refers to fibrous and bony swelling that results from chronic osteoarthritis of the proximal intertarsal, centrodistal, and tarsometatarsal joints. This swelling usually is seen in older horses and can be palpated and observed on the medial side of the hock (Fig. 6-32). Although the bony enlargement is the result of proliferation, it does not necessarily mean the horse is lame as the result of the condition. Most

Capped hock, a firm fibrous swelling of the proximal aspect of the calcaneus (point of the hock), is considered a blemish, but with effusion of the calcaneal bursa (not shown), lameness is substantial.

Fig. 6-28

horses with distal hock joint pain do not have palpable enlargement medially, and based on radiographic evaluation, the most common area of proliferation and bony change is dorsolateral. Blood spavin is an old term usually meaning enlargement of the saphenous vein,3 but it also may have been used to describe a prominent saphenous vein in horses with bog spavin. Saphenous distention is rare and the term is not used today. Occult or blind spavin is an obsolete term used to describe horses with clinical signs of hock lameness but no observable

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Fig. 6-29 Lateral dislocation (luxation) of the superficial digital flexor tendon. Instead of attaching to the tuber calcanei, the superficial digital flexor tendon (arrows) is now located lateral to the point of the hock. Initial swelling makes this diagnosis difficult.

Moderate to severe tarsocrural effusion, bog spavin, in this draft filly was caused by osteochondritis dissecans of the distal intermediate ridge of the tibia. Distention of the large dorsomedial pouch and swelling of the dorsolateral, plantarolateral, and plantaromedial pouches was present.

Fig. 6-31

bony swelling.3 High spavin is also an obsolete term used to describe bone spavin located close to the tarsocrural joint.3 Curb describes swelling along the distal, plantar aspect of the hock and has often erroneously been blamed on long plantar desmitis. In most horses the swelling is actually enlargement of the SDF tendon or subcutaneous tissues. The swelling is often firm, but in some horses subcutaneous fluid can be present (see Fig. 79-1). In horses with acute severe injury the swelling may feel soft and mushy. In some normal horses the proximal aspect of MtIV is prominent and should not be confused with curb. Swelling restricted to the medial or lateral aspect of the hock may reflect collateral ligament injury. Localized heat on the medial aspect of the hock or on the proximal aspect of the metatarsus may be important findings.

THE CHURCHILL HOCK TEST • Dan L. Hawkins

Thoroughpin, swelling located in the distal, caudal crus, usually is caused by distention of the tarsal sheath and must be differentiated from effusion of the plantarolateral pouch of the tarsocrural joint (bog spavin).

Fig. 6-30

The Churchill hock test was developed by Dr. E.A. Churchill in the 1950s as a rapid, non-invasive, specific method to screen and identify distal tarsal pain in athletic horses. Although the test has been used by Dr. Churchill and me primarily in STBs, TBs, and Three-Day Event horses, it is equally reliable when applied to other equine athletes. Digital pressure is applied on the plantar aspect of the head of the second metatarsal bone (MtII) and fused first and second tarsal bones with the limb in a non–weight-bearing position. Abduction of the limb is a positive response. To

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Correct left hand placement in the left proximal metatarsal region to perform the Churchill hock test. (Courtesy Dan Hawkins, Dubai, United Arab Emirates.)

Fig. 6-33

Fig. 6-32 Bone spavin (arrows), fibrous and bony swelling on the medial aspect of the distal hock joint (left hindlimb) caused by chronic osteoarthritis of the distal hock joints, sometimes appears in older sport horses but is rare in young racehorses. The presence of bone spavin should be noted and this area should be palpated carefully, but horses can have distal hock pain without bone spavin, and horses with bone spavin can have lameness elsewhere in the limb. Previous cunean tenectomy causes chronic fibrosis in this region. examine the left tarsus, the clinician approaches the horse facing caudally. The left hindlimb is picked up and brought forward, supported by the clinician’s right hand cupped under the fetlock or hoof. Holding the limb so that the hoof is approximately 25 to 30 cm above the ground is most comfortable for the horse. The heel of the left hand is positioned on the proximodorsal surface of the third metatarsal bone (MtIII) while the third phalanges of the index and middle or middle and ring fingers are placed around the medial side of the tarsus to engage the bony ridge formed by the head of MtII and the first and second tarsal bones (the area of insertion of the cunean tendon) (Fig. 6-33). The thumb is rested on the dorsal lateral aspect of the tarsus and proximal MtIII. Gentle, firm pressure is applied to the bony ridge by flexing the phalanges of only the index and middle fingers (Fig. 6-34). The hand does not squeeze the hock. Pressure is applied three times approximately 1 second apart, each time with increasing intensity to a maximum effort on the third time. Proficiency requires patience and routine practice. Consistent diagnostic information can be obtained safely from

The Churchill test is demonstrated on an anatomy specimen. The index and middle fingers are flexed and positioned on the bony ridge formed by the third metatarsal bone and the fused first and second tarsal bones, and the heel of the hand rests on the proximodorsal aspect of the third metatarsal bone. The thumb rests against the dorsolateral aspect of the tarsus. (Courtesy Dan Hawkins, Dubai, United Arab Emirates.)

Fig. 6-34

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more than 90% of fit racehorses. If the limb cannot be picked up, the test cannot be performed. Fussing and repeatedly flexing the hock and limb in an agitated manner while the procedure is performed should not be misinterpreted as a positive response. The Churchill hock test is useful for horses that are not visibly lame, but the trainer or rider has a complaint that the horse is doing something uncharacteristic during work or competition associated with decreased performance. The horse may have a changed attitude toward work, lugs in, is rough in the turns, refuses to change leads, stops at jumps, jumps to one side, or is stiff going in one direction. Although these horses cannot be blocked out at a slow gait, the Churchill hock test may suggest hock pain.

SAPHENOUS FILLING TIME • Mike W. Ross The veterinarian should assess the saphenous vein filling time. Blood flow in the saphenous vein is prevented using digital compression in the proximal metatarsal region, and the blood accumulated in the vein over the tarsocrural joint is pushed proximally to completely collapse the vein. The finger compressing the vein distal to the hock is then removed, and the time it takes for the saphenous vein to fill is observed. Normally, it takes less than 1 second for the vein to fill, but in horses with reduced circulation, prolonged filling time is seen. Pulse quality of the dorsal metatarsal artery, located on the dorsolateral aspect of MtIII just dorsal to the fourth metatarsal bone (MtIV), can be useful, especially if the history suggests lameness is caused by vascular compromise. The arterial pulse quality is compared with the contralateral limb.

The Metatarsal Region The veterinarian should palpate the flexor tendons and SL. Tendonitis is unusual in the hindlimb, but occasionally SDF tendonitis occurs in the proximal metatarsal region. This is most common in horses with curb, and tendonitis progresses distally to involve the metatarsal area. The hock angle is evaluated carefully. Occasionally horses with severe curb or those with SDF tendonitis of the metatarsal region have reduced hock angle (obvious unilateral sickle-hocked conformation), indicating loss of support in the SDFT. Once a general palpation for the presence of heat, swelling, exostoses associated with the MtIII, MtII, MtIV, and the proximal aspect of the DFTS is completed, the limb is lifted and deep palpation is performed. The clinician should carefully palpate the origin and body of the SL, keeping in mind that both false-positive and false-negative responses can occur (Fig. 6-35). Much of the palpation of the SL laterally is indirect, since MtIV hides the origin and proximal body. Because the presence of the splint bones and dense metatarsal fascia prevents substantial swelling, or at least the clinical recognition of swelling of the SL, even mild swelling in the proximal, medial metatarsal region should be carefully interpreted. With the limb in flexion, the axial borders of splint bones are palpated. The dorsal aspect of MtIII should also be assessed with the limb in flexion, because bony injury of MtIII does occur and includes dorsal cortical trauma from external injury or interference, dorsal cortical and spiral fractures, and proximal dorsolateral fractures.

Metatarsophalangeal Joint Many of the common problems of the metatarsophalangeal joint, such as short, mid-sagittal fractures of the proximal phalanx, sesamoiditis, stress or non-adaptive remodeling of MtIII, and osteochondrosis, cause very few clinical signs and while palpation is quite important, diagnostic analgesia is often needed to localize pain to this area. Nonetheless, careful

Fig. 6-35 Deep palpation of the proximal suspensory ligament can be performed only with the limb in flexion. The close association of the suspensory origin to the Churchill site explains the need to differentiate proximal plantar metatarsal pain from distal hock joint pain using diagnostic analgesia. (Courtesy Howard “Gene” Gill, Pine Bush, New York.)

palpation of the fetlock region is mandatory. Some horses have concurrent metatarsophalangeal joint and stifle pain and when suspicious findings exist in one site, the veterinarian should look carefully at the other for additional, secondary, or complimentary problems. The metatarsophalangeal or hind fetlock joint, is evaluated with the limb bearing weight and in flexion. The clinician should assess the metatarsophalangeal joint capsule and the DFTS for the presence of effusion or fibrosis (Fig. 6-36). Incidental effusion of both the metatarsophalangeal joint and DFTS is common in the hindlimb of older performance horses therefore this finding should not be over-interpreted. In younger horses, particularly racehorses, the presence of effusion can be an important clinical sign associated with osteoarthritis or other problems and should be interpreted accordingly. The clinician should carefully palpate for the presence of heat and mild swelling over the surface of both PSBs, subtle but important signs of sesamoiditis. This problem is more prevalent in the hindlimb and causes few clinical signs. The digital pulse should be assessed. With the fetlock joint in flexion, the veterinarian should palpate the proximal, dorsal aspect of the proximal phalanx for the presence of pain or exostoses (Fig. 6-37) and should apply pressure to the PSBs, avoiding aggressive compression

CHAPTER 6

• Palpation

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clinically important areas that were pointed out for the forelimb. High and low ringbone (osteoarthritis of the proximal interphalangeal and distal interphalangeal joints, respectively), osteochondrosis of the pastern joint, and soft tissue problems such as SDF branch tendonitis, distal sesamoidean desmitis, and plantar injury of the pastern joint occur, but with reduced frequency when compared with the forelimb.

Foot

Fig. 6-36 The metatarsophalangeal joint region often is overlooked during lameness examination. This joint should be palpated carefully with the limb in the standing and flexed (shown) positions. (Courtesy Ross Rich, Cave Creek, Arizona.)

A similar approach to the evaluation of the hind foot as that described for the front foot is used. I spend considerably less time evaluating the hind foot than the front foot, unless the history or horse type dictates otherwise, because this area is relatively infrequently the source of pain. In the Draft horse, hind foot pain is as common as in the forelimb, and therefore the hind feet merit considerable attention. Unless specifically indicated by the lameness history, or the horse is severely lame without an obvious cause in the upper limb, I do not routinely perform a hoof tester examination of the hind foot. Pressure with hoof testers over the frog and across the heels in the hind foot often causes a false-positive response in normal horses. The position needed to perform an unassisted hoof tester examination in the hindlimb can be dangerous. The presence of an assistant to elevate the limb may obviate some of the risk. The examiner should assess the shape, balance, and contour of the foot, and observe the shoe (or lack of one) carefully. Hoof angle in the hindlimb ranges from 48° to 58°, and the hoof and pastern axis should be straight. A common finding is low or under-run heels. An interesting relationship between low heels and the presence of PSD has been noted.2 In these horses a lateral radiograph of the foot shows the plantar aspect of the distal phalanx is lower than the dorsal aspect.2 Shoe wear is extremely important in the hindlimb and can give clues to the source of lameness. For instance, horses with distal hock joint pain tend to stab the lower hindlimb during advancement, causing excessive wear of the lateral branch of the shoe (Fig. 6-38). Other lower hindlimb lameness, such as osteoarthritis of the metatarsophalangeal joint, can cause a similar gait, but usually abnormal shoe wear is less pronounced. Horses with stifle lameness often wear the medial branch of the shoe. The presence of heel and toe caulks or borium cause additional shear stress on many of the lower limb joints and can exacerbate lameness.

THE ROLE OF PHYSICAL EXAMINATION IN THE LAMENESS EXAMINATION

Fig. 6-37 Palpation of the proximal, dorsal aspect of the proximal phalanx can elicit pain in horses with incomplete mid-sagittal fracture of the proximal phalanx. In trotters, interference injury from the ipsilateral front foot causes pain and swelling in this region. (Courtesy Ross Rich, Cave Creek, Arizona.) that may cause false-positive results. The range of motion of the metatarsophalangeal joint is noted.

Pastern When the limb is elevated, the reciprocal apparatus causes constant flexion of the digit, which makes palpation of the plantar aspect of the pastern exceedingly difficult. Subtle swelling in the plantar pastern is easy to miss. Bony and softtissue structures should be palpated with the horse in the standing position and the veterinarian should note the same

Body temperature may assist with a clinical diagnosis. The normal temperature range is 37.5º to 38.6º C (99.5 to 101.3º F), although in a foal the upper limit may normally be slightly higher. Body temperature in foals rises more abruptly than in adult horses in response to stress, infection, and inflammation. Thus transport of a foal may cause transient low-grade pyrexia, but fever in an adult horse after transport is abnormal. Localized infection in a foal usually causes pyrexia but rarely does in an adult. The examiner should not exclude infectious arthritis in an adult horse simply because fever is not present. However, adult horses usually are pyrexic during the early stages of cellulitis or lymphangitis. Elevation in the pulse and respiratory rates often accompanies severe lameness because of pain. Systemic diseases such as endotoxemia may cause abnormal vital parameter findings in any horse and can lead to conditions such as laminitis. It is important to remember that diseases of other body systems can cause clinical signs that mimic lameness or cause true gait deficits. For instance, abnormal or stiff gaits can be seen in horses with pleuritis and peritonitis, abdominal, sublumbar, inguinal, thoracic inlet, and pectoral abscesses or

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Diagnosis of Lameness tumors. Proliferative new bone associated with hypertrophic osteopathy may be associated with a thoracic or abdominal mass. If an unusual situation arises, the veterinarian should step back and think of the exception rather than the rule, because the “red herring” may be just around the corner.

REFERENCES

It is imperative to observe the hind shoes for wear during lameness examination. This right hind shoe (lateral is to the right) has wear along the dorsal and lateral aspects (lateral aspect of toe grab and fullering are worn) consistent with a lower hindlimb lameness, such as distal hock joint or proximal metatarsal region pain.

Fig. 6-38

CHAPTER •

1. Strand E, Martin G, Crawford M, et al: Intra-articular pressure, elastance and range of motion in healthy and injured racehorse metacarpophalangeal joints, Equine Vet J 30:520, 1998. 2. Dyson SJ: Personal communication, 2001. 3. Kane AJ, Stover SM, Gardner IA, et al: Horseshoe characteristics as possible risk factors for fatal musculoskeletal injury of Thoroughbred racehorses, Am J Vet Res 57:1147, 1996. 4. Kobluk CN, Robinson RA, Gordon BJ, et al: The effect of conformation and shoeing: a cohort study of 95 Thoroughbred racehorses, Proc Am Assoc Equine Pract 36:259, 1990. 5. Maddren L: Personal communication, 1984. 6. Turner TA: Predictive value of diagnostic tests for navicular pain, Proc Am Assoc Equine Pract 42:201, 1996. 7. Delahanty DD: Manipulative procedures in detecting horse lameness, Cornell Vet 64:443, 1974. 8. Jeffcott LB, Kalin G, Drevemo S, et al: Effect of induced back pain on gait and performance of trotting horses, Equine Vet J 14:129, 1982. 9. Stashak TS: Adam’s lameness in horses, Philadelphia, 1987, Lea & Febiger. 10. Barnhart CL: The American college dictionary, New York, 1970, Random House.

7

Movement Mike W. Ross “The best time for examining a lame horse is while he is in action. An attendant should lead him on a trot, preferably on hard ground, in a straight line, allowing him freedom of his head, so that his movements may all be natural and unconstrained.” A. Liautard, 18881 t would be difficult to improve on Liautard’s insistence that the lame horse be examined during movement or his description for how it is best accomplished. Although all parts of the lameness examination are important, the key is the determination of the limb or limbs involved. Not all horses with musculoskeletal problems exhibit lameness that is perceptible under normal conditions, or even by use of high-speed or slow-motion cinematography, gait analysis, or other sophisticated imaging devices. Under most circumstances, however, lameness from pain or a mechanical defect in gait is discernible, and the essence of the lameness examination is to determine the source of the pain. This discussion includes relevant experimental findings to support clinical

I

observations, but sometimes experimental finds are confusing rather than informative.

GAIT Gait, defined as the “manner or style of walking”2 or “the manner of walking or stepping,”3 is used to describe the speed and characteristics of a horse in motion. The natural gaits, those exhibited when a horse is free in a field, are the walk, trot, and gallop.4 The canter is a collected gallop. Other gaits including the pace, running walk, rack (a singlefoot or broken amble), fox trot, and amble are artificial gaits, although some

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Diagnosis of Lameness tumors. Proliferative new bone associated with hypertrophic osteopathy may be associated with a thoracic or abdominal mass. If an unusual situation arises, the veterinarian should step back and think of the exception rather than the rule, because the “red herring” may be just around the corner.

REFERENCES

It is imperative to observe the hind shoes for wear during lameness examination. This right hind shoe (lateral is to the right) has wear along the dorsal and lateral aspects (lateral aspect of toe grab and fullering are worn) consistent with a lower hindlimb lameness, such as distal hock joint or proximal metatarsal region pain.

Fig. 6-38

CHAPTER •

1. Strand E, Martin G, Crawford M, et al: Intra-articular pressure, elastance and range of motion in healthy and injured racehorse metacarpophalangeal joints, Equine Vet J 30:520, 1998. 2. Dyson SJ: Personal communication, 2001. 3. Kane AJ, Stover SM, Gardner IA, et al: Horseshoe characteristics as possible risk factors for fatal musculoskeletal injury of Thoroughbred racehorses, Am J Vet Res 57:1147, 1996. 4. Kobluk CN, Robinson RA, Gordon BJ, et al: The effect of conformation and shoeing: a cohort study of 95 Thoroughbred racehorses, Proc Am Assoc Equine Pract 36:259, 1990. 5. Maddren L: Personal communication, 1984. 6. Turner TA: Predictive value of diagnostic tests for navicular pain, Proc Am Assoc Equine Pract 42:201, 1996. 7. Delahanty DD: Manipulative procedures in detecting horse lameness, Cornell Vet 64:443, 1974. 8. Jeffcott LB, Kalin G, Drevemo S, et al: Effect of induced back pain on gait and performance of trotting horses, Equine Vet J 14:129, 1982. 9. Stashak TS: Adam’s lameness in horses, Philadelphia, 1987, Lea & Febiger. 10. Barnhart CL: The American college dictionary, New York, 1970, Random House.

7

Movement Mike W. Ross “The best time for examining a lame horse is while he is in action. An attendant should lead him on a trot, preferably on hard ground, in a straight line, allowing him freedom of his head, so that his movements may all be natural and unconstrained.” A. Liautard, 18881 t would be difficult to improve on Liautard’s insistence that the lame horse be examined during movement or his description for how it is best accomplished. Although all parts of the lameness examination are important, the key is the determination of the limb or limbs involved. Not all horses with musculoskeletal problems exhibit lameness that is perceptible under normal conditions, or even by use of high-speed or slow-motion cinematography, gait analysis, or other sophisticated imaging devices. Under most circumstances, however, lameness from pain or a mechanical defect in gait is discernible, and the essence of the lameness examination is to determine the source of the pain. This discussion includes relevant experimental findings to support clinical

I

observations, but sometimes experimental finds are confusing rather than informative.

GAIT Gait, defined as the “manner or style of walking”2 or “the manner of walking or stepping,”3 is used to describe the speed and characteristics of a horse in motion. The natural gaits, those exhibited when a horse is free in a field, are the walk, trot, and gallop.4 The canter is a collected gallop. Other gaits including the pace, running walk, rack (a singlefoot or broken amble), fox trot, and amble are artificial gaits, although some

CHAPTER 7 pacers pace “free-legged” (without the use of hobbles) while on the track, either at a slow speed or racing speed, and occasionally a Standardbred (STB) paces free-legged in a field. In some instances a trotter switches from a trot to the pace, but this change usually is exhibited while the horse is performing at speed and may be associated with lameness or interference. The term beat describes the number of foot strikes in a single stride cycle regardless of whether one or more feet strike the ground simultaneously. The following abbreviations are used for limbs: left forelimb (LF), right forelimb (RF), left hindlimb (LH), and right hindlimb (RH). The walk is a fourbeat gait in which all four feet strike the ground independently without a period of suspension (in which no feet are on the ground). Depending on the part of the stride during which observations begin, the walk can appear to be lateral or diagonal. In general, in a lateral gait, both feet on one side strike the ground before the feet on the contralateral side. In a diagonal gait, one foot strike is followed by a strike of the foot located diagonal and contralateral to the initial foot (e.g., LF followed by the RH). Lame horses should always be evaluated at the walk. Stride length should be evaluated and compared with observations at the trot. Stride length and sequence of footfalls are easier to see while horses are walking than while trotting. Horses with hindlimb lameness may be admitted for evaluation for failure to track up.5 Horses normally track up, or over track. The hind foot is placed in or in front of the imprint of the ipsilateral front foot. Failure to track up usually is caused by hindlimb lameness or poor impulsion, and the hind foot imprint is seen behind that of the ipsilateral front foot.5 Backing is a diagonal, two-beat gait. Horses seldom back up naturally, but backing commonly is required of horses during performance events, while exiting from a trailer, or while driving. Backing is useful during lameness examination to evaluate certain gait deficits, such as shivers, stringhalt, and neurological disease. The trot is a diagonal, two-beat gait and diagonal pairs of limbs move simultaneously. The trot is theoretically a symmetrical gait, meaning both “halves” (beats) of the stride are identical, and at low speed in a sound horse, symmetry is likely achieved. However, at speed perfect balance and fine management of weight (of the shoes) are necessary for a trotter to be perfectly symmetrical. There is a moment of suspension between impact of each diagonal pair of limbs. Hindlimb lameness is present in a higher percentage of horses that perform at speed at the trot compared with galloping horses because of differences in weight distribution in the trot and gallop. Compensating lameness develops in the diagonal paired limb. LF lameness predisposes to RH lameness. The pace is a symmetrical, lateral, two-beat gait predominantly in STB racehorses and is characterized by movement of lateral pairs of limbs simultaneously (LH and LF; RH and RF), with a moment of suspension between lateral pairs. Pacers also have a high percentage of hindlimb lameness, but compensatory lameness usually develops in the lateral paired limb. RH lameness predisposes to RF lameness. The gallop or run is a four-beat gait. In the gallop and the canter the horse leads with the left or right forelimb, the forelimb that strikes the ground last in the stride sequence. An unrestrained horse usually leads with the LF turning to the left, or the RF turning to the right. Fatigue also plays a role. A Thoroughbred (TB) racehorse racing counterclockwise leads with the LF on the turns, but immediately after entering the stretch, switches to the right lead. Failure to switch leads, or constantly switching leads in the gallop or canter, may reflect fatigue or lameness. In a left lead gallop, the RH strikes the ground first, followed in sequence by the LH, RF, and LF followed by a period of suspension. When a horse is on the right lead, the RF strikes

• Movement

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the ground last, propelling the horse into the suspension phase of the stride. It is often assumed that a horse with RF lameness is reluctant to take the right lead. However, bone stress measured in the radius and McIII is greater on the nonlead (trailing) forelimb, and thus a lame horse may change leads to protect the non-lead forelimb.6 Ground reaction forces are greater in the trailing (non-lead) forelimb, a fact that supports the clinical observation that horses with forelimb lameness may select leads to protect the lame forelimb. A horse with a RF lameness may prefer the right lead, allowing the LF to assume the greater forces and bone stress.5 The canter (lope) is a three-beat gait. In left lead canter the RH strikes the ground first, then the LH and RF land simultaneously, followed by the LF and then a period of suspension. A horse reluctant to take a lead may be trying to compensate for hindlimb lameness. In the right lead the LH must absorb a considerable amount of concussion and then generate propulsive forces. Proneness of this limb to fatigue seems logical, but a consistent change in stride characteristics of fatigued horses to protect the LH was not seen.7 Although the LH strikes the ground first, stance time, flexion of the upper limb joints, and ground reaction force are greater in the RH.5 It could be assumed that a horse lame in the RH would be reluctant to take the right lead and may prefer the left lead.5 Lead and stride characteristics of fatigued and lame horses are complex because of asymmetry of the gait, and forelimb and hindlimb problems could account for failure or reluctance to take a particular lead and inappropriate lead switching. Young horses early in training or trained horses that are lame may exhibit a disunited canter. The horse may spontaneously change legs behind, but not in front. In changing from left to right lead canter, or vice versa, the forelimbs and hindlimbs should change simultaneously. Horses with back pain or hindlimb lameness may be reluctant to change leads, or may change in front, but not behind.

The Lameness Examination: Which Gait Is Best? The trot is the most useful gait to determine the location of the lame limb or limbs. Forelimb lameness in particular is difficult to observe at the pace, especially in horses that are led in hand. Lame trotters may pace, supporting the supposition that the pace is an easier gait in a lame STB. I have seen horses with severe forelimb lameness at the trot that looked barely lame when pacing.

Relevance of Lameness at a Trot in Hand Is lameness seen at a trot in hand the same lameness that compromises performance at speed? Is the lameness seen at a trot in hand in a jumping horse the same problem that causes the horse to refuse fences? The answer is usually, but not invariably, yes. For instance, I have seen many STBs show subtle unilateral hindlimb lameness at a trot in hand, but when the horse was later examined at the track and hooked to a cart, pronounced contralateral hindlimb lameness was noted. Differences include the track surface, pulling a cart, the additional weight of the driver, and a faster gait. Lameness often is evaluated on a smooth hard surface useful in exacerbating even subtle problems, but most horses perform on softer surfaces, when other problems may be apparent. More than one lameness problem may exist, one evident at a trot in hand and another while the horse is ridden or driven. Horses can show lameness from one problem when trotted in a straight line, but lameness from an entirely different problem while being trotted in a circle.

Horse Temperament and Lameness Examination Safety of the handler, observers, and the horse must always be considered throughout a lameness examination, and with a difficult horse the examination may need to be modified,

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especially on cold, windy days. In some female horses and geldings, judicious use of the tranquilizer acetyl promazine (0.02 to 0.04 mg/kg, IV) permits continuation of the examination. I avoid use of this tranquilizer in stallions, although the possibility of paraphimosis is remote. Low doses of sedatives such as xylazine can be used (0.15 to 0.30 mg/kg, IV) in stallions or other horses but can produce mild ataxia. Detomidine may be a better choice than xylazine, since the drug lasts longer, thus allowing diagnostic analgesic procedures to be performed.5 I try to avoid using tranquilization and sedation, although some clinicians use them frequently and report that lameness in most horses may be more pronounced and easier to observe. Mild muscle relaxation may reduce the tendency of the horse to guard the lame leg. In big moving, exuberant Warmblood horses, especially dressage horses (particularly stallions), sedation may be essential to accurately assess lameness.5

Leading the Horse during Lameness Examination The horse must be led with a loose lead shank so that it can move the head and neck freely. It is impossible to see a head nod in a fractious or excited horse that is held tightly. Use of a chain lead shank over the nose facilitates control but is resented by some horses, and use of a bridle with a lunge line attached may be preferable.5 Horses should move at a consistent speed, not too fast and not too slow. A lazy horse may need encouragement with a whip. Constantly changing speed can make assessment of lameness difficult, but occasionally, assessing a horse during deceleration may reveal useful information about the existence of subtle lameness.5 A horse may have to be trotted up and down many times. It is sometimes useful for the examiner to lead the horse to assess subtle forelimb lameness, since gait abnormalities may become more obvious.

Surface Characteristics and Lameness Examination The horse should be examined on a smooth, flat surface. I prefer a hard surface, such as pavement or concrete, that creates maximal concussion and may exacerbate subtle lameness. However, the clinical relevance of mild lameness seen on hard surfaces, especially on turns, should not be over-interpreted. Many horses that are actively competing successfully show mild lameness on hard surfaces; it is important to understand that the horse does not perform on a surface of pavement, and foot strike patterns and gait could be much improved if the horse performs on firm, but forgiving surfaces. Crushed rock, cobblestone, deep sand, or undulating grassy areas and potentially dangerous slippery surfaces should be avoided. It is important that the surface is non-slip because some horses appear to lack confidence while moving on hard surfaces and alter the gait. In these situations, horses may shorten the stride for protection rather than from lameness.5 Horses with studs or caulks on the shoes may develop induced lameness unrelated to the baseline lameness when trotting on hard surfaces.5 Ideally the gait on hard and soft surfaces should be compared to help differentiate soft tissue from bony problems. Horses with foot pain usually perform worse on a hard surface. Lameness from soft tissue injuries, such as suspensory desmitis or tendonitis, tends to be worse on soft or deep ground.

DETERMINATION, GRADING, AND CHARACTERIZATION OF LAMENESS Six basic steps are necessary to determine, grade, and characterize lameness. The clinician should determine the following: 1. Primary or baseline lameness or lamenesses 2. Possibility of involvement of more than one limb and presence of compensatory lameness

3. Classification of lameness as a supporting, swinging, or mixed 4. Grading of lameness or lamenesses 5. Alteration of the cranial or caudal phase of the stride 6. Presence of abnormal limb flight The primary or baseline lameness is the gait abnormality before flexion or manipulative tests are used. The practitioner attempts to abolish baseline lameness using analgesic techniques. Lameness in more than one limb may complicate determination of the worst affected limb. It is important to trot a horse even if it is quite lame at a walk, unless an incomplete or stress fracture is suspected. A horse may take a short step with a limb at walk, or can appear very lame, but trot reasonably sound. Horses with scratches (palmar/plantar pastern dermatitis) or superficial wounds in the palmar or plantar pastern may appear quite lame at walk but trot well. A STB pacer may walk extremely short both in front and behind but pace or trot without lameness. However, only the degree of lameness usually differs between a walk and trot. A horse may appear sound at walk and trot in hand, but lameness may be apparent trotting in a circle, in hand or on the lunge, or while being ridden. This lameness now becomes the baseline lameness, and under these conditions, the results of nerve blocks should be evaluated. The clinician should try to recognize if the horse has bilateral forelimb or hindlimb lameness, which is manifest as shortness of stride or poor hindlimb impulsion, or if concurrent forelimb and hindlimb lameness is present. Moderate to severe hindlimb lameness can mimic ipsilateral forelimb lameness, although ipsilateral forelimb and hindlimb lameness also occurs. In these horses the veterinarian should perform diagnostic analgesia in the hindlimb first.

Compensatory Lameness Compensatory (secondary or complimentary) lameness results from overloading of the other limbs as a result of a primary lameness. It must be differentiated from the stride-to-stride compensation by a horse to avoid interference injury because of a gait deficit, or lameness, or to shift weight (load) during examination. A compensatory problem develops as the result of predictable compensation a horse may make over time for a primary lameness in a single limb. However, a horse may compensate for lameness in one limb by shortening the stride in another, a stride-to-stride change in gait that is not the result of lameness. A horse with severe LF lameness is reluctant to extend the LF and must shorten the cranial phase of the LH limb, creating what appears to be a hike in the LH. If the veterinarian looks only at the hindlimbs, LH lameness may be diagnosed. A trotter performing at speed with a LF lameness is likely to develop compensatory lameness in the RF or RH, but not in the LH. However, the horse may appear to be hiking (lame) in the LH to avoid interfering with the LF. Elimination of obvious unilateral forelimb lameness usually resolves an ipsilateral pelvic hike. Experimental results appear to contradict this clinical impression. In 6 of 10 horses with stance phase forelimb lameness, compensatory movements of horses created a false lameness in the contralateral hindlimb (see following text).8 It is often difficult to know which lameness came first, but it is important to understand how horses compensate for lameness and which limbs are at risk to develop compensatory problems. Compensatory problems range from obvious lameness to only mild palpable abnormalities that may still compromise performance. Several predictable patterns of compensatory lameness are possible; the most common is bilateral forelimb or hindlimb lameness. Horses with a specific lameness in one forelimb are at risk to develop the same condition in the opposite forelimb. This tendency may not always be compensation for the primary lameness but may be simultaneous injury or degeneration of bone or soft tissue of both limbs. Abnormal loading of forelimbs or hindlimbs, faulty

CHAPTER 7 bilateral conformation, and the same shoeing or foot conditions all likely contribute to bilateral, simultaneous lameness. In horses with bilateral lameness, eliminating lameness in one limb usually results in contralateral limb lameness. Bilateral lameness may affect both limbs equally, resulting in a short, choppy gait. The horse may be lame in one limb while being circled in one direction and lame in the contralateral limb in the opposite direction. Racehorses that gallop are most likely to develop compensatory lameness on the contralateral limb or the ipsilateral forelimb or hindlimb. A TB racehorse with a left metatarsophalangeal joint lameness is most likely to develop a similar problem in the RH but may also develop LF lameness. In a trotter the contralateral limb is most at risk, followed by the diagonal forelimb or hindlimb. If a trotter has a right carpal lameness, the left carpus should be examined carefully; compensatory lameness also may occur in the diagonal LH limb. In a pacer the ipsilateral forelimb or hindlimb should be considered after the contralateral limb. In a pacer with LH lameness the RH and LF are at risk. The most common compensatory lameness is the same problem in the contralateral limb. However, suspensory desmitis is a common compensatory problem in both the contralateral and other limbs. In a TB racehorse or a jumper with LF lameness, RF suspensory desmitis is common. Primary RH lameness may result in suspensory desmitis in the RF. It is logical that soft tissue structures are particularly vulnerable to the effects of over-load. Superficial digital flexor tendonitis

A

B

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may develop secondary to a primary problem in the contralateral limb. In trotters a common pattern is primary carpal lameness and compensatory osteoarthritis of the medial femorotibial joint in the diagonal hindlimb, or vice versa. Compensatory lameness also can develop in the same limb. In horses with front foot lameness the suspensory ligament (SL) often is sore, and some horses have suspensory desmitis. In horses with lameness abolished by palmar digital analgesia, most with navicular syndrome, scintigraphic examination revealed increased radiopharmaceutical uptake (IRU) in the proximal palmar aspect of the third metacarpal (McIII) bone in 30% of horses, indicating possible abnormal loading of the proximal SL (Fig. 7-1).9 Complete resolution of lameness may not be achieved until high palmar analgesia is performed. Horses with primary metatarsophalangeal joint lameness often have associated ipsilateral stifle pain.10 Determination of the primary site of lameness may be difficult without use of diagnostic analgesia and observing that blocking one site abolishes the majority of lameness. This phenomenon may be most common in trotters, but I have recognized it in all types of sport horses.

Supporting, Swinging, and Mixed Lameness Lameness has classically been divided into three categories in an attempt to characterize the motion associated with the lame leg and to assign etiology to the lameness condition. These categories are described and discussed, but I firmly believe that adequate characterization of most lameness conditions is impossible and may be unnecessary.

C

A, Lateral delayed-phase scintigraphic view showing focal, mild increased radiopharmaceutical uptake (IRU) of the navicular bone (bottom arrow) and proximal aspect of the third metacarpal bone (McIII; top arrow). Normal modeling is seen in the dorsal aspect of the proximal phalanx. B, Dorsal delayed-phase scintigraphic image, and C, dorsomedial palmarolateral oblique xeroradiograph of a dressage horse with lameness abolished by palmar digital analgesia. IRU of the medial aspect of the distal phalanx (bottom arrow) corresponds to the area of subchondral radiolucency seen in the xeroradiographic projection (C, arrowhead). Notice the focal area of mild IRU involving the proximal aspect of McIII (top arrow, A and B). Abnormal loading of the suspensory ligament may occur as a compensatory problem in some horses with navicular syndrome or other sources of palmar heel pain.

Fig. 7-1

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Diagnosis of Lameness

Supporting limb lameness describes a lameness that is painful during the weight-bearing phase of the stride. Most lameness conditions are of this type. Supporting limb lameness also has been referred to as stance phase lameness, but this term is inappropriate because the swing phase of the stride is also altered. Swinging limb lameness describes lameness that primarily affects the way the horse carries the lame limb. However, most horses with painful lameness conditions alter the swing phase of the stride in a typical and repeatable fashion, and it is difficult to make a clear separation between supporting and swinging limb lameness. Swinging limb lameness should be a term reserved for mechanical defects of gait, such as fibrotic myopathy, upward fixation of the patella, stringhalt, or other lameness conditions causing a mechanical restriction of gait. In these horses, lameness is manifested in the swing phase of the stride with no apparent pain. Unfortunately, the term swinging limb lameness often is used inappropriately to describe the gait deficit in horses with painful, supporting limb lameness. Lameness associated with osteochondrosis of the scapulohumeral joint is often described as a swinging limb lameness because of a marked shortened cranial phase of the stride. Dramatic improvement in the shortened cranial phase of the stride can be achieved by diagnostic analgesia, eliminating pain associated with lameness. Thus the gait deficit is the direct result of pain and no clear differentiation between supporting and swinging limb lameness can be made. Horses with painful forelimb lameness almost always shorten the cranial phase of the stride, although perhaps not to the extreme as in a horse with authentic scapulohumeral joint lameness. Because the terminology is confusing and often erroneous, I prefer to avoid use of these terms and simply describe lameness as accurately as possible. For instance, describing a horse as grade 2 of 5 LF lame, with a marked shortening of the cranial phase of the stride reminiscent of other horses I have seen with shoulder region lameness, gives the most accurate and useful information. There is an erroneous tendency to equate a swinging limb lameness with one that is more evident when the lame limb is on the outside of a circle. Upper limb lameness is often presumed, yet not confirmed by diagnostic analgesia. It is logical that if a horse is reluctant to swing a limb forward, the lameness may be most prominent when the lame limb is on the outside of a circle. However, many horses with painful weightbearing lameness show more pronounced lameness with the limb on the outside of the circle, a finding that neither suggests that lameness originates from the upper limb nor indicates the presence of swinging limb lameness (see following text). The outer limbs must stretch further and cover a larger circumference circle than the inside limbs. Slight temporal differences in the stance and swing phases of the inside and outside limbs are necessary to maintain gait symmetry.5 The results of cinematographic analysis of gait in lame horses seem to support reservation of the term swinging limb lameness for horses with authentic mechanical gait deficits, rather than those induced by painful lameness. In a horse with a supraglenoid tubercle fracture examined at a trot in hand, a marked decrease in the cranial phase of the stride (protraction) was observed, along with a marked head and neck nod. A markedly shortened stride could be equated with swinging leg lameness, but high-speed cinematography showed that the cranial and stance phases of the stride were shorter than in the sound limb.11 A horse with unilateral semitendinosus fibrotic myopathy had a shortened stride length and a shortened cranial phase of the stride, but the stance phase did not differ from that of the unaffected contralateral limb.12 In my experience, most lameness conditions can be considered mixed lameness, with changes in gait during weight bearing or the stance phase and during the swing phase of the

stride. With the exception of mechanical defects in gait, I have not been able to categorize the clinical characteristics of most lameness conditions into swinging or supporting limb types. However, it has been suggested that swinging limb lameness is caused by muscle injury, supporting limb lameness is caused by bone, tendon and ligament injury, and mixed lameness is caused by joint, tendon sheath and periosteal injury.13 A shortened cranial phase of the stride is a common characteristic in forelimb and hindlimb lameness and should not be considered pathognomonic for the location or type of lameness.

DETERMINING THE LOCATION OF LAMENESS The horse should be observed at both the walk and the trot from the front, behind, and side. I spend most of my time watching the horse move away and then back toward me. Medial-to-lateral limb flight and foot strike can be evaluated only from this perspective, although cranial and caudal aspects of the stride can be evaluated only from the side. Most important, evaluation of lameness from this perspective allows the veterinarian to use the horse as a frame of reference. I find it quite useful to evaluate forelimb lameness when the horse is traveling away from me and hindlimb lameness when the horse is traveling toward me. This perspective allows use of the horse’s top line to see a subtle head and neck nod or pelvic hike. Only by observing the horse from the side can the cranial and caudal phases of the stride be determined. When first learning to assess lameness from the side, a linear frame of reference, such as a fence or wall in the background, may be helpful to notice head nod and pelvic hike against a non-moveable background. Application of pieces of tape or other markers to the horse’s head or a fixed point on the pelvis can assist recognition of upward and downward movement of that body part. Independent observation of the forelimbs and hindlimbs is needed to understand whether a horse has forelimb or hindlimb lameness or a combination. These observations then are amalgamated to form a final clinical impression.

Recognition of Forelimb Lameness Forelimb lameness often is easier to recognize than hindlimb lameness. Understanding the concept of the head nod is vital to the correct interpretation of equine lameness. The head and neck elevate or rise when the lame forelimb is bearing weight or hits the ground and nod down or fall when the sound forelimb hits the ground. “…When the [forelimb] is the lame one, the movements of the foot and head occur somewhat in unison. When the lame foot is raised, the head is elevated, but only to fall when the sound leg is brought to a rest.”1 Some clinicians find it easier to appreciate the head nod, while others find it easier to recognize elevation of the head. When evaluating slow-motion videotape of lame horses, it is immediately obvious that the elevation of the head and neck is much easier to see than the head nod down. In slow motion the horse appears to be elevating the head and neck just before the lame limb hits the ground, and then, during the later portion of the support or stance phase, the head and neck nod down. The head and neck nod occurs as the contralateral limb begins the support or stance phase. Both head elevation and falling are present, but head elevation is much easier to detect when it occurs in unison with the lame limb hitting the ground. It is likely that a combination of visual clues allows the clinician to decide the primary forelimb lameness. Quantification of lameness and description of the actions of the lame and compensatory limbs have been attempted using gait analysis systems. In horses with amphotericin-induced carpal lameness, head movements were the most consistent indicator of lameness, followed by sinusoidal

CHAPTER 7 motion, or a rising and falling action, of the head and withers.14 The motion of the lame limb was assessed, and a falling of the head and withers during the support phase of the lame limb was noted, contrary to clinical perception and evaluation of slow-motion videotape of lame horses. It was suggested that an uncoupling of the weight from the lame forelimb and a “free fall–like” phenomenon occurred during weight bearing.14 The problem with this description is that it considers only the lame limb and is confusing. When evaluating a lame horse, the observer “sees” both forelimbs. During the later portion of the support phase of the lame limb, the sound limb is in the later portion of the swing phase and beginning the support or stance phase. Thus the head and withers drop described experimentally appears to occur concomitant with the sound limb hitting the ground. The observer perceives the early portion of the stance or support phase. In general a good correlation between clinical evaluation of forelimb lameness and that described using motion analysis has been observed. There was complete agreement between clinical determination of location of forelimb lameness and that detected by motion analysis using a computerized threedimensional motion measurement system. However, the degree of lameness differed in 6 of 29 horses.15 The maximal vertical acceleration of the head was the best indicator of forelimb lameness.16 Although horses with forelimb lameness shifted weight in a caudal direction to the diagonal hindlimb, the amount of withers motion was minimal. The authors reasoned that the tremendous mobility of the head and neck, allowing the horse to asymmetrically elevate the neck and thus load the non-lame forelimb, accounted for the lack of withers movement and the horse’s adaptation to forelimb lameness.16 A similar compensatory ability is not present in the hindlimb. Vertical displacement of the tuber coxae and forward motion or translation of the pelvis occur in horses with hindlimb lameness, since a mechanism such as head and neck movement does not exist.16 In a computer-generated model of a trotting horse the dynamic effects of head and neck movement accounted for the majority of load shift to the contralateral forelimb and diagonal hindlimb in horses with unilateral forelimb lameness.17 Load shift and compensation by the diagonal hindlimb in horses with unilateral forelimb lameness lends support to the clinical findings of compensatory lameness in the diagonal limbs in trotters. Instrumented shoes have been used experimentally to study motion in horses by quantifying ground reaction forces (GRF) but have had limited clinical use.18,19 Although this system is not currently widely available, in the future this or similar systems may be useful to objectively assess lameness and the response to diagnostic analgesic techniques in clinical patients.

Recognition of Hindlimb Lameness Historically descriptions of hindlimb lameness have been confusing. An important principle in the recognition of hindlimb lameness is the concept of the pelvic hike or asymmetrical movement of the pelvis. This has also been termed hip hike, but I prefer the term pelvic hike because it accurately describes how the pelvis moves in a horse with unilateral hindlimb lameness. The entire pelvis, not just the lame side of the pelvis, appears to undergo elevation. Because the horse has two “hips” and only one pelvis, the term pelvic hike seems preferable. Pelvic hike is the vertical elevation of the pelvis when the lame limb is weight bearing. In other words, the pelvis “hikes” upward when the lame limb hits the ground and moves downward when the sound limb hits the ground. “… the haunch settles downward when the sound leg touches the ground…”.1 Some clinicians find it easier to see the downward movement of the pelvis, on the side of the lame limb, rather than the pelvic hike.5 It may be simpler to determine which side has the most

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movement, rather than looking for either a hike or a drop.5 The clinician must keep in mind that the pelvic hike is the clinical impression of the change in height of the pelvis, not the absolute or measured height. It is the shifting of weight or load that occurs as the horse tries to reduce weight bearing in the lame limb and transfer weight to the sound limb. Another explanation for asymmetrical movement of the pelvis involves one of the protective or compensatory mechanisms used by the horse to assist in break over and minimize load on the lame limb. Many horses with hindlimb lameness drift away from the lame limb toward the sound limb. Drifting may decrease the magnitude of the observed pelvic hike, but more important, makes the lame side look lower than the sound side. This is why it is important to watch the entire pelvis as a unit rather than the individual sides of the “hips.” In most horses with hindlimb lameness, particularly those without a substantial tendency to drift away from the lame limb, the elevation of the pelvis (pelvic hike up) when the lame limb hits the ground surpasses that when the sound limb is weight bearing. This elevation can be seen readily in realtime and slow-motion videotape analysis, but it may not be as obvious during clinical examination. Observing horses with hindlimb lameness from the front as the horse trots toward you may be useful. This approach allows the pelvic hike to be seen clearly using the horse’s top line as a frame of reference. Subtle pelvic elevation is best seen from this perspective. The use of markers on a fixed part of the pelvis can help to identify asymmetry. Stride length characteristics, height of foot flight, sound, and fetlock drop are also helpful (see following text). Horses with bilateral hindlimb lameness may have a short, choppy gait that lacks impulsion, but they may have no pelvic hike. Other methods to exacerbate the baseline lameness should be performed, such as circling the horse at a trot in hand or while on a lunge line. Lameness may be accentuated when the lame or lamer limb is on the inside or outside of the circle (see following discussion).

Hindlimb Lameness Confused with Forelimb Lameness It is important to understand how a horse with unilateral hindlimb lameness modifies its gait so that hindlimb lameness can mimic forelimb lameness at the trot. When the lame limb hits the ground, the horse shifts its weight cranially to transfer load away from the lame limb. This causes the head and neck to shift forward and nod down at the same time. The contralateral forelimb bears weight simultaneously with the lame hindlimb and the head nod coincides, thus mimicking lameness in the forelimb ipsilateral to the lame hindlimb. Head and neck movement in horses with hindlimb lameness is not always observed. Horses generally must have prominent (>3 out of 5, see later grading discussion) hindlimb lameness before compensatory head and neck movement develops. At the pace, a lateral gait, LH lameness mimics RF lameness and RH lameness mimics LF lameness. Horses can have a head and neck nod at the trot caused by singular forelimb lameness, singular ipsilateral hindlimb lameness, or concurrent forelimb and ipsilateral hindlimb lameness. A prominent head nod is seen in horses with simultaneous LF and LH lameness. The examiner first must determine whether both limbs are affected. Problems arise because a horse with only LF lameness may shorten the LH stride at the trot, leading the veterinarian to question whether LH lameness also exists. Horses with only LH lameness can have a rather pronounced head nod, and thus the veterinarian may question the existence of LF lameness. Although a horse with LF lameness may have a compensatory shortened stride of the LH, in the absence of lameness a marked pelvic hike should not be

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Diagnosis of Lameness

present. A head nod consistent with a LF lameness may be inappropriately severe to be caused by mild LH lameness. If a horse has simultaneous LF and LH lameness, it is essential to perform diagnostic analgesia in the hindlimb first, because moderate to severe hindlimb lameness produces head and neck nod that is not abolished unless the hindlimb lameness is resolved. Resolution of the pelvic hike and reduction in the head nod should be expected with resolution of the hindlimb lameness. Simultaneous lameness of a diagonal pair of limbs is less common than simultaneous ipsilateral lameness, except in trotters, because many horses perform at gaits that induce compensatory lameness either in the contralateral or ipsilateral limb. With simultaneous LH and RF lameness the head nod reflects the forelimb component, a mandatory clinical sign for perception of RF lameness. The horse may drift away from the LH with shortening of the cranial phase of the stride. The horse may have a short, choppy stride in the forelimbs and hindlimbs. The horse may have a rocking gait. It cannot shift weight or compensate from stride to stride in the usual manner and thus tends to rock back and forth from the hindlimbs to the forelimbs. Reasonable agreement generally exists between clinical recognition of hindlimb lameness and that found experimentally. The use of markers placed on each tuber coxa of 13 horses with unilateral hindlimb lameness showed a consistent increase in vertical displacement of the pelvis during early weight bearing of the lame limb.20 Although the rise and fall of the pelvis was readily apparent and occurred consistently with weight bearing of the lame and sound limbs, respectively, the absolute height of the pelvis on the lame side did not rise above that of the lame limb.20 These findings are consistent with my clinical impressions. A head nod down when the diagonal forelimb was bearing weight further confirmed clinical observations that hindlimb lameness can mimic lameness of the ipsilateral forelimb.21 In a kinematic study using a three dimensional optoelectronic locomotion system, hip acceleration quotient increased in horses with hindlimb lameness.21 Vertical displacement corresponded to the pelvic hike up on the lame leg, with a simultaneous forward movement of the head and neck during the stance phase of the lame limb.21 GRF has been measured in normal horses and those with forelimb and hindlimb lameness.22-25 GRF is reduced in the lame forelimb or hindlimb with compensation by the other limbs. In horses with unilateral forelimb lameness, decreased horizontal GRF in the lame limb is compensated by increased GRF in the contralateral forelimb and ipsilateral hindlimb.26 Decreased vertical GRF in the lame limb is compensated by increased vertical GRF in the contralateral forelimb during the swing phase of the lame limb, and increased vertical GRF in both the ipsilateral and contralateral hindlimbs during the stance phase of the lame limb.26 During unilateral hindlimb lameness the decreased GRF in the lame limb is compensated by increased GRF in the contralateral hindlimb and the contralateral and ipsilateral forelimbs.26 These experimental data support the clinical impression that a lame horse adapts by shifting load to the contralateral limb or by shifting load in a caudal direction for forelimb lameness and in a cranial direction for hindlimb lameness. A study using an optoelectronic motion measurement system and expert vision analysis high-speed video system for motion analysis confirmed that horses with hindlimb lameness show false lameness in the ipsilateral forelimb. However, contrary to my clinical observations, 6 of 10 horses with severe forelimb lameness showed “false” lameness of the diagonal (contralateral) hindlimb.8 Review of videotape of lame horses reveals false lameness in the diagonal or ipsilateral hindlimb depending on several factors. Horses with pronounced forelimb lameness may look lame in the diagonal hindlimb. Horses with marked shortening of the cranial phase

of the stride may appear lame in the ipsilateral hindlimb. Horses with forelimb lameness circled with the lame limb on the inside may look lame in the ipsilateral hindlimb. Thus analysis of lameness can be complex, and determination of the lame limbs may not become clear until diagnostic analgesia is performed.

Bilaterally Symmetrical Forelimb or Hindlimb Lameness Bilateral lameness is a common cause of poor performance and may go unrecognized without additional movement, such as circling, lunging or riding. Horses with bilaterally symmetrical forelimb lameness may have a short, choppy gait when trotted in straight lines. Horses with hindlimb lameness may lack lift to the stride, have a subtle change of balance, or reduced hindlimb impulsion.5 If bilaterally symmetrical lameness is suspected, the veterinarian should select one limb and begin diagnostic analgesia. Horses often show pronounced lameness in the contralateral limb when the source of pain is desensitized.

THE LAMENESS SCORE: QUANTIFICATION OF LAMENESS SEVERITY I believe it is important to have a standardized lameness scoring system that allows the clinician to quantify lameness within and between horses. Ideally it should be consistent worldwide, but currently a scale from 0 to 5 generally is used in North America, and a scale from 0 to 10 is often used in Europe. Definitions vary within the grading systems. The system adopted by the American Association of Equine Practitioners (AAEP) provides a framework.27 Grade 1 lameness is difficult to observe and not consistently apparent regardless of circumstances (such as weight carrying, circling, inclines, hard surfaces). Grade 2 lameness is difficult to observe at a walk or trotting a straight line but is consistently apparent under certain circumstances (such as weight carrying, circling, inclines, hard surfaces). Grade 3 lameness is consistently observable at a trot under all circumstances. Grade 4 lameness is obvious lameness with marked nodding, hitching, or shortened stride. Grade 5 lameness is characterized by minimal weight bearing in motion or at rest and the inability to move. The AAEP system is potentially confusing because it grades lameness at both the walk and trot. It does not account for a horse that has a shortened stride at walk that trots sound. In my experience, many lame horses show consistently observable lameness at a trot and therefore would have to be scored at least 3, leaving only grades 3 and 4 for use for the majority of lame horses. Horses with bilateral lameness and a shortened stride but no obvious head nod or pelvic hike are difficult to score based on this system.5 It does not permit grading under different circumstances, such as straight lines, circles on the soft in each direction, and circles on the hard.5 An alternative lameness scoring system is listed in Box 7-1. Lameness is only scored at a trot, and the grading system is used most often to describe lameness at a trot in hand. The system is useful for both forelimb and hindlimb lameness and is based on a range of 0 (sound) to 5 (non–weight-bearing). In this system a horse with unilateral hindlimb lameness of grade 3 or worse would have a head nod that mimics ipsilateral forelimb lameness. There is a practical difference between this scoring system and that put forth by the AAEP. A horse with lameness grade 1 in this modified scoring system would have a lameness grade between 2 or 3 in the AAEP system. The

CHAPTER 7

Box • 7-1 Lameness Scoring Lameness grades from 0 to 5 are based on observation of the horse at a trot in hand, in a straight line, on a firm or hard surface. 0 Sound 1 Mild lameness observed while the horse is trotted in a straight line. When the lame forelimb strikes, a subtle head nod is observed; when the lame hindlimb strikes, a subtle pelvic hike occurs. The head nod and pelvic hike may be inconsistent at times. 2 Obvious lameness is observed. The head nod and pelvic hike are seen consistently, and excursion is several centimeters. 3 Pronounced head nod and pelvic hike of several centimeters are noted. If the horse has unilateral singular hindlimb lameness, a head and neck nod is seen when the diagonal forelimb strikes the ground (mimicking ipsilateral forelimb lameness). 4 Severe lameness with extreme head nod and pelvic hike is present. The horse can still be trotted, however. 5 The horse does not bear weight on the limb. If trotted, the horse carries the limb. Horses that are non–weight bearing at the walk or while standing should not be trotted.

modified scoring system is more flexible and allows clear differentiation between most lameness conditions. However, it does not account for a bilaterally symmetrical gait abnormality and may be difficult to apply in a horse with lameness in more than one limb. Many horses evaluated for subtle lameness or poor performance have a score between 0 and 1 because consistent lameness is not observed. Use of half grades provides greater flexibility and supports adoption of a scoring system from 1 to 10, assuming 0 denotes soundness.

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different shoe types, or disparity in foot size confounds interpretation. Listening for regularity of rhythm and sound of footfall are important, especially when evaluating the response of lame horses to diagnostic analgesia, particularly in horses with subtle lameness.5

Drifting Horses with hindlimb lameness generally drift away from the lame limb. Drifting is one of the earliest adaptive responses of a horse with unilateral hindlimb lameness, allowing the horse to break over easier or reduce load bearing. Drifting may alleviate the need for extensive pelvic excursion (hike). It may make pelvic drop on the lame side more obvious. The horse may mask the lameness by reducing pelvic excursion. In some horses a pelvic hike is undetectable or subtle, but consistent drifting away from the lame side indicates the presence of hindlimb lameness. Many driven STBs with hindlimb lameness drift away from the lame limb, or are “on the shaft.” Horses with LH lameness have a tendency to be on the right shaft and vice versa. Drifting away from the lame limb may be most evident when horses have pain from the tarsus distally, although some clinicians have different experiences.5 Drifting may result in the horse moving on three tracks. Horses with severe forelimb lameness also tend to drift away from the lame limb, but this tendency usually is less obvious than in horses with hindlimb lameness. Drifting is most common with carpal lameness when the horse tends to abduct the limb during the swing phase of the stride and appears to push-off with the limb, forcing the horse away from the lame side. Racehorses with either forelimb or hindlimb lameness tend to drift away from the lame limb while training or racing at speed. This finding is an important piece of the lameness anamnesis. Drifting toward the lame hindlimb is an unusual but important clinical sign. In horses that drift toward the lame limb, I suspect weakness and lameness exist simultaneously, suggesting a neurological component to the gait abnormality. However, a jumping horse at takeoff may push off more strongly with the non-lame hindlimb and drift across the fence toward the lame limb.5

EVALUATION OF LIMB FLIGHT LAMENESS DETECTION Fetlock Drop Assessment of fetlock drop, or extension of the metacarpophalangeal and metatarsophalangeal joints, may be helpful in recognition of the lame limb. In general, the fetlock joint of the sound limb drops farther when this limb is weight bearing than does the fetlock joint of the lame limb, because the horse is attempting to spare the lame limb by increasing load in the sound limb. This may be easier to detect by video analysis than in a clinical situation and may be more recognizable at the walk than a trot. However, in some horses with moderate or severe unilateral suspensory desmitis or tendonitis, the fetlock drops markedly on the lame limb when the horse is walking, but at a trot fetlock drop usually is more pronounced in the sound limb. With bilateral suspensory desmitis or severe tendonitis the fetlock may drop further in the lamer limb.

Use of Sound Sound can be useful in lameness evaluation. A lame horse usually lands harder on the sound limb, resulting in a louder noise. To appreciate this sound, the horse must be trotted on a firm or hard surface such as pavement or concrete. However, the sound a horse makes while landing depends greatly on symmetry of the front or hind feet, and the loss of one shoe,

Observation and characterization of limb flight can be useful in determining the lame limb or limbs and possibly the location of lameness within the limb. Abnormal limb flight also may predispose to lameness, especially in horses with faulty conformation. In my opinion, it is impossible to predict the site of lameness accurately based on limb flight and other characteristics, although some abnormalities lead to a high index of suspicion. I believe strongly that the location of pain should always be confirmed by diagnostic analgesic techniques whenever possible. Some abnormalities are consistently associated with specific lameness conditions, whereas others are general patterns of limb flight seen with many different conditions.

Cranial and Caudal Phases of the Stride Changes in limb flight in the cranial and caudal phases of the stride can be seen only when the horse is evaluated from the side. In a normal horse the length of the stride of the paired forelimbs and hindlimbs, measured from hoof imprint to hoof imprint, is nearly identical from side to side. Extension and flexion of the limbs is also similar. From a clinical perspective the length of the stride of the affected limb cranial to the stance position of the contralateral limb is called the cranial phase of the stride, and the length of the stride caudal to the stance position of the contralateral limb is called the caudal phase of the stride. Obviously in a normal horse these individual parts of the

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Diagnosis of Lameness

stride are symmetrical. In a lame horse the overall stride length does not appear to change. If stride length changed, the horse could not trot in a straight line. Drifting is associated with lameness and could be explained by a change in stride length, but shorter stride length would be expected in the lame limb, causing the horse to drift toward the lame side, in contrast to the usual observation, drifting away from the lame limb. In racehorses, some of the tendency to drift away or toward the inside of the track could be easily explained by mild differences in stride length. However, at a trot in hand we can assume that total stride length does not change. In many lame horses the cranial phase of the stride of the affected limb is shortened. The caudal phase is lengthened to maintain a near equal overall stride length side to side. Shortening of the cranial phase of the stride appears to be a learned response of the horse to reduce the time spent during the stance phase and to help during break-over. Loss of propulsion, or an unwillingness to push off with the lame limb, could also explain reduction in the cranial phase of the stride. Because most lame horses have a shortened cranial phase of the stride, this finding is not particularly useful in localizing or classifying lameness and is not synonymous with swinging limb lameness. It is also important to recognize that pain causing lameness results in altered proprioceptive responses, to protect the painful area, and these responses may persist for some time after pain has resolved.5 A classic example of attenuation of the cranial phase of the stride in the hindlimbs occurs mechanically in horses with fibrotic myopathy. This authentic swinging limb lameness causes a marked abrupt change in the later portion of the protraction phase of the affected hindlimb, shortening the cranial phase and causing a sudden downward and backward action of the limb. The caudal phase of the stride is lengthened in most lame horses since, to maintain overall equal stride length, this portion of the stride must compensate. I generally have not found evaluation of the caudal phase of the stride at the trot in hand clinically useful, but it is sometimes a useful observation in horses at a walk (see following text). Some horses with severe palmar foot pain have a shortened caudal phase of the stride at both walk and trot.5 Contrast of the cranial and caudal phases of the stride in the lame limb at a walk and a trot is useful. In most horses with forelimb lameness the cranial phase of the stride is slightly shortened at the walk but markedly shortened at a trot. Obviously, in horses with subtle lameness, this clinical sign is absent at the walk and only mildly apparent at the trot. Horses with pain in the dorsal aspect of the foot, such as hoof abscessation or laminitis, may have a shortened caudal phase of the stride at a walk. This response is an attempt to protect the painful area and to shorten during break-over. These horses walk with a marked camped-out appearance in the forelimbs. At the trot, however, the cranial phase of the stride is likely to be shortened, a clinical contrast useful in localizing lameness to the dorsal aspect of the hoof. Most horses with hindlimb lameness have a reduction in the cranial phase of the stride at the walk and the trot. Horses with pelvic fractures involving the acetabulum prefer to keep the lame limb ahead of the contralateral limb at the walk and have marked shortening of the caudal phase of the stride, but at the trot the horse has a shortened cranial phase of the stride. Horses with hoof abscessation, most commonly of the dorsal aspect of the hoof, walk similarly, only to trot with a pronounced shortening of the cranial phase of the stride. Unilateral or bilateral laminitis is rare in the hindlimbs and can cause similar clinical signs. Shortening of the cranial phase of the stride does not always indicate that lameness is present in that limb. At speed a trotter with forelimb lameness shortens the cranial phase of the stride in the ipsilateral hindlimb to avoid interference with the lame limb. This observation sometimes is also made

in horses being trotted in hand. This compensatory movement gives the impression that the horse may be lame in the ipsilateral hindlimb, with a subtle pelvic hike. Lameness of the foot and carpus in trotters most often causes this compensatory ipsilateral hindlimb pelvic hike. Once lameness is abolished in the ipsilateral forelimb, the pelvic hike and shortened cranial phase of the stride in the hindlimb abate. In trotters a shortened cranial phase of the stride and a pelvic hike may be related to faulty weight distribution and interference problems and not to lameness at all.

ABNORMALITIES OF LIMB FLIGHT Abnormalities of limb flight can cause interference of one limb with another, particularly in trotters and pacers (Fig. 7-2). However, horses performing at speed at any gait and those with faulty conformation also are at risk to develop interference injuries. In some horses, interference is of no consequence, but in others, especially trotters, it causes gait deficits. Skin lacerations, bruising, and underlying bone and soft tissue damage (interference injury) may occur. Various boots and other protective devices have been developed to protect the limbs from potential trauma. It is important to assess the presence and location of interference injuries. In some horses, only mild evidence of hitting is found, but other horse may have many painful areas. Chronic interference can be the sole reason for lameness or poor performance.

Front Foot Interference Front foot hitting the contralateral forelimb. Horses with toed-out conformation tend to wing-in during movement, predisposing to interference injuries. Horses with base-narrow conformation or those with a combination of base-narrow and toed-out conformation also are at risk. However, many horses with these conformational abnormalities do not interfere.

A

B Trotter

C Pacer D

Types of interference. A, Horses at any gait can be injured by interference of a forelimb with the opposite side. B, Interference is common in the trotter and usually involves the ipsilateral forelimb and hindlimb. Interference within a forelimb can be seen in horses that hit the elbow of the same limb. This usually occurs because of high action, excessive weight of the shoes, or a combination of these factors. C, Interference in the pacer can involve the forelimb and diagonal hindlimb, commonly called cross-firing. D, Forging occurs during trotting when the toe of the hind foot strikes the bottom of the ipsilateral front foot.

Fig. 7-2

CHAPTER 7 Some horses walk very closely but widen out at faster gaits. Interference injury from one hind foot hitting the medial side of the contralateral hindlimb occurs infrequently. All types of horses, especially STB racehorses, are at risk of interference. Interference can involve any level of the limb from the foot to the proximal antebrachium. Mild interference of this type is called brushing. STBs often “hit their knees,” which causes swelling, bruising, and lacerations of the skin on the distal medial aspect of the radius. In some horses, large, chronic swellings develop; these consist of mostly fibrous tissue. In others, osteitis of the distal radius or abscessation occurs. Even with protective gear, horses may be reluctant to perform at maximal speed to avoid injury or disruption of gait, or pain caused by interference induces the horse to go off-stride. Interference within the same limb. Horses can develop interference injuries within a limb when the hoof or shoe hits the ipsilateral elbow. This type of interference sometimes is seen in trotters with high action (excessive carpal flexion) and is common in gaited horses that perform with heavy shoes intended to cause high action of the forelimbs (Fig. 7-2, B). Front foot hitting the ipsilateral hindlimb. Interference in trotters usually involves the toe of a forelimb interfering (hitting) with the dorsal aspect of the ipsilateral hindlimb (see Fig. 7-1). Various names are given to the type of interference based on the location in which the injury occurs. Interference injury at the dorsal aspect of the hind foot or coronary band is called scalping; in the pastern region it is called speedy cutting; in the metatarsal region (shin) it is called shin-hitting; and in the dorsal or medial aspect of the tarsus, it is called hock-hitting. Because interference is common in trotters, it is important not to over-interpret signs of pain on palpation. Speedy cutting results in pain over the dorsal aspect of the proximal phalanx that should not be misinterpreted as pain associated with a mid-sagittal fracture. Front foot hitting the contralateral (the diagonal) hindlimb. Cross-firing, or the striking of the contralateral

(diagonal) hindlimb by the front foot, usually occurs only in pacers (Fig. 7-2, C).

Hind Foot Interference Interference as a result of a hind foot hitting the foot of the ipsilateral forelimb (forging) is common and usually does not result in injury. Many horses forge at a trot in hand or while being ridden. In horses with shoes the sound is unavoidable but may not be a sign of a pathological condition. Forging is most common in horses that are trotted in deep footing. Forging may reflect imbalance, lack of strength, incoordination, or poor foot triming.5

Forelimb: Common Abnormalities of Limb Flight Winging In and Winging Out Common limb flights observed during lameness examination include winging in and winging out movement of the front feet and are often related to conformation (see Fig. 4-12). Horses that are toed out tend to wing in, whereas those that are toed in tend to wing out. Such abnormalities do not necessarily compromise performance. However, such movement may result in uneven loading of the soft tissue structures and uneven hoof wear, leading to chronic imbalance. Horses that wing in tend to develop interference injuries and wear the medial aspect of the shoe excessively. Horses that wing out tend to develop lateral branch suspensory desmitis and wear the lateral aspect of the shoe excessively.

Lateral Placement of the Foot during Advancement (Abduction) Horses normally advance the forelimbs straight ahead. When advancing the limb, horses with articular carpal pain, and in some with pain in the proximal metacarpal region, the foot is placed lateral to the expected foot position. This action has

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been described as abduction of the limb, but this term may infer swinging the limb, and horses with carpal lameness seem to place the limb laterally rather than swing the limb. However, ankylosis associated with severe osteoarthritis of the carpus does necessitate swinging the limb during advancement. Horses with this abnormality of flight almost always have a shortened cranial phase of the stride. They tend to push off with the affected limb from the lateral location, resulting in a wide or peg leg type of motion at walk, and sometimes at trot. With bilateral carpal lameness the horse moves wide bilaterally. Not all horses with carpal pain move wide, and this gait change is seen more often in horses with middle carpal or carpometacarpal joint pain than in those with pain in the antebrachiocarpal joint. Some horses with upper limb lameness may carry the limb wide while walking, although this characteristic is not typical of horse with shoulder pain. A horse with a humeral stress fracture sometimes may travel wide, similar to a horse with carpal lameness, but the latter is more likely. A horse with pain in the lateral aspect of a foot may move wide in the affected limb to reduce load laterally. This characteristic is seen in STB and TB racehorses with subchondral bone trauma or early stress fractures of the distal phalanx in the LF.

Plaiting The verb to plait means to braid or pleat, or to make something by braiding.3 The term is used to describe horses that walk or trot by placing one foot directly ahead of the other foot. Plaiting in the forelimbs is not nearly as common as in the hindlimbs and usually is the result of base-narrow, toe-out conformation. Old horses (usually broodmares) with severe carpus osteoarthritis and carpus varus limb deformities occasionally may swing the limb laterally and place the foot far enough medially to end up in front of, or lateral to, the opposite foot. Some horses with shoulder region lameness guard the limb and travel very close in front. Plaiting in the forelimbs can be seen in horses with recent fractures of the thoracic dorsal spinous processes at the withers.5 Horses with neurological disease occasionally plait.

Limb Flight in Horses with Shoulder Region Lameness I include this section principally because the shoulder often is erroneously incriminated as the source of pain. Horses with moderate to severe lameness of the scapulohumeral joint or bicipital bursa have a marked shortening of the cranial phase of the stride. They also have an unusual motion of the shoulder joint that is difficult to describe. Since the cranial phase of the stride is shortened, during break-over the affected shoulder joint seems to drop or buckle forward, more so than the opposite side (assuming lameness is unilateral). There may be prominent lifting of the head and neck. Limb flight is either straight ahead or somewhat close to the opposite forelimb. However, racehorses with humeral stress fractures may travel wide in front. With mild lameness there are no typical gait characteristics.

Hindlimb: Common Abnormalities of Limb Flight Stabbing or “Stabby” Hindlimb Gait A common abnormality of limb flight seen in horses with hindlimb lameness is described as a stabbing or “stabby” gait. During protraction of the lame hindlimb or limbs the limb travels medially, close to the opposite hindlimb, and then moves laterally during the later portion of the swing phase and is placed lateral to the expected foot placement. This motion results in excessive wear of the lateral or dorsolateral aspects of the shoe. Although this gait often is seen in horses with distal hock joint pain, it can be seen with many other sites of pain from the distal tibia to the foot. Therefore diagnostic analgesia is required to localize the pain. However, horses with the most marked shoe wear consistent with this abnormality of limb flight are most likely to have tarsal

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lameness. Exaggerated stabbing hindlimb motion often is seen in horses with neurological disease.

Abduction of the Hindlimbs during Advancement In some horses with hindlimb lameness the limb is carried forward in a position lateral to the expected position (i.e., abducted). In some horses with this limb flight the limb swings outside the expected line of limb flight, only to strike the ground near the expected position. Lateral swinging of the limb begins immediately after the lame limb leaves the ground. I have observed this abnormality most consistently in horses with stifle lameness, but it also occurs with some other upper limb lameness conditions. Care must be taken when evaluating horses that normally travel wide behind, such as trotters. I have recognized lateral swinging of the hindlimb most commonly in pacers with articular lesions of the stifle, because the normal gait in these horses is to swing the hindlimb more than would be expected from other horses. Many horses with stifle lameness carry the limb forward lateral to the expected position, but just before impact may actually stab laterally. Therefore the veterinarian must pay close attention to limb flight directly after the lame limb leaves the ground and while it is passing the contralateral limb. Another common characteristic of horses with stifle lameness is a shortened cranial phase of the stride. The stifle joint also may appear unusually prominent and be carried somewhat away from the flank and slightly externally rotated.

Plaiting Plaiting is more common in the hindlimb than in the forelimb and usually results from lameness rather than faulty conformation, although plaiting can occur in a horse with severe base-narrow conformation. Plaiting can be seen in horses with unilateral or bilateral lameness. In horses with unilateral lameness, it appears that limb flight actually may be altered in both hindlimbs, resulting in both hind feet being placed ahead, or in some horses, lateral to the opposite foot. In horses with severe hindlimb lameness, it appears that the affected foot is being swung around and placed directly in front or lateral to the unaffected foot. Alternatively, the horse may be trying to support most of its weight on the unaffected limb and moves this limb inside to support the lame side. In horses with bilateral lameness, it is equally difficult to determine what exactly is causing the plaiting. The horse may be reluctant to bring either hindlimb along the expected line of flight, leaving the limb medially and forcing the opposite limb to the outside to avoid interference. A horse may swing each hindlimb around the other, ultimately ending placing one foot ahead or lateral to the other. An unusual rocking-type of gait is observed in horses with bilateral hindlimb lameness and plaiting. I have observed plaiting most commonly in horses with osteoarthritis of the coxofemoral joint or pelvic fractures, but I also have seen it in horses with bilateral distal hock joint pain or suspensory desmitis. Plaiting also is observed in some horses with sacroiliac joint pain.5

Mechanical Lameness of the Hindlimb and Limb Flight Mechanical conditions of the hindlimb can cause profound abnormalities of limb flight. These are termed lameness conditions because of the gait abnormality exhibited, although in many horses pain is not characteristic.

Stringhalt Stringhalt, an ill-defined neuromuscular disorder of the hindlimb, causes mild-to-severe hyperflexion of the tarsus. The condition can be unilateral or bilateral and usually is most obvious at a walk but can also be seen at the trot. In horses with severe stringhalt the dorsal aspect of the hoof comes close to or hits the ventral aspect of the abdomen. Horses may exhibit the clinical signs more prominently during backing or when initially moved after previous standing.

Fibrotic Myopathy Fibrotic myopathy is characterized by a sudden downward and backward motion of the limb (slapping motion) that occurs during, and restricts the length of, the cranial phase of the stride. Hyperflexion of the hock is not a clinical feature of this gait deficit, but the restriction of the cranial phase of the stride and the slapping motion and sound can be confused with the clinical signs of stringhalt. It is most obvious at the walk.

Upward Fixation of the Patella Upward fixation of the patella is a classic hindlimb gait deficit and one that displays the function of the stay or reciprocal apparatus. It can be intermittent or permanent and unilateral or bilateral. When the patella is locked in position over the medial trochlear ridge of the femur, the stifle and hock joints are held in extension, whereas the digit is held in partial flexion.

Shivers Shivers is an ill-defined neuromuscular disease and is most common in Warmbloods and Draft breeds; it can occur unilaterally or bilaterally. Clinical signs usually are most obvious when a horse is backed or first moves from the stall. Horses elevate and abduct the limb, and the limb may actually shiver or shake. The tail often is elevated. Signs may be accentuated if the horse is tense.

Other Hindlimb Gait Deficits Other unusual unexplained gait deficits affecting one or both hindlimbs are observed occasionally, and they often have characteristics similar to those seen with stringhalt, fibrotic myopathy, upward fixation of the patella, and shivers. However, some distinction usually prevents easy recognition and diagnosis. A gait deficit characterized by marked hindlimb abduction seen most prominently at the walk has been recognized. This is most similar to fibrotic myopathy, since a consistent abduction of the limb is observed, and signs tend to abate when the horse is trotted. It may be related to scarring, abnormal function of the biceps femoris and gluteal muscles, or neurological disease. Neurological disease can cause many different gait deficits, most commonly recognized in the hindlimbs but also in forelimbs. A complete neurological evaluation usually is not performed during lameness examination unless certain abnormalities are observed. Abnormal or excessive circumduction of the hindlimbs, a bouncy, stabby hindlimb gait noticed when the horse is trotted, knuckling over behind or crouching, stumbling, and lethargy are signs that should prompt further investigation.

EVALUATION OF FOOT PLACEMENT It is important to critically evaluate foot placement. Ideally, both the front and hind feet should land flat and level on a firm surface. Foot strike patterns change on soft footing. Evaluation of foot strike is most important in horses with lameness localized to the foot, but it can also give clues to other causes of lameness. Abnormal foot placement can be the result of a current lameness problem but may also cause lameness. In the forelimbs, horses commonly land on the lateral side of the foot first before rocking medially. This can be the result of abnormal conformation or hoof imbalance and can predispose to lameness in the digit and suspensory branch desmitis. Landing abnormalities in the dorsal-to-palmar direction are common but are difficult to recognize unless severe. Horses with profound pain in the toe caused by laminitis or hoof abscessation land heel first, giving a camped-out appearance, and have a shortened caudal phase of the stride. Horses with palmar heel pain may compensate by landing toe first and cause abnormal stress on the dorsal structures of the foot, but this characteristic is difficult to see, except in slow motion.

CHAPTER 7 In the hindlimbs, several patterns or abnormal landing or motion are recognized; not all of which are a cause or the result of lameness. Landing on the toe is commonly considered the result of heel pain, but many horses with severe hindlimb lameness land on the toe. This tendency is particularly prominent when the horse is first moved, and most horses warm out of the lameness. Horses may land on the toe when walking up an incline or at the walk on the flat, but generally place the heel on the ground when trotted. The most consistent lameness I see in horses that land on the toe is distal hock joint pain, but any cause of lameness from the tarsus to the foot can cause a horse to exhibit this abnormal landing pattern. Horses with lameness of the metatarsophalangeal joint region, including osteoarthritis, tenosynovitis of the digital flexor tendon sheath, or desmitis of the accessory ligament of the deep digital flexor tendon, have a tendency to land on the toe. Horses with adhesions within the digital flexor tendon sheath may have severe mechanical restriction that causes toe-first landing. Old Western performance horses with deep digital flexor tendonitis have severe toe-first landing and may stand on the toe and even rise up in the heels during the examination. The condition can be bilateral or unilateral and is difficult to manage. Mild or moderate tendency to land on the toe also has been attributed to stifle lameness.5 Abnormal movement of the lower or entire hindlimb occasionally is noted when horses are watched from behind. Horses may place one or both hind feet in an axial position and collapse or break-over the lateral aspect of the fetlock region.5 Another uncommon hindlimb motion is characterized by excessive rotation of the hindlimb. The horse plants the hind foot and rotates the heel laterally, causing abnormal loading or twisting of the distal limb.5 Although this movement can lead to lameness, it sometimes is seen in horses that are successful in various sporting endeavors. I have seen this type of hindlimb motion most often in TB racehorses.

ADDITIONAL MOVEMENT DURING LAMENESS EXAMINATION Further information about the character of lameness often can be obtained by observing the horse as it move in circles and is ridden or driven. Some lameness conditions are apparent only under these circumstances.

Hard and Soft Surfaces Comparison of movement on hard and soft surfaces is valuable. Foot lameness usually is worse when the horse is trotted on hard surfaces and better on a soft surface, such as grass or sand. Horses with suspensory desmitis or flexor tendonitis are more likely to show lameness on a soft surface. Deep sand may accentuate some lameness conditions, but an extended lameness examination under these conditions could cause proximal suspensory desmitis.5 A slight downward incline or an uneven, rough surface may make subtle lameness more apparent.5

Circling Lameness often is much more pronounced when a horse is circled. Horses should be circled in both directions: to the left (counterclockwise, LF and LH on the inside) and to the right (clockwise, RF and RH on the inside). Lameness may be more pronounced when circling at either the walk or the trot. In some horses with incomplete fractures, baseline lameness at a trot in straight lines in hand may be subtle or absent. Lameness may be readily apparent during circling, even at the walk. The additional forces of torsion and bending during circling are added to those of compression and tension. In horses

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with incomplete fractures, such as those involving the proximal or distal phalanges, torsion or bending forces during circling likely cause mild separation of the fracture fragments and exacerbate lameness. In horses with other lameness conditions, exacerbation of lameness may be caused by a change of load on the affected soft tissue structure or bone, redistribution of the forces of compression and tension in a medial to lateral direction, or additional forces of bending and torsion. From a clinical perspective the force of compression may be dominant to other forces in determining a horse’s response to circling, but it is not the only factor. Extension of the limb is also influential.5 When the lesion is on the outside of the circle and undergoing compression, exacerbation of the lameness occurs. For instance, lameness in horses with medially located lesions of the distal phalanx or of the third carpal bone is worse when the limb is on the outside of the circle and the lesion is being compressed. For some soft tissue injuries, tension forces may be more important. Lameness in horses with proximal suspensory desmitis often is worse with the limb on the outside of the circle, suggesting that tension is important in the expression of lameness. The same observation is not seen in horses with more distally located suspensory desmitis. Is lameness seen when in the horse while circling the same lameness seen while walking or trotting in straight lines? In most instances, circling exacerbates the primary lameness seen in straight lines. If lameness is subtle or non-existent when the horse is evaluated in a straight line, the lameness seen when circling becomes the baseline lameness. The clinician must recreate the same conditions of circling when evaluating the results of diagnostic analgesic techniques. There is always the possibility that lameness seen while circling may be different from the baseline lameness seen in straight lines. A horse may have a grade 1 RF baseline lameness when it moves in straight lines that increases to 3 when trotted in a circle to the left, but still has grade 1 lameness when trotted to the right. Lameness in straight lines and when trotting to the right is absent after palmar digital analgesia, but still is rated 3 when the limb is on the outside of the circle. The horse has two problems in the RF: palmar foot pain and an additional carpal lameness that becomes evident when the horse is trotted to the left (RF on the outside of the circle). With bilateral forelimb or hindlimb lameness, primary lameness often is seen in a single limb in straight lines, but while circling lameness is seen in whichever limb is on the inside (or outside) of the circle. Circling is useful in exacerbating the primary lameness problem and identifying an additional lameness not previously noted. This additional lameness must be recognized and treated separately from the baseline lameness. Good correlation usually exists between the cause of lameness seen on the straight and that seen while circling the horse; thus it is helpful to circle the horse to try to exacerbate lameness. Circling can be done at the walk and trot in hand and while lunging or riding the horse. Horses often move more freely and naturally when lunged rather than when being led.5 However, lunging is not possible in some horses, particularly racehorses, and circling while being led is better than no circling. The surface should be non-slip because horses may be hesitant to move freely on slippery surfaces and shorten or alter the stride even when lameness is not present.5 Soft footing is best when the horse is first being lunged, since the horse can buck and play without risk of injury. Hard or firm surfaces are best to exacerbate many lameness conditions, but the surface must be non-slip to avoid possible injury. That lameness of the upper forelimb or hindlimb is worse when the limb is on the outside of the circle is a common misconception. This is true in some horses, but a generalization cannot be made (see following text). Shortening of the cranial phase of the stride may appear more obvious with the limb on

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the outside of the circle, but exacerbation of lameness judged by the degree of head nod may not be observed. Another misconception is that horses with lameness of the foot are lamest when the limb is on the inside of the circle. Although a majority (65%) of those with lameness localized to the foot are most lame when the limb is on the inside of a circle, lameness can be worst with the lame limb on the outside of a circle. This depends in part on the location of pain within the foot.

Forelimb Lameness worsened with limb on the inside of the circle.

In many horses, lameness originating from the fetlock region to the foot is worse with the affected limb on the inside of the circle. Comparison of circling on hard and soft surfaces is useful. Baseline lameness associated with foot pain usually is dramatically increased when the horse is circling on a hard surface, but a less obvious response is seen when circling on softer surfaces. However, lameness in horses with medially located lesions can be worse with the limb on the outside of the circle. Horses with lameness of the metacarpal region vary in response to circling. Lameness in those with lameness related to metacarpal bony injury and distally located lesions in the suspensory ligament or digital flexor tendons tend to be worse with the limb on the inside of the circle, whereas lameness in those with proximal suspensory desmitis is worse with the limb on the outside. Horses with suspensory branch desmitis may show a different response depending on lesion severity and whether the injured branch is undergoing tension or compression. In my experience, in horses with lameness of the forearm, elbow joint, arm, and shoulder joint region, the lameness tends to be worse with the limb on the inside of the circle, but opinions and experiences do vary.5 Lameness in some horses with mechanical restriction of movement that dramatically decreases the cranial phase of the stride may be worse with the limb on the outside of the circle. Lameness worsened with limb on the outside of the circle.

Horses with medially based lesions of the lower limb, especially foot lameness, proximal metacarpal lesions (proximal suspensory desmitis or avulsion injury to McIII at the suspensory origin), or carpal pain often are more lame with the limb on the outside of the circle. Horses with lesions in the antebrachiocarpal joint are less consistent in response to circling compared with those with middle carpal joint lesions, since most of the common injuries involve the medial aspect of the latter. Upper limb lameness is accentuated in some horses.5

Lameness Improved when Circling Lameness that appears better on a circle than in straight lines is uncommon. Lameness in horses with medially located lesions in the foot or carpus may improve when the limb is on the inside of a circle. Baseline lameness in horses with middle carpal disease involving the third and radial carpal bones improves with the limb on the inside of the circle. A STB racehorse with grade 2 or 3 RF baseline lameness that increases to grade 3 or 4 when circled to the left, but is only grade 1 or 2 when circled to the right, may have lameness associated with the middle carpal joint, but pain in the medial aspect of the foot also is possible. A horse with bilateral forelimb lameness (e.g., a horse with grade 3 RF baseline lameness in straight lines) may show grade 3 to 4 RF lameness when trotting to the right, but grade 1 LF lameness when trotting to the left. The primary lameness is in the RF, and lameness is worse when the limb is on the inside of the circle. Circling to the left induced lameness in the LF, masking the RF lameness, because bilateral lameness existed that was not recognized when the horse was trotting in a straight line.

Hindlimb Lameness and Circling In my experience, baseline lameness in most horses with any hindlimb lameness is worse when the limb is on the inside of

the circle. Exceptions do exist, and some have different experiences and thus opinions.5 Lameness associated with proximal suspensory desmitis often is worse with the affected limb on the outside of the circle, and the horse may stumble or take bad steps. Lameness in some horses with stifle lameness appears worse with the affected limb on the outside of a circle, but in others it appears similar to the left and the right. Many conditions of the stifle involve the medial femorotibial joint, a location that would be compressed with the limb on the outside. Lameness in any horse with a medially located lesion involving the distal hindlimb could be worse with the limb on the outside of the circle. Circling may be useful in exacerbating a primary lameness but generally is not helpful in localizing lameness.

Observation during Riding Lameness may not be apparent when the horse is evaluated in hand in straight lines and circles but is obvious when the horse is ridden. This lameness becomes the baseline lameness for further investigation. The additional weight of a rider can exacerbate both forelimb and hindlimb lameness. Lameness in horses with primary back pain or those with substantial muscle pain secondary to hindlimb lameness usually is worse when they are ridden. Hindlimb gait restriction can occur in horses with back pain but may be apparent only when a horse is ridden.5 Problems related to an ill-fitting saddle or girth, behavioral problems, head shaking, abnormal posture or carriage of the head and neck, and refusal to take a lead or bend in certain directions may be evident only when a horse is ridden. A horse may be easier to control when ridden than when in hand or on the lunge. Performance of specific maneuvers by the horse may accentuate lameness. A collected trot that forces more weight onto the hindlimbs may exacerbate hindlimb lameness. An extended trot may reveal the horse’s inability to extend on limb compared with another and reveal lameness that was completely imperceptible under all other circumstances. The primary complaint, such as poor-quality flying changes of lead at canter, may require a riding assessment regardless of whether baseline lameness is evident under other circumstances. However, it is important for the veterinarian to separate his or her observations from those perceived by the rider. Identification of the lame limb may be difficult for a rider, although he or she may have a very strong opinion. If the veterinarian’s observations differ, the rider may be difficult to convince. It is also essential to recognize that bad riding can actually induce a false lameness that is completely unapparent if the horse is ridden well. Nonetheless, an experienced rider, trainer, or driver can be quite helpful in assessing the horse’s response to diagnostic analgesia or therapy, particularly in horses with thoracolumbar pain, subtle hindlimb lameness manifested only when ridden, and poor performance related to a musculoskeletal problem. Working regularly with a skilled, experienced, and reliable rider can be very helpful. Subtle differences in weight distribution of the rider may exacerbate or mask the presence of forelimb and especially hindlimb lameness. When the horse is performing the posting (rising) trot, lameness may be more or less prominent depending on which diagonal the rider is using. In the rising trot the rider sits on either the left or right diagonal. On the left diagonal the rider is sitting when the LF and RH are bearing weight and rising during the swing phase of these limbs. On the right diagonal the rider is sitting when the RF and LH are bearing weight. The correct diagonal is the outside diagonal (i.e., left diagonal on the right [clockwise] rein). Hindlimb lameness often is worse when the rider sits on the diagonal of the lame limb.5 Therefore if the horse is lame in the RH, the lameness appears and feel worse when the rider sits on the left diagonal.

CHAPTER 7 Horses with hindlimb lameness may try to force or throw the rider to sit on the more comfortable (for both horse and rider) diagonal.5 A horse with bilateral hindlimb lameness may appear lame in the RH when the rider sits on the left diagonal and lame in the LH when the rider sits on the right diagonal.5 Forelimb lameness is influenced less by the diagonal on which the rider sits, but a similar pattern exists. RF lameness is worse with the rider sitting on the right diagonal.5 This difference in lameness expression may be perceptible only by an experienced rider.

Observation of Inclines Walking or trotting a horse uphill or downhill may exacerbate lameness or identify previously unapparent lameness. Lameness in horses with suspensory desmitis may be worse when they walk uphill or downhill. Lameness associated with palmar heel pain may be worse when the horse walks downhill and the horse may show a tendency to stumble. Horses that tend to stumble or knuckle behind while walking downhill may have loose stifles (inability to maintain the position of the patella, usually caused by lack of muscle tone). Horses with neurological disease usually show more pronounced clinical signs when walking uphill or downhill. A superficially flat, hard surface may actually slope; this can influence lameness because the horse’s feet will be tilted with one side lower than the other. Thus the horse may appear different when trotting away from the observer than when returning.

EVALUATION OF LAMENESS WITH A TREADMILL OR GAIT ANALYSIS The use of a treadmill for poor performance evaluation is well recognized, and its use in lameness assessment is discussed in detail in Chapter 101. The clinical relevance of lameness apparent only on a treadmill is open to debate. I do not find lameness examinations on a treadmill at high speed particularly useful unless slow-motion videotape is available. I prefer to assess the horse while training or performing. A horse may modify its normal gait on a treadmill. Good correlation was demonstrated between gait regularity in horses exercised on a track and a treadmill, but treadmill strides and steps were shorter, and the swing phase of the stride was reduced.28 Horses require at least two training sessions on a treadmill before the gait becomes consistent.29 Stride characteristics of horses galloping on a treadmill change as the slope of the treadmill increases from 0% to 8%; horses reduced the suspension phase to maintain overall stride length.30 Gait analysis is discussed in Chapter 22. To date, assessment by an experienced, skilled observer has been more reliable in the identification of the lame limb or limbs than other more sophisticated methods of gait analysis.

REFERENCES 1. Liautard A: Lameness of horses, New York, 1888, William R Jenkins. 2. Dorland WAN, editor: Dorland’s illustrated medical dictionary, Philadelphia, 1974, WB Saunders. 3. Barnhart CL, editor: The American college dictionary, New York, 1970, Random House. 4. Adams OR: Natural and artificial gaits. In Stashak TS, editor: Adam’s lameness in horses, Philadelphia, 1987, Lea & Febiger. 5. Dyson S: Personal communication, 2000. 6. Biewener AA, Thomason J, Goodship A, et al: Bone stress in the horse forelimb during locomotion at different gaits: a comparison of two experimental methods, J Biomech 16:565, 1983.

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7. Leach DH, Sprigings E: Gait fatigue in the racing thoroughbred, J Equine Med Surg 3:436, 1979. 8. Uhlir C, Licka T, Kübber P, et al: Compensatory movements of horses with a stance phase lameness, Equine Vet J Suppl 23:102, 1997. 9. Ross MW: Observations in horses with lameness abolished by palmar digital analgesia, Am Assoc Equine Pract 44:230, 1998. 10. Evans LH: Personal communication, 1982. 11. Clayton HM: Cinematographic analysis of the gait of lame horses, J Equine Vet Sci 6:70, 1986. 12. Clayton HM: Cinematographic analysis of the gait of lame horses. V. Fibrotic myopathy, J Equine Vet Sci 8:297, 1986. 13. Wyman WEA: Lameness in the horse, New York, 1989, William R Jenkins. 14. Peloso JG, Stick JA, Soutas-Little RW, et al: Computerassisted three-dimensional gait analysis of amphotericininduced carpal lameness in horses, Am J Vet Res 54:1535, 1993. 15. Peham C, Licka T, Girtler D, et al: Supporting forelimb lameness: clinical judgement vs. computerized symmetry measurement, Equine Vet J 31:417, 1999. 16. Buchner HHF, Savelberg HHCM, Schamhardt HC, et al: Head and trunk movement adaptations in horses with experimentally induced fore- or hindlimb lameness, Equine Vet J 28:71, 1996. 17. Vorstenbosch MATM, Buchner HHF, Savelberg HHCM, et al: Modeling study of compensatory head movements in lame horses, Am J Vet Res 58:713, 1997. 18. Ratzlaff M, Hyde ML, Grand BD: Measurement of vertical forces and temporal components of the strides of horses using instrumented shoes, J Equine Vet Sci 10:23, 1990. 19. Judy CE, Galuppo LD, Snyder JR, et al: Evaluation of an in-shoe pressure measurement system in horses, Am J Vet Res 62:23, 2001. 20. May SA, Wyn-Jones G: Identification of hindleg lameness, Equine Vet J 19:185, 1987. 21. Buchner HHF, Kastner J, Girtler D, et al: Quantification of hindlimb lameness in the horse, Acta Anat 146:196, 1993. 22. Gingerich DA, Newcomb DM: Biomechanics in lameness, J Equine Med Surg 3:251, 1979. 23. Gingerich DA, Auer JA, Fackelman GE: Force plate studies on the effect of exogenous hyaluronic acid on joint function in equine arthritis, J Vet Pharmacol Ther 2:291, 1979. 24. Gingerich DA, Auer JA, Fackelman GE: Effect of exogenous hyaluronic acid on joint function in experimentally induced equine osteoarthritis: dosage titration studies, Res Vet Sci 30:192, 1981. 25. Schamhardt HC, Merkens HW: Quantification of equine ground reaction force patterns, J Biomech 20:443, 1987. 26. Merkens HW, Schamhardt HC: Evaluation of equine locomotion during different degrees of experimentally induced lameness. II. Distribution of ground reaction force patterns of the concurrently loaded limbs, Equine Vet J Suppl 6:107, 1988. 27. Guide to veterinary services for horse shows, ed 7, Lexington, Ky, 1999, American Association of Equine Practitioners. 28. Fredricson I, Drevemo S, Dalin G, et al: Treadmill for equine locomotion analysis, Equine Vet J 15:111, 1983. 29. Buchner HHF, Savelberg HCM, Schamhardt HC, et al: Habituation of horses to treadmill locomotion, Equine Vet J Suppl 17:13, 1994. 30. Kai M, Hiraga A, Kubo K, et al: Comparison of stride characteristics in a cantering horse on a flat and inclined treadmill, Equine Vet J Suppl 23:76, 1997.

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CHAPTER •

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Manipulation Mike W. Ross

lexion or other manipulative tests often are used to induce or exacerbate lameness during lameness or prepurchase examinations.

F

INDUCED AND BASELINE LAMENESS It is important to understand the concept of induced lameness and the possible difference between lameness seen at this stage and baseline lameness. During lameness examination, baseline lameness is established before any form of manipulation is performed. This may be difficult if more than one limb is involved, if lameness is subtle or sub-clinical, or if lameness is bilaterally symmetrical, which causes a gait abnormality without overt lameness. Lameness provocation is performed to exacerbate the baseline lameness or to provoke a hidden gait abnormality and attempt to localize the source of pain within a limb or limbs. Provocative tests create induced lameness that may not have any clinical relevance to the baseline lameness observed during initial movement. These tests are not sensitive or specific, and many times result in false-positive and false-negative findings. Many horses with palmar heel pain respond positively to the “fetlock flexion test” (or lower limb flexion test, see following text) and could erroneously be thought to have lameness of the metacarpophalangeal joint. A racehorse with baseline lameness as the result of a carpal chip fracture may have pre-existing low-grade osteoarthritis of the metacarpophalangeal joint and respond positively to lower limb flexion, but response to carpal flexion may be equivocal. Diagnostic analgesia is essential to localize the source or sources of pain. In the hindlimb, hock flexion, the so-called spavin test, causes many false-positive reactions.

FLEXION TESTS Flexion tests were first described early in the twentieth century, but information regarding the degree of flexion, force, or duration of the tests was lacking.1 Variations in technique persist and produce variable responses that can be misleading. There appear to be more false-positive reactions to flexion than there are false negatives, but the latter do occur. Flexion tests are useful during pre-purchase examinations because the horses being examined usually are relatively sound, and the tests are useful at uncovering hidden sources of pain. Flexion tests may be useful in exacerbating lameness, particularly when the primary or baseline lameness is in the region being flexed, but sensitivity is doubtful. Horses judged to be clinically sound underwent a “normal” and then a “firm” lower limb flexion test (fetlock flexion).2 Of the 50 horses tested, 20 had a positive response to normal flexion, and 10 of these horses were judged to be lame while trotting for about 15 m (50 ft) or more. Forty-nine of 50 horses had a positive response to firm flexion, and 35 of these remained lame for a minimum of 15 m. In this study the force applied

was not calibrated, 7 of the 50 horses developed lameness within 60 days of completion of the study, and 24 horses had radiographic abnormalities that could have contributed to a positive response to flexion.2 Although there may be an explanation for a positive response in some horses, the high percentage of positive results in the study is in agreement with my clinical impression. In a study using the Flextest (Krypton Electronic Engineering NV, Leuven, Belgium), an apparatus designed to control traction force and time during a lower limb flexion test, the optimal force and time for flexion were 100 N and 1 minute, respectively. There was a positive response to flexion in many horses that were considered sound, and a positive response in sound horses was more likely in those in active work than in horses that had been rested or turned out on pasture. Horses were more likely to manifest a positive response to flexion as the force used in the test was increased.3 A false-positive response to flexion can be observed in clinically normal horses and in those with unimportant low-grade problems. Lameness induced by flexion in these horses may have little clinical relevance. However, other evidence suggests that a positive response to lower limb flexion in sound horses may be useful to predict future lameness. In a retrospective study, 151 initially sound horses were followed for 6 months. Twenty-one percent of horses with a positive forelimb flexion test result developed lameness in the area being flexed, whereas only 5% of horses with a negative flexion test result subsequently developed lameness. In young Swedish Warmbloods there was a positive correlation between a positive response to flexion and a subsequent insurance claim related to lameness.4 Flexion tests lack specificity because it is nearly impossible to flex a single joint without flexing other joints or nearby tissues, particularly in any hindlimb or distal forelimb flexion tests. Elevation of a limb without flexion in severely lame horses may exacerbate the baseline lameness, since horses guard the limb or need to warm-out of the lameness for a number of steps while trotting, thus complicating interpretation. Hindlimb flexion tests are less specific than forelimb tests because the reciprocal apparatus prevents flexion of any joint without concomitant flexion of other joints. Hindlimb flexion tests are useful in exacerbating baseline lameness, but positive responses to individual lower limb and upper limb tests, in my opinion, only localize lameness to the entire hindlimb. I believe that flexion tests are useful in exacerbating lameness, and in some horses it is the baseline or relevant lameness that is being worsened. In general, unless the horse’s response is clearly pronounced and different from that of other manipulation, lameness cannot be localized based on response to flexion alone. Diagnostic analgesia should always be used, when possible, to localize pain.

Order, Duration, Force, and Venue during Flexion Tests Consistency in technique is essential. Although force exerted by individuals varies, the flexion technique of experienced practitioners is sufficient to objectively assess response to

CHAPTER 8 flexion.5 Response to flexion can and should be compared with the contralateral limb. Ideally the flexion test should be performed in the contralateral sound limb first, before performing the test in the suspect limb, to determine the horse’s response. Accurate assessment of response to flexion in the contralateral non-lame limb may not be possible if the horse is severely lame after flexion of the lame limb and lameness persists. In some instances, baseline lameness is actually increased by forcing the horse to stand for the contralateral flexion test, a useful observation seen most commonly in horses with forelimb lameness (see following text). Duration of flexion is somewhat controversial and may be an individual choice. In a study evaluating lower limb flexion, duration of 1 minute was considered ideal, because normal horses that underwent flexion at 100 N for 1 minute had few false-positive responses.3 Maintaining firm flexion for 1 minute while performing all flexion tests and repeating the tests in the contralateral limbs can make this portion of the lameness examination time-consuming. On the other hand, if the clinician takes the time to perform these tests, optimum chances of success are desired. A false-positive result is more useful than a false-negative test result. Some clinicians prefer to perform flexion tests with more force but for a shorter duration. This technique works well for lower limb flexion tests. Seldom is it possible to maintain some upper limb manipulative procedures for 1 minute. Thus some latitude is necessary. I believe that duration of flexion of 45 seconds to 1 minute is enough to elicit an accurate response in most horses. Force used during flexion varies considerably, but excessive force induces lameness in most normal horses. Forces in the range of 100 to 150 N represent a moderate degree of force for lower limb flexion tests. In studies using a dynamometer, the maximum amount of force that could be used without a consistent withdrawal response in normal horses was 150 N.6 The amount of force also depends on the size of the horse or the joint being flexed. The amount of force used in adult horses cannot be used in foals. Horses with obvious osteoarthritis or articular fracture, or those with substantial soft tissue injury likely to be affected by the flexion test, do not tolerate the same force as horses with more mild conditions. In a study of healthy and injured Thoroughbred (TB) racehorses, a positive correlation existed between decreased range of motion and joint injury.7 Loss of joint motion was most likely caused by joint capsule fibrosis, but pain associated with increased intra-articular pressure from effusion or flexion also may have limited joint motion.7 I recommend flexing a joint as much as possible with an amount of force just slightly less than that which consistently causes a withdrawal response. Proper evaluation of the results of flexion tests requires that the horse be observed while trotting in a straight line on a firm, non-slip surface. Horses usually are trotted in hand, although occasionally a horse’s response to flexion is evaluated while it is being ridden. The horse should be trotted immediately after the limb is placed to the ground, with care taken to avoid scaring the horse or providing any excessive encouragement to trot, because many horses will slip initially, gallop off, or balk, all of which necessitate test repetition. If possible, the horse should be trotted away from the examiner for a minimum of 12 to 15 m.

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Stretching or compression of the joint capsule, vascular constriction, and activation of pain receptors in the joints and surrounding soft tissues also can occur during flexion.3 It is rarely possible to attribute pain on static flexion or during movement after flexion to an individual articular surface. The “fetlock flexion test” is a misnomer because as it is commonly performed, it includes the interphalangeal joints and stresses surrounding soft tissue. Thus the names lower limb flexion test or fetlock region flexion test are more appropriate.

Positive Responses to Flexion Positive responses to flexion can be seen with static flexion (see Chapter 6) and when movement follows flexion. A positive flexion test result is defined as obvious lameness or an increase over baseline lameness that is observed for more than three to five strides while the horse trots in a straight line after flexion. A mild response, even in sound horses, often is seen in the first few strides, a finding that should be compared with the contralateral limb. Sound horses warm-out of this mild response quickly. A persistent, one- to two-grade increase over baseline lameness for several steps is a positive response. In horses with hindlimb lameness a marked positive response often is accompanied by reluctance to place the heel on the ground, and the horse may land only on the toe for several strides.

Forelimb Flexion Tests Lower Limb Flexion Test The lower limb flexion test often has been equated erroneously with the fetlock flexion test. The fetlock region can be flexed independently of interphalangeal joints (see following text). The lower limb flexion test is the most common test performed in the forelimb and involves placing a hand on the toe and forcing the fetlock and both interphalangeal joints into firm flexion (Fig. 8-1). A positive response to flexion can be observed with any condition of the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints; navicular bone or bursa; other causes of palmar heel pain; digital flexor tenosynovitis; any soft tissue problem in the palmar pastern region; and lameness associated with the

Causes of Pain during Flexion and Positive Flexion Test Results Forced flexion of a joint can induce pain in many potential sites. Force is being applied to both articular structures and surrounding soft tissues. The tissues on the flexion side of the joint are being compressed, whereas tissues on the extension side are under tension. During flexion, intra-articular pressure and intra-osseous pressure in subchondral bone are increased.3,7

Fig. 8-1 The lower limb flexion test often is erroneously called the fetlock flexion test. During the lower limb flexion test the fetlock, proximal interphalangeal, and distal interphalangeal joints are flexed; the palmar pastern and fetlock region soft tissue structures are compressed; and the dorsal structures are stretched.

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branches of the suspensory ligament (SL) or proximal sesamoid bones (PSBs). Horses with lesions of the PSBs usually have markedly positive responses to this test. This test is not specific for lameness of the metacarpophalangeal joint. I have seen marked responses in horses with navicular disease or osteoarthritis of the interphalangeal joints. However, horses with osteoarthritis, fractures of the metacarpophalangeal joint, or tenosynovitis usually also show a marked positive response. In a recent study of clinically sound horses in which lameness could consistently be induced by flexion with 250 N for 1 minute, lameness was alleviated by intra-articular analgesia of the metacarpophalangeal joint, but not by intraarticular analgesia of the proximal interphalangeal or distal interphalangeal joints or intra-thecal analgesia of the navicular bursa.8 The limb should be held as close to the ground as possible, and forced carpal flexion should be avoided (see Fig. 8-1). All soft tissue and bony structures in the palmar aspect of the distal limb are severely compressed, resulting in low specificity for the metacarpophalangeal joint. Some people use a hand as a fulcrum or grab the toe with both hands (Fig. 8-2), but this technique may result in application of excessive force, although it otherwise produces similar results.

Fetlock Flexion Test The specificity of the lower limb flexion test can be improved by applying force to the metacarpophalangeal joint and avoiding forced flexion of the interphalangeal joints. The fetlock flexion test is performed by placing one hand along the dorsal aspect of the pastern region and one hand along the dorsal aspect of the metacarpal region, while avoiding flexion of the carpus (Fig. 8-3). This test is more difficult to perform because it requires more force and the clinician’s effort to maintain a similar degree of flexion. The test is not specific for articular lameness of the metacarpophalangeal joint and horses with soft tissue problems respond positively.

Extreme lower limb flexion can be achieved by using both hands on the toe with the limb cradled between the clinician’s legs. With such extreme flexion even normal horses may manifest a positive response.

Fig. 8-2

Flexion of Interphalangeal Joints In my opinion, flexion of either the proximal interphalangeal or distal interphalangeal joint without concomitant flexion of the other, or of the metacarpophalangeal joint, is impossible. Varus or valgus stress can be applied to the interphalangeal joints, and when followed by trotting, this stress can be a suitable provocative test in horses with osteoarthritis or soft tissue injuries of these joints.

Carpal Flexion Test The carpal flexion test is the most specific of all forelimb flexion tests, and a positive response usually reflects baseline lameness associated with the carpal regions. Few false-positive results occur. A positive response may reflect intra-articular pain, but a positive response also is seen in horses with carpal tenosynovitis, accessory carpal bone fractures, proximally located superficial (SDF) and deep digital flexor (DDF) tendonitis, proximal suspensory desmitis (PSD), or avulsion fracture of the third metacarpal bone (McIII) at the SL insertion. Rarely, a horse with a problem in the scapulohumeral and cubital joints or the antebrachium responds positively. A negative response does not preclude an articular lesion of the carpus, including incomplete fractures or sclerosis of the carpal bones. The limb is elevated and the carpus is forced into full flexion by pushing the metacarpal region directly underneath the radius (Fig. 8-4). The distal limb can be pulled laterally to place the carpal joints in valgus stress or torsion. Horses sometimes trot off lame on the contralateral limb after the carpal flexion test is performed. I have seen this most commonly in young Standardbred or TB racehorses with subchondral bone pain in the middle carpal joint and call it the “Ross crossed-extensor phenomenon.” I believe that this reflects bilateral lameness, and flexion of the ipsilateral carpus causes less pain than making the horse stand for 1 minute on

A true fetlock flexion test can be performed by carefully flexing only the fetlock joint. The clinician’s hand grasps only the pastern and not the toe of the hoof while avoiding forced flexion of the proximal and distal interphalangeal joints (see Fig. 8-1).

Fig. 8-3

the contralateral limb. I have observed this response most commonly in horses with bilateral carpal lameness, but exacerbation of contralateral lameness is not restricted to carpal lesions. Dyson9 has called this a “paradoxical response to flexion” and has observed exacerbation of contralateral lameness in horses with navicular syndrome and distal hock joint pain.

Upper Limb Manipulation Because of the inverse but simultaneous movement of the elbow and shoulder joints, it is difficult to accurately name the

CHAPTER 8

Fig. 8-4 The carpal flexion test is the most specific of all flexion tests, but it applies concomitant mild flexion of the elbow and shoulder joints. Although false-negative results are possible, a positive carpal flexion test result usually means that lameness originates from the carpal region. flexion tests of these joints. For instance, when the limb is pulled in a caudal direction, the shoulder joint is flexed, but the elbow joint is extended. I call this manipulation upper limb flexion (Fig. 8-5). This maneuver requires both hands, one hand grasping the pastern region and one grasping the cranial aspect of the antebrachium to force the entire limb in a caudal direction. When the limb is pulled in a cranial direction, resulting in upper limb extension, the shoulder joint is extended, but the elbow joint is flexed (Fig. 8-6). Both hands are placed around the pastern region while forcing the entire forelimb into maximal extension. Maintenance of upper limb extension or flexion for even 45 seconds is difficult, so I try to maintain this position for as long as possible and then evaluate the horse while trotting. Many normal horses resist upper limb manipulation, and an alternative is to force the limb into hard flexion or extension in a rhythmical fashion six to eight times and then trot the horse. Even though the entire limb is being manipulated, there are few false-positive test results. However, false-negative test results can occur, probably because of the inability to place either the shoulder or the elbow joints in hard flexion. In my experience, horses with lameness originating from the elbow region are more likely to respond to upper limb extension, whereas those with lameness originating from the shoulder region are more likely to respond to upper limb flexion.

Hindlimb Flexion Tests Hindlimb flexion tests are not specific, but they may be useful to exacerbate the baseline lameness or detect hidden sources of potential lameness. I do not believe that hindlimb flexion tests are useful in differentiating the source of lameness in most horses, unless the response is dramatic, and diagnostic analgesia usually is required in all horses.

Lower Limb Flexion Test The lower limb flexion test is performed similarly to the forelimb flexion test, but with similar force the metatarsophalangeal joint can be flexed more extremely. The veterinarian should try to keep the limb as low as possible to avoid placing hard flexion on the upper limb, although all joints are flexed to a degree. The lower limb flexion test also affects the proximal interphalangeal and distal interphalangeal joints and the

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Fig. 8-5 Upper forelimb flexion is performed by grasping the antebrachium and pulling the entire limb caudally and slightly proximally. This maneuver flexes the shoulder joint and extends the elbow joint. Horses with shoulder region lameness often respond positively to this manipulative test.

Fig. 8-6 The upper limb extension test is performed by pulling the forelimb out in front of the horse and forcing it proximally. This places the elbow joint in flexion and the shoulder joint in extension. In my experience, lameness of the elbow region is exacerbated by this technique, but occasionally shoulder joint lameness also is worsened. surrounding soft tissues (Fig. 8-7). Horses with digital flexor tenosynovitis or DDF tendonitis show a marked response to the lower limb flexion test. False-positive results can occur, but these are less common in a hindlimb than in a forelimb, even in horses in active work. Horses with pain in the upper limb may show a mild or moderate response to lower limb flexion. This test is not specific for pain located in the lower limb, and lameness in horses with stifle pain often is worse after the lower limb flexion test.9 Horses with subchondral

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Fig. 8-7 The lower limb flexion test in the hindlimb is performed with the limb as close to the ground as possible. Flexion of one portion of the hindlimb is impossible without flexing the entire limb, a finding that explains many false-positive hindlimb flexion tests.

bone pain from non-adaptive or stress remodeling of the distal third metatarsal bone (MtIII) or those with incomplete fractures of MtIII or incomplete, mid-sagittal fractures of the proximal phalanx may show little response to this test (falsenegative result).

Fig. 8-8 The hindlimb upper limb flexion test is demonstrated. This test has been called the spavin or hock flexion test, but it is not specific for lameness of the hock. The hock and stifle joints are in forced flexion, the lower limb joints are flexed, the metatarsal region is compressed, and a small amount of forced flexion of the coxofemoral joint is induced.

Fetlock Flexion and Interphalangeal Joint Tests The metatarsophalangeal joint region can be flexed independently of the interphalangeal joints in the hindlimb, or the interphalangeal joints can be flexed independently, but these tests are difficult to perform and of limited value.

Upper Limb Flexion Test The so-called spavin or hock flexion test is not specific for lameness of the hock, because the stifle and coxofemoral joints also are stressed hard, and mild flexion of the lower joints is inevitable. The limb is held in hard flexion for at least 1 minute, but additional time for this test may improve its clinical value (Fig. 8-8). It may be necessary to have an assistant place a hand on the contralateral hip to steady the horse, because proper performance of this test requires that the limb be elevated substantially and the horse may lose its balance. The position of the hands in the metatarsal region is important to consider, since the force required to hold the hindlimb in this position may cause compression and pain in structures along the plantar aspect, potentially contributing to a false-positive response.

Hindlimb Flexion Test Alternatively, the entire hindlimb can be flexed simultaneously. This test is useless in differentiating potential sources of pain in a limb, but it is quite useful in exacerbating baseline lameness or uncovering occult lameness conditions. The clinician’s hands are placed on the toe and the entire limb is held in extreme flexion (Fig. 8-9). An assistant may be necessary to steady the opposite hip while the limb is elevated.

A hindlimb flexion test is a combination of the lower limb flexion and upper limb flexion tests.

Fig. 8-9

“Hock” Extension Test Hock extension may be useful in placing selective stress on the hock, independent of the stifle. Forced extension causes tension on the soft tissue structures on the dorsal, medial, and lateral aspects of the hock. Seldom is it possible to perform this test for 1 minute; six to eight attempts at forced exten-

sion followed by trotting the horse can be substituted for more lengthy manipulation (Fig. 8-10). False-positive and false-negative responses occur, which are caused mostly by the inelastic reciprocal apparatus. This maneuver can reveal laxity of a damaged fibularis (peroneus) tertius.

CHAPTER 8

Fig. 8-10 During the hock extension test the clinician forces the hock into extension by pushing down on the calcaneus while pulling up on the distal limb by using both the right arm and left leg. Pain from hock lameness can be exacerbated, but false-positive results from pain in other locations also can occur.

“Stifle Flexion” Test A modification of the upper limb flexion test can be used to place hard flexion on the stifle, independent of the hock (Fig. 8-11). This test can be somewhat difficult to perform but may exacerbate lameness in horses with osteoarthritis or other conditions of the stifle. Other proximal limb joints are also in flexion; therefore some false-positive results occur.

DIRECT OR LOCAL PALPATION FOLLOWED BY MOVEMENT Static palpation, in which the horse’s response to compression during palpation while standing is assessed, reveals useful information (see Chapter 6). Additional information can be gained by evaluating movement after palpation, dynamic provocation to induce lameness. Dynamic provocation usually is performed by digital palpation or use of hoof testers. Many horses manifest a positive response during static palpation, but the primary pain is located elsewhere. However, if lameness can be induced or baseline lameness can be increased by one or two grades by deep palpation, then the area may be relevant to the current cause of lameness. False-positive results do occur, but in my opinion, these are less frequent than with most flexion tests. There are few false-negative results.

Digital Compression of a Painful Area The veterinarian should elevate the limb and compress the painful or otherwise inflamed area for 15 to 30 seconds and then evaluate the horse at a trot in hand. Exacerbation of the baseline lameness by one or more grades is considered a positive response. This procedure is useful in differentiating the cause of lameness in both the forelimb and hindlimb. In the forelimb, I find it useful to compress the dorsal proximal aspect of the proximal phalanx (if a mid-sagittal fracture is suspected), the dorsal cortex of the McIII (for bucked shins or

• Manipulation

79

Fig. 8-11 A seldom-used test is the stifle flexion test. This test can be difficult and dangerous to perform in fractious horses. The forced flexion of the stifle joint used in this test attempts to differentiate stifle and hock joint pain.

a dorsal cortical fracture), exostoses involving the small metacarpal bones (for splints), the suspensory branches or digital flexor tendons, and the proximal palmar metacarpal region (for PSD or longitudinal or avulsion fracture). In horses with mild tendonitis of the superficial digital flexor tendon (SDFT), baseline lameness usually is mild or non-existent, but obvious lameness after digital compression suggests tendonitis as a substantial problem. In the hindlimbs, compression of the dorsal proximal aspect of the proximal phalanx can increase lameness from mid-sagittal fracture, but trauma from interference injury (of particular importance in trotters) or other forms can lead to a false-positive response. A dynamic Churchill test, compression followed by trotting (see Chapter 6), is useful in the diagnosis of lameness of the proximal metatarsal region and tarsus. In the hindlimb, compression of the proximal aspects of both the second and fourth metatarsal bones puts indirect pressure on the origin of the SL, and a positive response may indicate PSD. Compression of a “curb” followed by trotting may increase lameness. In some horses with tibial stress fractures, an induced lameness can be seen after deep palpation of the caudal tibial cortex. With the limb elevated, the veterinarian should apply deep pressure to the caudal cortex by wrapping the fingers around the tibia from the medial aspect. Most horses object to this maneuver, but in those with tibial stress fractures, the positive static response is followed by an exacerbation of the baseline lameness.

Axial Skeleton Application of direct local pressure to many parts of the axial skeleton is difficult, but in some instances this procedure can lead to the detection of pain both statically and while the horse is trotting (see Chapters 6, 94, 98, and 100). In the cervical area, forced lateral bending followed by walking or trotting may exacerbate neurological signs or gait deficits in horses with cervical instability or proliferative changes. Deep palpation over the thoracolumbar spine followed by trotting

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can induce hindlimb stiffness or other mild gait abnormalities. Direct and deep palpation over the tubera sacrale and tubera coxae can induce hindlimb lameness in horses with stress fractures or those with chronic lameness as a result of pelvic asymmetry from old fractures. Sacroiliac compression, or manipulation of the sacrum or tail head, can induce hindlimb stiffness or lameness in horses with injuries in these areas.

INDUCED LAMENESS AFTER HOOF TESTER EXAMINATION The hoof testers are applied in a suspected area for 15 to 30 seconds and the horse is evaluated for lameness while trotting. False-positive test results are quite common, but a marked difference between limbs can be an important clinical sign. Shoes and pad combinations may preclude complete hoof tester examination of the sole, so I often apply pressure across the heels. I have found this position to yield the most useful information in horses with palmar heel pain from most causes, but it also induces a positive response in horses with non-specific foot pain (sore feet). Most normal horses object to firm pressure placed across the heels using hoof testers, and mild lameness on the initial few steps is common, but severe lameness after this test is a useful indication that the foot is the source of baseline lameness.

THE WEDGE TEST The wedge test is a form of manipulation similar to the flexion or other varus or valgus stress tests, but it is used specifically to evaluate the digit and associated soft tissues. The wedge can be used to dramatically change the dorsal-to-palmar (heel) or medial-to-lateral hoof angles. Collateral ligaments, joint capsules, subchondral bone and articular surfaces, and surrounding soft tissues can be stretched or compressed when the horse stands on the wedge. Changes in hoof angles of this magnitude can greatly change the stress placed on the deep digital flexor tendon (DDFT), SDFT, and SL. Raising the heel reduces stress on the DDFT but increases stress on the SL. Raising the toe reduces stress on the SL but increases stress on the DDFT, navicular bone, and associated ligaments and bursa. The number of tissues affected by the wedge accounts for the lack of specificity of this test, and it likely accounts for many false-positive results. The wedge is placed in the desired position and the horse is made to stand in this position for 30 to 60 seconds with the contralateral limb elevated (Fig. 8-12). The horse is then trotted in a straight line on a firm surface. The test can be used in any limb but is performed most commonly in the forelimbs. In some horses, it is difficult to attain the desired duration regardless of whether they are lame. The horse’s response to simply standing on the wedge may not give an accurate indication of how lame it will be when it is trotted. In horses content to stand in such an abnormal position, a dramatic lameness may be seen at the trot. Horses with navicular syndrome or sore feet from many causes of palmar heel pain are most likely to manifest a positive response. In my experience, the direction of the wedge that elicits the most positive response from horses with palmar heel pain is with the apex (low end) directed medially (see Fig. 8-12). This substantial change in the medial-to-lateral hoof angle is likely to cause stretching of the suspensory apparatus of the navicular bone and collateral ligaments of the distal interphalangeal joint or compression on articular structures. Horses with palmar heel pain may show severe lameness, but diagnostic analgesia is required to confirm the foot as a source of pain. Horses with injuries of the DDFT, SDFT, and SL may show a milder response.

Fig. 8-12 A 15° to 20° wedge can be used to manipulate the joints and soft tissue structures of the digit. The most consistent response is elicited by directing the apex (low end) of the wedge medially (as shown). The wedge also can be used to raise the heel and toe. (Wedge courtesy Norman Ducharme, Ithaca, New York.)

VARUS OR VALGUS STRESS TESTS Evaluation for lameness after placing varus or valgus stress on an individual joint may incriminate this area as a potential source of pain and is used most commonly in the stifle. To perform the stifle valgus stress test, the clinician’s shoulder (or hand) is used as a fulcrum against the distal femur, and the distal limb is pulled laterally several times before the horse is trotted (see Fig. 6-24). False-positive results can be obtained because the entire distal extremity is manipulated during this test. Valgus or varus stress tests can be used in many joints in the distal limb, particularly the interphalangeal joints. Patellar manipulation followed by trotting (see Fig. 6-26) may be helpful but can be difficult to perform when horses resist forced proximal movement of the patella (frequently, the veterinarian’s wrist is forced into hyperextension). Although cranial and caudal drawer tests can be used to exacerbate stifle lameness, I have not found them particularly helpful, and they are dangerous to perform.

FLEXION TESTS AND DIAGNOSTIC ANALGESIA I do not generally recommend combining the results of flexion tests and diagnostic analgesia. I often hear that baseline lameness abated after a block, but the horse still had positive flexion test results. My usual comment is, “Why bother to flex the horse if baseline lameness has been abolished?” Flexion tests induce lameness that may be unrelated to the baseline lameness. Thus it is not unusual that a horse might have residual lameness after flexion, even if the baseline lameness has been eliminated.4 I usually do not recommend further investigation once baseline lameness has been eliminated. If baseline lameness is not obvious, but a low-grade gait deficit is present, or if a horse has bilaterally symmetrical lameness, flexion tests or other forms of manipulation or

CHAPTER 9

• Applied Anatomy of the Musculoskeletal System

provocation may be the only way of “seeing” lameness. In this instance, induced lameness from manipulation can be assumed to be the baseline lameness, and diagnostic analgesia can proceed. All involved parties should be well informed about the potential for misdiagnosis, but in certain circumstances this pathway may lead to a successful diagnosis.

REFERENCES 1. Nilsson G, Fredricson I, Drevemo S: Some procedures and tools in the diagnostics of distal equine lameness, Acta Vet Scand Suppl 44: 63, 1973. 2. Ramey DW: Prospective evaluation of forelimb flexion tests in practice: clinical response, radiographic correlation, and predictive value for future lameness, Am Assoc Equine Pract 43:116, 1997. 3. Verschooten F, Verbeeck J: Flexion test of the metacarpophalangeal and interphalangeal joints and flexion angle of the metacarpophalangeal joint in sound horses, Equine Vet J 29:50, 1997.

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4. Dyson SJ: Evaluation of the musculoskeletal system. Part 4. The use of flexion tests and small diameter lunging. In Mair T, editor: British Equine Veterinary Association manual: the pre-purchase examination, Newmarket, 1998, Equine Veterinary Journal. 5. Keg P, van Weeren PR, Back W, et al: Variations in the force applied to flexion tests of the distal limb of horses, Vet Rec 141:435, 1997. 6. Nilsson G: Lameness and pathologic changes in the distal joints and the phalanges of the Standardbred horse, Acta Vet Scand (Suppl) 43:83, 1973. 7. Strand E, Martin GS, Crawford MP, et al: Intra-articular pressure, elastance and range of motion in flexion of the equine metacarpophalangeal joint, Am J Vet Res 56:1362, 1995. 8. Meijer M, Busschers E, Van Weeren P: Which joint is most important for the positive outcome of a flexion test of the distal forelimb of a sound horse? Equine Vet Educ 13: 319, 2001. 9. Dyson SJ: Personal communication, 2001.

9

Applied Anatomy of the Musculoskeletal System Matt Durham and Sue J. Dyson

t is beyond the scope of this book to describe all aspects of musculoskeletal anatomy in depth, yet a detailed knowledge of anatomy is fundamental to a lameness diagnostician, as highlighted in the chapters on observation and palpation (Chapters 5 and 6). Some aspects of anatomy are considered in depth in individual chapters dealing with conditions of specific areas. This chapter considers some philosophical aspects of the importance of anatomical knowledge and describes some basic principles. It also provides illustrations that we hope will help the reader to understand better the three-dimensional aspects of anatomy. Accurate interpretation of what we see and feel during an examination requires knowledge of what structures we are looking at and palpating. For example, a swelling is noted over the dorsal aspect of the carpus. Is the swelling diffuse and possibly related to a hygroma, periarticular edema or cellulitis, or is there a discrete swelling, horizontally oriented, reflecting distention of the middle carpal joint? Or is it a longitudinal swelling reflecting distention of the common digital extensor tendon sheath or the tendon sheath of extensor carpi radialis? If the swelling is longitudinal, are any compressions in the swelling caused by normal retinaculum or adhesions within the sheath (Fig. 9-1)? If we examine the sheath by ultrasonography, is the echogenic band extending from the sheath wall to the enclosed tendon normal mesotendon, or is it an adhesion? If diffuse swelling is present around the dorsal aspect of the carpus associated with lameness, how can we tell if the middle carpal joint capsule is distended? We need to know that there is a palmar outpouching of the middle carpal joint on the palmarolateral aspect of the carpus, just distal to the accessory carpal bone. Thus during visual inspection and palpation the clinician should be constantly asking “what

I

ECRT ICB

C3

Fig. 9-1 Sagittal anatomical section through the carpus, transecting the extensor carpi radialis tendon (ECRT). ICB, Intermediate carpal bone; C3, third carpal bone.

CHAPTER 9

• Applied Anatomy of the Musculoskeletal System

provocation may be the only way of “seeing” lameness. In this instance, induced lameness from manipulation can be assumed to be the baseline lameness, and diagnostic analgesia can proceed. All involved parties should be well informed about the potential for misdiagnosis, but in certain circumstances this pathway may lead to a successful diagnosis.

REFERENCES 1. Nilsson G, Fredricson I, Drevemo S: Some procedures and tools in the diagnostics of distal equine lameness, Acta Vet Scand Suppl 44: 63, 1973. 2. Ramey DW: Prospective evaluation of forelimb flexion tests in practice: clinical response, radiographic correlation, and predictive value for future lameness, Am Assoc Equine Pract 43:116, 1997. 3. Verschooten F, Verbeeck J: Flexion test of the metacarpophalangeal and interphalangeal joints and flexion angle of the metacarpophalangeal joint in sound horses, Equine Vet J 29:50, 1997.

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4. Dyson SJ: Evaluation of the musculoskeletal system. Part 4. The use of flexion tests and small diameter lunging. In Mair T, editor: British Equine Veterinary Association manual: the pre-purchase examination, Newmarket, 1998, Equine Veterinary Journal. 5. Keg P, van Weeren PR, Back W, et al: Variations in the force applied to flexion tests of the distal limb of horses, Vet Rec 141:435, 1997. 6. Nilsson G: Lameness and pathologic changes in the distal joints and the phalanges of the Standardbred horse, Acta Vet Scand (Suppl) 43:83, 1973. 7. Strand E, Martin GS, Crawford MP, et al: Intra-articular pressure, elastance and range of motion in flexion of the equine metacarpophalangeal joint, Am J Vet Res 56:1362, 1995. 8. Meijer M, Busschers E, Van Weeren P: Which joint is most important for the positive outcome of a flexion test of the distal forelimb of a sound horse? Equine Vet Educ 13: 319, 2001. 9. Dyson SJ: Personal communication, 2001.

9

Applied Anatomy of the Musculoskeletal System Matt Durham and Sue J. Dyson

t is beyond the scope of this book to describe all aspects of musculoskeletal anatomy in depth, yet a detailed knowledge of anatomy is fundamental to a lameness diagnostician, as highlighted in the chapters on observation and palpation (Chapters 5 and 6). Some aspects of anatomy are considered in depth in individual chapters dealing with conditions of specific areas. This chapter considers some philosophical aspects of the importance of anatomical knowledge and describes some basic principles. It also provides illustrations that we hope will help the reader to understand better the three-dimensional aspects of anatomy. Accurate interpretation of what we see and feel during an examination requires knowledge of what structures we are looking at and palpating. For example, a swelling is noted over the dorsal aspect of the carpus. Is the swelling diffuse and possibly related to a hygroma, periarticular edema or cellulitis, or is there a discrete swelling, horizontally oriented, reflecting distention of the middle carpal joint? Or is it a longitudinal swelling reflecting distention of the common digital extensor tendon sheath or the tendon sheath of extensor carpi radialis? If the swelling is longitudinal, are any compressions in the swelling caused by normal retinaculum or adhesions within the sheath (Fig. 9-1)? If we examine the sheath by ultrasonography, is the echogenic band extending from the sheath wall to the enclosed tendon normal mesotendon, or is it an adhesion? If diffuse swelling is present around the dorsal aspect of the carpus associated with lameness, how can we tell if the middle carpal joint capsule is distended? We need to know that there is a palmar outpouching of the middle carpal joint on the palmarolateral aspect of the carpus, just distal to the accessory carpal bone. Thus during visual inspection and palpation the clinician should be constantly asking “what

I

ECRT ICB

C3

Fig. 9-1 Sagittal anatomical section through the carpus, transecting the extensor carpi radialis tendon (ECRT). ICB, Intermediate carpal bone; C3, third carpal bone.

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SDFT DDFT ICL

A SL

A

B

Sagittal views of the palmar metacarpal region. Proximal is to the right. A, FreeStyle Extended Imaging (Sequoia model, Acuson Co., Mountain View, CA) ultrasonographic image of the palmar metacarpal region. SDFT, Superficial digital flexor tendon; DDFT, deep digital flexor tendon; ICL, accessory ligament of the DDFT (inferior check ligament); SL, suspensory ligament. B, Corresponding anatomical section.

Fig. 9-2

structure am I seeing or palpating, what are its functions, and what would be the consequences of loss of function?” If it has abnormal contour or size, is this the result of swelling of that structure or an adjacent or underlying structure? Having established what structure is abnormal, the clinician then must consider the best imaging modality. If it is a tendonous or ligamentous structure, ultrasonography probably will provide the most information, but we must remember that it has bony attachments, and damage at those attachments might best be assessed by either radiography or nuclear scintigraphy. So we need to know not only what each structure is, but also the structures to which it is attached. During visual inspection and palpation, we also need to think logically. We know that the superficial and deep digital flexor tendons (SDFT, DDFT), the accessory ligament of the DDFT (ALDDFT), and the suspensory ligament (SL) lie on the palmar aspect of the third metacarpal bone (Fig. 9-2). Swelling confined to just the medial aspect of the metacarpal region is far more likely to reflect direct trauma to the medial aspect of the limb than sprain or strain of any of the ligamentous or tendonous structures. We need to know that the proximal aspect of the SL lies between the bases (heads) of the second (McII) and fourth (McIV) metacarpal bones and therefore is inaccessible to direct palpation, and that desmitis often may be present without discernible soft tissue swelling (Fig. 9-3). We must be aware of anatomy to realize the possible consequences of trauma to an area. The paucity of soft tissues over the cranial aspect of the stifle makes the patella and the tibial tuberosity vulnerable to direct trauma, hence the risk of fracture after hitting a fixed fence. The lack of soft tissues also means that if the horse hits a thorn hedge, the possibility of a thorn penetrating the femoropatellar joint capsule, resulting in contamination and infection, is quite high. We also need to think how structures move relative to one another while the horse is in motion. If a steeplechase horse sustains an interfer-

SL

B

ICL DDFT SDFT

Transverse sections through the proximal metacarpal region. Dorsal is to the top and lateral is to the left. SL, Suspensory ligament; ICL, accessory ligament of the deep digital flexor tendon (inferior check ligament); DDFT, deep digital flexor tendon; SDFT, superficial digital flexor tendon. A, Anatomical specimen. B, Computed tomographic scan using soft tissue windowing. (Courtesy Alamo Pintado Equine Medical Center, Los Olivos, California.)

Fig. 9-3

ence injury on the palmar aspect of the metacarpal region while galloping, the position of the skin laceration probably will not coincide with the level of the laceration in the SDFT (Fig. 9-4). We also need to know the relative positions of the laceration and the digital flexor tendon sheath (DFTS) to be aware of the likelihood that the sheath may have been traumatized, and thus the risk of infectious tenosynovitis. Faced with a contaminated wound on the dorsal aspect of a hind fetlock and severe lameness, and the possibility of infection of

CHAPTER 9

SL

• Applied Anatomy of the Musculoskeletal System

83

MC3

SDFT

P1 NF

P2

Lateral scintigraphic image of the metacarpal region acquired before the end of the vascular phase and at the beginning of the pool phase. This jumper had a history of low-grade chronic proximal suspensory ligament (SL) desmitis, and mild diffuse superficial digital flexor (SDFT) tendonitis. An acute interference injury to the mid-metacarpal region was evident on the skin. Note the proximal location of the acute injury to the SDFT. The linear area of uptake between the SL and SDFT is vascular artifact related to the time of acquisition. (Courtesy Alamo Pintado Equine Medical Center, Los Olivos, California.)

Fig. 9-4

the metatarsophalangeal joint, we need to know where to expect to see distention of the plantar pouch of the joint capsule and to know that this site is safely accessible for arthrocentesis. A fundamental principle of lameness investigation is the identification of the source or sources of pain. Although this may be possible through detailed clinical examination, in many instances it is essential to perform diagnostic analgesia (see Chapter 10). A detailed knowledge of the anatomy of nerves, joint capsules and the various out-pouchings, tendon sheaths, and bursae is fundamental to safe, accurate performance of perineural and intra-synovial injections. Given the knowledge of the close relationship among the distal interphalangeal joint capsule, the distal sesamoidean impar ligament, the collateral ligaments of the navicular bone and the distal phalanx, and the close proximity of branches of the palmar digital nerve, it is not surprising that intra-articular analgesia is not specific and that other structures can be affected, especially if interpretation of the response is delayed or an excessively large volume of local anaesthetic solution is used. Knowledge that the medial and lateral femorotibial joints do not normally communicate and that the cruciate ligaments usually are extra-articular structures is crucial for an understanding of why these joint compartments must be injected separately, and why the response to intra-articular analgesia may be both incomplete and delayed if a cruciate ligament is damaged. Knowledge of functional neuroanatomy also is important for interpretation of specific gait abnormalities. Inability to bear weight on a hindlimb after general anesthesia may be due to myopathy, but in the absence of marked pain and distress, it is more likely that the horse has lost extensor function and is unable to extend any of the hindlimb joints because of femoral nerve paresis. Loss of ability to extend the elbow may be due to loss of triceps function associated with a fracture of the olecranon but may also be due to radial nerve paresis.

Fig. 9-5 Sagittal anatomical section through the pastern demonstrating a common location for the nutrient foramen (NF) entering the proximal phalanx (P1). MC3, Third metacarpal bone; P2, middle phalanx. Vascular anatomy is important because many nerves lie close to vessels. With superficial nerves and vessels, identification of the vessel may facilitate palpation of the nerve and thus aid accurate perineural injection. Avoiding penetration of the vessel and causing hematoma formation also is desirable. With regard to deeper nerves the veterinarian may benefit by knowing that the needle must be in close proximity to the nerve if blood appears in the needle hub. This information can be helpful when performing perineural analgesia of the deep branch of the fibular nerve. Assessment of digital pulse amplitudes is an integral part of palpation. Increased pulse amplitude usually signifies a site of inflammation at, or distal to, the region of palpation, especially in association with inflammatory conditions of the foot, such as subsolar abscessation or laminitis. Palpation of the pulse in the dorsal metatarsal artery and assessment of saphenous vein filling can be helpful in the evaluation of a horse with suspected aortoiliac thrombosis. Knowledge of the sites of major vessels is important when considering the consequences of major laceration to an area and possible avascular areas, and in planning a surgical approach to an area. All bones have one or more nutrient foramina through which major vessels enter. These usually are in standard locations (Fig. 9-5). Knowledge of these sites is critical for accurate radiological interpretation because a nutrient foramen appears as a radiolucent area, which should not be confused with a pathological lesion. The position of these intra-osseous vessels also has important consequences in considering repair of major long bone fractures. Thermography relies on the detection of surface heat and is obviously greatly influenced by the position of superficial vessels. Interpretation may be misleading without knowledge of location. Thus it should be absolutely clear that anatomy is

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a dynamic subject and is not merely a function of knowing the origins and insertions of numerous structures. We also need to know some fundamentals of biomechanics. What is the biomechanical function of the SL? What are the implications of loss of function? For example, how may function be altered by a change in foot angle after application of a heel wedge? How is load in the distal limb joints affected by mediolateral foot imbalance? If the accessory ligament of the SDFT is cut (superior check desmotomy), how does this alter the function of not only the SDFT but also other tendonous and ligamentous structures? Does consequent overload of the SL predispose to an increased risk of suspensory desmitis? When orthopedic surgery is being considered, which is the tension side of the bone, to which a dynamic compression plate should be applied to take advantage of the tension band principle? In more general terms, how will lameness in the left hindlimb alter forces in the other limbs, and does this vary with the gait? Given the reciprocal apparatus of the hindlimb and the inability to flex and extend the limb joints independently, it is not surprising that the gait characteristics of hindlimb lameness are so similar, irrespective of the source of pain causing lameness. Understanding the reciprocal apparatus, in addition to the results of loss of its function (e.g., after damage to the fibularis tertius) are hugely important for an understanding of hindlimb lameness. After the source of pain causing lameness is isolated, then it is necessary to establish what is causing pain; this requires one

of a number of imaging modalities: radiography, ultrasonography, nuclear scintigraphy, magnetic resonance imaging (MRI), computed tomography (CT), and exploratory arthroscopy, bursoscopy, or tenoscopy. Accurate interpretation of any of these techniques requires specialist anatomical knowledge. With radiographic images, various structures are superimposed, resulting in potentially confusing radiolucent lines that can mimic a fracture (e.g., in the relatively complex carpus and tarsus). A frog shadow superimposed over the navicular bone may mimic a fracture. We must be cognizant of anatomical variations, for example, the shape and size of the crena of the distal phalanx. We have to know how best to image a specific anatomical location, such as the sustentaculum tali of the calcaneus (fibular tarsal bone) using a skyline projection. To interpret the significance of periosteal or entheseous new bone, detailed knowledge of the soft tissue structures that do (or do not) attach in that area is vital. Particularly in the fetlock and pastern areas, numerous ligamentous structures have discrete areas of attachment (Fig. 9-6). Radiography requires the awareness that we are looking at a three-dimensional structure in two dimensions, and thus images of the area must be obtained from several different angles. With ultrasonography, and more particularly with MRI and CT, structures can be imaged in three dimensions; this requires detailed knowledge of the shape, size, and relationships between structures. In the proximal metatarsal region the DDFT lies more medial than the SDFT and SL, and thus these structures cannot be imaged adequately by ultrason-

B

SB

PSB

SDSL

DDFT

SDFT branch

A ODSL B

C ODSL P2

C

Fig. 9-6 The oblique distal sesamoidean ligaments. A, Frontal magnetic resonance imaging (MRI) scan of the pastern showing the origins and insertions of the oblique distal sesamoidean ligaments (ODSL). SB, Suspensory branch; PSB, proximal sesamoid bone. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.) B, Frontal (left) and transverse (right) ultrasonographic images of the ODSL obtained at point B in part A. Proximal and dorsal are to the left. C, Transverse MRI scan obtained at point C in part A. DDFT, Deep digital flexot tendon; SDFT, superficial digital flexor tendon; SDSL, straight distal sesamoidean ligament; P2, middle phalanx.

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ography at the same time from the plantar aspect of the limb (Fig. 9-7). The transducer must be moved to a plantaromedial site to evaluate the DDFT in its entirety. A large vessel on the plantarolateral aspect of the SL can cause shadowing artifacts in the SL. The internal architecture of the joint becomes important during exploratory arthroscopy. What are the normal variations in cartilage thickness? Where do you expect to see a synovial fossa? Which parts of the synovial membrane are usually more vascular? Is it normal that the cranial cruciate ligament can be seen without synovial covering from the medial femoral tibial joint? A textbook of this type cannot possibly provide detailed descriptions of all aspects of anatomy, functional anatomy, and biomechanics, nor answer all of the questions posed earlier in this chapter. It is hoped that this overview will stimulate readers to have a thirst for more knowledge of these subjects, in the knowledge of their huge importance. Lameness clinicians are encouraged to acquire a set of boiled-out bones for reference and perform detailed dissections of cadaver limbs to improve knowledge of anatomy. Practicing nerve block techniques on cadaver limbs is very important for inexperienced clinicians or those performing a new block for the first time. If a lame horse must be humanely destroyed, clinicians should take the opportunity, whenever possible, to perform a post-mortem examination to correlate clinical findings with the actual lesions and revise anatomy at the same time. Each time a dissection is performed, new anatomical detail becomes apparent that had previously been missed. The remainder of this chapter provides some basic definitions of anatomical terms used elsewhere in the book, describes the reciprocal apparatus of the forelimb and hindlimb, and presents correlative illustrations of anatomical

MT3

85

specimens and images of those areas to assist in the understanding of three-dimensional anatomy.

The Language of Anatomy The system described in the Nomina Anatomica Veterinaria (NAV) according to the guidelines of the International Committee on Veterinary Anatomical Nomenclature has been used so that anatomical terminology is universal. English translations of NAV terms have been used whenever possible according to these guidelines.

Forces The interaction of anatomical structures allows for the conversion of chemical energy into purposeful movement. It is often useful to think of complex anatomical structures in terms of interactions between simplified structural units. The interaction of forces within these anatomical units dictates the abilities and the potential weaknesses of the equine athlete. In simple terms, the stresses acting on the body are compression, tension, shear, torsion, and bending. Compression is the force applied between two points to move them together. Examples of compression are seen in joints, such as within the middle carpal joint at the interface between the radial and third carpal bones, or that sustained by the digital cushion between the sole, frog, and the distal phalanx. Compression also is sustained within most bones, such as the third carpal bone, or the dorsal cortex of the third metacarpal bone (McIII). Tension is the force that tends to stretch or elongate a structure. Examples of tension are most obvious in tendons and ligaments, but bones such as the olecranon or within the palmar cortex of McIII also sustain tensile strain. Shear is a stress at the interface between two structures moving in opposite directions. Examples of shear are seen in the femoropatellar and tarsocrural joints, within bone, and within the hoof capsule. Torsion is the stress produced when a twisting motion is applied to an object. Examples of torsional strain are seen within joints, such as the distal hock joints, or within individual bones, such as McIII. Bending is a combination of compression on one side of a structure and tension on the other side. Structures submitted to bending are long bones such as McIII, where the dorsal cortex is submitted to compression, whereas the palmar cortex is submitted to tension.

Specialized Structures Synovial Structures MT2

MT4

SL DDFT

SDFT

Transverse anatomical section of the proximal metatarsal region demonstrating the lateral position of the superficial digital flexor tendon (SDFT) relative to the deep digital flexor tendon (DDFT). Lateral is to the left and dorsal to the top of the image. This arrangement is the opposite of that seen in the forelimb (compare with Fig. 9-3). SL, Suspensory ligament; MT2, MT3, and MT4, second, third, and fourth metatarsal bones, respectively.

Fig. 9-7

Synovial bursae, tendon sheaths, and joints have a similar function and generally similar structure. All are sacs containing synovial fluid produced by the lining of the sac. In simple terms, synovial structures facilitate the movement between independent structures by providing a hydraulic cushion of viscous fluid that limits the effects of friction to help dissipate compressive and shear forces. (For a more complete discussion on synovial structures, see Chapters 63 and 80.) A diarthrosis is a mobile joint containing a synovial membrane. This membrane is flexible enough to allow for movement of the joint. The synovial fluid lubricates, hydraulically equalizes pressure between cartilage plates, and nourishes the articular cartilage. A synovial sheath is a sac that completely surrounds a tendon, forming a synovial lining on the surface of the tendon and the lining of the sheath. The synovial reflection between these visceral and parietal layers is termed the mesotendon. This structure is similar to the mesentery in the abdominal cavity. Nerve and blood supply to the tendon is found within the mesotendon. In areas of great mobility within the synovial sheaths, the nerve and blood supply to the tendons is through

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Tibia

A

Calcaneus

DDF

Gastrocnemius

Calcanean bursa SDFT

Fig. 9-8 Transverse anatomical section through distal tibia and proximal calcaneus demonstrating the distinct calcanean bursa bounded by the collateral ligaments of the superficial digital flexor tendon (SDFT). DDF, Deep digital flexor muscle. PSB B

a vinculum, which is a modified mesotendon in the form of a narrow band connecting visceral and parietal layers. A synovial bursa is a simple sac lying between a tendon or muscle and an adjacent bony prominence. A bursa does not surround the tendon but acts as a cushion at the interface where pressure is concentrated (Fig. 9-8).

Intercalated Bones Intercalated bones are bones that arise within tendons or ligaments allowing for the interface between the tendonous structure and the underlying bone at an area of focal pressure, typically at the level of a joint. The interface between these bones is within a synovial sac. The navicular bone, proximal sesamoid bones (PSBs), and patella are intercalated bones. These bones allow for smooth movement and dissipation of focal pressure between the tendon or ligament and the underlying joint (Fig. 9-9).

Fibrocartilaginous Structures In general terms, there are four functional arrangements of fibrocartilage: interarticular, connecting, circumferential, and stratiform. Interarticular fibrocartilage. Menisci are fibrocartilaginous structures located between the articular cartilages of a diarthrosis. Menisci are not directly attached to the joint surfaces but are held in place by ligaments immediately adjacent to the articular surfaces. They provide congruency between the condyles, allow for a greater range of movement of the joint, and absorb concussion. Menisci are found in the stifle and temporomandibular joints of the horse. Connecting fibrocartilage. A symphysis is a fibrocartilaginous joint that allows minimal movement. The pelvic symphysis and intersternebral and intervertebral joints are examples of fibrocartilaginous joints. Circumferential fibrocartilage. In the coxofemoral joint the acetabular lip (labrum acetabulare) is a fibrocartilaginous ring extending the articular surface in a firm, semi-flexible manner. The transverse acetabular ligament is the portion of

ODSL

Fig. 9-9 A, Oblique radiographic projection of a normal proximal sesamoid bone (PSB). B, Parasagittal anatomical section through suspensory branch, PSB, and oblique distal sesamoidean ligament (ODSL).

the labrum crossing the acetabular notch. The glenoid labrum seen in other species is a poorly developed fibrous band in the shoulder of the horse. Stratiform fibrocartilage. Stratiform fibrocartilages arise within ligamentous structures at an interface with high focal pressure between soft tissue and bone, either within a ligament or as an extension of a bony surface. These structures are similar to intercalated bones in that they typically provide rigidity to help dissipate compressive forces, but the moderate elasticity allows for some flexibility of the structures. The parapatellar fibrocartilage on the medial aspect of the patella, portions of the biceps brachii tendon of origin within the intertubercular (bicipital) bursa, the manica flexoria, and portions of the DDFT adjacent to the proximal aspect of the middle phalanx are examples of stratiform cartilage formation

CHAPTER 9

• Applied Anatomy of the Musculoskeletal System

Serratus ventralis thoracis muscle

87

Patella

Lateral patellar ligament Biceps brachii muscle

Middle patellar ligament

Triceps brachii muscles

Medial patellar ligament Lacertus fibrosus

Medial collateral ligament

Extensor carpi radialis muscle

Peroneus (fibularis) tertius Tibial crest

Fig. 9-11

Common digital extensor tendon

Fig. 9-10

The passive stay apparatus of the forelimb.

Long digital extensor muscle

The patellar locking mechanism.

of the digit. The axial and abaxial palmar/plantar ligaments of the proximal interphalangeal joint, the SDFT branches, and the straight distal sesamoidean ligament support the palmar/plantar aspect of the proximal interphalangeal joint. The navicular bone and its suspensory apparatus, in combination with the distal sesamoidean impar ligament, stabilize the palmar/plantar aspect of the distal interphalangeal joint.

Forelimb within tendonous structures. The proximal, middle, and distal scuta are stratiform fibrocartilaginous structures associated with the intersesamoidean ligament, the palmar aspect of the middle phalanx, and the collateral ligaments of the navicular bone, respectively. These structures serve as semi-rigid pulleys primarily for the DDFT.

Passive Stay Apparatus Distal Limb The horse is uniquely equipped to be able to stand at rest while expending minimal muscular effort. In the forelimb and hindlimb the fetlock is prevented from over-extension by a combination of structures providing passive resistance. The suspensory apparatus is the main contributor, forming a sling that maintains the fetlock in extension. In addition, the SDFT, DDFT, and the associated accessory (check) ligaments (in the forelimb) act as tension bands providing passive support. The suspensory apparatus consists primarily of the SL and branches, PSBs, and distal sesamoidean ligaments. The intercalated PSBs provide a broad face at the point where focal pressure is high at the palmar/plantar aspect of the fetlock joint, enabling the ligamentous tension band to support the fetlock. Dorsal branches of the SL join with the common/long digital extensor tendon, helping to stabilize the dorsal aspect

In the forelimb the fibrous portion of the serratus ventralis thoracis acts as a sling suspending the thorax from the forelimb by its attachment to the scapula. The downward force applied by the serratus ventralis on the caudal aspect of the scapula causes slight flexion of the scapulohumeral joint, applying tension to the biceps brachii. A fibrous band of the biceps brachii extends from the supraglenoid tubercle of the scapula and continues as the lacertus fibrosus, which joins with the extensor carpi radialis to passively extend the carpus. Minimal muscular effort by the triceps on the olecranon maintains the elbow in extension (Fig. 9-10).

Hindlimb The stifle is maintained in extension by the patellar locking mechanism with minimal muscular effort. Slight muscular effort by the quadriceps and tensor fascia lata rotates the patella medially, where the cartilaginous process of the patella is caught caudal to the large prominence of the medial trochlear ridge of the femur. Slight relaxation of the quadriceps as a whole allows slight flexion of the stifle, which “locks” the patella in place by applying tension primarily to the medial and middle patellar ligaments (Fig. 9-11). When the stifle is extended, the hock is passively extended by the superficial digital flexor and the fibrous component of the lateral head of the gastrocnemius muscles, which extend from the femur to the tuber calcis.

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Tensor fascia lata

Middle and medial patellar ligaments

Lateral fibrous band of gastrocnemius Peroneus (fibularis) tertius and long digital extensor

SDFT DDFT

Fig. 9-12 The reciprocal apparatus. SDFT, Superficial digital flexor tendon; DDFT, deep digital flexor tendon.

The reciprocal apparatus forces the hock to flex and extend in unison with the stifle. The reciprocal apparatus transfers mechanical energy to the distal limb from the massive muscular structures of the upper limb without adding mass to the lower limb. The superficial digital flexor and the fibrous portion of the gastrocnemius serve as the caudal component of the reciprocal apparatus, along with the long plantar ligament, which acts as a tension band to make the calcaneus, distal tarsus, and metatarsal region a single functional lever arm. The fibularis (peroneus) tertius serves as the cranial component of the reciprocal apparatus, extending from the femur to the dorsal and lateral aspects of the tarsus (Fig. 9-12). Although the fibularis tertius is important as part of the reciprocal apparatus, it is not essential for function of the passive stay apparatus, as its function is flexion of the tarsus. A second reciprocal mechanism has been described for the lower limb of the hind limb, where the fetlock and digit are flexed at the same time as the stifle and hock. The long digital

extensor tendon and DDFT were the dorsal and plantar components suggested, but the SDFT probably also contributes.

Three-Dimensional Anatomy Major advances in lameness diagnosis are being made with the assistance of advanced imaging techniques. Radiography, nuclear scintigraphy, and ultrasonography are well established, whereas CT and MRI are growing in importance. CT and MRI in particular require a detailed knowledge of threedimensional anatomy. It is beyond the scope of this text to provide detailed correlative images of the entire musculoskeletal system. Figs. 9-13 through 9-18 give a flavor of what is possible. Figs. 9-13 through 9-16 highlight the complex anatomy of the navicular bone region, showing the close relationship between the collateral ligaments of the navicular bone, the distal sesamoidean impar ligament, the DDFT and the navicular bursa and distal interphalangeal joint capsule. Figs. 9-17 and 9-18 demonstrate the relationship between some aspects of the complex anatomy of the carpal region.

DFTS

DSCL

DIP P2

A

P3

B Nav

DSIL

NB

DDFT

D,E

DDFT DSCL DFTS

C

D P2 DIP Nav

F

E

F

DDFT

NAV BONE DDFT

NAV BONE

Fig. 9-13 Comparisons of the lateral view of the navicular bone and its relationship to neighboring structures. A, Sagittal anatomical section showing the digital flexor tendon sheath (DFTS), navicular bursa (NB), and distal interphalangeal (DIP) joint surrounding the navicular bone. DSIL, Distal sesamoidean impar ligament; DSCL, distal sesamoidean collateral ligament (axial union forming fibrous portion of T ligament); P2, middle phalanx; Nav, navicular bone; P3, distal phalanx. B, Lateral radiographic projection centered on the navicular bone. C, Sagittal magnetic resonance imaging scan of the foot. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.) D and E, Sagittal anatomical section and corresponding ultrasonographic image of the palmar aspect of the distal pastern obtained at points D and E on part C. Proximal is to the right. The arrows outline the distal sesamoidean collateral ligament. F, Frontal (left) and sagittal (right) ultrasonographic images obtained through the frog at point F in part C. The hypoechoic appearance to the portion of the deep digital flexor tendon (DDFT) is due to the off-incidence artifact because the fibers are not perpendicular to the line of the ultrasound beam. Lateral and proximal are to the right.

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A

C

DDFT

Nav bone

B

Fig. 9-14 Transverse sections through the navicular bone. A, Anatomical specimen, palmar view. B, Palmaroproximal-palmarodistal oblique radiographic projection of a normal navicular bone. C, Transverse magnetic resonance imaging scan. The deep digital flexor tendon (DDFT) is nearly as broad at this point as the navicular bone. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.)

P2

B A p

DSCL DDFT t

Fig. 9-15 Transverse sections through the foot at the level of the distal sesamoidean collateral ligaments (DSCL). A, Anatomical section showing the attachments of the DSCL to the deep digital flexor tendon (DDFT) marked at point t, and to the middle phalanx (P2) at point p. These attachments form the so-called T ligament, which forms the boundaries between the navicular bursa, distal interphalangeal joint, and digital flexor tendon sheath. B, Corresponding magnetic resonance imaging scan. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.)

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• Applied Anatomy of the Musculoskeletal System

91

DSIL insertion

A

B

ft fs (DDFT insertion)

C

D ft

Fig. 9-16 The insertions of the deep digital flexor tendon (DDFT) and distal sesamoidean impar ligament (DSIL). A, Isolated distal phalanx solar view, showing the point of insertion of the DDFT on the flexor surface. The flexor tubercle (see ft on part C) is relatively smaller than in other species but should be recognized as a normal structure as seen on computed tomographic (CT) imaging. B, Transverse anatomical section through the insertion of the DDFT. This slice is slightly distal to the site of insertion of the distal sesamoidean impar ligament. C, Transverse CT scan showing a normal flexor tubercle (ft). Avulsions here are difficult to demonstrate radiographically. Nuclear scintigraphy and ultrasonography can be helpful, but this area is best imaged using CT or magnetic resonance imaging (MRI). (Courtesy Alamo Pintado Equine Medical Center, Los Olivos, California). D, Transverse MRI scan. (Courtesy Alexia L. McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.)

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Joint capsule

ECRT CDET ICB

UCB RCB

A Medial palmar nerve

Accessory carpal bone Median artery

Carpal canal DDFT

B

ACB DDFT SDFT

SDFT

C

D

Fig. 9-17 Transverse slices through the proximal row of carpal bones. All images are oriented with dorsal to the top and lateral to the left. A, Diagram of carpal bones. B, Anatomical section. C, Computed tomographic scan. (Courtesy Alamo Pintado Equine Medical Center, Los Olivos, California.) D, Magnetic resonance imaging scan. (Courtesy Alexia L McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.) ACB, Accessory carpal bone; DDFT, deep digital flexor tendon; ICB intermediate carpal bone; RCB, radial carpal bone; SDFT, superficial digital flexor tendon; UCB, ulnar carpal bone; CDET, common digital extensor tendon; ECRT, extensor carpi radialis tendon.

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ECRT

ICB

A

B C3

Fig. 9-18 Lateral views of the carpus. Compare with Fig. 9-1. A, Flexed lateral radiograph. B. Flexed sagittal magnetic resonance imaging scan through the extensor carpi radialis tendon (ECRT). ICB, Intermediate carpal bone; C3, third carpal bone. (Courtesy Alexia L McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.).

SUGGESTED READING Ashdown R, Done S: Colour atlas of veterinary anatomy, vol 2, The horse, London, 1987, Balliere Tindall. Back W, Clayton H: Equine locomotion, ed 1, London, 2001, WB Saunders. Budras K, Sack WO, Rock S: Anatomy of the horse, ed 2, London, 1994, Mosby. Denoix JM: The equine distal limb: an atlas of clinical anatomy and comparative imaging, ed 1, London, 2000, Manson.

CHAPTER •

Freweined J, Habel RE, Sack WO, editors: Nomina anatomica veterinaria, ed 4, Ithaca, NY, 1994, World Association of Veterinary Anatomists. Getty R: Sisson and Grossman’s the anatomy of domestic animals, ed 5, vol 1, Philadelphia, 1975, Saunders. Weaver J, Stover S, O’Brien T: Radiographic anatomy of soft tissue attachments in the equine metacarpophalangeal and proximal interphalangeal region, Equine Vet J 24:310, 1992.

10

Diagnostic Analgesia Lance H. Bassage II and Mike W. Ross

espite the many technological advances in equine sports medicine over the past two decades, diagnostic analgesia arguably remains the most valuable tool in the equine clinician’s arsenal to localize lameness. Although the technique requires a thorough understanding of anatomy, basic technical skill, and clinical experience, the equipment and expense are minimal. In addition, diagnostic analgesia can

D

be performed on site, with the outcome immediately obvious. In this way, any lingering concern that a suspected “shoulder problem” exists is convincingly erased when the response to local analgesia of the digit is observed. This chapter reviews the various perineural, intrasynovial, and local (regional) infiltration techniques for application of local analgesia in the diagnosis of lameness in horses.

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• Diagnostic Analgesia

93

ECRT

ICB

A

B C3

Fig. 9-18 Lateral views of the carpus. Compare with Fig. 9-1. A, Flexed lateral radiograph. B. Flexed sagittal magnetic resonance imaging scan through the extensor carpi radialis tendon (ECRT). ICB, Intermediate carpal bone; C3, third carpal bone. (Courtesy Alexia L McKnight, University of Pennsylvania, Philadelphia, Pennsylvania.).

SUGGESTED READING Ashdown R, Done S: Colour atlas of veterinary anatomy, vol 2, The horse, London, 1987, Balliere Tindall. Back W, Clayton H: Equine locomotion, ed 1, London, 2001, WB Saunders. Budras K, Sack WO, Rock S: Anatomy of the horse, ed 2, London, 1994, Mosby. Denoix JM: The equine distal limb: an atlas of clinical anatomy and comparative imaging, ed 1, London, 2000, Manson.

CHAPTER •

Freweined J, Habel RE, Sack WO, editors: Nomina anatomica veterinaria, ed 4, Ithaca, NY, 1994, World Association of Veterinary Anatomists. Getty R: Sisson and Grossman’s the anatomy of domestic animals, ed 5, vol 1, Philadelphia, 1975, Saunders. Weaver J, Stover S, O’Brien T: Radiographic anatomy of soft tissue attachments in the equine metacarpophalangeal and proximal interphalangeal region, Equine Vet J 24:310, 1992.

10

Diagnostic Analgesia Lance H. Bassage II and Mike W. Ross

espite the many technological advances in equine sports medicine over the past two decades, diagnostic analgesia arguably remains the most valuable tool in the equine clinician’s arsenal to localize lameness. Although the technique requires a thorough understanding of anatomy, basic technical skill, and clinical experience, the equipment and expense are minimal. In addition, diagnostic analgesia can

D

be performed on site, with the outcome immediately obvious. In this way, any lingering concern that a suspected “shoulder problem” exists is convincingly erased when the response to local analgesia of the digit is observed. This chapter reviews the various perineural, intrasynovial, and local (regional) infiltration techniques for application of local analgesia in the diagnosis of lameness in horses.

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LOCAL ANESTHETICS: PHARMACOLOGY AND TISSUE INTERACTIONS Pain is transmitted specifically in the small, lightly myelinated, A-delta and non-myelinated C nerve fibers.1 All commonly used local anesthetics, regardless of the specific molecular structure, share the same basic mechanism of action, specifically, the ability to block or inhibit nociceptive nerve conduction by preventing the increase in membrane permeability to sodium ions.2 These agents consist of a lipophilic and a hydrophilic group, connected by an intermediate chain containing a carbonyl group of an amide or ester linkage, and have traditionally been categorized as either amide- or ester-type local anesthetics.3 Common local anesthetics used in horses— 2% solutions of lidocaine, mepivacaine, and bupivacaine—are of the amide type. Compared with most local anesthetics, lidocaine and mepivacaine are considered relatively fast-acting and have a reported duration of action of 1 1⁄ 2 to 3 hours and 2 to 3 hours, respectively. In contrast, bupivacaine is intermediate in onset but has a much longer duration of action (3 to 6 hours).4 Bupivacaine is most suited for providing therapeutic rather than diagnostic analgesia. The results in clinical practice vary, because in severely lame horses the degree and duration of local analgesia are decreased, regardless of the agent used. When local anesthetics are injected, tissue damage can occur but is extremely rare.3,4 Soft tissue swelling occurs occasionally and is likely caused by needle trauma or hematoma formation and not from a direct drug-tissue interaction. We suggest that alcohol and a clean wrap be applied to the injection sites when the diagnostic evaluation is complete to prevent or minimize swelling at injection sites. Cellulitis or other forms of infection are rare potential complications. Acute synovitis, or flare, is a rare complication that can occur after intrasynovial (most commonly intra-articular) injection of anesthetics. Synovitis from intrasynovial injection of local anesthetics is much less common than from injection of other medications. Mepivacaine is less irritating than lidocaine when administered intra-articularly, but we have not recognized this difference.3 However, Dyson reported that lidocaine may be considerably more irritating than mepivacaine, and clinical data documenting differences was used successfully in the licensing of mepivacaine in the United Kingdom.5 Like cellulitis after perineural injections of local anesthetics, infectious synovitis is a rare but possible sequela. To mitigate the possibility of contaminated solution, we use a new vial of local anesthetic solution when performing intrasynovial analgesic procedures. Systemic side effects from diagnostic analgesic techniques are exceedingly rare. Cardiovascular or central nervous system signs, including muscle fasciculation, ataxia, and collapse, were reported.3 Systemic intoxication would require a dose much higher than is commonly used, even for an extensive diagnostic evaluation. For example, the maximum single infiltration dose of lidocaine that can be safely administered to a 500-kg horse is about 6.0 g, or 300 ml of a 2% solution.6

Strategy, Methodology, and Other Considerations A few basic principles must be followed to ensure success. A thorough working knowledge of regional anatomy is required. Even for seasoned veterans a review of anatomy may be required before performing less common techniques. A most important principle when performing perineural analgesia is to start distally in the limb and work proximally (Figs. 10-1 to 10-4). If possible, sequential blocks from distal to proximal should always be used, but in certain circumstances a different strategy can be successful. Sequential blocking requires a fair amount of time, and in certain horses, selective intra-articular or local blocks can be performed without following this

“golden rule.” However, in most situations, blocking a large portion of the distal limb at a proximally located site may preclude accurate determination of the source of lameness and may require an additional visit to perform additional diagnostic procedures. It is important to test the efficacy of a perineural block before reevaluating the horse’s degree of lameness. If any question exists, the block should be repeated rather than assuming deep pain has been abolished, when skin sensitivity persists. If a horse shows partial improvement only minutes after injection, an additional few minutes should be allowed to achieve complete analgesia before proceeding with the next block. Alternatively, the block can be repeated. In so doing, the clinician minimizes the potential for misinterpretation and the tendency to ascribe the residual lameness to a “second problem” that does not exist. During this portion of the examination, we are attempting to eliminate baseline rather than induced lameness, and care must be taken when adopting the practice of “blocking out a positive flexion test” (see Chapter 8). Once baseline lameness has been eliminated, we rarely perform additional flexion tests or attempt to eliminate all induced lameness. How is the efficacy of the block assessed? Several methods are available, but the following points should be considered. Individual horses react differently to noxious stimuli applied to the skin. Therefore it is helpful to test the contralateral (unblocked) limb to establish the horse’s baseline response to the test. Similarly, covering a horse’s eye or feigning a few gestures with an instrument (pen tip, hemostatic forceps) without actually contacting the skin can help differentiate between a random or anticipatory response by an apprehensive horse and a true painful response. Positioning oneself on the contralateral side of the patient when testing for sensation also can help in making this determination. The clinician should avoid using sharp instruments that can penetrate the skin and cause hemorrhage, a situation not well understood by a concerned horse owner. Hemostatic forceps, used to pinch the skin, are ideal, because they are blunt and appear to consistently induce an appropriate amount of pain. Forceps are only useful in assessing superficial or skin sensation, however. Perineural blocks must be assessed for the amelioration of deep and not just superficial pain. To assess whether deep pain in the hoof has been ameliorated after palmar digital analgesia or other techniques, hoof testers can usually be applied with enough force to cause a painful response, even in the most stoic of horses. Physical strength of the operator must be considered. Extreme or hard joint flexion (combined with varus or valgus stress) can be used to assess whether deep pain has been abolished in more proximal locations. In some instances, however, it is impossible to avoid contacting the skin proximal to the site of anesthetic administration, leading the clinician to assume that the block has not worked. The application of firm digital pressure in the blocked area may be a viable alternative to flexion or manipulation to help avoid these potentially confounding factors. It is important to understand that the region of the limb that is actually desensitized may, in fact, differ from that which the clinician has intended.7 Proximal diffusion of local anesthetic solution appears to be the most likely cause, but other intangible factors may play a role. Using a small volume of anesthetic (1 to 5 ml for most perineural blocks) can minimize but not abolish this phenomenon. To further minimize the potential for diffusion of anesthetic, the horse should be reevaluated no more than 10 minutes after the injection (exceptions apply in certain situations). Complete analgesia, and thus 100% improvement in lameness score, is the goal when performing diagnostic analgesia, but in many horses this level of pain relief is never achieved. Improvement in degree of lameness greater than 70% to 80%

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Anatomical Diagnosis

• Diagnostic Analgesia

95

Final Diagnosis

Differential Procedures

Proceed to Proximal Limb (–) (+)

Middle carpal joint block

MC/CMC joint problem Suspensory origin problem (unlikely if Wheat negative)

Osteoarthritis/synovitis Articular fracture

(–) Palmar metacarpal problem Carpal sheath problem

(+)

Wheat block

(+) Carpal sheath

Tenosynovitis/tendonitis (–) Proximal suspensory desmitis Proximal palmar McIII lesion Small metacarpal lesion

(+)

High palmar block

Metacarpal problem Carpal problem (MC/CMC joints)

Wheat block (–) Middle carpal joint block (see above for details) (+)

Digital flexor tendon sheath block

(–)

Dorsal metacarpal disease

(–)

(–)

Subchondral bone lesion Extraarticular problem

(–) Low palmar block

(+)

Distal metacarpal problem MCP region problem

MCP joint block

Digital flexor tendon sheath block

(+)

(+)

(–)

(–)

(–) PIP joint block

(+)

Dorsal foot problem Pastern problem

DIP joint block

PIP joint block

DIP joint block

(+)

Foot problem Distal pastern problem

Navicular bursa block

Dorsal laminar disease Distal sesamoidean desmitis Other soft tissue problem? Fetlock region problem?

(+)

P3 Extensor process fracture P3 Midsagittal fracture

(+)

Osteoarthritis Osteochondrosis

(–)

(–) Palmar digital (PD) block

Tenosynovitis/tendonitis (distal aspect DFTS)

Osteoarthritis Osteochondrosis

(–)

(–)

Osteoarthritis/synovitis Osteochondrosis Articular fracture

(+)

(–) Mid-pastern ring block or Abaxial sesamoid block

Tenosynovitis/tendonitis (proximal aspect DFTS)

Navicular disease Osteoarthritis P3 Fracture Pedal osteitis Soft tissue problem

(+) Navicular disease

Blocking strategy in the forelimb: foot to carpus. CMC, Carpometacarpal; DFTS, digital flexor tendon sheath; McIII, third metacarpal bone; MC, middle carpal; MCP, metacarpophalangeal; PIP, proximal interphalangeal; Mc3, third metacarpal bone; P3, distal phalanx.

Fig. 10-1

after most perineural or intra-articular techniques should be considered a positive response in most horses. The quintessential response is the horse “switching lameness” to the contralateral limb, indicating that now, pain arising from the opposite limb is greater than that originating from the baseline lameness. However, complete response may not occur,

and the clinician must decide when to stop sequential blocks or when the horse has “blocked out.” The clinician hopes for an obvious difference in lameness score when the horse is blocked, but in some horses, serial improvement occurs with each successive block, a situation that makes assessing the primary source of lameness difficult.

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Primary Analgesic Procedure

Anatomical Diagnosis

Final Diagnosis

Differential Procedures

Proceed to advanced imaging? Cervical vertebral OA? Neurological disease? Reassess?

(–) Bicipital bursa block

(+)

Bursitis Tendonitis Humeral osteitis

Bicipital bursa/tendon problem Proximal humeral problem

(–)

Shoulder joint block

(+)

Synovitis Osteoarthritis Osteochondrosis

Shoulder joint

(–) Cubital (elbow) joint block

(+)

Synovitis Osteoarthritis

Elbow joint

(–) (–) Median and ulnar blocks

(+) Distal antebrachium

(–)

Antebrachiocarpal joint

Fig. 10-2

(+)

Antebrachiocarpal joint

Carpal joint blocks Carpal sheath block (see below and Fig.10–1)

(–)

Periarticular soft tissue problem Distal radial trauma/fracture Superior check desmitis/enthesitis Synovitis Osteoarthritis Articular fracture

Blocking strategy in the forelimb: antebrachium to shoulder joint, OA, Osteoarthritis.

Incomplete response to local analgesics in some horses may be explained by the fact that chronic pain, particularly deep bone pain, may remain resistant to complete analgesia when perineural techniques are used. For example, horses with laminitis tend to remain lame despite blocking many times at the appropriate level. Mechanical gait deficits do not improve after diagnostic analgesia because pain is minimal. Horses may continue to show lameness even with pain abolition, a situation that appears to be caused by habit. These horses tend to show mild residual lameness initially, only to warm out of it quickly during examination. Other factors affecting response to diagnostic analgesia include individual variation in neuroanatomy, the intermittent nature of certain lameness conditions, and the inherent difficulty in assessing and abolishing pain in horses with subtle lameness.8 Articular lesions may not be desensitized by intra-articular analgesia. Sensory innervation of joints is complex and involves three classes of neurons that transmit information from four receptor types, each of which has a specific distribution throughout the joint.9-12 Articular pain can arise from several sources, including the synovium (inflammation, effusion), fibrous joint capsule (increased intra-articular pressure), articular and periarticular ligaments, periosteum, and subchondral bone (injury, osseous vascular engorgement).8,10,13 Other than small branches in the perichondrium, articular cartilage is devoid of innervation. In osteoarthritic joints, however, erosion channels, formed in the calcified layer of cartilage, are invaded by subchondral vasculature.10 Putative nociceptive neurotrans-

mitters were identified in these areas, and therefore it is plausible that in horses with advanced osteoarthritis, pain could be emanating from the deep cartilage layers.14,15 On occasion, lameness from an articular lesion abates after perineural analgesia but shows minimal or only partial response after intra-articular analgesia. In some horses, this can be explained by the fact that pain is originating from articular and periarticular tissues.8 Subchondral bone pain— caused by stress or non-adaptive remodeling, cystic or erosive lesions, incomplete fractures, and osteoarthritis—is inconsistently abolished by intra-articular analgesia. In fact, subchondral bone pain is abolished much more consistently by perineural techniques. Subchondral bone receives innervation from endosteal branches of peripheral nerves that enter the medullary cavity through the nutrient foramen.8,9,16,17 Intra-articularly administered local anesthetic solutions may not penetrate subchondral bone sufficiently to completely block these nerves. This shortcoming is presumably even more likely in situations in which the overlying articular cartilage is intact. Unfortunately, intra-articular analgesia, although easier to perform, inconsistently abolishes pain from many of the common articular problems. This fact, however, is either overlooked or misunderstood by many practitioners. Whenever possible, perineural analgesia should be performed, particularly in the distal limbs, because this type of analgesia more consistently abolishes pain from all aspects of the joint and surrounding soft tissue structures.

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Anatomical Diagnosis

• Diagnostic Analgesia

97

Final Diagnosis

Differential Procedures

Proceed to proximal limb (–) Tarsocrural joint block

(+)

Tarsocrural joint problem

Synovitis Osteochondrosis Osteoarthritis Articular fracture

CD joint problem

Osteoarthritis Articular fracture

(–) (+) CD joint block (–) (+) TMT joint block

TMT joint problem (± Proximal plantar metatarsal problem?)

Suspensory origin infiltration

(–)

Metatarsal problem Tarsal problem? (TMT, ± CD joints) Tarsal sheath problem?

TMT joint block Tarsal sheath block (see Fig. 10-4)

(–)

(–) (+)

High plantar block

(+)

Digital flexor

(–)

Osteoarthritis Articular fracture

Suspensory desmitis Proliferative periostitis MtII/IV Fracture MtIII Other metatarsal problem Tenosynovitis/tendonitis (proximal aspect DFTS)

(–) Subchondral bone lesion Extraarticular problem

(–) (+)

Low plantar block

Distal metatarsal problem MTP region problem

(+)

MTP joint block

(+)

Digital flexor tendon Sheath block

(–)

(–) (–) PIP joint block

Osteoarthritis/synovitis Osteochondrosis Articular fracture

Tenosynovitis/tendonitis (distal aspect DFTS) Dorsal laminar disease Distal sesamoidean desmitis Other soft tissue problem? Fetlock region problem?

(+) Osteoarthritis Osteochondrosis

(–) Mid-pastern ring block or Abaxial sesamoid block

(+)

Dorsal foot problem Pastern problem

DIP joint block

PIP joint block

(–)

(+)

P3 Extensor process fracture P3 Mid-sagittal fracture

(+)

Osteoarthritis Osteochondrosis

(–) Plantar digital block

(+)

Foot problem Distal pastern problem

DIP joint block

(+)

Osteoarthritis P3 Fracture Pedal osteitis Soft tissue problem

Fig. 10-3 Blocking strategy in the hindlimb: foot to hock joint. CD, Centrodistal; DFTS, digital flexor tendon sheath; DIP, distal interphalangeal; MtII, MtIII, MtIV, second, third, and fourth metatarsal bones, respectively; MTP, metatarsophalangeal; P3, proximal phalanx; PIP, proximal interphalangeal; TMT, tarsometatarsal.

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Primary Analgesic Procedure

Anatomical Diagnosis

Final Diagnosis

Differential Procedures

Proceed to advanced imaging? Pelvic/sacroiliac problem? Back/vertebral problem? Neurological disease? Reassess? (–) (+)

Trochanteric bursa block

Trochanteric bursa problem Gluteal tendon problem Greater trochanter problem

Bursitis Tendonitis Trochanteric osteitis

Coxofemoral joint problem

Synovitis Osteoarthritis Articular fracture

(–) (+)

Coxofemoral joint block

(–) Stifle joint blocks

(+)

Stifle joint problem

Block joints sequentially

(+)

Synovitis Osteoarthritis Osteochondrosis Articular fracture Cruciate/meniscal injury

SBC distal tibia Calcanean tendonitis Distal tibial fracture Other distal crural problem? Calcanean bursa block

(–)

Calcanean bursitis Gastrocnemius enthesitis Osteitis – Tuber calcanei

(–)

Tarsal sheath block

(+)

Tenosynovitis DDF tendonitis Osteitis – sustaculum tali

(+)

Various articular problem (see Fig.10–3)

(–) Fibular and tibial blocks

(+)

Distal crural problem Tarsal problem

Tarsal joint blocks (see Fig.10–3)

Blocking strategy in the hindlimb: crus to coxofemoral joint. DDF, Deep digital flexor; SBC, subchondral bone cyst.

Fig. 10-4

Perception of Diagnostic Analgesia by Laypersons One of the intangible factors that can complicate the lameness examination is the layperson’s perception of diagnostic analgesia or nerve blocking. In many instances the opportunity for an owner or trainer to observe the outcome of diagnostic analgesia provides the concrete evidence that finally convinces him or her of the diagnosis. The classic example is the acute shoulder injury that is actually chronic navicular disease. However, for many reasons, misunderstanding about diagnostic analgesia can lead to frustration for everyone involved. Many laypersons are not fully able to recognize the baseline lameness and therefore may not be capable of seeing that the horse’s lameness improves after the block. Another difficulty is trying to explain why lameness in a horse with an articular problem is better after a perineural block but no better when local anesthetic solution is placed directly into a joint. Similarly, many layper-

sons do not understand why a horse with an articular lameness may “block sound” but does not respond satisfactorily to therapeutic injection. This finding that a horse blocks sound but does not inject sound is quite common in young racehorses with subchondral bone pain. Most experienced practitioners have learned to deal with these issues, but the new graduate may need fortitude and ingenuity when explaining the results of diagnostic analgesia is difficult.

Role of Chemical Restraint Whenever possible, use of physical (nose or shoulder twitch) rather than chemical restraint is best when performing diagnostic analgesia. This is particularly important in horses with low-grade lameness. The analgesic properties of α2-agonists (xylazine, detomidine) and synthetic opiates (e.g., butorphanol) are well recognized and may lead to false-positive

CHAPTER 10 results. Ataxia after sedation can complicate lameness interpretation. However, in some horses mild sedation or tranquilization may be necessary to perform diagnostic analgesia and may improve the clinician’s ability to evaluate the baseline lameness. Acetylpromazine (0.02 to 0.04 mg/kg intravenously) can calm a highly strung horse and facilitate the lameness examination. Extra care must be taken when performing hindlimb procedures, and the safety of everyone involved and the horse must be considered. In horses with moderate or severe lameness, xylazine (0.15 to 0.30 mg/kg intravenously) may not interfere appreciably with lameness interpretation. Similarly, extremely fractious horses can be sedated with an α2-agonist, which then is reversed with the prescribed α2antagonist (e.g., yohimbine) before reevaluation. Alternatively, sedation can simply be allowed to wear off before reevaluating the horse, but diffusion of anesthetic may occur or the effect may wear off, both of which may potentially cause misinterpretation of results.

Patient Preparation Before perineural analgesia is performed, the skin and hair should be cleaned of any gross debris such as mud, bedding, feces, or poultice. Clipping usually is not necessary unless the hair coat is long and prohibits accurate palpation of anatomical landmarks or adequate cleaning of the site. The site should then be scrubbed with an antiseptic, such as povidone-iodine or chlorhexidine, using clean gauze sponges or cotton. If the clinician has any concern about inadvertent penetration of a synovial cavity, a 5-minute aseptic preparation should be performed. This is followed by isopropyl alcohol administration over the site using cotton or gauze sponges. Aseptic preparation should always be performed before any intrasynovial injection. Considerable debate and variation exists among clinicians regarding the need to clip the hair over the site. Some clinicians always clip the hair, whereas others never do. Still others shave the hair in a small area directly over the injection site. The results of a recent study indicated no significant difference in the number of post-scrub colonyforming units (bacterial flora) between clipped and unclipped skin over the distal interphalangeal (DIP) and carpal joints.18 Nonetheless, we still clip the hair over all proposed intrasynovial injection sites before undertaking a 5-minute aseptic preparation. The only time we deviate from this policy is when we are specifically asked not to clip the hair, a situation that arises in some sport horses actively competing, in claiming horses, or in those being sold. Similar variation among clinicians exists regarding wearing of sterile latex gloves when performing an intrasynovial injection. However, we recommend wearing sterile gloves during these procedures. Science aside, clipping hair and wearing sterile gloves project a positive impression to all in attendance. How does, or should, the practitioner attempt perineural or intrasynovial analgesia in a horse with contact or chemical dermatitis (scurf) over the proposed injection site? A superficial wound or abrasion with a localized infection presents a similar quandary. For obvious reasons, these areas are difficult, if not impossible, to clean effectively. If possible, an alternative site, away from the area of dermatitis, should be used. If not, then the procedure should be delayed until the skin condition (or wound) has resolved. In many instances, dermatitis can be treated with topical medications (medicated sweats such as nitrofurazone-dimethylsulfoxide) for a few days to facilitate resolution of the problem.

Injection Techniques Perineural injections are typically performed using needles ranging in size from 25 gauge, 1.6 cm ( 5⁄ 8 inch) to 20 gauge, 2.5 or 4 cm (1 to 1 1⁄ 2 inches). Small needles cause less pain but carry the risk of breaking off within tissues if the horse

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99

kicks out or otherwise misbehaves. For this reason, we recommend using 18-or 19-gauge needles for injections or blocks within the proximal metatarsal or plantar tarsal regions. In the distal limb the needle is inserted subcutaneously directly over and parallel to the nerve. We generally direct the needle proximally rather than distally, although this portion of the procedure differs among clinicians. The needle is inserted before the syringe is attached. To avoid excessive manipulation once the needle is inserted, a slip-type syringe hub is preferred. Syringes with screw-on hubs can be difficult to attach, requiring additional manipulation in a sometimes fractious horse, and are not generally used. However, when dense tissue requires that additional force be used for injection, the seal between the hub and the needle can be broken, a complication minimized by using a screw-on hub (see the following discussion of lateral palmar block). Volume of local anesthetic solution varies, but for a majority of blocks in the distal limb 1 to 5 ml is injected at each site. Larger volumes are used to perform the median/ulnar and fibular (peroneal)/tibial techniques and when infiltrating the proximal palmar (plantar) metacarpal (metatarsal) region. After injection, we briefly massage the sites with gauze sponges or clean cotton soaked in alcohol. Skin sensation and deep pain are assessed between 5 and 10 minutes after injection. More time is allowed under certain circumstances (see specific comments throughout the chapter). At the completion of the examination an alcohol wrap should be applied to minimize swelling, a common sequela resulting from local irritation and bleeding from nearby vessels. For “ring” blocks, circumferential subcutaneous infiltration of local anesthetic solution, and other local or regional infiltration techniques, we most commonly use 18- to 22-gauge, 4-cm needles. To perform a ring block, the needle is inserted perpendicular to the long axis of the limb, and local anesthetic solution is injected as the needle is advanced, leaving a clearly visible wheal or subcutaneous bleb in most locations. The needle then is reinserted at the leading edge of this wheal, a practice that minimizes the number of injections and the horse’s discomfort. However, most horses object to needle insertion even when it is performed well within the bleb. The injection is continued around the limb in this manner. For most ring blocks in the distal limb, 10 to 15 ml of local anesthetic solution is used, but larger volumes may be preferred for surgical procedures. Ring blocks can be done as a substitute for or in combination with perineural injections (see the specific blocking techniques discussed in the chapter). However, simply placing anesthetic in a subcutaneous location is not a substitute for the preferred approach, direct perineural injection. To block a local area such as a splint or curb, the needle is typically inserted in one or two locations, and local anesthetic solution is deposited in a fan-shaped pattern. As with the perineural analgesia, the sites are massaged briefly and the horse is reevaluated in 5 to 10 minutes. Intrasynovial injections typically are performed using needles ranging in size from 22 gauge, 2.5-cm to 18 gauge, 4-cm. If marked effusion is present, drainage of synovial fluid is advised, either by allowing the fluid to drip from the hub of the needle or by aspirating with a sterile syringe before proceeding with injection. We prefer the former procedure unless fluid analysis is necessary. The manipulation required to attach the syringe may cause the horse discomfort and potentially dislodge the needle but, if successful, may hasten withdrawal of synovial fluid. Brief evaluation of the color and viscosity of synovial fluid can shed some light on the disease process within and is expected practice among most racehorse trainers. Volume of local anesthetic solution varies considerably between synovial cavities, but the clinician should keep in mind that small volumes might contribute to a false-negative result. False-negative results are common in horses with

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severe osteoarthritis, and larger volumes of local anesthetic solution should be used. We routinely spray or wipe antiseptic solution over the injection site. After the examination a light bandage is applied over the injection sites from the metacarpophalangeal/metatarsophalangeal joint, distally. Initial reevaluation is done 5 to 10 minutes after injection. Additional evaluations may be necessary depending on the response during the initial time period. General practice is to have the horse walked in hand or with a rider after perineural or intrasynovial analgesia is administered, a procedure thought to hasten local distribution of anesthetic solution and potentially improve success. Excessive diffusion of local anesthetic solution is a potential drawback to this practice, particularly with techniques such as distal interphalangeal or middle carpal analgesia (see the following discussion), although it would be a complication difficult to quantify. Another issue to consider when performing diagnostic analgesia is whether riding or driving a horse after blocks have been performed is safe. In general, riding on the flat or driving a horse at slow speed after any of the common blocks are performed is safe. Stumbling or knuckling can be a concern after upper limb perineural techniques, such as the median/ulnar and fibular (peroneal)/tibial techniques. Common sense should prevail, however, with regard to the horse and rider negotiating fences or performing at high speed. Horses at risk of lameness from stress or incomplete fracture are candidates for imaging before evaluation at speed after diagnostic analgesic techniques have been performed.

PERINEURAL ANALGESIA IN THE FORELIMB Palmar Digital Analgesia Palmar digital analgesia (or palmar digital block) is the most common diagnostic analgesic procedure performed. The medial and lateral digital neurovascular bundles, consisting, in a dorsal to palmar direction, of the digital vein, artery, and nerve, course in an abaxial location to the digital flexor tendons. With the exception of small breeds or Draft horses with exceptionally long-haired pasterns (feathers), the palmar digital nerve is easily palpable between the proximal sesamoid bones and the cartilages of the foot. The palmar digital block can be performed with the horse in a standing position or with the limb held off the ground. We prefer the latter. If held by an assistant, the limb should be grasped in the midmetacarpal region, with the fetlock and digit hanging in neutral position. The palmar digital nerve is easily palpated in this extended position. Alternatively, the clinician performing the block can hold the limb, a technique that requires practice. The clinician can stand facing backward with a hand grasping the mid-pastern region or can stand behind the limb and clutch the hoof between both legs. A 25-gauge, 1.6-cm needle is inserted subcutaneously, directly over the nerve, just proximal to the cartilages of the foot (Fig. 10-5). One of us (L.H.B.) directs the needle in a distal direction, whereas the other (M.W.R.) directs the needle in a proximal direction to avoid deeper penetration or laceration of digital vessels if the horse withdraws the limb. Alternatively, a 22-gauge, 4-cm needle can be inserted on the palmar midline in the mid-pastern region, and local anesthetic solution is then infiltrated in a V-shaped pattern. This modification of the PD block is quite difficult to perform in the hindlimb, but when done in the forelimb, provides maximal analgesia to the bulbs of the heel and minimizes the potential of depositing local anesthetic solution dorsal to the nerve. Loss of skin sensation in the midline between the bulbs of the heels should be assessed, because this area seems most recalcitrant to palmar digital analgesia. Deep pain is assessed using hoof testers.

Traditionally the PD block was felt consistently to desensitize only the palmar (plantar) one third to one half of the foot.19 However, in clinical practice, this block desensitizes 70% to 80% of the foot. Most of the distal interphalangeal joint is affected, with the exception of the proximodorsal aspect. Horses with fractures of the extensor process of the distal phalanx may show partial improvement after palmar digital analgesia, however. Our clinical observations have been substantiated in a recent study. Setscrews were placed near the medial and lateral aspects of the toe to simulate pain from the sole. Lameness in these horses was abolished using palmar digital analgesia performed just proximal to the heel bulbs.20 Classically, most horses that responded positively to palmar digital analgesia were thought to have navicular syndrome, but this block desensitizes many lameness conditions within and outside the hoof capsule (Table 10-1). This is an important and common misconception. Lameness in horses with mid-sagittal fracture of the proximal phalanx or other conditions involving the fetlock joints can be abolished using palmar digital analgesia.7 Although using small volumes of anesthetic solution and performing the block just above the cartilages of the foot may help to minimize the area of analgesia, these procedures do not prevent inadvertent diagnosis in some horses. Diffusion of anesthetic solution is the most likely explanation, and even a small volume can readily spread in a proximal direction, but the normal anatomy of the digit prevents distal placement of anesthetic solution (Fig. 10-6). The concept that palmar digital analgesia abolishes lameness in an area considerably more than the palmar (plantar) one third of the foot appears to be difficult for many to accept. Although results of studies are widely published and this finding has been emphasized at international meetings, most veterinary students still graduate today armed with this common misconception. Diffusion of anesthetic solution easily explains why lameness conditions in the proximal aspect of the pastern or fetlock regions are desensitized by palmar digital analgesia. But what about the innervation of the hoof itself? Skeptics should consider the anatomy of the palmar digital nerve. Most practitioners have severed the palmar digital nerve while performing neurectomy. Can the clinicians recall any instance of having identified a large dorsal branch, or for that matter, any branching of the nerve at all? The lack of nerve branches in the mid-pastern region is circumstantial evidence that important innervation to the structures located dorsally within the hoof capsule occurs farther proximally (ill-defined dorsal branches) or after the nerve courses deep to the collateral cartilages of the foot. It makes little sense that ill-defined dorsal branches would innervate the dorsal two thirds of the foot, leaving the robust palmar digital nerve to innervate only the palmar one third. Accurately quantifying the contribution of the palmar digital nerve to the innervation of the foot or, for that matter, the exact percentage of structures desensitized by palmar digital analgesia may be impossible. Clinical experience will undoubtedly convince practitioners of the broad nature of palmar digital analgesia. Finally, it is imperative to develop expertise in diagnostic imaging of the entire digit, because the many lameness conditions affected by palmar digital analgesia require detective-like differential diagnostic skills.

Mid-Pastern Ring Block Traditionally the diagnostic blocks performed after palmar digital analgesia are the basisesamoid or abaxial sesamoid techniques. The basisesamoid block provides little additional information compared with palmar digital analgesia, unless, of course, the dorsal branch, originating from the digital nerve at the level of the proximal sesamoid bone, is blocked. If, however, the dorsal branch is blocked, then the basisesamoid block is in reality an abaxial sesamoid block. For this reason, we rarely

CHAPTER 10

• Diagnostic Analgesia

Lateral palmar vein, artery, and nerve

A

Lateral palmar vein, artery, and nerve

Dorsal branch of lateral palmar nerve

Dorsal branch of lateral palmar nerve

101

b

c Lateral palmar digital nerve

B

b

Lateral palmar digital nerve

a a

A, Palmarolateral view of the distal limb showing site for needle penetration for palmar (plantar) digital analgesia (a). The clinician directs the needle as shown or in a proximal direction. The palmar (plantar) digital nerve is blocked more proximally at the level of the abaxial surface of the proximal sesamoid bone (b). At this level the palmar (plantar) and dorsal branches are both blocked. B, Dorsolateral view of the distal limb demonstrating needle positions for palmar (plantar) digital analgesia (a) with an additional dorsally directed subcutaneous ring block to desensitize the dorsal aspect of the pastern region and foot (b). A block at the base of the proximal sesamoid bone (c) likely desensitizes the palmar (plantar) and dorsal branches of the digital nerve (note close association of both branches to the site of the block) and provides the same region of analgesia as does the palmar digital block with the dorsal ring, or the abaxial sesamoid block. C, Alternative technique used for palmar digital nerve block. The clinician inserts the needle on the palmar midline and places a line of anesthetic solution in a proximal dorsal direction to the level of each of the medial and lateral palmar nerves in an approximate V-shaped pattern. This technique confines anesthetic solution to the palmar aspect of the limb. This blocking technique is difficult to perform in the hindlimb.

Fig. 10-5

C

Medial palmar digital nerve

Lateral palmar digital nerve

perform the basisesamoid block. When performing the abaxial sesamoidean technique in racehorses or, for that matter, any sport horse with a propensity to develop lameness of the metacarpophalangeal or metatarsophalangeal joints, the veterinarian runs the risk of an additional misdiagnosis. When local

anesthetic solution is deposited in a location abaxial to the proximal sesamoid bones, pain from the metacarpophalangeal or metatarsophalangeal joints can be inadvertently blocked, explained most likely because of anesthetic diffusion, leading the clinician to assume the horse has a problem in the foot or

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Table • 10-1 Differential Diagnostic Analgesia of the Equine Foot DISEASE

Navicular disease Synovitis DIP joint Osteoarthritis DIP joint Subchondral bone DIP joint P3 Fracture (wing) P3 Fracture (midsagittal) Extensor process fracture (P3) Pedal osteitis Subsolar abscess Solar pain (heel/quarter) Solar pain (toe) DDF tendonitis DDF enthesitis (P3 insertion) Sheared heels Quittor Laminitis (toe) Laminitis (quarter/heel) Toe crack Quarter crack/heel crack Distal sesamoidean desmitis PIP joint problem DFTS problem P2 Fracture P1 Fracture

PALMAR DIGITAL NERVE BLOCK

DISTAL INTERPHALANGEAL JOINT BLOCK

NAVICULAR BURSA BLOCK

+ + + + + ± ± + + + + + + + + – + – + ± ± ± ± ±

± + + ± + + + ± ± ± ± – ± – – – ± – ± – – – ± –

+ – – – – – – – – – – – – – – – – – – – – – – –

DIP, Distal interphalangeal; P3, distal phalanx; DDF, deep digital flexor; PIP, proximal interphalangeal; DFTS, digital flexor tendon sheath; P2, middle phalanx; P1, proximal phalanx.

digit, but in reality the pain originated from these joints. For these reasons, we prefer to use a blocking sequence as follows: palmar digital nerve, followed by a dorsally directed subcutaneous ring block, followed by the low palmar or plantar block. The mid-pastern ring block affects the dorsal branches of the digital nerves and desensitizes any remaining areas of the foot and pastern region that were not affected by palmar digital analgesia. In most horses, this includes the dorsal 20% of the foot (dorsal laminar and extensor process regions of the distal phalanx), and dorsal pastern region (middle phalanx, proximal interphalangeal joint, and distal portions of the proximal phalanx). Although desirable, performing the dorsal ring block just above the cartilages of the foot usually is not possible. Instead the block is performed at the level of the mid-pastern region. A 20- to 22-gauge, 4-cm needle is used to deposit subcutaneously 10 to 12 ml of local anesthetic solution, beginning near the injection site used for palmar digital analgesia over the lateral neurovascular bundle and continuing dorsally and medially, ending over the medial neurovascular bundle (see Fig. 10-5). Resistance to needle advancement and injection of local anesthetic solution will invariably be encountered dorsally, if the block is done just proximal to the coronary band, because of the dense tissue (proximal interphalangeal joint capsule, extensor branches of the suspensory ligament, and extensor tendons). Performing the block in the mid-pastern region minimizes this problem and mitigates the potential for inadvertent penetration of the proximal interphalangeal joint.

Abaxial Sesamoid Block Radiograph showing palmar digital anesthesia performed with positive contrast material. The clinician performed palmar digital anesthesia as far distal as possible, but the injection site is still at the level of the proximal interphalangeal joint, explaining why palmar digital anesthesia desensitizes most of the foot and the pastern region in some horses.

Fig. 10-6

Desensitizing the medial and lateral palmar nerves at the level of the proximal sesamoid bones is commonly referred to as the abaxial sesamoid block but may provide the same information as the basisesamoid block, if the dorsal branch of the palmar digital nerve is blocked. To avoid redundancy, we rarely perform the basisesamoid technique before progressing to the

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DDFT SDFT

c b

a b A SL

Common and lateral digital extensor tendons

a

B

SL

Fig. 10-7 A, This lateral view shows needles positioned for a low palmar (plantar) nerve block. The clinician inserts a needle (a) just distal to the distal aspect of the fourth metacarpal or metatarsal bone and directs it axially to block the lateral palmar (plantar) metacarpal (metatarsal) nerve. The clinician then inserts a needle (b) between the suspensory ligament (SL) and deep digital flexor tendon (DDFT) to block the lateral palmar (plantar) nerve. The clinician repeats the two injections on the medial side. A subcutaneous ring block from the first injection site around to the dorsal midline (c) completely abolishes skin sensation. B, Transverse view of the distal left metacarpal region demonstrating an alternative technique for low palmar (plantar) analgesia. The clinician inserts a needle (a) in a lateral-to-medial direction between the deep digital flexor tendon and the SL to block the lateral and medial palmar (plantar) nerves. The palmar (plantar) metacarpal (metatarsal) nerves are blocked as depicted in A (not shown in this diagram), which also shows the subcutaneous ring block. The clinician inserts a needle (b) in a lateral-to-medial direction dorsal to the digital extensor tendons to block the dorsal metatarsal nerves of the hindlimb.

abaxial sesamoid block (see previous comments). A block done at this level essentially provides analgesia of the entire digit, because the block is performed at the level of or just proximal to the origin of the dorsal branch of the palmar digital nerve. Response to this block may vary, however. Some horses retain skin sensation in the dorsoproximal aspect of the pastern region. In others, pain arising from lesions involving the fetlock joint or peri-articular tissues is abolished. In part, these phenomena can be explained by proximal diffusion of anesthetic, affecting the palmar digital nerves proximal to the fetlock joint. Branches of the palmar digital nerves supplying the proximal sesamoid bones, the sesamoidean nerves, could easily be blocked using an analgesic technique in this abaxial position.21 The abaxial sesamoid block can be performed in the standing horse or with the limb held by the clinician or an assistant. The palmar digital nerve can easily be palpated over the rigid proximal sesamoid bones and in fact is in its most superficial position in this location. A 25-gauge, 1.6-cm needle, directed in a proximal or distal direction, and typically 1 to 3 ml of local anesthetic solution is used for the medial and lateral injection. Deep pain is assessed by hard flexion of the interphalangeal joints.

Low Palmar Analgesia Analgesia of the metacarpophalangeal joint region and distal limb is induced using the low palmar block or low palmar analgesia (low four-point). This technique blocks the medial and lateral palmar nerves and the medial and lateral palmar

metacarpal nerves. In the forelimb a subcutaneous, dorsally directed ring block and block of the dorsal branch of the ulnar nerve completely abolishes skin sensation. Disagreement exists about whether abolishing skin sensation is necessary when performing perineural techniques. Abolition of skin sensation does not necessarily mean deep pain is abolished, which is particularly relevant when a nerve responsible for skin sensation is blocked independently from nerves contributing to deep pain sensation, as in the case of the low palmar technique. When using these techniques for diagnostic purposes, it may be best to avoid blocking nerves that only contribute skin sensation, thus minimizing the number of needle insertions. For therapeutic interventions, however, these nerves need to be blocked. The low palmar block is performed at the level of the distal end (button) of the second and fourth metacarpal bones (splint bones), with the limb in a standing position or held off the ground (Fig. 10-7). A 20- or 22-gauge needle is used to inject 1.5 to 5 ml of local anesthetic solution at each injection site. To block the palmar metacarpal nerves, the needle is inserted perpendicular to the skin, just distal to the end of the splint bones, to a depth of 1 to 2 cm. It is important to deposit anesthetic solution deep in the injection site, rather than simply in a subcutaneous location. While continuously injecting local anesthetic solution, the needle is slowly withdrawn, leaving a visible bleb in the subcutaneous space. To block the medial and lateral palmar nerves, the needle is inserted subcutaneously, in the palmar aspect of the space between the

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suspensory ligament and deep digital flexor tendon (DDFT) at the level of or slightly more proximal to the distal end of the splint bone. To improve the accuracy of the injection, using a fan-shaped injection technique is helpful. To complete this block, local anesthetic solution is placed in the subcutaneous tissues from the bleb at the distal end of the splint bone to the dorsal midline. Alternatively, some clinicians prefer to use a longer needle first to deposit local anesthetic solution over the palmar metacarpal (metatarsal) nerves. The needle is then pushed subcutaneously to deposit local anesthetic solution over the palmar nerves (see Fig. 10-7). When performing this modification, incompletely blocking the palmar metacarpal (metatarsal) nerves or lacerating the digital vessels is possible. The lateral and medial palmar nerves can be blocked using only the lateral injection site by advancing the needle in a medial direction, palmar to the DDFT. Although each of these modifications may theoretically decrease the number of injections needed to perform this technique, they have the disadvantages of potential hemorrhage and incomplete analgesia. mc

High Palmar Block To provide analgesia to the metacarpal region, the high palmar block (high four-point, sub-carpal block) is the most common technique, but a modified block (lateral palmar or Wheat block) can be performed. Inadvertent penetration of the carpometacarpal joint is a potential complication with the high palmar block. A similar complication can occur in the hindlimb but is less frequent (see the following discussion). Inadvertent penetration of the carpometacarpal joint occurred in 17% of specimens, in which a conventional high palmar block was performed, because of extensive distopalmar outpouchings (Figs. 10-8 and 10-9). However, when the high palmar block was performed within 2.5 cm of the carpometacarpal joint, inadvertent penetration of this joint occurred in 67% of specimens. The carpometacarpal joint always communicates with the middle carpal joint, and therefore penetration of the carpometacarpal joint during high palmar analgesia would lead the clinician to diagnose a metacarpal problem, when in reality, the authentic lameness condition exists in the carpus. Moving the injection site in a distal direction decreases the possibility of entering the carpometacarpal joint but also narrows the scope of the technique. Two ways around this likely complication are these: first, the clinician could perform middle carpal analgesia before performing high palmar analgesia; second, the clinician could perform a lateral palmar block in lieu of the conventional high palmar technique. In an experimental study, it was unlikely to enter the carpal joints inadvertently when performing the lateral palmar block, although in every specimen, local anesthetic solution would have entered the carpal canal.22 Unless the clinician is familiar with the lateral palmar block, the most straightforward approach to reduce the possibility of misdiagnosis in this region is to perform middle carpal analgesia before proceeding to the high palmar block. When local anesthetic solution is placed in the middle carpal joint, not only is the carpometacarpal joint blocked, but also the possibility exists of providing local analgesia to the proximal palmar metacarpal region. Using this approach, abolishing pain associated with proximal suspensory attachment avulsion injury (desmitis, fracture), stress remodeling, and longitudinal fracture is possible (see Chapter 38). The palmar metacarpal nerves and suspensory branches from the lateral palmar nerve are closely associated with the distopalmar outpouchings of the carpometacarpal joint, and anesthetic diffusion from this area could explain in part this clinical finding (Fig. 10-10). It is important for the clinician to understand that interpretation of analgesic techniques in the proximal palmar metacarpal region or carpus can be somewhat complex.

cmc

Positive contrast arthrogram of the middle carpal (mc) and carpometacarpal (cmc) joints (dorsal is to the right). Contrast material injected into the middle carpal joint flows freely distally into the carpometacarpal joint and fills the extensive distopalmar outpouchings of the joint (arrow).

Fig. 10-8

Correct diagnosis is always the key, and comprehensive evaluation using multiple imaging modalities is a must in differentiating lameness in this region. From the clinical perspective, one is more likely to assume incorrectly that one is dealing with a carpal problem, when the authentic lameness condition resides in the proximal palmar metacarpal region, than vice versa. Numerous techniques are used to perform high palmar analgesia; some provide partial and others provide complete analgesia to the metacarpal region. For complete analgesia, blocking the following nerves is necessary: the medial and lateral palmar nerves, the medial and lateral palmar metacarpal nerves, the suspensory branches, and nerves providing skin sensation along the dorsum (dorsal branch of ulnar nerve and musculocutaneous nerve). To block these nerves effectively, one must use a site close to the carpometacarpal joint, at the level where the splint bones begin to taper (Fig. 10-11). If the block is done at a lower level, the region of the suspensory attachment will be missed. A 20- or 22-gauge needle at least 2.5 cm long is necessary to reach the palmar metacarpal nerves in this location. The needle is inserted axial to the splint bones just abaxial to the suspensory ligament and then guided to the palmar cortex of the third metacarpal bone (McIII). Five milliliters of local anesthetic solution is deposited, first deep within the tissues, and continued as the needle is withdrawn, ending with a bleb in the subcutaneous tissues. To block the medial and lateral palmar nerves between the suspensory ligament and DDFT, a smaller gauge needle can be used to deposit 3 to 5 ml of local anes-

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Median nerve Ulnar nerve

Ulnar nerve

Palmar branch of ulnar nerve Lateral palmar nerve

A

Lateral palmar metacarpal nerve

Medial palmar nerve

Median nerve Ulnar nerve Lateral palmar nerve

Deep branch of lateral palmar nerve Branches to the suspensory ligament

Dorsal branch of ulnar nerve

Deep branch of lateral palmar nerve

Lateral palmar nerve

Medial palmar nerve

B

Lateral and medial palmar metacarpal nerves

Fig. 10-12 A, This diagram of the left carpus in a flexed position shows the location of the lateral palmar nerve block and parent nerves (inset) contributing to the origin of the lateral palmar and other important nerves. B, Palmar view of the limb showing nerves in situ and the site for needle penetration for lateral palmar nerve block.

and the origin of the suspensory ligament. Pain associated with the carpal canal is abolished, however. The lateral palmar block can be performed in the standing position or with the limb held off the ground, with the carpus in 90° of flexion. The nerve cannot be palpated because it courses in the accessorial-metacarpal ligament, dense connective tissue distal to the accessory carpal bone. A 25-gauge, 1.6-cm needle is inserted to the hub, perpendicular to the skin, just distal to the accessory carpal bone, and 5 ml of local anesthetic solution is deposited within this dense tissue. Injection can be difficult to perform, and breaking the seal between the needle and syringe is common, so a screw-type hub should be used. The medial palmar nerve is then blocked as described previously. If desired, a dorsal, circumferential subcutaneous ring block provides complete analgesia to the dorsum.

Median, Ulnar, and Medial Cutaneous Antebrachial Block Although not frequently performed, analgesia of the distal antebrachium and carpus can be induced by blocking the median, ulnar, and medial cutaneous antebrachial (musculocutaneous) nerves.19 Because the latter nerve supplies only skin sensation, for diagnostic purposes it does not need to be included in the technique. In our practices, this block is most commonly performed to facilitate lavage of the carpal joints or carpal canal or to perform regional limb perfusion of antibiotics in standing horses. We generally default to intrasynovial analgesia in these structures, however. The median, ulnar, and medial cutaneous antebrachial nerve block is occasionally useful in diagnosing subchondral carpal bone pain or lameness involving the carpal canal. Although the prevalence of lameness in the distal antebrachium is low, this block can be used to diagnose distal radial bone cysts or enthesitis at the origin of the accessory ligament of the superficial digital flexor tendon (SDFT) (superior check ligament). This block can be used to eliminate the entire distal limb as a potential source of pain. Alternatively, this block can be used alone to elimi-

nate pain distal to the injection site, or the median and ulnar nerves can be blocked independently to improve specificity of the technique. The ulnar nerve is blocked about 10 cm proximal to the accessory carpal bone on the caudal aspect of the antebrachium (Fig. 10-13). A 20- or 22-gauge, 4-cm needle is inserted to the hub, perpendicular to the skin, in the groove between the flexor carpi ulnaris and the ulnaris lateralis muscles. Needle contact with the ulnar nerve may cause the horse to strike forward.5 Ten milliliters of local anesthetic solution is injected as the needle is slowly withdrawn. Skin sensitivity along the lateral aspect of the limb from the carpus to the metacarpophalangeal joint will be eliminated.19 The median nerve is blocked 5 cm distal to the cubital (elbow) joint on the medial aspect of the antebrachium. At this level, the nerve lies along the caudal aspect of the radius, just cranial to the flexor carpi radialis muscle. A 20- or 22-gauge, 4cm needle is inserted to the hub, in a lateral direction, along the caudal aspect of the radius, just distal to the superficial pectoral muscle, and 10 ml of local anesthetic solution is used (see Fig. 10-13). Rarely in large horses, a 9-cm (3 1⁄ 2-inch) spinal needle may be necessary to reach the median nerve. Often the needle hits the median nerve, a useful indicator that the tip is in the proper location.5 In any event the needle should be kept close to or against the caudal cortex of the radius to avoid inadvertent puncture of the median artery or vein, which lies caudal to the nerve.19,24 To facilitate these deep injections, the skin can be first desensitized by using a small volume of local anesthetic solution. A more distal injection site for the median nerve may eliminate the possibility of inadvertently eliminating elbow joint pain using the suggested approach.5 Finally (for therapeutic applications), to block the cranial and caudal branches of the medial cutaneous antebrachial (musculocutaneous) nerve, 3 ml of local anesthetic solution is injected, subcutaneously, on the cranial and caudal aspect of the accessory cephalic and cephalic veins, about halfway between the carpus and elbow (see Fig. 10-13).19 Alterna-

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Flexor carpi ulnaris muscle

b Extensor carpi radialis

Median nerve

Ulnar nerve

a

Cephalic and accesory cephalic vein

A

Lacertus fibrosus

B

b

Ulnaris lateralis muscle

Median nerve Flexor carpi ulnaris muscle

Ulnar nerve

Musculocutaneous nerve

Radius

a A, This caudal view of the left antebrachium shows the sites of needle insertion for the median and ulnar nerve blocks. A needle placed between the ulnaris lateralis and flexor carpi ulnaris muscles (a), about 10 cm proximal to the accessory carpal bone, blocks the ulnar nerve. A needle inserted along the caudal aspect of the radius about 10 cm distal to the elbow joint (b) blocks the median nerve. The inset shows the orientation between the radius, median artery, vein, and nerve at the site of needle insertion (b) and shows the orientation of the needle for the ulnar nerve block (a), which is performed distally. B, This medial view of the proximal left antebrachium shows the technique for a musculocutaneous nerve block. The nerve is blocked as it crosses the lacertus fibrosus on the cranial aspect of the proximal antebrachium. This block abolishes skin sensation on the medial and dorsal aspects of the antebrachium.

Fig. 10-13

tively, this nerve can be blocked before it branches, as it courses across the lacertus fibrosus. At this location, the nerve is easily palpable in most horses. A third method to completely abolish skin sensation is using a circumferential subcutaneous ring block, a technique that can effectively block all four cutaneous antebrachial nerves but requires a large volume of local anesthetic solution.

INTRA-ARTICULAR ANALGESIA IN THE FORELIMB Distal Interphalangeal Joint The assumption is that analgesia of the DIP joint is specific for intra-articular pain, but clinical experience and the results of recent clinical and anatomical investigations have convinced us otherwise (see Fig. 10-1). Of great clinical interest is the comparative accuracy of analgesia of the DIP joint and navicular (podotrochlear) bursa in the diagnosis of navicular syndrome. Overall, analgesia of the navicular bursa is likely the most specific technique to diagnose navicular syndrome. However, analgesia of the distal interphalangeal joint lacks specificity for intra-articular pain and in fact can eliminate pain associated with many conditions of the foot.25,26 For instance, using highperformance liquid chromatography to study the effects of 8 ml of mepivacaine injected into the distal interphalangeal joint, there was local anesthetic solution in the synovium of the navicular bursa in all horses and in the medullary cavity of the navicular bones in 40% of horses.27 Anatomical studies showed that nociceptive neurofibers are present in the dorsal and palmar aspects of the collateral sesamoidean ligaments, within the distal sesamoidean impar ligament, and directly innervating the navicular bone, in the periarticular connective

tissues of the distal interphalangeal joint and proximal intramedullary portions of the distal phalanx.28,29 The close anatomical relationship between these structures and the palmar digital neurovascular bundles to the distal interphalangeal joint capsule makes them susceptible to desensitization by local anesthetics injected into the DIP joint.29 In a recent study using a setscrew model to create solar pain at the toe, distal interphalangeal intra-articular analgesia abolished lameness, leading to the conclusion that pain in distant sites can be abolished using this technique.20 Therefore a positive response to distal interphalangeal intra-articular analgesia could mean lameness is caused by an articular problem, navicular syndrome, or for that matter, solar pain. Close juxtaposition between the palmar synovial extensions of the distal interphalangeal joint and digital nerves at this level was theorized as the reason that these nerves were blocked, secondary to diffusion of local anesthetic solution from the joint.20 Therefore a protocol to examine a lame horse no longer than 5 minutes after intra-articular analgesia of the distal interphalangeal joint may minimize diffusion and improve accuracy. Because diffusion of local anesthetic solution may be hastened by moving the horse, some clinicians prefer the horse to stand until the results of the block are evaluted.5 Traditionally, arthrocentesis of the distal interphalangeal joint has been performed in the dorsal pouch, either medial or lateral to the common digital extensor (CDE) tendon. A 20gauge, 2.5- to 4-cm needle is inserted about 1.5 cm proximal to the coronary band, abaxial to the CDE tendon, and directed in a distal and axial direction (Fig. 10-14). An easier approach, however, is to insert the needle, angled just slightly distal from horizontal, on the dorsal midline, through the CDE. Synovial fluid is consistently obtained using this approach. To open up the dorsal aspect of the distal interphalangeal joint,

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a b

a

CDET

b Dorsal pouch of DIP joint

c Palmar pouch of DIP joint

c

Fig. 10-14 A, Lateral view of the foot showing our preferred approach for arthrocentesis of the digital interphalangeal joint using a dorsal midline needle insertion site (a) and directing the needle slightly distally through the common (long) digital extensor tendon. Alternatively, the clinician approaches the digital interphalangeal joint using a site medial or lateral to the extensor tendon (b). The top inset shows the needle positions from the dorsal aspect. The clinician may use a palmar (plantar) approach by positioning the needle between the distal palmar (plantar) border of the middle phalanx and a palpable notch in the proximal border of the cartilage of the foot. The clinician directs the needle (c) in a palmaroproximolateral to dorsodistomedial direction. The lower inset shows the notch into which the needle is inserted. DIP, Distal interphalangeal; CDET, common (long) digital extensor tendon.

the limb should be positioned slightly ahead of the contralateral limb, and the horse should be in a standing position. Five to 10 ml of local anesthetic solution has been used traditionally, but a maximum of 6 ml may prevent leakage from the joint. The horse is examined after 5 minutes. Alternatively, a lateral approach to the distal interphalangeal joint can be used (see Fig. 10-14). Landmarks include the distal palmar border of the middle phalanx dorsally and the palpable notch in the proximal border of the lateral cartilage of the foot distally. A 4-cm needle is inserted laterally and directed in a dorsodistomedial direction. This technique, however, is less reliable than the dorsal approach, because contrast material entered exclusively the distal interphalangeal joint in only 13 of 20 specimens and in 7 specimens inadvertently entered the navicular bursa or digital flexor tendon sheath.30

Proximal Interphalangeal Joint Arthrocentesis of the proximal interphalangeal joint is most commonly performed in the dorsal pouch. Effusion is rarely present even in horses with severe lameness, a situation that makes arthrocentesis challenging. The injection site is just lateral (or medial) to the CDE tendon at a level of or just distal to the distal, palmar process of the proximal phalanx, located and easily palpable on the distopalmar aspect of this bone. With the horse in the standing position, a 20-gauge, 2.5-cm needle is directed slightly distally and medially (using the dorsolateral approach) and inserted until articular cartilage is encountered (Fig. 10-15). Although a desirable sign, synovial fluid appearing in the hub of the needle is an unusual occurrence. Five to 10 ml of local anesthetic solution is injected, and the horse is examined after 5 minutes. Alternatively, the proximal interphalangeal joint can be approached using the proximal palmar pouch, from the lateral aspect. The injection location is a V-shaped notch, located dorsal to the neurovascular bundle and between the distal palmar process of the proximal phalanx the insertion of the

lateral branch of the SDFT (see Fig. 10-15). The limb is held off the ground with the digit in flexion, and a 2.5- or 4-cm needle is directed distomedially (and slightly dorsally), at an angle of about 30° from the transverse plane, until fluid is collected (generally at a depth of 2 to 3 cm).31 Advantages of this compared with the dorsal approach include less needle manipulation, a larger injection volume, and more frequent recovery of synovial fluid. Diffusion into palmar soft tissue structures could confound interpretation of results, however.5

Metacarpophalangeal Joint Four sites commonly used for arthrocentesis of the metacarpophalangeal joint include the dorsal, proximopalmar, distopalmar, and approach through the collateral ligament of the proximal sesamoid bone. The two most commonly used, the dorsal and proximopalmar sites, have potential disadvantages compared with the less commonly used sites. The dorsal pouch can be prominent in horses with effusion, but inadvertently stabbing articular cartilage repeatedly is common using this approach. The proximopalmar pouch or recess is large and easily identified, but prominent synovial villi often occlude the needle end, complicating retrieval of synovial fluid, even in horses with severe effusion. Hemorrhage associated with large intra-capsular vessels is also a common complication with the proximopalmar approach. The palmar pouch is located dorsal to the suspensory branch, palmar to McIII, proximal to the collateral sesamoidean ligament, and distal to the bell of the splint bone (Fig. 10-16). Arthrocentesis using the proximopalmar approach can be performed with the limb in the standing position or being held. An 18- to 22-gauge, 2.5- to 4-cm needle is inserted in the center of the pouch and directed slightly distally in the frontal plane, until synovial fluid is recovered (Fig. 10-17). It may be necessary to aspirate synovial fluid if the joint capsule is not distended. Dorsally, arthrocentesis is performed medial or lateral to the CDE tendon (see Fig. 10-17). With the limb in a standing or

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Lateral palmar process

CDET

Palmar recess of PIP joint

Dorsal pouch of PIP joint

A

B

Joint capsule

Fig. 10-15 A, Dorsolateral view of the digit showing the site for arthrocentesis of the dorsal pouch of the proximal interphalangeal joint. The clinician inserts the needle just abaxial to the digital extensor tendon at a site level with the palpable distal palmar (plantar) process of the proximal phalanx. B, Flexed lateral view of the digit indicating the site for arthrocentesis of the palmar (plantar) aspect of the proximal interphalangeal joint. The clinician inserts the needle into the V-shaped notch formed by the distal palmar (plantar) aspect of the proximal phalanx dorsally, the bony eminence associated with the attachment of the lateral collateral ligament to the distal aspect of the proximal phalanx and proximal aspect of the middle phalanx distally, and the insertion of the lateral branch of the superficial digital flexor tendon palmaro- (plantaro) distally. The clinician directs the needle distomedially (in a slightly dorsal direction) at an angle of about 30° from the transverse plane until fluid appears. CDET, Common (long) digital extensor tendon; PIP, proximal interphalangeal. flexed position, the clinician can insert a needle in the distal aspect of the palmar pouch, through the collateral sesamoidean ligament, a less common but effective approach for arthrocentesis of the metacarpophalangeal joint. The technique is more easily performed with the joint held in flexion. This approach for arthrocentesis was shown to be associated with less subcutaneous and synovial inflammation than was the proximopalmar approach.32 Under most circumstances we prefer to perform arthrocentesis of the metacarpophalangeal joint using the distopalmar approach. The injection site is in a small but reliable recess bounded by a triad of structures. Just proximal to the readily palpable proximal, palmar process of the proximal phalanx is a distinct depression. The dorsal aspect of the proximal sesamoid bone and the palmar condyle of McIII complete the triad but are not readily palpable. The injection site is dorsal to the neurovascular bundle. Synovial fluid is consistently retrieved because the injection site is in the most distal aspect of the joint, and hemorrhage is rare. A large volume of fluid can be collected, if desired, because this area is devoid of the large synovial villi that complicate the proximopalmar approach. With the horse in a standing position, a 20-gauge, 2.5-cm needle is inserted, parallel to the ground, in a dorsomedial direction until fluid is obtained (see Fig. 10-17). The needle can be advanced to the hub, but the joint is quite superficial in this location. This technique can also readily be performed with the limb being held in a flexed position. Ten milliliters of local anesthetic solution is injected, and the horse is reexamined in 5 to 10 minutes. In horses with subchondral bone pain, additional time may be necessary, but perineural analgesia may be necessary to abolish lameness in

Fig. 10-16 Positive contrast arthrogram of the metacarpophalangeal joint showing the extensive nature of the palmar pouch that extends proximally to the level of the distal end of the splint bones. The distopalmar outpouchings are reliable sites for retrieval of synovial fluid and injection.

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b a Collateral sesmoidean ligament

A

Proximal palmar process of proximal c phalanx

B

d Joint capsule

a

Suspensory ligament

C

Palmar annular ligament

Distal digital annular ligament

Proximal digital annular ligament

b

Fig. 10-17 A, Palmaro (plantaro) lateral view of the left metacarpophalangeal (metatarsophalangeal) joint and digit showing the sites for arthrocentesis of the proximal palmar (plantar) pouch (a), the dorsal pouch (b), the distal palmar (plantar) pouch (c), and the palmar (plantar) pouch through the collateral ligament of the proximal sesamoid bone (d). B, Our preferred site for metacarpophalangeal (metatarsophalangeal) joint arthrocentesis, the distopalmar approach, using a site just proximal to the palmar (plantar) process of the proximal phalanx, is easily located in the standing or flexed position. C, Palmaro (plantaro) lateral view of the digit indicating sites for synoviocentesis of the proximal (a) and distal (b) aspects of the digital flexor tendon sheath. Proximally, the clinician inserts the needle proximal to the palmar (plantar) annular ligament, and distally inserts the needle on the palmar (plantar) midline into an outpouching of the digital flexor tendon sheath between the proximal and distal digital annular ligaments.

these horses. Diffusion of local anesthetic solution may account for partial improvement in lameness in horses with suspensory branch desmitis or sesamoiditis. Therefore timely evaluation of horses after metacarpophalangeal analgesia is necessary.

Carpal Joints Arthrocentesis of the middle carpal or antebrachiocarpal joints is one of the easiest and most straightforward of all

joint injection techniques. With the carpus in flexion, injection sites are easily identified, and large portals exist through which to access the joints. Portals can be found either medial to the extensor carpi radialis tendon or between the ECR and the CDE tendons (Fig. 10-18). The middle carpal and carpometacarpal joints always communicate, but a communication between the middle carpal and antebrachiocarpal joints rarely exists. A communication between the middle carpal joint and carpal sheath rarely is encountered clinically but

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a ECRT

CDET

c b B

A

b a a

Carpal sheath

d

c

A, Dorsal view of the left carpus in a flexed position showing the sites for arthrocentesis of the middle carpal (a) and antebrachiocarpal (b) joints. Needles are usually positioned between the extensor carpi radialis and common digital extensor tendons (as shown) but sites for injection of both joint cavities located medial to the extensor carpi radialis tendon can be used. B, Lateral view of the left carpus demonstrating sites for arthrocentesis of the proximal palmar pouch of the antebrachiocarpal joint (a), the palmarolateral pouch of the middle carpal joint (b), and the proximal (c) and distal (d) pouches of the distended carpal sheath. The inset shows the relative needle positions to enter the palmar pouch of the antebrachiocarpal joint and the carpal sheath. CDET, Common (long) digital extensor tendon; ECRT, extensor carpi radialis tendon.

Fig. 10-18

was not seen in a study using cadaver limbs. Analgesia of the middle carpal and antebrachiocarpal joints should be performed separately to differentiate lameness between these independent cavities. Distopalmar outpouchings of the carpometacarpal joint complicate interpretation of analgesic techniques, because these extend a mean distance of 2.5 cm distal to the carpometacarpal articulation and are closely associated with the suspensory ligament origin and the palmar metacarpal nerves (see Figs. 10-8 to 10-10).33 Careful differential analgesic techniques and comprehensive imaging are necessary for accurate diagnosis of lameness in the carpal and proximal metacarpal regions. Typically, a 20-gauge, 2.5-cm needle is used to inject 5 to 10 ml of local anesthetic solution into the middle carpal and antebrachiocarpal joints. If the skin can be prepared aseptically on the dorsal aspect, the injections are most commonly performed with the joint in 90° to 120° of flexion. The clinician can maintain flexion, but having an assistant hold the limb securely is easier. If the dorsal aspect of the carpus cannot be prepared aseptically, as occurs commonly in racehorses with chemically induced dermatitis (scurf), or if an additional site is needed for thorough lavage, the palmarolateral pouch of the middle carpal and antebrachiocarpal joints can be used. The palmar pouch of the antebrachiocarpal joint is bounded by the lateral digital extensor tendon dorsally and the ulnaris lateralis tendon palmarly. In horses with substantial effusion, this pouch is easily identified but must be differentiated from the lateral outpouching of the carpal sheath. Arthrocentesis can be performed either proximally or distally in the palmar

pouch (see Fig. 10-18). The distal injection site is located in a shallow recess between the distal lateral radius (ulna) and the ulnar carpal bone, just distal to the V-shaped convergence of the lateral digital extensor and ulnaris lateralis tendons. With the horse in a standing position, a 20-gauge, 2.5-cm needle is inserted perpendicular to the skin and advanced until synovial fluid is recovered. The palmar pouch of the middle carpal joint is similarly accessed in a shallow depression between the ulnar and fourth carpal bones, located 2 to 2.5 cm distal to the recess palpated to access the antebrachiocarpal in the palmar aspect (see Fig. 10-18). The shallow depression in the middle carpal joint is difficult to palpate, but in horses with severe effusion an outpouching of the joint is palpable. This approach is done with the limb in a standing position, decreases the potential for iatrogenic cartilage injury, and is less dangerous to the clinician because the procedure is performed on the side, rather than in front of the limb.34 The injection is more difficult and less commonly used, however.

Cubital (Elbow) Joint Two sites are used for arthrocentesis of the elbow joint. The cranial pouch is accessed at the level of the radiohumeral articulation, just cranial to the lateral collateral ligament. The lateral collateral ligament courses between the palpable lateral tuberosity of the radius and the lateral epicondyle of the humerus (Fig. 10-19). An 18- or 20-gauge, 6- to 9-cm needle is directed medially and slightly caudally to a depth of 5 to 6 cm, beginning in the adult horse, about 3.5 cm proximal to the lateral tuberosity of the radius and 2.5 cm cranial to the

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Infraspinatus muscle

d Deltoid tuberosity Triceps brachii muscle

b c d

Biceps brachii muscle

a Scapula

e

Olecranon

Fig. 10-19 Lateral view of the left elbow and shoulder regions. For arthrocentesis of the cranial pouch of the elbow (cubital) joint, the clinician directs the needle (a) medially and slightly caudally to a depth of about 5 to 6 cm at a point about 3.5 cm proximal to the lateral tuberosity of the radius and 2.5 cm cranial to the lateral collateral ligament. Arthrocentesis of the proximal, caudal pouch (b) is performed at a site in the palpable depression between the cranial aspect of the olecranon and the caudal aspect of the lateral epicondyle of the humerus. One injection site is for the rarely performed technique of synoviocentesis of the olecranon bursa (c). Proximally is the site for arthrocentesis of the scapulohumeral joint (d). A needle is inserted cranial to the infraspinatus tendon in the notch between the cranial and caudal eminences of the greater tubercle of the humerus and advanced in a caudomedial direction, roughly parallel to the ground and about 45° to the long axis of the body (inset). For the bicipital bursa (e), the clinician inserts the needle at a point about 4 cm proximal to the palpable distal aspect of the deltoid tuberosity of the humerus (or alternatively, a point about 3 to 4 cm distal and 6 to 7 cm caudal to the palpable aspect of the cranial process of the greater tubercle) and directs it proximally and medially, and in some patients slightly cranially.

lateral collateral ligament.19 To account for differences in horse size, the injection site is generally located two thirds of the distance between the humeral epicondyle and the lateral tuberosity of the radius. This block may be more easily performed closer to the lateral collateral ligament, and at this site the joint is penetrated in a more superficial location.5 Before injection, every effort should be made to verify the needle is actually in the joint. Peri-articular deposition of anesthetic solution in this location can induce temporary radial nerve dysfunction, and horses may lose the ability to extend the carpus and digit.35 Twenty to 25 ml of local anesthetic solution is used. An older approach relied on injection of local anesthetic solution into the ulnaris lateralis bursa, once universally thought to communicate with the elbow joint. The frequency of communication between the elbow joint and ulnaris lateralis bursa was deter-

mined to be 37.5%, and therefore this approach is no longer recommended.36 We prefer to perform arthrocentesis in the proximolateral aspect of the caudal pouch in the palpable depression cranial to the olecranon process and caudal to the lateral epicondyle of the humerus. In most horses the site of needle penetration is 3 to 3.5 cm caudal to the lateral epicondyle (see Fig. 10-19). In small horses and ponies, an 18- or 20-gauge, 4-cm needle is sufficient, but in large horses a 9-cm spinal needle is often necessary. The needle is advanced for 5 to 7 cm in a distal, slightly cranial, and medial direction until synovial fluid is recovered. Elimination of skin sensitivity at the site of needle insertion by depositing a small volume of local anesthetic solution may facilitate elbow arthrocentesis, because multiple attempts

CHAPTER 10 may be necessary. Synovial fluid is consistently retrievable from the joint with proper needle positioning.

Scapulohumeral (Shoulder) Joint The shoulder joint is frequently blamed for lameness in many horses but, based on the results of diagnostic analgesia, is an uncommon source of lameness. Arthrocentesis of this joint is most commonly performed at a site between the cranial and caudal prominences of the greater tubercle of the humerus, just cranial to the infraspinatus tendon. This tendon is easily palpated in most horses and serves as the primary landmark. Firm, careful palpation between the cranial and caudal prominences reveals a depression or notch, which is the point of needle insertion (see Fig. 10-19). Identification of landmarks is easier in horses with muscle atrophy resulting from chronic lameness. In most horses an 18- to 20-gauge, 9-cm spinal needle is preferred, although using the entire length is not necessary. Elimination of skin sensitivity is usually not necessary. The needle is inserted in a caudomedial direction (about 45° from lateral), and directed slightly distal. Attaching a syringe to aspirate synovial fluid is sometimes necessary, because in joints with minimal effusion, confirming intra-articular position of the needle may be difficult. Twenty-five to 30 ml of local anesthetic solution is used and the horse is assessed 10 and 30 minutes after injection, because severe pain associated with osteochondrosis may resolve slowly. Analgesia of the suprascapular nerve and subsequent supraspinatus and infraspinatus muscle paralysis was reported following attempts at intra-articular shoulder analgesia.35 This complication is rare, in our experience, and may result from anesthetic diffusion to nerves of the brachial plexus.5 Trauma from multiple needle insertions or injection of large volumes of anesthetic solution (>30 ml) may increase the likelihood of this complication. In fact, some have recommended using only 8 to 10 ml, but false-negative results from the block would likely occur.35 Our opinion is that the most likely cause of this rare complication is malposition of the needle or iatrogenic trauma. Rarely, a communication between the bicipital bursa and the shoulder joint occurs.37 Thinking a horse has shoulder joint pain is possible then, but in reality the diagnosis is bicipital bursitis or tendonitis. Rather than a communication between the structures, the most likely explanation is inadvertent penetration of the bicipital bursa from a misdirected needle.

ANALGESIA OF FORELIMB BURSAE AND TENDON SHEATHS In most instances, analgesia of bursae and tendon sheaths is achieved using perineural techniques, but in some horses, selective intrasynovial analgesia is indicated. Pain sensation from bursae and sheaths is likely complex, and lameness after intra-bursal or intrathecal (within a sheath) analgesia may improve but not completely resolve. In fact, horses with severe lameness resulting from bursitis or tenosynovitis often have other associated soft tissue damage, a fact that explains partial improvement after intrasynovial analgesia. Extra time is usually given, after blocking, to reassess the horse’s clinical signs.

Podotrochlear (Navicular) Bursa A palmar midline approach is most commonly used for analgesia of the navicular bursa. Because needle position is difficult to assess and fluid recovery varies, radiographs should be used to confirm proper needle position. Positioning the foot on a wooden block can minimize the problems of manipulation at the bulbs of the heel and helps to maintain aseptic

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technique. Subcutaneous deposition of a small volume (1 to 2 ml) of local anesthetic solution can improve patient compliance during this procedure. An 18- to 20-gauge, 9-cm spinal needle is inserted on the palmar midline, just proximal to the hairline, and directed parallel to the sole until the needle contacts bone (Fig. 10-20).23,25,38 Others describe a similar approach, although they direct the needle parallel to the coronary band.19,39,40 Because redirection of the needle proximally or distally often is necessary, these approaches differ little. Success depends most on personal experience, but radiographs can be critical in confirming successful entry into the navicular bursa. The direction in which the needle is inserted is often dictated by the shape of the horse’s foot, and the projected position of the navicular bone.5 Plotting and marking the navicular position on the hoof wall can be helpful in determining needle direction and depth of insertion. The navicular position is located at a site 1 cm distal to and halfway between the dorsal and palmar aspects of the coronary band.41,42 However, with experience and after identifying the navicular position, the procedure can be done blindly. In most horses the flexor surface of the navicular bone will be contacted at a depth of 4 to 5 cm. The needle is likely improperly positioned if resistance is encountered at a depth of less than 3 to 4 cm or if the needle can be advanced more than 6 to 7 cm. Spontaneous retrieval of synovial fluid is rare and usually indicates that the needle is in the distal interphalangeal joint capsule or the digital flexor tendon sheath (DFTS). To avoid penetrating these structures, the needle should be placed in the middle of the flexor surface of the navicular bone.5 Three to 5 ml of local anesthetic solution is used. If navicular syndrome is suspected, some clinicians combine injection of local anesthetic solution with a corticosteroid. Alternatively, navicular bursography can be performed in combination with diagnostic analgesia by adding 1 to 2 ml of sterile, iodinated contrast material (see Chapter 30). Because in the standing horse the navicular bursa is under compression by the DDFT, suspending the foot and having the foot in partial flexion during actual injection are useful. Without using radiographs, being confident of accurate needle placement is difficult. A proximal, palmar injection technique has been described. A needle is inserted into the deepest part of the hollow between the heel bulbs and advanced dorsodistally, about 30° from horizontal, until contact with the bone is made.38,43 A lateral (or medial) approach is also described. A needle is inserted just proximal to the cartilage of the foot, between the neurovascular bundle and the DFTS and directed axially, distally, and slightly dorsally until contact with bone is made (see Fig. 10-20).38,40,44 Recently, these five techniques were compared in an in vitro study. The most reliable technique was determined to be the distal palmar approach, with the needle being directed to the navicular position and the limb in a non–weight-bearing position.45

Digital Flexor Tendon Sheath Two sites for intrasynovial injection of the DFTS are just proximal to the palmar annular ligament (PAL) or in the palmar aspect of the pastern region in an outpouching of the sheath located between the proximal and distal digital annular ligaments (see Fig. 10-17). Effusion facilitates identification of these sites, and rarely would an intrathecal injection be contemplated without the presence of effusion. Proximal to the PAL, villous hypertrophy of synovial membrane can complicate the procedure, because even with severe distention of the sheath, synovial fluid may be difficult to retrieve. For this reason, we favor the palmar pastern approach. In some horses, the sheath appears to be compartmentalized and distended proximal to the PAL, but not below, and therefore injections are easier to perform

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50% 1cm

b Navicular bone A B

a

Fig. 10-20 A, Lateral view showing two techniques for synoviocentesis of the navicular bursa of the foot. In the palmar (plantar) approach (a) the needle is placed just proximal to the hairline between the bulbs of the heels and inserted to the navicular bursa using the navicular position as a guide. The navicular position (arrow) is located by determining the point on the outside of the hoof wall that is 50% of the distance from the dorsal to the palmar (plantar) extent of the coronary band and 1 cm below (inset). An approach slightly more proximal (b) requires placing the needle in the depression between the heel bulbs and advancing the needle in a dorsodistal direction, about 30° from horizontal toward the navicular position. B, Palmaro (plantaro) lateral view of the digit showing the lateral approach for synoviocentesis of the navicular bursa. The needle is inserted just proximal to the cartilage of the foot between the digital neurovascular bundle and the digital flexor tendon sheath and directed axially, distally, and slightly dorsally.

proximally. A 20-gauge, 2.5-cm needle and 10 to 15 ml of local anesthetic solution are used. Alternatives to these approaches for intrasynovial injection of the DFTS are described. The procedure can be performed at a site just distal to the proximal sesamoid bones, between the distal aspect of the PAL and the proximal aspect of the proximal digital annular ligament (see Fig. 10-17). Recently the palmar axial sesamoidean approach was described. With the metacarpophalangeal joint held in flexion (225° angle between McIII and the proximal phalanx), a 20-gauge, 2.5-cm needle is inserted at an angle of 45°, 3 mm axial to the palmar border of the proximal sesamoid bone (mid-body) and just palmar to the neurovascular bundle. Putative advantages included more reliable access to the DFTS when effusion is absent and reduced time required for successful entry.46

Carpal Sheath The carpal sheath (carpal flexor sheath) envelops the SDFT and DDFT in the carpal canal. Distention of the carpal sheath is most easily recognized laterally, just proximal to the accessory carpal bone, between the lateral digital extensor and ulnaris lateralis tendons (see Fig. 10-18). Effusion of the carpal sheath must be differentiated from that of the antebrachiocarpal joint. Concurrent distention of the dorsal aspect of the antebrachiocarpal joint or distention of the distal aspect of the carpal sheath (lateral or medial, distal to the flexor retinaculum on the palmar aspect of the metacarpal region) are signs that are helpful in determining this. Ultrasonographic evaluation or positive contrast radiography can be useful adjunct diagnostic techniques. Synoviocentesis can be performed either in the proximal or distal aspect of the sheath, using a 20-gauge, 2.5-cm needle and 10 to 15 ml of local anesthetic.

Olecranon Bursa This technique is mentioned to be complete, but we have never found an indication to perform analgesia of this bursa (see Fig. 10-19). If distended, this bursa could be entered using the same techniques described for other bursae. Rarely, local analgesia over implants used to repair olecranon process fractures is necessary to investigate whether implant removal is indicated.

Bicipital Bursa Bicipital bursitis and shoulder lameness are frequently diagnosed but in reality are uncommon causes of lameness, if the clinician religiously adheres to the principles of diagnostic analgesia. However, bicipital bursitis and tendonitis, and proximal humeral osteitis, fractures, or osseous cyst-like lesions can cause lameness, and are diagnosed using analgesia of the bicipital bursa. The bicipital bursa is located between the greater and lesser tubercles of the humerus and the overlying tendon of origin of the biceps brachii muscle. Synoviocentesis of the bicipital bursa is routinely performed from a lateral approach, but if severe effusion exists, the bursa can be accessed medially. The injection site is located just cranial to the humerus, 4 cm proximal to the distal aspect of the deltoid tuberosity.38 Alternatively the site can be located by finding a point 3 to 4 cm distal and 6 to 7 cm caudal to the cranial process of the greater tubercle (see Fig. 10-19).19 Subcutaneous infiltration of local anesthetic solution at the site can be used but is rarely needed. An 18-gauge, 9-cm needle is directed in a proximal, medial, and slightly cranial direction and can be “walked off” (shaft of the needle in contact with the bone) the cranial cortex of the humerus. A change in resistance is felt, and synovial fluid may be seen in the needle hub or can be aspirated. Ten to 20 ml of local anesthetic solution is used. If injection is difficult, synovial fluid cannot be retrieved, and retrieving

CHAPTER 10 anesthetic solution already injected is not possible, the bursa likely has not been entered. An alternative is to use an ultrasound-guided technique.

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response to the block will be interpreted as lameness in the foot, when in reality lameness involves the metatarsophalangeal joint).

Low Plantar Block

PERINEURAL ANALGESIA IN THE HINDLIMB Perineural analgesia in the distal hindlimb is similar to that described for the forelimb. Minor differences in innervation and anatomy must be taken into consideration, however. Technical differences in whether, or how, the limb is held and other intangible differences exist. Most clinicians are not as familiar, or frankly as comfortable, with performing hindlimb analgesic techniques, and this is particularly true with perineural analgesia. It takes a dedicated lameness detective to be enthusiastic about hindlimb analgesia, particularly in fractious or highly strung horses. Obviously, safety for the veterinarian and assistants is paramount, and physical and chemical restraint become important. Performing intraarticular analgesia is far easier, but the clinician must keep in mind that perineural techniques are much more effective in abolishing subchondral bone pain. Therefore false-negative results will likely be obtained if one is limited to only intraarticular procedures. We generally recommend that most perineural techniques distal to the tarsus be performed with the limb held off the ground by an experienced assistant, but personal preference can of course prevail. In some instances, such as when performing plantar digital analgesia, the anatomy is much easier to identify when the limb is bearing weight. To limit the number of hindlimb injections in horses that lack clinical signs referable to the digit, starting with the low plantar block may be reasonable, in lieu of performing sequential blocks starting with palmar digital analgesia. Of course, performing blocks distal to this site at another time may be necessary if baseline lameness is discovered using this approach. The clinician should take care when testing the efficacy of hindlimb blocks, and using a pole or similar device may be safer than using forceps.5 Complete abolition of skin sensation in the hindlimb is less likely than in the forelimb, because the distribution of cutaneous innervation varies.

Plantar Digital Analgesia This analgesic technique is essentially the same as in the forelimb (see Fig. 10-5). The prevalence of lameness abolished by palmar digital analgesia in the hindlimb is considerably lower than in the forelimb but is not zero, and therefore this block should still represent a good starting point for a horse with undiagnosed lameness. Because of the reciprocal apparatus, the digit is constantly flexed when the limb is held off the ground, and this block can be slightly more difficult to perform in this position.

Dorsal Ring Block of the Pastern The section on the dorsal ring block of the pastern in the forelimb describes this technique (see Fig. 10-5). This block requires several needle insertions and can be difficult to perform if the limb is held off the ground, because the dorsal aspect of the pastern is constantly flexed, making subcutaneous injection difficult.

Basisesamoid and Abaxial Sesamoid Blocks Basisesamoid and abaxial sesamoid blocks present no essential differences between the forelimbs and hindlimbs (see Fig. 10-5). Our philosophical points about the basisesamoid block (see forelimb) hold true in the hindlimb as well. The abaxial sesamoid block is avoided, if possible, in racehorses, because of the high prevalence of lameness involving the metatarsophalangeal joint may lead to inadvertent misdiagnosis (a positive

Analgesia of the metatarsophalangeal joint region is achieved using the low plantar block, a procedure similar to the low palmar block (see Fig. 10-7). This block is one of the most overlooked but most useful of all perineural techniques. It is essential to block the medial and lateral plantar, the medial and lateral plantar metatarsal, and the dorsal metatarsal nerves. Anecdotal information suggests that some practitioners may not include the plantar metatarsal nerves when performing this block. The plantar metatarsal nerves supply innervation to the subchondral bone of the distal third metatarsal bone (MtIII), and to provide analgesia to this important area, these nerves need to be blocked. In fact a modification of this technique can be used in horses suspected of having subchondral, non-adaptive remodeling of MtIII, a common diagnosis in the Standardbred and Thoroughbred racehorse (see Chapters 108 and 109). A positive response to an independent block of the lateral plantar metatarsal nerve can help establish this syndrome as the cause of lameness. The only difference between the low palmar and low plantar blocks involves the dorsal aspect of the limb (see Fig. 10-7). Skin sensation laterally and medially is retained after this block, unless a circumferential, subcutaneous ring block is used. In the forelimb, it is only necessary to use subcutaneous infiltration to the dorsal midline. Alternatively, the dorsal metatarsal nerves can be blocked individually.

High Plantar Nerve Block The high plantar or sub-tarsal block is one of the most important but often overlooked perineural analgesic procedures in the horse. This block is used to diagnose suspensory desmitis, arguably one of the most important lameness conditions in the hindlimb. However, suspensory desmitis can be a catchall diagnosis in some horses with occult hindlimb lameness, and the high plantar block must be done to confirm the authentic location of pain. The tarsometatarsal joint has distoplantar outpouchings (similar to but less extensive than the distopalmar outpouchings of the carpometacarpal joint) that may complicate tarsometatarsal intra-articular or high plantar analgesic techniques (Fig. 10-21). However, this is certainly less of a problem in the hindlimb than in the forelimb. For example, inadvertent penetration of the tarsometatarsal joint occurred in only 5% of limbs in which high plantar analgesia was performed, at a level of 1.5 cm distal to the tarsometatarsal joint. However, contrast material was found in the tarsal sheath in 40% of limbs, adding yet another dimension to this already somewhat difficult blocking technique. False-negative results have been attributed to inadvertent injection into blood or lymphatic vessels.47 The clinician should take care in preparing the limb for this procedure and interpreting the results. It is possible, although not likely, that when performing a high plantar block, local anesthetic solution could be inadvertently placed in the tarsometatarsal joint. A good chance also exists, however, of inducing analgesia of the tarsal sheath. Comprehensive evaluation using multiple imaging modalities is needed when attempting to differentiate causes of lameness in this important area. The medial and lateral plantar and the medial and lateral plantar metatarsal nerves are blocked, and a circumferential dorsal ring block provides complete analgesia to the metatarsal region. Blocking only the plantar metatarsal nerves can abolish pain associated with the suspensory ligament. Most clinicians do not include the dorsal ring block, but it is necessary to do so to eliminate lameness resulting from injury of the dorsal cortex of MtIII or to suture lacerations in this

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Diagnosis of Lameness Tibial nerve Medial plantar nerve

Lateral plantar metatarsal nerve Lateral plantar nerve

Medial plantar metatarsal nerve Medial plantar nerve

Lateral plantar nerve Deep branch of lateral plantar nerve

Lateral and medial plantar metatarsal nerves

The high plantar block is performed at a level 4 cm distal to the proximal aspect of fourth metatarsal bone and on the medial side 3 cm distal to the proximal aspect of second metatarsal bone. The needles are inserted axial to the respective splint bone and advanced deep to contact the plantar surface of the third metatarsal bone. Anesthetic solution is deposited in this location to block the lateral (medial) plantar metatarsal nerves and in a more superficial position as the needle is withdrawn blocks the lateral (medial) plantar nerves (inset).

Fig. 10-22

Positive contrast arthrogram of the tarsometatarsal joint showing short, distoplantar outpouchings extending distally toward the origin of the suspensory ligament. Inadvertent penetration of these pouches occurs during subtarsal or high plantar analgesic techniques.

Fig. 10-21

area. This block is performed most commonly and safely with the limb held off the ground. Although uncommon to rare, needle breakage is a complication during high plantar analgesia, and for this reason we prefer to use needles no smaller than an 18- to 20-gauge and 4 cm long. At this level on the plantar aspect of the limb, it is impossible to palpate nerves, and unlike the high palmar block, only one injection site exists for each, on the medial and lateral aspects of the limb. The needle is placed just distal to the tarsometatarsal joint and axial to the fourth metatarsal bone and inserted until contact is made with MtIII (Fig. 10-22). A minimum of 5 ml of local anesthetic solution is deposited at this deep location, and an additional 5 ml is deposited as the needle is withdrawn, leaving a definite bleb in the subcutaneous tissues. Some clinicians prefer lower volumes of local anesthetic solution. Additional local anesthetic solution can be used without risk, and a common modification is flooding the origin of the suspensory ligament with an additional 5 to 10 ml of local anesthetic solution. The procedure is then repeated medially, and the needle is inserted axial to the second metatarsal bone. To complete the block, a circumferential subcutaneous ring block is performed. The clinician must take care not to lacerate the dorsal metatarsal artery or the saphenous vein during this procedure.

Fibular (Peroneal) and Tibial Nerve Block Analgesia of the distal crus and tarsus or entire distal hindlimb is induced using the fibular and tibial nerve blocks. These blocks are used most commonly in horses with distal hock joint pain, in which intra-articular analgesia is difficult or impossible to perform. The fibular and tibial nerve blocks, when completed successfully, are more effective in eliminat-

ing pain from the complex hock joint than is intra-articular analgesia. The fibular and tibial nerve blocks also are useful in eliminating pain associated with subchondral trauma of the distal tibia and talus, distally located tibial stress fractures, the tarsal sheath, the distal aspect of the common calcaneal tendon, the calcaneal bursa, and the plantar aspect of the hock. The clinician should keep in mind that if the high plantar block has not already been performed, the fibular and tibial nerve blocks eliminate pain associated with proximal suspensory desmitis. The deep fibular nerve is blocked at a site located laterally, 10 cm proximal to the point of the hock (tuber calcanei), in the groove between the long and lateral digital extensor muscles (Fig. 10-23). In this groove the superficial fibular nerve is easily palpated and can be rolled against the fascia of the crus. An 18- to 22-gauge, 4-cm needle is inserted to the hub or until it contacts the lateral tibial cortex, and 10 to 15 ml of local anesthetic solution is injected, beginning deep and continuing as the needle is withdrawn. The needle can be re-directed in a fan-shaped pattern if desired to ensure complete block of the deep branch of the fibular nerve. Seeing blood in the needle hub is common, a reliable sign of accurate needle placement, because the cranial tibial vein and artery are located close to the deep peroneal nerve.48 Performing the tibial block first is therefore preferable, as is warning the client that blood may appear.5 The superficial fibular nerve is blocked as the needle is withdrawn from deep within the injection site. Additional local anesthetic solution (5 to 10 ml) is placed in this subcutaneous location. The tibial nerve is blocked at a site 10 cm proximal to the tuber calcanei, cranial to the common calcaneal tendon, and caudal to the deep digital flexor tendon (see Fig. 10-21). The nerve can be palpated as a firm cord-like structure with the limb in a flexed position. For this reason, performing this block is easier with the leg not bearing weight. Although the tibial nerve is slightly more superficial, medially, the injection can be performed either medially or laterally. A 20-gauge, 2.5-cm needle is inserted laterally, and 15 ml of local anes-

CHAPTER 10 Deep fibular (peroneal) nerve

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b Tibial nerve

a Superficial fibular (peroneal) nerve

Lateral digital extensor

Lateral view of the left crus and tarsus showing the fibular (peroneal) and tibial nerve block. The deep and superficial fibular nerves are blocked by finding the groove between the long and lateral digital extensor muscles, 10 cm proximal to the tarsus, in which the superficial fibular nerve is palpable. The needle (a) is advanced deep to block the deep branch and withdrawn to a more superficial position to deposit local anesthetic solution subcutaneously to block the superficial branch. The tibial nerve block (b) is performed by palpating the nerve just cranial to the common calcaneal tendon (from either a lateral or medial approach) in a location about 10 cm proximal to the tuber calcanei.

Fig. 10-23

thetic solution is injected over the nerve. The needle tip should be palpated under the skin, medially, to ensure the proper depth of penetration. Local anesthetic solution can be placed using a fan-shaped injection technique, but the horse will object if the tibial nerve is penetrated. Although deep pain will be abolished if these nerves are successfully blocked, superficial sensation persists on the medial aspect and occasionally in the caudal (plantar) aspect of the limb. To use the fibular and tibial nerve blocks therapeutically, it is necessary to perform a circumferential subcutaneous ring block to completely abolish skin sensation. After the fibular and tibial nerve blocks, paradoxically, pre-existing toe drag may persist or increase, despite resolution of weight-bearing lameness.5 Some horses stumble or knuckle, indicating loss of extensor muscle function, but this is not common and certainly not a necessary sign to suggest complete analgesia has been obtained. However, exercising a horse at speed or over fences should be avoided. Because of nerve size and depth, we suggest that additional time be given, as much as 20 to 30 minutes, to evaluate the effect of this block before reaching a final conclusion. Dyson has recognized improvement in horses up to 1 hour after blocking and warns that proceeding with a stifle block too soon leads to false-positive results.5 The fibular and tibial nerve blocks are not commonly performed in practice, at least in the United States, and at best may result in only 50% to 80% improvement in lameness score, particularly in those horses with severe distal hock joint pain. Allowing more time for maximal response and taking a realistic approach to the percent improvement expected are warranted when using the fibular and tibial nerve blocks. Intrasynovial analgesic techniques are certainly more specific than are the fibular and tibial nerve blocks, and although the fibular and tibial nerve blocks have limitations, the lameness diagnostician should become familiar and comfortable with this procedure. Proficiency in performing these blocks is a must for accurate diagnosis of hindlimb lameness. Performing the fibular and tibial components can independently improve specificity of the fibular and tibial nerve blocks.

Analgesia of the distal interphalangeal and proximal interphalangeal joints in the hindlimb is exactly the same as that described for the forelimb. Analgesia of the metatarsophalangeal (metatarsophalangeal) joint is the same as that described for the metacarpophalangeal joint. Perineural analgesic techniques should be used, whenever possible, because subchondral pain is more completely abolished using these techniques, and false-negative results are less likely.

Tarsus Tarsometatarsal Joint The most reliable site for arthrocentesis of the tarsometatarsal joint is a lateral approach, just proximal to the fourth metatarsal bone. At this site is a subtle but consistent depression that can reliably be palpated. A 20-gauge, 2.5-cm needle is inserted in a craniomedial and slightly distal direction (Fig. 10-24). The needle can usually be inserted to the hub, but occasionally it hits articular cartilage. Synovial fluid is consistently retrieved, but we find it interesting that even in horses without lameness of the tarsometatarsal joint, the fluid is generally watery, lacking what is thought to be normal viscosity. In most horses, 4 to 8 ml of local anesthetic solution can be injected without encountering elevated intra-articular pressures and patient discomfort. Anecdotal reports of a subtle pop or sudden decrease in pressure have been attributed to communication between the tarsometatarsal and centrodistal (distal intertarsal) joints. In reality, this most often results from rupture of the tarsometatarsal joint capsule and subsequent deposition of anesthetic solution (or medication) extraarticularly into the tarsal space and not the centrodistal joint. We recommend using no more than 4 to 8 ml of local anesthetic solution or injecting only that amount of local anesthetic solution necessary to develop moderate intra-articular resistance to avoid inadvertent deposition into the intertarsal space. An alternative site for tarsometatarsal arthrocentesis is a medial approach, similar to that described for the centrodistal joint. The issue of communication between the distal tarsal joints is important from diagnostic and therapeutic standpoints. Studies have shown that the tarsometatarsal and centrodistal joints communicate in 8% to 35% of normal horses.47,49,50 Communication between the tarsometatarsal joint (and presumably the centrodistal joint) and the talocalcaneal-centroquatral (proximal intertarsal) and tarsocrural joints was shown to be about 4% in an in vivo study, after injection of latex in the tarsometatarsal joint.50 A common misconception is that a single injection into the tarsometatarsal joint also provides analgesia or treats the centrodistal joint. In addition, some clinicians preferentially inject a large volume of anesthetic solution, hoping to block or medicate the tarsometatarsal and centrodistal joints. However, based on the low communication rate, the clinician should consider the tarsometatarsal and centrodistal joints to be separate synovial cavities. Because the tarsometatarsal joint has distoplantar outpouchings, abolishing pain associated with the proximal suspensory attachment or lesions involving the proximal aspect of the third metatarsal bone is also possible when performing tarsometatarsal analgesia. Accurate differential diagnosis for pain involving the lower hock joints and proximal metatarsus depends on careful interpretation of response to diagnostic analgesia and evaluation of ancillary images.

Centrodistal Joint Compared with the tarsometatarsal joint, arthrocentesis of the centrodistal joint is relatively difficult. The centrodistal joint is small, and in fact inserting a needle any larger than 22 to 25 gauge into this joint is difficult, even in horses with

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Joint capsule

c

c a

A

b

Tendon sheath

a

B Joint capsule

a

Mt IV Joint capsule

Cunean tendon

Cunean bursa

Saphenous vein

b A, Lateral and plantar (inset) views of the left tarsus showing sites for tarsal arthrocentesis. The tarsometatarsal joint is entered by locating the depression just proximal to the proximal aspect of the fourth metatarsal bone (Mt IV) and inserting a needle (a) in the plantar aspect of this depression, directing it dorsomedially. The dorsomedial pouch of the tarsocrural joint (b) is entered either just lateral or medial to the dorsal branch of the saphenous vein or, alternatively, using the plantarolateral pouch (c). B, Medial view of the left tarsus. The centrodistal joint is entered by placing the needle (a) in the depression formed between the fused first and second tarsal bones, the third tarsal bone, and the central tarsal bone, which is at the proximal edge or just slightly distal to the proximal edge of the cunean tendon. The cunean bursa (dotted ellipse) is entered by locating the distal border of the cunean tendon and inserting the needle (b) under the tendon from the distal aspect or placing it directly through the tendon. The distended tarsal sheath (c) can be entered proximal, just caudal to the tarsocrural joint capsule or distal (not shown) to the tarsus.

Fig. 10-24

normal width of joint space. We have tried several alternative sites, including dorsomedial and dorsolateral approaches. Anecdotal reports suggest the dorsomedial approach, about 1 cm distal to the distal end of the medial trochlear ridge, is a consistent, reliable injection site, but we often enter the proximal intertarsal joint from this approach. An outpouching of the centrodistal joint exists dorsolaterally, but the perforating tarsal artery precludes use of this site in vivo. For these reasons, we use a medial approach at the distal aspect of, or through, the cunean tendon (medial tendon of insertion of the cranialis tibialis muscle), a structure that can be readily palpated. Using the fingertip, the distal edge of the cunean tendon is moved proximally to reveal an ill-defined concavity, the articulation of the fused first and second tarsal bones, with the third and central tarsal bones (see Fig. 10-24). This depression is sometimes located in a slightly more proximal location. This injection technique is one of the few commonly performed by standing on the opposite side of the horse. A skin bleb is useful because in most horses inserting a needle directly into the joint is difficult, and multiple attempts may be necessary. A 22- to 25-gauge, 2.5-cm needle is inserted directly in a lateral direction, horizontally, roughly parallel to the central and third tarsal articulation, perpendicular to the skin. Slight redirection of the needle may be necessary, and in many horses joint fluid is not obtained. If the needle can be inserted to a depth of 1 to 1.5 cm, it is likely properly positioned even if synovial fluid cannot be retrieved. Fluid retrieved in a more superficial location likely indicates penetration of the cunean bursa. In horses in which diagnostic information or therapeutic injection is critical and any question of needle placement exists, radiographs are warranted. A maximum of 4 to 5 ml can be injected. If a larger volume can be comfortably injected, the needle tip is likely in the tarsal space or in the proximal intertarsal joint, or a commu-

nication with the tarsometatarsal joint exists. If the injection is difficult to perform, the needle is likely malpositioned in the subcutaneous tissues, or the needle tip is touching articular cartilage. Most clinicians attempt injection of the centrodistal joint after first injecting the tarsometatarsal joint, and in some instances, medication or local anesthetic solution readily flow from the needle. The typical response is, “There must be a communication between the tarsometatarsal and centrodistal joints.” However, this clinical finding most often results from inadvertent penetration of the distended medial pouch of the tarsometatarsal joint. Fluid accumulation in the tarsal space from the tarsometatarsal joint injection can cause the same result, if the needle enters the tarsal space rather than the centrodistal joint space. In horses with advanced osteoarthritis or even in horses with early distal hock joint pain, it may be difficult or impossible to be confident that intra-articular analgesia has been achieved. An alternative approach to provide tarsal analgesia is first to perform sequential, intra-articular analgesia of the tarsometatarsal and tarsocrural joints, and then to perform the fibular and tibial nerve blocks if lameness persists. If lameness abates after the fibular and tibial nerve blocks, a presumptive diagnosis of centrodistal joint pain can be made, assuming other sources of pain abolished by this block can be ruled out.

Tarsocrural Joint Arthrocentesis of the tarsocrural joint is straightforward and easy compared to some joints, because of extensive and multiple dorsal and plantar outpouchings. In horses with moderate to severe effusion, identifying four distinct outpouchings—the dorsolateral, dorsomedial, plantarolateral, and plantaromedial pouches—is easy. The clinician must keep in mind that the tarsocrural and proximal intertarsal joints communicate through a large fenestration at the dorsal aspect of the joints in adult horses, although in weanlings and yearlings

CHAPTER 10 the fenestration cannot be seen during arthroscopic examination. Any one of the tarsocrural joint pouches can be used, but the most common site of entry is on either side of the saphenous vein, in the dorsomedial pouch (see Fig. 10-24). This particular site is preferred in horses without obvious effusion. An alternative site is the plantarolateral pouch. The most consistent site to use is the distal aspect of the dorsomedial pouch, just distal to the medial malleolus of the tibia and medial to the saphenous vein. An 18- to 20-gauge, 2.5- or 4-cm needle is used to deposit 20 to 30 ml of local anesthetic solution into the tarsocrural joint. In horses with severe osteoarthritis of the tarsocrural joint or those with subchondral bone pain, as much as 30 to 50 ml of local anesthetic solution is necessary to abolish pain. In these horses, a falsenegative result is common if only 10 to 20 ml of local anesthetic solution is used. The plantar pouches can be useful alternative sites for arthrocentesis, if the dorsomedial pouch is unsuitable, as sometimes occurs with a wound, swelling associated with trauma of the fibularis (peroneus) tertius, or superficial dermatitis. The plantar pouches must be differentiated from distention of the tarsal sheath or other forms of thoroughpin. Although the dorsal and plantar pouches freely communicate, anatomically, flushing from one aspect of the tarsocrural to the other when the horse is in a weight-bearing position may be difficult. Fluid flow between articular surfaces and joint spaces under collateral ligaments is likely restricted when horses are in a weight-bearing position. This same phenomena occurs in other joint spaces.

Stifle Joint The three compartments of the equine stifle joint are the medial femorotibial, lateral femorotibial, and femoropatellar joint compartments. Most consider that the femoropatellar and medial femorotibial joints communicate in almost all horses and that the lateral femorotibial compartment is solitary, but recent anatomical studies have shed new light on this time-honored concept. The frequency of communication between the medial femorotibial and femoropatellar compartments was found to be 60% to 74% in normal horses, when the injection was performed from the femoropatellar compartment.51,52 The frequency of communication was higher (80%) when the injection was performed in the medial femorotibial compartment.51 It is important to realize, however, that the medial femorotibial and femoropatellar compartments did not communicate in all horses. Inconsistency in communication depending on which compartment was injected was attributed to directionality in the normal foramen or slit between the two compartments (flow easier from the medial femorotibial to the femoropatellar compartment). The time-honored assumption that the lateral femorotibial joint is a solitary compartment was also challenged. The lateral femorotibial joint communicated with the femoropatellar joint in 3% to 18% of horses but was indeed solitary in the majority of normal horses51,52 Communication may be more frequent after trauma and certainly after arthroscopic surgical procedures. We recommend that each compartment of the stifle joint be injected independently, either sequentially or simultaneously, to avoid confusing results during stifle analgesia. The variable degree of communication will obviously cause some degree of uncertainty in diagnosis. The same principle is recommended for therapy as well. Needle insertion in the stifle joints is complicated by a natural tendency of horses to react inappropriately to manipulation compared with other areas of the limbs. Horses seem to object to simple palpation of the stifle and may become fractious during arthrocentesis. To avoid excessive manipulation during injection, we have found it useful to attach an extension set to the needle, a procedure

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that obviates the need to touch the needle or skin when attaching the syringe. If necessary, the extension set may be useful for many diagnostic procedures, particularly in the hindlimbs. In general, 20 to 30 ml of local anesthetic solution is used in each of the medial femorotibial, lateral femorotibial, and femoropatellar compartments. A common misconception is that long needles are needed to perform arthrocentesis of the stifle joint compartments. In fact, some racehorse trainers will insist that “the long needles, Doc” are necessary to achieve success in medicating the femoropatellar joint. If arthrocentesis is performed with the limb in a weight-bearing position, the joint capsules can easily be penetrated with needles no longer than 4 cm. In the flexed position, using a spinal needle when performing femoropatellar arthrocentesis is necessary. We prefer to have the horse in a weight-bearing position, with the limb slightly ahead of the contralateral limb, a position that allows the clinician to palpate landmarks readily without undue tension on patellar and collateral ligaments. Arthrocentesis of the medial femorotibial joint is performed at a site located just caudal to the medial patellar ligament, cranial to the medial collateral ligament, and 1 to 2 cm proximal to the medial tibial plateau (Fig. 10-25). In the normal horse a distinct depression occurs at this location, but in horses with effusion, a considerable bulge in the joint capsule can be present. An 18-gauge, 4-cm needle is inserted perpendicular to the skin and can be redirected or rotated if synovial fluid is not immediately retrieved. A common mistake is to insert the needle too far distally, and in this position the needle tip enters ligaments or the medial meniscus. Arthrocentesis of the lateral femorotibial joint is more challenging than for the other two compartments, because the lateral joint pouch is small and located deep within tissue. The site is caudal to the long digital extensor tendon and cranial to the lateral collateral ligament, just proximal to the lateral tibial plateau (see Fig. 10-25). These landmarks are easily palpated, but distention of the joint capsule is not, in contrast to the medial femorotibial joint. An 18-gauge, 4-cm needle is inserted horizontally and directed in a slight caudomedial direction. Retrieval of synovial fluid varies, and redirecting or rotating the needle is often necessary. An alternate site can be used, located caudal to the lateral patellar ligament and cranial to the long digital extensor tendon, and just proximal to the tibial plateau. Arthrocentesis of the femoropatellar joint is most commonly performed at a sub-patellar site and either lateral or medial to the middle patellar ligament. The joint capsule can be easily palpated even in most normal horses, if the horse is in a weight-bearing position. With the horse in a weightbearing position, an 18-gauge, 4-cm needle is inserted perpendicular to the skin, or directed slightly proximally, until joint fluid is obtained or the needle tip contacts articular cartilage of the distal femur (see Fig. 10-25). The clinician does not need to angle the needle sharply proximally using this technique. What is sometimes frustrating is that even in horses with obvious femoropatellar effusion, a steady flow of synovial fluid cannot be obtained, and attempting aspiration of fluid with a syringe is seldom helpful, because synovial villi readily plug the needle, making aspiration impossible. Some clinicians perform femoropatellar arthrocentesis with the limb in a non–weight-bearing position, in which case a 9-cm spinal needle is used and the needle is directed severely proximally, between the patella and distal femur. An alternative lateral approach to the femoropatellar joint was described.53 An 18-gauge, 4-cm needle is inserted into the lateral cul-desac of the femoropatellar compartment, located about 5 cm proximal to the lateral tibial plateau, caudal to the lateral patellar ligament and the lateral trochlear ridge of the femur. The needle is directed perpendicular to the long axis of the femur until bone is contacted (about 1.5 to 2 cm in most

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e

Medial patellar ligament

Lateral patellar ligament

Lateral collateral ligament

Medial collateral ligament

a d b

c

A Long digital extensor muscle

B

A, Cranial view of the left stifle. The medial femorotibial joint (a) is approached from a site between the medial patellar and medial collateral ligaments, about 2 cm proximal to the proximal aspect of the tibia. The femoropatellar joint (b) most commonly is injected either between the lateral and middle patellar ligaments or between the middle and medial patellar ligaments (not shown). The needle is directed proximally in this subpatellar position. B, Lateral view of the left stifle. The lateral femorotibial joint can be approached by placing the needle caudal to the long digital extensor tendon and cranial to the lateral collateral ligament (c) or inserting it between the lateral patellar ligament and the cranial edge of the long digital extensor tendon (d). An alternative site for arthrocentesis of the femoropatellar joint (e) can be used by passing the needle through the lateral femoropatellar ligament.

Fig. 10-25

horses) and then withdrawn slightly until synovial fluid is collected. Proposed advantages of this approach are a reduced potential for iatrogenic injury to the articular cartilage and more reliable recovery of synovial fluid compared to the subpatellar approach.54

Coxofemoral (Hip) Joint Although the coxofemoral joint is relatively large and the landmarks for needle insertion are consistent, injection is considered to be a daunting task. Few of us perform this injection technique on a regular basis, and depth of penetration makes accurate needle placement difficult. An 18-gauge, 15-cm (6inch) spinal needle is adequate for all but the largest of draft horses. A needle of this length should be inserted carefully, and if the horse is moving or fractious, it may be necessary to provide sedation. The site is in the angle formed between the long caudal and short cranial processes of the greater trochanter of the femur (Figs. 10-26 and 10-27). This site can be difficult to palpate in heavily muscled horses, and ultrasonographic evaluation can be useful to identify the injection site. The most difficult landmark to palpate consistently, but an important one nonetheless, is the cranial process. The site is between the two processes and not caudal to the trochanter.

Before the needle is inserted, blocking the injection site may be useful. Because the shaft of the needle is handled, sterile gloves are recommended. Needle direction is important. The needle is inserted in a slightly craniomedial direction and slightly distally and directed just dorsal to the femoral neck, until the joint capsule is penetrated. In most horses, a subtle pop can be felt as this occurs. “Walking” the needle off the femoral neck may be useful, using the bone as a guide to the coxofemoral joint. In most adult light breed horses, this occurs within 3 to 5 cm of the hub of the needle. Synovial fluid is reliably retrieved from the coxofemoral joint, spontaneously or by aspiration. A large volume of local anesthetic solution should not be injected if synovial fluid is not readily obtained, but injecting a small volume and attempting retrieval with a syringe is useful. It is possible inadvertently to inject local anesthetic solution around the sciatic nerve, causing temporary paresis, if the needle is caudally malpositioned, and therefore anesthetic solution should not be injected if any doubt exists that the needle is correctly positioned. Twenty-five to 30 ml of local anesthetic solution is used. Most patients are evaluated in 20 to 30 minutes, but in horses with fractures of the acetabulum the clinician should expect only 50% improvement in lameness score, and improvement may be short lasting (15 to 30 minutes).

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Joint capsule (cut)

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Sciatic nerve

Cranial process of greater trochanter

a Caudal process of greater trochanter

Sciatic nerve

a Gluteus medius muscle

b

Greater trochanter of femur

Lateral and dorsal (inset) views of the left coxofemoral joint. Arthrocentesis of the coxofemoral joint is performed by inserting the needle (a) in the angle formed between the caudal and cranial processes of the greater trochanter of the femur. The needle is inserted slightly cranially, distally, and medially just dorsal to the shaft of the femoral neck (inset). This view (b) shows the seldom used diagnostic technique of synoviocentesis of the trochanteric bursa.

Fig. 10-26

ANALGESIA OF HINDLIMB BURSAE AND TENDON SHEATHS Analgesia of the navicular bursa and digital flexor sheath in the hindlimb is the same as in the forelimb.

Cunean Bursa Occasionally, injecting the cunean bursa is necessary to assess the role of the cunean bursa and tendon in horses with distal hock joint pain, to perform cunean tenectomy, or to medicate the structure. The cunean bursa is seldom the sole source of distal hock joint pain, but can play a role, so analgesia or medication of this structure is sometimes combined with other injections. The cunean bursa is between the distal tarsal bones and the medial branch of the cranialis tibialis tendon (called the jack tendon or cord) but is seldom palpable (see Fig. 10-24). The distal aspect of the cunean tendon is usually easily palpated, however, by starting at the distal aspect of the hock and sliding the fingertip in a proximal direction. Retrieving synovial fluid is unusual but possible, but during injection the clear outline of the bursa can be seen as it distends. A 20- to 22-gauge needle is inserted deep to the distal edge of the cunean tendon and directed in a proximal direction, and 3 to 5 ml of local anesthetic solution is injected. We prefer this approach, but alternatively the needle can be inserted perpendicular to

Fig. 10-27 Arthrocentesis of the right coxofemoral joint. Using an extension set between needle and syringe, a technique that reduces the amount of manipulation necessary during the procedure, facilitates arthrocentesis of this and other joints.

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the skin and directly through the tendon itself until bone is contacted.

Tarsal Sheath Analgesia of the tarsal sheath is performed to confirm the structure as a source of lameness associated with traumatic and infectious tenosynovitis (although the response may be limited in face of infection) and various osseous lesions, such as those involving the sustentaculum tali, or unusual exostoses (osteochondroma). The tarsal sheath surrounds the deep digital flexor tendon from a point approximately level with the tuber calcanei and extends to a point 2 to 3 cm distal to the tarsometatarsal joint. Distention of the tarsal sheath is commonly called thoroughpin, but occasionally, thoroughpin appears as fluid swelling proximal to the tarsus that does not involve the tarsal sheath. The deep digital flexor tendon is located medial to the calcaneus as it crosses the sustentaculum tali. The heavy tarsal retinaculum medially and the calcaneus laterally restrict outpouching of the tarsal sheath to the proximal and distal aspects. The clinician should take care to differentiate tarsal sheath effusion from distention of the plantar pouches of the tarsocrural joint. A 20-gauge, 2.5-cm needle is used to inject 10 to 15 ml of local anesthetic solution.

localized area of pain, into which a needle can be inserted safely, is fair game for local analgesia. The clinician must be aware, however, that local infiltration may not provide total analgesia to the region, mostly because the entire nerve supply to the region cannot be blocked. Incomplete analgesia is common in horses with bony lesions, such as bucked shins, because deep pain from the cortex of McIII is difficult if not impossible to eliminate using subcutaneous infiltration of local anesthetic solution. In most instances, perineural analgesia for this particular condition is preferred. Local infiltration is performed in many horses in lieu of perineural technique, or in horses in which perineural analgesia has localized pain to a general region, but conflicting or numerous clinical problems exist. An advantage of local infiltration is that proprioception is not lost, and horses can be moved at speed for re-evaluation after this form of analgesia. Efficacy can be assessed by deep, direct digital palpation, to confirm that the previously identified source of pain was eliminated by local analgesia.

Splints

Indications for analgesia of the calcaneal bursa include traumatic and infectious bursitis, tendonitis of the gastrocnemius or SDFT at this level, and osseous lesions of the tuber calcanei. The bursa is located between the SDFT and tuber calcanei. Proximal to the tuber calcanei, the bursa is interposed between the SDFT and the gastrocnemius tendon. When distended, an unusual clinical finding, the bursa is palpable as medial and lateral outpouchings just proximal to the tuber calcanei. Smaller outpouchings are often discernable just distal to the tuber calcanei but are inconsistent. The bursa can be accessed for injection at any of these outpouchings. A 20- to 22-gauge, 2.5- or 4-cm needle is used to inject 10 ml of local anesthetic solution, after retrieving fluid for analysis if indicated (see Fig. 10-24). Pain may take 20 to 30 minutes to abate in horses with osseous lesions or with severe lameness.

A common suspected cause of lameness in many horses are exostoses associated most commonly with the second (McII) and fourth (McIV) metacarpal or metatarsal bones (MtII, MtIV) or in combination with the McIII or MtIII. A 20- to 22-gauge, 2.5- to 4-cm needle is used to deposit 5 ml of local anesthetic solution, subcutaneously, over the painful exostosis. The needle is slid directly alongside the proliferative lesion, between skin and bone. For splints involving McII/MtII and McIV/MtIV, it is important to deposit local anesthetic solution abaxial and axial (between the suspensory ligament and splint bones) to the lesion. In some horses proliferative changes involve only the axial aspect of McII/MtII or McIV/MtIV (blind splints), and it is critical to block in this location. In others with primary proliferation between McII/MtII, McIV/MtIV, and McIII/MtIII, subcutaneous injection will suffice. When local anesthetic solution is infiltrated on the axial aspect of the splint bones, the palmar/plantar metacarpal/ metatarsal nerves are likely blocked, making it possible to abolish pain from a more distal site and leading to misinterpretation of results.

Trochanteric Bursa

Suspensory Ligament Origin

Seldom does an indication exist to block the trochanteric bursa, although injections in this region are commonly performed to manage bursitis and muscle pain (see Chapter 48). The trochanteric bursa is located between the tendon of insertion of the gluteus accessorius muscle and the cranial process of the greater trochanter of the femur (see Fig. 10-26; see also Chapter 48). In normal horses, this bursa is small and likely has minimal synovial fluid. Synoviocentesis is performed using an 18- to 20-gauge, 4-cm needle, although in larger, more heavily muscled horses, a longer needle may be necessary. The needle is inserted perpendicular to the skin, directly over the cranial aspect of the greater trochanter until contact with bone is made. We have had difficulty retrieving fluid even in lame horses that have a positive response to analgesia. Generally, 5 to 10 ml of local anesthetic solution is injected until pressure is felt. If local anesthetic solution can be aspirated, the needle was likely in the bursa, but if not, the injection was likely performed in the surrounding tissues.

Local infiltration or flooding the palmar/plantar metacarpus/metatarsus at the origin of the suspensory ligament is often done in lieu of perineural analgesia, as described previously. This is also referred to by some as sub-tarsal or subcarpal blocks. An 18- to 22-gauge, 2.5- to 4-cm needle can be used to distribute 5 to 15 ml of local anesthetic solution in a fan-shaped pattern, usually from a lateral injection site just axial to McIV/MtIV. It is important to use adequate restraint and have the limb in a flexed position when performing this technique. In the hindlimb an 18- to 19-gauge needle should be used to minimize the potential for needle breakage, should the horse kick during the procedure. False-positive results, attributed to inadvertent analgesia of palmar/plantar metacarpal/metatarsal nerves, penetration of the distal outpouchings of the carpometacarpal and tarsometatarsal joints, or penetration of the tarsal sheath can occur.22,47 Compared with high palmar analgesia, the incidence of inadvertent injection of the distal palmar outpouchings of the carpometacarpal joint was highest when local infiltration of the suspensory origin was performed.22

Calcaneal Bursa

LOCAL INFILTRATION IN THE FORELIMB AND HINDLIMB

Curb

Local infiltration of local anesthetic solution in painful soft tissues or over painful bony swellings can be performed at any location, although some areas deserve special mention. Any

Curb, the term used for swelling of the distal, plantar aspect of the tarsus, is a complex condition involving superficial digital flexor tendonitis, long plantar desmitis, subcutaneous swelling, or various combinations of these soft tissue injuries

CHAPTER 10 (see Chapter 79). Local infiltration can partially abolish pain associated with curb and usually involves depositing local anesthetic solution subcutaneously. Completely blocking deep pain associated with the long plantar ligament or SDFT is not possible without using the fibular and tibial nerve blocks. A tibial nerve block may be more specific.5 A 20gauge, 2.5- to 4-cm needle is used to inject 15 to 20 ml of local anesthetic solution with the limb in a flexed position. Adequate restraint and the help of an assistant are mandatory. Local anesthetic solution is infiltrated subcutaneously along the plantar, medial, and lateral aspects of the swelling, but deep injection into or between the SDFT and long plantar ligament is avoided. The medial injection is most comfortably and safely performed by standing on the opposite side of the horse.

Dorsal Spinous Process Impingement This local infiltration technique is performed when attempting to confirm or rule out lameness or poor performance associated with back pain caused by impingement or other pain originating from the dorsal spinous processes of the thoracolumbar vertebrae.55 The horse is usually evaluated under saddle or in harness or on a lunge line, because lameness associated with this condition may be subtle and only manifested under these conditions. The hair along the dorsal midline is clipped, and the site or sites are prepared aseptically. We prefer to use 22-gauge, 9-cm spinal needles, although in most instances shorter needles can easily reach the tops of the dorsal spinous processes. Needles are inserted on the dorsal midline and directed ventrally to the dorsal spinous processes or the inter-spinous space. Markers placed after scintigraphic or radiographic examination are helpful to determine the precise location for blocking or to administer medication. The interspinous space can be located by redirecting the needle in a cranial or caudal direction. If impingement of the dorsal spinous processes exists, it may be impossible to infiltrate between them, but placing local anesthetic solution around the processes is satisfactory.5 Seven to 10 ml (per site) of local anesthetic solution is deposited as the needle is slowly withdrawn, and the horse is reevaluated 10 to 15 minutes later.

Orthopedic Implants Occasionally, pain associated with orthopedic implants is suspected to cause lameness. This is most commonly seen in horses after distal McIII/MtIII condylar fracture repair but can occur after repair of proximal phalanx or olecranon process fractures. Low-grade lameness is most common. Differentiating pain arising from negative interaction of implants with bone or surrounding soft tissue is nearly impossible based on the results of any diagnostic analgesia technique, because innervation to the joint or surrounding tissues is complex. Local anesthetic solution can be injected around screw heads, next to pins and wires or bone plates, and the horse is then re-evaluated. Because lameness is often subtle, improvement is often difficult to judge. A combination of clinical findings and those from ancillary diagnostic techniques is used to determine the role of implant pain.

REFERENCES 1. Melzak R, Wall PO: Pain mechanisms: a new theory, Science 150:971, 1965. 2. Butterworth JF IV, Strichartz GR: Molecular mechanisms of local anesthesia: a review, Anesthesiology 72:711, 1990. 3. Day TK, Skarda RT: The pharmacology of local anesthetics, Vet Clin North Am Equine Pract 7:489, 1991. 4. Jones EW: Veterinary anesthesia, ed 2, Philadelphia, 1987, Lea & Febiger. 5. Dyson S: Personal communication, 2001.

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6. Zotterman Y: Studies in peripheral mechanisms of pain, Acta Med Scand 80:185, 1933. 7. Ross MW: Observations in horses with lameness abolished by palmar digital analgesia. Proc Am Assoc Equine Pract 44:230, 1998. 8. Dyson SJ: Problems associated with the interpretation of the results of regional and intra-articular anaesthesia in the horse, Vet Rec 118:419, 1986. 9. Todhunter RJ: Anatomy and physiology of synovial joints. In McIlwraith CW, Trotter GW, editors: Joint disease in the horse, Philadelphia, 1996, WB Saunders. 10. Caron JP: Neurogenic factors in joint pain and disease pathogenesis. In McIlwraith CW, Trotter GW, editors: Joint disease in the horse, Philadelphia, 1996, WB Saunders. 11. Wyke B: The neurology of joints: a review of general principles, Clin Rheum Dis 7:223, 1981. 12. Dee R: The innervation of joints. In Sokoloff L, editor: The joints and synovial fluid New York, 1978, Academic Press. 13. Fessler JF: The musculoskeletal system—functional anatomy and physiology of diarthrodial joints. In Jennings PB, editor: The practice of large animal surgery, vol 2, Philadelphia, 1984, WB Saunders. 14. Wojtys EM, Beaman DN, Glover RA, et al: Innervation of the human knee joint by substance-P fibers, Arthroscopy 6:254, 1990. 15. Beaman D, Graziano G, Glover R, et al: Substance P innervation of the lumbar facet joints, Spine 18:1044, 1993. 16. Herskovits MS, Singh IJ, Sandhu HS: Innervation of bone. In Hall BK, editor: Bone, vol 3, Bone matrix and bone specific products, Boca Raton, 1991, CRC Press. 17. Reimann I, Christensen SB: A histological demonstration of nerves in subchondral bone, Acta Orthop Scand 48:345, 1977. 18. Hague BA, Honnas CM, Simpson RB, et al: Evaluation of skin bacterial flora before and after aseptic preparation of clipped and nonclipped arthrocentesis sites in horses, Vet Surg 26:121, 1997. 19. Stashak TS: Diagnosis of lameness. In Stashak TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 20. Schumacher J, Steiger R, Schumacher J, et al: Effects of analgesia of the distal interphalangeal joint or palmar digital nerves on lameness caused by solar pain in horses, Vet Surg 29:54, 2000. 21. Cornelissen BPM, Burma P, Rijkenhuizen ABM, et al: Innervation of the equine mature and immature proximal sesamoid bone by calcitonin gene-related peptide and substance P-containing nerve fibers, Am J Vet Res 59:1378, 1998. 22. Ford TS, Ross MW, Orsini PG: A comparison of methods for proximal palmar metacarpal analgesia in horses, Vet Surg 18:146, 1989. 23. Wheat JD, Jones KJ: Selected techniques of regional anesthesia, Vet Clin North Am Large Anim Pract 3:223, 1981. 24. Dyce KM, Sack WO, Wensing CJG: The forelimb of the horse. In Dyce KM, Sack WO, Wensing CJG, editors: Textbook of veterinary anatomy, Philadelphia, 1987, WB Saunders. 25. Dyson SJ, Kidd L: A comparison of responses to analgesia of the navicular bursa and intra-articular analgesia of the distal interphalangeal joint in 59 horses, Equine Vet J 25:93, 1993. 26. Pleasant RS, Moll HD, Ley WB, et al: Intra-articular anesthesia of the distal interphalangeal joint alleviates lameness associated with the navicular bursa in horses, Vet Surg 26:137, 1997. 27. Keegan KG, Wilson DA, Kreeger JM, et al: Local distribution of mepivacaine after distal interphalangeal joint injection in horses, Am J Vet Res 57:422, 1996.

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28. Bowker RM, Rockerhouser SJ, Vex KB, et al: Immunocytochemical and dye distribution studies of nerves potentially desensitized by injections into the distal interphalangeal joint or the navicular bursa of horses, J Am Vet Med Assoc 203:1708, 1993. 29. Bowker RM, Linder K, Van Wulfen KK, et al: Anatomy of the distal interphalangeal joint of the mature horse: relationships with navicular suspensory ligaments, sensory nerves and neurovascular bundle, Equine Vet J 29:126, 1997. 30. Vasquez de Mercado R, Stover SM, Taylor KT, et al: Lateral approach for arthrocentesis of the distal interphalangeal joint in horses, J Am Vet Med Assoc 212:1413, 1998. 31. Miller SM, Stover SM, Taylor KT, et al: Palmaroproximal approach for arthrocentesis of the proximal interphalangeal joint in horses, Equine Vet J 28:376, 1996. 32. Misheff MA, Stover SM: A comparison of two techniques for arthrocentesis of the equine metacarpophalangeal joint, Equine Vet J 23:273, 1991. 33. Ford TS, Ross MW, Orsini PG: Communications and boundaries of the middle carpal and carpometacarpal joints in horses, Am J Vet Res 49:2161, 1988. 34. Keily RG, McMullan W: Lateral arthrocentesis of the equine carpus, Equine Pract 9:22, 1987. 35. Lewis RD: Techniques for arthrocentesis of equine shoulder, elbow, stifle, and hip joints, Proc Am Assoc Equine Pract 42:55, 1996. 36. Sams AE, Honnas CM, Sack WO, et al: Communication of the ulnaris lateralis bursa with the equine elbow joint and evaluation of caudal arthrocentesis, Equine Vet J 25:130, 1993. 37. Moyer W: A guide to equine joint injections, Trenton, NJ, 1983, Veterinary Learning Systems. 38. Grant BG: Bursal injections, Proc Am Assoc Equine Pract 42:64, 1996. 39. Scrutchfield W: Injection of the navicular bursa, Southwestern Vet 30:161, 1977. 40. Turner TA: Diagnosis and treatment of navicular syndrome in horses, Vet Clin North Am Equine Pract 5:131, 1989. 41. Verschooten F, Desmet P, Peremens K, et al: Navicular disease in the horse: the effect of controlled intrabursal corticoid injection, J Equine Vet Sci 11:8, 1991.

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42. Butler JA, Colles CM, Dyson SJ, et al: Clinical radiology of the horse, Oxford, 1993, Blackwell Science. 43. Bishop HW: A clinical review: navicular disease, J Royal Army Vet Corps 31:61, 1960. 44. Dietz O, Wiesner E: Diseases of the horse, part 1, New York, 1984, Karger. 45. Schramme MC, Boswell JC, Hamhougias KT, et al: An in vitro study to compare 5 different techniques for injection of the navicular bursa in the horse, Equine Vet J 32:263, 2000. 46. Hassell DM, Stover SM, Yarbrough TB, et al: Palmar-plantar axial sesamoidean approach to the digital flexor tendon sheath in horses, J Am Vet Med Assoc 217:1343, 2000. 47. Dyson SJ, Romero JM: An investigation of injection techniques for local analgesia of the equine distal tarsus and proximal metatarsus, Equine Vet J 25:30, 1993. 48. Dyce KM, Sack WO, Wensing CJG: The hindlimb of the horse. In Dyce KM, Sack WO, Wensing CJG, editors: Textbook of veterinary anatomy, Philadelphia, 1987, WB Saunders. 49. Sack WO, Orsini PG: Distal intertarsal and tarsometatarsal joints in the horse: communication and injection sites, J Am Vet Med Assoc 179:355, 1981. 50. Bell BTL, Baker GJ, Foreman JH, et al: In vivo investigation of communication between the distal intertarsal and tarsometatarsal joints in horses and ponies, Vet Surg 22:289, 1993. 51. Reeves MJ, Trotter GW, Kainer RA: Anatomical and functional communications between the synovial sacs of the equine stifle joint, Equine Vet J 23:215, 1991. 52. Vacek JR, Ford TS, Honnas CM: Communication between the femoropatellar and medial and lateral femorotibial joints in horses, Am J Vet Res 53:1431, 1992. 53. Hendrickson DA, Nixon AJ: A lateral approach for synovial fluid aspiration and joint injection of the femoropatellar joint of the horse, Equine Vet J 24:397, 1992. 54. Hendrickson DA, Nixon AJ: Comparison of the cranial and a new lateral approach to the femoropatellar joint for aspiration and injection in horses, J Am Vet Med Assoc 205:1177, 1994. 55. Marks D: Medical management of back pain, Vet Clin North Am Equine Pract 15:179, 1999.

11

Neurological Examination and Neurological Conditions Causing Gait Deficits Jill Beech and William V. Bernard

ifferentiating neurological gait deficits from lameness can sometimes be a dilemma for the clinician. Many repeated examinations and ancillary testing may be necessary, and even then experienced clinicians may give varied opinions about the same horse. Lack of definitive diagnostic tests to identify the origin of subtle gait changes, which in some horses may be perceived only by a rider or driver and not visible, promote diagnoses that are based purely on opin-

D

ions and individual prejudices. This chapter discusses the examination of the horse with gait deficits caused by disease of either the spinal cord, the most frequently documented cause of neurological gait deficits, or peripheral nerves. The chapter does not consider neurological syndromes characterized by signs of brain dysfunction, such as vestibular, cerebral, and cerebellar disorders. We also refer readers to a recent review on the equine spinal cord.1

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28. Bowker RM, Rockerhouser SJ, Vex KB, et al: Immunocytochemical and dye distribution studies of nerves potentially desensitized by injections into the distal interphalangeal joint or the navicular bursa of horses, J Am Vet Med Assoc 203:1708, 1993. 29. Bowker RM, Linder K, Van Wulfen KK, et al: Anatomy of the distal interphalangeal joint of the mature horse: relationships with navicular suspensory ligaments, sensory nerves and neurovascular bundle, Equine Vet J 29:126, 1997. 30. Vasquez de Mercado R, Stover SM, Taylor KT, et al: Lateral approach for arthrocentesis of the distal interphalangeal joint in horses, J Am Vet Med Assoc 212:1413, 1998. 31. Miller SM, Stover SM, Taylor KT, et al: Palmaroproximal approach for arthrocentesis of the proximal interphalangeal joint in horses, Equine Vet J 28:376, 1996. 32. Misheff MA, Stover SM: A comparison of two techniques for arthrocentesis of the equine metacarpophalangeal joint, Equine Vet J 23:273, 1991. 33. Ford TS, Ross MW, Orsini PG: Communications and boundaries of the middle carpal and carpometacarpal joints in horses, Am J Vet Res 49:2161, 1988. 34. Keily RG, McMullan W: Lateral arthrocentesis of the equine carpus, Equine Pract 9:22, 1987. 35. Lewis RD: Techniques for arthrocentesis of equine shoulder, elbow, stifle, and hip joints, Proc Am Assoc Equine Pract 42:55, 1996. 36. Sams AE, Honnas CM, Sack WO, et al: Communication of the ulnaris lateralis bursa with the equine elbow joint and evaluation of caudal arthrocentesis, Equine Vet J 25:130, 1993. 37. Moyer W: A guide to equine joint injections, Trenton, NJ, 1983, Veterinary Learning Systems. 38. Grant BG: Bursal injections, Proc Am Assoc Equine Pract 42:64, 1996. 39. Scrutchfield W: Injection of the navicular bursa, Southwestern Vet 30:161, 1977. 40. Turner TA: Diagnosis and treatment of navicular syndrome in horses, Vet Clin North Am Equine Pract 5:131, 1989. 41. Verschooten F, Desmet P, Peremens K, et al: Navicular disease in the horse: the effect of controlled intrabursal corticoid injection, J Equine Vet Sci 11:8, 1991.

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42. Butler JA, Colles CM, Dyson SJ, et al: Clinical radiology of the horse, Oxford, 1993, Blackwell Science. 43. Bishop HW: A clinical review: navicular disease, J Royal Army Vet Corps 31:61, 1960. 44. Dietz O, Wiesner E: Diseases of the horse, part 1, New York, 1984, Karger. 45. Schramme MC, Boswell JC, Hamhougias KT, et al: An in vitro study to compare 5 different techniques for injection of the navicular bursa in the horse, Equine Vet J 32:263, 2000. 46. Hassell DM, Stover SM, Yarbrough TB, et al: Palmar-plantar axial sesamoidean approach to the digital flexor tendon sheath in horses, J Am Vet Med Assoc 217:1343, 2000. 47. Dyson SJ, Romero JM: An investigation of injection techniques for local analgesia of the equine distal tarsus and proximal metatarsus, Equine Vet J 25:30, 1993. 48. Dyce KM, Sack WO, Wensing CJG: The hindlimb of the horse. In Dyce KM, Sack WO, Wensing CJG, editors: Textbook of veterinary anatomy, Philadelphia, 1987, WB Saunders. 49. Sack WO, Orsini PG: Distal intertarsal and tarsometatarsal joints in the horse: communication and injection sites, J Am Vet Med Assoc 179:355, 1981. 50. Bell BTL, Baker GJ, Foreman JH, et al: In vivo investigation of communication between the distal intertarsal and tarsometatarsal joints in horses and ponies, Vet Surg 22:289, 1993. 51. Reeves MJ, Trotter GW, Kainer RA: Anatomical and functional communications between the synovial sacs of the equine stifle joint, Equine Vet J 23:215, 1991. 52. Vacek JR, Ford TS, Honnas CM: Communication between the femoropatellar and medial and lateral femorotibial joints in horses, Am J Vet Res 53:1431, 1992. 53. Hendrickson DA, Nixon AJ: A lateral approach for synovial fluid aspiration and joint injection of the femoropatellar joint of the horse, Equine Vet J 24:397, 1992. 54. Hendrickson DA, Nixon AJ: Comparison of the cranial and a new lateral approach to the femoropatellar joint for aspiration and injection in horses, J Am Vet Med Assoc 205:1177, 1994. 55. Marks D: Medical management of back pain, Vet Clin North Am Equine Pract 15:179, 1999.

11

Neurological Examination and Neurological Conditions Causing Gait Deficits Jill Beech and William V. Bernard

ifferentiating neurological gait deficits from lameness can sometimes be a dilemma for the clinician. Many repeated examinations and ancillary testing may be necessary, and even then experienced clinicians may give varied opinions about the same horse. Lack of definitive diagnostic tests to identify the origin of subtle gait changes, which in some horses may be perceived only by a rider or driver and not visible, promote diagnoses that are based purely on opin-

D

ions and individual prejudices. This chapter discusses the examination of the horse with gait deficits caused by disease of either the spinal cord, the most frequently documented cause of neurological gait deficits, or peripheral nerves. The chapter does not consider neurological syndromes characterized by signs of brain dysfunction, such as vestibular, cerebral, and cerebellar disorders. We also refer readers to a recent review on the equine spinal cord.1

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DIAGNOSIS History is important but depends not only on asking the appropriate questions but also on many uncontrollable factors, such as how closely, impartially, and astutely the horse has been observed. The time of onset of signs and rate of progression, whether the gait deficit waxes and wanes or is affected by exercise or rest, whether one or more limbs are affected, whether the affected limb varies, what the horse was doing before onset of signs occurred, whether exercise or management has changed, whether the horse has been moved geographically, whether signs occurred after transport, what medications may have been given and any observed effects, and whether other horses on the farm or in the stable have had any recent illnesses or fever should be determined. It is also important to know if other horses on the same farm have similar clinical signs. For instance, a history of fever, respiratory disease, or abortions in horses in contact with the patient would make one suspect equine herpes virus I (EHVI) infection.

Clinical Examination The clinician should observe whether the horse displays cranial nerve dysfunction; muscle hypertrophy, atrophy, or asymmetry; muscle trembling; abnormal hoof wear; or abnormal posture. Muscle atrophy may be due to disease of the ventral horn cells of the gray matter of the spinal cord, peripheral nerve, or the muscle itself; it also can occur with disuse. Palpation can reveal abnormalities such as altered skin temperature, sweating, muscle fasciculations, abnormal sensitivity, or soreness. The horse should be observed on a flat surface, at a walk and trot, and in straight and curving lines. The horse should be evaluated on a surface that allows detection of abnormal hoof flight and placement, toe dragging, or excessive force when landing. The sound of the feet landing should be noted for consistency and loudness. Hard surfaces also may enhance abnormal hyperflexion in horses with stringhalt. Evaluation on a soft surface may be necessary if the horse is unstable or if the clinician is trying to determine whether the horse could have sore feet. Any abnormal head or neck movement associated with limb movement should be noted. It is important to permit normal neck and head movement when the horse is being led. The person leading the horse should hold the horse as loosely as is safely possible. Collapsing or sinking on a limb, knuckling, hyperflexion, spasticity, hesitance in any part of the stride, dragging of a toe, landing excessively hard, leaning to one side, or failing to track straight can indicate a neurological deficit. Various manipulations are used to diagnose whether proprioceptive or motor deficits exist and to localize the lesion. While being led, the horse should be evaluated while stopping and starting from a walk and trot, backing up, circling tightly in both directions, walking while sideway traction is applied and released on the tail, being pushed sideways from a standstill, and walking with its head elevated. Some clinicians also evaluate repositioning of the foot after placing the horse’s hoof in an abnormal position. We do not find this particularly helpful because a horse’s disposition, age, training, and distractions can affect its response. A horse with a normal gait may stand with its feet placed in an abnormal position for what seems an abnormally long time. Some clinicians also use wheelbarrowing and hopping reactions.1 We do not use these tests in mature horses because we believe responses may be inconsistent and difficult to evaluate accurately and safely. Observation of the horse walking or trotting up and down inclines can be helpful in revealing whether the horse “knows where its limbs are” (proprioception) and can adjust limb movement appropriately. It may be helpful to observe the horse while it is being ridden or lunged, and in some horses while it is loose in an enclosure. Watching the horse stop and start, turn, back up, and maintain

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its balance during many postural maneuvers allows detection of neurological deficits that may not be obvious when the horse is being led. Are errors in range of movement of the limb (dysmetria) apparent? Is the horse extending its limbs to the full extent, or is the range decreased (hypometria)? Does the horse lift its limbs excessively high (hypermetria)? Is spasticity or stiffness of movement apparent? In some horses it is necessary to observe the horse performing its usual activity, providing it is capable. However, gait deficits may be much less apparent at speed than when the horse is walking or trotting slowly. Basically, the clinician is trying to determine whether the horse moves symmetrically and smoothly with normal stride length and height of foot flight appropriate to the breed and use, whether it appears strong and consistently places its feet in the appropriate positions, and whether it moves in balanced harmonious fashion. It is sometimes difficult to determine whether certain postural or gait changes are due to pain or weakness, or associated with motor or proprioceptive deficits. Is the horse flexing its hindlimbs excessively and holding its croup more ventrally and flexed because of pain or weakness? If the horse is shifting weight between the hind feet, is it because of weakness, as seen for example in lower motor neuron disease, or because of pain? When both limbs are affected, manipulation of a limb to try to localize pain may not be possible. Gaited horses can be extremely difficult to evaluate, especially if one is unfamiliar with the specific gaits. Conformation also can confound interpretation of clinical signs. It may be necessary to observe the horse on many occasions and compare its gait before and after exercise. Is the deficit consistent, or does it vary? If it worsens with exercise, is it because of pain or inability to compensate for a neurological deficit as the horse tires? Perineural analgesia may be helpful. Is there palpable evidence of muscle cramping with exercise or an increase in creatine kinase (CK) level, indicating rhabdomyolysis? A variable gait deficit and inconsistent alterations in foot flight or placement are more likely to represent a neurological deficit than lameness; single limb lameness may vary in intensity but usually remains similar in character. Painful and neurological conditions could coexist but may be difficult to differentiate even with use of commonly used analgesics such as phenylbutazone. If the horse buckles in a limb, especially on turns, is easily pulled sideways by the tail when standing or walking, or trembles its limb, weakness of the extensor muscle groups should be suspected. When the flexor muscles are weak, the horse is unable to lift its limb normally, and the toe may be worn from dragging. Pushing the horse sideways or trying to pull on the halter and tail simultaneously can reveal weakness. If the horse is weak or has pain in one limb, it is not able to bear weight normally when the contralateral hoof is lifted from the ground. Neck flexion sideways and vertically should be evaluated for ease and range of movement. Skin sensation and the cutaneous trunci reflex and cervical reflexes should be evaluated. Tapping the trunk should elicit contraction of the cutaneous trunci muscle. Abnormalities can delineate a thoracic spinal cord lesion, because afferent input is through the dorsal thoracic nerves and cranially through the spinal cord white matter, and the efferent pathway involves the cranial thoracic motor neurons in the first thoracic and eighth cervical segments and the lateral thoracic nerve. Hypalgesia of the cutaneous trunci as assessed by response to a two-pinch test with a hemostat is rare and occurs only with severe thoracic spinal cord disease.1 Lack of a cervicofacial reflex (failure of the facial muscles to twitch when the ipsilateral side of the proximal neck is tapped) can suggest a lesion in the cervical cord or a branch of cranial nerve VII. If tapping the side of the neck fails to elicit contraction of the cutaneous coli muscle, a cervical cord lesion could exist. If any abnormal response to skin stimulation is detected, the test should be repeated because

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the horse’s disposition can influence its responses. Limb reflexes usually are not used, although patellar reflexes can be elicited in horses. We do not consider the thoracolaryngeal reflex (slap test) to be helpful. Response is inconsistent in horses with cervical spinal cord lesions and may be absent in normal horses. Blindfolding the horse usually is not part of our routine neurological examination unless vestibular disease is suspected. A complete physical examination should always be conducted. In some horses with hindlimb gait deficits, palpation per rectum of the pelvic bones, lumbar region, distal aorta, and iliac vessels may be necessary. Simple observation may not differentiate hindlimb weakness caused by spinal cord disease from that caused by partial aortoiliac thrombosis. Horses that do not “feel right” to the rider yet show no obvious deficits to the observer whether observed saddled or in hand are problematic. It may be necessary to observe a horse from the jog cart or carriage if the gait deficit about which a driver complains is not visible to the bystander. In attempting to differentiate between a musculoskeletal and neurological condition causing a gait deficit in a limb, diagnostic analgesia may be necessary. Obviously, this does not help differentiate pain from lameness emanating from a lesion proximal to the coxofemoral or scapulohumeral joints. A course of non-steroidal anti-inflammatory drugs (such as moderate doses of phenylbutazone for days or even several weeks) may be helpful in determining whether a gait deficit is caused by pain.

Hematology and Serology In most horses serum chemistry screens and hematological tests are not particularly helpful; however, in horses with a gait deficit caused by an underlying muscle disease, evaluation of aspartate aminotransferase (AST) and CK levels may be helpful. Stage of training, exercise pattern, and whether the blood specimen is obtained after exercise preceded by a day of rest must be considered in evaluation of enzyme levels. If a horse consistently has abnormally elevated enzyme levels, the horse has rhabdomyolysis, and the clinician must decide whether the condition is causing or contributing to the horse’s abnormal gait. Plasma CK and AST levels do not increase simply because of muscle atrophy; rhabdomyolysis must occur to increase the enzyme levels in the blood (see Chapter 84). Elevated plasma concentrations of CK and AST in horses that are not being exercised suggest a primary muscle disorder, such as (but not limited to) polysaccharide storage myopathy (see Chapter 84). An elevation in white blood cell count and fibrinogen level indicates inflammation. In our experience, elevation in fibrinogen level is a more consistent indicator of inflammation in the adult horse than is elevation in white blood cell count. If clinical signs suggest equine lower motor neuron disease, serum levels of vitamin E (α-tocopherol) should be measured because levels consistently have been low unless the horse has been given supplements.2 Low vitamin E levels are not specific for equine lower motor neuron disease. Tocopherol concentrations can decrease during winter when horses lack access to green pasture.3 Daily variations in plasma levels may occur.4 Low levels also have been reported in clinically normal horses5-7 and in one horse with chronic gastrointestinal disease.8 The laboratory that performs the test should be contacted for any specific requirements for submission of samples and to ensure they have an established normal range for vitamin E levels. Serological testing for antibodies to various infectious agents may be indicated. In EHVI infection, detection of an increase in antibody titer is considered diagnostic of the disease. A horse that shows signs of neurological disease secondary to EHVI should have an elevated serum antibody titer, and single high titers have been the basis for initial diagnosis

in individual horses. Recent vaccination confounds interpretation. Rarely, high titers may be measured in horses with no history of recent vaccination and no obvious clinical signs of EHVI infection. Antibody titers for Borrelia burgdorferi, the cause of Lyme disease, sometimes are measured in serum from horses with ill-defined gait deficits. High titers, or rising titers, have been used as a basis for treatment of the disease. A positive titer, however, does not mean the horse has active disease. Because of the geographical variation in exposure to B. burgdorferi, titers may vary greatly. Serological surveys in the United States have demonstrated positive test results in 1% of samples from non-endemic areas and up to 68% in endemic areas.9-11 Reports of horses “responding” to treatment exist,12,13 but to date we are unaware of any horses with Lyme disease in in which neurological deficits mimic primary lameness. Currently the importance of Lyme disease as a cause of equine gait deficits is unclear. Serological testing for the presence of antibodies to Sarcocytis neurona can be used only to indicate exposure to the organism. Serological surveys in certain areas of the United States have shown that a high percentage of horses have positive antibody titers. A positive test result does not mean the horse has equine protozoal myelitis (EPM). A negative test result could theoretically occur in horses with peracute disease or perhaps in severely immunocompromised animals. However, a negative test result usually indicates that disease caused by S. neurona is highly unlikely. The test result also could be negative in a horse with signs of EPM if another protozoan, such as Neospora, causes the spinal cord lesions. In a U.S. study of several hundred horses with neurological disease, test sensitivity was 89%, but specificity was only 71%, because 30% of horses with other neurological diseases also had antibodies to S. neurona. Although the positive predictive value was only 72% in horses with neurological diseases, the negative predictive value was almost 90%, indicating that a negative test result is useful in this population.14 In one study of 44 horses on a farm sampled for more than 1 year, all horses were seropositive for at least 50 weeks yet showed no neurological signs.15

Cerebrospinal Fluid Aspiration and Analysis Cerebrospinal fluid (CSF) can be obtained from either the atlanto-occipital or the lumbosacral space. The advantage of lumbosacral centesis is that it can be performed in the standing sedated horse, whereas atlanto-occipital centesis requires general anesthesia. Fluid from the atlanto-occipital site is considered easier to obtain and not as likely to be contaminated with blood. The atlanto-occipital site is identified by palpating the cranial edge of the wings of the atlas. The hair is clipped and the site prepared aseptically. Atlanto-occipital centesis is performed at the intersection of the median plane and a line drawn across the cranial edge of the wings of the atlas. In the adult horse a 9-cm (3 1⁄ 2-inch), 18- or 20-gauge spinal needle is directed toward the horse’s lower lip with the head held in a flexed position. It is important that the needle remain on the midline as it is advanced, because otherwise it will be too far lateral to enter the sub-arachnoid space. The needle is initially inserted to a depth of approximately 2.5 cm (1 inch) and then gradually advanced. While the needle is gradually advanced to the sub-arachnoid space, it should be held carefully to prevent penetrating the spinal cord when advancing through the atlanto-occipital membrane and the dura mater. Usually a “pop” is felt as the needle advances through the dura; however, this finding is not consistent and the stylette should be frequently removed to observe for flow of CSF. CSF usually flows from the needle once the sub-arachnoid space is entered; however, once a substantial depth has been reached (about 5 to 8 cm [2 to 3 inches] in the average-size horse),

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some clinicians advise gentle and frequent aspiration with a small syringe. In preparation for aspiration from the lumbosacral space the type and degree of restraint is guided by the horse’s behavior, the horse’s stability, and the clinician’s personal preference. A nose twitch, stocks, sedation, or a combination of physical and chemical restraint are options. We prefer to use light sedation with xylazine, sometimes combined with butorphanol. However, lumbosacral CSF pressure can be transiently decreased up to 15 minutes after administration of a high dose of xylazine (1.1 mg/kg intravenously).16 The puncture site for lumbosacral centesis is identified by combining several landmarks, realizing that individual variation exists. A line drawn between the caudal edge of the tuber coxae and the intersection with the midline can be used to locate the lumbosacral space. The lumbosacral space is bordered cranially by the caudal edge of the sixth lumbar vertebra, caudally by the cranial edge of the sacrum, and laterally by the medial rim of the tubera sacrale. The dorsal spinous process of the last lumber vertebra is lower than the dorsal spinous process of the fifth lumbar vertebra. The V formed by the medial rim of the tubera sacrale is one of the more useful landmarks, and the appropriate site for puncture is within this V. The site should be prepared aseptically, and local anesthetic solution is placed subcutaneously. A small skin stab incision is usually made. The needle is inserted on the midline, at the depression palpated just caudal to the last lumbar vertebra, in the middle of the V formed by the tubera sacrale. A 15-cm, 18-gauge spinal needle is generally adequate for a horse that is 16 hands or less. A 20-cm needle may be necessary in a horse greater than 16 to 17 hands. While the clinician advances the needle, it is critical to remain on the midline. The needle can be advanced until a pop indicates it is advancing through the dura or until the patient responds as the needle stimulates nervous tissue. These responses can be unreliable and occasionally dangerous for the horse, handler, and the individual performing the tap. Because horses can react unpredictably (including rearing, bolting, collapsing, or kicking), it is safer to advance the needle gradually until it is near the spinal canal, approximately 12.5 cm (5 inches) in a 15- to 16-hand horse. Once the needle is near the canal, it should be advanced slowly with repeated frequent removal of the stylette and aspiration with a small syringe. The horse may move its tail when the dura is penetrated, but usually minimal reaction occurs. If fluid is obtained, but the amount is small, the needle can be rotated 180°. Jugular vein compression for at least 10 seconds (Queckenstedt’s test) is thought to elevate intra-cranial CSF pressure and aid fluid collection, provided flow is not obstructed. If a hemorrhagic sample is thought to be from iatrogenic causes, the syringe can be changed frequently until subsequent aliquots are clear. If fluid is not obtained on the first attempt, the needle is withdrawn and the procedure is repeated slightly cranial or caudal to the original location. CSF samples should be placed in sterile tubes and rapidly processed after collection. Normal CSF is clear and colorless, and red discoloration indicates hemorrhage. However, normal fluid can sometimes appear mildly hazy when grossly examined, especially in a tube with ethylenediamine tetraacetic acid. Hemorrhage can be iatrogenic or caused by underlying disease. Fluid may appear clear even with red blood cell contamination, and studies indicate that subjective evaluation of spinal fluid is sensitive in detecting blood only when the red blood cells number more than 1200/μl.17,18 Centrifugation of a bloody sample should produce a clear fluid with a pellet of red blood cells on the bottom of the sample tube. If hemorrhage occurred before collection and lysis of cells has occurred, the supernatant may be slightly pink or xanthrochromic (orange/yellow or yellow). Lysis of red blood cells reportedly

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can occur within 1 to 4 hours.19 Xanthochromic CSF results from red blood cell breakdown products (bilirubin) and suggests hemorrhage or vasculitis. A centrifuged xanthochromic sample does not become clear. Turbid CSF may appear with hypercellularity or epidural fat contamination. The latter is not uncommon with lumbosacral aspirates. Formulas used to differentiate between white cell or protein elevations caused by iatrogenic blood contamination of CSF versus pathological increases have been shown to be unreliable. Contamination with a few thousand red blood cells results in minimal increase in white blood cell count or protein content.18 The normal reported range for leukocyte counts has been variable; usually a range of 0 to 6/μl is cited,20 but higher values have been reported.21,22 Diversity in techniques can account for different values in normal CSF. Undiluted fluid can be assayed in a hemocytometer, or acidified crystal violet can be added to accentuate the cells.20 It is important that equine reference values be determined in the laboratory the practitioner uses. As previously stated, the cell quality rapidly deteriorates in CSF, and samples for cytological testing should be processed rapidly or a portion fixed in 40% ethanol if processing must be delayed. For morphological and differential evaluation, cytocentrifugation or filtration through a glass fiber membrane filter is the preferred method of processing spinal fluid. In our experience, cell and differential counts are often normal in horses with spinal cord disease. Small lymphocytes and monocytes are normally seen. Neutrophils may be seen with blood contamination or inflammation. Eosinophilia is rarely seen in equine CSF but could occur secondary to parasite migration. Rarely, eosinophils have been seen in samples from horses with protozoal encephalomyelitis,21 but frequently spinal fluid from horses with EPM is normal. A relative neutrophilia, with or without an increase in cell count, indicates inflammation, and intracellular bacteria may be seen in horses with bacterial meningitis. Reported values for protein content of CSF vary considerably between laboratories, probably because of diversity in measurement techniques. A range of 10 to 120 mg/dl is generally acceptable, although some authors consider 100 to 105 mg/dl the high end of normal range.20,23 Protein may increase because of vascular leakage (vasculitis), inflammatory lesions, trauma, iatrogenic blood contamination, or intrathecal globulin production. High-resolution protein electrophoresis of CSF has been reported in a small number of horses, but its value as a diagnostic test remains to be determined. Compared with normal horses (n = 18), horses with cervical cord compression (n = 14) often had a decreased β fraction and post-β peaks.24 However, divergent findings have been reported. Because CK is abundant in neural tissue (and in skeletal tissue and cardiac muscle) and is a large macromolecule that does not cross the blood-brain barrier, measurement was suggested to be a sensitive index of central nervous system lesions. Horses with EPM were reported to frequently have increased CSF CK concentrations, unlike horses with cervical vertebral malformation.25 However, another study showed the sensitivity and specificity of CSF CK activity are inadequate for diagnostic use. Also, CSF simultaneously collected from the atlanto-occipital and lumbosacral sites had disparate values for CK activity, which was not associated with site or other CSF parameters. Contamination of CSF with either epidural fat or dura, which is possible during collection, increases CK activity.26 Albumin is the predominant protein in normal CSF. Elevated albumin concentration can indicate hemorrhage or altered blood-brain barrier integrity. To eliminate serum albumin as a source of increased CSF protein and albumin, the following albumin quotient (AQ) has been suggested27: AQ =

CSF albumin × 100 Serum albumin

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The AQ cited for normal equine CSF 1.4 ± 0.04,23,27 and it was suggested that an increase above reference range indicated blood contamination during sample collection or compromise of the blood-brain barrier. The immunoglobulin G (IgG) index CSF IgG concentration CSF albumin concentration ÷ Serum IgG concentration Serum albumin concentration was suggested to be useful for differentiating intrathecal IgG production from an increase secondary to blood contamination or increased blood-brain barrier permeability. Normal reference range has been reported to be 0.14 to 0.24.27 However, we do not consider these to be specific, and a recent study has shown that blood contamination can increase the IgG index without a concomitant change in AQ.18 Although CSF cell count, cytological examination, and total protein often do not represent the extent or type of spinal cord or brain tissue disease, when abnormal, the values can be useful. For example, in CNS disease caused by EHVI infection the fluid may be xanthochromic with a high protein level but normal cell count. This disassociation between elevation in protein level and normal cell count may help differentiate EHVI infection from EPM. Also, xanthochromic CSF indicates an alteration in the blood-brain barrier and could explain false-positive CSF immunoblot findings for S. neurona in a horse with positive serological test results. Unfortunately, except for EHVI infections and meningitis, CSF analysis with currently available tests frequently is not helpful in diagnosing spinal cord disease in horses. In the United States the frequency of performing CSF aspirates increased with the introduction of a Western immunoblot test for detecting S. neurona antibodies. Although limited data are available, the specificity and sensitivity of the immunoblot test on CSF from horses with clinical signs consistent with EPM were reported to be approximately 90%.14 However, positive test results have been found in clinically normal horses and in horses with neuropathological lesions other than EPM. Even minute amounts of contamination of CSF with blood can cause the test result to be positive in a horse with high serum antibody levels.19 When CSF was contaminated by even minute amounts of strongly immunoreactive blood (10–3 μL of blood/ml of CSF), the fluid was falsely positive even though the AQ was normal.18 This small amount of blood contamination is grossly undetectable and can correlate with as little as eight red blood cells per microliter of CSF. Also, blood contamination, without increasing the AQ, can increase the IgG index. The IgG index is not specific for intrathecal IgG production. Although the red blood cell count may be a more sensitive indicator of blood contamination than the AQ, it does not correlate with the amount of antibody contamination. Minute amounts of highly immunoreactive blood may have a greater impact on CSF Western blot analysis than a greater amount of contamination with blood with low immunoreactivity.18 Any compromise to the bloodbrain barrier regardless of cause allows antibodies to leak into the CSF from the serum, causing a false-positive test result. Although the test for immunoblot S. neurona antibodies was reported to have 85% positive predictive value in a study of horses with neurological disease,14 in the general equine population the test has poor positive predictive value. Many normal horses have positive antibody test results. In contrast the negative predictive value for the test is high. With what is currently known, interpretation of positive Western blot results must be made with caution. Negative Western blot tests are generally useful to rule out EPM. Polymerase chain reaction (PCR) testing detects DNA of infectious organisms and has been applied to CSF. Its value in the diagnosis of EPM is controversial, especially when positive results have been reported on CSF samples that were negative for S. neurona antibodies and from horses that did not exhibit

overt neurological deficits. We do not find PCR testing for the diagnosis of EPM useful. PCR technique on CSF has been useful in diagnosing neuroborreliosis in a horse. Similar to some human cases, the PCR test result was positive yet the CSF had a negative antibody titer.12

Radiography The use of radiographs in evaluating traumatic or infectious injuries, congenital lesions, and developmental malformations of the spinal column is limited by the size of the patient. Radiographs are useful in diagnosing congenital abnormalities of vertebrae, narrowing of intervertebral disk spaces, stenosis of the cervical spinal canal, osteoarthritic changes, osteomyelitis or osseous cysts, vertebral neoplasia, malalignment, and fractures. However, in most mature horses, except for the cervical spine, anesthesia may be required for adequate radiographs of the spine. Computed tomography (CT) and magnetic resonance imaging have tremendous potential for evaluating the equine central nervous system but also are limited by the size of the horse. At present, except in foals, CT is available only for evaluating the head and cranial–mid-cervical regions. The primary use of radiography in evaluating horses with neurological disease is localization of cervical vertebral lesions or cervical vertebral malformation and diagnosis of cervical compressive myelopathy or stenotic myelopathy (see Chapter 62). Survey radiography is useful in the diagnosis of cervical vertebral malformation and cord compression but can be misleading. Standing lateral radiographic views of the cervical vertebrae are routinely evaluated to detect vertebral malformation and to measure spinal canal diameter and can suggest the likelihood of cervical compressive myelopathy.1,29,30 In horses with cervical compressive myelopathy, malformations that characteristically may be identified include flare of the caudal epiphysis of the vertebral body (vertebral endplate remodeling), caudal extension of the dorsal laminae, vertebral non-alignment, and osteoarthritis of articular facets. Remodeling of the articular processes of the caudal cervical vertebrae is a common malformation identified in horses with cervical compressive myelopathy and in horses not affected with cervical compressive myelopathy. Interpretation of changes is more difficult in older horses, because obvious changes may be seen radiographically, without impingement on the spinal canal. Subjective evaluation of articular facet abnormalities can result in a false-positive diagnosis of cervical compressive myelopathy. Identification of characteristic vertebral malformations supports, but does not confirm, the diagnosis of cervical compressive myelopathy, and subjective evaluation of radiographic malformation does not reliably differentiate between horses affected or not affected with cervical compressive myelopathy. Objective assessment of vertebral canal diameter is a more reliable indicator of cervical compressive myelopathy than the subjective evaluation of vertebral malformation. The minimum sagittal diameter (MSD) is the first described method of assessment of canal diameter based on lateral cervical radiographs.29 Determination of canal diameter using the sagittal ratio improves on the original measurements by adjusting for magnification and providing a more accurate adjustment for body size.30 The sagittal ratio measurements were developed using a population of affected (confirmed by myelogram or histopathological studies) versus non-affected horses.30 The sagittal ratio is determined by dividing the MSD by the width of the corresponding vertebral body. Although a sagittal ratio percent at any cervical vertebra from the third to seventh cervical vertebrae less than 50% is a strong predictor of spinal cord compression, a few horses with no pathological evidence of spinal cord compression have had sagittal ratios of less than 50%. Recently intervertebral measurements of canal diameters were shown to improve diagnosis of cord compression, and addition of intervertebral sagittal ratio measurements was recommended to increase accuracy of plain radiographs.1

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A semi-quantitative scoring system for evaluating cervical radiographs in horses younger than 1 year of age has been published. This scoring system used neurological examination alone to determine affected versus non-affected foals and combined subjective determination of radiographic vertebral malformation and objective determination of canal diameter.29 Vertebral canal stenosis is determined by measurement of intervertebral and intravertebral MSD. Dividing the MSD by the length of the vertebral body corrects for magnification. Malformation is determined by the subjective assessment of five categories. The most discriminating factors in the semi-quantitative scoring system in differentiating affected from non-affected foals are canal stenosis and the angle between adjacent vertebrae. The disadvantage of the semi-quantitative scoring system is the inclusion of subjective determinations. Myelographic examination is advised to obtain the best evidence of compression.1,31-33 Myelograms also can demonstrate compression from soft tissue masses, which are not evident on radiographs, and suggest transverse compression. However, myelography may not be definitive and occasionally is misleading. A study to evaluate myelography critically and compare the results with necropsy findings in a large number of horses has not been done. A diagnosis of cord compression is assumed if a 50% reduction in the width of the dorsal dye column exists. However, the diagnostic criterion of 50% decrease in width of the dorsal dye column is not well documented32 and has been found in horses with no histological evidence of cord compression at the site of dye column decrease. Iohexol is currently the preferred contrast medium for myelography. It is important that the owner understands the advantages and disadvantages (including risks) of a myelogram before the procedure is undertaken.

Electromyography and Nerve Conduction Studies Recording electrical activity of muscles can indicate whether evidence of denervation or a myopathy exists, although the distinction is not always clear-cut. Electromyographic examination in the early stages of disease or injury may be normal. Certain abnormal patterns can indicate denervation. However, depending on the specific areas to be examined, electromyography may require anesthesia or heavy sedation. It may be helpful in identifying abnormal muscles and indirectly the affected nerves. In a standing, awake horse, spontaneous muscle movement can hinder interpretation. Values for sensory and motor nerve conduction velocities in horses and ponies have been reported.34-37 Differences in speed of conduction occur in different nerves and horses’ sensory nerve conduction velocities are slower than those of ponies.37 However, similar motor nerve conduction velocities have been reported for the median and radial nerves of ponies and horses.35 Location of the segment being measured may be important, because distal tapering of nerves may be associated with slower velocity. Skin temperature significantly affects nerve conduction velocity,37 and variability in technique can alter findings. Slower motor nerve conduction velocities were reported in horses older than 18 years of age.34 The procedure usually requires the horse be anesthetized and, similar to electromyography, should be performed by a skilled person. The technique mainly has been used in research.

Nuclear Scintigraphy Nuclear scintigraphy has been helpful in identifying lesions in the thoracic and lumbar spinal column and pelvic areas not readily evaluated by radiography. It also has been used to evaluate vertebral changes identified radiographically, to determine whether active bone change has occurred. It has revealed hairline fractures and other unsuspected bone lesions in the appendicular skeleton as the cause of gait deficits,

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which sometimes had been suspected to be caused by spinal cord disease. Scintigraphic imaging from both sides of the horse can differentiate which side may have a lesion. The role of nuclear scintigraphy in diagnosing equine spinal cord disease is limited.

Ultrasonography Ultrasonography has been used to diagnose aortoiliac thrombosis and to identify soft tissue masses near the spine or deep within muscles. It has also revealed bony proliferation or fractures of the pelvis in horses with obscure gait deficits, which were originally suspected to be due to spinal cord disease.

Virus Isolation If horses die or are euthanized with neurological signs thought to be caused by viral disease, the spinal cord, brain, or both should be sent for virus isolation. In horses with acute disease, nasal swabs and whole blood samples can be collected.

Immunohistochemistry and Polymerase Chain Reaction Testing Immunohistochemistry and PCR testing can be used to detect the antigen of certain infectious organisms and are applied most commonly to tissues collected at necropsy but can also be used on affected tissues obtained by biopsy.

SPECIFIC DISEASES AND SYNDROMES Equine Protozoal Myelitis EPM was first reported in 197438-41 and appeared to be the same condition originally reported as segmental myelitis of unknown cause.42 It is caused by infection with S. neurona. EPM currently appears to be limited to the Western hemisphere. It is particularly of concern in the United States, where in some regions a high percentage of horses are infected. The actual number of horses confirmed as having neurological disease from EPM is much lower than the actual number of horses infected, but the disease does have a substantial and serious impact. EPM has not been confirmed in horses younger than 6 months of age, although antibodies were detected in serum from a 2-month-old foal.43 A recent comprehensive review of this disease should be consulted for details.44 Neospora species have been identified as a cause of EPM in horses from the western United States.45-48 CSF testing was positive for S. neurona antibodies by Western blot test, and no antemortem features distinguished Neospora infection from Sarcocystis infection. The disease caused by S. neurona tends to occur in warm, temperate, non-arid areas with resident opossums. The horse is a “dead-end” host and the disease is not contagious. The life cycle is not completely understood, although opossums have been identified as the definitive host. The proportion of infected horses that show clinical signs is low. This disease can cause gait deficits affecting one or all limbs and may be difficult or impossible to differentiate from musculoskeletal or other neurological diseases. Signs ascribed to EPM by veterinarians in the United States have been seen in horses in the United Kingdom, where horses have no known exposure to the organism.1 Infected horses and horses with confirmed EPM seen in Europe, Asia, or South Africa have been imported from the Western hemisphere.44 Horses frequently show asymmetrical deficits and may have focal or multifocal muscle atrophy or cranial nerve deficits. Horses may have profound or mild motor or proprioceptive gait deficits, and onset of signs can be acute or chronic, with slow or rapid progression. It may be difficult or impossible to differentiate subtle neurological deficits from those caused by subtle lameness or musculoskeletal pain. Behavior may change. Focal sweating

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may occur. Diagnosis is based on clinical signs and history, by eliminating other potential causes by radiography and other diagnostic tests, and by testing of serum or CSF for antibodies to S. neurona. No definitive antemortem test exists, although absence of serum antibodies to S. neurona makes it highly unlikely that a horse has EPM. If a horse demonstrates classic signs (e.g., asymmetrical motor deficits and muscle atrophy in the hindlimbs, asymmetrical motor deficits in one or more limbs, a limb deficit combined with cranial nerve deficits not deemed caused by peripheral nerve trauma) and has no other organ dysfunction, we would treat the horse for EPM if it has been in the United States and serological findings are positive. We would forgo CSF testing for reasons outlined earlier. To date, drugs used to treat EPM have been a combination of trimethoprim sulfa (sulfadiazine or sulfamethoxazole) and pyrimethamine, or sulfas and pyrimethamine, diclazuril, toltrazuril, and nitazoxanide. Because no definitive antemortem test exists to confirm the disease, evaluation of response to therapy is problematic, especially because the clinical syndrome as treated is so variable and often poorly defined. To date, no treatment trials of experimental infections have been reported. Confounding assessment of drug response is the fact that experimentally infected horses develop clinical signs that decrease over time, despite receiving no treatment.49 Numbers of organisms ingested, virulence factors, and the horse’s own immune status (which depends on heredity, previous exposure to S. neurona, stresses such as transport and parturition, lack of adequate nutrition, and other factors) all presumably can affect development of and recovery from the disease. In the United States the most widely used drug combination is one of the sulfa drugs and pyrimethamine. Because pyrimethamine reaches higher concentrations in the CSF and neural tissue, it is considered superior to trimethoprim. The usual dosage regimen is 20 mg/kg of sulfadiazine once or twice daily and 1 mg/kg of pyrimethamine once daily, both by mouth for at least 2 to 3 months. Diarrhea occasionally occurs in horses treated with trimethoprim-sulfamethoxazole, and anemia and leukopenia have been observed in some horses receiving 1 mg/kg twice daily of pyrimethamine with sulfas. Whether horses require such a prolonged course of treatment or continued high levels of pyrimethamine is unknown. Earlier treatment regimens used a lower dose, but to our knowledge no observations comparing dosages have been reported. A syndrome of bone marrow aplasia and hypoplasia, renal nephrosis or hypoplasia, and epithelial dysplasia was reported in three foals born from mares given sulfonamides, trimethoprim, pyrimethamine, vitamin E, and folic acid during gestation. The authors of that report suggested that administration of the folic acid reduced absorption of active folic acid and combined with the folic acid inhibitors (trimethoprim and pyrimethamine) induced folic acid deficiency and lesions in the foals.50 We do not routinely add supplements for horses being treated with trimethoprim or pyrimethamine, but if sequential blood tests indicate anemia or leukopenia, the horse should be given folinic acid, a form of bioactive tetrahydrofolate. Folic acid should not be used because it is poorly absorbed in the horse, conversion to its active form is prevented by the dihydrofolate reductase inhibitors pyrimethamine and trimethoprim, and it can competitively decrease absorption of the active form of folic acid.44,50 Diclazuril, a coccidiostat, has anti–S. neurona activity in cell cultures infected with S. neurona51 and has been used to treat horses with suspected EPM.52 It is absorbed quickly after feeding. Dosage and therapeutic efficacy is being evaluated. Toltrazuril, like diclazuril, is a triazine-based anti-coccidial drug. Because the drug has good lipid solubility and oral absorption and is absorbed into the CSF, it has potential for treating EPM.53 Ponazuril, a metabolite of toltrazuril, has in

vitro activity against S. neurona,54 and the latter appeared to have favorable clinical results in a multicenter treatment study.44 Nitazoxanide kills S. neurona in cell cultures and has been tested in a field trial. Safety studies showed lethargy at twice the recommended dose and illness and death at four times the recommended dose. In seven horses with clinical signs compatible with EPM and positive immunoblot results for S. neurona antibodies in the CSF, clinical signs improved in six horses by the end of the trial (85 to 140 days).55 Clinical signs recurred in two horses when treatment was stopped, but signs improved when treatment was re-initiated. Another report described two horses with a diagnosis of EPM that improved after 28 to 42 days of treatment with 50 mg/kg nitazoxanide once daily.56 Anorexia and depression were reported as side effects.56 The CSF remained positive for S. neurona antibodies. Until more information is available about this drug, we do not recommend its use. To our knowledge, no evidence shows that concurrent use of immune stimulants, oral anti-oxidants, and antiinflammatory drugs has any beneficial effect. The use of corticosteroids is controversial, because some clinicians claim corticosteroid administration can exacerbate infection. Severity of neurological signs in horses infected with S. neurona reportedly was increased by corticosteroids,57 but in another study of induced disease, signs were less severe in horses given corticosteroids.58 Providing an accurate prognosis is difficult, given the inherent diagnostic problems. Some horses that recover or respond to treatment may not have EPM, and others may recover spontaneously. Economic factors influence duration of treatment and time allowed for convalescence. Even when a severely affected horse improves dramatically, if recovery of function is not complete, a return to previous performance levels is not possible. Signs also may recur in the same horse; whether this is caused by recrudescence of infection or reinfection is unknown. We usually give a guarded prognosis for full recovery of horses showing moderate gait deficits compatible with EPM. Because the exact life cycle and natural intermediate hosts are unknown, definitive recommendations for control of the disease are difficult. Because the opossum is the definitive host and sheds sporocysts, which the horse ingests, fecal contamination of feedstuffs or water sources by this animal should be prevented. The role of other intermediate mammalian hosts is unclear. The efficacy of a recently introduced vaccine remains to be determined.

Cervical Spinal Cord Compression Cervical vertebral malformations of various types have been described as the cause of cord compression and neurological signs.1,59,60 Occasionally it may be difficult to decide if a horse is mildly affected with cervical cord compression or is bilaterally lame in the hindlimbs. Mildly affected horses may show only a slightly stiff, stabbing gait at a walk and trot, only mild circumduction of the outside hindlimb when turning, and equivocal hindlimb dysfunction at a canter. Horses with bilateral osteochondrosis dissecans of the hocks or stifles may show similar signs but usually also have joint capsule distention. Thorough lameness and neurological examinations and radiographs are needed. With more severe compression, the gait deficits increase. Circumduction may be severe, and the horse may strike the distal limb with the opposite hoof, causing hair loss or wounds from interference. A horse may lose balance or fall, especially when backing up or turning. If the caudal cervical spinal cord is compressed, thoracic limb motor deficits and hypometria, frequently asymmetrical, may occur. The horse may severely scuff or drag its toes and have abnormal hoof wear. Occasionally, substantial bony proliferation at the

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synovial articular facets can result in neck stiffness and decreased ability to turn in one direction. Cervical muscle atrophy is rare but can occur if the nerves or lower motor neurons are affected. An affected horse usually lacks hindlimb impulsion and may have a somewhat stiff, bouncy canter. The horse frequently is imprecise when stopping, and the hindquarters may sway or bounce. When compression of the cranial cervical spinal cord occurs, the horse may hold its neck and head higher than normal, in an extended position, and in horses with severe clinical signs all limbs may be affected. Signs may occur suddenly or have a more gradual onset, and progression is variable. Various vertebral abnormalities have been reported in young horses, but clinical signs can be delayed, even when radiographs reveal chronic lesions. We suspect that trauma may cause a pre-existing lesion to become clinically relevant. If a horse with vertebral malformation falls, acute spinal cord compression can occur. Acute cervical spinal cord compression caused by trauma can cause tetraparesis or recumbency, but signs may be delayed in the initial stages after injury and may become apparent only when muscle spasms subside, the unstable fracture displaces, or progressive hemorrhaging is present. In the neck the occipito-atlantoaxial and caudal cervical regions are predilection sites for spinal cord injury.1 Synovial cysts may also cause severe sudden signs of spinal cord compression, often asymmetrical and sometimes intermittent.1 The diagnosis of synovial cysts is usually made at necropsy. Diagnosis of cervical cord compression is based on radiography and myelography. Numerous types of vertebral abnormalities have been described. Management depends on the nature of the lesion, severity of clinical signs, intended use of the horse, and financial considerations. Horses affected with cervical vertebral malformation and cord compression at less than a year of age may improve when exercise and energy intake are restricted.61 Although no controlled studies of a paced diet and restricted exercise program have been conducted, clinical experience supports its use in young horses with radiographic evidence of cervical vertebral malformation.1,61 This treatment is not helpful for young horses with very severe stenosis, for defects such as occipito-atlantoaxial or other cranial cervical malformations, or for older horses. Prognosis with conservative management is poor. Surgical fusion of vertebrae is indicated in some horses and has been used successfully.60,62,63 This subject is discussed in Chapter 62.

Equine Degenerative Myeloencephalopathy and Neuroaxonal Dystrophy Horses mildly affected with equine degenerative myeloencephalopathy and neuroaxonal dystrophy may be misdiagnosed as being lame. Clinical signs may be somewhat similar to those of cervical spinal cord compression. Because no definitive antemortem test exists, clinical diagnosis is based on clinical signs, sometimes supported by the presence of other affected horses on the same farm or in the same family. Equine degenerative myelopathy is thought to be a vitamin E deficiency, with a likely genetic predisposition.64,65 Neuroaxonal dystrophy appears to have a genetic basis in Morgan horses.66 Various breeds and also Przewalski’s horses and Zebras can be affected, and no geographical restriction is apparent. When horses are affected at a young age (i.e., < 6 to 12 months old), signs are more severe and progressive than when signs are first noted in horses 2 years old or older. However, because signs can be mild and only slowly progressive, owners may not be aware of the abnormality. When a severely affected horse is identified on an individual farm, other more mildly affected horses are often found on the same premises or among relatives. Signs tend to be most noticeable in the hindlimbs. Affected horses usually lift the hind feet too

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high and slap them down on the ground and frequently lift the hoof toward the midline and then place it more laterally. The gait is jerky and asynchronous and sometimes ataxic, with excessive sideways sway of the hindquarters. Interference may occur, with a hind hoof hitting the opposite hind fetlock or pastern region. The horse may have a jerky foot placement when stopping and may pivot on the hindlimbs when turning. Severely affected horses may show forelimb ataxia and weakness of all limbs. The gait lacks impulsion. Occasionally, middle-aged horses are examined because of inability to perform at collected gaits with impulsion and precision. No musculoskeletal cause is found, but the hindlimb gait is characteristic of mild equine degenerative myeloencephalopathy or neuroaxonal dystrophy. Mildly affected mature horses appear to function without substantial progression of signs. No ancillary diagnostic test confirms the disease. Vitamin E supplementation (5000 to 6000 units by mouth daily) has been used to treat affected horses, with some, but not total, improvement reported.67 Horses at risk for the disease should be given vitamin E supplements. Supplementation on farms with a number of affected horses was associated with a subsequent decrease in the incidence of disease.64 Mares and foals should have access to grass pasture, because lack of access to green pasture has been identified as a risk factor.

Equine Lower Motor Neuron Disease Equine lower motor neuron disease has been diagnosed in many countries.68 Older horses and those lacking access to green pasture appear to be at risk to develop equine lower motor neuron disease. The disease is thought to be caused by deficiency of antioxidant activity in the central nervous system, leading to degeneration and loss of lower motor neurons in the brainstem and spinal cord.69 Affected horses lose muscle mass and have generalized muscle trembling, which may be more severe in the triceps and quadriceps and is exacerbated by transport. Other clinical signs include stiffness, shifting of weight between the hindlimbs, standing with all feet excessively under the body, excessive sweating, holding the tail elevated and trembling, long periods of recumbency, and sometimes excessively low head carriage. Trembling disappears when the horse lies down. Although the gait may be choppy, the horse has no lameness or ataxia. Horses move better than they stand, and therefore the condition is unlikely to be confused with lameness. Muscle atrophy may be profound. Ophthalmoscopic examination of horses with chronic equine lower motor neuron disease may reveal abnormal pigment deposition in the tapetum with a horizontal band of pigment at the tapetal-nontapetal junction.70 Diagnosis is based on clinical signs and low serum vitamin E concentrations in unsupplemented horses or biopsy of the sacrocaudalis dorsalis medialis (dorsolateral coccygeal) muscle. Affected horses that have not been given vitamin E usually have serum vitamin E concentrations less than or equal to 1 μg/ml.71 Biopsy of a branch of the spinal accessory nerve, which had a high specificity and sensitivity in diagnosis of equine lower motor neuron disease, has been replaced by the muscle biopsy, which is technically much easier, can be performed in the standing horse and has a similar diagnostic specificity and sensitivity.72 However, false-positive test results can occur in horses that have had “tail blocks.”72 The dorsolateral coccygeal muscle is ideal for biopsy because it contains a high percent of type I oxidative fibers, which are the main muscle fibers affected in the disease. Other muscles with a high proportion of type I fibers are not accessible for biopsy. Most limb muscles have high percentages of type II fibers and are not suitable for diagnosis of the disease. Oral vitamin E supplementation (6000 to 10,000 units by mouth daily) improves horses, and green pasture is also helpful. However, athletic ability may remain impaired.69

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Equine Herpes Virus I Infection Neurological disease caused by EHVI can occur in individual horses or as an outbreak. Ataxia is variable but usually symmetrical. The hindlimbs are more severely affected, and recumbency can occur. Signs occur acutely and usually stabilize within 24 to 48 hours. Because this condition is unlikely to be confused with lameness, it is not discussed further and readers are referred to a review.1

Miscellaneous Diseases of the Spinal Cord Spinal cord disease from migrating parasites could manifest as an asymmetrical gait deficit. Incidence appears to vary geographically, and clinical signs reflect the path of migration. Antemortem diagnosis is usually not possible, although eosinophilia in the CSF supports the diagnosis. Various parasites including Setaria species, Halicephalobus (Micronema) deletrix, Hypoderma, and Strongylus species have been identified. Treatment includes anti-parasitic and antiinflammatory drugs. Vertebral osteomyelitis, neoplasia, and diskospondylitis are rare causes of spinal cord disease. Signs reflect location of the lesion, which may be confirmed by radiography or scintigraphy. CSF may reflect the disease condition if it extends through the dura. Traumatically induced diskospondylitis has been described and may be difficult to differentiate from bacterial diskospondylitis.1,73 Spinal cord traumas may occur directly or from instability of intervertebral joints. External trauma can affect any horse, and clinical signs reflect the site of the lesions. Three predilection sites for injury are the occipito-atlantoaxial region, the caudal cervical region (the fifth cervical to the first thoracic vetebrae) and mid-thoracolumbar region.1 Clinical signs may initially be mild or peracute, and some horses develop severe progressive signs. It is often not possible to perform an adequate or accurate neurological examination or form a prognosis on an acutely injured horse. Initial treatment includes first aid care, sedation if needed, and the administration of analgesics, anti-inflammatory drugs, and mannitol. Radiographs can be useful, depending on site of injury and size of the horse. Repeated neurological evaluations are used for prognosis.

Peripheral Nerve Injuries Except for stringhalt and radial nerve injury, peripheral nerve diseases affecting the gait are rarely diagnosed. Suprascapular nerve injury by itself does not alter the gait but results in atrophy of the supraspinatus and infraspinatus muscles (“sweeney”).74-76 However, injury to the nerve usually occurs with more general trauma to the region such as a collision or fall. This type of injury frequently can lead to damage to other nerves of the limb and soft tissue structures. If other nerve roots of the brachial plexus are simultaneously damaged, the shoulder joint may be unstable and subluxate laterally. The horse may circumduct the limb during protraction. Rest and anti-inflammatory drugs are usually used. Several surgical procedures have been advocated for suprascapular nerve injury.77 Radial nerve paresis or paralysis is recognized, usually secondary to trauma. Horses with radial nerve paralysis cannot flex the shoulder joint or extend the elbow, knee, fetlock, or interphalangeal joints. The dorsum of the toe rests on the ground, and the elbow is dropped. Severely affected horses have difficulty rising and often collapse on the limb if it bears weight. More mildly affected horses may advance the leg by flinging or jerking it forward from the shoulder. Evaluation of skin sensation may not be helpful. Atrophy of the triceps and other limb extensor muscles occurs after 2 weeks, and denervation potentials can be found on electromyographic examination 3 to 4 weeks, or sooner, after radial nerve injury.77,78 Because of the difficulty of knowing whether the gait deficits

are due solely to radial nerve injury or muscle damage, an accurate prognosis can be difficult in horses with acute clinical signs. Signs of radial paralysis occurring after recumbency or general anesthesia are probably caused by ischemic myopathy, with possible ischemic neuropraxia, and these horses generally recover. Prognosis depends on the cause and extent of radial nerve injury, neither of which may be identified. Prognosis is obviously better in horses that are less severely affected and those that show early signs of improvement. However, some severely affected horses completely recover. Prognosis is worse if rapid severe atrophy of extensor muscle occurs. Signs of radial nerve dysfunction can also occur from lesions in the caudal cervical and cranial thoracic ventral gray matter, but other signs of spinal cord disease usually coexist, especially in EPM. Physical therapy, including splinting to avoid flexor deformity, is very important, and electrical stimulation of muscles may also help prevent atrophy. Irreversible fibrosis and contracture are likely without intervention. Lesions in the nerves supplying the flexor muscles of the thoracic limb are extremely rare, although signs of dysfunction can accompany brachial plexus or spinal cord lesions.75 If the ulnar nerve is sectioned, the horse may move its foot in a jerking fashion with decreased flexion of the fetlock and carpal joints. When the median nerve is cut, the horse drags the toe because of decreased flexion of the fetlock and carpus. Hypalgesia of the medial pastern occurs, whereas with ulnar neurectomy, hypalgesia of the lateral metacarpal region occurs.75,77 After neurectomy of the proximal musculocutaneous nerve, the horse drags its toe because of decreased elbow flexion. Since natural disease syndromes affecting these nerves are not described, prognosis is difficult because gait deficits improve with time after neurectomy.77 If the femoral nerve is damaged, the horse cannot extend its stifle and rests the leg in a flexed position. The hip is lower than the opposite limb, and the horse cannot support weight normally or at all when walking. When both limbs are affected, the horse will appear crouched and have great difficulty rising. The patellar reflex is absent or depressed, and with time the quadriceps muscles atrophy. Damage to the nerve has occurred during anesthesia with horses positioned in dorsal or lateral recumbency (usually with the affected limb having been positioned uppermost) or after over-extension of the limb, pelvic or femoral fractures, or in association with space-occupying masses impinging on the nerve.77,79,80 Lesions in the spinal cord ventral gray matter or nerve roots at L5 or L6 lumbar vertebrae can also cause signs of femoral paralysis. Complete neurological evaluation to detect other deficits may be difficult if signs of femoral nerve paralysis are severe. Because the condition is rare and rhabdomyolysis and postoperative myopathy can mimic the signs of femoral nerve damage, giving a prognosis is difficult. Anti-inflammatory drugs are usually used. Most horses with post-anesthetic femoral nerve paresis make a complete recovery.80 Signs of paresis or paralysis of the sciatic nerve can occur in horses with pelvic fractures, with deep muscle injections in foals, or with spinal cord lesions affecting the ventral gray matter or nerve roots of the fifth lumbar to third sacral nerves. Signs reflect flexor muscle weakness. The horse can support weight on the limb if the hoof is placed flat on the ground under the pelvis. Otherwise, the horse stands with the hock and stifle extended and the dorsum of the hoof on the ground behind it. When the horse walks, it drags or jerks the limb forward. With time all muscles distal to the stifle and those of the caudal thigh atrophy. The prognosis is very poor if the nerve is severed. If the fibular (peroneal) nerve is damaged (usually because of blunt trauma), the horse cannot extend the fetlock and interphalangeal joints or flex the tarsus normally. At rest it stands with the hoof behind it, resting on its dorsal surface. If the hoof is placed flat on the ground under

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the horse, the horse can support weight. When the horse moves, it drags the foot cranially, then jerks it caudally, sliding it on the ground. Skin sensation is decreased over the front and lateral aspects of the tarsus and metatarsal region. With time muscle atrophy in the craniolateral crus can occur. Treatment involves support and protection of the distal limb. Electrical stimulation of muscles might help prevent muscle atrophy. Many horses recover with time. Gait had returned to virtually normal within 3 months of experimental transection of the fibular nerve.77 Tibial nerve injury is uncommonly diagnosed, but a stringhalt-like gait has been described. When walking, the horse over-flexes the limb and drops the foot straight to the ground when it reaches the end of the cranial phase of the stride. The gastrocnemius muscle reportedly atrophies. The horse stands with the fetlock flexed or partly knuckled, the tarsus flexed, and the hip lower than that of the unaffected leg.79 Obturator nerve damage, which can occur after foaling, results in signs varying from abduction or circumduction and stiffness of the affected limb when walking to paraplegia. Prognosis depends on severity of signs, whether both limbs are affected, and whether adequate supportive care can be provided. Stringhalt is easily recognized with its exaggerated flexion of the hock, which can result in a bizarre hopping, jerking, and propulsive gait when both hindlimbs are affected (see Chapter 49). Horses may be so severely affected that they “freeze” in the abnormal position or are very reluctant or unable to move. They may strike the ventral abdomen with the hoof. The gait usually is worse when the horse is walking on a hard surface and when it is anxious or frightened. Horses with mild signs may show the exaggerated hock flexion only when backing, turning, or during the first few strides after walking from a standstill. Atrophy of the distal limb muscles may occur in horses with chronic stringhalt. Spasticity, toe scuffing, and stumbling of the thoracic limbs and left laryngeal hemiplegia have been described in some affected horses.81,82 A distal axonopathy of peripheral nerves has been described.83,84 The condition can be sporadic or occur in outbreaks. The cause frequently is unknown, especially when only one horse is affected. Outbreaks have been associated with particular pastures, and mycotoxins are a suspected cause.81,82 Lathyrism can also be a cause. Phenytoin and baclofen have been used with some success to decrease clinical signs.85,86 Tenectomy of the lateral digital tendon has also been used. The course is variable and some horses recover spontaneously. However, because it is difficult to predict which horses will recover, the prognosis is guarded, especially in horses with severe clinical signs or in those which are and not associated with a pasture outbreak. Shivers is somewhat similar to stringhalt, and the origin and pathogenesis are unknown (see Chapter 49). Affected horses tremble one or both pelvic limbs, primarily when backing up or lifting a hoof, and they elevate the tail. Some affected horses cannot stand to have the hooves trimmed, even though the hindlimb gaits are relatively normal and otherwise functional. The clinical course seems variable, and the disease is thought to be progressive, at least in Draft breeds.77 However, we have seen affected horses remain relatively static and functional, although hoof care can be difficult because of the inability to stand for the farrier. A group of horses exists with mild hindlimb deficits resembling a combination of stringhalt and shivers. Although they may continue to be functional for riding, the gait disability impairs the dressage performance. The cause usually is undiagnosed.

REFERENCES 1. Mayhew IG: The equine spinal cord in health and disease (Milne lecture), Proc Am Assoc Equine Pract 45:56, 1999.

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2. Divers TJ, Mohammed HO, Cummings JF, et al: Equine motor neuron disease: findings in twenty-eight horses and proposal of a pathophysiological mechanism for the disease, Equine Vet J 26:409, 1994. 3. Maylin GA, Rubin DS, Lein DH: Selenium and vitamin E in horses, Cornell Vet 70:272, 1980. 4. Craig AM, Blythe LL, Lassen ED, et al: Variations of serum vitamin E, cholesterol and total serum lipid concentrations in horses during a 72-hour period, Am J Vet Res 50:1527, 1989. 5. Beech J: Equine degenerative myeloencephalopathy, Vet Clin North Am Equine Pract 3:379, 1987. 6. Mayhew IG, Brown CM, Stowe HD, et al: Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial, J Vet Intern Med 1:45, 1987. 7. Steiss JE, Traber MG, Williams MA, et al: Alpha tocopherol concentrations in clinically normal adult horses, Equine Vet J 26:417, 1994. 8. Traber MG, Steiss JE, Williams MA, et al: Vitamin E deficiency in horses, FASEB J 9:A473, 1995. 9. Marcus LC, Patterson MM, Gilfillan RE, et al: Antibodies to Borrelia burgdorferi in New England horses: serologic survey, Am J Vet Res 46:2570, 1985. 10. Cohen ND, Bosler EM, Bernard W, et al: Epidemiologic studies of Lyme disease in horses and their public health significance, Ann N Y Acad Sci 539:244, 1988. 11. Lindenmayer J, Weber M, Onderdonk A: Borrelia burgdorferi infection in horses, J Am Vet Med Assoc 194:1384, 1989. 12. Hahn CN, Mayhew IG, Whitwell KE, et al: A possible case of Lyme borreliosis in a horse in the UK, Equine Vet J 28:84, 1996. 13. Browning A, Carter SD, Barnes A, et al: Lameness associated with Borrelia burgdorferi infection in the horse, Vet Rec 132:610, 1993. 14. Granstrom DE: Equine protozoal myeloencephalitis: parasite biology, experimental disease, and laboratory diagnosis. Proceedings of the International Equine Neurology Conference, Ithaca, NY, March 1997. 15. Saville WJA, Reed SM, Granstrom DE, et al: Response of horses exposed to Sarcocystis neurona when monitored biweekly, Proc Am Assoc Equine Pract 43:8, 1997. 16. Moore RM, Trims CM: Effect of xylazine on cerebrospinal fluid pressure in conscious horses, Am J Vet Res 53:1558, 1992. 17. Patten B: How much blood makes the cerebrospinal fluid bloody? JAMA 206:378, 1968 (letter). 18. Miller MM, Sweeney CR, Russell GE, et al: Effects of blood contamination of cerebrospinal fluid on Western blot analysis for detection of antibodies against Sarcocystis neurona and on albumin quotient and immunoglobulin G index in horses, J Am Vet Med Assoc 215:67, 1999. 19. Calabrese VP: The interpretation of routine CSF tests, Vir Med Month 103:207, 1976. 20. Mayhew IG, Whitlock RH, Tasker JB: Equine cerebrospinal fluid: reference values of normal horses, Am J Vet Res 38:1271, 1977. 21. Beech J: Cytology of equine cerebrospinal fluid, Vet Pathol 20:553, 1983. 22. Behrens H: Cerebrospinal liquor of horses, its withdrawal, examination, and diagnostic importance. Proceedings of the fifteenth annual International Veterinary Congress, Stockholm, Sweden, 1953. 23. Green EM, Constantinescu GM, Kroll RA: Equine cerebrospinal fluid: analysis, Comp Cont Educ Pract Vet 15:288, 1993. 24. Furr M, Chicoring WR, Robertson J: High resolution protein electrophoresis of equine cerebrospinal fluid, Am J Vet Res 58:939, 1997.

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25. Furr MO, Tyler RD: Cerebrospinal fluid creatine kinase activity in horses with central nervous system disease: 69 cases, J Am Vet Med Assoc 197:245, 1990. 26. Jackson C, de Lahunta A, Divers T, et al: The diagnostic utility of cerebrospinal fluid creatine kinase activity in the horse, J Vet Intern Med 10:246, 1996. 27. Andrews FM, Maddux JM, Faulk D: Total protein, albumin quotient, IgG and IgG index determinations for horse cerebrospinal fluid, Prog Vet Neurol 1:197, 1990. 28. Cohen ND, McKay RJ: Interpreting immunoblot testing of cerebrospinal fluid for equine protozoal myeloencephalitis, Comp Contin Educ Pract Vet (Equine) 19:1176, 1997. 29. Mayhew IG, Donawick WJ, Green SL, et al: Diagnosis and prediction of cervical vertebral malformation in thoroughbred foals based on semi-quantitative radiographic indicators, Equine Vet J 25:435, 1993. 30. Moore BR, Reed SM, Biller DS, et al: Assessment of vertebral canal diameter and bony malformations of the cervical part of the spine in horses with cervical stenotic myelopathy, Am J Vet Res 55:5, 1994. 31. Beech J: Metrizamide myelography in the horse, J Am Vet Radiol Soc 20:22, 1979. 32. Papageorges M, Gavin P, Sande RD, et al: Radiographic and myelographic examination of the cervical vertebral column in 306 ataxic horses, Vet Radiol 28:53, 1987. 33. Maclean AA, Jeffcott LB, Lavelle RB, et al: Use of iohexol for myelography in the horse, Equine Vet J 20:286, 1988. 34. Henry RW, Diesem CD, Wiechers DO: Evaluation of equine radial and median nerve conduction velocities, Am J Vet Res 40:1406, 1979. 35. Henry RW, Diesem CD: Proximal equine radial and median motor nerve conduction velocity, Am J Vet Res 42:1819, 1981. 36. Blythe LL, Kitchell RL, Holliday TA, et al: Sensory nerve conduction velocities in forelimb of ponies, Am J Vet Res 44:1419, 1983. 37. Blythe LL, Engel HN, Rose KE: Comparison of sensory nerve conduction velocities in horses versus ponies, Am J Vet Res 49:2138, 1988. 38. Beech J, Dodd DC: Toxoplasma-like encephalomyelitis in the horse, Vet Pathol 11:87, 1974. 39. Beech J: Equine protozoan encephalomyelitis, Vet Med Small Anim Clin 69:1562, 1974. 40. Cusick PK, Sells DM, Hamilton DP, et al: Toxoplasmosis in two horses, J Am Vet Med Assoc 164:77, 1974. 41. Dubey JP, Davis GW, Koestner A, et al: Equine encephalomyelitis due to a protozoan parasite resembling Toxoplasma gondii, J Am Vet Med Assoc 154:249, 1974. 42. Rooney JR, Prickett ME, Delaney FM, et al: Focal myelitis-encephalitis in horses, Cornell Vet 50:494, 1970. 43. Saville WJA, Reed SM, Granstrom DE, et al: Seroprevalence of antibodies to Sarcocystis neurona in horses residing in Ohio, J Am Vet Med Assoc 210:519, 1997. 44. Dubey JP, Lindsay DS, Saville WJA, et al: A review of Sarcocystis neurona and equine protozoal myeloencephalitis (EPM), Vet Parasitol 95:89, 2001. 45. Daft BM, Barr BC, Collins N, et al: Neospora encephalomyelitis and polyradiculoneuritis in an aged mare with Cushing’s disease, Equine Vet J 28:240, 1996. 46. Marsh AE, Barr BC, Madigan J, et al: Neosporosis as a cause of equine protozoal myeloencephalitis, J Am Vet Med Assoc 209:1907, 1996. 47. Marsh AE, Barr BC, Packham AE, et al: Description of a new Neospora species (Protozoa: Apicomplexa: Sarcocystidae), J Parasitol 84:983, 1998. 48. Hamir AN, Tornquist SJ, Gerros TC, et al: Neospora caninum associated equine protozoal myeloencephalitis, Vet Parasitol 79:269, 1998.

49. Reed SM: Diagnosing equine protozoal myeloencephalitis, Comp Cont Educ Pract Vet 22(Suppl 7A):1, 2000. 50. Toribio RE, Bain FT, Mrad DR, et al: Congenital defects in newborn foals of mares treated for equine protozoal myeloencephalitis during pregnancy, J Am Vet Med Assoc 212:697, 1998. 51. Lindsay DS, Dubey JP: Determination of the activity of diclazuril against Sarcocystis neurona and Sarcocystis falcatula in cell cultures, J Parasitol 86:164, 2000. 52. Granstrom DE, McCrillis S, Wulff-Strobel C, et al: Diclazuril and equine protozoal myeloencephalitis, Proc Am Assoc Equine Pract 43:13, 1997. 53. Furr M, Kennedy T: Cerebrospinal fluid and blood levels of toltrazuril 5% suspension (Baycox) in the horse following oral dosing, Vet Therapeutics 1:125, 1999. 54. Lindsay DS, Dubey JP, Kennedy TJ: Determination of the activity of ponazuril against Sarcocystis neurona in cell cultures, Vet Parasitol 92:165, 2000. 55. Vatistas N, Fenger C, Palma K, et al: Initial experiences with the use of nitazoxanide in the treatment of equine protozoal encephalitis in northern California, Vet Clin North Am Equine Pract 21:18, 1999. 56. McClure SR, Palma KG: Treatment of equine protozoal myeloencephalitis with nitazoxanide, J Equine Vet Sci 19:639, 1999. 57. Cutler TJ, MacKay RJ, Ginn PE, et al: Immunoconversion against Sarcocystis neurona in normal and dexamethasone-treated horses challenged with S. neurona sporocysts, Vet Parasitol 95:197, 2001. 58. Saville WJA, Stich RW, Reed SM, et al: Utilization of stress in the development of an equine model for equine protozoal myeloencephalitis, Vet Parasitol 95:211, 2001. 59. Rooney JR: Clinical neurology of the horse, Kennett Square, Pa, KNA Press, 1971. 60. Nixon AJ: Cervical vertebral malformation and malarticulation. In Colahan PT, Mayhew IG, Merritt AM, et al, editors: Equine medicine and surgery, ed 5, St Louis, Mosby, 1999. 61. Donawick WJ, Mayhew IG, Galligan DT, et al: Early diagnosis of cervical vertebral malformation in young thoroughbred horses and successful treatment with restricted paced diet and confinement, Proc Am Assoc Equine Pract 35:525, 1989. 62. Moore BR, Reed SM, Robertson JT: Surgical treatment of cervical stenotic myelopathy in horses: 73 cases (19831992), J Am Vet Med Assoc 203:108, 1993. 63. Wagner PC, Grant BD, Bagby GW, et al: Evaluation of cervical spinal fusion as a treatment in the equine “wobbler syndrome,” Vet Surg 8:84, 1979. 64. Mayhew IG, Grown CM, Stowe HD, et al: Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial, J Vet Intern Med 1:45, 1987. 65. Blythe LL, Craig AM: Equine degenerative myeloencephalopathy. I. Clinical signs and pathogenesis, Comp Cont Educ Pract Vet 13:1215, 1922. 66. Beech J, Haskins M: Genetic studies of neuroaxonal dystrophy in the Morgan, Am J Vet Res 48:109, 1987. 67. Blythe LL: Equine degenerative myeloencephalopathy: genetics and treatment. Proceedings of the International Equine Neurology Conference, Ithaca, NY, 1997. 68. Divers TJ, Mohammed HO, Cummings JF: Equine motor neuron disease, Vet Clin North Am Equine Pract 13:97, 1997. 69. Divers TJ, Mohammed HO, Cummings JF, et al: Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease, Equine Vet J 26:409, 1994. 70. Riis RC, Jackson C, Rebhun W: Ocular manifestations of equine motor neuron disease, Equine Vet J 31:99, 1999.

CHAPTER 12 71. De la Rùa-Doménech R, Mohammed HO, Cummings JF, et al: Association between plasma vitamin E concentration and the risk of equine motor neuron disease, Vet J 154:203, 1997. 72. Divers TJ, Valentine BA, Jackson CA, et al: Simple and practical muscle biopsy test for equine motor neuron disease, Proc Am Assoc Equine Pract 42:180, 1996. 73. Hillyer MH, Innes JF, Patteson MW, et al: Diskospondylitis in an adult horse, Vet Rec 139:519, 1996. 74. Dyson S: The differential diagnosis of shoulder lameness in the horse, fellowship thesis, London, 1986, Royal College of Veterinary Surgeons. 75. Henry RW: Gait alteration in the equine pectoral limb produced by neurectomies, master’s thesis, Stillwater, Okla, 1976, Oklahoma State University. 76. Dyson S: Personal communication, 2001. 77. Hahn CN, Mayhew IG, Mackay RJ: Diseases of the peripheral (spinal) nerves. In Colahan PT, Mayhew IG, Merritt AM, et al, editors: Equine medicine and surgery, ed 5, St Louis, Mosby, 1999.

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78. Cauvin E, Munroe GA, Mitsopoulos A: Peripheral neuropathy involving brachial plexus nerves in 2 horses, Equine Vet Educ 5:90, 1993. 79. Mayhew IG: Large animal neurology: a handbook for veterinary clinicians, Philadelphia, 1989, Lea & Febiger. 80. Ross MW: Personal communication, 2001. 81. Cahill JI, Goulden BE, Pearce HG: A review and some observations on stringhalt, N Z Vet J 33:101, 1985. 82. Pemberton DH, Caple IW: Australian stringhalt in horses, Vet Annual 20:167, 1980. 83. Slocombe RF, Huntington PJ, Friend SCE: Pathological aspects of Australian stringhalt, Equine Vet J 24:174 1992. 84. Cahill JI, Goulden BE, Jolly RD: Stringhalt in horses: a distal axonopathy, Neuropathol Appl Neurobiol 12:459, 1986. 85. Huntington PJ, Seneque S, Slocombe RF, et al: Use of phenytoin to treat horses with Australian stringhalt, Aust Vet J 68: 221, 1991. 86. Kannegieter NJ, Malik R: The use of baclofen in the treatment of stringhalt, Aust Vet J 10:90, 1992.

12

Unexplained Lameness Sue J. Dyson

ameness diagnosis is a never-ending challenge, even for an experienced clinician, since despite a logical and thorough investigation it still may prove difficult to reach a satisfactory conclusion. This chapter discusses some of the reasons that a definitive diagnosis may remain elusive. In some horses it may be possible to isolate the source of pain reasonably accurately, but it may not be possible to determine the cause of pain. In other horses the source of pain cannot be determined (see Chapter 100).

L

FALSE-NEGATIVE RESPONSES TO LOCAL ANALGESIC TECHNIQUES A false-negative response to local analgesic techniques may occur for a variety of reasons, including the following: • Inaccurate injection • Inadequate time for the local anesthetic solution to be effective • Failure to appreciate improvement in the lameness • Very severe pain • Failure to alleviate subchondral bone pain after intraarticular injection • Extra-articular pain • Aberrant nerve supply • Failure, in an unshod horse, to appreciate the extent of foot soreness contributing to lameness • Failure to appreciate the degree of lameness fluctuatation within an examination period The following are common case examples: 1. It is misleading to conclude that pain does not arise from the centrodistal and tarsometatarsal joints and the

central and third tarsal bones after a negative response to intra-articular analgesia of the centrodistal and tarsometatarsal joints. Intra-articular analgesia has only a limited ability to alleviate subchondral bone pain. In moderate to advanced osteoarthritis, subchondral bone pain is a significant contributor to pain. Hock pain may be missed if it is concluded that a negative response to intraarticular analgesia precludes the existence of hock pain and if there is a failure to desensitize the hock region using regional analgesia. It should also be recognized that perineural analgesia of the fibular and tibial nerves may only result in partial improvement in lameness associated with moderate to severe osteoarthritis of the centrodistal and or tarsometatarsal joints. 2. Laminitis, a fracture of either the distal phalanx or the navicular bone, and a subsolar abscess are all common causes of severe foot pain. Desensitization of the foot by perineural analgesia of the palmar (plantar) nerves at the level of the proximal sesamoid bones may have a negligible effect or result in only mild improvement in lameness. Foot pain in the hindlimb is often more difficult to alleviate than in a forelimb. If clinical signs point to foot pain, but apparent desensitisation of the foot fails to markedly alter the lameness, further investigation of the foot should be performed with other means (e.g., radiographic examination). The horse in Fig. 12-1 was admitted with suspected back pain, but showed obvious blateral forelimb lameness, with right forelimb lameness predominating. Digital pulse amplitudes were increased in the right forelimb, but there was no response to hoof testers. Nonetheless, the horse appeared clinically to have foot

CHAPTER 12 71. De la Rùa-Doménech R, Mohammed HO, Cummings JF, et al: Association between plasma vitamin E concentration and the risk of equine motor neuron disease, Vet J 154:203, 1997. 72. Divers TJ, Valentine BA, Jackson CA, et al: Simple and practical muscle biopsy test for equine motor neuron disease, Proc Am Assoc Equine Pract 42:180, 1996. 73. Hillyer MH, Innes JF, Patteson MW, et al: Diskospondylitis in an adult horse, Vet Rec 139:519, 1996. 74. Dyson S: The differential diagnosis of shoulder lameness in the horse, fellowship thesis, London, 1986, Royal College of Veterinary Surgeons. 75. Henry RW: Gait alteration in the equine pectoral limb produced by neurectomies, master’s thesis, Stillwater, Okla, 1976, Oklahoma State University. 76. Dyson S: Personal communication, 2001. 77. Hahn CN, Mayhew IG, Mackay RJ: Diseases of the peripheral (spinal) nerves. In Colahan PT, Mayhew IG, Merritt AM, et al, editors: Equine medicine and surgery, ed 5, St Louis, Mosby, 1999.

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78. Cauvin E, Munroe GA, Mitsopoulos A: Peripheral neuropathy involving brachial plexus nerves in 2 horses, Equine Vet Educ 5:90, 1993. 79. Mayhew IG: Large animal neurology: a handbook for veterinary clinicians, Philadelphia, 1989, Lea & Febiger. 80. Ross MW: Personal communication, 2001. 81. Cahill JI, Goulden BE, Pearce HG: A review and some observations on stringhalt, N Z Vet J 33:101, 1985. 82. Pemberton DH, Caple IW: Australian stringhalt in horses, Vet Annual 20:167, 1980. 83. Slocombe RF, Huntington PJ, Friend SCE: Pathological aspects of Australian stringhalt, Equine Vet J 24:174 1992. 84. Cahill JI, Goulden BE, Jolly RD: Stringhalt in horses: a distal axonopathy, Neuropathol Appl Neurobiol 12:459, 1986. 85. Huntington PJ, Seneque S, Slocombe RF, et al: Use of phenytoin to treat horses with Australian stringhalt, Aust Vet J 68: 221, 1991. 86. Kannegieter NJ, Malik R: The use of baclofen in the treatment of stringhalt, Aust Vet J 10:90, 1992.

12

Unexplained Lameness Sue J. Dyson

ameness diagnosis is a never-ending challenge, even for an experienced clinician, since despite a logical and thorough investigation it still may prove difficult to reach a satisfactory conclusion. This chapter discusses some of the reasons that a definitive diagnosis may remain elusive. In some horses it may be possible to isolate the source of pain reasonably accurately, but it may not be possible to determine the cause of pain. In other horses the source of pain cannot be determined (see Chapter 100).

L

FALSE-NEGATIVE RESPONSES TO LOCAL ANALGESIC TECHNIQUES A false-negative response to local analgesic techniques may occur for a variety of reasons, including the following: • Inaccurate injection • Inadequate time for the local anesthetic solution to be effective • Failure to appreciate improvement in the lameness • Very severe pain • Failure to alleviate subchondral bone pain after intraarticular injection • Extra-articular pain • Aberrant nerve supply • Failure, in an unshod horse, to appreciate the extent of foot soreness contributing to lameness • Failure to appreciate the degree of lameness fluctuatation within an examination period The following are common case examples: 1. It is misleading to conclude that pain does not arise from the centrodistal and tarsometatarsal joints and the

central and third tarsal bones after a negative response to intra-articular analgesia of the centrodistal and tarsometatarsal joints. Intra-articular analgesia has only a limited ability to alleviate subchondral bone pain. In moderate to advanced osteoarthritis, subchondral bone pain is a significant contributor to pain. Hock pain may be missed if it is concluded that a negative response to intraarticular analgesia precludes the existence of hock pain and if there is a failure to desensitize the hock region using regional analgesia. It should also be recognized that perineural analgesia of the fibular and tibial nerves may only result in partial improvement in lameness associated with moderate to severe osteoarthritis of the centrodistal and or tarsometatarsal joints. 2. Laminitis, a fracture of either the distal phalanx or the navicular bone, and a subsolar abscess are all common causes of severe foot pain. Desensitization of the foot by perineural analgesia of the palmar (plantar) nerves at the level of the proximal sesamoid bones may have a negligible effect or result in only mild improvement in lameness. Foot pain in the hindlimb is often more difficult to alleviate than in a forelimb. If clinical signs point to foot pain, but apparent desensitisation of the foot fails to markedly alter the lameness, further investigation of the foot should be performed with other means (e.g., radiographic examination). The horse in Fig. 12-1 was admitted with suspected back pain, but showed obvious blateral forelimb lameness, with right forelimb lameness predominating. Digital pulse amplitudes were increased in the right forelimb, but there was no response to hoof testers. Nonetheless, the horse appeared clinically to have foot

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A

B

A, Lateral and B, solar scintigraphic images of the front feet of a horse with suspected back pain but clinical signs of laminitis. There is reduced uptake of the radiopharmaceutical in the toe region (arrows). The horse showed no improvement in lameness after apparent desensitization of the lamer right front foot by palmar (abaxial sesamoid) nerve blocks, despite the firm focal pressure applied with artery forceps around the coronary band. However, the horse responded well to symptomatic treatment for laminitis.

Fig. 12-1

pain typical of laminitis. Apparent desensitization of the foot, performed to convince the owner that the horse had foot pain, produced absolutely no change in the lameness. The horse responded rapidly to treatment for laminitis. 3. Inadvertent intrasynovial injection may result in misleading results. For example, accidental injection into the tarsal sheath when attempting to deposit local anesthetic solution around the plantar metatarsal nerves distal to the hock may result in proximal suspensory lesions being missed. 4. Failure to allow sufficient time for local anesthetic solution to be effective may result in a false-negative response in some circumstances. Premature assessment of the response to intra-articular analgesia of the femorotibial joints may result in a false-negative result in association with a cruciate ligament injury. These ligaments have an extrasynovial location and it may take up to an hour after injection for cruciate ligament pain to be significantly improved. Failure to allow sufficient time may in some circumstances result in a false-positive response and then confusion. The tibial and fibular nerves are relatively large, and it takes time for the local anesthetic solution to diffuse into them and take effect. This time requirement, combined with the deep location of the deep fibular nerve and thus difficulty in precisely locating the site for injection, may result in a response delayed for up to an hour after injection. Testing the efficacy of these blocks through evaluation of cutaneous sensation is unreliable. If the response is deemed to be negative after 30 minutes, and intra-articular analgesia of the compartments of the stifle is then performed and the lameness improves, it may be wrongly inferred that pain originated in the stifle. However, the improvement in lameness may reflect alleviation of pain arising from the hock region. Much wasted time and money may then be spent trying to establish a cause of stifle pain. Blocking each compartment of the stifle joint separately (e.g., the medial femorotibial joint), may not result in substantial clinical improvement in the lameness, despite the

presence of stifle pain. A considerably better response is frequently seen after blocking the medial and lateral femorotibial joints and the femoropatellar joint in combination. The importance of the clinical examination and repeated observations of a horse cannot be overemphasised. Each clinician has to learn how much to trust nerve blocks. This depends on experience and the frequency of performing blocks. An inexperienced clinican is far more likely to encounter false-negative responses. The results of nerve blocks must be compared with the clinical signs, and if the interpretation is doubtful, the block should be repeated or the area desensitized with a different technique. The clinician must develop experience in the interpretation of improvement in lameness compared with complete alleviation of pain and lameness. This contrast depends to some extent on the degree of the baseline lameness and whether the forelimbs or hindlimbs are involved.

Failure to Perform the Appropriate Nerve Blocks Failure to perform nerve blocks in a logical and complete sequence can lead to confusion. If the response to a low 6point block in a hindlimb is negative and is followed by a positive response to tibial and fibular nerve blocks, the clinician may conclude that pain arose from the hock. Lesions of the proximal aspect of the suspensory ligament (SL) may be completely overlooked.

Blocking the Wrong Limb Failure to appreciate that a head nod reflects hindlimb lameness and is not always a sign of forelimb lameness may result in a blocking a forelimb with negative results, when the primary source of pain is in the ipsilateral hindlimb.

Sources of Pain that Cannot Be Desensitized by Nerve Blocks Many regions of the limbs proximal to the carpus and tarsus cannot be satisfactorily desensitized. In young horses, stress fractures are now well-recognized causes of lameness that in many circumstances cannot be blocked out. In young or older horses a fracture of the deltoid tuberosity of the humerus

CHAPTER 12

Lateral scintigraphic image of the shoulder region of a 6-year-old Warmblood with acute onset of moderate right forelimb lameness. Note the marked focal increased uptake of the radiopharmaceutical in the region of the deltoid tuberosity of the humerus. There was a slightly displaced fracture of the deltoid tuberosity of the humerus, which healed satisfactorily with conservative management.

Fig. 12-2

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Caudocranial view of the left stifle of a general purpose riding horse with recent-onset, episodic, and transient severe left hindlimb lameness. There is a fracture of the proximal aspect of the fibula (large arrow). The lucent line separating the different centers of ossification further distally (small arrow) should not be confused as a fracture. There was little evidence of bony union after 6 weeks, but after 12 weeks the fracture healed satisfactorily.

Fig. 12-3

A

B

Fig. 12-4 A, Dorsal oblique and B, caudal scintigraphic image of the tubera ischii of an 8-yearold Grand prix show jumper with loss of hindlimb power and a tendency to jump to the right. There is increased uptake of the radiopharmaceutical in the right tuber ischium and a change of contour compatible with a fracture.

(Fig. 12-2), the proximal aspect of the fibula (Fig. 12-3), the third trochanter of the femur, and the tuber ischium (Fig. 12-4) are all causes of lameness that are unaffected by nerve blocks. Muscle injuries, such as tearing or fibrosis of brachiocephalicus or the pectoral muscles, may have no localizing signs (see page 141). Associated lameness cannot be influenced by nerve blocks.

POTENTIALLY CONFUSING RESPONSES TO LOCAL ANALGESIC TECHNIQUES Improvement without complete alleviation of lameness after perineural analgesia is not always easy to interpret. It may reflect failure to completely alleviate pain from a single source, or it may be due to additional sources of pain. Sometimes lameness improves with each successive block

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(e.g., palmar digital, palmar [abaxial sesamoid], low 4-point, and subcarpal nerve blocks). However, the lameness is not associated with any detectable radiographic, ultrasonographic, or scintigraphic abnormalities. Sometimes further useful information can be obtained by performing intra-articular analgesia of the interphalangeal and metacarpophalangeal joints, but if the response is negative the diagnosis remains inconclusive. Isolation of pain to a region but failure to define the cause is particularly frustrating. For example, intra-articular analgesia of the femorotibial joints may be positive, but no radiographic or ultrasonographic abnormalities may be detectable. Nuclear scintigraphy may reveal a generalized increased uptake of the radiopharmaceutical in the distal femur and proximal tibia compared with the contralateral limb. Medication of the joints may result in no improvement. Exploratory arthroscopy may reveal minor findings (e.g., mild fibrillation of the cranial meniscal ligaments) of questionable significance, but evaluation of all the joint surfaces and meniscal cartilages is impossible. The definitive diagnosis for the cause of pain remains elusive. The importance of subchondral bone pain as a cause of lameness must not be overlooked. Such pain frequently is present without associated radiological change. A comparison of the responses to intra-articular analgesia and perineural analgesia (and the response to intra-articular medication) may be helpful. With subchondral pain, intra-articular analgesia may have a limited effect. Nuclear scintigraphy is a sensitive indicator of increased remodeling in the subchondral bone. Magnetic resonance imaging (MRI) has the potential to show subtle structural changes in the subchondral bone. Until recently, soft tissue lesions within the hoof capsule have proved elusive to definitive diagnosis. Diagnostic ultrasonography, although possible, has marked limitations. Pool-phase scintigraphic images sometimes are helpful. Examination of the navicular bursa may yield useful information about the bursa, the deep digital flexor tendon, and the distal sesamoidean impar ligament. Advanced imaging techniques such as computed tomography and MRI have the best potential to demonstrate soft tissue pathological conditions, although determining the clinical significance of lesions is not necessarily easy. False-positive results may be obtained if the horse is only mildly lame at investigation but has a history of a more obvious lameness. The detectable mild lameness may not necessarily reflect the original cause. Lameness that is induced when a horse is lunged in small circles on a concrete surface may not reflect the primary cause of lameness. Thus eliminating this lameness by nerve blocks may be misleading. Lameness induced by flexion also may not reflect the principal cause of lameness. Blocking the flexion response does not necessarily identify the primary cause of lameness. A pony had moderate forelimb lameness that was markedly accentuated by lower limb flexion. The response to flexion was eliminated by either regional or intra-articular analgesia of the fetlock joint. However, the baseline lameness was unchanged and did not respond to any of the nerve blocks that were repeated on several occasions. Surgical removal of a large osseous fragment from the fetlock joint did not improve the lameness.

Multiple Sources of Pain in a Limb and More than One Lame Limb Problems can arise in interpretation of nerve blocks in a horse that is lame in more than one limb, especially if there is more than one source of pain in a limb. Perineural nerve blocks usually last for up to 2 to 3 hours unless a long-acting local anesthetic agent, such as bupivacaine, is used. If a horse is lame in several limbs it is usually easiest to start with the lamest limb and block it first. Interpretation becomes difficult if there is a failure to desensitize all the lame limbs simulta-

neously. If the blocks in one limb are wearing off, then lameness in the least lame limb becomes less apparent. The horse’s tolerance for nerve blocks may also compromise how much can be done. It may be necessary to start again on another occasion using bupivacaine. If simultaneous lameness of the ipsilateral forelimb and hindlimb is suspected, blocking should begin in the hindlimb. In this situation a substantial amount of the head nod probably originates from the hindlimb component. Because elimination of head nod is vital to improvement after blocking, forelimb diagnostic procedures cannot be fairly evaluated.

Very Low-Grade Lameness Nerve blocks, especially in hindlimbs, often result in improvement rather than complete alleviation in lameness. Assessing improvement in subtle lameness is nearly impossible. If the horse has a history of more severe lameness previously, delaying further investigation often is worthwhile. The horse should be worked to accentuate the lameness and simplify interpretation of the response to local analgesic techniques.

Improvement of Lameness in Some Situations, but Unrelieved Lameness under All Situations: Which Is the Baseline Lameness? Sometimes a horse has lameness that appears different in nature under different circumstances. Such findings may be related to more than one cause of lameness, and it is important to recognize this fact. For example, a dressage horse was admitted with left forelimb lameness that was only apparent to the rider when the horse was ridden on the right rein (to the right). Clinical examination revealed left forelimb lameness on the right rein on the lunge on a hard surface. This was alleviated by desensitization of the foot. However, desensitization did not alter the lameness that was apparent when the horse was ridden. The cause of the lameness could not be identified. It is vitally important to relate the results of the investigation to the history.

CHALLENGES TO LAMENESS DIAGNOSIS Very Intermittent or Sporadic Lameness Sometimes lameness is intermittent, and the horse may be perfectly normal between episodes. Lameness may be provoked only by maximal exercise in competition. It is very important to carefully assess the history and get the owner to pay great attention to any clinical features of the lameness when present. For example, mild, transient diffuse swelling in the midmetacarpal region medially may reflect axial impingement of a splint on the SL (Fig. 12-5) (see Chapter 73). Spontaneous resolution of hindlimb lameness after standing still is suggestive of aorto-iliaco-femoral thrombosis (see Chapter 52). Ask the owner to assess the reaction to manipulation of specific joints when the horse is lame. Pain on manipulation may suggest a joint problem such as hemarthrosis. If it is not possible to examine the horse when it is lame, nuclear scintigraphic examination can be helpful but also has the potential to mislead (see page 141). For example, an Arab endurance horse had episodic right forelimb lameness that was present only immediately after rides longer than 30 miles. Comprehensive clinical evaluation revealed no evidence of lameness and no suggestions of the cause of previous lameness. Scintigraphic examination revealed increased uptake of the radiopharmaceutical in the third carpal bone of the lame limb (Fig. 12-6). Radiographic examination revealed marked sclerosis of the third carpal bone in the lame limb only, an unusual finding in an endurance horse and thought likely to be of clinical significance. Another Arab endurance horse had an acuteonset, severe right hindlimb lameness that resolved within

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48 hours, but mild, extremely transient, and episodic lameness persisted over the next 3 weeks. Clinical evaluation revealed no suggestion of the cause and no current lameness. Nuclear scintigraphic examination revealed focal increased uptake of the radiopharmaceutical in the medial wing of the distal phalanx, and radiographic examination confirmed a recent fracture (Fig. 12-7). If nuclear scintigraphic findings are negative, it is necessary to try to recreate the circumstances under which the horse exhibits lameness. For example, hemarthrosis can cause a very severe but extremely transient lameness. The horse may be completely normal between episodes. Diagnosis can be reached only by arthrocentesis at the time of acute episode, when there is usually some degree of joint capsule distention and pain on manipulation of the affected joint. Working the horse on a treadmill sometimes is helpful (see Chapter 101).

Lameness that Varies within and between Examinations Sometimes lameness varies considerably in degree both within an examination period and between examinations. This variation makes interpretation of the response to nerve blocks potentially difficult, unless the veterinarian is aware of the fluctuation. It is important to watch a horse move for a sufficient length of time to appreciate any spontaneous changes in the degree of lameness. Horses with a subchondral bone cyst in either the distal scapula or the medial femoral condyle may behave in this way. Within a single examination period the horse may appear sound or lame. In such circumstances it is vital to compare the response to nerve blocks with the clinical signs exhibited. For example, if the characteristics of the lameness are suggestive of shoulder pain, but the lameness is apparently improved after desensitization of the foot, consider the possibility of spontaneous improvement in the lameness that is unrelated to the nerve block. This is, however, an unusual clinical situation, and generally it is best to rely on the results of the diagnostic blocks. A combination of nerve blocks, scintigraphic examination, and radiographic examination may enable a conclusive diagnosis to be reached.

Fig. 12-5 Transverse ultrasonographic image of the palmar metacarpal soft tissues of the right forelimb of an endurance horse at 10 cm distal to the accessory carpal bone. Medial is to the left. The horse had low-grade lameness at the end of endurance rides that resolved completely within 24 hours. Note the echogenic tissue (arrowhead) next to the suspensory ligament (SL). This was a granulomatous reaction between an exostosis on the second metacarpal bone (McII) and the SL. The distal half of the McII was excised and the granulomatous tissue removed. The horse made a complete recovery.

C

A

B

A, Dorsal scintigraphic image of the carpi of an endurance horse with episodic lameness that occurred only during endurance rides. The right forelimb is on the left. There is a focal increased uptake of the radiopharmaceutical in the middle of the distal row of carpal bones in the right forelimb. B, Lateral scintigraphic image of the right carpus. There is increased uptake of the radiopharmaceutical in the dorsal aspect of the third carpal bone. C, Dorsoproximal-dorsodistal oblique radiographic view of the right carpus showing marked sclerosis of the radial facet of the third metacarpal bone.

Fig. 12-6

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A

B

C

A, Plantar scintigraphic image of the hind feet of an endurance horse with recent onset of left hindlimb lameness that was only apparent after an endurance ride. The horse appeared clinically normal at the time of the examination. There is moderate focal increased uptake of the radiopharmaceutical in the medial aspect of the left hind foot (left). B, Solar scintigraphic image of the left hind foot. Medial is to the right. There is marked increased uptake of the radiopharmaceutical in the medial plantar process of the distal phalanx. C, Plantarodorsal radiographic view of the left hind foot. There is a fracture of the medial plantar process (arrow). The horse was treated conservatively and made a complete recovery.

Fig. 12-7

The Dangerous Horse and Nerve Blocks Some horses do not tolerate needle placement and cannot be restrained safely. Nuclear scintigraphic examination sometimes indicates a diagnosis, but the results may be negative. Under such circumstances the horse can be sedated for each block. This approach obviously is time consuming and may be of low specificity, because time must be allowed for the sedative to wear off adequately before the response to the block can be assessed. During this time the local anesthetic solution has the potential to diffuse away from the site of injection and influence more remote pain. Sedation may result in a rather sloppy gait, which can hinder interpretation, especially with mild hindlimb lameness characterized only by a toe drag. Therefore patient selection is important. However, bearing in mind these limitations, it may be the only way to proceed. Xylazine is the shortest-acting α2-agonist available and is the drug of choice, but with a difficult horse, combination with an opioid such as butorphanol may be necessary.

NEGATIVE RESPONSES Negative Response to All Nerve Blocks: Where Next? Occasionally a horse is evaluated for forelimb or hindlimb lameness that is not influenced by any local analgesic technique. Clinical signs may be suggestive of a source of pain (e.g., the foot). The reason for nerve blocks that result in apparent desensitization of a region but fail to eliminate or improve pain is not understood, but it does occur occasionally.1 Alternatively, there may be no clinical clues for the source of pain. Nuclear scintigraphic examination may be helpful in either situation if the pain is bony in origin but is likely to be less helpful for soft tissue injuries.

Negative Responses to Nerve Blocks, No Clinical Clues, and Negative Scintigraphic Findings Consideration may be given to systematic radiographic examination, bearing in mind that not all bony lesions are sufficiently active to yield positive scintigraphic findings. However, com-

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prehensive radiographic examination is time consuming, expensive, and frequently unrewarding, and potentially results in unnecessary exposure to radiation. Thus it is usually discouraged. In the forelimb, unusual causes of lameness such as neurological disease (usually lower motor neuron diseases, such as equine protozoal myelitis), cervical nerve root pain (radiculitis), spondylosis of the cranial thoracic vertebrae, and pectoral, sternal, or rib pain may be considered. In the hindlimb, neurological disease and thoracolumbar or pelvic soft tissue injuries visible neither on pool nor bone phase scintigraphic images should be considered. Keep in mind that horses with forelimb or hindlimb lameness could potentially have a distant source of pain and comprehensive imaging (whole body bone scan, for instance) may be necessary.

NECK LESIONS AND FORELIMB LAMENESS Forelimb lameness that is unassociated with primary limb pain has been recognized in association with bony lesions of the mid-cervical and caudal cervical vertebrae and the cranial thoracic vertebrae (see Chapter 55).2 There are not necessarily any detectable clinical signs that can be related to the neck. In horses with confusing forelimb lameness, evaluation of the neck with radiography, scintigraphy, or both modalities is certainly indicated.

Lateral scintigraphic image of the right elbow region of a 4-year-old Warmblood stallion with right forelimb lameness evident only at the walk, which was unaltered by any local analgesic technique. Uptake of the radiopharmaceutical was increased in the biceps brachii muscle (arrow), which corresponded to an area of increased echogenicity compatible with fibrosis.

Fig. 12-8

REFERRED PAIN The concept of referred pain is well recognized in people but is more difficult in the horse. We must accept that referred pain originating from a lesion far removed from the lame limb may contribute to pain and thus cause lameness.

PREVIOUSLY UNRECOGNIZED CAUSES OF LAMENESS PROXIMAL TO THE CARPUS AND TARSUS I think it is naive to consider that all potential causes of lameness proximal to the tarsus and carpus have been recognized. Injuries that primarily involve bone usually can be identified with nuclear scintigraphic examination. However, scintigraphy is rather insensitive in the identification of soft tissue injuries, although it may help identify some muscle injuries (Fig. 12-8). Muscles can be examined ultrasonographically, but we need to know where to look for damage. Acupuncture trigger point sensitivity may provide information. Use of muscle stimulators may help to identify superficial muscles that are damaged. We know that the horse can tear fibularis tertius, resulting in pathognomonic clinical signs. We do not know if minor injuries to this modified muscle could cause lameness. Tendonous and ligamentous pain without palpable abnormalities and therefore without a specific indication for ultrasonographic examination must always be considered. We must remain open-minded and search for other means of diagnosis.

MISINTERPRETED IMAGING FINDINGS THAT RESULT IN MISDIAGNOSIS In horses in which the results of local analgesic techniques are equivocal or negative, it may be tempting to rely on the results of other diagnostic techniques, such as radiography, ultrasonography, and nuclear scintigraphy, without necessarily relating them to the initial clinical signs. Although these imaging modalities may help to confirm a clinical diagnosis, they also have the potential to mislead, especially if interpreted in isolation.

Fig. 12-9 Lateral scintigraphic image of the tarsus of a 7-yearold riding horse. Note the marked focal increased uptake of the radiopharmaceutical in the hock. Lameness was completely alleviated by desensitization of the fetlock region. There was no radiographic abnormality of the hock. The horse illustrated in Fig. 12-9, with focal increased uptake of the radiopharmaceutical in the hock, was admitted with left hindlimb lameness that was alleviated by desensitization of the fetlock region. The horse illustrated in Fig. 12-10, which has increased uptake of the radiopharmaceutical in the distal tibia, was admitted with forelimb lameness. No hindlimb lameness

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Fig. 12-11 Solar view of the right front foot of a 6-year-old Warmblood. There is increased uptake of the radiopharmaceutical in the region of insertion of the deep digital flexor tendon on the distal phalanx. The gait characteristics were typical of proximal limb lameness and lameness was unaltered by desensitization of the foot. The horse had a fracture of the deltoid tuberosity of the humerus.

Fig. 12-10 Lateral radiographic view of the tarsus and tibia of a 12-year-old advanced event horse with bilateral forelimb lameness associated with distal interphalangeal joint synovitis. The horse had no history or evidence of hindlimb lameness and competed successfully thereafter. Note the intense increased uptake of the radiopharmaceutical in the tibia. The horse was reexamined approximately 8 months later with similar results. The horse had been competing successfully but had recurrent forelimb lameness.

was observed at any time, even after alleviation of the forelimb lameness. The horse in Fig. 12-11, with increased uptake of radiopharmaceutical in the region of insertion of the deep digital flexor tendon, had lameness associated with a fracture of the deltoid tuberosity of the humerus.

ODD LAMENESS APPARENT ONLY DURING RIDING Some causes of lameness are apparent only when the horse is ridden. Some of these are easy to block, but a minority fail to respond to local analgesic techniques. Consideration must always be given to rider-induced lameness (see page 144 and Chapter 100), discomfort caused by tack, and gait abnormalities arising through thoracolumbar (see Chapter 54), sacral, and sacroiliac pain (see Chapters 52 and 53). The possibility of the rider’s weight compressing muscles in the saddle and caudal neck region and nerve compression should be considered as potential causes of forelimb pain.

articular margin of the tibial plateau, and a complete fracture of the proximal aspect of the fibula [Fig. 12-3]). It is likely that acute lameness is related to the fibular fracture. The horse in Fig. 12-3 had been coping despite radiographic evidence of both ostechondrosis of the femoropatellar joint and osteoarthritis of the medial femorotibial joint.

OTHER CAUSES OF LAMENESS Lacerations and Occult Spiral Fractures Acute-onset, moderate to severe lameness sometimes develops within 2 to 3 weeks of trauma to, or laceration over, a long bone (see Figs. 3-3 and 3-4). Sometimes lameness is first observed when the horse is still restricted to box rest and controlled exercise while the wound heals. There may or may not be any detectable focus of pain. Consideration must always be given to the possibility of an occult spiral fracture of, for instance, the radius, which was obviously sustained at the time of the initial injury. Occult spiral fractures are most common in the radius but can involve the third metacarpal or metatarsal bones and tibia. Radiographic examination should be performed to eliminate this possibility.

Rib Lesions A fracture of one or more cranial ribs is a rather unusual cause of forelimb lameness that usually is a sequel to direct trauma, such as a collision with another horse or a gate post, or a fall. There are usually no localizing clinical signs, although secondary neurogenic muscle atrophy may develop within the next 10 to 14 days. The lameness may suggest an upper limb problem. Diagnosis is dependent on radiographic or scintigraphic identification of the fracture.

Sternal Injury

IDENTIFIABLE LESIONS: WHICH CONTRIBUTE TO THE CURRENT LAMENESS? The presence of radiographic lesions is not necessarily synonymous with pain, or the pain may be low grade and not compromise the horse’s gait sufficiently to be recognized by the rider. For example, a horse may have an acute lameness referable to the stifle. Several lesions may be identified radiographically (e.g., smooth flattening of the middle of the lateral trochlear ridge of the femur, modeling of the medial

Sternal injury usually causes a change in behavior, such as a tendency to buck when first tacked up and mounted (i.e., extreme cold back behavior) rather than lameness. Frequently it is not possible to elicit pain by deep palpation.

Fracture of the Summits of the Dorsal Spinous Processes in the Withers Region Acute fractures of the withers usually result in a very shortened forelimb stride and a tendency to move very closely in front (“the mini-skirt walk”). There is usually obvious palpa-

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ble deformity of the withers region. Diagnosis is confirmed radiographically.

Temporomandibular Joint Pain Pain associated with one or both temporomandibular joints may cause reluctance for the horse to take the bit properly, crookedness in the head and neck carriage, and secondary gait irregularities. The joints can be assessed by applying firm pressure over each joint, which may cause pain, and by opening the mouth and moving the upper and lower jaws relative to one another and assessing mobility. Thermography may be a sensitive indicator of local inflammation. If temporomandibular pain is suspected, further investigation can be performed using nuclear scintigraphic examination and diagnostic ultrasonography.3 Radiography is relatively insensitive unless major bony changes are present.4

Neurological Problems and Lameness or Stiffness Early compressive lesions of the cervical spinal cord can cause an apparent low-grade hindlimb lameness that is characterized by slight toe drag and asymmetrical movement of the hindquarters. Signs of weakness or ataxia may not be evident unless a comprehensive neurological examination is performed, especially if the horse is quite fit and fresh. Neurological signs may only be seen when the horse is tired and not compensating for its gait deficits. Equine protozoal myelitis can cause rather bizarre forelimb or hindlimb gait abnormalities, either unilaterally or bilaterally. It should be considered in the differential diagnosis of odd gait abnormalities in horses that reside or have spent time in America. Damage to the branch of the radial nerve, which results in an innervation of the extensor muscles of the carpus and digits, may cause a subtle gait abnormality that is characterized by a tendency to stumble and associated with slight knuckling of the carpus and distal limb joints. Stiff horse syndrome5-7 and equine motor neuron disease8 are unusual neurological conditions in which the horse moves better in the trot and canter than at a walk and may stand abnormally. Shivering behavior often is seen in one or both hindlimbs in association with hindlimb lameness. The two conditions generally are unrelated. Shivering behavior may be more apparent when the horse is stressed. The behavior can make it difficult to assess whether any manipulation of the limb causes pain, or whether the horse is uncomfortable with one hindlimb picked up. Stringhalt, or exaggerated flexion of a limb, usually a hindlimb, results in a gait abnormality most obvious at the slower speeds of walk and trot. It is not usually directly associated with any other form of lameness. It may be sudden or insidious in onset. Congenital abnormalities of the first ribs in association with abnormalities of the adjacent brachial plexus have been seen as a cause of persistent forelimb lameness (Fig. 12-12). Acute-onset, severe, and persistent forelimb lameness has been seen in association with a mediastinal abscess that encroached on the nerve roots of the seventh cervical and first thoracic vertebrae, the stellate ganglion, and the first rib (Fig. 12-13). Measurement of fibrinogen may help to identify the presence of an infective or inflammatory process.

Fig. 12-12 Post-mortem specimen showing an anomalous first rib from a 3-year-old Thoroughbred with right forelimb lameness that was not altered by any local analgesic technique. There was an abnormal web of fibrous tissue that extended from this anomalous rib to incorporate part of the brachial plexus on the right side.

A 7-year-old pony with severe right forelimb lameness that progressively deteriorated. The pony had an increased fibrinogen level and intermittent pyrexia. There was a mediastinal abscess that encroached on the roots of the seventh cervical and first thoracic nerves, the stellate ganglion, and the first rib.

Fig. 12-13

Lyme Disease Lyme disease has frequently been incriminated as a cause of shifting lameness that involves several limbs, but confirmed cases are extremely rare.9 Many horses that are in areas where there are many ticks have relatively high antibody titers to Borrelia burgdorferi,9,10 but this is not consistent with clinical disease. Lyme disease may be suspected in adult horses in endemic areas when unusual synovitis develops in absence

of any known injection history or presence of a wound (see Chapter 67).

Immune-Mediated Polysynovitis Immune-mediated polysynovitis is relatively uncommon but may result in generalized stiffness associated with transient synovial distention of several joint capsules. It is frequently not

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possible to identify the underlying cause, but this condition usually responds to corticosteroid medication (see chapter 67).

be aware that there may be a placebo effect. Not all pain responds to phenylbutazone, so a negative response does not preclude a pain-induced problem (see Chapter 100.)

Tack-Induced Pain An ill-fitting saddle can induce back pain and restricted action or poor performance. The bit can induce pain through poor fit (too narrow or too wide), being too low in the horse’s mouth, banging on the canine teeth, pinching the corners of the horse’s mouth, or being too severe. Any oral pain related to the bit, sharp teeth, or lacerations of the tongue, cheeks, or corners of the horse’s mouth may cause reluctance to accept the bit properly and gait irregularities.

Rider-Induced Problems The rider has a potentially huge influence on the gait of the horse. If a horse is not going forward properly, either because the rider is restricting it or because the rider is not asking it to go forward properly, the forelimb and hindlimb gaits may appear irregular, mimicking pain-induced lameness. An overweight rider who is too heavy for the horse may induce hindlimb lameness. A rider who constantly sits crookedly may induce back pain and hindlimb lameness. (Rider-related problems are discussed further in Chapter 100.)

Physical Limitations of the Horse, Temperament, and Confidence With appropriate handling and training, most horses are cooperative. However, a previously compliant horse can very rapidly change if regularly handled and ridden by someone who lacks confidence, technique, or strength. Such a horse can quickly develop evasions, such as not going forward properly, rearing, bucking, or taking off. These problems may be pain related, but not necessarily. A horse that has never been trained properly may be very difficult and even potentially dangerous to the rider. Horses homebred by amateur enthusiasts are high-risk candidates. Some horses are innately lazy and unwilling to go forward. Others are very exuberant and excessively forward going and “fizzy.” The veterinarian may be asked to investigate any of these behavioral features as a potentially pain-related problem. It is important to establish how the horse was previously. It may be useful to see a video. Determine if there has been a change in rider or management. Establish what the horse is being fed and how much work it is getting: there is a tendency for people to overfeed and underwork horses. A comprehensive clinical evaluation may need to be repeated on several occasions before you can determine if it is a pain-related problem. Nuclear scintigraphic examination of selected areas may be useful to eliminate the presence of any underlying problems and to convince the owner that there is not a physical problem. A change of rider or work pattern may be necessary. The use of high doses of non-steroidal, anti-inflammatory drugs (e.g., 2 to 3 g twice daily for at least 7 to 10 days) can be helpful to determine if the problem is pain related, but

Reproductive Problems Some mares become more difficult to handle and ride when in season and the judicious use of a synthetic progestagen such as altrenogest (Regumate, Intervet, Millsboro, DE) to stop the mare’s cycling can sometimes be helpful. While some stallions can be used successfully for both competition and breeding, especially if the management is good and a very clear distinction is made with handling routines, others cannot focus adequately and thus perform athletically below expectations. Performance may be enhanced by castration. However, although malorientation of testicles is frequently blamed for lameness or poor performance, in the Editors’ experience this is highly unusual. A schirrhous cord in a gelding or mastitis in a mare can cause loss of hindlimb action and hindlimb stiffness. Chronic episodic, transient hindlimb lameness associated with strenuous work (jumping) has been seen in a stallion with large internal inguinal rings.11 The lameness resolved after herniorrhaphy.

REFERENCES 1. Dyson S: Problems associated with the interpretation of the results of regional and intra-articular anaesthesia in the horse, Vet Rec 118:419, 1986. 2. Ricardi G, Dyson S: Forelimb lameness associated with radiographic abnormalities of the cervical vertebrae, Equine Vet J 25:422, 1993. 3. Weller R, Cauvin E, Bowen I, et al: Comparison of radiography, scintigraphy and ultrasonography in the diagnosis of a case of temporomandibular joint arthropathy in a horse, Vet Rec 144:377, 1999. 4. Weller R, Taylor S, Maierl J, et al: Ultrasonographic anatomy of the equine temporomandibular joint, Equine Vet J 31:529, 1999. 5. Nollet H, Vanderstraeten G, Sustronck B, et al: Suspected case of stiff-horse syndrome, Vet Rec 146:282, 2000. 6. Mayhew I: Personal communication, 2000. 7. Dyson S: Unpublished data, 1988-2002. 8. Divers T, Mohammed H, Cummings J, et al: Equine motor neuron disease: findings in twenty-eight horses and proposal of a pathophysiological mechanism for the disease, Equine Vet J 26:409, 1994. 9. Clegg P: Lyme disease, Proc Br Equine Vet Assoc Congress 39:155, 2000. 10. Lindenmayer J, Weber M, Onderdonk A: Borrelia burgdorferi infection in horses, J Am Vet Med Assoc 194:1384, 1989. 11. Marien T: Standing laparoscopic herniorrhaphy in stallions using cylindrical polypropylene mesh prosthesis, Equine Vet J 33:91, 2001.

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Assessment of Acute-Onset, Severe Lameness Sue J. Dyson

FIELD DIAGNOSIS OF THE INJURED HORSE The assessment of an acutely lame horse presents a challenge in diagnosis and in dealing with the people associated with the animal, particularly if lameness occurs at a competition. The horse may have fallen and been lame immediately or may have pulled up lame, and the veterinary surgeon may be called to examine the horse on course in full view of the public. Ideally the horse should be transported to an examination area for comprehensive evaluation, but the veterinary surgeon must establish whether the injured limb requires support, before moving the horse. Although the horse may be very lame, establishing a definitive diagnosis for the cause of the lameness at this stage may be difficult. This may surprise riders, trainers, and owners, and maintaining their confidence in what is an emotionally charged situation can be quite difficult. If a fracture is suspected, pressure to destroy the horse humanely without delay may be felt. Although some fractures are catastrophic and horses merit immediate destruction on humane grounds (e.g., a spiral fracture of the humerus), other serious fractures can be repaired. Therefore as much information as possible about the site of the fracture and its configuration should be obtained before a decision is made. The limb should be supported appropriately before the horse is moved for radiographic examination. If a horse must be destroyed on humane grounds at a competition, this should be done off the course. Although a diagnosis may be obvious in some horses immediately after the onset of lameness, the veterinarian must recognize that severe lameness may occur without an evident cause. Serial re-examinations over the following hours or days may be required before a diagnosis can be reached. Sometimes the lameness resolves spontaneously within 12 to 18 hours and its cause is never established. The clinician must be aware of the most common causes of acute-onset, severe lameness, which include the following: • Sub-solar abscess • Fracture • Laminitis • Intra-synovial sepsis • Periarticular cellulitis When lameness occurs during training or competition, a spectrum of other injuries must be considered. However, a history of acute-onset, severe lameness during exercise must not mislead the clinician into thinking that lameness must be caused by internal or external trauma associated with exercise. Lameness may still be caused by pain from a sub-solar abscess. This chapter describes a systematic approach to management of a horse with sudden-onset, severe lameness and focuses particularly on injuries that occur during work.

ASSESSMENT Medical History While performing an initial visual appraisal of the horse, establishing a history is useful. The examiner must determine the following:

• Any previous lameness, tendon or ligament injury, or history of tying up • Date of last shoeing • Circumstances of lameness: whether the horse was performing normally, fell, hit a fixed fence, or collided with a fixed object such as a guide rail or a tree. The horse may have reared in the starting stalls or reared and fallen over backward. Another horse may have kicked it. The clinician should also be aware of common injuries in the discipline in which the horse is competing. The horse may be distressed because of the severity of pain and excited because of the atmosphere of a competition and thus difficult to restrain and examine adequately. Sedation with romifidine or detomidine, with or without butorphanol, may be necessary to facilitate examination of the horse. The horse’s posture should be observed while it stands still and walks a few steps. If the horse bears weight only on the toe, it may be inapparent that a horse has lost some support of the fetlock because of rupture of the superficial digital flexor tendon (SDFT) in the metacarpal region or at the musculotendonous junction in the antebrachium, unless it walks a few steps.

Limb Examination The veterinarian should establish whether the horse is able and willing to bear weight on the limb, bearing in mind that after a fall, a neurological component may contribute to the lameness, in addition to the pain. The horse’s demeanor should be assessed; the degree of pain and distress usually but not invariably reflects the severity of the injury. The horse may be greatly distressed, shifting weight constantly between limbs, and may be reluctant to move. Reluctance to move may be due to a bilateral problem (e.g., bilateral severe superficial digital flexor [SDF] tendonitis) or a more generalized problem such as equine rhabdomyolysis (tying up). The horse should be carefully appraised visually to identify areas of swelling or a laceration. If the horse’s limbs are covered in mud or grease (commonly applied to the limbs during the speed and endurance phase of a Three-Day Event), this should be washed off before proceeding with the evaluation. Boots, bandages, and the saddle and martingale should also be removed. Temporary studs in the shoes should be removed, because they may be more difficult to remove later if the injury is severe. The horse may be obviously lame on a hindlimb or forelimb, but this may mask a similar, less severe injury in a contralateral limb or a different injury; therefore all limbs should be assessed carefully. For example, a racehorse may develop a lateral condylar fracture of the third metacarpal bone in one limb and SDF tendonitis in the contralateral limb. Although the former injury results in a more severe lameness, the latter may be more important to the horse’s long-term prognosis. Occasionally, forelimb and hindlimb lameness are concurrent. Each limb should be palpated systemically with the horse bearing weight and not bearing weight. The examiner should pay careful attention to heat, swelling, abnormal muscle texture, pain on firm pressure, pain induced by manipulation of a joint, restriction of flexibility of a joint, an abnormal range

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of motion of the joint, audible or palpable crepitus, and the intensity of the digital pulse amplitudes. The position of the shoe should be assessed carefully. A shoe that has moved slightly may result in nail bind. Hoof testers should be systemically applied across the wall and sole, gently at first and then firmly. Percussion should also be applied to the sole of the foot with the limb picked up and to the wall with the limb bearing weight. The clinician should not forget that if the sole is very hard, eliciting pain with hoof testers may not be possible, despite the presence of a sub-solar abscess. The limbs should be carefully assessed for lacerations. Serious damage may occur to underlying structures if the laceration was sustained while the horse was moving at speed, and the position of the laceration and the site of damage to underlying structures may not coincide.

Shoulder and Chest Injuries to the shoulder region usually result from a fall or collision, which may result in severe bruising only or a fracture. A fracture of the supraglenoid tubercle of the scapula results in severe lameness (Fig. 13-1). Slight soft tissue swelling may develop, usually without audible or palpable crepitus, and pain on palpation may be difficult to differentiate from that caused by severe bruising alone. Articular fractures of the scapula may be associated with audible crepitus on manipulation of the limb. Fractures of the body of the scapula or the humerus are usually associated with severe lameness, soft tissue swelling, and pain in that area. After collision with a fixed object, or occasionally a fall, the scapulohumeral joint may become luxated or subluxated, with or without a fracture of the glenoid cavity of the scapula. The horse bears weight on the limb reluctantly, soft tissue swelling develops rapidly, and the distal aspect of the scapular spine may become more difficult to palpate. The limb may appear straighter than usual. A collision also may result in collateral instability of the shoulder, so-called shoulder slip, usually caused by trauma to nerves of the brachial plexus. The horse may have pain-related lameness because of bruising, together with mechanical lameness caused by neurological dysfunction (Fig. 13-2). Although major fractures of the scapula and humerus are usually readily evident by clinical signs, most other shoulder injuries require radiographic and sometimes ultrasonographic examination to reach a diagnosis. Pectoral muscle tears may result in similar clinical signs, with severe lameness and distress. Repeated clinical examinations may reveal the site of muscle rupture, with increasing evidence of hemorrhage, inflammatory effusion, and edema. Rib fractures can also result from direct trauma or from falls and occur most commonly in steeplechasers and polo ponies. Fractures in the region of the scapula and triceps result in acute, severe forelimb lameness. More caudal fractures may result in extreme stiffness and may cause severe respiratory embarrassment. Lameness associated with the upper forelimb may also be caused by strain of the biceps brachii or brachiocephalicus muscles or hematoma formation. Careful, deep palpation of these muscles is required to identify focal pain and possibly swelling or abnormal muscle texture.

Elbow and Carpus Acute-onset lameness associated with pain arising from the elbow region is rare, except as the result of a fall or kick. Fracture of the olecranon process of the ulna is the most common injury (Fig. 13-3). If the fracture is non-displaced, the horse may stand normally, but with severe pain or if the fracture is complete with loss of triceps function, the horse stands with a dropped elbow.

Fig. 13-1 Mediolateral radiographic view of the left shoulder of an advanced event horse that fell during competition 3 days previously and developed severe left forelimb lameness from a displaced comminuted fracture of the supraglenoid tubercle of the scapula.

Fig. 13-2 Lateral radiographic view of the mid-cervical region of a 6-year-old event horse that fell on a cross-country course. The horse was not bearing weight on the left forelimb and showed moderate hindlimb ataxia. The synovial facet joints were fractured between the sixth and seventh cervical vertebrae (arrow). A cause of the forelimb lameness was not identified and the lameness resolved within 24 hours. The horse had a complete functional recovery but had some residual neck stiffness. Acute-onset lameness associated with the carpus occurs most commonly, in racehorses, both flat racehorses and steeplechasers, and usually is associated with a chip or slab fracture or, less commonly with hemarthrosis. Synovial effusion within the antebrachiocarpal or middle carpal joint usually develops rapidly. The horse may resent maximal flexion of the carpus,

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Mediolateral radiographic view of left elbow of an event horse that was very lame after a fall and stood with the elbow dropped. The olecranon of the ulna sustained a displaced, comminuted fracture.

Fig. 13-3

and direct palpation of the carpal bones may elicit pain. Fracture of the accessory carpal bone usually results from a fall and occurs most commonly in steeplechasers; such fractures may be associated with effusion within the carpal sheath. Acute tears of the accessory ligament of the SDFT sometimes occur in polo ponies, with associated distention of the carpal sheath.

Forelimb Soft Tissue Injuries Injuries of the forelimb suspensory ligament (SL) (proximal, mid-body, and branch lesions), and of the forelimb SDFT occur most commonly in racehorses and event horses, whereas desmitis of the accessory ligament of the deep digital flexor tendon (ALDDFT) occurs more commonly in show jumpers, older steeplechasers, and polo ponies. Severe, apparently acute onset lesions of the SDFT occasionally occur in show jumpers, especially those of international standard. Evaluation of the posture of the limb and the presence of heat, pain, and swelling are important for accurate diagnosis. Clinical signs associated with these injures can vary markedly. Substantial lesions of the SDFT can develop without detectable lameness, whereas a large tear can result in acute, severe, non–weight-bearing lameness. Bilateral tears may result in extreme distress, a reluctance to move, and a laminitic-like stance. In event horses, lameness can develop after the speed and endurance phase of a Three-Day Event, associated with SDF tendonitis, but no clinical signs may suggest the injury. Swelling or localized heat and pain may take several days to develop despite improvement or resolution of the lameness. Therefore careful re-appraisal of the horse over the next few days is strongly recommended if an event horse develops an acute-onset, forelimb lameness for which no diagnosis can be identified. Rupture of the SDFT results in hyperextension of the fetlock with normal foot placement. Elevation of the toe with normal angulation of the fetlock indicates disruption of the deep digital flexor tendon (DDFT). Hyperextension of the fetlock and elevation of the toe reflect laceration or rupture of the SDFT and the DDFT. Sinking of the fetlock to the ground indicates disruption of the suspensory apparatus, with or without the flexor tendons. Severe lameness and distress, with hyperextension of the fetlock, without obvious swelling in the metacarpal region suggests rupture of the SDFT at the musculotendonous junction. This injury occurs most commonly in steeplechasers. Rupture of the SDF tendon usually is a sequel to a previous

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injury; therefore the tendon is generally chronically enlarged. Detection of the rupture is easiest at the peracute stage, before exudate and hemorrhage fill the deficit. The site of rupture is usually in the mid-metacarpal region. Desmitis of the ALDDFT usually causes acute-onset, moderate to severe lameness with rapid development of soft tissue swelling in the region of the ligament. However, recurrent injuries can develop with no detectable alteration of a chronically enlarged ligament. The degree of lameness associated with a SL injury varies from mild to moderate but may be worse if a concurrent fracture of the second or fourth metacarpal bone or of the apex of a proximal sesamoid bone exists, and these structures should be evaluated carefully. Some severely lame horses with proximal suspensory desmitis have no palpable abnormalities. Each of the tendons and ligaments in the metacarpal region should be palpated carefully, from proximally to distally with the limb bearing weight and picked up. The size, shape, and consistency of the tendons and ligaments and any pain on palpation should be carefully assessed. With severe SDF tendonitis the horse may be distressed, and peritendonous edema rapidly develops, which makes accurate palpation of the tendon difficult. Bilateral SDF tendonitis sometimes occurs, with the only detectable palpable abnormality being slight enlargement of each tendon and rounding of its margins. The clinician must be aware of this, because these lesions may be missed if one assumes that because the limbs feel symmetrical, the tendons are normal.

Fractures of the Distal Aspect of the Limbs A fracture of the lateral, or more rarely the medial, condyle of the third metacarpal or metatarsal bone results in acute-onset, severe lameness. If the fracture is incomplete and non-displaced, no palpable abnormality may be detectable, although some effusion in the metacarpophalangeal joint usually develops within 12 to 24 hours. The horse may resent fetlock flexion; however, some horses become so distressed that in the acute phase, determining whether pressure or joint manipulation causes pain is impossible. The same can apply for a fracture of the proximal phalanx. Subluxation of the metacarpophalangeal joint occasionally occurs, with disruption of a collateral ligament, with or without an associated fracture. The horse may be very lame, but during normal load bearing the joint may appear to be aligned normally. Instability of the joint may only be detectable with the joint stressed with the limb not bearing weight.

Feet Trauma to the palmar aspect of the pastern may result in an innocuous skin wound but severe damage to the underlying soft tissue structures. The branches of the SDFT, the DDFT, and the digital flexor tendon sheath are particularly vulnerable. Posture of the limb should be carefully assessed to determine which structure or structures may be involved. An over-reach on the bulb of the heel can result in severe, deep-seated bruising and lameness, especially on hard ground. Injuries of the foot are common, especially in event horses. The differential diagnosis should include sub-solar hemorrhage (especially corns), nail bind, a sub-solar abscess, and a fracture of the distal phalanx. If the horse shows any reaction to percussion of the foot or pressure applied with hoof testers, the shoe should be removed for further exploration of the foot. If the horse is very lame, removal of each nail individually using nail pullers may be preferable to levering off the shoe.

Hindlimb Injuries When presented with a horse with acute hindlimb lameness that developed during exercise, consideration should always

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be given to tying up, even if the hindlimb musculature feels soft and local pain cannot be elicited and the horse is not unduly distressed. The clinical manifestations of tying up vary considerably from acute, severe bilateral or unilateral hindlimb lameness with obvious firmness of the muscles of the hind quarter, with or without swelling, to a moderate unilateral hindlimb lameness that developed after the horse was not moving as freely as normal, with no detectable palpable abnormality. This lameness may persist for several hours but usually resolves within 12 to 18 hours. Occasionally, tying up can affect forelimbs, alone or together with the hindlimbs. Measurement of substantially raised serum creatine kinase concentration 3 to 24 hours after the onset of lameness may be the only way to reach a definitive diagnosis. Alternatively, a horse may not be moving as freely as normal during the competition and subsequently may be withdrawn; further clinical signs may not develop. Major hindlimb muscle rupture of quadriceps, semimembranosus, gastrocnemius, adductor, or belly muscles results in severe lameness and distress, but diagnosis may be difficult. Careful palpation may reveal a site of rupture. Detection of acute muscle strains may be possible when superficial muscles are involved. Pain on palpation and sometimes swelling may be present; however, this is not always the case, and evaluation of deep muscles is limited. Stifle trauma is common in horses that jump fixed fences at speed, even if the rider cannot recollect the horse hitting a fence. Lameness caused by a fracture may be sudden and severe in onset, and the horse may pull up, but in some horses it does not become apparent until the horse has finished. Because the cranial aspect of the stifle is relatively poorly covered with soft tissues, the bones are particularly susceptible to bruising or fracture (Fig. 13-4). The degree of pain on palpation does not necessarily reflect accurately the severity of the injury. Development of femoropatellar or femorotibial effusion or marked periarticular soft tissue swelling suggests a fracture. Sometimes a displaced fragment of bone can be palpated. The superficial location of the femoropatellar joint capsule also makes it vulnerable to puncture and the introduction of infection, and effusion and severe lameness may develop rapidly.

Most horses with stifle injuries require radiographic examination to establish or confirm the presence of a fracture. Although lameness associated with bruising may initially be severe, the horse generally rapidly improves within 24 to 48 hours, whereas with most fractures the lameness usually persists unchanged. The horse may be reluctant to extend the stifle and tends to stand with the limb semi-flexed and the weight on the toe, a posture also typical of severe foot pain. Occasionally severe ligamentous injury occurs in the stifle, which cannot be detected radiographically. Rupture of fibularis tertius usually results from a traumatic episode, with the limb getting trapped in an extended position, and results in a severe lameness with the horse unwilling to load the limb fully. Passive extension of the hock is pathognomonic. Acute injuries to the hock are uncommon, unless the horse has a severe fall resulting in damage to the hock joint capsules and the collateral ligaments or a lateral malleolar fracture of the distal tibia. The horse usually is severely lame and rapidly develops distention of the tarsocrural joint capsule and periarticular soft tissue swelling. Radiographic examination is indicated to determine the extent of the damage. Less commonly, slab fractures of the central or third tarsal bone cause acute, severe lameness. Kick injuries may result in a fracture. Displacement of the SDFT from the tuber calcanei may occur suddenly, resulting in marked distress, especially if the tendon continues to move on and off the tuber calcanei. The tendon may slip laterally, or less commonly medially, and occasionally splits. Peritendonous soft tissue swelling develops rapidly. The horse is reluctant to bear weight on the limb and characteristically shows extreme distress, caused by pain or instability. Careful palpation usually confirms the diagnosis, although acute soft tissue swelling may make this difficult in the initial period after injury. Periarticular cellulitis of the tarsal region results in an extreme lameness associated with the rapid development of extensive soft tissue swelling, which is exquisitely sensitive to touch. The horse is often lamer than with a fracture, and swelling is more extensive than with synovial infection. Injuries to the soft tissue structures of the metatarsal and pastern regions are less common than those of the metacarpal and forelimb pastern regions. Suspensory branch injuries are the most common injuries resulting from direct blunt trauma. Acute tears of the DDFT may occur within the digital flexor tendon sheath, with rapid development of effusion. Fractures of the third metatarsal bone and phalanges are also less common than in the forelimbs, except in barrel racing or cutting horses or polo ponies. Plantar process fractures of the proximal phalanx are rare but do occur in racehorses and result in moderate to severe lameness, with pain on manipulation of the fetlock, effusion, and in some horses periarticular soft tissue swelling especially on the plantar aspect. Stability of the fetlock should be assessed carefully.

Stress Fractures

Fig. 13-4 Cranioproximal-craniodistal oblique radiographic view of right stifle of an event horse that hit the penultimate fence at the World Equestrian games. The horse completed the course, pulled up slightly lame, and was very lame within a few hours. The arrows show an articular fracture of the medial pole of the patella (arrows).

In young Thoroughbred racehorses the possibility of a fatigue or stress fracture must always be considered. The most common sites are the humerus, radius, ilial wing, tibia, third metacarpal bone, and tarsus. With the exception of ilial wing fractures, in which asymmetry of the tubera sacrale and pain on palpation in this area may be obvious, localizing clinical signs may otherwise be absent. A definitive diagnosis can rarely be made by clinical examination alone.

Hemarthrosis Hemarthrosis may occur in any joint and results in acute onset, non–weight-bearing lameness associated with distention of the joint capsule. Lameness often improves rapidly

CHAPTER 13

• Assessment of Acute-Onset, Severe Lameness

within the following 48 hours. Diagnosis is based on ultrasonography and synoviocentesis. Draining blood from the joint produces rapid relief of clinical signs.

TRANSPORTATION In any horse with severe lameness in which making a tentative diagnosis based on a preliminary but thorough clinical examination is not possible, a decision has to be made about whether the horse is fit to travel, whether any risks are involved in travel, and whether the horse should be stabled as close as possible and be reassessed later or the following day (if this is practical). Whether the horse is insured should be established, together with the terms of the insurance policy. The majority of horses can be taken safely to the nearest adequate diagnostic facility, which ideally should have a loading ramp, a veterinarian experienced in orthopedics, facilities for hospitalization, and high-standard radiographic, ultrasonographic, and possibly nuclear scintigraphic, equipment. Facilities for orthopedic surgery are not necessarily essential, although desirable, because the first step must be to reach an accurate diagnosis. Having reached a diagnosis, the limb may then be appropriately supported to minimize risks of exacerbating the injury, if the horse is to be treated conservatively, or during induction of general anesthesia or for transfer to a suitable surgical facility. If a hindlimb fracture is suspected, the horse should be tied up (cross tied). For transport for further diagnostic investigation or surgical treatment the injured limb should usually be supported using a Robert Jones bandage,1 with or without splints, or an appropriate commercial splint, bearing in mind the proposed site of injury2 (see Chapter 87). For forelimb injuries the horse should ideally travel facing backward, although some low-loading ambulances are not designed for loading from the front.3 When possible a low-loading trailer should be used, but if this is not available, the ramp of the vehicle should be placed on a slope to minimize the gradient for loading and unloading. If a diagnosis has been made for a horse with an injury that requires rapid surgical treatment, the limb should be supported in the most appropriate way and the horse referred to the nearest surgical facility, or to the best surgical facility in close proximity to the horse’s place of origin, or to the person with the most expertise and experience dealing with that kind of injury. Provided that the limb is adequately immobilized and adequate pain relief is possible, the horse should be fit to travel several hours safely and humanely.

GUIDELINES FOR HUMANE DESTRUCTION OF AN INJURED HORSE If the horse is insured for all risks of mortality, owners, trainers, and other interested people may request humane destruction. The American Association of Equine Practitioners (AAEP) and the British Equine Veterinary Association (BEVA) have issued guidelines indicating the requirements that should be fulfilled to satisfy a claim under a mortality insurance policy. Nonetheless, the decision to advise an owner to destroy a horse on humane grounds must be the responsibility of the attending veterinary surgeon, based on the assessment of clinical signs at the time of the examination or examinations, regardless of whether the horse is insured. The veterinary surgeon’s primary responsibility is always to ensure the welfare of the horse. On occasion the attending veterinary

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surgeon will advise euthanasia, but such a decision may not necessarily lead to a successful insurance claim. It is important that all parties are aware of these potential conflicts of interests before a horse is destroyed. The owner’s responsibility is to ensure compliance with any policy contract with an insurer. The AAEP has issued the following guidelines for recommending euthanasia: The AAEP recommends that the following criteria should be considered in evaluating the immediate necessity for intentional destruction of a horse. It should be pointed out that each case should be addressed on its individual merits and that the following are guidelines only. Not all criteria must be met in each case. 1. Is the condition chronic, incurable and resulting in unnecessary pain and suffering? 2. Does the immediate condition present a hopeless prognosis for life? 3. Is the horse a hazard to itself or its handlers? 4. Will the horse require continuous medication for the relief of pain for the remainder of its life? Justification for euthanization of a horse for humane reasons should be based on medical grounds, not economic considerations; and further the same criteria should be applied to all horses regardless of age, sex or potential value.

The BEVA guidelines for compliance for a mortality insurance policy are as follows: That the insured horses sustains an injury, or manifests an illness or disease, that is so severe as to warrant immediate destruction to relieve incurable and excessive pain, and that no other options of treatment are available to that horse, at that time. If immediate destruction cannot be justified, then the attending veterinary surgeon should provide immediate first aid treatment before: 1. Requesting that the insurance company be contacted, or, failing that 2. Arranging for a second opinion from another veterinary surgeon.

It is essential that the attending veterinary surgeon keep a written record of the injuries sustained by the horse, its identification, and the date, time, and place. The owner or agent should whenever possible sign a form consenting to euthanasia. Insurance companies frequently require some form of examination after death and may request an independent postmortem examination, and this must be borne in mind when arranging for disposal of the carcass.

REFERENCES 1. Campbell N: Application of a Robert Jones bandage. In Dyson S, editor: A guide to the management of emergencies at equine competitions, Newmarket, UK, 1996, Equine Veterinary Journal. 2. Walmsley J: Management of a suspected fracture. In Dyson S, editor: A guide to the management of emergencies at equine competitions, Newmarket, UK, 1996, Equine Veterinary Journal. 3. Ellis D: Transporting an injured horse. In Dyson S, editor: A guide to the management of emergencies at equine competitions, Newmarket, UK, 1996, Equine Veterinary Journal.

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CHAPTER •

14

The Swollen Limb Sue J. Dyson

he development of diffuse or more localized swelling in one or more limbs can present a diagnostic challenge, requiring a systematic approach to identify the cause. Although the metacarpal, metatarsal, and pastern regions are most commonly affected, an entire limb may be swollen, or swelling may initially be restricted to the antebrachium or crus or the carpus or tarsus, with swelling subsequently spreading distally. This chapter discusses an approach to diagnosis and management but does not provide exhaustive differential diagnoses and treatments. Some conditions are discussed in more detail in other chapters.

T

DIAGNOSIS Many stabled horses develop some degree of enlargement of the distal limbs, especially the hindlimbs, that dissipates with work. Termed filled legs or cold edema (stocked-up, stovedup), this swelling may be controlled by applying stable bandages and is of no consequence.

History Accurate diagnosis of the cause of limb swelling requires knowledge of the history. • Was the problem sudden or gradual in onset? • What is the duration of the swelling? It may be pertinent to establish when the owner last thought that the horse was normal, especially in horses that are not inspected reguarly while kept at pasture. The actual duration of swelling may be longer than the owner recognized. The veterinarian also should bear in mind that some owners are remarkably unobservant, despite maintaining that they veterinarian and groom the horse thoroughly daily. • Were any swellings pre-existing? • What was the initial distribution of the swelling and has this changed? • Has similar swelling appeared previously (lymphangitis may be a recurrent problem)? • Does any history of trauma exist? • Has the limb been bandaged, or have boots or bandages been used for exercise? Overly tight bandages can rapidly result in severe cellulitis, skin excoriation, and hair loss. Sand or grit inside a boot can provoke severe skin inflammation and diffuse soft tissue swelling. • Has the horse had tendonitis or desmitis? Recurrent injury may be much more severe and result in diffuse swelling, prohibiting accurate palpation of the injured structure. • Has the horse had any other recent clinical problems (strangles may predispose to purpura hemorrhagica)? • Does the horse show any other clinical signs, and could the limb swellings reflect systemic disease? • Is the horse lame, and when did lameness develop relative to the recognition of swelling? If swelling preceded the lameness, more than one problem may exist.

• Has the horse received any treatment, and what was the response? Has anything topical been applied to the limb that may be irritant? Swelling in a single limb usually reflects a local problem, whereas swelling in several limbs may be due to systemic disease or a primary skin problem. The differential diagnosis should include the following: sub-solar abscess (see Chapter 28); mud fever or scratches; scabby skin lesions on the palmar aspect of the fetlock; other bacterial pyodermas; hemorrhage or thrombosis (see Chapter 38); desmitis or tendonitis (see Chapters 70, 72, and 73); cellulitis associated with superficial digital flexor tendonitis (see Chapter 70); skin necrosis and cellulitis after topical application of proprietary products; infected tendon or tendon sheath; cold edema; cellulitis caused by trauma or infection; fracture; or hypertrophic osteopathy (see Chapter 38); muscle rupture (see Chapter 13); muscle trauma resulting in compartment syndrome (see Chapter 84); lymphangitis; photosensitization; equine viral arteritis; heart failure; and hypoproteinemia.

Clinical Examination A systematic clinical examination should be performed by careful observation and palpation. The veterinarian should assess the horse’s posture, demeanor, and attitude. Depression may reflect pain or infection. • Is the horse febrile? The clinician should determine whether one or more limbs are involved. • What is the distribution of the swelling? Is it localized or more diffuse? Swelling associated with a sub-solar abscess is usually diffuse and involves the pastern and metacarpal or metatarsal region, extending a variable degree proximally, and is symmetrically distributed around the limb. In contrast, swelling associated with direct trauma may be restricted to the metacarpal region in the acute phase and only later spread distally. • Does the swelling relate to a joint or to a long bone and the surrounding soft tissues? • Where is swelling maximal? Is swelling predominantly on one side of the limb, which may reflect trauma, because of the horse becoming cast? • Does the metacarpal (metatarsal) region have a straight palmar (plantar) contour? Diffuse swelling in the metacarpal region is unlikely to reflect superficial digital flexor tendonitis if the palmar aspect of the limb is straight. • Is the swelling cool, warm, or hot? Hot swelling is most likely to be associated with infection. • Is the swelling tense, often reflecting infection, or soft? • Is evidence of pitting edema present? • Does light digital pressure or firm pressure elicit pain? Pain caused by only light pressure is often associated with cellulitis caused by infection or less commonly by intra-tendonous infection. • How does the location of pain relate to the site of maximal swelling? • How easily can underlying anatomical structures be palpated, and does palpation cause pain? The

CHAPTER 14 veterinarian should note that scabby skin lesions overlying soft tissue swelling can in themselves be remarkably painful. • Does a draining tract suggest an abscess, cellulitis, or infectious osteitis or osteomyelitis? • Does joint manipulation cause pain? • Do any skin lesions exist through which infection may have entered? This may not be readily apparent in a horse with a long hair coat, and clipping may be necessary. In a horse kept at pasture the limb may be caked in mud, and thorough cleaning may be necessary before an accurate clinical examination can be made. • Do any other skin lesions reflect a primary dermatological problem? The clinician should try to categorize any lesions identified. The digital pulse amplitudes should be assessed: any increase highly suggests a primary foot problem. The response to pressure and percussion applied with hoof testers should be evaluated. Pulse rate, the quality of the peripheral pulses, capillary refill time, and careful auscultation of the heart and lungs should reveal whether a primary cardiac problem exists. The mucous membranes should be examined for evidence of petechial hemorrhages, which can be seen with purpura hemorrhagica. The veterinarian should relate the swelling to the color of the limbs; swelling confined to white limbs may result from photosensitization. The clinician should establish the degree of lameness and bear in mind that mild stiffness may result from extensive limb swelling and mechanical restriction. Extremely severe lameness often reflects infection, either periarticular (e.g., peritarsal cellulitis; see Chapter 45), intra-articular, intra-thecal, intra-tendonous, or sub-solar. A horse with a fracture may be less lame. The results of this clinical examination should suggest the likely causes of the swelling, but definitive diagnosis might not be possible without further investigation. This may include radiography, ultrasonography, routine hematological testing, measurement of total protein and fibrinogen, and liver enzyme levels if indicated. Paired serum samples may be required to confirm equine viral arteritis. Treating the horse symptomatically to reduce the soft tissue swelling may be helpful to facilitate more accurate palpation. This may include the use of non-steroidal anti-inflammatory drugs (NSAIDs), hydrotherapy, poulticing or leg sweats, bandaging, and walking, with or without antimicrobial medication. Without evidence of a primary infectious process the response to corticosteroids may be helpful diagnostically, because limb filling may be an immune-mediated response. The clinician should be prepared to make repeated examinations if a primary diagnosis is not readily apparent. Early periosteal new bone associated with hypertrophic osteopathy is readily overexposed, and greatly reduced exposure factors are required for its radiographic detection. On the first day of examination the results of radiographic and ultrasonographic examinations may be misleading, and repeated examinations may be necessary. Following trauma, laceration, or both injuries, to the antebrachium, crus, and metacarpal or metatarsal regions, delayed-onset lameness caused by an occult spiral fracture of the radius, tibia, or third metacarpal or metatarsal bones is possible. Many oblique radiographic views or follow-up examination be may be necessary to identify the fracture. If extensive cellulitis occurs around a joint or tendon sheath, but intra-articular or intra-thecal infection are suspected, the examiner should be cautious about performing synoviocentesis through infected tissues, because iatrogenic intra-articular or intra-thecal infection may ensue. If skin lesions are identified as a possible primary cause of limb swelling, but these fail to respond to topical or systemic treatment, obtaining skin biopsies for culture and histological examination or seeking specialist advice from a dermatologist may be necessary.

• The Swollen Limb

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MANAGEMENT Mud Fever Mud fever (scratches or pastern dermatitis) is associated with bacterial or fungal skin infection and usually is restricted to the palmar or plantar aspect of the pastern but sometimes extends farther proximally if severe. Mud fever is associated with many excoriated skin lesions, which may develop severe crusting. Deep fissures may develop in the skin, especially if the condition goes unrecognized or in horses with many skin folds in the pastern region. Extensive edematous swelling often extends up the metacarpal and metatarsal regions. If the condition is mild, no associated lameness may occur, but severe lesions are associated with marked stiffness. The condition can occur in horses kept out in wet, muddy conditions or in horses that are stabled but work in a muddy environment. Certain soil types seem to be associated with a higher occurrence. Some horses seem prone to recurrent episodes, although this may in part reflect management practices. The condition is difficult to manage if the horse is left in wet, muddy pasture and it must be stabled. The affected areas should be clipped and thoroughly cleaned with chlorhexidine solution. The scabs should be softened to facilitate removal. If the condition is mild, no further treatment may be required, but if the condition is more severe, daily topical application of lanolin-based emollient cream with trimethoprim and sulfadiazine and dexamethasone is indicated, sometimes combined with systemic antimicrobial treatment. Alternatively, a proprietary topical preparation can be used. The limbs should be carefully cleaned and dried after exercise.

Scabs on the Palmar Aspect of the Fetlock Some horses seem prone to develop many small skin scabs on the palmar or plantar aspects of the fetlock. The scabs appear to be related to work on specific surfaces, which presumably cause skin irritation and subsequent bacterial infection. These skin lesions are often associated with diffuse swelling and can be exquisitely painful. The lesions rarely resolve spontaneously but usually resolve with penicillin therapy.

Cellulitis Caused by Trauma Direct trauma to a limb may result in extensive edematous soft tissue swelling unassociated with infection. If skin abrasion is concurrent, the site of the wound relative to synovial structures susceptible to infection must be evaluated carefully. Lameness may vary in degree, but if severe, the possibility of fracture must be considered. If little soft tissue covers the underlying bones, radiographic examination is prudent to eliminate the possibility of a fracture. With primary cellulitis, treatment with NSAIDs and rest and controlled exercise is usually all that is required.

Cellulitis Caused by Infection Cellulitis associated with infection from a penetrating wound usually results in fairly extensive soft tissue swelling, which tends to be warmer and more painful than noninfectious cellulitis (see Fig. 5-8). Associated lameness may also be severe, depending in part on the location of infection. If untreated, abscessation may develop in muscular areas and may require surgical drainage. Cellulitis may also be concurrent with infectious osteitis or osteomyelitis (see Chapter 38). Horse with acute infectious cellulitis usually respond well to systemic broad-spectrum antimicrobial treatment, unless clostridial organisms are involved (see Chapter 84).

Lymphangitis So-called lymphangitis occurs more commonly in hindlimbs than forelimbs and is often unilateral but may be bilateral. Diffuse soft tissue swelling occurs throughout the limb, often

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extending distad from immediately below the stifle. The superficial lymphatic vessels may appear more prominent than usual. Serum may ooze through taut skin. The degree of swelling usually results in mechanical stiffness that improves with progressive walking. Careful inspection may reveal some small skin lacerations, often in the more distal part of the limb. Once a horse has had a severe attack of lymphangitis, it seems prone to recurrence, often after seemingly innocuous skin abrasions. Although the condition appears to be triggered by infection, antimicrobial treatment alone is inadequate and usually must be combined with long-term corticosteroid treatment (dexamethasone 0.05 to 0.2 mg/kg once daily intravenously or intramuscularly, using the lowest dose necessary to control edema, and replacing with prednisolone 0.5 to 1 mg/kg intramuscularly or by mouth twice daily, when the dexamethasone dose is 30 minutes a day or walk on a mechanical walker. We believe horses usually are more active walking on a mechanical walker than in hand. Thoroughbred (TB) and Standardbred (STB) racehorse, event horse (EV), and sport horse (SH): exercise level- 1A/B plus trotting in hand for 5 to 10 minutes a day. TB racehorse, SH, and EV: trot under saddle 10 to 15 minutes once a day or swim. STB racehorses: walk only in the bike or swim. This level also includes 10 to 15 minutes of trotting on a treadmill. Small paddock turnout for all horses. Small paddock implies small enough not to be able to work up to a sustained canter or gallop. Large paddock turnout for all horses. TB and SH: 15 to 20 minutes a day of walk, trot, and canter under saddle, 3 days per week, plus any of the above levels. This level does not apply to most STBs. TB: 20 to 30 minutes a day of walk, trot and canter under saddle, 3 to 4 days a week. TB racehorse: “ponying” (being led from another horse) on the racetrack. This level does not apply to most STBs.

5

TB racehorse and EV: all of the above plus normal galloping. STB racehorse: all of the above plus jogging. SH: all of the above plus normal arena flat work with limited low fence jumping where applicable. Dressage horses: normal work minus lateral movements and special gaits. TB racehorse: all of the above plus faster gallops. EV: all of the above plus jumping. STB racehorse: all of the above plus training miles ≥2:10. SH: all of the above plus unlimited low fence jumping where applicable. Dressage: all of the above plus lateral movements and special gaits. Contest horses (reiners, cutters, and so on): all of the above plus practicing specific turns and movements. In essence, this is the maximal work level for any type of athletic horse. TB and EV: racing, fast works, and competing. STB racehorse: training miles 35%

*All have a total type or echo score > 3.

zones (Fig. 16-40). Zone 2A was designated the maximal injured zone because it had the lesion with the largest CSA (37%). The MIZ-CSA of 166 mm2 was 47% larger than the same zone of the contralateral normal SDFT. T-CSA of the 7 zones was 1179 mm2, 31% greater than the contralateral SDFT. Additional measurements included T-TS of 11, T-FAS score of 8, and %T-lesion of 22% (i.e., category V). Unlike many newly injured tendons or ligaments with similar T-TS and T-FAS scores, this re-injured SDFT had a difference in these scores. This may serve as a means to identify new versus re-injured structures ultrasonographically. Category VI Category VI injuries have substantial MIZCSA or T-CSA enlargement with more extensive hypoechogenic or anechogenic lesions than category V. The range of %T-lesion to qualify for category VI varies depending on the number of zone used to determine the “total” (Table 16-3). A 4-year-old TB racehorse gelding developed swelling of the left fore SDFT after a race 6 days earlier. Physical examination revealed slight swelling (2/5), moderate SDFT thickening (3/5), slight sensitivity to direct digital palpation (2/5), slight heat (2/5), and low-grade lameness (2/5). A large type 3 anechogenic lesion of the lateral half of the SDFT was seen in zone 2B, the maximal injured zone (MIZ-LCA 92 mm2 representing 54% of the tendon CSA). The MIZ-CSA was

114% larger than the contralateral normal zone 2B SDFT (see Fig. 16-15). Six of the 7 zones had hypoechogenic or anechogenic contiguous fiber bundles, with a 65% increase compared with the contralateral SDFT. T-LCSA was 300 mm2, resulting in a 28% T-lesion. T-TS (14) and T-FAS (14) were the same, a common finding in newly injured tendons, although not acute SL injuries.

Summary Tendon and ligament injuries can be graded from 1 to 6 to reflect the severity of injury. Advantages of using quantitative assessment in conjunction with clinical findings and qualitative evaluation include the following: 1. Confirmation or addition to a qualitative diagnosis. 2. Improved detection of subtle structural enlargement not accompanied by detectable echogenicity abnormalities, thus reducing interpretive errors. 3. Establishment of an objective means to categorize the severity of an injury, which can be used to determine prognosis for intended use and whether continued use or extended rest is the optimal choice. It also provides baseline information that can be compared with follow-up examinations.

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FAS

Zone

Structure SIze (mm2)

Lesion Size (mm2)

Type/Echo Score

0

1A

115

5 (3.86%)

1

1

1B

127

17 (12.60%)

1

2

2A

166

61 (36.57%)

2

3

2B

238

83 (34.88%)

3

1

3A

201

1.64 (32.34%)

3

1

3B

173

1.28 (16.24%)

1

0

3C

159

—

1179 (11.79 cm2)

258 (2.53 cm2)

Total 8 Maximal injury score (MIZ) MIZ-cross-sectional area (MIZ-CSA) MIZ-lesion cross-sectional area (MIZ-LCA) MIZ-echo (type) score (MIZ-TS) MIZ-fiber alignment score (MIZ-FAS)

2A 166 mm2 (+41%) 61 mm2 (37%) 2 2

Total (7 levels) cross-sectional area (TCSA) Total lesion cross-sectional area (TLCSA) Percent total lesion (% T-Hypoechoic) Total echo (type) score (TTS) Total fiber alignment score (TFAS) Average fiber alignment score (AFAS) Present category

1179 mm2 (+31%) 258 mm2 22% 11 8 1.1 V

STAGE SWEL 1/5 SEN 2/5 ANK. SINK

L H 0/5

11

Initial exam 2/5 THIC 3/5 1/5 T.SH 0/5 FLEX Neg.

A computer graphic of the left metacarpal region of the same horse as Fig. 16-39 shows seven data points for quantitative evaluation. The superficial digital flexor tendon is 31% larger than the normal limb, has a 22% T-lesion, a T-echo or type score of 11, a T-fiber alignment score of 8, and an average fiber alignment score of 1.1. The maximal injury zone is 2A. The overall category of fascicle compromise is V. ANK. SINK; Ankle sinking; FLEX, flexion; H, heat; L, lameness; SWEL, swelling; THIC, Thickening; T.SH, tendon sheath.

Fig. 16-40

4. Enhanced veterinary participation in the rehabilitation of a tendon or ligament injury. 5. Improved client appreciation of the injury and improved compliance for suggested exercise restraint and treatment. 6. Creation of a common ultrasonographic interprofessional language and provision of a valid tool for research purposes to evaluate treatment responses.

Exceptions As with most attempts to categorize medical injuries, exceptions most always are possible. The following are three common exceptions to quantitative categorization of tendons and ligaments: 1. Diffuse tendonitis/desmitis. This is an uncommon clinical presentation of SDFT thickening, which is seen mostly in 2-year-old TB racehorses and older event horses and show jumpers. The T-CSA measurements indicate substantial enlargement if the contralateral SDFT is normal. However, injury may be bilateral; therefore CSA measurements are compared with normal values for the breed, size, and age of the horse. Two-year-old TB racehorses in training tend to have larger T-CSA values than similar,

older horses. In these horses, not only is the SDFT enlarged, but the entire CSA has a subtle reduction in echogenicity that extends through several zones. Although the %T-lesion is high, it does not necessarily indicate severe tendon fiber disruption because the echogenicity score for each zone is type 1 or 2 and the FAS score is 1or 2. This indicates a diffuse tendonitis with little loss of tensile strength. Given time and restricted exercise, documentation with serial ultrasonography indicates that most 2-year-old horses generally do well (Fig. 16-33). 2. If the SDFT or SL is totally disrupted, fiber bundles in adjacent zones may appear artificially more hypoechogenic or anechogenic because of the loss of tension in the structure, which is otherwise known as relaxation effect.22 Clinically, tension is lost and the structure can be moved medially and laterally with ease. Ultrasonography shows a loss of parallel fiber alignment and a decrease in echogenicity. Measurement of CSA is difficult and can even be decreased at the maximal injured zone (Fig. 16-41). The diagnosis of complete rupture of a tendon or ligament is usually readily made clinically.

CHAPTER 16

•

Ultrasonographic Evaluation of the Equine Limb: Technique

16-41 Transverse (left) and longitudinal (right) images of zone 1B obtained with a standoff pad. The borders of the superficial digital flexor tendon (SDFT) are not defined, and most of the echoes present represent hematoma. The SDFT was completely ruptured. DDFT, Deep digital flexor tendon; ICL, accessory ligament of the DDFT; SL, suspensory ligament. 3. Total collapse of the SL is characterized clinically by an extreme extension of the metacarpophalangeal or metatarsophalangeal joint (4/5 ankle sink), with little swelling or significant thickening of the SL or SL branch, and no sensitivity to direct palpation. Rupture cannot be palpated, and it appears as though the entire suspensory system has lost its cross-links and stretched, although ultrasonography shows little evidence of fiber tearing. Ultrasonographic images do not reflect the severity of the clinical signs.

Clinical Applications If clinical evidence of swelling or thickening, with or without lameness, is present, the basic objective of an ultrasonographic evaluation is to determine the cause. Every effort must be made to determine whether tendons and ligaments are normal or abnormal and whether the lameness can be directly attributed to a soft tissue abnormality. Lameness may only be visible at high speeds in a racehorse or during special gait movements in a high-level dressage horse. In some instances the ultrasonographic data are insufficient to confirm the suspected cause, especially in subtle injury, although thorough evaluation and serial ultrasonographic examinations may provide clues. Incidental abnormalities may be identified that have no bearing on the lameness or represent old, stable injuries of no clinical significance. Careful identification of these abnormalities and serial ultrasonographic monitoring may determine their significance. Sometimes other imaging techniques, such as radiography or nuclear scintigraphy, also are required to completely appreciate an injury process. For example, evaluation of SL insertion injuries should also include radiographic assessment.

Timing of Ultrasonographic Examinations: When to Scan Timing of the initial ultrasonographic examination is critical. A clinician may be requested to examine a limb within hours of an injury. Peritendonous edema may obscure fiber damage because of acoustic enhancement, and the continued release of destructive enzymes may result in further ongoing fiber injury. Thus an examination shortly after an injury may not reveal the true extent of fiber damage. Ideally, an ultrasono-

187

graphic evaluation should be delayed until at least 48 to 72 hours after the injury. If an ultrasonographic examination is performed before this time, the time after injury should be recorded, exercise restricted to walking, and symptomatic therapy instituted. Physical and ultrasonographic evaluations should be repeated after an additional 72 hours. Significant hypoechogenic, anechogenic, or both types of lesions may be seen in an injury less than 72 hours old. The areas of reduced echogenicity may represent a combination of hemorrhage (seroma), edema, and fiber bundle injury. The diagnostic dilemma at this stage is that the clinician cannot accurately determine the relative contribution of each. It should not necessarily be assumed that the hypoechoic areas only represent fiber bundle injury. In most horses this assumption is true, but not always. We administer symptomatic antiinflammatory treatment and advise complete stall rest (exercise level 0) or limited hand walking (exercise level 1A) for 14 to 30 days, followed by an ultrasonographic re-evaluation. (The exception to this advice would be if tendon splitting surgery were the treatment of choice to attempt to decompress a core lesion). When the horse is re-examined, persistent hypoechoic areas represent fiber bundle compromise, because most inflammatory edema and hemorrhage will have resolved. The severity of the injury can now be determined, and we refer to this as the baseline evaluation. The baseline evaluation often reveals the same or increased severity of injury compared with the initial scan (especially in core lesions caused by enzymatic degradation of damaged fiber bundles or pressure necrosis). As an example, we can compare ultrasonographic images of a SDFT injury after 24 hours and after 22 days. The initial examination determined that the SDFT was 32% larger than the normal contralateral limb and had a 17% T-lesion (category V), a T-TS of 17, and a T-FAS of 16. After symptomatic therapy and a reduction of exercise to exercise level 1A, the baseline scans (22 days later) revealed a 12% increase in size of the SDFT compared with the normal limb, a 13% T-lesion (now category IV), a T-TS of 10, and a T-FAS of 12. The apparent decrease in severity was due to the resolution of the inflammatory response and absorption of the seroma. The baseline data represent the actual severity of fiber bundle compromise and serve as the starting point for rendering prognosis for intended use, treatment programs, and longterm rehabilitation exercise regimens.

Serial Ultrasonographic Examinations as Part of Case Management Serial ultrasonographic examinations are best performed when it is anticipated that the exercise level may be increased. This justifies the examination to the owner or trainer. In addition to the ultrasonographic assessment, the clinician must always consider the physiological principles of tendon and ligament healing and the necessary physiological time for healing for the severity of an injury before advising exercise level increases. With time and as quantitative ultrasonographic analysis is more commonly used to evaluate tendon and ligament repair, more definitive recommendations will develop concerning convalescent time based on the severity and location of an injury and the intended athletic function of the horse. The same applies to the quality of the repair. Horses destined for light work will be able to perform with a less than perfect repair, but racehorses and other high-level athletes will require optimal repair and a reasonable time to give the best chance for return to athletic use without reinjury. During rehabilitation a qualitative ultrasonographic evaluation of the clinically injured tendon is done to detect obvious lesions, evidence of re-injury, restricting peritendonous tendon sheath fibrosis, or restriction by the PAL. Objective, or quantitative, ultrasonographic assessments should also be determined.

188

PART I

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Diagnosis of Lameness

Guidelines for an optimum chance to return to racing include the following23: 1. At least a 60% decrease in category IV %T-lesion and 50 g/L) and other clinical signs of infectious arthritis (lameness, effusion, and heat) persist. In my experience these are horses that developed infectious arthritis after injection with a corticosteroid, were treated with systemic antibiotics and lavage, but not aggressive drainage, have a nidus of infected subchondral bone that keeps seeding the joint, or have a joint with severe cartilage erosion. The distribution of nucleated cells in synovial fluid is an important aid to diagnosis. In horses with early infectious arthritis, almost always nucleated cells comprise more than 80% neutrophils and commonly more than 90% neutrophils.

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Arthritis

The neutrophils usually appear healthy and not degenerate, although in overwhelming or aggressive infection, degeneration of neutrophils is seen. If synovial fluid has less than 75% neutrophils, infection is usually resolving. Techniques that may be useful clinically in the future for diagnosis include polymerase chain reaction (PCR) analysis for detecting base pairs of bacterial or viral DNA in the synovial fluid18,19 and determining enzyme and cytokine release that may be specific for infection.20,21 Benefits of PCR include rapid (80%6 and, we hope, will achieve success rates close to 100%. Aggressive surgical debridement and use of implantable elution materials for chronic administration and multiple site delivery of antimicrobial agents have improved prognoses. The prognosis in foals is more guarded. Septicemia, osteomyelitis, and hypogammaglobulinemia result in a lower prognosis for life in foals, and infection is eliminated in only 50%.7 Elimination of infection was achieved in 70%,1,6 50% survived,6,10 and 30% reached racing performance.1

FUTURE TREATMENTS Newer biodegradable polymers impregnated with antimicrobial drugs for direct joint insertion through an arthroscopic portal could greatly enhance the process of sustained drug delivery. Arthroscopic instrumentation can be used to insert the beads into the joints of standing horses. Medical therapies for intra-articular drug therapy in the future may focus on prevention of S. aureus adhesion. A prominent feature of S. aureus virulence is the production of a bacterial surface marker that recognizes adhesive matrix molecules in collagen, precipitating bacterial adherence.70,71 Monoclonal antibody, receptor antagonists, and vaccination challenges reduce the risk of obtaining infection with S. aureus in experimental animals.70-72 These therapies may also be useful in the horse, since S. aureus is the most common cause of joint infection in adult horses.

REFERENCES 1. Steel CM, Hunt AR, Adams PL, et al: Factors associated with prognosis for survival and athletic use in foals with septic arthritis: 93 cases (1987-1994), J Am Vet Med Assoc 215:973, 1999. 2. Palmer JL, Bertone AL: Joint structure, biochemistry and biochemical disequilibrium in synovitis and equine joint disease, Equine Vet J 26:263, 1994. 3. Bertone AL: Infectious arthritis. In Mcllwraith CW, Trotter GW, editors: Joint disease in the horse, Philadelphia, 1996, WB Saunders. 4. Cohen ND: Causes of and farm management factors associated with disease and death in foals, J Am Vet Med Assoc 204:1644, 1994. 5. Schneider RK, Bramlage LR, Moore RM, et al: Open drainage, intraarticular acid systemic antibiotics in the treatment of septic arthritis/tenosynovitis in horses, Equine Vet J 24:436, 1992. 6. Meijer MC, van Weeren PR, Rijkenhuizen AB: Clinical experiences of treating septic arthritis in the equine by repeated joint lavage: a series of 39 cases, J Vet Med Physiol Pathol Clin Med 47:351, 2000. 7. Schneider RX, Bramlage LR, Moore RM, et al: A retrospective study of 192 horses affected with septic arthritis/tenosynovitis, Equine Vet J 24:436, 1992.

8. Clegg PD: Idiopathic infective arthritis of the coxofemoral joint in a mature horse, Vet Rec 137:46, 1995. 9. Moore RM, Schneider RK, Kowalski J, et al: Antimicrobial susceptibility of bacterial isolates from 233 horses with musculoskeletal infection during 1979-1989, Equine Vet J 24:450, 1992. 10. Raisis AL, Hodgson JL, Hodgson DR: Equine neonatal septicaemia: 24 cases, Aust Vet J 73:137, 1996. 11. Madison JB, Reid BV, Raskin RE: Amphotericin B treatment of Candida arthritis in two horses, J Am Vet Med Assoc 206:338, 1995. 12. Kenney DG, Robbins SC, Prescott JF, et al: Development of reactive arthritis and resistance to erythromycin and rifampin in a foal during treatment for Rhodococcus equi pneumonia, Equine Vet J 26:246, 1994. 13. Bertone AL, McIlwraith CM, Jones RL: Comparison of various treatments for experimentally induced equine infectious arthritis, Am J Vet Res 48:519, 1987. 14. Hague BA, Honnas CM, Simpson RB, et al: Evaluation of skin bacterial flora before and after aseptic preparation of clipped and nonclipped arthrocentesis sites in horses, Vet Surg 26:121, 1997. 15. Madison JB, Sommer M, Spencer PA: Relations among synovial membrane histopathologic findings, synovial fluid cytologic findings and bacterial culture results in horses with suspected infectious arthritis: 64 cases (19791987), J Am Vet Med Assoc 198:1655, 1991. 16. Tulamo R-M, Bramlage L, Gabel A: Sequential clinical and synovial fluid changes associated with acute infectious arthritis, Equine Vet J 21:325, 1989. 17. Tulamo R-M, Bramlage L, Gabel A: The influence of corticosteroids on sequential clinical and synovial fluid parameters in joints with acute infectious arthritis in the horse, Equine Vet J 21:332, 1989. 18. Crabill MR, Cohen ND, Martin LJ, et al: Detection of bacteria in equine synovial fluid by use of the polymerase chain reaction, Vet Surg 25:195, 1996. 19. Stahl HD, Hubner B, Seidl B, et al: Detection of multiple viral DNA species in synovial tissue and fluid of patients with early arthritis, Ann Rheum Dis 59:342, 2000. 20. Spiers S, May SA, Harrison LJ, et al: Proteolytic enzymes in equine joints with infectious arthritis, Equine Vet J 26:48, 1994. 21. Arican M, Coughlan AR, Clegg PD, et al: Matrix metalloproteinases 2 and 9 activity in bovine synovial fluids, J Vet Med A Physiol Pathol Clin Med 47:449, 2000. 22. Bertone AL, Palmer JL, Jones J: Synovial fluid cytokines and eicosanoids as markers of joint disease in horses, Vet Surg 30:258, 2001. 23. Pilleul F, Garcia J: Septic arthritis of the spine facet joint: early positive diagnosis of magnetic resonance imaging: review of two cases, Joint Bone Spine 67:234, 2000. 24. Graif M, Schweitzer ME, Deely D, et al: The septic versus nonseptic inflamed joint: MRI characteristics, Skeletal Radiol 28:616, 1999. 25. Bertone AL, Tremaine WH, Macoris DG, et al: Effect of the chronic systemic administration of an injectable enrofloxacin solution on physical, musculoskeletal, and histologic parameters in adult horses, Am J Vet Res 217:1514, 2000. 26. Baldessari A, Bermingham E, Bargar A, et al: Evaluation of the gross and histologic changes in articular cartilage of neonatal foals dosed with enrofloxacin, Equine Vet J 2001 (in review). 27. Zhanel GG: Influence of pharmacokinetic and pharmacodynamic principles on antibiotic selection, Curr Infect Dis Rep 3:29, 2001. 28. Godber LM, Walker RD, Stein GE, et al: Pharmacokinetics, nephrotoxicosis, and in vitro antibacterial activity associated with single versus multiple (three times) daily gentamicin treatments in horses, Am J Vet Res 56:613, 1995.

CHAPTER 66 29. Green SL, Conlon RD: Clinical pharmacokinetics of amikacin in hypoxic premature foals, Equine Vet J 25:276, 1993. 30. Wichtel MG, Breuhaus BA, Aucoin D: Relation between pharmacokinetics of amikacin sulfate and sepsis score in clinically normal and hospitalized neonatal foals, J Am Vet Med Assoc 200:1339, 1992. 31. Raisis AL, Hodgson JL, Hodgson DR: Serum gentamicin concentration in compromised neonatal foals, Equine Vet J 30:324, 1998. 32. Firth EC, Klein WR, Nouws JF, et al: Effect of induced synovial inflammation on pharmacokinetics and synovial concentration of sodium ampicillin and kanamycin sulfate after systemic administration in ponies, J Vet Pharmacol Ther 11:56, 1988. 33. Lloyd KCK, Stover SM, Pascoe JR, et al: Synovial fluid pH, cytologic characteristics and gentamicin concentration after intra-articular administration of the drug in an experimental model of infectious arthritis in horses, Am J Vet Res 51:1363, 1990. 34. Wininger DA, Fass RJ: Antibiotic-impregnated cement and beads for orthopedic infections, Antimicrob Agents Chemother 40:2675, 1996. 35. Bertone AL, Caprile KA, Davis DM, et al: Serum and synovial fluid concentration of gentamicin administered chronically to horses with experimentally induced infectious arthritis, Vet Surg 19:57, 1990. 36. Lloyd KCK, Stover SM, Pascoe JR, et al: Plasma and synovial fluid concentrations of gentamicin in horses after intraarticular administration of buffered and unbuffered gentamicin, Am J Vet Med Res 49:644, 1988. 37. Beluche LA, Bertone AL, Anderson DE, et al: Dosedependent effect of enrofloxacin on equine articular cartilage, Am J Vet Res 60:571, 1999. 38. Klohnen A, Wilson DG, Hendrickson DA, et al: Effects of potentiated chlorhexidine on bacteria and tarsocrural joints in ponies, Am J Vet Res 57:756, 1996. 39. Wilson DG, Cooley AJ, MacWilliams PS, et al: Effects of 0.05% chlorhexidine lavage on the tarsocrural joints of horses, Vet Surg 23:442, 1994. 40. Swalec Tobias KM, Schneider RK, Besser TE: Use of antimicrobial-impregnated polymethylmethacrylate, J AmVet Med Assoc 208:841, 1996. 41. Ostermann PA, Seligson D, Henry SL: Local antibiotic therapy for severe open fractures: a review of 1085 consecutive cases, J Bone Joint Surg Br 77B:93, 1995. 42. Schneider RK, Andrea R, Barnes HG: Use of antibioticimpregnated polymethylmethacrylate for treatment of an open radial fracture in a horse, J Am Vet Med Assoc 207:1454, 1995. 43. Holcombe SJ, Schneider RK, Bramlage LR, et al: Use of antibiotic-impregnated polymethylmethacrylate in horses with open or infected fractures or joints: 19 cases (19871995), J Am Vet Med Assoc 211:889, 1997. 44. Butson RJ, Schramme MC, Garlick MH, et al: Treatment of intrasynovial infection with gentamicin-impregnated polymethylmethacrylate beads, Vet Rec 138:460, 1996. 45. Gerhart TN, Roux RD, Hanff PA, et al: Antibiotic-loaded biodegradable bone cement for prophylaxis and treatment of experimental osteomyelitis in rats, J Orthop Res 11:250, 1993. 46. DiMaio FR, O’Halloran JJ, Quale JM: In vitro elution of Ciprofloxacin from polymethylmethacrylate cement beads, J Orthop Res 12:79, 1994. 47. Mehta S, Humphrey JS, Schenkman DI, et al: Gentamicin distribution from a collagen carrier, J Orthop Res 14:749, 1996. 48. Cook VL, Bertone AL, Kowalski JJ, et al: Biodegradable drug delivery systems for gentamicin release and treatment of synovial membrane infection, Vet Surg 28:233, 1999.

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49. Nie L, Nicolau DP, Tessier PR, et al: Use of bioabsorbable polymer for the delivery of ofloxacin during experimental osteomyelitis treatment, J Orthop Res 16:76, 1998. 50. Laurencin CT, Gerhart T, Witschger R, et al: Bioerodible polyanhydrides for certibiotic drug delivery: in vivo osteomyletis treatment in a rat model system, J Orthop Res 11:256, 1993. 51. Nelson CL, Hickmon SG, Skinner RA: Treatment of experimental osteomyelitis by surgical debridement and implantation of bioerodable, polyanhydride-gentamicin beads, J Orthop Res 15:249, 1977. 52. Cook VL, Bertone AL, Kowalski JJ, et al: Gentamicinimpregnated biodegradable polymer for the treatment of equine joint infection in vivo: preliminary study, Vet Surg 26:411, 1997. 53. Benoit MA, Moussatt B, Delloye C, et al: Antibioticloaded plaster of Paris implants coated with polylactideco-glycolide as a controlled release delivery system for the treatment of bone infections, Int Orthop 21:403, 1997. 54. Whitehair KJ, Blevins WE, Fessler JF, et al: Regional perfusion of the equine carpus for antibiotic delivery, Vet Surg 21:279, 1993. 55. Whitehair KJ, Bowersock T, Blevins WE, et al: Regional limb perfusion for antibiotic treatment of experimentally induced septic arthritis, Vet Surg 21:367, 1992. 56. Bertone AL, Davis DM, Cox HU, et al: Arthrotomy versus arthroscopy and partial synovectomy for treatment of experimentally induced infectious arthritis in horses, Am J Vet Res 53:585, 1992. 57. Theoret CL, Barber SM, Moyana T, et al: Repair and function of synovium after arthroscopic synovectomy of the dorsal compartment of the equine antebrachiocarpal joint, Vet Surg 25:142, 1996. 58. Palmer J, Bertone AL, Malemud CJ, et al: Changes in third carpal bone articular cartilage after synovectomy in normal and inflamed joints, Vet Surg 27:321, 1998. 59. Yarborough TB, Lee MR, Hornof WJ, et al: Evaluation of samarium-153 for synovectomy in an osteochondral fragment-induced model of synovitis in horses, Vet Surg 29:252, 2000. 60. Ross M, Orsisni J, Richardson D, et al: Closed suction drainage in the treatment of infectious arthritis of the equine tarsocrural joint, Vet Surg 30:21, 1991. 61. Groom LJ, Gaughan EM, Lillich JD, et al: Arthrodesis of the proximal interphalangeal joint affected with septic arthritis in 8 horses, Can Vet J 41:117, 2000. 62. Wisner ER, O’Brien TR, Pool RR, et al: Osteomyelitis of the axial border of the proximal sesamoid bones in seven horses, Equine Vet J 23:383, 1991. 63. Honnas CM, Welch RD, Ford TS, et al: Septic arthritis of the distal interphalangeal joint in 12 horses, Vet Surg 21:261, 1992. 64. Smith R, Kajiyama G, Schurman DJ: Staphylococcal septic arthritis: antibiotic and nonsteroidal anti-inflammatory drug treatment in a rabbit model, J Orthop Res 15:919, 1997. 65. Moses V, Hardy J, Bertone AL, et al: The effect of various nonsteroidal antiinflammatory drugs on lipopolysaccharide challenged and unchallenged equine synovial membrane explants, Am J Vet Res 162:54, 2001. 66. Moses VS, Bertone AL: Nonsteroidal anti-inflammatory drugs, Vet Clin North Am Equine Pract 18:21, 2002. 67. Sysel AM, Pleasant RS, Jacobson JD, et al: Efficacy of an epidural combination of morphine and detomidine in alleviating experimentally induced hindlimb lameness in horses, Vet Surg 25:511, 1996. 68. Sysel AM, Pleasant RS, Jacobson JD, et al: Systemic and local effects associated with long-term epidural catheterization and morphine-detomidine administration in horses, Vet Surg 26:141, 1997.

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69. Smith G, Bertone AL, Kaeding C, et al: Anti-inflammatory effects of topically applied dimethylsulfoxide gel on endotoxin-induced synovitis in horses, Am J Vet Res 59:1149, 1998. 70. Visai L, Xu Y, Casolini F, et al: Monoclonal antibodies to CNA, a collagen-binding microbial surface component recognizing adhesive matrix molecules, detach Staphylococcus

CHAPTER •

aureus from a collagen substrate, J Biol Chem 275:39837, 2000. 71. Smeltzer MS, Gillaspy AF: Molecular pathogenesis of staphylococcal osteomyelitis, Poult Sci 79:1042, 2000. 72. Balaban N, Collins LV, Cullor JS, et al: Prevention of diseases caused by Staphylococcus aureus using the peptide RIP, Peptides 21:1301, 2000.

67

Non-Infectious Arthritis Alicia L. Bertone

on-infectious arthritis is characterized by pain, heat, swelling (effusion), erythema, and lameness. Joint structure and function, aspects of diagnosis and management of joint disease, and osteoarthritis are discussed in Chapters 63 and 64. This chapter focuses on normal and abnormal joint physiology and other specific non-infectious joint diseases.

N

JOINT PHYSIOLOGY Fluid flow from the vascular space into the interstitium and joint space (third compartment space) and out into venules and lymphatics is tightly governed by Starling forces, which are a balance of arterial and venous pressures and colloid osmotic forces across the joint. The resultant fluid flow through the joint is modified by permeability of the synovium (osmotic reflection coefficient) and the vessel surface area available for fluid transport (filtration coefficient). Even in normal joints these forces are influenced by gravity (joint dependency), motion (exercise), and structure (joint compliance).1-7 Horses are unique in needing joint motion to maintain isogravimetric states of the joints (no fluid gain or loss), especially in peripheral joints.1 In normal stationary equine limbs, lymphatic drainage from joints approximates zero until joint pressure exceeds 11 mm Hg for the fetlock joint (transitional microvascular pressure). In standing animals without counter forces, such as motion or external bandages to increase lymph flow forces, gravitational pressures increase arterial pressure to the joint and venous and lymphatic pressure from the joint. The result is tissue edema and joint effusion.

JOINT PATHOPHYSIOLOGY (SYNOVITIS) The balance of these forces is altered in horses with synovitis because of the increased blood flow, altered synovial permeability, structural joint capsular changes, and loss of joint motion because of pain.1,3,5,8,9 These factors profoundly affect joint physiology, contribute to clinical signs, and result in damage to the synovium and articular cartilage. Early signs of effusion that precede clinical detection of inflammation are related to changes in the hemodynamics of the joint, including increased blood flow and reduced joint motion.8,9

In chronic arthritis, capsular thickening, fibrosis, and altered synovial function likely influence fluid dynamics. Capsular fibrosis and joint enlargement produce decreased tissue compliance and an increase in intra-articular pressure occurs, even with slight increases in joint effusion. Articular cartilage is avascular and depends on synovial fluid for nutrition, so alteration in fluid flux affects nutritional exchange between the articular cartilage and synovium. Reduced nutrition exchange to articular cartilage exacerbates articular surface fibrillation and degenerative changes.10,11

JOINT PATHOLOGICAL CONDITIONS ASSOCIATED WITH ARTHRITIS Effusion Increased blood flow and capillary leakage occur early and contribute to increased fluid volume in the joint interstitium and synovial fluid, recognized as effusion. The condition is stimulated by vascular changes and neurotransmitter release, particularly β2-adrenergic stimulation.2,8,9 Because of low intra-articular pressures in normal equine joints (–5 mm Hg6; –1.25 mm Hg12), effusion precedes interstitial edema, until intra-articular pressure is greater than 11 mm Hg.1 These physiological circumstances make detection of effusion one of the most sensitive indicators of early joint stress. Effusion, although common, is not normal and alters joint function. Congruent motion of joint surfaces depends on normal negative pressure and is important in decreasing shear force (side to side, sloppy movement).7 Effusion is not painful as long as capsular tension is normal. Through the phenomenon of creep-relaxation, capsular tension is reduced in distended joints. Normal joints are relatively compliant and can accommodate fairly large changes in fluid volume with minimal increase in pressure, but elastance profiles of these joints may be permanently altered.13 Joints with high structural congruence, such as the tarsocrural joint, are less affected biomechanically by joint effusion than are less congruent joints.7 High synovial fluid volume becomes more important during joint motion. Joint pressure profiles are profoundly altered by joint angle.6,7,13 With effusion, as initial intra-articular pressure is increased, the capacity to accommodate rapid changes in pressure goes down, causing a rapid rise in intraarticular pressure and capsular wall tension at extreme joint

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69. Smith G, Bertone AL, Kaeding C, et al: Anti-inflammatory effects of topically applied dimethylsulfoxide gel on endotoxin-induced synovitis in horses, Am J Vet Res 59:1149, 1998. 70. Visai L, Xu Y, Casolini F, et al: Monoclonal antibodies to CNA, a collagen-binding microbial surface component recognizing adhesive matrix molecules, detach Staphylococcus

CHAPTER •

aureus from a collagen substrate, J Biol Chem 275:39837, 2000. 71. Smeltzer MS, Gillaspy AF: Molecular pathogenesis of staphylococcal osteomyelitis, Poult Sci 79:1042, 2000. 72. Balaban N, Collins LV, Cullor JS, et al: Prevention of diseases caused by Staphylococcus aureus using the peptide RIP, Peptides 21:1301, 2000.

67

Non-Infectious Arthritis Alicia L. Bertone

on-infectious arthritis is characterized by pain, heat, swelling (effusion), erythema, and lameness. Joint structure and function, aspects of diagnosis and management of joint disease, and osteoarthritis are discussed in Chapters 63 and 64. This chapter focuses on normal and abnormal joint physiology and other specific non-infectious joint diseases.

N

JOINT PHYSIOLOGY Fluid flow from the vascular space into the interstitium and joint space (third compartment space) and out into venules and lymphatics is tightly governed by Starling forces, which are a balance of arterial and venous pressures and colloid osmotic forces across the joint. The resultant fluid flow through the joint is modified by permeability of the synovium (osmotic reflection coefficient) and the vessel surface area available for fluid transport (filtration coefficient). Even in normal joints these forces are influenced by gravity (joint dependency), motion (exercise), and structure (joint compliance).1-7 Horses are unique in needing joint motion to maintain isogravimetric states of the joints (no fluid gain or loss), especially in peripheral joints.1 In normal stationary equine limbs, lymphatic drainage from joints approximates zero until joint pressure exceeds 11 mm Hg for the fetlock joint (transitional microvascular pressure). In standing animals without counter forces, such as motion or external bandages to increase lymph flow forces, gravitational pressures increase arterial pressure to the joint and venous and lymphatic pressure from the joint. The result is tissue edema and joint effusion.

JOINT PATHOPHYSIOLOGY (SYNOVITIS) The balance of these forces is altered in horses with synovitis because of the increased blood flow, altered synovial permeability, structural joint capsular changes, and loss of joint motion because of pain.1,3,5,8,9 These factors profoundly affect joint physiology, contribute to clinical signs, and result in damage to the synovium and articular cartilage. Early signs of effusion that precede clinical detection of inflammation are related to changes in the hemodynamics of the joint, including increased blood flow and reduced joint motion.8,9

In chronic arthritis, capsular thickening, fibrosis, and altered synovial function likely influence fluid dynamics. Capsular fibrosis and joint enlargement produce decreased tissue compliance and an increase in intra-articular pressure occurs, even with slight increases in joint effusion. Articular cartilage is avascular and depends on synovial fluid for nutrition, so alteration in fluid flux affects nutritional exchange between the articular cartilage and synovium. Reduced nutrition exchange to articular cartilage exacerbates articular surface fibrillation and degenerative changes.10,11

JOINT PATHOLOGICAL CONDITIONS ASSOCIATED WITH ARTHRITIS Effusion Increased blood flow and capillary leakage occur early and contribute to increased fluid volume in the joint interstitium and synovial fluid, recognized as effusion. The condition is stimulated by vascular changes and neurotransmitter release, particularly β2-adrenergic stimulation.2,8,9 Because of low intra-articular pressures in normal equine joints (–5 mm Hg6; –1.25 mm Hg12), effusion precedes interstitial edema, until intra-articular pressure is greater than 11 mm Hg.1 These physiological circumstances make detection of effusion one of the most sensitive indicators of early joint stress. Effusion, although common, is not normal and alters joint function. Congruent motion of joint surfaces depends on normal negative pressure and is important in decreasing shear force (side to side, sloppy movement).7 Effusion is not painful as long as capsular tension is normal. Through the phenomenon of creep-relaxation, capsular tension is reduced in distended joints. Normal joints are relatively compliant and can accommodate fairly large changes in fluid volume with minimal increase in pressure, but elastance profiles of these joints may be permanently altered.13 Joints with high structural congruence, such as the tarsocrural joint, are less affected biomechanically by joint effusion than are less congruent joints.7 High synovial fluid volume becomes more important during joint motion. Joint pressure profiles are profoundly altered by joint angle.6,7,13 With effusion, as initial intra-articular pressure is increased, the capacity to accommodate rapid changes in pressure goes down, causing a rapid rise in intraarticular pressure and capsular wall tension at extreme joint

CHAPTER 67 angles, resulting in sharp pain during maximal joint excursion and simultaneous reduction in synovial perfusion.14 These effects could be present even if synovitis is not recognized clinically. The influence of intermittent synovial ischemia is not elucidated fully, but it may be important in diseases of synovial proliferation.

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production by synovial cells matches elevation in synovial fluid volume.23 When inflammation increases, synovial cell production decreases and degradation of hyaluronan increases. In horses with severe joint inflammation or hemarthrosis, hyaluronan concentration may be negligible.

Pain in Arthritis Inflammation Inflammation causes a humoral (vascular) and a cellular response. In early arthritis, cells are up-regulated to produce inflammatory mediators. Gene transcriptional profiles may be unique to certain forms of arthritis and potentially could be used in the future to recognize and prevent arthritis. Upregulation of genes causes protein production, initiation of the inflammatory cascade, and further release of inflammatory mediators. Important mediators include cytokines interleukin-1, interleukin-6, and tumor necrosis factor.2-4,15,16 Secondary mediators such as the eicosanoids (prostaglandin E2 and leukotrienes),2-4,15 free oxygen radicals,17 substance P,3 and nitric oxide3,4 are also pro-arthritic and amplify pain. Cellular influx causes effusion and subsequent clinical recognition of synovitis. The degree of synovitis and articular cartilage damage are directly proportional to synovial fluid nucleated cell count in infectious and non-infectious arthritis. Neutrophils are highly migratory and can move into joint fluid within 3 hours after a chemotactic stimulus, such as interleukin-1, paclitaxel, or endotoxin.2,8,9,15,18 These cells are damaging to surrounding tissue because they have destructive enzymes and alter synovial fluid environment. In non-infectious arthritis, nucleated cell count is usually less than 30,000 nucleated cells per microliter,15 but values greater than 100,000 nucleated cells per microliter occur in autoimmune arthritis,19 endotoxin-induced arthritis,16,20 and early in reactive arthritis.

Ischemia Intra-articular pressures greater than 30 mm Hg cause significant reduction in the perfusion of the synovium and fibrous layer of the joint capsule.14 Pressures of this magnitude occur in horses with palpable effusion of the fetlock joint and are present when synovitis is prominent.12 Pressures greater than 60 mm Hg can reduce blood flow profoundly, and pressures approximating 100 mm Hg can cause capsule joint rupture (carpus and fetlock21). Clinically, joint rupture is uncommon but was hypothesized to contribute to dorsal fetlock capsular thickening.12 I have seen this as a rare occurrence in the plantar pouch of the tarsocrural joint and the palmar pouch of the antebrachiocarpal joint. Intra-articular pressure can reach high levels during maximal flexion and extension, particularly in horses with resting pressures greater than 30 mm Hg.6 Ischemia has been hypothesized to be a component of synovitis particularly in the proliferative form.22 Low oxygen tension stimulates angiogenesis and granulation tissue formation, resulting in fibrosis. In chronically inflamed joints, clubbed and thickened synovial membrane often is seen during arthroscopic surgery, supporting the concept of synovial ischemia.

Synovial Fluid Lubrication: Hyaluronan Synovial cells produce hyaluronan. A protective layer of high concentration hyaluronan remains close to the surface of the synovium and the remainder diffuses into the joint space, creating the unique viscosity of synovial fluid.3,7 Adequate hyaluronan concentration is critical to provide lubrication of synovial soft tissues, particularly synovial villi. During inflammatory synovitis, lubrication of the soft tissues is reduced because of dilution of hyaluronan and a reduction in hyaluronan production. Swollen, edematous villi cause an elevated coefficient of friction. In horses with mild effusion, hyaluronan concentration can be normal because increased

Sensory and motor innervation help maintain joint stability, and in the absence of these protective reflexes, severe arthropathy may develop.24 When activated, the peripheral nervous system can initiate the major features of acute inflammation, such as vasodilation and effusion, and lower the threshold for pain.25 The C and A nerve fibers responsible for pain sensation in arthritis are activated by amines (such as serotonin) and neuropeptides (calcitonin gene-related peptide and substance P) that also act locally to exert pro-inflammatory effects on synovium. A role of substance P in joint pain is supported by the clinical effectiveness of the substance P depleting substance, capsaicin. Capsaicin initially activates C fibers, resulting in substance P release and pain, but subsequently desensitizes or causes degeneration of C fibers.26 The contribution of neuropeptides may be different in acute and chronic inflammatory arthritis. Edema formation in denervated limbs may indicate that loss of sensory innervation could play a role in acute arthritis.27 Increased edema formation and decreased permeability to macromolecules were observed in denervated limbs subjected to interleukin-1 induction of synovitis.2 The role of innervation in chronic arthritis is complex, because the neuropeptide substance P and calcitonin gene-related peptide were increased in sciatic nerve, dorsal root ganglia, and peri-articular tissues but were decreased in synovium. The therapeutic implications are intriguing. Intramuscular gold or topically applied capsaicin could selectively destroy C fibers, thus lowering substance P levels, and these have been found to be clinically useful. Non-steroidal anti-inflammatory drugs (NSAIDs) decrease prostanoid production, and intra-articular corticosteroids inhibit the arachidonic acid cascade, thus having direct and indirect effects.28 In addition, stimulation of primary afferent nociceptive fibers causes release of glutamate and substance P from central spinal pathways. This nociceptive input can be inhibited by stimulation of proprioceptive and tactile type I and II fibers. Stimulation of these fibers can be accomplished by highfrequency, low-intensity transcutaneous neural stimulation, frequently used in physiotherapy.

AUTOIMMMUNE-MEDIATED ARTHRITIS Rheumatoid arthritis is a steroid-responsive arthritis, associated with high synovial nucleated cell counts, progressing to bone erosion and pannus formation. To establish a diagnosis of rheumatoid arthritis, an autoimmune component and production of rheumatoid factor must be documented. According to these criteria rheumatoid arthritis has not been reported in horses. In human systemic lupus erythematosus (SLE), systemic disease is also present and auto-antibodies are directed toward nuclear cellular material. An SLE-like disease was described in a young horse.29 In horses, anti-collagen type II antibodies and immune complexes were identified in synovial fluid of horses with osteoarthritis and joint trauma. However, these immune complexes are much less common in horses with mild synovitis and have been found in sera. Relationship of cause and effect of these immunological findings is unclear, because immune complexes were found in many disease types. Although these auto-antibodies may be associated with equine diseases, it is unlikely that they initiate arthritis in horses.30 They may develop after exposure to type II collagen,

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after articular cartilage trauma or wear. Specific assays of synovial fluid for immunoglobulin M–rheumatoid factor (a feature of rheumatoid arthritis), antibodies to heat-shock protein, and anti-nuclear antibodies (ANA), a feature of SLE, revealed only modestly low levels of rheumatoid factor without correlation to disease and no ANA.31

IMMUNE-MEDIATED ARTHRITIS The presence of synovitis and immunoglobulin G complex deposition in the synovium of foals has been reported.32-34 This form of synovitis is called immune-mediated arthritis and may be associated with circulating immune complexes formed as a result of systemic disease.32 Using specific monoclonal antibody techniques, immune-mediated arthritis was diagnosed in a 6-week-old pony foal infected with equine herpes virus-4.33 Three horses were hyperimmunized with Streptococcus equine M protein vaccine and subsequently injected intra-articularly with purified streptococcal M protein. Severe suppurative synovitis developed, and synovial fluid nucleated cell counts were greater than 100,000 cells per microliter.34 Eosinophils were prominent in the synovial fluid and synovial membrane in two horses. A clinical syndrome of polysynovitis and vasculitis secondary to high circulating M protein (after streptococcal infection), or associated with Rhodococcus equi infections, is recognized and thought to be caused by immune-mediated arthritis. Seventeen (35%) of 48 foals with R. equi pneumonia infection had chronic active non-infectious arthritis. Pathogenesis involves immunocomplexes in the synovium. The hallmark of immune-mediated arthritis in foals is effusion in one or more joints but minimal lameness.35 Synovitis often resolves in several weeks with or without treatment. Foals should be restricted to box rest, but no other specific treatment is necessary. Corticosteroids are contraindicated, because bacterial infection may be perpetuated.

REACTIVE SYNOVITIS Reactive synovitis may occur after intra-articular injection of any product. Any intra-articular injection incites at least mild synovitis. The activated drug or a product in the solution may chemically induce reactive synovitis. Endotoxin contamination of multiple-dose vials or even single-dose products may cause reactive synovitis. In the case of a multiple-dose vial, a suspicion of endotoxin contamination should be high if more than one horse shows clinical signs within a short period. Horses are exquisitely sensitive to endotoxin, and concentrations above 0.125 ng per joint incite synovitis.36 After intra-articular injection of methylprednisolone acetate, inflammatory cells surrounding vehicle crystals were identified in synovium 6 weeks later.37 Reactive synovitis associated with methylprednisolone acetate may be most common in the distal interphalangeal joint. Although unusual, within a few hours after injection, horses can show severe lameness. Steroid arthropathy may be a form of reactive synovitis. The distal interphalangeal and tarsocrural joints appear most at risk to develop reactive arthritis after intraarticular injection of polysulfated glycosaminoglycans.38 Reactive synovitis must be distinguished from early infectious arthritis. Distinguishing features of reactive arthritis include early onset after injection (about 24 hours), synovial nucleated counts less than 30,000 cells per microliter, and resolution within 1 to 3 days. Lameness ranges from mild to severe, and in some horses distinguishing reactive arthritis from infectious arthritis may be difficult, and prompt management with intra-articular lavage, systemic and local antimicrobial drug administration, and anti-inflammatory therapy should be instituted. Culture and susceptibility testing should

be performed if any suspicion exists that a bacterial infection is present, if synovitis does not resolve quickly, or in horses in which lameness persists. Eosinophilic synovitis is rare and may represent an allergic reaction to an injected product, or to parasite migration, or could be truly idiopathic.34,39 Joint lavage to assist in removing foreign material, and the administration of non-steroidal anti-inflammatory medication and anthelmintic treatment are indicated. Foreign bodies rarely may be present within a joint or tendon sheath and incite chronic reactive synovitis. Broken needles, plant or seed awns or thorns, and debris from nearby wounds can cause reactive synovitis. Radiographic and ultrasonographic examinations can be helpful to identify the nature of the foreign material.40 Cellulitis close to a joint may cause reactive synovitis that resolves with successful treatment of the primary infection.

TRAUMATIC SYNOVITIS Primary traumatic synovitis is an early form of osteoarthritis. Horses at risk are usually in active sports training. Lameness usually is managed by intra-articular and systemic medication. Early medical intervention and appropriate joint rest and physiotherapy are critical to prevent loss of glycosaminoglycan from articular cartilage and permanent joint wear. Early loss of articular cartilage proteoglycan is reversible with medication and joint rest. If training is continued, some horses will develop proliferative synovitis, chip fractures, intra-articular ligament injury, and osteoarthritis. Intermittent hemarthrosis (see below) may be detected with primary traumatic synovitis, but often it indicates injury to subchondral bone, such as chip fracture or cartilage elevation.

PROLIFERATIVE (VILLONODULAR) SYNOVITIS Chronic traumatic synovitis and continued exercise result in a painful thickening of the synovium, proliferative synovitis, particularly in areas of compression trauma.41-45 The most common location is the dorsal fibrous pad (synovial pad) of the metacarpophalangeal joint, directly under the broad, flat common digital extensor tendon and joint capsule.41 At maximal extension and flexion, pad compression results in intrasynovial hemorrhage, granulation tissue formation, fibrosis, and mineralization. Diagnosis and management are discussed in Chapter 37. Chronic proliferative synovitis is a frequent finding in the carpal and tarsocrural joints during arthroscopic examination. Diffuse proliferative synovitis can be seen in horses that have had frequent intra-articular injections and have continued in exercise. Capsular fibrosis and loss of fine villous architecture occur. I do not recommend radical synovectomy, but removal of fibrotic tufts of capsule and synovium prone to pinching or demonstrating signs of internal hemorrhage and edema is warranted. See Chapters 56 and 58 for a discussion of osteochondrosis.

IDIOPATHIC ARTHRITIS Synovitis can occur without any known cause or associated trauma and can be truly idiopathic, although synovitis may be related to circulating toxins, including endotoxin, streptococcal cell wall, M protein, and viruses. In people, bacterial and viral deoxyribonucleic acid and bacterial peptidoglycans have been located in joints of patients with early rheumatoid and other non-infectious arthritides.46,47 In horses synovitis can be associated with vasculitis, such as that seen with equine viral arteritis.

CHAPTER 67 HEMARTHROSIS Bleeding into a joint (hemarthrosis) causes joint capsule distention, severe pain, and lameness.48 Draining the blood from the joint usually results in rapid relief of clinical signs. The cause of hemorrhage may be trauma to proliferative hemorrhagic synovium, an intra-articular fracture, or tearing of an intra-articular ligament. Hemorrhage may occur on a single occasion or may be recurrent. Diagnosis of hemorrhage is simple, by arthrocentesis, but identification of the primary cause can be more difficult. In the absence of radiological abnormalities, exploratory arthroscopy is warranted in a horse with recurrent episodic severe lameness associated with hemarthrosis. Hemorrhage associated with proliferative synovitis may be managed successfully by subtotal synovectomy.

13. 14. 15. 16.

17.

LYME DISEASE Although strictly speaking an infectious disease, Lyme disease is discussed in this section because it should be considered a differential diagnosis in tick-endemic areas in a horse with shifting limb lameness associated with synovitis in several joints.49,50 However, many clinically normal horses have antibody titers to Borrelia burdorferi, and high titers are not synonymous with clinical disease. True Lyme disease is poorly documented in the horse, and definitive diagnosis would require identification of significantly raised titers in paired serum samples.

REFERENCES 1. Bertone AL, Hardy J, Simmons EJ, et al: Transsynovial forces of the isolated stationary equine joint, Am J Vet Res 59:495, 1998. 2. Hardy J, Bertone AL, Weisbrode SE, et al: Cell trafficking, mediator release, and articular metabolism in acute inflammation of innervated or denervated isolated equine joints, Am J Vet Res 59:88, 1998. 3. Palmer J, Bertone AL: Joint structure, biochemistry and biochemical disequilibrium in synovitis and equine joint disease, Equine Vet J 26:263, 1994. 4. Bertone AL, Palmer J, Jones J: Synovial fluid cytokines and eicosanoids as markers of joint disease in horses, Vet Surg 30:528, 2001. 5. Levick JR: Blood flow and mass transport in synovial joints. In Handbook of physiology. II. The cardiovascular system, vol 4, Bethesda, Md, 1984, American Physiological Society. 6. Macoris D, Bertone AL: Intra-articular pressure profiles of the cadaveric equine fetlock joint in motion, Equine Vet J 33:1, 2001. 7. Palmer J, Bertone AL: Joint biomechanics in the pathogenesis of traumatic arthritis. In McIlwraith CW, Trotter G, editors: Joint disease in the horse, Philadelphia, 1996, WB Saunders. 8. Bragdon B, Bertone AL, Hardy J, et al: Use of an isolated joint model to detect early changes induced by intraarticular injection of paclitaxel-impregnated microspheres, J Invest Surg 14:169, 2001. 9. Simmons EJ, Bertone AL, Muir WW: Receptor mechanisms of enhanced vascular responsiveness of isolated equine osteoarthritic joints, Vet Surg 28:405, 1999. 10. Lane Smith R, Rusk SF, Ellison BE, et al: In vitro stimulation of articular chondrocyte mRNA and extracellular matrix synthesis by hydrostatic pressure, J Orthop Res 14:53, 1996. 11. Edwards JCW, Winchester R, Henderson B, et al: Consensus statement, Ann Rheum Dis 54:389, 1995. 12. Strand E, Martin GS, Crawford MP, et al: Intra-articular pressure, elastance and range of motion in healthy and

18. 19. 20.

21. 22.

23.

24.

25. 26. 27. 28.

29. 30. 31.

32. 33.

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injured racehorse metacarpophalangeal joint, Equine Vet J 30:520, 1998. Hardy J, Bertone AL, Muir WW: Pressure-volume relationships in equine midcarpal joint, J Appl Physiol 78:1977, 1995. Hardy J, Bertone AL, Muir WW: Joint pressure influences synovial tissue blood flow as determined by colored microspheres, J Appl Physiol 80:1225, 1996. Hardy J, Bertone AL, Muir WW: Local hemodynamics, permeability and oxygen metabolism of innervated or denervated isolated equine joints, Am J Vet Res 59:1307, 1998. Hawkins DL, MacKay RJ, Gum GG, et al: Effects of intra-articularly administered endotoxin on clinical signs of disease and synovial fluid tumor necrosis factor; interleukin 6, and prostaglandin E2 values in horses, Am J Vet Res 54:379, 1993. Auer DE, Ng JC, Seawright AA: Free radical oxidation products in plasma and synovial fluid of horses with synovial inflammation, Aust Vet J 70:49, 1993. Todhunter RJ, Fubini SL, Vernier-Singer M, et al: Acute synovitis and intra-articular methylprednisolone acetate in ponies, Osteoarthritis Cartilage 6:94, 1998. Furst DE, Breedveld FC, Burmester GR, et al: Access to disease modifying treatments for rheumatoid arthritis patients, Ann Rheum Dis 58(Suppl)1:I129, 1999. Hawkins DL, Cargile JL, MacKay RJ, et al: Effect of tumor necrosis factor antibody on synovial fluid cytokine activities in equine antebrachiocarpal joints injected with endotoxin, Am J Vet Res 56:1292, 1995. Bertone A: Unpublished data, 1996. Sanchis-Alfonso V, Villanueva-Garcia E: Localized pigmented villonodular synovitis as a rare cause of chronic anterolateral ankle pain in an equestrienne, Arthroscopy 16:E15, 2000. Tulamo RM, Heiskanen T, Salonen M: Concentration and molecular weight distribution of hyaluronate in synovial fluid from clinically normal horses and horses with diseased joints, Am J Vet Res 55:710, 1994. Vilensky JA, O’Connor BL, Brandt KD, et al: Serial kinematic analysis of the canine knee after L4-S1 dorsal root ganglionectomy: implications for the cruciate deficiency model of osteoarthritis, J Rheumatol 21:2113, 1994. Basbaum AI, Levine JD: The contribution of the nervous system to inflammation and inflammatory disease, Can J Physiol Pharmacol 69:647, 1991. Colpaert FC, Donnerer J, Lembeck F: Effects of capsaicin on inflammation and on the substance P content of nervous tissues in rats with adjuvant arthritis, Life Sci 32:1827, 1983. Cambridge H, Brain SD: Calcitonin gene-related peptide increases blood flow and potentiates plasma protein extravasation in the rat knee, Br J Pharmacol 106:746, 1992. Konttinen YT, Kemppinen P, Segerberg M, et al: Peripheral and spinal neural mechanisms in arthritis, with particular reference to treatment of inflammation and pain, Arthritis Rheum 37:965, 1994. Geor RJ, Clark EG, Haines DM, et al: Systemic lupus erythematosus in a filly, J Am Vet Med Assoc 197:1489, 1990. Osborne AC, Carter SD, May SA, et al: Anti-collagen antibodies and immune complexes in equine joint disease, Vet Immunol Immunopathol 45(1-2):19, 1995. Carter SD, Osborne AC, May SA, et al: Rheumatoid factor, anti-heat shock protein (65 kDa) antibodies and anti-nuclear antibodies in equine joint diseases, Equine Vet J 27:288, 1995. Madison JB, Scarratt K: Immune-mediated polysynovitis in four foals, J Am Vet Med Assoc 192:1581, 1988. Blunden AS, Smith KC, Binns MM, et al: Replication of equid herpesvirus 4 in endothelial cells and synovia of a field case of viral pneumonia and synovitis in a foal, J Comp Pathol 112:133, 1995.

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34. Madison JB, Ziemer EL: Eosinophilic synovitis following the intra-articular injection of bacterial antigen in horses, Res Vet Sci 54:256, 1993. 35. Sweeney CR, Sweeney RW, Divers TJ: Rhodococcus equi pneumonia in 48 foals: response to antimicrobial treatment, Vet Microbiol 14:329, 1987. 36. Palmer J, Bertone AL, Malemud CJ, et al: Changes in third carpal bone articular cartilage after synovectomy in normal and inflamed joints, Vet Surg 27:321, 1998. 37. Carter BG, Bertone AL, Weisbrode SE, et al: Influence of methylprednisolone acetate on osteochondral healing in exercised tarsocrural joints of horses, Am J Vet Res 57:914, 1996. 38. Ross M: Personal communication, 2001. 39. Turner AS, Gustafson SB, Zeider NS, et al: Acute eosinophilic synovitis in a horse, Equine Vet J 22:215, 1990. 40. Crabill MR, Watkins JP, Morris EL, et al: Lead foreign body arthropathy in a horse, J Am Vet Med Assoc 205:864, 1994. 41. Dabareiner RM, White NA, Sullins KE: Metacarpophalangeal joint synovial pad fibrotic proliferation in 63 horses, Vet Surg 25:199, 1995. 42. Vickers KL, Ross MW: Atypical villonodular synovitis in a horse, J Am Vet Med Assoc 209:1602, 1996.

CHAPTER •

43. Roneus B, Andersson AM, Ekman S: Racing performance in standardbred trotters with chronic synovitis after partial arthroscopic synovectomy in the metacarpophalangeal, metatarsophalangeal and intercarpal (midcarpal) joints, Acta Vet Scand 38:87, 1997. 44. Kannegieter NJ: Chronic proliferative synovitis of the equine metacarpophalangeal joint, Vet Rec 127:8, 1990. 45. van Veenendaal JC, Moffatt RE: Soft tissue masses in the fetlock joint of horses, Aust Vet J 56:533, 1980. 46. van der Heijden IM, Wilbrink B, Tchetverikov I, et al: Presence of bacterial DNA and bacterial peptidoglycans in joints of patients with rheumatoid arthritis and other arthritides, Arthritis Rheum 43:593. 2000. 47. Stahl HD, Hubner B, Seidle B, et al: Detection of multiple viral DNA species in synovial tissue and fluid of patients with early arthritis, Ann Rheum Dis 59:342, 2000. 48. Dyson S: Lameness associated with recurrent hemarthrosis in a horse, Equine Vet J 18:224, 1986. 49. Clegg P: Lyme disease, Proc Br Equine Vet Assoc 39:150, 2000. 50. Lindermayer J, Weber M, Onderdonk A: Borrelia burgdorferi infection in horses, J Am Vet Med Assoc 194:1384, 1989.

68

Other Joint Conditions Chris E. Kawcak and Gayle W. Trotter

everal types of joint diseases are rare and have been presented only in case reports or small retrospective studies. This makes generalizations about these diseases difficult and searching for information a tedious process.

S

sible for maintaining joint support and provides a barrier for synovial fluid. Because the capsule surrounds the entire joint, appropriate elasticity is needed to maintain joint flexibility (see Chapter 67).

Ligament Injuries

DISEASES OF SOFT TISSUES OF THE JOINT Soft tissue structures serve to support the joint, and disease can result in abnormal stresses to the articular cartilage and hence chronic progression of articular cartilage degeneration and osteoarthritis (see Chapter 63). Preoperative diagnosis of some soft tissue injuries is difficult, often leaving the surgeon with little to do other than evaluate the injury and debride fibrillated tissue during arthroscopic surgery. With the advent of newer diagnostic techniques such as magnetic resonance imaging (see Chapter 21) and increased use of ultrasonography (see Chapter 17), soft tissue injuries can be characterized better preoperatively. Most soft tissues of joints, such as ligaments, menisci, and joint capsule, function to support joints. Joint ligaments maintain alignment of opposing and adjacent bones in joints. They form a connection between opposing bones (such as the tibia and femur in the stifle) and between adjacent bones in more complex joints (such as between the carpal bones in the carpus). They function to maintain alignment and allow for movement of the joint. The meniscal cartilages function as cushions between the tibia and femur of the femorotibial joints. Proper material characteristics are necessary for maintenance of the joint environment. Joint capsule is also respon-

Joint ligament injury can be an incidental finding during surgery or a devastating cause of lameness. For instance, medial palmar intercarpal ligament damage can be an incidental finding during arthroscopic surgery and has been seen incidentally in necropsy specimens (see Chapter 39).1 Injury to cruciate ligaments and menisci of the stifle usually cause significant pain (see Chapter 47), but cutting the cranial cruciate ligament in an attempt to create a model of osteoarthritis did not lead to osteoarthritis in horses. Therefore further destabilization of the joint beyond cruciate injury must usually occur, with possible damage to other soft tissue structures, including the joint capsule. Collateral ligament injury caused by a bad step or laceration can result in subtle or severe lameness. We have seen lowgrade lameness in a horse that had complete tearing of the medial collateral ligament of the metatarsophalangeal joint (Fig. 68-1). Laxity of the joint was detected by manipulation and stressed radiographs. The joint was immobilized in a cast for 6 weeks, followed by a splint for an additional 6 weeks. Reinjury occurred after splint removal and the joint was recast. After immobilization for 16 weeks the injury healed well enough for trail riding. Ligament injuries usually heal slowly, and gradual return to function is needed to strengthen the tissues. The conse-

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34. Madison JB, Ziemer EL: Eosinophilic synovitis following the intra-articular injection of bacterial antigen in horses, Res Vet Sci 54:256, 1993. 35. Sweeney CR, Sweeney RW, Divers TJ: Rhodococcus equi pneumonia in 48 foals: response to antimicrobial treatment, Vet Microbiol 14:329, 1987. 36. Palmer J, Bertone AL, Malemud CJ, et al: Changes in third carpal bone articular cartilage after synovectomy in normal and inflamed joints, Vet Surg 27:321, 1998. 37. Carter BG, Bertone AL, Weisbrode SE, et al: Influence of methylprednisolone acetate on osteochondral healing in exercised tarsocrural joints of horses, Am J Vet Res 57:914, 1996. 38. Ross M: Personal communication, 2001. 39. Turner AS, Gustafson SB, Zeider NS, et al: Acute eosinophilic synovitis in a horse, Equine Vet J 22:215, 1990. 40. Crabill MR, Watkins JP, Morris EL, et al: Lead foreign body arthropathy in a horse, J Am Vet Med Assoc 205:864, 1994. 41. Dabareiner RM, White NA, Sullins KE: Metacarpophalangeal joint synovial pad fibrotic proliferation in 63 horses, Vet Surg 25:199, 1995. 42. Vickers KL, Ross MW: Atypical villonodular synovitis in a horse, J Am Vet Med Assoc 209:1602, 1996.

CHAPTER •

43. Roneus B, Andersson AM, Ekman S: Racing performance in standardbred trotters with chronic synovitis after partial arthroscopic synovectomy in the metacarpophalangeal, metatarsophalangeal and intercarpal (midcarpal) joints, Acta Vet Scand 38:87, 1997. 44. Kannegieter NJ: Chronic proliferative synovitis of the equine metacarpophalangeal joint, Vet Rec 127:8, 1990. 45. van Veenendaal JC, Moffatt RE: Soft tissue masses in the fetlock joint of horses, Aust Vet J 56:533, 1980. 46. van der Heijden IM, Wilbrink B, Tchetverikov I, et al: Presence of bacterial DNA and bacterial peptidoglycans in joints of patients with rheumatoid arthritis and other arthritides, Arthritis Rheum 43:593. 2000. 47. Stahl HD, Hubner B, Seidle B, et al: Detection of multiple viral DNA species in synovial tissue and fluid of patients with early arthritis, Ann Rheum Dis 59:342, 2000. 48. Dyson S: Lameness associated with recurrent hemarthrosis in a horse, Equine Vet J 18:224, 1986. 49. Clegg P: Lyme disease, Proc Br Equine Vet Assoc 39:150, 2000. 50. Lindermayer J, Weber M, Onderdonk A: Borrelia burgdorferi infection in horses, J Am Vet Med Assoc 194:1384, 1989.

68

Other Joint Conditions Chris E. Kawcak and Gayle W. Trotter

everal types of joint diseases are rare and have been presented only in case reports or small retrospective studies. This makes generalizations about these diseases difficult and searching for information a tedious process.

S

sible for maintaining joint support and provides a barrier for synovial fluid. Because the capsule surrounds the entire joint, appropriate elasticity is needed to maintain joint flexibility (see Chapter 67).

Ligament Injuries

DISEASES OF SOFT TISSUES OF THE JOINT Soft tissue structures serve to support the joint, and disease can result in abnormal stresses to the articular cartilage and hence chronic progression of articular cartilage degeneration and osteoarthritis (see Chapter 63). Preoperative diagnosis of some soft tissue injuries is difficult, often leaving the surgeon with little to do other than evaluate the injury and debride fibrillated tissue during arthroscopic surgery. With the advent of newer diagnostic techniques such as magnetic resonance imaging (see Chapter 21) and increased use of ultrasonography (see Chapter 17), soft tissue injuries can be characterized better preoperatively. Most soft tissues of joints, such as ligaments, menisci, and joint capsule, function to support joints. Joint ligaments maintain alignment of opposing and adjacent bones in joints. They form a connection between opposing bones (such as the tibia and femur in the stifle) and between adjacent bones in more complex joints (such as between the carpal bones in the carpus). They function to maintain alignment and allow for movement of the joint. The meniscal cartilages function as cushions between the tibia and femur of the femorotibial joints. Proper material characteristics are necessary for maintenance of the joint environment. Joint capsule is also respon-

Joint ligament injury can be an incidental finding during surgery or a devastating cause of lameness. For instance, medial palmar intercarpal ligament damage can be an incidental finding during arthroscopic surgery and has been seen incidentally in necropsy specimens (see Chapter 39).1 Injury to cruciate ligaments and menisci of the stifle usually cause significant pain (see Chapter 47), but cutting the cranial cruciate ligament in an attempt to create a model of osteoarthritis did not lead to osteoarthritis in horses. Therefore further destabilization of the joint beyond cruciate injury must usually occur, with possible damage to other soft tissue structures, including the joint capsule. Collateral ligament injury caused by a bad step or laceration can result in subtle or severe lameness. We have seen lowgrade lameness in a horse that had complete tearing of the medial collateral ligament of the metatarsophalangeal joint (Fig. 68-1). Laxity of the joint was detected by manipulation and stressed radiographs. The joint was immobilized in a cast for 6 weeks, followed by a splint for an additional 6 weeks. Reinjury occurred after splint removal and the joint was recast. After immobilization for 16 weeks the injury healed well enough for trail riding. Ligament injuries usually heal slowly, and gradual return to function is needed to strengthen the tissues. The conse-

CHAPTER 68

A 3-year-old Paint gelding had acute swelling on the medial aspect of the metatarsophalangeal joint. A stressed dorsoplantar radiograph shows subluxation of the metatarsophalangeal joint caused by complete rupture of the medial collateral ligament.

Fig. 68-1

quences of collateral ligament injury depend on the severity of damage to the ligament, contamination in the joint, and damage to other structures in the joint and may be difficult to predict at the time of injury. Long-term instability may place abnormal stresses on the joint and lead to progressive osteoarthritis. Cutting the lateral collateral and lateral collateral sesamoidean ligaments of the metacarpophalangeal joint resulted in lameness, increased joint circumference, decreased range of motion, and osteophyte formation in 8 weeks, resulting in osteoarthritis.1

Fig. 68-2

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611

A synovial hernia on the dorsum of the carpus.

hygroma is an isolated structure. Although preoperative contrast radiographs may show no communication between a hygroma and a joint or tendon sheath, one might exist in the form of a one-way valve from the joint into the mass.5 Drainage of the mass with a Penrose drain and bandaging has been used successfully for treatment of recurrent hygromas. Drains usually are removed once drainage stops, 2 to 7 days after placement.6 Surgical excision can be performed in horses with chronic hygroma and is best accomplished if the fluid sac is left intact and dissected from the other tissues (see Chapter 39).7 Soft tissue and skin closure are routine, and a splint can be used to prevent flexion for better healing. Prognosis for resolution of hygroma is often good, although some degree of thickening usually persists.

Hygroma A hygroma is an adventitious or acquired bursa on the dorsum of the carpus caused by trauma from falling, getting up and down, or hitting a fence; or by chronically pawing and hitting the dorsum of the carpus.2-4 Non-painful, fluctuant, uniform soft tissue swelling occurs on the dorsal aspect of the carpus. Pressure does not induce swelling in any associated joints or tendon sheaths. Range of motion of the carpus may be reduced, but lameness is unusual. Injection of radiopaque contrast agent into the hygroma confirms its extra-articular position. Spontaneous resolution of hygromas may occur, but treatment is often necessary. Drainage and injection of antiinflammatory agents has been used with varying success; in many horses repeated injection is necessary.3,4 We have seen spontaneous resolution after injection of the contrast agent. Injection of atropine (7 mg) may resolve the swelling. Owners should be warned that bandaging is an essential component of treatment and that long-term chronic thickening may occur. Other treatments include incisional drainage; injection of irritants, such as iodine or Lugol’s solution; and blistering,3,4 but contrast radiography should be performed to ensure that the

Synovial Hernia A synovial hernia is a defect in a joint capsule or tendon sheath through which the synovial membrane can protrude. The condition rarely causes lameness but is a cosmetic blemish. A welldefined, round, soft tissue mass can be palpated over a joint, and with palpation fluid often can be moved between the hernia and the underlying joint or tendon sheath (Fig. 68-2). The hernia may disappear with joint flexion. Contrast agent injected into the hernial sac is detected in the underlying joint or tendon sheath, although a one-way valve may be present, limiting movement of contrast material. If the synovial hernia is of cosmetic concern, surgical excision can be performed, with a good prognosis for soundness provided no other joint diseases are present.8

Ganglion A ganglion is defined as a fluid-filled structure that connects to a joint or tendon sheath through a one-way tract from the joint into the mass.2 Unlike a synovial hernia, the mass lacks a synovial lining and often is filled with mucin. Ganglions are rare in

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the horse, but common in people, and they have been reported around the stifle and the carpus.2 A ganglion adjacent to the fetlock was associated with lameness that was alleviated by regional analgesia and after surgical excision of the mass.9 However, communication with the tendon sheath and joint was not demonstrable by ultrasonography. Demonstrating connection between a ganglion and an adjacent joint by injection of radiographic contrast agent into the mass may or may not be possible.6

Occasionally a fistula can be seen during arthroscopic surgery, but closure of the fistula requires an arthrotomy. However, arthroscopic surgery for treatment of a primary problem, without repair of the fistula, has resulted in resolution of lameness, without resolution of the swelling. We do not close these fistulae unless a cosmetic effect is important, if the swelling itself is impeding performance, or if medical therapy fails to alleviate lameness.

Synovial Fistula

NEOPLASIA

Synovial fistulae are communications between two synovial structures, usually a joint and tendon sheath. They have occurred between the antebrachiocarpal joint and the common digital extensor tendon; the middle carpal joint and the extensor carpi radialis tendon sheath or the common digital extensor tendon sheath; the proximal interphalangeal joint and long digital extensor tendon sheath; and the extensor carpi radialis tendon sheath and a carpal hygroma.5,10-12 Additional joint damage is often present in association with the fistula, causing lameness referable to the area. Swelling in the joint and nearby tendon sheath occurs, and fluid is often movable between the structures (Fig. 68-3). Radiography may reveal additional joint or tendon sheath damage, and contrast agent injected into one of the structures is visible in the other.10

Joint-associated tumors in horses are rare and consequently behave unpredictably, and relying on treatment information from other species is difficult. Soft tissue tumors in horses are vascular, fibrous, or synovial in origin. Benign vascular masses such as hemangiomas have been seen in carpal and digital tendon sheaths of horses.2 The tendon sheaths were distended with blood-stained fluid, but no associated lameness occurred, and surgical excision of the masses was curative. Fibromas may occur as slow-growing masses near the tarsus, stifle, and distal radius. These masses are rarely erosive to associated bone. Complete surgical excision may be curative, but incomplete excision can result in recurrence.11,13 A fibroma on the proximal lateral aspect of the tarsus was incompletely resected, and over a 4-month period the mass regrew to larger than its original size.14 Villonodular (proliferative) synovitis is a common traumatic injury on the proximal dorsal aspect of the metacarpophalangeal joints of racehorses and is not a tumor (see Chapters 36 and 67). Keratinization of a villonodular synovitis was associated with severe lameness.15 It was suggested that this was a form of epidermal inclusion cyst, the result of inadvertent introduction of epidermal tissue into the joint after repeated arthrocentesis for previous infectious arthritis, resulting in a foreign body reaction. Surgical resection resulted in resolution of lameness. Pigmented villonodular synovitis has occurred in the metatarsophalangeal and femoropatellar joints resulting in chronic lameness in a mule.16 Synovial cell sarcomas have been identified in the antebrachium,14 a digital sheath,17 and proximal interphalangeal joint associated with soft tissue swelling and variable lameness. The masses had infiltrated the soft tissues and caused localized inflammatory bone loss because of pressure. Recurrence may occur after surgical excision.18 Chondrosarcomas are rare, but they have been described in a metacarpophalangeal joint19 and the carpal region,20 associated with expansible radiolucent lesions. A hemangiosarcoma occurred in the tarsal sheath, and surgical excision resulted in relief of lameness.21 A secondary melanosarcoma in a shoulder joint caused severe lameness.22

OSTEOCHONDROMATOSIS

Fig. 68-3 Dorsal view of carpus with effusion of the antebrachiocarpal joint and common digital extensor tendon sheath. A synovial fistula was seen during arthroscopic surgery.

Synovial chondromatosis and osteochondromatosis describe pieces of uncalcified and calcified hyaline cartilage, respectively. Synovial chondromatosis is a disease in which hyaline cartilage can occur in the joint in pedunculated form, within the synovial membrane, or free within the joint. Osteochondromatosis results when endochondral ossification of the mass occurs, often making it difficult to differentiate from osteochondral fragmentation. Osteochondromatosis has occurred in the femorotibial joint.2,23 Secondary osteochondromatosis also occurs within joints with osteoarthritis. The condition is often painful in people, and surgical removal is indicated. Osteochondromatosis has occurred incidentally in horses without lameness.

CHAPTER 68 CALCINOSIS CIRCUMSCRIPTA For a discussion of calcinosis circumscripta, see Chapter 47.

REFERENCES 1. Simmons EJ, Bertone AL, Weisbrode SE: Instabilityinduced osteoarthritis in the metacarpophalangeal joint of horses, Am J Vet Res 60:7, 1999. 2. Pool R: Tumors and tumorlike lesions of joints and adjacent soft tissues. In Moulton JE, editor: Tumors in domestic animals, ed 3, Berkeley, 1990, University of California Press. 3. Stashak T: Lameness. In Stashak T, editor: Adams’ lameness in horses, Philadelphia, 1987, Lea & Febiger. 4. van Veenendaal JC, Speirs VC, Harrison I: Treatment of hygromata in horses, Aust Vet J 57:513, 1981. 5. Jann H: Treatment of acquired bursitis (hygroma) by enbloc resection, Equine Pract 12:8, 1990. 6. Andren L, Eiken O: Arthrographic studies of wrist ganglions, J Bone Joint Surg Am 53:299, 1971. 7. Adams OR: Lameness in horses, Philadelphia, 1974, Lea & Febiger. 8. Kawcak C, Trotter G: Other conditions affecting equine joints, In McIlwraith C, Trotter G, editors: Joint disease in the horse, Philadelphia, 1996, WB Saunders. 9. Hay WP, Baskett A: Lameness caused by a ganglion in a mare, Comp Cont Educ Pract Vet 18:1352, 1996. 10. Llewellyn HR: A case of carpal intersynovial fistula in a horse, Equine Vet J 11:90, 1979.

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11. McIlwraith C: Diseases of joints, tendons, ligaments and related structures. In Stashak T, editor: Adams’ lameness in horses, Philadelphia, 1987, Lea & Febiger. 12. Johnson JE, Ryan GD: Intersynovial fistula in the carpus of a horse, Cornell Vet 65:84, 1975. 13. Adams SB, Fessler JF, Thacker HL: Tendon fibromas in 2 horses, Equine Vet J 14:95, 1982. 14. Lillich J, Gaughan E: Personal communication, 2001. 15. Vickers KL, Ross MW: Atypical villonodular synovitis in a horse, J Am Vet Med Assoc 209:1602, 1996. 16. Kawcak C, Goltz K: Pigmented villonodular synovitis in a mule, Unpublished date, 1999. 17. Cheli R, Zaraga L: Synovioma della grande sesamoidea nel cavallo, La Clinica Veterinaria 100:280, 1977. 18. Lewis R: Personal communication, 2001. 19. Riddle WE Jr, Wheat JD: Chondrosarcoma in a horse, J Am Vet Med Assoc 158:1674, 1971. 20. Bertone AL, Powers BE, Turner AS: Chondrosarcoma in the radius of a horse, J Am Vet Med Assoc 185:534, 1984. 21. Van Pelt RW, Langham RF, Gill HE: Multiple hemangiosarcomas in the tarsal synovial sheath of a horse, J Am Vet Med Assoc 161:49, 1972. 22. Grant B, Lincoln S: Melanosarcoma as a cause of lameness in a horse (a case report), Vet Med Small Anim Clin 67:995, 1972. 23. Kirk MD: Radiogrpahic and histologic appearance of synovial osteochondromatosis of the femorotibial bursae in a horse: a case history report, Vet Radiol 23:168, 1982.

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CHAPTER •

69

Pathophysiology of Tendon Injury Roger K.W. Smith

FUNCTIONS OF TENDONS AND LIGAMENTS Tendons passively transfer force generated by muscle to bony attachments on the opposite side of a joint, or joints, to provide movement. In contrast the function of a ligament is to resist distraction of its two bony attachments (e.g., collateral ligaments and suspensory ligament [SL]). Although this function is true for most tendons and ligaments, the horse has evolved its digital flexor tendons and SL to exhibit additional functions. These tendons and ligaments, situated on the palmar aspect of the equine distal limb, receive large weightbearing loads because of the hyperextended metacarpophalangeal and metatarsophalangeal joints. As a result the tendons and ligaments on the palmar aspect act to support the metacarpophalangeal and metatarsophalangeal joint during normal weight bearing. In addition, the equine digital flexor tendons exhibit considerable elasticity that is used to store energy for energyefficient locomotion.1 In the case of the superficial digital flexor tendon (SDFT), its muscle is highly pennate (the muscle fibers are arranged at an oblique angle to the line of pull of the muscle, which maximizes power and minimizes contraction distance) and is unable to contract by more than a few millimeters. Therefore the action of the muscle, together with its accessory ligament, is largely passive to fix the origin of the SDFT in space. Although the muscle contracts only a short distance, its action, together with the tendon elasticity, also provides shock absorption. The gait of a horse at speed can be compared with a weight (the horse’s body) bouncing up and down on elastic springs (the digital flexor tendons) in a similar fashion to a pogo stick.2 This arrangement allows horses to reach and maintain high speeds while minimizing energy expenditure.

and what parts of the tendon are responsible for this linear deformation is unclear. 3. Yield region, in which irreversible lengthening of the tendon occurs at these strains, possibly arising from covalent cross-link rupture and slippage of collagen fibrils. 4. Rupture, in which the stress falls quickly to zero as the collagen cross-links or fibrils sequentially rupture.

Biomechanical Parameters A number of simple biomechanical parameters can be ascribed to tendons that are derived from its stress-strain characteristics: ultimate tensile stress (force per unit area at the point at which the tendon breaks), ultimate tensile strain (the percentage extension of the tendon at its breaking point), and the modulus of elasticity (E, a constant determined from the ratio of stress to strain for the linear part of the stress/strain curve). Some of the values of these parameters for the palmar supporting structures of the distal limb are shown in Table 69-1. A parameter not frequently calculated, but probably more relevant to the in vivo situation, is the force/stress at the yield point, after which irreversible damage is occurring. Ultimate tensile force/stress. The SDFT receives in excess of 1 metric ton of weight (10 kN) at maximum weight bearing on a structure only about 1 cm2 in cross-sectional area. The ultimate tensile stress (force at failure per area) for the SDFT (rupturing at the mid-metacarpal region) in the horse is therefore close to 100 MPa, which is at the upper limit of previously documented figures for other species (45 to 125 MPa).3,4 However, within any population of horses, large variation occurs in the ultimate tensile force, with up to a twofold dif-

FUNCTIONAL CHARACTERISTICS 4

Biomechanical Properties Stress-Strain Curves Stress-strain curves for the tendon in which the force per unit area (stress) is plotted against the percentage of elongation (strain) can be used to provide values for the elastic modulus of tendon. Variation in the slopes between tendons and tendon sites occurs, but Fig. 69-1 shows a simplified stressstrain curve for tendon. The curve has four regions: 1. The toe region, where stretch to the tendon is nonlinear. This is associated with the elimination of the undulating pattern of the collagen fibrils (known as crimp; see the following discussion). 2. Linear deformation, which is this area of the curve from which the modulus of elasticity is determined and that characterizes the elastic stiffness of the tendon. The mechanism for this elongation is unclear, but it involves elongation of the collagenous network, with possible movement of collagen fibrils or fascicles relative to one another. A tendon is not homogeneous,

3 Stress 2

1

Strain Fig. 69-1 Simplified stress-strain curve for tendon. 1, Toe region; 2, linear deformation; 3, yield, 4, rupture. (From Goodship AE, Birch HL, Wilson AM: The pathobiology and repair of tendon and ligament injury, Vet Clin North Am Equine Pract 10:323, 1994.)

CHAPTER 69 ference between the weakest and strongest tendons.5 This variation also exists for ultimate tensile stress,6 indicating that the variation is not just due to differences in cross-sectional area. It is hypothesized that the horses with weaker tendons are more prone to tendon injury. Modulus of elasticity/stiffness. The structural stiffness of a tendon is the force required to extend it by a unit length. This material property, the modulus of elasticity, is derived from the linear portion of the stress-strain curve for tendon, and for the SDFT it is about 1000 Mpa. It is normally correlated with ultimate tensile stress, so that the stronger the tendon, the stiffer it is. Ultimate tendon strain. In vitro testing of equine flexor tendons indicates that they usually extend by 10% to 12% of the original length before they rupture, although values of up to 20% have been reported.7 However, the ultimate tensile strain reflects only the final strain before rupture and includes that yield portion of the stress-strain curve that represents irreversible damage to the tendon tissue (Fig. 69-1). In addition the ultimate tensile strain is not constant along the length of the SDFT in vitro,8 with the highest ultimate tensile strain in the metacarpal region (the region most frequently injured). In vivo, the normal strains in the digital flexor tendons (in ponies) are about 2% to 4% at the walk and 4% to 6% at the trot.9 At the gallop in the Thoroughbred, maximum strains in the metacarpal region of the SDFT can reach 16%.10 Such strains are far greater than usually expected in tendons from most species and reflect the highly specialized nature of the equine digital flexor tendon. If these high strains are truly representative of the strains within the tendon, they indicate that equine tendon is operating at or close to its ultimate tensile strain. This suggests little tolerance in the system, which would explain the high incidence of injury in this structure. However, some caution in the interpretation of in vitro measurements is necessary, because studies have shown different results obtained between in vivo and in vitro tests.9

Hysteresis Hysteresis refers to the energy loss between the loading and unloading cycles of tendon (Fig. 69-2), determined from the area between these two curves. Hysteresis is usually about 5% in equine tendons.11 Some of this energy is responsible for the rise in temperature within the tendon core associated with repeated loading (as in an exercising horse), which has been

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suggested as a causative factor in equine superficial digital flexor tendonitis12 (see the following discussion).

Classification of Tendons and The Relationship to Function Recent research has demonstrated that tendons possess different properties depending on function. The tendons in the horse, like those in people, can be divided into two broad categories: those with the primary function of withstanding the weight of the horse (weight-bearing tendons) and those with the primary function of flexing, extending, or rotating joints (positional tendons). Weight-bearing tendons, such as the equine digital flexor tendons, are more elastic than positional tendons (e.g., the equine digital extensor tendons), which reflects the function of the digital flexor tendons as elastic energy stores. Positional tendons require stiffness for accurate positioning of the limb or digit. Human finger tendons are stiff for such a purpose, and although equine digital extensor tendons are not required for accurate placement of the digit, they nevertheless resemble this category of positional

6 5 Loading

4 Force (kN)

3 Energy loss 2 Unloading 1 0 0

2

4

6

8

Strain (%)

Hysteresis loop for tendon. (From Goodship AE, Birch HL, Wilson AM: The pathobiology and repair of tendon and ligament injury, Vet Clin North Am Equine Pract 10:323, 1994.)

Fig. 69-2

Table • 69-1 In Vitro Biomechanical Parameters Quoted for the Palmar/Plantar Supporting Structures of the Equine Distal Limb TENDON

SDFT

SDFT (HL) DDFT DDFT (HL) CDET ALDDFT SL SL (HL)

ULTIMATE TENSILE FORCE (kN)

ULTIMATE TENSILE STRESS (MPa)

ULTIMATE TENSILE STRAIN (%)

E (MPa)

REFERENCE

12.43 12.37 12.34 13.6 (range 9.5-20) — 17.00 19.27 — 6.72 8.71 17.15 17.43 —

— 128.5 —

— 17.8 12.5

1096.5 1188.9 1189.0

— — 89 — 179

12.3 — — 10.0 — — 10-12 — 11.0

1000-1282 1585 613 738-1398 1523 490 1100 510 576-669

63 67 8 5 11 63 6 11 6 63 63 6 11

— 78 —

SDFT, Superficial digital flexor tendon; HL, hindlimb; DDFT, deep digital flexor tendon; CDET, common digital extensor tendon; ALDDFT, accessory ligament of the deep digital flexor tendon; SL, suspensory ligament.

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tendons.13 These differences in biomechanical properties are reflected in the anatomical features of the tendons.

ANATOMICAL STRUCTURE Morphology of Tendons Tendon is composed of a hierarchical structure of subunits. To the naked eye, in cross-section the tendon substance is divided into a number of fascicles, which are in turn composed of ever decreasingly sized subunits: fibers and then fibrils. The fascicles are held together by the loose connective tissue, the endotenon, which is confluent with the outside of the tendon, the epitenon. The endotenon contains vascular and neural elements and separate cell populations, which may be a source of pluripotential cells. In regions where the tendons are not surrounded by a tendon sheath, a thick fibrous layer, the paratenon, further surrounds the tendon.

Crimp In longitudinal section, under the light microscope, the collagen fibers in tendon have a wavy appearance known as crimp. This pattern is responsible in part for the elasticity of the tendon, and the toe region of the stress-strain curve when the mechanical behavior of the tendon is non-linear. A generalized reduction in the crimp angle occurs with aging, with a differentially greater reduction in the central fibers.14,15 As the tendon stretches, the central fibers straighten first and therefore receive differentially greater load than the peripheral fibers, which may explain the site of pathological damage in those horses with centrally positioned core lesions. The reason for lesions situated peripherally at the tendon is less clear, unless these are also focal regions of the tendons that have developed atypically straightened fibers. Lesions involving the entire cross-section of the tendon represent a more generalized disruption of the tendon matrix.

Collagen Fibril Diameter The collagen fibrils are composed of many triple helical collagen molecules arranged in a quarter stagger, which gives a characteristic banding pattern on electron microscopy. These collagen molecules are secreted through pores in the cell membrane as triple helical procollagen, which is subsequently assembled into fibrils extracellularly, by covalent intermolecular cross-linking (see the following discussion). Fusion of adjacent fibrils is responsible for the increasing size of collagen fibrils with age.16,17 Foals at birth already have a bimodal or trimodal pattern of fibril diameters, and in the adult the fibrils can be grouped into two or three populations: small (40 nm), medium (120 nm), and large (>200 nm).7

with paratenon blood vessels, although removal of the paratenon blood supply in the horse failed to produce gross pathological damage. However, ligation of the intratendonous supply in the mid-metacarpal region produced ischemic pathological damage, demonstrating the importance of the intratendonous supply. The deep digital flexor tendon (DDFT) also has an anastomosing vascular network, except for its dorsal aspect as it passes over the metacarpophalangeal joint, where it has a more fibrocartilagenous phenotype to resist the compressive forces in this region.19 Tendon has been shown to have a good blood supply based on a number of techniques, usually involving clearance measurements of various radionuclides injected intratendonously (most commonly 133Xe and 24Na). The SDFT appears to have good blood supply similar to that of resting skeletal muscle, although findings have been inconsistent between studies and between animals on successive measurements. The large variation in the blood flow under different circumstances may indicate that external factors, as yet undefined, influence blood flow on a day-to-day basis. Differences in blood flow between tendons are affected by age, exercise, and injury (Fig. 69-3).20 The SDFT has a slightly higher blood flow than the DDFT, which reflects its good vascular anatomy (see the previous discussion). However, studies have shown similar functional blood flow throughout the metacarpal region of the SDFT although, histologically and microangiographically, the mid- and distal regions are less well vascularized.21 However, not surprisingly, the DDFT in the metacarpophalangeal joint region has a significantly lower blood flow, associated with its fibrocartilagenous phenotype, with few blood vessels because of the high compressive forces in this region, which would limit any blood flow. The blood flow appears to be considerably higher in foals than in adult horses, with a gradual decline in blood flow to the adult level by 3 years of age. Exercise induces an increase in blood flow (about 200%), although this increase is delayed in animals not previously trained. The tendon blood supply therefore appears to exhibit a fitness memory. Injury provokes a considerable increase in blood flow (>300%), which occurs in the clinically affected and the clinically unaffected limb, consistent with the bilateral nature of tendonitis in the horse, even though one limb is more severely affected than the other. Other measurements carried out in injured tendons have yielded variable results, which have been interpreted as representing the coexistence of fibrous tissue with low blood flow and hyperemic areas of acutely inflamed tendon.

Cellular Components Associated Structures Blood Supply Tendons obtain nutrients from two primary processes: perfusion and diffusion. Diffusion of nutrients from compartments other than blood occurs predominantly where the tendon is enclosed in a sheath, the synovial fluid playing an important role in tendon nutrition. The principal blood supply in tendon arises from three sources: proximally, the musculotendonous junction; distally, the osseous insertion; and between these two, the tendon is supplied by intratendonous and extratendonous vessels. The extratendonous supply arises from the paratenon in extrasynovial tendon and from mesotenon attachments within synovial tendon sheaths (such as the vinculum between the fetlock annular ligament and the SDFT). The predominance of either source in the mid-tendon region depends on the species and the tendon. In the equine SDFT, two major parallel vessels run longitudinally in the lateral and medial borders of the mid-metacarpal tendon accompanied by an extensive anastomosing network of vessels.18 These vessels anastomose

Although the biomechanical characteristics of tendon are determined by the composition and organization of the extracellular matrix, tenocytes are essential for the formation and maintenance of tendon tissue. At least three different populations of tenocytes are identifiable within normal equine tendon and ligament7,22 (Fig. 69-4): • Type I: Cells with thin, spindle-shaped nuclei • Type II: Groups of cells with more rounded, thick, cigar-shaped nuclei • Type III: Cartilage-like cells with round nuclei and visible nucleoli The proportion of these cells varies between tendons and ligaments, with tendon site, and with age. Young tendon has considerably larger numbers of type II cells arranged between the collagen bundles. With aging, type I cells predominate, whereas in the areas subjected to compressive forces, type III cells can be identified. The activity of these different cell types is unknown. The different cell types identifiable histologically may represent different cell lines or different states of extracellular matrix

CHAPTER 69

• Pathophysiology of Tendon Injury 5

6

1

20

5

1

3 4 14

3 37

2

36

20

37

37

DDFT-MC

36

Adult

Blood flow (ml/min/100 g)

619

36 37

2

1

Normal metacarpal region

Effect of age DDFT-MC

Effect of site

Effect of exercise

SDFTcl

SDFTi

SDFT

DDFT-E

DDFT-NE

SDFT-E

SDFT-NE

DDFT-MCP

Yearling

Foal

SL

DDFT

SDFT

0

Effect of injury

Absolute blood flow in equine digital flexor tendons derived from 133Xe clearance half-times. Numbers above the columns indicate the numbers of tendons evaluated. DDFT, Deep digital flexor tendon; E, exercised; MC, metacarpal region; MCP, metacarpophalangeal region; NE, not exercised; SDFT, superficial digital flexor tendon; SDFTcl, contralateral “normal” SDFT; SDFTi, superficial digital flexor tendonitis. (From Jones AJ: Normal and diseased equine digital flexor tendon: blood flow, biochemical and serological studies, PhD thesis, 1993, University of London.)

Fig. 69-3

production. A reasonable assumption is to suppose that type II and III cells are metabolically more active and are responsible for maintaining the tendon extracellular matrix, although the metabolic activity of the type I cells cannot be discounted. Ligament has a much higher cell population, with a predominance of type II cells arranged in columns. In the SDFT of the horse, which has greater numbers of cells during growth, total tendon cell numbers remain relatively constant after skeletal maturity. However, acellular areas develop, especially in the center of the SDFT in the metacarpal region, although the degree of acellularity is not particularly related to age.23 More active, type II cells can be found surrounding the fibrils in these regions. Chondroid metaplasia can also be identified associated with these areas. Other areas, typified by the DDFT in the metacarpophalangeal region, also have acellular regions associated with a fibrocartilagenous phenotype (type III cells and cartilage-like matrix) as a result of concurrent compressive forces as the tendon wraps around the metacarpophalangeal joint. Other cells are associated with the tendon, namely the paratenon, epitenon, and endotenon fibroblasts and the synovial-like cells of the epitenon within the tendon sheaths. These cell populations may also play important roles in maintaining tendon tissue, especially because the endotenon harbors certain growth factors, such as transforming growth factor-β (TGF-β) (Fig. 69-5).24 The regulation of tenocyte metabolism still is not understood fully but probably relies on a combination of mechanical and cytokine stimuli. Tenocytes have been shown to sense and react rapidly to mechanical stimuli in vitro.25 However, equine tenocytes in culture require the addition of a suitable growth factor to initiate a synthetic response to load.26 Recently, the use of confocal microscopy has provided an insight into the relationship between tenocytes. Staining with a membrane dye has revealed extensive cytoplasmic extensions from tenocytes, which form a complex meshwork around the collagen bundles. Gap junctions have been shown to exist between these cytoplasmic extensions, which would provide an ideal arrangement for the coordinated biosynthetic reactions to mechanical stimuli.27

Of the multitude of growth factors having effects on connective tissues, TGF-β and insulin-like growth factor 1 have been investigated the most in equine tendon.28,29 The synthesis and distribution of TGF-β isoforms in equine digital flexor tendon vary with age. The highest levels are observed in young equine digital flexor tendon, especially within the endotenon.24 Levels decline after skeletal maturity, especially in the tendon fascicles themselves, and this may result in a relative lack of tenocyte synthetic activity after skeletal maturity. However, it is not yet clear which are the most fundamental growth factors in equine tendons and how the growth factor milieu acts to cause tendon matrix synthesis and repair.

Molecular Composition of Tendon Matrix Tendons are composed predominantly of extracellular matrix, within which is a wide array of proteins, organized and interacting to produce the mechanical properties of tendon. The tendon extracellular matrix is composed predominantly of water (about 65% wet weight), collagen (about 30% wet weight), and non-collagenous glycoproteins (about 5% wet weight).

Collagen About 80% of the dry weight of the tendon is collagen, of which the predominant collagen type is type I (>95%).7 Type III collagen is present in the endotenon and appears to increase as the animal ages. Type II (the collagen of articular cartilage) is likely to occur at the same sites in the horse as described in other species; namely, tendon insertions and where tendons develop fibrocartilage-like tissue associated with a change in the direction of pull around bony prominences (e.g., at the metacarpophalangeal joint). Collagen fibrils are strong, but the bonds formed between these fibrils and the higher order subunits are more likely to determine the strength of the tissue. The major covalent crosslink of type I collagen in tendon is between hydroxylysine and lysine residues.30 Lysine and hydroxylysine are converted to the respective aldehydes by the action of the enzyme lysyl oxidase, which is inhibited by β-aminopropionitrile fumarate, a chemical that has been used in the treatment of equine

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A

B

C

D

E

Fig. 69-4 Histological features of equine tendon and ligament. A, Foal superficial digital flexor tendon showing obvious crimp and predominantly type II cells (arrow). B, Young superficial digital flexor tendon showing reduction in crimp and increased number of type I cells (arrow). Note also the endotenon septa (star). C, Aged deep digital flexor tendon from the metacarpophalangeal region showing acellular regions and type III cells (arrow), resembling the chondrocyte phenotype associated with compressive loading in this region. D, Chondroid metaplasia (arrow) in an aged superficial digital flexor tendon. The acellular areas are visible between the regions of chondroid metaplasia. E, Suspensory ligament branch showing the lines of type II cells (arrows) characteristic of ligament.

tendon injuries. These lysine and hydroxylysine aldehydes then can form a number of different types of cross-links: reducible (e.g., dihydroxylysinonorleucine and hydroxylysinonorleucine) or non-reducible (hydroxylysylpyridinoline). The reducible cross-links become reduced with age so that at maturity their level is less than 10% of the level in the foal.31

Non-covalent cross-links (electrostatic in nature) are provided by the proteoglycans and other glycoproteins, especially the small proteoglycan decorin, which coats the collagen fibril. Although individually these cross-links are less strong than the covalent cross-links, the high number and involvement in the higher order organization of the collagen network

CHAPTER 69

make them potentially major determinants of tendon mechanical properties.

Non-Collagenous Glycoproteins Cartilage oligomeric matrix protein. The large cartilage oligomeric matrix protein (COMP) consists of five subunits, bound via disulfide bonds at their N-termini to form a fivearmed protein, with a bouquet of arms with globular Cterminal domains that can interact with other matrix components32,33 (Fig. 69-6). Although initially thought to be restricted in distribution to cartilage, COMP subsequently has been found largely in tissues whose function primarily is to resist load. Thus COMP is found in significant amounts in tendon, ligament, cartilage, intervertebral disk, and meniscus. In equine digital flexor tendons COMP shows large variation with site and age.34 Levels are low at birth but accumulate rapidly associated with weight bearing. Levels peak in the metacarpal region of the SDFT (at about 3% dry weight of tendon) at skeletal maturity and subsequently decline (Fig. 69-7). Levels peak at a lower level in the metacarpophalangeal regions and in the DDFT but are maintained in the former. The function of COMP has not yet been elucidated completely, but COMP is known to bind fibrillar collagens (I, II, and IX),35,36 and a mutation in the human COMP gene is responsible for pseudoachondroplasia, characterized by lax tendons and ligaments, short stature, and early-onset osteoarthritis.37,38 Although COMP may have a structural role, present research data suggest that it also may also act to bring collagen molecules together to form fibrils, and it may assist in the organization of the collagen network. This role may explain the decline in COMP levels after skeletal maturity in the metacarpal region, because the collagen matrix has been formed and limited remodeling occurs in the adult. Preliminary data on equine SDFT show a significant correlation between ultimate tensile stress and COMP levels at skeletal maturity.39 Thus high levels of COMP during development potentially enable the formation of a high-quality tendon matrix. Proteoglycans. Proteoglycans are a group of molecules that possess a protein core and a side chain of sugars (glycosaminoglycans, or GAGs). The sugar side chains are highly variable in type and length so that great diversity exists even within a given tissue. Work on a variety of soft tissues, especially articular cartilage, has demonstrated a large number of different proteoglycans that are vital to maintaining the structural integrity of the tissue by playing structural roles or by regulating the metabolism of the tissue.

621

Cartoon of the cartilage oligomeric matrix protein molecule. (Courtesy K. Rosenberg, Lund, Sweden.)

Fig. 69-6

Cartilage oligometric matrix protein content (mg/g tendon wet weight)

Immunohistochemical staining for transforming growth factor-β3 in equine superficial digital flexor tendon. Note the concentration of stain (arrow) in the endotenon septa. (Courtesy Eddy Cauvin, Lyon, France.)

Fig. 69-5

• Pathophysiology of Tendon Injury

11 10 9 8 7 6 5 4 3 2 1 0

0

5

10 15 Age (years)

20

25

The variation of cartilage oligomeric matrix protein levels with age in the metacarpal region of the superficial digital flexor tendon. (Modified from Smith RK, Zunino L, Webbon PM, et al: The distribution of cartilage oligomeric matrix protein (COMP) in tendon and its variation with tendon site, age and load, Matrix Biol 16:255, 1997.)

Fig. 69-7

Proteoglycans are largely divided into two broad categories, the large and small proteoglycans. The large proteoglycans are exemplified by the major proteoglycan of cartilage, aggrecan, and the fibroblast-derived large proteoglycan, versican. These molecules possess a large number of GAG side chains and can form aggregates with hyaluronic acid. With the repulsion of the negatively charged GAG chains, this molecule has a bottle-brush shape and can trap large quantities of water. The swelling potential for this molecule, when restrained by the collagen network of cartilage, produces a structural matrix ideally suited to resisting compression. In tendon, areas subjected to compressive forces develop a matrix rich in these large proteoglycans, such as in the DDFT and SDFT in the metacarpophalangeal region. The small proteoglycans such as decorin, biglycan, fibromodulin, and lumican usually have only one or two GAG side chains. Many of these proteoglycans have wide tissue distribution and have been shown to have structural and regulatory roles. A number of these proteoglycans bind to other members of the extracellular matrix. Thus decorin, the most common proteoglycan in tensional tendon (e.g., metacarpal region of the digital flexor tendons), has been shown to bind to fibrils of type I collagen.40 Decorin is thought to be respon-

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sible for regulating collagen fibril diameter and, together with the other small proteoglycans, may be responsible for providing electrostatic cross-links between fibrils, thus being also an important determinant of tendon strength. Targeted disruption of the genes for some of these small proteoglycans has confirmed a suggested role in maintaining tissue structural integrity. Deleting or knocking out the decorin gene results in variably sized collagen fibrils and poor mechanical strength in skin,41 whereas targeted disruption of the fibromodulin gene causes altered collagen fibril morphology and reduced mechanical strength in tendon.42 Furthermore the small proteoglycans have been shown to bind various growth factors, especially TGF-β,43 which may be important in regulating tendon homeostasis, adaptation, and response to injury. Other non-collagenous glycoproteins. A number of other non-collagenous glycoproteins have been described in tendon, including elastin (not thought to be important for tendon elasticity in the horse),31 fibronectin (which is upregulated after injury), thrombospondin 4, PRELP (proline arginine-rich end leucine-rich repeat protein), and tenascin-C. However, the functions of these, and others that have yet to be characterized, have not been determined fully.

Types of Tendon Injury Tendons can suffer intrinsic (strain) or extrinsic (percutaneous) injury or displacement. The most common injury in the horse is the intrinsic injury of the SDFT in the metacarpal region. Recent epidemiological data have indicated an incidence of 43% in National Hunt horses in training.44 Much of our understanding of tendon physiology (as described previously) and pathogenesis relates to this tendon. Insertional injuries, although common in the human athlete, are rarer in the horse and most commonly are seen associated with the SL rather than the SDFT. Clinical superficial digital flexor tendonitis varies in severity from individual fibril or fiber slippage to individual fibril or fiber rupture and ultimately to complete rupture of tendon with progressive involvement of more groups of fibers and fascicles. Many horses with clinical tendonitis are believed to be preceded by subclinical degeneration of the tendon matrix. This is based on a number of observations. First, post-mortem examination of tendons of horses euthanized for reasons other than tendonitis revealed low-grade pathological damage ranging from acellular areas, chondroid metaplasia, and cyst formation.23,45 Second, tendonitis is frequently a bilateral

disease, although one limb is more severely affected than the other. Although bilateral changes sometimes can be difficult to identify clinically, ultrasonography invariably confirms some degree of bilateral involvement. Thirdly, recent research has identified a number of changes that occur within tendons associated with aging and exercise.

Mechanisms of Tendon Injury: Effect of Aging and Exercise A number of controlled exercise studies in adult and young horses (Table 69-2) has provided considerable information on the effect of exercise on normal equine tendons. In none of these studies was there any indication of clinical tendonitis induced by the exercise protocols. Regional differences in collagen fibril diameter were seen in long-term exercised older horses, but not in the short-term exercised, or younger horses.46 Within the central region of the SDFT there was a higher proportion of smaller fibrils in comparison with the controls (Fig. 69-8). The higher proportion of small fibrils did not correlate with new collagen formation and thus appears to result from disassembly of the larger diameter fibrils, rather than the formation of new collagen, which would indicate an adaptive response. The reduction in crimp pattern seen with aging was accelerated by the exercise protocols in the adult.47 Changes in molecular composition also occurred in the long-term exercise studies, with a reduction in GAG content and an accelerated loss of COMP in the center of the tendon.48,49 In contrast, molecular analysis of tendons recovered post mortem with central discoloration but no prior diagnosis of superficial digital flexor tendonitis demonstrated an increase in type III collagen and GAG.50 Because these tendons appear to be enlarged significantly and have central hypoechoic lesions when examined by ultrasonography in vitro (Fig. 69-9), these molecular changes probably more reflect a reparative response rather than a degenerative change associated with aging and exercise. In young growing animals, removal of load from tendon results in a lack of COMP accumulation in tendon, whereas removal of load after COMP has accumulated does not alter its levels in the tendon. Because recent data have shown an association between COMP levels and tendon strength at skeletal maturity,39 too little exercise may inhibit the ability of the tendon to develop quality tendon matrix. However, exercise studies during skeletal development indicated that tendons are more easily damaged if the exercise level is too high.51

Table • 69-2 Studies Aimed at Investigating the Effect of Exercise of Equine Digital Flexor Tendons

POPULATION

STUDY NAME

Thoroughbred

Bristol, long-term study Bristol, short-term study Utrecht study

Thoroughbred Warmblood

AGE OF ANIMAL AT ONSET OF EXERCISE

DURATION OF EXERCISE

NATURE OF EXERCISE

AGE AT ANALYSIS

REFERENCES FOR PROTOCOL

21 months

18 months

Treadmill

46, 49

19 months

41⁄2 months

Treadmill

3 years 3 months 231⁄2 months

1 week

19 weeks (high intensity) followed by 6 months (low intensity)

Over ground

5 months (first group) 11 months (second group)

68

49

CHAPTER 69

• Pathophysiology of Tendon Injury

A

623

B

Fig. 69-8 Difference in collagen fibril populations in control and treadmill-exercised yearlings. A, Control. B, Treadmill exercised. Note the increased proportion of small-diameter fibrils compared with the non-exercised cohort (A). (From Patterson-Kane JC, Firth EC, Parry DAD, et al: Comparison of collagen fibril populations in the superficial digital flexor tendons of exercised and nonexercised thoroughbreds, Equine Vet J 29:121, 1997.)

A

A, Transverse section of the superficial digital flexor tendon from the mid-metacarpal region, showing asymptomatic central discoloration observed in some tendons at post mortem. B and C, Note the abnormalities demonstrated when the tendon is examined by ultrasonography in a water bath. The central hypoechoic region and increase in the tendon cross-sectional area in the transverse scans (B) and the central disruption of the fiber alignment pattern in the longitudinal view (C) resemble the changes observed with ultrasonography in clinical tendonitis. (From Goodship AE, Birch HL: Exercise effects on the skeletal tissues. In Back W, Clayton H, editors: Equine locomotion, London, 2001, WB Saunders.)

B

Fig. 69-9

C

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These controlled exercise studies have demonstrated that exercise accelerates a degenerative change that occurs inevitably with aging. Thus the research data would suggest that after skeletal maturity the tendon has limited ability to adapt. Instead, cumulative fatigue damage weakens the tendon matrix and allows the initiation of clinical tendonitis when loading overcomes the resistive strength of the tendon. Epidemiological studies have supported a strong association of age and exercise with the incidence of tendon injury in horses and people.44,52 Further confirmation of cellular activity during growth, but not after skeletal maturity, has been provided by studies of matrix turnover and gene expression. The turnover of collagen has been determined for experimental animals, but no definitive data are present for the horse. In experimental animals, collagen turnover is high in the neonate and growing animal, but it declined to low levels in the adult.53 In bovine digital flexor tendons matrix gene expression, as determined by in situ hybridization, was easily detectable in young, growing animals, but no gene activity was present in the metacarpal region in the adult.54 Interestingly, gene activity did persist in the metacarpophalangeal region, which may explain the relative resistance to injury of this region, because of its capability to remodel microdamage. In support of this hypothesis, COMP levels in this region of the equine SDFT and DDFT do not decline after skeletal maturity. The absence of gene activity in the metacarpal region may be from a lack of appropriate growth factors or cellular senescence. Certainly in these studies investigating TGF-β in equine tendons, young equine tendon had high levels, but amounts declined after skeletal maturity.24 In contrast, young growing tendon does appear to be sensitive to the effects of loading and exercise. The adaptive response of the growing animal may not be constant, and research data suggest that response may be pronounced most early in life and decline with growth. The level and amount of work necessary to induce this response is unknown and currently is being evaluated. However, by analogy with bone remodeling in response to load, high strain rates may be the most effective. An interesting note is that the natural exercise performed by a group of young foals at pasture includes a large amount of jumping activity at play, which is perfectly suited to these high strain rates on the digital flexor tendons. Thus, as with other skeletal tissue development, such as cartilage, a window of opportunity apparently may be exploited to optimize conditioning of tendons for athletic performance (Fig. 69-10). The large variation seen in the mechanical properties within a population could be accounted for by variation in tendon development, caused by environmental factors, or genetic determinants. From these observations a strategy for preventing tendonitis can be proposed. Maximizing the quality of tendon before skeletal maturity with the early introduction of controlled exercise may be possible, thereby reducing the incidence of tendon injury in subsequent racing and competition (Fig. 69-11).

Hypothesized Mechanisms of Tendon Degeneration Mechanical Influences Sudden over-extension of the metacarpophalangeal joint causes mechanical disruption of the tendon. Although this may be the mechanism of certain tendon injuries, such as deep digital flexor tendonitis, direct low-grade mechanical forces, such as experienced under maximal loading, could be responsible for the cumulative fatigue microdamage of the tendon matrix. Subsequent clinical tendonitis is initiated by similar, or sudden supra-maximal, loading after the accumulation of microdamage.

Physical Influences: Exercise-Induced Hyperthermia Because of the hysteresis loop, when a tendon is loaded and unloaded, a loss of stored energy as heat results in temperature increases within the equine digital flexor tendons.

Training ‘window’

Training level Immature adaptation Immature injury risk

Adult adaptation Adult injury risk

Hypothesized schematic representation of the adaptive response and injury risk for growing (immature) and adult (>2 years of age) equine digital flexor tendons. (Modified from Goodship AE, Birch HL: Exercise effects on the skeletal tissues. In Back W, Clayton H, editors: Equine locomotion, London, 2001, WB Saunders.)

Fig. 69-10

Tendon strength

624

Training

Tendonitis risk level

Skeletal maturity

Racing career Age

Strategy for the prevention of tendonitis in the horse. The dotted line refers to a horse that develops strong tendons, whereas the dashed line represents a horse with poorquality tendons at skeletal maturity (which appears to be at about 2 years of age). The latter suffers tendonitis during its racing/competitive career because of inevitable and cumulative fatigue damage to the tendon, whereas the former, although suffering the same degeneration, starts from a stronger point and therefore does not suffer tendonitis. The early introduction of exercise during development potentially improves tendon quality (arrow), thereby subsequently reducing the incidence of tendonitis.

Fig. 69-11

Thermocouples have been placed inside the SDFT, and these have recorded temperatures of up to 45º C during periods of galloping.12 Such temperatures are used to kill neoplastic cells therapeutically and so it was hypothesized that these temperatures would interfere with tenocyte metabolism and possibly destroy the cells. However, in vitro experiments have shown that tenocytes are much more resistant to these temperature increases in comparison with other fibroblastlike cells.55 Interestingly, tenocytes tolerate such temperature increases even in utero, suggesting a genetically determined, rather than acquired, characteristic. Although

CHAPTER 69 the cells remain viable with such temperature increases, hyperemia may still influence tendon matrix quality. A reduction in the normal synthetic activity of tenocytes or a direct denaturing effect on tendon extracellular matrix still may occur.

Vascular Theories Blood flow through tendon is a complex issue and its relevance to clinical injury is still unsubstantiated. Under maximal loading, blood flow is limited or abolished within the tendon because of the compressive forces generated by the lengthening of the tendon, and this may give rise to relative hypoxia. Some areas of equine flexor tendon are relatively poorly perfused (e.g., the dorsal portion of the DDFT in the metacarpophalangeal joint region), and this level (but not just the dorsal surface) is a site predisposed to deep digital flexor tendonitis. However, this area also shows histological adaptation to the relatively ischemic environment, with fewer cells and increased amounts of the compression-resisting extracellular matrix components. Furthermore the tendon may receive some of its nutrition at this site by diffusion from the digital sheath synovial fluid. Similar alterations in the extracellular matrix composition are seen at the corresponding positions in the SDFT, and one could assume that the forces on this tendon would be similar to those of the DDFT at the same site. Therefore, a reduced blood flow would also be expected at this level, and yet clinically this region is invariably spared injury in all but the most severe tendonitis. Equine tendon cells do rely at least in part on oxidative metabolism, although blocking aerobic metabolism does not prevent normal cell proliferation.56 Based on studies in other species, tenocytes may be more resistant to hypoxia than other similar fibroblast-like cells. Laser Doppler flowmetry has suggested that a change in blood supply is not the initiating cause in human Achilles tendonitis,57 in contrast to the previously proposed hypoxic cause for tendonitis based on electron microscopic investigations of normal and diseased Achilles tendons.58 Another result of poor perfusion under loading is the generation of toxic free radicals when perfusion is restored. Such reperfusion injury also has been proposed as a causative factor for tendonitis through the destruction of tenocytes or tendon matrix by the free radicals, although this at present remains a speculative mechanism.

Proteolytic Enzymes Various stimuli, including those mentioned previously, could result in the synthesis, release, or activation of proteolytic enzymes. Relatively little information is available on the constitutive or induced expression of proteases in tendon, although activity of procollagenase and aggrecanase has been described in human and bovine tendon explants in vitro.59,60 An imbalance between the matrix synthesis and degradation of various extracellular matrix proteins is a possible mechanism whereby the tendon can be weakened and predisposed to clinical tendonitis.

Factors Affecting the Loading of the Superficial Digital Flexor Tendon and Initiation of Clinical Tendonitis Peak SDFT forces are responsible for initiating clinical tendonitis. When the tendon has been weakened sufficiently by the preceding degenerative change, factors that increase the peak loading of the SDFT therefore also act to increase the risk of clinical tendonitis. The SDFT is loaded preferentially at the early stage of the stride,7,9,61 which represents the time of highest injury risk. External factors, such as the rider’s weight or hard ground, increase these peak forces, although possibly only in certain tendons.9 Recent data have suggested that landing from a jump increases the peak forces in the SDFT but not the SL.62

• Pathophysiology of Tendon Injury

625

The greater the height and number of fences jumped at Grand Prix–level show jumping would explain the higher incidence of injury in these horses to those competing at a lower level (see Chapters 70 and 116). Foot conformation is also critical for affecting the loading of the SDFT (and SL). The lowering of the toe with respect to the heels, or the raising of the heels with respect to the toe, results in reduced loading of the DDFT and increased loading of the SL (and possibly the SDFT), often only detectable at the trot.10,63,64 As a corollary to this, the long-toe, low-heel conformation characteristic of the Thoroughbred may actually protect the horse from superficial digital flexor tendonitis.64 The ground surface also influences the loading of the SDFT. Soft ground may predispose to increased strains in the SDFT by allowing the toe to sink. However, using sand has been shown largely to have little effect on the strains in the SDFT and DDFT.9 The effect of ground surface on the incidence of tendonitis is probably more related to determining the speed of the horse. Speed is correlated with strains in the SDFT and also has been correlated with the incidence of SDFT tendonitis in racehorses (see Chapters 70, 107, 108, and 113). Thus ground surfaces that slow the horse tend to be protective of SDFT tendonitis, whereas the driest and hardest racecourses are associated with the highest incidence of tendonitis. Many horses suffer tendonitis toward the end of a race or event when horses are fatigued. Fatigue will cause greater incoordination, which can result in increased peak loads on the SDFT, thereby increasing the risk of tendonitis. Because tendon degeneration appears to be related to the number of loading cycles, the greater the exercise history and age, the more at risk the horse becomes. This certainly explains the strong association between age and tendonitis and may explain why older, sedentary horses still can develop tendonitis. Because the subclinical phase of tendon degeneration affects both limbs similarly, clinical superficial digital flexor tendonitis is frequently bilateral. Changes are frequently observed with ultrasonography on both limbs, although one limb is usually more severely affected than the other.

Pathological Conditions and Phases of Tendon Healing Tendonopathy can be divided into four phases. The subclinical phase of tendon degeneration, described previously, is difficult to identify clinically at present by palpation or ultrasonographic examination, because it causes minimal, if any, inflammatory reaction. In the future, serological assays, currently being developed to detect matrix proteins released from the tendon, may prove useful for detecting and monitoring this phase. The clinically detectable pathological condition is divided into three phases: the acute inflammatory phase, the subacute reparative phase, and the chronic remodeling phase. The acute inflammatory phase begins with the onset of the clinical injury and lasts usually only 1 to 2 weeks, although this is in part determined by the severity of the injury and the antiinflammatory therapy initiated. This phase is characterized by substantial inflammation, with intratendonous hemorrhage, increased blood supply and edema, and the infiltration of leukocytes, initially neutrophils, but followed by macrophages and monocytes. The pronounced inflammation, if unchecked, results in the release of proteolytic enzymes, which, although directed at removing necrotic collagen, also digest relatively intact tendon collagen, which may cause the expansion of the lesion in the few days after the onset of the clinical tendonitis. The sub-acute reparative phase begins within a few days of the injury, overlapping with the acute phase, and peaks after about 3 weeks.65 This phase is characterized by a strong angiogenic response and the accumulation of fibroblasts within

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the damaged tissue. These fibroblasts probably are derived from a number of sources including the resident tenocytes, endotenon and paratenon cells, and monocytes of vascular origin. These cells are then responsible for synthesizing scar tissue (tendon tissue is not regenerated), characterized by haphazardly arranged collagen, predominantly type III. The scar tissue formed is initially weaker than tendon tissue and hence healing tendon is predisposed to re-injury at the injury site. Such episodes of re-injury perpetuate the first two phases and increase the amount of damaged tendon and hence the severity of the injury. The absence of a paratenon and an externally derived blood supply within a tendon sheath may explain the relative poor response in healing in these areas. The formation of adhesions within tendon sheaths, although responsible for limiting the movement of the tendons subsequently, provide a method of allowing angiogenesis and the infiltration of cells into damaged tendon tissue within a tendon sheath. Hence, although adhesions have deleterious effects on the function of tendons, they are a normal response to encourage tendon healing in this region. During the chronic remodeling phase, which begins several months after the injury, the scar tissue slowly remodels over a number of months. This remodeling process is associated with a conversion of type III collagen to type I collagen, the major component of normal tendon. However, in spite of this conversion the tissue never becomes normal tendon tissue, although it is probably more functional. Controlled loading (exercise) during this phase may help promote this conversion and, even more importantly, align the collagen fibrils in the direction of force, which further improves the mechanical properties of the scar tissue. This aspect of the remodeling process is followed by assessing the fiber alignment score on ultrasound (see Chapter 70). Re-injury is unfortunately common, even after healing is complete, in the same tendon, the contralateral tendon, or other supporting structures of the metacarpophalangeal joint. As the injured tendon remodels, it becomes stronger, so that fully healed tendon (15 to 18 months after injury) is frequently stronger than normal tendon.66 However, remodeled tendon has poor elasticity, resulting in increased strain in adjacent, relatively undamaged regions of the tendon. Therefore if re-injury occurs in the same tendon, it frequently occurs at adjacent or remote sites to the original injury. Subsequent injury to the contralateral tendon is also effectively a re-injury because of the bilateral nature of the preceding degeneration and clinical tendonitis. Subsequent injury to the SL may be the consequence of some loss of support of the metacarpophalangeal joint, caused by significant lengthening of the SDFT, which can occur with severe superficial digital flexor tendonitis. The SL may also suffer cumulative microdamage, which would increase further its susceptibility to injury.

REFERENCES 1. Alexander RM: Energy-saving mechanisms in walking and running, J Exp Biol 160:55, 1991. 2. Wilson AM, van den Bogert AJ, McGuigan MP: Optimization of the muscle-tendon unit for economical locomotion in cursorial animals. In Herzog W, editor: Skeletal muscle mechanics: from mechanisms to function, Chichester, England, 2000, John Wiley & Sons. 3. Viidik A: Tensile strength properties of Achilles tendon systems in trained and untrained rabbits, Acta Orthop Scand 40:261, 1969. 4. Woo SL-Y: Mechanical properties of tendons and ligaments. I. Quasi-static and nonlinear viscoelastic properties, Biorheology 19:385, 1982.

5. Wilson AM: The effect of exercise intensity on the biochemistry, morphology, and mechanical properties of tendon, PhD thesis, 1991, University of Bristol, UK. 6. Birch HL: Personal communication. 7. Goodship AE, Birch HL, Wilson AM: The pathobiology and repair of tendon and ligament injury, Vet Clin North Am Equine Pract 10:323, 1994. 8. Crevier N, Pourcelot P, Denoix J-M, et al: Segmental variations of in vitro mechanical properties in equine superficial digital flexor tendons, Am J Vet Res 57:1111, 1996. 9. Riemersma DJ, van den Bogert AJ, Jansen MO, et al: Tendon strain in the forelimbs as a function of gait and ground characteristics and in vitro limb loading in ponies, Equine Vet J 28:133, 1996. 10. Stephens PR, Nunamaker DM, Butterweck DM: Application of a Hall-effect transducer for measurement of tendon strains in horses, Am J Vet Res 50:1089, 1989. 11. Riemersma DJ, Schamhardt HC: In vitro mechanical properties of equine tendons in relation to cross-sectional area and collagen content, Res Vet Sci 39:263, 1985. 12. Wilson AM, Goodship AE: Exercise induced hyperthermia as a possible mechanism for tendon degeneration, J Biomech 27:899, 1994. 13. Batson EL, Paramour RJ, Smith T, et al: The elastic modulus of the equine superficial digital flexor tendon and common digital extensor tendon. Proceedings of the seventeenth meeting of the Federation of European Connective Tissue Societies, Patras, Greece, July 2000. 14. Wilmink J, Wilson AM, Goodship AE: Functional significance of morphology and micromechanics of collagen fibres in relation to partial rupture of the superficial digital flexor tendon in racehorses, Res Vet Sci 53:354, 1991. 15. Patterson-Kane JC, Parry DA, Birch HL, et al: An agerelated study of morphology and cross-link composition of collagen fibrils in the digital flexor tendons of young thoroughbred horses, Connect Tissue Res 36:253, 1997. 16. Kadler KE, Holmes DF, Trotter JA, et al: Collagen fibril formation, Biochem J 316:1, 1996. 17. Kadler KE, Holmes DF, Graham H, et al: Tip-mediated fusion involving unipolar collagen fibrils accounts for rapid fibril elongation, the occurrence of fibrillar branched networks in skin and the paucity of collagen fibril ends in vertebrates, Matrix Biol 19:359, 2000. 18. Kraus-Hansen AE, Fackelman GE, Becker C, et al: Preliminary studies on the vascular anatomy of the equine superficial digital flexor tendon, Equine Vet J 24:46, 1992. 19. Kraus BLH, Kirker-Head CA, Kraus KH, et al: Vascular supply of the tendon of the equine deep digital flexor muscle within the digital sheath, Vet Surg 24:102, 1995. 20. Jones AJ: Normal and diseased equine digital flexor tendon: blood flow, biochemical and serological studies, PhD thesis, 1993, University of London. 21. Strömberg B: The normal and diseased superficial digital flexor tendon in racehorses: a morphologic and physiologic investigation, Acta Radiol 305(Suppl):1, 1971. 22. Smith RK, Webbon PM: The physiology of normal tendon and ligament. Rantanen NW, Hauser ML, editors: Proceedings of the 1996 Dubai International Equine Symposium, Bonsall, Calif, 1996, Matthew R. Rantanen Design. 23. Webbon PM: A histological study of macroscopically normal equine digital flexor tendons, Equine Vet J 10:253, 1978. 24. Cauvin ERJ: An investigation into the roles of transforming growth factor beta (TGFβ) in the development, adaptation, and repair of equine tendon. PhD dissertation, London, 2001, University of London.

CHAPTER 69 25. Banes AJ, Tsuzaki M, Yamamoto J, et al: Mechanoreception at the cellular level: the detection, interpretation, and diversity of responses to mechanical stimuli, Biochem Cell Biol 73:349, 1995. 26. Goodman SA, May SA, Smith RK: Cyclical strain and TGFβ modulate the synthesis of collagen types I and III in equine tenocytes in vitro. Proceedings of the seventeenth meeting of the Federation of European Connective Tissue Societies, Patras, Greece, July 2000. F17. 27. McNeilly CM, Banes AJ, Benjamin M, et al: Tendon cells in vivo form a three dimensional network of cell processes linked by gap junctions, J Anat 189:593, 1996. 28. Murphy DJ, Nixon AJ: Biochemical and site-specific effects of insulin-like growth factor I on intrinsic tenocyte activity in equine flexor tendons, Am J Vet Res 58:103, 1997. 29. Smith RK, Williams L, Cauvin E, et al: TGFβ-1 stimulates cartilage oligomeric matrix protein (COMP) synthesis by tenocytes in vitro: a hypothesis for tendon failure, Vet Surg 27:518, 1998. 30. Frank C, Woo S, Andriacchi T, et al: Normal ligament: structure, function, and composition. In Woo SL-Y, Buckwalter JA, editors: Injury and repair of musculoskeletal soft tissues, Park Ridge, Ill, 1987, American Academy of Orthopaedic Surgeons. 31. Silver IA, Brown PN, Goodship AE, et al: A clinical and experimental study of tendon injury, healing, and treatment in the horse Equine Vet J Suppl 1, 1983. 32. Hedbom E, Antonsson P, Hjerpes A, et al: Cartilage matrix proteins: an acidic oligomeric protein (COMP) detected only in cartilage, J Biol Chem 267:6132, 1992. 33. Mörgelin M, Heinega[o]rd D, Engel J, et al: Electron microscopy of native cartilage oligomeric matrix protein purified from the Swarm rat chondrosarcoma reveals a five-armed structure, J Biol Chem 267:6137, 1992. 34. Smith RK, Zunino L, Webbon PM, et al: The distribution of cartilage oligomeric matrix protein (COMP) in tendon and its variation with tendon site, age and load, Matrix Biol 16:255, 1997. 35. Rosenberg K, Olsson H, Morgelin M, et al: Cartilage oligomeric matrix protein shows high affinity zincdependent interaction with triple helical collagen, J Biol Chem 273:20397, 1998. 36. Thur J, Rosenberg K, Nitsche DP, et al: Mutations in cartilage oligomeric matrix protein causing pseudoachondroplasia and multiple epiphyseal dysplasia affect binding of calcium and collagen I, II, and IX, J Biol Chem 276:6083, 2001. 37. Hecht JT, Nelson LD, Crowder E, et al: Mutations in exon 17B of cartilage oligomeric matrix protein (COMP) cause pseudoachondroplasia, Nat Genet 10:325, 1995. 38. Briggs MD, Hoffman SM, King LM, et al: Pseudoachondroplasia and multiple epiphyseal dysplasia due to mutations in the cartilage oligomeric matrix protein gene, Nat Genet 10:330, 1995. 39. Smith RK, Gerard M, Dowling B, et al: A proposed role for cartilage oligomeric matrix protein (COMP) in determining function and specific mechanical characteristics of locomotor tendons in the horse, Equine Vet J (in press). 40. Brown DC, Vogel KG: Characteristics of the in vitro interaction of a small proteoglycan (PG II) of bovine tendon with type I collagen, Matrix 9:468, 1989. 41. Danielson KG, Baribault H, Holmes DF, et al: Targeted disruption of decorin leads to abnormal collagen fibril morphology and skin fragility, J Cell Biol 136:729, 1997. 42. Svensson L: The role of leucine-rich repeat glycoproteins/proteoglycans in the assembly of collagen matrices, PhD thesis, 1999, University of Lund, Sweden.

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43. Yamaguchi Y, Mann DM, Ruoslahti E: Negative regulation of transforming growth factor-β by the proteoglycan decorin, Nature 346:281, 1990. 44. Pickersgill C: Epidemiological studies into orthopaedic conditions of the equine athlete, MVM thesis, 2000, University of Glasgow, UK. 45. Webbon PM: Post mortem study of equine digital flexor tendons, Equine Vet J 9:61, 1977. 46. Patterson-Kane JC, Firth EC, Parry DAD, et al: Comparison of collagen fibril populations in the superficial digital flexor tendons of exercised and nonexercised thoroughbreds, Equine Vet J 29:121, 1997. 47. Patterson-Kane JC, Wilson AM, Firth EC, et al: Exerciserelated alterations in crimp morphology in the central regions of the superficial digital flexor tendons from young thoroughbreds: a controlled study, Equine Vet J 30:61, 1998. 48. Birch HL, Wilson AM, Goodship AE: Physical training induces alterations in tendon matrix composition which are structure specific, J Bone Joint Surg Br 80(Suppl 2):17, 1998. 49. Smith RKW, Birch H, Patterson-Kane J, et al: Should equine athletes commence training during skeletal development? changes in tendon matrix associated with development, ageing, function, and exercise, Equine Vet J Suppl 30:201, 1999. 50. Birch HL, Bailey AJ, Goodship AE: Macroscopic “degeneration” of equine superficial digital flexor tendon is accompanied by a change in extracellular matrix composition, Equine Vet J 30:534, 1998. 51. Cherdchutham W, Becker C, Smith RK, et al: Age-related changes and the effect of exercise on the molecular composition of immature equine superficial digital flexor tendons, Equine Vet J Suppl 31:86, 1999. 52. Haglund-Akerlund Y, Eriksson E: Range of motion, muscle torque and training habits in runners with and without Achilles tendon problems, Knee Surg Sports Traumatol Arthrosc 1:195, 1993. 53. Neuberger A, Slack HGB: Metabolism of collagen from liver, bone, skin and tendon in normal rat, Biochem J 53:47, 1953. 54. Perez-Castro AV, Vogel KG: In situ expression of collagen and proteoglycan genes during development of fibrocartilage in bovine deep flexor tendon, J Orthop Res 17:139, 1999. 55. Birch HL, Wilson AM, Goodship AE: The effect of exercise-induced localised hyperthemia on tendon cell survival, J Exp Biol 200:1703, 1997. 56. Birch HL, Rutter GA, Goodship AE: Oxidative energy metabolism in equine tendon cells, Res Vet Sci 62:93, 1997. 57. Anstrom M, Westlin N: Blood flow in chronic Achilles tendinopathy, Clin Orthop 308:166, 1994. 58. Józsa L, Bálint BJ, Réffy A, et al: Hypoxic alterations of tenocytes in degenerative tendinopathy, Arch Orthop Trauma Surg 99:243, 1982. 59. Dalton S, Cawston TE, Riley GP: Human shoulder tendon biopsy samples in organ culture produce procollagenase and tissue inhibitor of metalloproteinases, Ann Rheum Dis 54:571, 1995. 60. Rees SG, Flannery CR, Little CB, et al: Catabolism of aggrecan, decorin and biglycan in tendon, Biochem J 350:181, 2000. 61. Platt DP, Wilson AM, Timbs A, et al: An investigation of the biomechanics of equine flexor tendon using an implantable microforce leaf, J Biomech 24:449, 1991. 62. Meershoek L: Calculation of forelimb tendon forces in horses, PhD thesis, 2001, University of Utrecht, Holland.

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63. Denoix J-M: Functional anatomy of tendons and ligaments in the distal limbs (manus and pes), Vet Clin North Am Equine Pract 10:273, 1994. 64. Riemersma DJ, van den Bogert AJ: Influence of shoeing on ground reaction forces and tendon strains in the forelimbs of ponies, Equine Vet J 28:126, 1996. 65. Fackelmann GE: The nature of tendon damage and its repair, Equine Vet J 5:141, 1973. 66. Crevier-Denoix N, Collobert C, Pourcelot P, et al: Mechanical properties of pathological equine superficial digital flexor tendons, Equine Vet J 23:23, 1997.

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67. Birch HL, Smith TJ, Lawes TJ, et al: Mechanical properties of equine flexor tendons show symmetry between right and left forelimbs within individuals but a wide variation in strength and stiffness between individuals. Proceedings of the seventeenth meeting of the Federation of European Connective Tissue Societies, Patras, Greece, July 2000. L13. 68. van Weeren PR, Barneveld A: Study design to evaluate the influence of exercise on the development of the musculoskeletal system of foals up to 11 months, Equine Vet J 31:4, 1999.

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Superficial Digital Flexor Tendonitis he first two sections of this chapter consider the general clinical manifestations of tendonitis and then the specific surgical management of tendonitis in racehorses. The third section discusses some of the variable clinical presentations in other competition horses and factors influencing treatment and prognosis.

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SUPERFICIAL DIGITAL FLEXOR TENDONITIS IN RACEHORSES • Joan S. Jorgensen and Ronald L. Genovese Superficial digital flexor tendon (SDFT) injuries significantly compromise athletic performance and may culminate in a career-ending injury. The incidence of SDFT injuries in Thoroughbred (TB) racehorses ranges from 7% to 43%,1,2 and such horses are most at risk because of high racing speeds or high speeds associated with jumping (steeplechase racing, see Chapter 113).3 Other performance horses, including upperlevel event horses (see Chapter 118), have an increased risk of SDFT injury (see page 639). Horses used for dressage, high-level show jumpers (see Chapter 116), racing Arabians (see Chapter 112) and Quarter Horses (see Chapter 111) , polo ponies (see Chapter 120) , and fox hunters incur SDFT injuries less frequently.3-5 SDFT injury from athletic use in racehorses commonly is seen because of repetitive speed cycles over distance and possibly genetic predisposition to SDFT injury.6 We are aware of several TB racehorse mares and at least one TB stallion and one Standardbred (STB) stallion that are known to have progeny with an increased susceptibility to SDFT injury compared with the normal racehorse population. Additional factors that may predispose a horse to SDFT injury include conformation, working surfaces, shoeing, training methodology, and the relationship between the level of physical fitness and the current exercise. SDFT injury also occurs spontaneously in sedentary or lightly used horses more than 15 years of age. These tendon injuries often are severe and generally involve the proximal metacarpal region and the carpus and extend to the musculotendonous junction in the antebrachium. Many of these injuries result in overt lameness, tendon thickening, and carpal sheath effusion. Sometimes, however, the only pre-

senting sign is lameness, with little palpable thickening. These injuries occasionally can be difficult to diagnose, requiring local analgesia and ultrasonography. SDFT injuries from athletic use occur in the forelimb far more frequently than in the hindlimb. In one American study of 143 TB racehorses, 58% of SDFT injuries occurred in the left forelimb and 42% in the right forelimb.7 Bilateral injury is common and has been recognized more frequently since veterinarians have been examining both limbs routinely by ultrasonography. Most injuries in the SDFT caused by athletic use occur in the mid-metacarpal region (zones 2B to 3B), but injuries also occur at the musculotendonous junction of the antebrachium, in the carpal canal and subcarpal region, and in the pastern (see Chapter 83). The plantar hock region is the most common site of SDFT injury in hindlimbs, especially in the STB racehorse (see Chapters 79 and 109). Occasionally this injury extends into the mid-metatarsal region. Infrequently, a subtle SDFT injury is associated with tenosynovitis of the digital flexor tendon sheath (DFTS) in hunters, jumpers, and dressage horses. Racehorses with SDFT injuries in racehorses traditionally have been regarded as having a guarded to poor prognosis for return to racing, although the prognosis for other athletic disciplines is more optimistic. Before ultrasonography was used routinely, documentation of SDFT injury was limited. Diagnosis was based on gait evaluation and palpation of a swollen or thickened tendon. The injury was referred to as a bowed tendon, and morphological abnormality and severity of injury were little appreciated. Recently, substantial progress has been made in understanding the nature of tendon injury and the mechanisms of healing. During repair, injured elastic tendon fibers are replaced with modified fibrous scar tissue, resulting in a tendon repair that is never totally normal. The quality of repair can vary greatly. Some tendon injuries repair and resolve with enough mature collagen so that they return to nearly normal size, with sufficient remodeling that results in approximately parallel alignment of the repair tissue. Other injuries develop a scar, with an overall increase in tendon size, poor or random fibrous tissue alignment, and peritendonous fibrosis. Many of the proposed therapeutic approaches are directed at maximizing the chances for a more physiologically functioning tendon. Therapy requires a multifaceted approach

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63. Denoix J-M: Functional anatomy of tendons and ligaments in the distal limbs (manus and pes), Vet Clin North Am Equine Pract 10:273, 1994. 64. Riemersma DJ, van den Bogert AJ: Influence of shoeing on ground reaction forces and tendon strains in the forelimbs of ponies, Equine Vet J 28:126, 1996. 65. Fackelmann GE: The nature of tendon damage and its repair, Equine Vet J 5:141, 1973. 66. Crevier-Denoix N, Collobert C, Pourcelot P, et al: Mechanical properties of pathological equine superficial digital flexor tendons, Equine Vet J 23:23, 1997.

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67. Birch HL, Smith TJ, Lawes TJ, et al: Mechanical properties of equine flexor tendons show symmetry between right and left forelimbs within individuals but a wide variation in strength and stiffness between individuals. Proceedings of the seventeenth meeting of the Federation of European Connective Tissue Societies, Patras, Greece, July 2000. L13. 68. van Weeren PR, Barneveld A: Study design to evaluate the influence of exercise on the development of the musculoskeletal system of foals up to 11 months, Equine Vet J 31:4, 1999.

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Superficial Digital Flexor Tendonitis he first two sections of this chapter consider the general clinical manifestations of tendonitis and then the specific surgical management of tendonitis in racehorses. The third section discusses some of the variable clinical presentations in other competition horses and factors influencing treatment and prognosis.

T

SUPERFICIAL DIGITAL FLEXOR TENDONITIS IN RACEHORSES • Joan S. Jorgensen and Ronald L. Genovese Superficial digital flexor tendon (SDFT) injuries significantly compromise athletic performance and may culminate in a career-ending injury. The incidence of SDFT injuries in Thoroughbred (TB) racehorses ranges from 7% to 43%,1,2 and such horses are most at risk because of high racing speeds or high speeds associated with jumping (steeplechase racing, see Chapter 113).3 Other performance horses, including upperlevel event horses (see Chapter 118), have an increased risk of SDFT injury (see page 639). Horses used for dressage, high-level show jumpers (see Chapter 116), racing Arabians (see Chapter 112) and Quarter Horses (see Chapter 111) , polo ponies (see Chapter 120) , and fox hunters incur SDFT injuries less frequently.3-5 SDFT injury from athletic use in racehorses commonly is seen because of repetitive speed cycles over distance and possibly genetic predisposition to SDFT injury.6 We are aware of several TB racehorse mares and at least one TB stallion and one Standardbred (STB) stallion that are known to have progeny with an increased susceptibility to SDFT injury compared with the normal racehorse population. Additional factors that may predispose a horse to SDFT injury include conformation, working surfaces, shoeing, training methodology, and the relationship between the level of physical fitness and the current exercise. SDFT injury also occurs spontaneously in sedentary or lightly used horses more than 15 years of age. These tendon injuries often are severe and generally involve the proximal metacarpal region and the carpus and extend to the musculotendonous junction in the antebrachium. Many of these injuries result in overt lameness, tendon thickening, and carpal sheath effusion. Sometimes, however, the only pre-

senting sign is lameness, with little palpable thickening. These injuries occasionally can be difficult to diagnose, requiring local analgesia and ultrasonography. SDFT injuries from athletic use occur in the forelimb far more frequently than in the hindlimb. In one American study of 143 TB racehorses, 58% of SDFT injuries occurred in the left forelimb and 42% in the right forelimb.7 Bilateral injury is common and has been recognized more frequently since veterinarians have been examining both limbs routinely by ultrasonography. Most injuries in the SDFT caused by athletic use occur in the mid-metacarpal region (zones 2B to 3B), but injuries also occur at the musculotendonous junction of the antebrachium, in the carpal canal and subcarpal region, and in the pastern (see Chapter 83). The plantar hock region is the most common site of SDFT injury in hindlimbs, especially in the STB racehorse (see Chapters 79 and 109). Occasionally this injury extends into the mid-metatarsal region. Infrequently, a subtle SDFT injury is associated with tenosynovitis of the digital flexor tendon sheath (DFTS) in hunters, jumpers, and dressage horses. Racehorses with SDFT injuries in racehorses traditionally have been regarded as having a guarded to poor prognosis for return to racing, although the prognosis for other athletic disciplines is more optimistic. Before ultrasonography was used routinely, documentation of SDFT injury was limited. Diagnosis was based on gait evaluation and palpation of a swollen or thickened tendon. The injury was referred to as a bowed tendon, and morphological abnormality and severity of injury were little appreciated. Recently, substantial progress has been made in understanding the nature of tendon injury and the mechanisms of healing. During repair, injured elastic tendon fibers are replaced with modified fibrous scar tissue, resulting in a tendon repair that is never totally normal. The quality of repair can vary greatly. Some tendon injuries repair and resolve with enough mature collagen so that they return to nearly normal size, with sufficient remodeling that results in approximately parallel alignment of the repair tissue. Other injuries develop a scar, with an overall increase in tendon size, poor or random fibrous tissue alignment, and peritendonous fibrosis. Many of the proposed therapeutic approaches are directed at maximizing the chances for a more physiologically functioning tendon. Therapy requires a multifaceted approach

CHAPTER 70 that reduces the acute inflammatory response and hemorrhage in the acute phase and improves fiber alignment during the long rehabilitation phase. The ultimate goal of any treatment and management programs is to maximize the chances for a tendon to repair with adequate strength and elasticity for a return to a similar level of performance with the lowest risk of re-injury. It is important to recognize the variables that may affect the ultimate prognosis when managing SDFT injuries. Not all tendon injuries are the same, and case management depends on the specific injury, medical factors, and other non-medical factors.

CLINICAL SIGNS Clinical signs of SDFT injury in racehorses vary considerably depending on the location of the primary injury, type of injury, severity, and the timing of the examination. Occasionally, clinical signs may be delayed by days or weeks. Furthermore, a lack of correlation may exist between the severity of the injury and the severity of tendonitis in any given individual, especially in the more common core tendon injuries experienced by TB racehorses. In contrast, STB racehorses more often experience lateral and medial border tendon injuries that result in significant swelling but less severely injured tendon fascicles. Identification of subtle, yet significant, re-injury by clinical evaluation may be difficult because of previous tendon thickening. Thus ultrasonographic imaging is essential to confirm clinical signs and to evaluate the extent of injury to the SDFT.

Lameness In our experience the degree of lameness associated with a tendon lesion in the mid-metacarpal region is correlated with the severity of the injury. Slight to high-slight (category II to IV) injuries generally are not associated with any appreciable lameness, whereas mid-moderate to high-moderate (category V) injuries cause only transient lameness. Most severely injured tendons (category VI), or total rupture of the SDFT, result in at least transient lameness, which may be severe. In contrast, lesions in the carpal canal or proximal metacarpal region (zones 0 and lA) consistently are associated with lameness.

Swelling For assessing tendon injuries, swelling is defined as subcutaneous or peritendonous fluid accumulation. Digital palpation reveals a soft or semi-firm, diffuse or focal fluid accumulation that may prohibit exact palpation of the SDFT. Subcutaneous swelling can be associated with tendon injury, especially in the acute stage of injury. Careful digital palpation of the limb held in a semi-flexed position may reveal slight crepitus in an acutely injured tendon. However, subcutaneous inflammation or hemorrhage is not associated invariably with tendon injury. Examples of focal edema or hemorrhage without significant SDFT injury include swelling associated with cording of the mid-metacarpal region secondary to a malpositioned bandage or subcutaneous swelling in the proximal or distal metacarpal region caused by malpositioned tendon boots or stable (stall) bandages. An example of diffuse swelling is pitting edema (see Chapter 14), occasionally caused by external blistering. Diffuse filling also may reflect a sub-solar abscess or cellulitis.

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the normal contralateral limb may be required to identify SDFT enlargement. In more severely injured tendons examined in the subacute phase, enlargement generally can be felt. Two clinical situations in which assessing SDFT thickening is difficult are a focal SDFT injury in the sub-carpal region, where the tendon is enveloped by the retinaculum, especially in colder climates when limb hair is long, and instances of SDFT injury within the DFTS that also is associated with tenosynovitis. Tenosynovitis makes distinguishing between tendon thickening and sheath fibrosis difficult. When palpating the SDFT, one should always determine if the medial and lateral borders of the SDFT can be separated clearly from the accessory ligament of the deep digital flexor tendon and the tendon itself. If both digital flexor tendons are slightly enlarged, detection of abnormality is more difficult; however, frequently the margins of both tendons are more rounded than normal. Assessing the flexibility of the SDFT also is useful, because abnormal stiffness usually reflects previous injury.

Heat Increase in surface temperature often can be the earliest and most subtle clinical sign of SDFT injury or re-injury. Digital appreciation of an increase in skin temperature, or thermography, often can indicate tendon inflammation. Because extensive use of liniments and daily bandaging in racehorses also increases skin temperature, one must be careful when making this assessment.

Sensitivity to Direct Digital Palpation A painful response to direct digital palpation is often a reliable clinical test for tendon injury. Examination is best performed by holding the limb in a semi-flexed position and palpating with the thumb and forefinger systematically from proximal to distal in the metacarpal region in an effort to elicit a painful response. When a sensitive area is palpated, the horse generally flinches. The examination has many caveats. If a sensitive response is elicited bilaterally, the horse may merely be hyperresponding to increased pressure and possibly has no injury. Not all horses with tendon injury have a painful response. Horses with blistering of the skin, adverse local drug reaction, infection, or cording are also hyper-responsive and more reactive than those with a tendon injury. In addition, extreme sensitivity to direct palpation coupled with focal or diffuse swelling may indicate a problem not related to the tendon.

Tendon Profile Evaluation of the tendon profile with the limb in a full weightbearing position can provide valuable information. In a normal limb the metacarpal region has a straight palmar profile. A normal SDFT should be superficial and parallel to the deep digital flexor tendon. It is important to examine the profile from all possible angles. With a slight injury, the tendon often has a normal profile when viewed from the lateral aspect and a convex or bowed profile from the medial aspect, or vice versa. In an acute total rupture, little swelling and thickening may be present if the leg is examined within 2 hours of the injury. However, with the limb in full weight-bearing position, one may note hyperextension of the metacarpophalangeal joint. In this case, digital palpation along the palmar aspect of the tendon reveals a 1- to 2-cm defect in the SDFT. Digital palpation with the limb in a semi-flexed position also reveals laxity and excessive mobility of the tendon.

Thickening Thickening, or enlargement specifically indicates SDFT swelling secondary to injury or a thickened end-stage repair from a previous injury. In this context, subcutaneous swelling is not appreciable, but a palpable enlargement of the SDFT occurs. In many slightly and diffusely injured tendons thickening may be difficult to appreciate and careful comparison to

Tenosynovitis of the Carpal Sheath or Digital Flexor Tendon Sheath Tenosynovitis may be associated with a tendon injury or may be a clinical entity without tendon injury (see Chapters 75 and 76). Ultrasonographic evaluation is required to appreciate tendon injury in the presence of tenosynovitis.

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Tendon Injury Limited to the Pastern Injury to one or both of the SDFT branches of the pastern generally is associated with branch thickening and a painful response to direct digital pressure (see also Chapter 83). This is best appreciated with the limb held in a semi-flexed position and direct pressure placed on the branch with the clinician’s thumb. Injury to the SDFT branch(s) may be associated with tenosynovitis.

MANAGEMENT OF THE ACUTE PHASE OF TENDON INJURY IN RACEHORSES In most horses with sub-total SDFT injuries in the acute phase, anti-inflammatory and supportive management are instituted. A variety of treatment regimens are available. For the most part, systemic non-steroidal anti-inflammatory drugs (NSAIDs) such as phenylbutazone (4.4 mg/kg per day) for 7 to 10 days and a single dose of systemic corticosteroids such as dexamethasone (0.04 mg/kg) are included in the initial therapy. Perilesionally administered corticosteroids are considered contraindicated in tendon injuries, especially long-term usage, because they are thought to delay collagen formation. However, some clinicians use a single perilesional dose of triamcinolone (6 to 9 mg) or methylprednisolone acetate (40 mg) (dystrophic mineralization occasionally has been associated with methylprednisolone therapy) in horses with slight, peripheral tendon injuries in STB racehorses, especially when associated with a curb (see Chapter 79). Practitioners often administer a course of polysulfated glycosaminoglycans (PSGAGs; 1 vial per week for 4 weeks) in the acute stage. Physical therapy is indicated, and we recommend icing for 1 to 2 hours once or twice a day, with application of a poultice, or simple support bandaging for subtotal injuries. Casting may be indicated for total ruptures. Exercise generally is restricted to stall (box) rest or limited hand walking. In horses with subtotal injuries, we prefer to keep the injured limb shod in a fully grooved bar shoe, with a straight hoof-pastern axis, so that the metacarpophalangeal joint position is normal in a standing position. We do not advocate raising or lowering the heel to an exaggerated position. We perform an ultrasonographic examination within the first few days and then again 3 to 4 weeks later. Sometimes tendon splitting is advised for small core lesions.

INJURY ASSESSMENT AND GOALS FOR ATHLETIC OUTCOME Qualitative assessment combines the physical findings and a subjective ultrasonographic appraisal. This gives an accurate diagnosis, but we also strongly encourage the use of quantitative ultrasonographic evaluation. This includes data such as cross-sectional area (CSA) and echogenicity and fiber alignment scores (see Chapter 16). Optimal healing of SDFT injuries depends on managing a number of variables including the personality of the horse, its age, sex, athletic use, conformation, injury episode number, maximal level of exercise attained, and severity of the injury. For instance, a 4-year-old TB gelding racehorse that has an upright conformation, has never raced, and suffers a severe (category VI) SDFT injury after one gallop has a poor prognosis with any treatment. If this horse sustained a small core lesion of the SDFT, its prognosis would be more guarded because of its conformation and the exercise level at which injury occurred compared with a similar injury in a well-conformed, seasoned racehorse. Athletic outcome of a racehorse may be divided into three categories: successful, meaning completion of five or more

races (I); partially successful, completion of one to four races (II); and failure, meaning re-injury occurred before the first race was completed (III). Successful horses can be further subdivided into those with re-injury or no re-injury. Partially successful can be further subdivided into those suffering re-injury or those injuring the contralateral SDFT or a forelimb suspensory ligament.

ULTRASONOGRAPHIC EVALUATION AND CATEGORIZATION OF INJURIES If clinical evaluation indicates a possible SDFT injury, ultrasonography should be used to confirm the diagnosis and objectively assess the severity of injury. Sequential examinations provide a guide to controlled exercise management and are used to assess progress of repair and attempt to establish an optimal time to return to full work. The acquisition and assessment of accurate ultrasonographic data requires high-quality images, and it is important to develop a rigid, standardized technique (see Chapter 16). The ultrasonographer must take primary responsibility for image interpretation. For a second person to give an opinion on images previously obtained by someone else is often difficult. Quantitative ultrasonographic data includes CSA, percentage of CSA occupied by a lesion, grade of echogenicity of a lesion (type or echo score, TS), and assessment of fiber bundle alignment in longitudinal images (fiber alignment score, FAS). Each of these data points is assessed at every defined level of the limb (zone) and then summed to provide total scores. These scores then can be used to categorize an injury as minimal (category III), slight (category IV), moderate (category V), or severe (category VI) (see Chapter 16). The following comments apply to forelimb and hindlimb injuries, although reference is only made to the metacarpal region.

Initial Evaluation Early examination of a suspected new injury of the SDFT may not reveal any anechoic or hypoechoic lesions. However, if the CSA of a single zone is more than 39% larger than the contralateral limb, or if the total of 6 of 7 zones is more than 14% larger than the contralateral limb, then tendonitis should be suspected (category II). If tendonitis cannot be substantiated by ultrasonography, despite soft tissue swelling, then conservative management is indicated. The horse should be restricted to walking exercise for at least 72 hours and then reevaluated clinically and by ultrasonography. Symptomatic therapy includes systemic NSAIDs, daily icing, and mild leg liniments or sweats with limb bandaging. One must recognize that sometimes a lesion(s) cannot be appreciated by ultrasonography for at least several days or longer. Within 7 days of injury a hypoechoic or anechoic lesion may represent tendon fascicle damage, hemorrhage, or inflammatory exudates and is most likely a combination of all three. Distinguishing the relative contributions of each or determining accurately the severity of injury, which may be underestimated or overestimated, is not possible. Initially, damaged collagen fibers may be grossly intact but non-functional, resulting in reflecting echoes. Ongoing enzymatic degradation and further injury caused by pressure necrosis may result in a lesion deteriorating over 3 to 4 weeks. In contrast, infrequently the hemorrhage and inflammatory exudates resolve over the following 3 to 4 weeks and result in a great improvement of the lesion, and the injury to fiber bundles may not be as serious as initially indicated.

Baseline Evaluation If an initial examination is done within 1 to 7 days of a new injury or a re-injury, we strongly advise that a second ultra-

CHAPTER 70 sonographic evaluation be performed 2 to 4 weeks (preferably 4 weeks) later to obtain baseline data about the severity of injury (see Chapter 16).

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optimum therapy for specific lesions and better equip the veterinarian to provide accurate prognostic information.

Symptomatic Treatment with Continued Exercise

SUBACUTE PHASE TREATMENT AND LONG-TERM REHABILITATION History of Treatment in Racehorses A wide variety of short-term and long-term treatment programs for superficial digital flexor tendonitis have been used, sometimes implemented regardless of the severity of the injury or re-injury, and with or without prolonged rest or controlled exercise. No comprehensive reports comparing various treatments of similarly injured tendons are available, and therefore proposing specific recommendations that will give the best prognosis for return to racing is difficult. A comprehensive retrospective study of TB and STB racehorses currently is being performed to compare the rate of return to racing between a variety of therapeutic regimens for minimal (category III), slight (category IV), moderate (category V), and severe (category VI) tendon injuries documented by ultrasonography. Therapies include pasture turnout, external blistering, internal blistering, intralesional therapies (excluding β-aminoproprionitrile fumarate [Bapten]), or a combination of these. In addition, the amount of layup time is being considered for each category of injury. If all therapeutic regimens are combined (Fig. 70-1), preliminary data indicate that few racehorses successfully return to racing without re-injury (athletic outcome I, completed five or more races), especially with severe injuries.8 In addition, these data demonstrate that few racehorses are able to return to racing and not experience reinjury of the SDFT, sustain injury to the contralateral SDFT, or injure the suspensory apparatus (subcategories IB and IC). Ultimately, we hope that this research helps to determine

Injury Category

Percentage of tendons in each injury category

80 70

IV (n = 213)

60 50

V (n = 97) VI (n = 141)

40 30 20 10 0

IA

II IB+C One race Athletic outcome category

III

Fig. 70-1 A successful return to racing becomes increasingly difficult as the severity of tendon injury increases. Treatments for slight (category IV), moderate (category V), and severe (category VI) superficial digital flexor tendon injuries including pasture turnout, external or internal blistering, intralesional injections (excluding β-aminoproprionitrile fumarate), or a combination of these were assessed for their success in return to racing. Athletic outcome categories (AOCs) were separated into five groups. AOC IA refers to those horses that have successfully raced at least five times with no re-injury. AOC IB + C includes those that have raced at least five times but have re-injured the same tendon (group B) or the contralateral tendon (group C). AOC II includes those that have raced successfully one to four times and includes tendons that have been re-injured, whereas horses with tendon injuries in AOC III have never raced successfully. An additional group of all those that completed at least one race was included. Data are represented as the percentage of tendons in each injury category that resulted in the ultimate AOC.

If the decision is made to treat a horse with an injured tendon symptomatically and continue exercise (racing), serial ultrasonographic examinations should be performed, because changes in size or echogenicity may be detected before clinical signs are obvious. If the ultrasonographic examination demonstrates progressive injury or instability and the horse is not athletically (economically) productive, stopping racing and considering long-term rehabilitation would be wise. Naturally, any racehorse racing with an injured tendon is risking more serious injury. A retrospective study of 209 tendons from 207 TB racehorses was performed to determine if quantitative ultrasonographic assessment could aid in accurately defining a SDFT injury and provide evidence for determining a prognosis for racing in patients that underwent symptomatic treatment with continued exercise. Eighty-eight percent of horses that had no or minimal injury (categories I and III) started more than three races, whereas 12% failed. Thirty-five percent of horses with slight (IV), moderate (V), or severe (VI) injuries started more than three races, but 82% had recurrent injury.7 Ultrasonography is therefore helpful to determine the prognosis for returning to racing. Symptomatic therapy while continuing to race is a viable therapeutic option for minimal tendon injuries. Consider a 3-year-old TB gelding racehorse with a swollen left front SDFT after a race (Fig. 70-2). Quantitative ultrasonographic analysis revealed a total lesion area of 13%, TS of 7, and total FAS of 7, indicating a mildly injured (category IV) tendon. The horse was treated symptomatically with antiinflammatory medication and continued to race. After 41⁄2 months and 6 races the horse was racing well, having earned more than $34,000. After two additional races, the total lesional area increased and the horse’s performance decreased. Long-term therapy with time off was instituted. STB racehorses are generally more successful than TBs in continued performance with a tendon injury.8 A retrospective study of pre-training (exercise level 5) ultrasonographic data from 106 injured racehorses provided four criteria that we use as a guideline for an optimum return to racing9: 1. At least a 60% decrease in category IV total lesional area, or 30 × 109/L, with more than 90% neutrophils), and a total protein concentration of more than 40 g/L. Contrast radiography (Fig. 78-2) or ultrasonography may be useful to confirm communication between a penetrating wound and the tendon sheath, especially if horses are presented soon after injury. The primary aim of treatment of horses with infectious tenosynovitis is the rapid elimination of bacteria and rapid return of the normal synovial environment. This is best achieved by wound debridement, lavage of the tendon sheath with copious amounts of sterile isotonic fluids, and the provision of bactericidal levels of appropriate antibiotics within the sheath. Appropriate systemic and intra-thecal antibiotic therapy should be initiated immediately. The presence of Enterobacteriaceae most commonly is associated with tendon sheath infection caused by a penetrating wound, whereas staphylococci are most commonly identified as the cause of iatrogenic infections of the tendon sheath.25 The most effective combination of antibiotics for the treatment of infectious tenosynovitis is amikacin and cephalosporin (>85% effective).28 However, the cost of these drugs may be prohibitive, and other drug combinations, such as penicillin and gentamicin, may be considered. The initial selection of antibiotic may be altered according to bacterial sensitivity, if a positive culture is obtained from the synovial fluid. Wound debridement and lavage of the affected tendon sheath with copious amounts of sterile isotonic fluids is important to reduce concentrations of bacteria and inflammatory mediators. Early in the infection, effective lavage maybe achieved by through-and-through lavage using 16-gauge needles or arthroscopic egress cannulae. In more established infectious tenosynovitis, leukocytes and fibrin accumulate

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Fig. 78-3 Chronic distention of the tendon sheath of the extensor carpi radialis in a horse with chronic tenosynovitis. Lateromedial radiographic view of a carpus. Dorsal is to the left. Positive-contrast medium has been injected into the extensor carpi radialis tendon sheath and antebrachiocarpal joint in a horse that had sustained a deep puncture wound over the dorsal aspect of the carpus. Radiopaque contrast agent is near the skin surface (solid arrow), outside the tendon sheath (small arrows), confirming penetration of the extensor carpi radialis sheath. The antebrachiocarpal joint (open arrow) was not involved.

Fig. 78-2

within the sheath, necessitating tenoscopic debridement. If satisfactory debridement and lavage have been achieved, primary closure of the sheath may be performed. The horse should be monitored closely for lameness, and repeated synovial fluid samples should be taken at 2- to 3-day intervals to monitor for return of infection. Alternatively the sheath may be left open, or a closed suction drain system may be inserted into the sheath for further elimination of inflammatory mediators and fibrin. The drain should be left in place for 3 to 5 days, but careful management is important to prevent ascending suprainfection. Systemic antibiotic therapy should be continued for at least 2 weeks after the resolution of clinical signs. Once the infection has been eliminated, intrathecal injection of corticosteroids or hyaluronan may be used, with physiotherapy, to reduce adhesion formation and restore the normal gliding movement of the tendon within its sheath. However, both drugs may cause immunosuppression within the sheath and may potentiate dormant infection. Early return to controlled exercise is also important to reduce intrathecal adhesion formation. If chronic infectious tenosynovitis becomes established, exploration of the tendon sheath and radical synovectomy may be required (see the following discussion). Successful outcome has been reported after complete resection of the

intrasynovial part of the common digital extensor tendon in a horse with chronic infectious tenosynovitis and tendonitis.29 The prognosis for return to soundness after infectious extensor tenosynovitis appears to be more favorable than for infectious flexor tenosynovitis,25,27 possibly because extensor tendons are non–weight bearing compared with flexor tendons. The prognosis for return to soundness is generally good after early surgical intervention and appropriate antibiotic therapy for horses with infectious extensor tenosynovitis.

Chronic Tenosynovitis Chronic tenosynovitis of the extensor tendon sheaths is characterized by persistent synovial effusion, fibrous thickening of the sheath, and subcutaneous edema.30,31 Chronic tenosynovitis results in variable, sometimes severe, lameness; restricted carpal flexion; and a gait characterized by circumduction of the affected limb during protraction.31 However, in some horses there is no gait abnormality. Chronic tenosynovitis commonly arises after penetrating injuries to the carpal extensor sheaths, which may result in the inoculation of foreign material or bacteria into the synovial cavity, and establishment of an infectious or non-infectious chronic tenosynovitis. The condition commonly occurs in horses jumping natural fences, because of penetration of the sheath by thorns.31 Chronic tenosynovitis also may occur after acute tenosynovitis and may be associated with partial tendon rupture.21,30 Chronic inflammation of the tendon sheath causes granulomatous proliferation of the synovial membrane, connective tissue deposition in the fibrous capsule, and fibrous adhesion formation between the tendon and its sheath, resulting in restriction of movement and pain on carpal flexion.30,31 Diagnosis of chronic tenosynovitis is based on clinical signs of effusion and thickening of the affected sheath (Fig. 78-3)

CHAPTER 78

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required. Full flexion of the carpus should be achieved by 30 days after surgery. The prognosis for soundness after surgical exploration and radical synovectomy is excellent, but the resultant scar may cause a substantial blemish. In a retrospective study of 15 horses with chronic tenosynovitis treated by surgical exploration and radical synovectomy, all were sound and all but one horse returned to the former use.31

Osteochondromatosis Synovial osteochondromatosis of the extensor carpi radialis tendon sheath has been reported. Synovial osteochondromatosis is characterized by the formation of multiple small osseous bodies within a synovial-lined structure. The cause is unclear, but it may be associated with trauma. Clinical signs include swelling on the dorsal surface of the carpus characterized by multiple, firm subcutaneous nodules and crepitus during joint movement, and lameness is usually evident. Diagnosis is confirmed by radiography and ultrasonography.32 Although no information is available for the surgical treatment of osteochondromatosis of the extensor tendon sheaths in horses, partial synovectomy and arthroscopic removal of the osteochondral bodies has been used successfully in other synovial cavities in horses and other species.33

Intersynovial Fistulae

Fig. 78-4 A craniolateral-caudomedial oblique radiographic view of the distal radius in a horse with chronic tenosynovitis of the extensor carpi radialis tendon sheath. There is palisading new bone formation (arrows) on the craniomediodistal ridge of the radius adjacent to the tendon sheath.

and restricted carpal flexion. Radiography of the carpus often reveals palisading new bone formation on the craniodistal ridges of the radius adjacent to the affected sheaths (Fig. 78-4) and entheseous new bone formation on the dorsal aspect of the carpal bones.31 Synovial fluid aspirates vary from serosanguineous to turbid, with an increased nucleated cell count and total protein concentration. Ultrasonography may demonstrate tendon damage, synovial membrane hypertrophy, foreign bodies, and intrathecal adhesions. Conservative treatment with antibiotics, analgesics, intrathecal corticosteroids, and symptomatic physiotherapeutic procedures such as bandaging, cold hosing, massage, and forced exercise is usually unrewarding.18,21,30,31 The results of surgical treatment have been good, however. Surgical treatment involves exposing the entire length of the tendon within its sheath, radical synovectomy of the hyperplastic synovial membrane, removal of intrathecal adhesions, debridement of damaged tendon, and primary closure of the fibrous layer of the tendon sheath and skin. Postoperatively the carpus should be kept bandaged and the horse confined to its box for 10 days. After suture removal on the fourteenth post-operative day, an intensive program of physiotherapy involving manual flexion and extension of the carpus and an ascending program of in-hand walking exercise should be initiated. Early passive motion to stimulate cavitation and reformation of the synovial lining and prevent adhesion formation is considered an essential part of the treatment.31 Initially, carpal flexion is resented and administration of non-steroidal anti-inflammatory drugs and sedatives may be

Intersynovial fistulae are uncommon, but they have been documented between the common digital extensor tendon sheath and antebrachiocarpal joint,34 the common digital extensor tendon sheath and middle carpal joint,14 and the extensor carpi radialis tendon sheath and middle carpal joint.5 The cause of these fistulae is unclear, but they are considered to be traumatic in origin and may occur with carpitis or carpal fractures.5,34 Typically, horses with intersynovial fistulae have chronic lameness and distention of the affected tendon sheath. Synovial fluid can be massaged from the joint to the tendon sheath. Diagnosis may be confirmed by contrast radiography6 and intrasynovial analgesia. Surgical treatment is advocated in the management of intersynovial fistulae,14 but little information concerning the prognosis of affected horses is available, because reports of this condition are rare. Surgical treatment involves exposure of the fistula, removal of redundant synovial membrane, and closure of the fibrous layers of the joint and tendon sheath.

Infectious Bursitis Infectious bursitis may occur in any of the bursae associated with the extensor tendons over the dorsal aspect of the fetlock. The condition is seen most commonly in horses that jump natural obstacles (e.g., eventers and National Hunt horses). Typically these horses have swelling of the dorsal aspect of the fetlock (Fig. 78-5) and mild to severe lameness. Infectious bursitis may affect the subtendonous bursae or more commonly affects an acquired subcutaneous (supratendonous) bursa on the dorsal aspect of the long digital extensor tendon in the fetlock region.35 Occasionally both bursae may communicate around the lateral or medial aspect of the long digital extensor tendon. Some horses have a severe, non–weight-bearing lameness, and this condition frequently is confused with infectious arthritis of the metacarpophalangeal or metatarsophalangeal joints. Diagnosis is confirmed by ultrasonographic examination or contrast radiography6 and synoviocentesis. Synoviocentesis from the palmar or plantar pouch of the adjacent metacarpophalangeal or metatarsophalangeal joint should be used to rule out joint infection. Treatment consists of surgical drainage and debridement and appropriate antibiotic therapy. The prognosis for return to soundness is good.

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Prominent soft tissue swelling over the dorsal aspect of the fetlock region in the hindlimb of a horse with severe lameness. This is a supratendonous infectious bursitis and should not be confused with infectious arthritis of the metatarsophalangeal joint. Arthrocentesis of the metatarsophalangeal joint through a dorsal approach may result in iatrogenic infectious arthritis.

Fig. 78-5

REFERENCES 1. Getty R: Equine myology. In Sisson and Grossman’s the anatomy of the domestic animals, ed 5, Philadelphia, 1975, WB Saunders. 2. Rooney JR: Biomechanics of lameness in horses, New York, 1977, Kreiger Publishing. 3. Hago BED, Vaughan LC: Radiographic anatomy of tendon sheaths and bursae in the horse, Equine Vet J 18:102, 1995. 4. Denoix J-M: The equine fetlock. In The equine distal limb: an atlas of clinical anatomy and comparative imaging, London, 2000, Manson Publishing. 5. Llewellyn HR: A case of carpal intersynovial fistula in a horse, Equine Vet J 11:90, 1975. 6. Hago BED, Vaughan LC: Use of contrast radiography in the investigation of tenosynovitis and bursitis in horses, Equine Vet J 18:375, 1986. 7. Tnibar M, Kaser-Hotz B, Auer J: Ultrasonography of the dorsal and lateral equine carpus: technique and normal appearance, Vet Radiol Ultrasound 34:413, 1993. 8. Baxter GM: Retrospective study of lower limb wounds involving tendons, tendon sheaths or joints in horses, Proc Am Assoc Equine Pract 33:715, 1987. 9. Foland JW, Trotter GW, Stashak TS, et al: Traumatic injuries involving tendons of the distal limbs in horses: a retrospective study of 55 cases, Equine Vet J 23:422, 1995.

10. Belknap JK, Baxter GM, Nickels FA: Extensor tendon lacerations in horses (1982-1988), J Am Vet Med Assoc 203:428, 1993. 11. Bertone AL: Tendon lacerations, Vet Clin North Am Equine Pract 11:293, 1995. 12. Crabill MR, Honnas CM, Taylor DS, et al: Stringhalt secondary to trauma to the dorsoproximal region of the metatarsus in horses: 10 cases (1986-1991), J Am Vet Med Assoc 205:867, 1994. 13. Yovich JV, Stashak TS, McIlwraith CW: Rupture of the common digital extensor tendons in foals, Comp Cont Educ Pract Vet 6:S373, 1984. 14. Stashak TS: Lameness. In Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 15. Myers VS, Gordon GW: Ruptured common digital extensor tendon associated with contracted flexor tendons on foals, Proc Am Assoc Equine Pract 21:67, 1975. 16. Dyson SJ: Personal communication, 2001. 17. Kirker-Head C: Rupture of the common digital extensor tendon. In Colahan PT, Mayhew IG, Merritt AM, et al, editors: Equine medicine and surgery, vol 2, St Louis, 1999, Mosby. 18. Mason TA: Chronic tenosynovitis of the extensor tendons and tendon sheaths of the carpal region in the horse, Equine Vet J 9:186, 1997. 19. Kirker-Head C: Rupture of the extensor carpi radialis muscle. In Colahan PT, Mayhew IG, Merritt AM, et al, editors: Equine medicine and surgery, vol 2, St Louis, 1999, Mosby. 20. Catlin JE: Rupture of the tendon of the extensor carpi radialis muscle in the horse, Vet Med Small Animal Clin 59:1178, 1964. 21. Wallace CE: Chronic tendosynovitis of the extensor carpi radialis tendon in the horse, Aust Vet J 48:585, 1972. 22. Ross MW, Martin BB: Dorsomedial articular fracture of the proximal aspect of the third metacarpal bone in standardbred racehorses: seven cases (1978-1990), J Am Vet Med Assoc 201:332, 1992. 23. Van Pelt RW: Idiopathic tenosynovitis in foals, J Am Vet Med Assoc 155:510, 1969. 24. Dyson SJ, Dik KJ: Miscellaneous conditions of tendons, tendon sheaths and ligaments, Vet Clin North Am Equine Pract 11:315, 1995. 25. Schneider RK, Bramlage LR, Moore RM, et al: A retrospective study of 192 horses affected with septic arthritis/tenosynovitis, Equine Vet J 24:436, 1992. 26. Hawkins JE, Lescun TB: Sepsis of the common digital extensor tendon sheath secondary to hemicircumferential periosteal transection in a foal, J Am Vet Med Assoc 211:331, 1997. 27. Honnas CM, Schumacher J, Cohen ND, et al: Septic tenosynovitis in horses: 25 cases (1983-1989), J Am Vet Med Assoc 199:616, 1991. 28. Moore RM, Schneider RK, Kowalski JJ, et al: Antimicrobial sensitivity of microorganisms isolated from 233 horses with musculoskeletal infection during 19791989, Equine Vet J 24:450, 1992. 29. Booth TM, Clegg PD, Singer ER, et al: Resection of the common digital extensor tendon in a gelding, Vet Rec 146:373, 2000. 30. McIlwraith CW: Diseases of joints, tendons, ligaments and related structures. In Stashak TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 31. Platt D, Wright IM: Chronic tenosynovitis of the carpal extensor sheaths in 15 horses, Equine Vet J 29:11, 1997. 32. Newell S, Roberts RE, Baskett A: Presumptive tenosynovial osteochondromatosis in a horse, Vet Radiol Ultrasound 37:112, 1996.

CHAPTER 79 33. Smith RK, Coumbe A, Schramme MC: Bilateral synovial chondromatosis of the metatarsophalangeal joints in a pony, Equine Vet J 27:234, 1995. 34. Johnson JE, Ryan GD: Intersynovial fistula in the carpus of a horse, Cornell Vet 65:84, 1975.

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35. Voute LC, Schramme MC, Boswell JC, et al: Subcutaneous abscessation on the dorsal aspect of the metatarsophalangeal joint in six horses, Proc 39th Br Equine Vet Assoc Annual Congress 207, Birmingham, 2000.

79

Curb Mike W. Ross and Ronald L. Genovese

he historical definition of curb is enlargement on the plantar aspect of the fibular tarsal bone (calcaneus), caused by inflammation and thickening of the (long) plantar ligament.1 However, by ultrasonographic evaluation, we have redefined curb as a complex of soft tissue injuries that occurs on the distal plantar aspect of the tarsus. Long plantar desmitis is only one of many injuries that causes curb. However, the term curb is useful to describe swelling of the distal, plantar aspect of the tarsus (excluding the calcaneal bursa and proximal aspect of the calcaneus). In the rest of this chapter, curb is used specifically to mean soft tissue swelling of the plantar aspect of the tarsus. Conformational abnormalities or bony exostoses can mimic or contribute eventually to formation of curb.

T

sometatarsal joints or fractures of the central tarsal bone, or more commonly the third tarsal bone. Horses can have curby conformation without developing curb, and horses with normal hindlimb conformation can develop curb. The proximal aspect of the fourth metatarsal bone (MtIV) is often prominent in horses with sickle-hock conformation. The most dramatic example of altered joint morphology occurs in young foals with tarsal crush syndrome, the result of delayed or incomplete ossification of the tarsal cuboidal bones (see Chapter 45).

CLINICAL APPEARANCE OF CURB The convex profile typical of curb is best seen from the side (Fig. 79-1). Careful evaluation of swelling from all perspectives, palpation, and thorough lameness examination are critical. Curb must be differentiated from other swellings of the hock, including capped hock, effusion, edema and fibrosis of the calcaneal bursa (see Chapter 80), tarsal tenosynovitis (see Chapter 77), thoroughpin (with or without involvement of the tarsal sheath), and bony enlargements of the distal hock region (see Chapter 45). Injuries of the deep digital flexor tendon (DDFT) as it courses along the plantaromedial aspect of the hock within the tarsal sheath can produce typical signs of curb, but they account for only a small percentage injuries in horses with curb. Horses with sickle-hock conformation are said to be curby (see Chapter 4). Sickle-hock and in-at-the-hock conformation lead directly to curb, a finding most common in the Standardbred (STB) and Thoroughbred (TB) racehorse. Prognosis for STB racehorses with sickle-hock conformation and curb is worse in the trotter than in the pacer. Trotters with sickle-hock conformation are usually fast early in training and racing, but this conformation is often career limiting. Sicklehock conformation is also undesirable in the TB racehorse. Horses with sickle-hock conformation often develop curb first, but they then independently or concomitantly develop other lameness associated with the distal hock joints. Tarsal region lameness begins with curb in 2- and 3-year-olds and progresses to osteoarthritis of the centrodistal and tar-

A Standardbred racehorse with typically appearing curb. Swelling associated with the distal, plantar tarsus is centered over the centrodistal and tarsometatarsal joints. In this horse swelling was caused by superficial digital flexor tendonitis.

Fig. 79-1

CHAPTER 79 33. Smith RK, Coumbe A, Schramme MC: Bilateral synovial chondromatosis of the metatarsophalangeal joints in a pony, Equine Vet J 27:234, 1995. 34. Johnson JE, Ryan GD: Intersynovial fistula in the carpus of a horse, Cornell Vet 65:84, 1975.

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35. Voute LC, Schramme MC, Boswell JC, et al: Subcutaneous abscessation on the dorsal aspect of the metatarsophalangeal joint in six horses, Proc 39th Br Equine Vet Assoc Annual Congress 207, Birmingham, 2000.

79

Curb Mike W. Ross and Ronald L. Genovese

he historical definition of curb is enlargement on the plantar aspect of the fibular tarsal bone (calcaneus), caused by inflammation and thickening of the (long) plantar ligament.1 However, by ultrasonographic evaluation, we have redefined curb as a complex of soft tissue injuries that occurs on the distal plantar aspect of the tarsus. Long plantar desmitis is only one of many injuries that causes curb. However, the term curb is useful to describe swelling of the distal, plantar aspect of the tarsus (excluding the calcaneal bursa and proximal aspect of the calcaneus). In the rest of this chapter, curb is used specifically to mean soft tissue swelling of the plantar aspect of the tarsus. Conformational abnormalities or bony exostoses can mimic or contribute eventually to formation of curb.

T

sometatarsal joints or fractures of the central tarsal bone, or more commonly the third tarsal bone. Horses can have curby conformation without developing curb, and horses with normal hindlimb conformation can develop curb. The proximal aspect of the fourth metatarsal bone (MtIV) is often prominent in horses with sickle-hock conformation. The most dramatic example of altered joint morphology occurs in young foals with tarsal crush syndrome, the result of delayed or incomplete ossification of the tarsal cuboidal bones (see Chapter 45).

CLINICAL APPEARANCE OF CURB The convex profile typical of curb is best seen from the side (Fig. 79-1). Careful evaluation of swelling from all perspectives, palpation, and thorough lameness examination are critical. Curb must be differentiated from other swellings of the hock, including capped hock, effusion, edema and fibrosis of the calcaneal bursa (see Chapter 80), tarsal tenosynovitis (see Chapter 77), thoroughpin (with or without involvement of the tarsal sheath), and bony enlargements of the distal hock region (see Chapter 45). Injuries of the deep digital flexor tendon (DDFT) as it courses along the plantaromedial aspect of the hock within the tarsal sheath can produce typical signs of curb, but they account for only a small percentage injuries in horses with curb. Horses with sickle-hock conformation are said to be curby (see Chapter 4). Sickle-hock and in-at-the-hock conformation lead directly to curb, a finding most common in the Standardbred (STB) and Thoroughbred (TB) racehorse. Prognosis for STB racehorses with sickle-hock conformation and curb is worse in the trotter than in the pacer. Trotters with sickle-hock conformation are usually fast early in training and racing, but this conformation is often career limiting. Sicklehock conformation is also undesirable in the TB racehorse. Horses with sickle-hock conformation often develop curb first, but they then independently or concomitantly develop other lameness associated with the distal hock joints. Tarsal region lameness begins with curb in 2- and 3-year-olds and progresses to osteoarthritis of the centrodistal and tar-

A Standardbred racehorse with typically appearing curb. Swelling associated with the distal, plantar tarsus is centered over the centrodistal and tarsometatarsal joints. In this horse swelling was caused by superficial digital flexor tendonitis.

Fig. 79-1

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Firm, fibrous soft tissue swelling can develop just proximal to MtIV as a sequela to injection or local analgesia of the tarsometatarsal joint, presumably from local trauma, hemorrhage, or leakage into the subcutaneous tissues. Mild bony proliferation or fragmentation of proximal MtIV, or of the fourth tarsal bone, can cause focal swelling easily mistaken for curb. Considerable variation in clinical signs occurs, and the injury cannot be categorized, or a management program and prognosis established, without thorough clinical and ultrasonographic examinations. Historically, owners and trainers consider curb to be an annoying, self-limiting problem that rarely causes lameness or poor performance, that responds to a single treatment that is uniformly effective, and that is cured once curb is treated. Most racehorse trainers are opposed to resting a horse with curb unless lameness is performance limiting, so veterinarians often are faced with management decisions without an option for even short-term rest or a reduction in training intensity. Many traditional therapies have no data to support efficacy. Lameness ranges from none, mild, or severe depending on the structure involved and extent of injury. Lameness tends to be worse if the soft tissue structure involved is located dorsal to the superficial digital flexor tendon (SDFT) in the plantar tarsus (DDFT, long plantar ligament), if SDFT injury is diffuse, or if a mixed injury involves more than one structure. Diagnosis is straightforward in horses with obvious lameness seen at a trot in hand and painful swelling, but lameness may be evident only as a slight loss of performance or unlevelness when performing at maximum and may be perceived only by trainers, drivers, or riders. A horse with chronic curb may not exhibit signs of pain during palpation, or lameness at a trot in hand, but can show lameness at speed, and convincing a trainer that the long-term swelling is a source of pain may be difficult. The area should be palpated carefully with the limb bearing weight and flexed. Swelling may be firm and fibrous, with few signs of active inflammation, or may be warm, painful, and edematous. Acute, compliant or mushy swelling is associated with hemorrhage or other subcutaneous fluid accumulation and sometimes deeper soft tissue injury. Horses with this form of curb usually have acute, moderate to severe lameness. Horses with distal hock joint pain often exhibit a painful response when direct pressure is placed on plantar hock structures, including the SDFT, proximal aspect of MtIV, second metatarsal bone, and proximal aspect of the suspensory ligament. Often swelling is not detected in these horses. Response to upper limb flexion varies and is non-specific. Direct digital palpation followed by trotting is useful, because horses with active curbs show increased lameness. Because horses with curb can have concomitant osteoarthritis or other problems of the lower hock joints, differentiation of the source of pain is important but difficult. Diagnostic analgesia is useful but not foolproof. If horses are lame at a trot in hand, local infiltration of local anesthetic solution subcutaneously over the curb is effective. A minimum of 20 to 30 ml of local anesthetic solution should be infiltrated along the lateral, plantar, and medial aspects of the curb. Small-gauge needles should be avoided (to avoid needle breakage), and the injection should be performed with the limb in flexion, because horses may object to several injections. If horses are not visibly lame at a trot in hand, examination at the track or under saddle should be performed. Selective intra-articular analgesia of the lower hock joint and sequential perineural analgesia to rule out the lower limb are essential. A tibial nerve block alleviates pain with curb, but it is seldom done because other common sources of pain are abolished similarly.

Radiography and scintigraphy help differentiate other sources of pain, but ultrasonography is the imaging method of choice to determine which structures are involved and the extent of damage.

APPLIED ANATOMY AND NORMAL ULTRASONOGRAPHIC EXAMINATION OF THE PLANTAR TARSUS Plantar to the calcaneus are skin, subcutaneous tissues, a thin fibrous tissue layer, the SDFT, and the long plantar ligament. Medially the DDFT courses distally over the sustentaculum tali, within the tarsal sheath. Normally the tarsal sheath has a small amount of fluid that can be seen during ultrasonographic examination, but it is not felt. The long plantar ligament originates from the calcaneus, closely adheres to this bone, and inserts distally on the plantar surface of the fourth tarsal bone and MtIV. The plantar tarsus can be divided into zones to classify findings (Fig. 79-2) or the distance measured from the proximal aspect of the calcaneus (point of hock). Transverse and longitudinal images of both limbs should be obtained from the plantar midline, plantaromedial (to evaluate the DDFT), and slightly plantarolateral (to evaluate the distal aspect of the long plantar ligament). Measurement of cross-sectional area (CSA) is important to confirm lesions in which enlargement has occurred but with no overt fiber damage. Precise placement of the ultrasound transducer is important since the long plantar ligament changes size and shape as it courses distally. Knowledge of normal ultrasonographic anatomy is crucial (Figs. 79-3 to 79-6).

Zone 1A

Zone 1B1 Zone 1B2

The plantar aspect of the tarsus is divided into zones lA and lB. Because zone lB is rather large and important, the zone is sometimes subdivided into 1B1 and 1B2. An alternative technique for recording level of injury is to measure distally from the proximal aspect of the calcaneus.

Fig. 79-2

CHAPTER 79

Fig. 79-3 Transverse (left) and longitudinal (right) midline ultrasonographic images at 5 cm distal to the point of the hock. A thin subcutaneous fibrous tissue layer runs along the plantar surface of the superficial digital flexor tendon. The superficial digital flexor tendon (SDFT, crescent shape) is narrower in a medial to lateral direction and somewhat thickened from that seen proximally. In the longitudinal scan the normal SDFT has a dense parallel fiber pattern. Deep to the SDFT the long plantar ligament (PL) is at full thickness (plantar to dorsal direction), is rectangular in shape, and is attached firmly to the calcaneus (CAL). At this level the deep digital flexor tendon is out of view medially and must be evaluated by placing the transducer plantaromedially.

Fig. 79-5

Transverse (left) and longitudinal (right) ultrasonographic images from the plantaromedial aspect of the left hock 5 cm distal to the point of the hock. In the transverse image the tarsal sheath surrounds the deep digital flexor tendon (DDFT). The tendon is oval and has a large eccentric hypoechoic region composed of residual muscle tissue, but this defect could be caused by incident angle artifact.

Fig. 79-6

Fig. 79-4

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701

Transverse (left) (medial is to the right) and longitudinal (proximal is to the left) (right) plantarolateral ultrasonographic images 9 cm distal to the point of the hock at the level of the fourth tarsal bone (T4). The long plantar ligament (PL) is a multi-septated ligamentous structure, and large plantar fiber bundles are not normally perfectly aligned with dorsal bundles. In transverse images the long plantar ligament normally may appear to lack echogenicity, and the size and shape changes at the insertion on the fourth tarsal bone. The long plantar ligament is wide at the insertion on the fourth tarsal bone (longitudinal scan).

Transverse (left) (medial is to the right) and longitudinal (right) (proximal is to the left) plantarolateral ultrasonographic images 14 cm distal to the point of the hock, just distal to the insertion of the long plantar ligament (PL) on the fourth tarsal bone (T4). The long plantar ligament is thick in the plantar to dorsal direction. A midline image would show the superficial digital flexor tendon (SDFT) and deep digital flexor tendon (DDFT), but at this level a plantarolateral transducer placement is needed to assess the long plantar ligament. In the longitudinal image the long plantar ligament is seen attaching to the fourth tarsal bone proximally and fourth metatarsal bone (MtIV) distally.

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CURB: A COLLECTION OF SOFT TISSUE INJURIES Seventy-three horses with a curb were examined using ultrasonography, comprising 58 (80%) racehorses (48 STB and 10 TB) and 15 non-racehorse sport horses (hunters, jumpers, Tennessee walking horses, reining horses, Three-Day Event horses, barrel racing, and general-use horses).2 Twenty-two horses (30%) had thickening, inflammation, swelling, or fluid accumulation in peritendonous and periligamentous tissues, without obvious injury of the SDFT, DDFT, and long plantar ligament. Eighteen horses (25%) had a combination of fluid accumulation of peri-tendonous and periligamentous tissues with superficial digital flexor tendonitis, and 25 (34%) had a combination of fluid accumulation of peritendonous and periligamentous tissue and long plantar ligament desmitis. Six horses (8%) had fluid accumulation of peritendonous and periligamentous tissues and DDFT injury, and two horses (3%) had peritendonous and periligamentous tissue infection. This incidence of injury is considered typical. Curb is primarily an injury of racehorses, especially STBs. Gait, speed, and training methods differ between racing breeds, and STB racehorses have a higher prevalence of conformational abnormalities, such as sickle hock and in at the hock. Weight and load distribution are considerably different. Curb develops frequently in STB racehorses that train and race on a thin, near-hard surface, contrary to many soft tissue injuries that result from work on deep surfaces. Many curbs develop in young STB racehorses early in training. In some instances track surfaces are inconsistent and perhaps slippery, since early training is done in the winter months. Nonracehorse sport horses develop curb, but only sporadically, and lameness is often moderate to severe and most commonly is associated with peritendonous and periligamentous tissue swelling, although other structures are sometimes involved.

Fig. 79-7 Transverse midline ultrasonographic image (medial is to the left) of the plantar aspect of the hock of 2-year-old Standardbred gelding obtained in zone lB. There is subcutaneous edema (arrows) and thickening. The superficial digital flexor tendon (SDFT), deep digital flexor tendon (DDFT), and long plantar ligament (PL) were normal. This horse was managed using a peritendonous injection of corticosteroids.

Peritendonous and Periligamentous Inflammation Peritendonous and periligamentous tissue swelling occurs alone or with abnormalities of one or more of the SDFT, DDFT, or long plantar ligament. Peritendonous and periligamentous tissue injury can occur secondary to direct trauma from horses kicking a wall or trailer door, or rarely from a direct kick or interference injury from another horse, resulting in acute, large, painful swelling. Ultrasonographic examination most often reveals frank hemorrhage and edema. More commonly the horse has neither history of trauma nor clinical findings suggesting trauma. We suspect that peritendonous and periligamentous tissue injury reflects excess loading or strain of the plantar tarsal soft tissue structures from race training. Extensive jogging of young STBs early in training may cause dramatic increase in hock loading, and tension and overstretching of thin peritendonous and periligamentous tissue occurs. Peritendonous and periligamentous tissue injury may be an accumulated overload injury and may develop secondarily to other lameness. The peritendonous and periligamentous tissue is most plantar in location, is thin, may be most vulnerable to injury from abnormal strain, and may be the first tissue in progression to be injured. Conformational abnormalities may predispose the horse to such injuries. The cause of such soft tissue injury in mature non-racehorses is unknown, and although swelling can develop with relatively mild lameness, more often lameness is moderate to severe. Clinical examination reveals localized soft tissue swelling, often with heat and pain on palpation, with or without lameness. Previous application of liniments or blisters, or pin firing may create sore skin and considerable soft tissue swelling. Ultrasonographic findings depend on the duration of the injury. Acute lesions have an accumulation of anechoic fluid subcutaneously; in more chronic injuries, swelling is from sub-

Fig. 79-8 Transverse midline ultrasonographic images of the left hindlimb (left) and right hindlimb taken in zone lB in 2-yearold Standardbred colt pacer with bilateral curb showing subcutaneous fibrosis (arrows) (LH, RH) and mild fluid accumulation (RH) typical of that seen in curb from peritendonous and periligamentous tissue injury. cutaneous echogenic material (Figs. 79-7 to 79-9). The SDFT, DDFT, and long plantar ligament should be inspected carefully, but they are frequently normal. Management depends on the degree of lameness, the stage of training, the race or competition schedule and the owner’s or trainer’s wishes. Blistering is used widely, but we question its value. Although not supported by scientific evidence, thermocautery (pin firing) appears to be an effective management tool, perhaps because it enforces rest. However, prolonged rest is rarely necessary in racehorses, and many horses can be managed by local injection of corticosteroids (triamcinolone acetonide, 9 mg) without significant interruption of training. More than one treatment may be required if the swelling and

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• Curb

703

Fig. 79-9

Transverse (left) (medial is to the right) and longitudinal midline ultrasonographic images of the hock in zone lB in a 5-year-old Thoroughbred racehorse. There is soft tissue swelling of heterogeneous echogenicity of the peritendonous and periligamentous tissues and fibrous adhesion (double-headed arrow) plantaromedial to the superficial digital flexor tendon (SDFT). The SDFT, deep digital flexor tendon (DDFT), and long plantar ligament (PL) are normal.

Fig. 79-10 Transverse (left) and longitudinal midline ultrasonographic images of the plantar aspect of the hock of 2-year-old Standardbred racehorse with curb resulting from peri-tendonous and peri-ligamentous tissue injury and superficial digital flexor tendonitis. Subcutaneous fibrous tissue accumulation (top arrow) plantar to the superficial digital flexor tendon (SDFT) and a central anechoic lesion of the SDFT can be seen, findings verified in the longitudinal view. Cross-sectional area of the affected superficial digital flexor tendon was 33% greater than the normal tendon.

lameness do not resolve. A lame horse must be rested to prevent injury to deeper structures. In non-racehorses with moderate to severe lameness, lameness may take several weeks to resolve. If the swelling becomes firm, fibrous, and pain free but lameness recurs, further investigation is warranted, because other causes of tarsal pain often develop in STB and TB racehorses with curb. Infection can occur from direct trauma with skin penetration, previous injection, or severe topical counterirritation. If infection is suspected, cytological examination and culture are indicated. If a hematoma resulting from trauma is large or recurrent, or the curb is infected, establishing drainage is often necessary. A distal incision is made to provide drainage and fibrin and debris are removed. Care must be taken to avoid penetration of the tarsal sheath when creating the incision. A drain is inserted if necessary and the hock is bandaged. Culture usually reveals Staphylococcus species and appropriate antimicrobial and non-steroidal anti-inflammatory drug (NSAID) therapy is instituted. Horses are rested for 2 to 3 weeks to allow the tissues to heal, even though lameness from peritendonous and periligamentous tissue injury was not present before infection developed. Prognosis in horses with infection of peritendonous and periligamentous tissues is excellent but is far worse in those with infection of the SDFT, DDFT, or tarsal sheath.

stage of a progressive legion that eventually involves the SDFT or long plantar ligament. Progressive injury occurs frequently if horses with peritendonous and periligamentous tissues injury are treated with cryotherapy, internal blisters, or corticosteroids, and training intensity is accelerated before mature fibrous tissue can form. In horses with peritendonous and periligamentous tissue injury and superficial digital flexor tendonitis lameness varies, but it is much more likely to be observed than in horses with only peritendonous and periligamentous tissue injury. Lameness may be acute in onset and often is seen at fast speeds, but it can be seen in some horses at a trot in hand. Superficial digital flexor tendonitis occurs commonly in young STB racehorses but usually at a later stage of training than peritendonous and periligamentous tissue injury. Ultrasonographic examination reveals enlargement of the CSA of the SDFT, with a variable change in echogenicity and fiber pattern, depending on the severity of the injury (Fig. 79-10). Often subcutaneous edema or fibrosis occur, depending on the chronicity of the injury. In horses with superficial digital flexor tendonitis, rest is an important part of management. Lesions usually are localized to the plantar tarsus, and those extending farther distally are associated with more severe lameness and horses have a poorer prognosis. Horses with localized lesions have a fair prognosis, although the prognosis is worse in trotters than in pacers. Horses with mild acute superficial digital flexor tendonitis, with enlargement of the tendon without fiber tearing, should be rested for 3 to 4 weeks. Without rest, progressive fiber damage may occur, resulting in prolonged recovery. Horses with more severe injuries may require up to 4 months of stall rest and controlled walking exercise. In some STB racehorses, superficial digital flexor tendonitis in horses actively racing can be managed symptomatically, without giving rest, if the lesion is well localized and mild. Mild lameness may be observed at speed or while the horse is trotting in hand, but severe lameness should not be evident. Ultrasonographic examination often reveals peritendonous and periligamentous tissue injury with enlargement of the SDFT, but core lesions are not present. In most horses local

Superficial Digital Flexor Tendonitis A common finding in horses with curb is superficial digital flexor tendonitis. Sickle-hock conformation may predispose the horse to tendonitis, which can occur alone, but rarely is seen without concomitant inflammation of the peritendonous and periligamentous tissues. Pathogenesis likely involves progressive or accumulated overload injury of first the thin, fragile peritendonous and periligamentous tissues and later the SDFT. Previous peritendonous and periligamentous tissue injury appears to predispose to subsequent superficial digital flexor tendonitis if the training level is increased quickly. Peritendonous and periligamentous injury may simply be an early

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therapy using cold water hosing and poultice application, NSAID therapy, and subcutaneous injection of a corticosteroid preparation is successful. Subcutaneous injection of methylprednisolone acetate (200 mg) and Sarapin (25 ml) medial, plantar, and lateral to the SDFT is often done by practitioners with apparent success. Horses are given 10 to 14 days of jogging and light training before racing again. Non-racehorses with localized lesions usually respond well to rest for up to 3 months and have a favorable prognosis. Horses with severe superficial digital flexor tendonitis have severe mushy swelling. If not given rest, these horses develop progressive tearing of the SDFT distal to the hock in the metatarsal region and lose support of the hock. Long-term rest (9 to 12 months) is recommended, but prognosis for return to previous race class is poor and in trotters, grave.

Deep Digital Flexor Tendonitis Deep digital flexor tendonitis is a rare cause of curb. Horses with curb resulting from deep digital flexor tendonitis are usually acutely lame and have substantial swelling. Mixed injury with deep digital flexor tendonitis accompanying superficial digital flexor tendonitis and long plantar ligament desmitis occurs, but it is unusual. Horses with deep digital flexor tendonitis have concomitant peritendonous and periligamentous tissue inflammation and effusion of the tarsal sheath (tenosynovitis). The DDFT simply can be enlarged compared with the contralateral limb or have anechoic or hypoechoic core lesions. During ultrasonographic examination, the DDFT should be evaluated carefully from the midline and plantaromedial aspects. Lameness often is pronounced, and rest is recommended for a minimum of 4 to 6 months, but prognosis is guarded because lameness can recur. Serial ultrasonographic examination, corrective shoeing, and controlled exercise are given.

Long Plantar Desmitis Long plantar ligament injury usually causes acute lameness, but chronic soft tissue swelling and progressive lameness can occur. Soft tissue swelling often is pronounced. Although long plantar desmitis can occur in racehorses, this form of curb appears to be equally common in other types of horses, such as Western performance horses. Long plantar desmitis can be well localized or diffuse. Cross-sectional measurements of the long plantar ligament are critical, because desmitis typically is often manifested as ligament enlargement rather than overt fiber tearing. Subtle thickening of the long plantar ligament may cause high-speed lameness, and evaluation of the crosssectional area may be the only method to identify early lesions in these horses. Lesions can occur at any level within zones 1A and 1B, and injury may involve the insertion of the long plantar ligament on MtIV (Fig. 79-11). Conservative management is best for horses with long plantar desmitis, because lameness and swelling often are pronounced. Owners and trainers of non-racehorses are often open to a conservative approach involving ample rest (3 months) to rehabilitate horses with curb properly. Intervening with therapy to enforce rest is not necessary. Controlled return to exercise is straightforward in this type of horse, because walking and trotting under saddle can be given easily. Graded exercise programs are not administered as easily or desired in the STB racehorse compared with non-racehorse sport horses. Lunging and walking and trotting under saddle are usually not practical,

Transverse plantarolateral ultrasonographic images of the left hindlimb (LH) (abnormal) and right hindlimb (RH) (normal) plantar tarsi in zone lB of 3-year-old Standardbred pacer. The left long plantar ligament (PL) is enlarged, with an indistinct central hypoechoic lesion. SDFT, Superficial digital flexor tendon; DDFT, deep digital flexor tendon.

Fig. 79-11

although riding trotters is popular among trainers originally from Europe. Walking and light jogging in the jog cart is the best way to give graded exercise in the STB racehorse. We do not recommend turnout exercise in any horse with soft tissue injury, because we feel strongly this prolongs recovery and may lead to re-injury, but we realize our recommendations may not be followed. Cryotherapy, topical counterirritants, subcutaneous injections, and thermocautery are less likely to influence inflammation and healing of the long plantar ligament than more superficial causes of curb, but these treatments are sometimes requested. Curb can result from long plantar desmitis at its insertion on MtIV. These horses do not have extensive swelling but focal thickening just proximal to MtIV. Mild soft tissue swelling must be differentiated from a prominent but normal MtIV seen in yearlings with sickle-hock conformation. Horses with curb resulting from distally located long plantar desmitis show lameness and mild, focal swelling and are managed with rest.

Mixed Soft Tissue Injuries Ultrasonographic examination of curb nearly always identifies peritendonous and periligamentous tissue inflammation and in many horses an abnormality of the SDFT, DDFT, or the long plantar ligament. Occasionally, however, simultaneous injury of the SDFT and long plantar ligament occurs in addition to peritendonous and periligamentous tissue inflammation. This is most common in non-racehorse sport horses, in which lameness and swelling are severe.

REFERENCES 1. Stashak TS: Curb. In Stashak TS, editor: Adam’s lameness in horses, Philadelphia, 1987, Lea & Febiger. 2. Genovese R: Unpublished data, 2001.

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• Bursae and Other Soft Tissue Swellings

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Bursae and Other Soft Tissue Swellings Sue J. Dyson

bursa is a flattened, closed sac interposed between structures subject to friction or at points of unusual pressure, such as bony prominences and tendons. Bursae are lined with a cellular membrane resembling synovium and are classified according to position (subcutaneous, subligamentous, submuscular, and subtendonous) and according to the method of formation (congenital or acquired). Acquired bursae develop because of pressure and friction over bony prominences. Tearing of the subcutaneous tissues results in accumulation of transudative fluid, which becomes encapsulated by a fibrous tissue. In chronic injuries fibrous bands may develop within the capsule.

A

SUPRASPINOUS BURSA The supraspinous bursa overlies the summits of the dorsal spinous process of the second to fifth thoracic vertebrae, under the funicular part of the nuchal ligament. Inflammation of the supraspinous bursa and surrounding soft tissues, so-called fistulous withers, is usually infectious in origin and may be a sequel to trauma. Streptococcus and Staphylococcus species, Brucella abortus, and Onchocerca cervicalis have been considered important causative agents.1-3 Clinical signs of supraspinous bursitis are generalized soft tissue swelling, heat and pain, and often draining tract(s). Osteitis or osteomyelitis of the dorsal spinous processes of the cranial thoracic vertebrae may be concurrent. Care must be taken not to misinterpret the normal granular radiopaque appearance of normal, incompletely ossified summits of the dorsal spinous processes.4 Diagnostic ultrasonography and radiography are useful for determining the extent of the infection, for identifying a foreign body, and for evaluating signs of osteitis or osteomyelitis. Treatment is by aggressive surgical debridement of all infected tissue and establishment of adequate drainage, taking care not to penetrate the dorsoscapular ligament. Several surgical procedures may be required to resolve the infection successfully.1-3

INTERTUBERCULAR (BICIPITAL) BURSA

TROCHANTERIC BURSA The Editors have no clinical experience of trochanteric bursitis. This condition is discussed further in Chapter 48.

CALCANEAL BURSA The calcaneal bursa lies between the tendons of the gastrocnemius and the superficial digital flexor muscles, proximal to the hock, and extends distally on the plantar aspect of the calcaneus to the distal aspect of the hock (Fig. 80-1). In some horses a communication exists between the calcaneal bursa and the gastrocnemius bursa. Injuries of the calcaneal bursa are not common and are usually the result of trauma. However, mild distention of the calcaneal bursa often is seen with gastrocnemius tendonitis (see page 709). Mild distention also may be seen unilaterally or bilaterally, as an incidental finding unassociated with lameness.5 Primary inflammation of the bursa results in acute onset lameness associated with distention of the bursa. Hemorrhage into the bursa also may occur. Conservative management by rest, with or without injection of short-acting corticosteroids, usually results in resolution of lameness, although enlargement of the bursa may persist. More commonly infection of the bursa is caused by a penetrating injury or is secondary to infectious osteitis of the calcaneus6 (see Chapter 45).

Gastrocnemius bursa Calcanean bursa

Plantaroproximal pouch of tarsocrural joint capsule

Dorsal pouch of tarsocrural joint capsule

The intertubercular (bicipital) bursa is discussed in Chapter 41.

HYGROMA Hygroma is discussed in Chapters 39 and 68.

NAVICULAR BURSA The navicular bursa is discussed in Chapters 24 and 30.

Fig. 80-1 Diagram of sagittal section of the hock region showing the relative positions of the calcaneal and gastrocnemius bursae.

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Chronic distention of the calcaneal bursa also has been seen with well-circumscribed osteolytic lesions on the tuber calcanei, which were thought to represent enthesopathy at the insertion of gastrocnemius.7 Further investigation should include diagnostic ultrasonography, radiography of the calcaneus, and synoviocentesis. Radiographic examination should include a flexed skyline view of the calcaneus.8 The internal structure of the bursa may be evaluated endoscopically,9 but some underlying bony lesions may not be visible if the insertion of gastrocnemius is intact.7 Endoscopy has been used diagnostically and therapeutically in horses with infectious osteitis, or bursitis, and in those with osteolytic lesions. Horses with primary infection of the calcaneal bursa should be treated by debridement and lavage of the bursa and broad-spectrum antimicrobial therapy. Horses with infectious and non-infectious lesions of the calcaneus have been managed conservatively and surgically, with rather disappointing results.6,7 A substantial number of treated horses have persistent lameness.

GASTROCNEMIUS BURSA The gastrocnemius bursa lies between the superficial digital flexor tendon and the tuber calcanei. Mild distention may be present, unassociated with lameness. Primary injuries of the gastrocnemius bursa are rare. The bursa may be distended in association with gastrocnemius tendonitis, resulting in a capped hock appearance (see page 709). Occasionally, infection may occur because of a puncture wound or extension of infection from the calcaneal bursa.

CUNEAN BURSA The cunean bursa lies underneath the cunean tendon on the medial aspect of the hock. Inadvertently penetrating the bursa is easy if one is inexperienced in injecting the centrodistal joint. Although the potential for primary bursitis exists, neither of the Editors of this text recognizes primary bursitis as a cause of lameness in racehorses or other sports horses. Gabel recognized a syndrome, “cunean tendonitis and bursitisdistal tarsitis syndrome of harness racehorses,” but appreciated that horses showed substantially better improvement in gait after local analgesia of the distal hock joints than after infiltration of the cunean bursa alone.10 Nonetheless, a component of peri-articular soft tissue pain may occur in Standardbred trotters and pacers with distal hock joint pain, and treatment of the cunean bursa with cortiscosteroids frequently is used as part of management. Cunean tenectomy is practiced by some, but it has largely fallen from favor. Subcutaneous injection of corticosteroids and Sarapin over the proximal aspect of the second metatarsal bone may yield better results than medication of the cunean bursa.11

CAPPED ELBOW A capped elbow is an acquired bursa that develops over the olecranon of the ulna. The bursa results from repeated trauma from the heel of the shoe on the ipsilateral forelimb when the horse is lying down. The condition generally is not associated with lameness and is merely a cosmetic blemish. The use of a sausage boot around the pastern prevents trauma from the shoe, and usually the swelling diminishes significantly and rapidly in size. Chronic injuries have been treated by injection of corticosteroids, orgotein, or dysprosium-165, with disappointing results, or surgically, with better cosmetic results.12

CAPPED HOCK A capped hock appearance may be caused by distention of the gastrocnemius bursa or by development of an acquired bursa over the tuber calcanei. An acquired bursa develops because of repetitive trauma, such as the horse kicking the stable walls or leaning backward on its hindlimbs when traveling. Capped hock usually has no associated lameness. Protection of the hocks with hock boots may help to prevent deterioration.

ACQUIRED BURSA ON THE DORSAL ASPECT OF A HIND FETLOCK Firm swelling on the dorsal aspect of the hind fetlocks of horses that jump fixed fences is common. These lesions are false bursae that overlie the extensor tendon and are usually of no consequence, except cosmetically. However, a puncture wound may result in infection, resulting in enlargement of the bursa and surrounding soft tissue swelling, localized heat, and pain on palpation.5 In contrast to infection in a joint or tendon sheath, lameness is usually only mild to moderate. Ultrasonography is useful to identify better the causes of the soft tissue swelling, and diagnosis is confirmed by synoviocentesis and identification of many nucleated cells. Surgical treatment is required and the prognosis is good.

FALSE THOROUGHPIN A thoroughpin is the colloquial name for distention of the tarsal sheath, but more commonly the term is misused to describe a variety of swellings that may develop in the distal crus cranial to the gastrocnemius tendon. These conditions are otherwise called false thoroughpins and should be differentiated from distention of the tarsal sheath, tarsocrural joint capsule (see Chapter 45), or calcaneal bursa (see page 705). A false thoroughpin occurs laterally more commonly than medially and may develop unilaterally or bilaterally. A false thoroughpin varies in size from small to large. In contrast to distention of the tarsal sheath or the plantar outpouching of the tarsocrural joint capsule, these swellings cannot be balloted from laterally to medially and do not extend distal to the hock (Fig. 80-2). They may be sudden or insidious in onset and may or may not be associated with lameness. The causes vary and are poorly understood. False thoroughpins are usually solitary, fluid-filled sacs (Fig. 80-3), unilocular or multilocular, with a wall of variable thickness, with or without large echogenic fibrous bands traversing them (Fig. 80-4). They may develop secondary to local hemorrhage or because of herniation of the tarsal sheath or the calcaneal or gastrocnemius bursae.13-15 Diagnostic ultrasonography is useful to identify the nature and extent of the swelling (Fig. 80-4). Unlike the tarsal sheath, no tendon is within the cavity. Positive-contrast radiography can be used to demonstrate whether any communication exists between adjacent structures (Fig. 80-3). A false thoroughpin may be an incidental clinical finding unassociated with lameness. They are seen commonly in horses with a base-narrow hindlimb conformation.5 Other causes should be excluded before one concludes that a false thoroughpin is the cause of lameness. Even if the swelling is acute in onset, in the absence of lameness I have maintained horses in work with no deleterious effects. Sometimes such swellings spontaneously reduce in size, but some swelling is likely to persist. Long-term lameness associated with a false thoroughpin has been seen in a number of horses with chronic hindlimb

CHAPTER 80

A false thoroughpin (arrow). The swelling in this horse was acute in onset, but it was unassociated with lameness. The horse was maintained in full work, and despite this the swelling reduced in size. Ultrasonographic evaluation revealed a unilocular fluid-filled cavity.

Fig. 80-2

Fig. 80-4 Longitudinal ultrasonographic image of false thoroughpin. Proximal is left. There is a thick-walled fluid-filled cavity with some echogenic bands.

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Dorsolateral-plantaromedial oblique radiographic view of a hock. A positive-contrast radiographic study of false thoroughpin. This fluid-filled cavity did not communicate with the tarsal sheath.

Fig. 80-3

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lameness that has not responded to conservative management. Surgical excision of large multiloculated cyst-like lesions has resolved lameness successfully in some horses,5 although cosmetic results may be disappointing.

REFERENCES 1. Cohen N, Carter G, McMullan W: Fistulous withers in horses: 24 cases (1984-1990), J Am Vet Med Assoc 201:121, 1992. 2. Gaughan E, Fubini S, Dietze A: Fistulous withers in horses: 14 cases (1984-1990), J Am Vet Med Assoc 193:964, 1988. 3. Hawkins J, Fessler F: Treatment of supraspinous bursitis by use of debridement in standing horses: 10 cases (19681999), J Am Vet Med Assoc 217:74, 2000. 4. Butler J, Colles C, Dyson S, et al: The spine. In Clinical radiology of the horse, ed 2, Oxford, 2000, Blackwell Science. 5. Dyson S: Unpublished data, 1980-2002. 6. MacDonald M, Honnas C, Meagher D: Osteomyelitis of the calcaneus in horses: 28 cases (1972-1987), J Am Vet Med Assoc 194:1317, 1989.

CHAPTER •

7. Bassage L, Garcia-Lopez J, Currid E: Osteolytic lesions of the tuber calcanei in two horses, J Am Vet Med Assoc 217:710, 2000. 8. Butler J, Colles C, Dyson S, et al: The tarsus. In Clinical radiology of the horse, ed 2, Oxford, 2000, Blackwell Science. 9. Ingle-Fehr J, Baxter G: Endoscopy of the calcaneal bursa in horses, Vet Surg 27:561, 1998. 10. Gabel A: Lameness caused by inflammation in the distal hock, Vet Clin North Am Large Anim Pract 2:101, 1980. 11. Ross M: Personal communication, 2001. 12. Honnas C, Schumacher J, McClure S, et al: Treatment of olecranon bursitis in horses: 10 cases (1986-1993), J Am Vet Med Assoc 206:1022, 1995. 13. Dik K, Leitch M: Soft tissue injuries of the tarsus, Vet Clin North Am Equine Pract 11:235, 1995. 14. Dik K, Merkens H: Unilateral distension of the tarsal sheath in the horse: a report of 11 cases, Equine Vet J 19:307, 1987. 15. Whitton C, Kannegeiter N: Tarsal sheath rupture in a horse, Aust Equine Vet 13:50, 1995.

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Other Soft Tissue Injuries Sue J. Dyson

RUPTURE OF FIBULARIS (PERONEUS) TERTIUS Anatomy Fibularis (peroneus) tertius is an entirely tendonous muscle that lies in the craniolateral muscle group of the crus, between the subcutaneous long digital extensor and the cranialis tibialis, which cover the craniolateral aspect of the tibia. The muscle originates from the extensor fossa of the femur. Distally the fibularis tertius divides into branches that enfold the tendon of insertion of tibialis cranialis and insert on the dorsoproximal aspect of the third metatarsal bone, the calcaneus, and the third and fourth tarsal bones. The tendon is an important part of the reciprocal apparatus of the hindlimb, which coordinates flexion of the stifle and hock. Fibularis tertius is the most echogenic structure on the craniolateral aspect of the crus and is identified readily by ultrasonography as a well-demarcated hyperechoic structure relative to the surrounding muscles (Fig. 81-1).

History and Clinical Signs Rupture of fibularis tertius invariably is caused by trauma resulting in hyperextension of the limb; for example, a horse trying to jump out of a stable and getting one hindlimb caught on the top of the stable door. This usually results in rupture of the tendon in the middle of the crus but occasionally farther distally. Alternatively, rupture may be caused by a laceration on the dorsal aspect of the tarsus, resulting in transection of the tendon. Occasionally, partial tearing of the tendon occurs, usually at the level of the tarsocurual joint, with prominent swelling. Occasionally the reciprocal apparatus is partially but

not totally disrupted. Avulsion injuries of the origin of the tendon rarely occur in young foals. The clinical signs are pathognomonic, because rupture of this tendon allows the hock to extend while the stifle is flexed. When standing at rest, the horse may appear clinically normal, although with acute injury careful palpation may reveal some muscle swelling on the craniolateral aspect of the crus or further distally. When the horse walks, it should be viewed carefully from behind and from the side. The hock may extend more than usual. The tendons of gastrocnemius and the superficial digital flexor tendon may appear unusually flaccid, and a dimple is seen on the caudal aspect of the crus about one hand’s breadth proximal to the tuber calcanei. At the trot the horse appears severely lame, with apparent delayed protraction of the limb because of over-extension of the hock. If the limb is picked up and pulled backward, the hock can be extended gradually and “clunks” into complete extension while the stifle remains flexed. A characteristic dimple appears in the contour of the caudal distal aspect of the crus (Fig. 81-2). If rupture is only partial, or if lameness is chronic and some repair has taken place, clinical signs may be less severe and the diagnosis less obvious. Presumably, strain of this tendon can occur, resulting in lameness, but I have no experience of this, and to my knowledge this condition has not been documented.

Diagnosis The diagnosis of rupture of fibularis tertius is based on the pathognomonic clinical signs. The site of rupture can be iden-

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lameness that has not responded to conservative management. Surgical excision of large multiloculated cyst-like lesions has resolved lameness successfully in some horses,5 although cosmetic results may be disappointing.

REFERENCES 1. Cohen N, Carter G, McMullan W: Fistulous withers in horses: 24 cases (1984-1990), J Am Vet Med Assoc 201:121, 1992. 2. Gaughan E, Fubini S, Dietze A: Fistulous withers in horses: 14 cases (1984-1990), J Am Vet Med Assoc 193:964, 1988. 3. Hawkins J, Fessler F: Treatment of supraspinous bursitis by use of debridement in standing horses: 10 cases (19681999), J Am Vet Med Assoc 217:74, 2000. 4. Butler J, Colles C, Dyson S, et al: The spine. In Clinical radiology of the horse, ed 2, Oxford, 2000, Blackwell Science. 5. Dyson S: Unpublished data, 1980-2002. 6. MacDonald M, Honnas C, Meagher D: Osteomyelitis of the calcaneus in horses: 28 cases (1972-1987), J Am Vet Med Assoc 194:1317, 1989.

CHAPTER •

7. Bassage L, Garcia-Lopez J, Currid E: Osteolytic lesions of the tuber calcanei in two horses, J Am Vet Med Assoc 217:710, 2000. 8. Butler J, Colles C, Dyson S, et al: The tarsus. In Clinical radiology of the horse, ed 2, Oxford, 2000, Blackwell Science. 9. Ingle-Fehr J, Baxter G: Endoscopy of the calcaneal bursa in horses, Vet Surg 27:561, 1998. 10. Gabel A: Lameness caused by inflammation in the distal hock, Vet Clin North Am Large Anim Pract 2:101, 1980. 11. Ross M: Personal communication, 2001. 12. Honnas C, Schumacher J, McClure S, et al: Treatment of olecranon bursitis in horses: 10 cases (1986-1993), J Am Vet Med Assoc 206:1022, 1995. 13. Dik K, Leitch M: Soft tissue injuries of the tarsus, Vet Clin North Am Equine Pract 11:235, 1995. 14. Dik K, Merkens H: Unilateral distension of the tarsal sheath in the horse: a report of 11 cases, Equine Vet J 19:307, 1987. 15. Whitton C, Kannegeiter N: Tarsal sheath rupture in a horse, Aust Equine Vet 13:50, 1995.

81

Other Soft Tissue Injuries Sue J. Dyson

RUPTURE OF FIBULARIS (PERONEUS) TERTIUS Anatomy Fibularis (peroneus) tertius is an entirely tendonous muscle that lies in the craniolateral muscle group of the crus, between the subcutaneous long digital extensor and the cranialis tibialis, which cover the craniolateral aspect of the tibia. The muscle originates from the extensor fossa of the femur. Distally the fibularis tertius divides into branches that enfold the tendon of insertion of tibialis cranialis and insert on the dorsoproximal aspect of the third metatarsal bone, the calcaneus, and the third and fourth tarsal bones. The tendon is an important part of the reciprocal apparatus of the hindlimb, which coordinates flexion of the stifle and hock. Fibularis tertius is the most echogenic structure on the craniolateral aspect of the crus and is identified readily by ultrasonography as a well-demarcated hyperechoic structure relative to the surrounding muscles (Fig. 81-1).

History and Clinical Signs Rupture of fibularis tertius invariably is caused by trauma resulting in hyperextension of the limb; for example, a horse trying to jump out of a stable and getting one hindlimb caught on the top of the stable door. This usually results in rupture of the tendon in the middle of the crus but occasionally farther distally. Alternatively, rupture may be caused by a laceration on the dorsal aspect of the tarsus, resulting in transection of the tendon. Occasionally, partial tearing of the tendon occurs, usually at the level of the tarsocurual joint, with prominent swelling. Occasionally the reciprocal apparatus is partially but

not totally disrupted. Avulsion injuries of the origin of the tendon rarely occur in young foals. The clinical signs are pathognomonic, because rupture of this tendon allows the hock to extend while the stifle is flexed. When standing at rest, the horse may appear clinically normal, although with acute injury careful palpation may reveal some muscle swelling on the craniolateral aspect of the crus or further distally. When the horse walks, it should be viewed carefully from behind and from the side. The hock may extend more than usual. The tendons of gastrocnemius and the superficial digital flexor tendon may appear unusually flaccid, and a dimple is seen on the caudal aspect of the crus about one hand’s breadth proximal to the tuber calcanei. At the trot the horse appears severely lame, with apparent delayed protraction of the limb because of over-extension of the hock. If the limb is picked up and pulled backward, the hock can be extended gradually and “clunks” into complete extension while the stifle remains flexed. A characteristic dimple appears in the contour of the caudal distal aspect of the crus (Fig. 81-2). If rupture is only partial, or if lameness is chronic and some repair has taken place, clinical signs may be less severe and the diagnosis less obvious. Presumably, strain of this tendon can occur, resulting in lameness, but I have no experience of this, and to my knowledge this condition has not been documented.

Diagnosis The diagnosis of rupture of fibularis tertius is based on the pathognomonic clinical signs. The site of rupture can be iden-

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Fig. 81-1 Transverse ultrasonographic images of the craniolateral aspect of the mid-crus of 7-year-old horse with left hindlimb lameness of 2 months’ duration. Fibularis tertius is the most echogenic structure in the center of the image of the right (R) hindlimb (solid arrow). Compare this with the image of the left (L) hindlimb in which fibularis tertius is markedly hypoechoic (open arrow). Note also that the overlying muscle is increased in echogenicity compared with the right hindlimb. recognition of the clinical signs and failure to confine the horse may result in a chronic lesion, which fails to heal satisfactorily. However, compensatory hypertrophy and or fibrosis of surrounding muscles may permit functional recovery.1

COMMON CALCANEAL TENDONITIS

A horse with rupture of the fibularis tertius. The hock can be extended while the stifle is flexed. Note also the characteristic dimple in the contour of the caudodistal aspect of the crus. Clinical signs developed after the horse had attempted to jump out of its stable and had got hung up on the door. The horse made a complete recovery.

Fig. 81-2

tified with ultrasonography (Fig. 81-1). The normally echogenic structure is not clearly identifiable and may be replaced by a region hypoechoic relative to the surrounding muscles. In chronic injuries the surrounding muscles may become hypertrophied. Usually no associated radiological abnormalities are apparent in adult horses, although avulsion fracture of the origin has been described in foals.

Treatment Confinement to box rest for 3 months, followed by a slow resumption of work usually results in total resolution of clinical signs. Most horses are able to return to full athletic function without recurrence of clinical signs. However, delayed

The common calcaneal tendon comprises components from the superficial digital flexor and gastrocnemius tendons and from biceps femoris, soleus, semimembranosus, and semitendinosus muscles. Contributions from the latter two muscles are called the axial and medial tarsal tendons. Socalled common calcaneal tendonitis has been described as resulting from a kick in the hock region.2 Unfortunately the horse was not examined with ultrasonography until 5 months after injury, at which time soft tissue swelling was marked. Ultrasonographic examination revealed that the superficial digital flexor and gastrocnemius tendons appeared normal, but the axial and medial tarsal tendons were enlarged. The horse made a complete functional recovery.

GASTROCNEMIUS TENDONITIS Tendonitis of gastrocnemius is a relatively unusual cause of hindlimb lameness in the horse.3-5

Anatomy The gastrocnemius muscle arises from two heads that terminate in the mid-crus in a common tendon. Proximally the tendon lies caudal to the superficial digital flexor tendon (SDFT); farther distally the tendon lies laterally and is ultimately cranial, inserting on the tuber calcanei. The SDFT and gastrocnemius tendons are separated by a bursa, the calcaneal bursa, that extends to the mid-tarsal region. A small bursa, the gastrocnemius bursa, also lies cranial to the insertion of the gastrocnemius tendon on the tuber calcanei. A communication may exist between these bursae.

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The tendon of gastrocnemius may still contain some muscular tissue as far distally as the level at which it lies lateral to the SDFT. This results in hypoechoic regions within the tendon. Gastrocnemius tendonitis usually occurs distally, distal to the musculotendonous junction. Rarely, damage occurs at the musculotendonous junction.6 Occasionally, injuries occur at the origin of the gastrocnemius on the femur.7

History and Clinical Signs Lameness may be acute or gradual in onset and varies from mild to severe. Distention of the calcaneal bursa frequently is associated with gastrocnemius tendonitis, and the horse often develops a capped-hock appearance also because of distention of the gastrocnemius bursa (Fig. 81-3). However, these swellings can occur without lameness or detectable pathological conditions of the gastrocnemius or SDFT (see page 706). Mild enlargement of the gastrocnemius tendon may occur, but this can be difficult to appreciate. Eliciting pain by palpation usually is not possible. Severe lameness is characterized by a reduced height of arc of foot flight, shortened cranial phase of the stride, and a tendency to hop off the caudal phase of the stride. Horses with less severe lameness have no specific gait characteristics. Lameness often is accentuated by proximal or distal limb flexion. Two of four horses with injury to the origin of the gastrocnemius muscle had an unusual gait characterized by internal rotation of the affected limb (outward movement of the calcaneus).7

Diagnosis Lameness is improved substantially by perineural analgesia of the tibial nerve, possibly because of local diffusion of the local anesthetic solution, unless the injury is at the origin. Diagnosis is confirmed by ultrasonographic examination. Comparison with the contralateral limb is useful. The tendon usually is damaged in the distal aspect of the crus, where it lies cranial to the SDFT. Ultrasonographic abnormalities include enlargement of the tendon, poor definition of the margins, and focal or diffuse hypoechoic or anechoic regions (Fig. 81-4). Usually no detectable radiographic abnormalities are apparent. Radiographic (proliferative changes) and scintigraphic (increased radiopharmaceutical uptake) abnormalities may exist in horses with chronic injury at the origin of the gastrocnemius muscle on the caudal femur.7

Treatment and Prognosis Conservative treatment with box rest and controlled exercise for up to 12 months generally has resulted in progressive improvement in lameness and improvement in the ultrasonographic appearance of the tendon. Horses with mild lesions have been able to return to full athletic function without recurrent lameness, but more severe lesions have a more guarded prognosis.4,5 Three of four horses with injury of the origin returned to athletic use, but recurrent injury occurred in the fourth horse.7

SUBLUXATION AND LUXATION OF THE SUPERFICIAL DIGITAL FLEXOR TENDON FROM THE TUBER CALCANEI Lateral (see Fig. 6-29), or less commonly medial, luxation or subluxation of the SDFT from the point of hock may occur along with damage to or rupture of the tendonous bands that insert medially and laterally on the tuber calcanei. Although usually a unilateral injury, the condition can occur bilaterally. Lateral displacement of the SDFT occasionally occurs secondarily to hyperextension of the hind fetlock associated with

Medial view of the left hock of 7-year-old Thoroughbred with acute-onset lameness associated with gastrocnemius tendonitis. Note the capped-hock appearance (black arrowhead) and the distention of the calcaneal bursa (white arrowhead).

Fig. 81-3

Fig. 81-4 Transverse ultrasonographic image of the caudal aspect of the distal crus of 6-year-old mare with left hindlimb lameness that was alleviated by perineural analgesia of the tibial nerve. Medial is to the left. The gastrocnemius tendon is enlarged, its plantar lateral aspect is poorly defined (arrowheads), and there is a large hypoechoic region consistent with gastrocnemius tendonitis.

CHAPTER 81 progressive breakdown of the suspensory apparatus (see Fig. 73-24 and page 671).

Anatomy The SDFT lies caudally in the distal crus and broadens to form a cap over the tuber calcanei. At this level, broad tendonous bands extend medially and laterally to insert on the tuber calcanei. The calcaneal bursa is interposed between the SDFT and the tendon of gastrocnemius.

History and Clinical Signs Partial or complete disruption of one of the retinacular bands that attach the SDFT to the tuber calcanei can result in subluxation, or more commonly, luxation of the SDFT laterally or medially. Lameness is usually sudden in onset and severe, although occasionally mild lameness precedes this, associated with soft tissue swelling in the region of the point of hock. Frequently no history of trauma is apparent, and the injury often occurs as the horse is being worked. The horse may suddenly stop and may become extremely distressed, especially if the tendon repeatedly moves on and off the tuber calcanei. The horse may kick out repeatedly with the limb. The tendon may return to its normal position when the horse bears weight. Soft tissue swelling rapidly ensues, making accurate palpation difficult. If the horse is kicking repeatedly when moving, one may conclude wrongly that the soft tissue swelling developed as the result of trauma caused by kicking. With subluxation of the SDFT, the tendon is usually positioned normally at rest. Careful observation of the tendon as the horse moves may reveal instability. With luxation it may be possible to see that the SDFT has been displaced laterally or, less commonly, medially. If the tendon remains luxated, then the horse tends to be less agitated, although obviously in pain in the acute stage. Careful palpation may reveal instability of the tendon or its displacement to an abnormal position. In horses in which lateral displacement occurs secondary to hyperextension of the fetlock, the condition may be insidious in onset and slowly progressive and unassociated with acute lameness.8

Diagnosis Ultrasonographic examination is helpful if the tendon is displaced by confirming its abnormal position, but such examination can add to confusion if the tendon is in the normal position when the horse stands still.

Treatment In the acute stage pain relief is essential and tranquilization may be necessary to calm the horse. If the SDFT is unstable and is moving constantly on and off the tuber calcanei, management in the acute and chronic phases may be difficult. If the tendon is permanently dislocated laterally or medially, the distress usually resolves rapidly. Anti-inflammatory drugs are best avoided, because the surrounding soft tissue swelling helps stabilize the tendon. If the tendon has luxated laterally,

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prolonged rest (6 months) usually results in resolution of pain, although a mechanical lameness may persist. This limits the horse’s function for dressage, but these horses may be able to race or show jump at a high level. The prognosis associated with medial luxation is more guarded and tends to be associated with a greater degree of mechanical lameness. If the SDFT is unstable initially, the tendon may with time and progressive further disruption of the attaching retinacular bands become more stable in a luxated position. Peritendonous injection of a sclerosing agent, P2G (Martindale Pharmaceuticals, Romford, Essex, England), has been helpful in stabilizing the luxated tendon in a limited number of horses.8 Surgical transection of a partially torn band has helped in chronic subluxation.9 Attempts at surgical stabilization of the SDFT in its normal position often have been disappointing, although successful results have been reported.10,11 Surgical stabilization is only worth considering if the horse is temperamentally suited to a full-limb cast. Prognosis is influenced by the ease of reconstruction of the torn retinaculum, which depends on the site of the tear (close to the tendon, close to the bone, or mid-way) and its age. Only four of nine horses were sound.12

BICEPS BRACHII TENDONITIS Biceps brachii tendonitis is discussed in Chapter 41.

REFERENCES 1. Dik K: Ultrasonography of the equine crus, Vet Radiol Ultrasound 34:28, 1995. 2. Proudman C: Common calcaneal tendonitis in a horse, Equine Vet Educ 4:277, 1992. 3. Dyson S, Kidd L: Five cases of gastrocnemius tendonitis in the horse, Equine Vet J 23:25, 1991. 4. Dyson S: Gastrocnemius tendonitis in the horse. Proceedings of the fifteenth Bain-Fallon Memorial Lectures, Canberra, Australia, 1993. 5. Dyson S, Dik K: Miscellaneous conditions of tendons, tendons sheaths and ligaments, Vet Clin North Am Equine Pract 11:315, 1995. 6. Ross M: Personal communication, 2001. 7. Swor TM, Schneider RK, Ross MW, et al: Injury to the origin of the gastrocnemius muscle as a possible cause of lameness in four horses, J Am Vet Med Assoc 219:215, 2001. 8. Dyson S: Unpublished data, 1980-2002. 9. Ordidge R: Personal communication, 1998. 10. Scott E, Breuhas B, Gertsen K: Surgical repair of dislocated superficial digital flexor tendon in a horse, J Am Vet Med Assoc 181:171, 1982. 11. Phillips T: Dislocation of the superficial digital flexor tendon from the tuber calcanei, Proc Br Equine Vet Assoc Congress 39:82, 2000. 12. Phillips T: Personal communication, 2000.

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Tendon Lacerations Sue J. Dyson and Alicia L. Bertone

endon lacerations are serious injuries in horses because of the loss of the biomechanical function of the tendon, the slow return of tendon strength, the immediate strenuous loading demanded by the equine patient, and the complications of scarring. Nonetheless, early diagnosis, wound management, limb support, and long-term surgical and medical management have resulted in a good prognosis for most extensor tendon lacerations and a fair prognosis for most flexor tendon lacerations.1,2 The extensor (dorsal) aspect of the limb is often damaged by wire or a sharp object over which the horse has jumped. The flexor (palmar or plantar) aspect of the limb may be traumatized by circumferential wire injuries, landing on a sharp object, or being struck. The latter may be self-inflicted or from another horse.

T

Proximal to the carpus, transection of the extensor carpi radialis and common digital extensor tendons is most frequent. Flexion of the carpus may cause pain. The tendon sheath often is often involved. Proximal or dorsal to the tarsus, transection of the long digital extensor, cranial tibialis, and fibularis (peroneus) tertius tendons is most frequent. If the fibularis tertius is disrupted, the hock can be extended while the stifle is flexed, indicating loss of the reciprocal apparatus. The gastrocnemius tendon develops a characteristic wrinkle in this extended position (see Fig. 81-2 and page 708). The degree of gait abnormality may be mild. Transection of all the extensors over the tarsus still allows full weight bearing with the foot flat on the ground. A greater tarsal extension during the swing phase of the stride and intermittent knuckling of the digit can be detected.

Flexor Tendons

DIAGNOSIS Any laceration over the dorsal or palmar/plantar surface of the limb distal to the stifle or elbow, especially across the dorsal tarsus, distal dorsal tarsus, dorsal metatarsal region, distal radius, dorsal metacarpal region, and dorsal fetlock region may involve a tendon (Fig. 82-1). Extensor tendons and the superficial digital flexor tendon (SDFT) are positioned directly under the skin; therefore minor-appearing wounds can transect these tendons completely. Direct visual inspection may reveal transected tendon fibers protruding from the wound. However, injuries sustained at the gallop may result in a skin wound removed from the site of tendon damage, because of the movement of the skin during exercise. The position of the wound relative to synovial structures should be evaluated with care, because concurrent synovial contamination or sepsis reduces the prognosis and necessitates specific emergency treatment.

Transection of flexor tendons below the carpus or tarsus produces pain on weight bearing and therefore lameness and gait abnormality. Transection of the SDFT is most common, because it has the most superficial position of the two flexor tendons. The suspensory ligament (SL) is deep to the deep digital flexor tendon (DDFT) and is therefore least commonly injured with lacerations. A horse with complete transection of the SDFT may stand normally, or it may bear weight on the toe of the hoof to minimize movement of the tendon ends with fetlock joint extension. Administration of phenylbutazone for pain may eliminate lameness, and a gait abnormality may become hard to detect. The DDFT and SL support the fetlock joint together with the SDFT. Therefore slight hyperextension of the fetlock because of disruption of the SDFT may be difficult to detect unless the contralateral limb is picked up. The greater the number of structures transected, the less support to the fetlock and other distal joints and the greater the likelihood of vessel and nerve transection. Elevation of the toe is pathognomonic for transection of the DDFT.

Evaluation of Gait

Digital Palpation of the Wound

Each tendon serves a biomechanical function. Complete severance of a tendon results in a posture or gait change, which may be pathognomonic for disruption of the tendon integrity.

Digital palpation is a simple and direct way to determine the extent of damage to structures below the skin. Integrity of the tendons is readily determined by feel. Partial tears can be distinguished from complete tears, and this affects treatment (see “Partial Tendon Lacerations”). The tendon ends are often palpable beneath the skin proximal and distal to the wound, but they may be removed from the wound if the injury was sustained while the horse was galloping. The muscular attachment to the proximal end pulls the proximal tendon end farther from the wound. The wound should be shaved around the edges and cleansed thoroughly with a dilute antiseptic solution such as chlorhexidine before exploration. Gross debris can be debrided manually from the wound. Sterile gloves should be worn for the digital exploration after the wound is clean. Digital palpation may reveal involvement of a tendon sheath or joint capsule; however, small tears of these synovial structures may not be palpable. Sterile preparation of the skin and injection of a balanced electrolyte solution into the synovial structure in question at a site distant from the

Gross Appearance of the Wound

Extensor Tendons Transection of an extensor tendon below the carpus produces a reduced ability to extend the digit, which is detected as an exaggerated, rapid (uncontrolled) dorsal flip of the hoof at the walk. This subtle change is easiest to detect if the lateral and common (or long) digital extensor tendons are transected completely. Intermittently the horse knuckles at the fetlock joint and places the digit on the dorsal surface of the pastern and fetlock joint. The gait abnormality is more obvious in the hindlimb and with lacerations in close proximity to the fetlock. Remaining peritendonous fascial attachments provide some support in the more proximal injuries. Horses with extensor tendon lacerations fully bear weight in a normal posture, unless other aspects of the wound create lameness and pain. Transection of extensor tendons proximal to the carpus and at, or just proximal to, the tarsus also commonly occurs.

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ECRM Lateral digital extensor muscle

CDE

DDFM

LDE

Long digital extensor muscle

SDFM

3 3

Tibialis cranialis muscle

4

A Lateral

2

SL

5 C

B

1

2

6 4

1

Medial

D Lateral

Medial

Diagram illustrating common sites of tendon injury. A, Lateral forelimb. B, Medial forelimb. C, Lateral hindlimb. D, Medial hindlimb. 1, Dorsal tarsus; 2, dorsal metatarsal region; 3, distal radius; 4, dorsal metacarpal region; 5, dorsal fetlock region; 6, palmar metacarpal region; ECRM, Extensor carpi radialis muscle; CDE, common digital extensor muscle; LDE, lateral digital extensor muscle; DDFM, deep digital flexor muscle; SDFM, superficial digital flexor muscle; SL, suspensory ligament. (Adapted from Bertone AL: Tendon laceration. In Tendon and ligament injuries. Part II, Vet Clin North Am Equine Pract 11:293, 1995.)

Fig. 82-1

wound may demonstrate communication if solution exits the wound. Synovial fluid also can be obtained and submitted for cytological evaluation. Hemorrhage or inflammation is usually present in the synovial fluid if the sheath has been penetrated. Mild inflammatory changes can be seen in synovial structures adjacent to tendon injuries, even if no actual communication with the wound occurs.

Ultrasonographic Evaluation Ultrasonographic evaluation of the tendons can quantitate the degree of tendon damage, particularly in horses with partial tears. Ultrasonographic examination is not necessary for diagnosing complete tears and therefore is performed rarely. Ultrasonographic evaluation can be useful during the healing phases of horses with partial or complete tendon lacerations.3 The amount of repair tissue should increase early in repair and then decrease as the tissue matures and gains strength. In flexor tendons, about 6 weeks are required for the tendon to gain the strength to support 450 kg, and the strength of the repair tissue is largely because of an increase in tissue mass. The repair tissue cross-sectional area is greater than the original tendon area, but the strength of that tissue per unit area is reduced.4 The quality of the repair tissue can be monitored with ultrasonography. Ultrasonographic examinations should show progressively increased homogeneity of echogenicity, reduction in the hypoechoic areas of damaged tendon or early immature repair tissue, and appearance of parallel arrangements of fibers.

EMERGENCY MANAGEMENT Treatment of Shock Trauma is often severe in horses with lacerated tendons, particularly flexor tendons. Some horses may be trapped for hours in wire or entangled in equipment. Blood loss may be extensive if major arteries to the distal limbs have been tran-

sected. The loss of the function of a limb is painful and stressful. Initial management of these horses can be lifesaving. If possible, the horse should be caught and brought into a warm, clean area for examination and further treatment. If the horse has severe tachycardia (>100 beats/min), with pale mucous membranes and is reluctant to move, initial treatment should be performed on site. If the wound is still bleeding, a clean pressure bandage should be applied to stop the bleeding and provide some support to the limb. If the function of the limb is impaired mechanically, a splint should be applied over the bandage to minimize further damage with movement. Use of tranquilizers and sedatives should be kept to a minimum until the degree of blood loss and shock can be assessed and treated. Most sedatives are peripheral vasodilators and may produce significant hypotension in a hypovolemic patient. Some horses may be in stress-induced shock from pain, with extreme catecholamine release. The effect of tranquilizers may be unpredictable and potentially worsen the bleeding. Securing the horse in a familiar, warm, clean environment and stabilizing the injured limb may resolve the stress-related shock and allow assessment of hemorrhagic shock by evaluating peripheral pulse strength and quality, heart rate, and mucous membrane color. If hemorrhagic shock is severe, the most important treatment is intravenous fluid volume replacement, which can be in the form of high-volume isotonic fluids (20 to 60 L minimum per 450 kg of horse), or hypertonic saline (9% NaCl; 1 L per 450 kg of horse), followed by isotonic fluid replacement. Hypertonic fluid therapy can be effective for rapid expansion of the vascular space in hemorrhagic shock, but hypertonic solutions dehydrate the interstitium and induce a profound renal diuresis. Therefore it is critical that isotonic fluid therapy begins within 30 minutes to 1 hour after hypertonic fluid administration. Hypertonic fluid therapy is practical because of the convenience of the small volumes necessary and works well if the horse is referred or transported to a facility that has access for fluid administration.

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Transportation

Extensor Tendons

For transportation the injured limb should be placed toward the back of the trailer. The horse’s weight shifts to the front of the trailer during braking, which is often less controlled than acceleration. The horse’s head should not be tied tightly, so the head and neck can be used for balance. The limb should be supported with a padded pressure bandage and a splint for transport.

Transected extensor tendons heal well without primary suturing of the tendon, even if a large gap has formed between the tendon ends. Serial ultrasonographic evaluations show fibrosis occurring between the tendon ends that eventually becomes more organized and regains the linear arrangement of collagen along the pattern of the original tendon. This fibrous tissue seems to provide a mechanical link between the tendon ends, because extensor function of the digit returns in most horses. In our experience, a palpable thinning of the new tendon and an enlargement at the old tendon ends usually remains, even after 1 year. Horses with lacerated extensor tendons have a good prognosis, with 73% of injured horses returning to athletic soundness and 18% to pasture soundness.2 In that study, 62% of the affected limbs were treated with a 3-layer cotton bandage, 23% with a splint and bandage, and 10% with fiberglass casts. It is important that the horse is confined to box rest for at least 6 weeks so that lameness does not ensue. With lameness the hoof may be positioned on the toe, and the force of the flexor tendons maintains this position, particularly without the counter-force of the extensor tendon. Chronic flexor pull may result in permanent flexor deformity and lameness. If flexor dominance is noted, a splint or cast should be applied (see Chapter 87). In our experience, the best cosmetic outcome, and chances of achieving primary wound closure, occur with using a fiberglass cast for 3 to 6 weeks. The cast provides the most immobility to the limb and the lacerated tendon ends. Early fibrosis matures more quickly, without disruption of the early granulation tissue.

MEDICAL MANAGEMENT All horses with tendon lacerations need medical therapy, whether surgery to re-appose tendon ends is elected or not. If tendon laceration, partial or complete, is diagnosed, a more thorough aseptic preparation of the wound should be performed. These procedures require sedation, restraint of the patient, and local or regional analgesia.

Wound Cleansing and Debridement The hair should be clipped circumferentially around the limb from above the wound (to the estimated top of the bandage) and the entire limb distal to the wound. Drainage of serum and exudate from the wound is often voluminous, and removal of the hair makes subsequent cleaning of the limb easier and more thorough, thereby minimizing bacterial growth and contamination. A 10-minute scrub of the wound with an antiseptic solution should be performed. If bone and tendon are exposed, care must be taken to minimize trauma to these tissues. A minor sterile instrument pack may be helpful in trimming heavily contaminated tissues, macerated tendon ends and removing hair and debris from deep in the wound. Lacerated tendons should be trimmed at the edges to remove traumatized tissue that is expected to become necrotic. Debridement of tendon ends should be most conservative in horses with flexor tendon lacerations, for which apposition of tendon ends with suture is recommended.

Systemic and Local Medications Tetanus toxoid should be administered to any horse with a tendon laceration, and tetanus antitoxin if no vaccination history exists. Because all wounds are contaminated at injury and compound wounds have extensive soft tissue injury, broad-spectrum antimicrobial drugs should be administered systemically for a minimum of 3 days. Metronidazole should be considered in horses with grossly contaminated distal extremity wounds. The duration of antimicrobial therapy may be longer in horses with heavily contaminated wounds, wounds healing by second intention, infected wounds, wounds involving a tendon sheath, or wounds with delayed treatment (>24 hours). Wound lavage should be copious, usually with a minimum of 5 L of a balanced electrolyte solution.

SURGICAL TREATMENT Surgery in the form of wound closure is performed in most horses with compound wounds involving tendons. Primary closure is preferred, if possible, to provide the best success of obtaining primary wound healing, minimal scar formation, and the fewest complications associated with the transected tendon. However, wounds that are heavily contaminated, older than 24 hours, or heavily traumatized should have a delayed closure (1- to 3-day delay) performed to reduce the contamination and necrotic debris before closure. The decision to close a wound older than 24 hours must be made based on the condition of the wound and surrounding structures. Wounds in horses that have been managed appropriately from the time of injury until surgery can be closed at any time, if tissue loss is minimal and infection is not present.

Flexor Tendons Horses with complete laceration of one or more flexor tendons are best treated with tendon suturing, wound closure, and post-operative immobilization for about 6 weeks. Flexor tendons support the weight of the horse on loading. Thus healing and return to full strength is a slow process, one that does not return to normal for at least 6 months. In studies investigating methods of tendon repair, immobilization of the limb in a cast without suturing produced a significantly weaker repair that resulted in the clinical sequela of a hyperextended fetlock joint.4,5 The amount of scar tissue filling the tendon gap was significantly less in this group compared with the sutured groups and was the reason for the reduced strength. Suturing of flexor tendon injuries is therefore recommended. Monofilament suture (nylon or polyglyconate) produced the greatest strength of repair compared with carbon fiber suture, when placed in a double-locking loop pattern (nylon) or threeloop pulley pattern (polyglyconate) for apposition of tendon ends, or for spanning tendon gaps.4-6 The limb should be cast for at least 6 weeks, with the fetlock joint in mild flexion, by building a heel support with casting tape or plaster to provide a level weight-bearing surface with the ground. Repairs of flexor tendon lacerations above the hock (i.e., gastrocnemius tendon, DDFT, or SDFT) should follow the same principles, but the prognosis is decreased because of the greater difficulty in maintaining a full-limb cast, larger size of the tendons at this location, and greater biomechanical stresses to support the hock with weight bearing.

Partial Tendon Lacerations Tendons that are partially transected can be treated successfully without suturing but with wound closure and limb immobilization in most horses. Partial transection of flexor tendons usually involves the SDFT only or the axial margin (medial or lateral) of the SDFT and DDFT. If the limb is immobilized, the remaining fibers of tendon provide the stability for the torn tendon ends to remain in apposition and

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provide the strength to prevent further tendon tearing during healing. Anecdotally, if greater than 75% of the SDFT is lacerated, tendon suturing may provide a reduced gap and faster healing and improve the repair. If the SDFT is completely transected along with a partial laceration of the DDFT, the SDFT should be treated with suturing as previously described and the DDFT left unsutured.

given after the horse is sound at the walk and trot and ultrasonographic examination demonstrates extensive fibrosis and mature scar tissue. Heavy athletic use should not begin until 8 to 12 months after the injury.

Lacerations in Tendon Sheaths

Successful outcome (soundness) occurs in about 75% of horses with extensor tendon lacerations and up to 54% of horses with flexor tendon lacerations.1,2,8 The prognosis for horses with partial disruption of the SDFT, or the DDFT, or both is better than those with complete lacerations.8 Long-term failures are attributable to continued pain from extensive adhesions, joint pain, other injury at the time of laceration, tendon sheath adhesions, tendon contracture, annular ligament constriction, re-injury, and failure of the repair to regain adequate strength to support the joint, leading to breakdown. Re-injury to a damaged tendon may occur during healing, but such a tendon can heal successfully, although convalescence is prolonged. In general the prognosis is better for pleasure riding horses than for sports horses, but especially with injuries involving the flexor tendons of a hindlimb, complete function may be restored. An association exists between lacerations of either or both the long and lateral digital extensor tendons in the proximal part of the metatarsal region and the subsequent development of stringhalt several months later.9

If a laceration enters a tendon sheath, then therapy is altered to include aggressive lavage of the sheath and wound, intrathecal administration of antibiotics, close monitoring of sheath fluid cytological condition, longer use of systemic antibiotics, and limb immobilization. If tissue loss is minimal, wounds entering tendon sheaths should be closed primarily. Primary closure and fiberglass cast application offer the best chance of early healing and minimize the potential for the complications of ascending infection, chronic drainage and fistulae formation, and fibrosis.

CONVALESCENT THERAPY Shoeing After removal of a cast or splint for extensor tendon lacerations, a gradual return to full weight bearing is recommended. Shoeing recommendations are simple and include trimming or shoeing level, without toe extensions that may catch and produce knuckling. For flexor tendon lacerations, an elevated and extended heel shoe can be applied and the heel lowered sequentially over the next 6 weeks to a flat position. For severe lacerations involving the DDFT, SDFT, or SL, an extended heel shoe may always be required for additional flexor support.7

Graduated Exercise Horses with extensor tendon injuries have not been evaluated as closely during the healing process to assess tissue maturation and return of strength as those with flexor tendons injuries Because the function of the extensor tendon is to extend the digit and not endure a load on weight bearing, return to full strength may occur sooner than for flexor tendons. Horses should remain in a box stall or a confined area during the wound healing phases and early fibroblastic repair phases of tendon healing (3 to 6 weeks). After this time, hand walking and controlled exercise such as swimming can begin to strengthen the tendon and improve gliding function. After 10 to 12 weeks of controlled exercise, and if no signs of knuckling or flexor dominance are present, gradual return to athletic use can begin. Horses with flexor tendon lacerations require a more gradual convalescent period. After the first 6 weeks of immobilization, the next 6 weeks should be spent in confinement and regaining a normal foot posture and full weight bearing. Heel support shoes are applied during this time. After 12 weeks, hand walking can begin and gradually increase in frequency and duration over the next 3 to 6 weeks. Controlled exercise with walking, lunging, swimming, or ponying (leading from another horse) is preferred to turnout. Turnout can be

PROGNOSIS

REFERENCES 1. Foland JW, Trotter GW, Stashak TS, et al: Traumatic injuries involving tendons of the distal limbs in horses: a retrospective study of 55 cases, Equine Vet J 23:422, 1991. 2. Belknap JK, Baxter GM, Nickels FA: Extensor tendon lacerations in horses: 50 cases (1982-1988), J Am Vet Med Assoc 203:428, 1993. 3. Crass JR, Genovese RL, Render JA, et al: Magnetic resonance, ultrasound and histopathologic correlation of acute and healing equine tendon injuries, Vet Radiol Ultrasound 33:206, 1992. 4. Bertone AL, Stashak TS, Smith FW, et al: A comparison of repair methods for gap healing in equine flexor tendon, Vet Surg 19:254, 1990. 5. Jann HW, Good JK, Morgan SJ, et al: Healing of transected equine superficial digital flexor tendons with and without tenorrhaphy, Vet Surg 21:40, 1992. 6. Easley KJ, Stashak TS, Smith FW, et al: Mechanical properties for four suture patterns for transected equine tendon repair, Vet Surg 19:102, 1990. 7. Flecker RH, Wagner PC: Therapy and Corrective shoeing for equine tendon disorders, Comp Cont Educ Pract Vet 8:970, 1986. 8. Taylor S, Pascoe J, Meagher D, et al: Digital flexor tendon lacerations in horses: 50 cases (1975-1990), J Am Vet Med Assoc 206:342, 1995. 9. Crabhill M, Honnas C, Taylor S, et al: Stringhalt secondary to trauma to the dorsoproximal region of the metatarsus in horses: 10 cases (1986-1991), J Am Vet Med Assoc 205:867, 1994.

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Soft Tissue Injuries of the Pastern Virginia B. Reef and Ronald L. Genovese

njuries to the flexor tendons and ligaments in the pastern are a common cause of lameness in horses.1-6 Injuries to the collateral ligaments or the palmar or plantar ligaments of the proximal interphalangeal joint are a less frequent cause of lameness.1,7-9 Swelling, heat, and sensitivity of the affected tendon or ligament to palpation often accompany lameness. Ultrasonographic evaluation of the pastern is indicated when local swelling, heat, and sensitivity are detected, or when effusion occurs in the digital flexor tendon sheath (DFTS). The cause of the swelling can be determined by ultrasonography, and the severity of the injury can be characterized. If injury occurs to the superficial or deep digital flexor tendons (SDFT, DDFT) in the metacarpal or metatarsal region, ultrasonographic examination should include an evaluation of these structures in the pastern. Lameness associated with soft tissue injuries of the pastern also can occur without localized soft tissue swelling, and ultrasonographic examination is indicated if pain is localized to the region using diagnostic analgesia and no radiographic abnormality is detected, or entheseous new bone is seen. The clinician should bear in mind that intraarticular analgesia of the metacarpophalangeal or metatarsophalangeal joints and the proximal interphalangeal joint is not necessarily specific and may influence closely related structures such as the distal sesamoidean ligaments and the palmar ligaments of the proximal interphalangeal joint. It also may be important to use diagnostic analgesia to determine whether any injury causing soft tissue swelling in the pastern region is the source of pain causing lameness. Perineural analgesia of the palmar nerves at the level of the base of the proximal sesamoid bones (PSBs) should remove lameness if the soft tissue swelling is the sole cause of lameness. Nuclear scintigraphy may help to determine if entheseous new bone is active, and magnetic resonance imaging has the potential to provide additional information.

I

ANATOMY Most of the soft tissue structures in the pastern are on the palmar or plantar aspects and are similar in the forelimbs and hindlimbs. The following describes the forelimb but applies equally to the hindlimb. The SDFT forms a thin ring around the DDFT at the ergot and in the proximal most portion of the pastern and then bifurcates into medial and lateral branches. The origin of the branches have a teardrop shape. The cross-sectional area (CSA) of each SDFT branch gradually enlarges as the branch extends distally along the palmarolateral and palmaromedial aspects of the pastern, until the branches insert on the distal aspect of the proximal phalanx and on the proximal aspect of the middle phalanx. The DDFT lies immediately dorsal to the SDFT and extends along the midline to its insertion on the distal phalanx.1-6,10-14 The DDFT has a bilobed shape in the pastern and is surrounded by the DFTS. The oblique (middle) distal sesamoidean ligaments originate from the base of the lateral and medial PSBs as two large, round to oval branches. These branches become

smaller in CSA as they extend distally. The branches join in the proximal to mid aspect of the proximal phalanx and insert as a broad band on the palmar aspect of the middle of the proximal phalanx. The straight distal sesamoidean ligament also has its origin at the base of the PSBs and the palmar ligament and extends distally in the midline, palmar to the oblique distal sesamoidean ligament, to insert on the scutum medium of the middle phalanx.1-6,10-12 The straight distal sesamoidean ligament lies dorsal to the DDFT and has an hourglass shape, larger proximally and distally, and narrowest in the middle. The DFTS surrounds the SDFT and DDFT throughout the proximal aspect of the proximal phalanx to the bifurcation of the SDFT.1-6,10-15 The entire length of the DDFT is included in the DFTS, except for a small area in the distal palmar pastern, just proximal to the bulbs of the heel. The dorsal aspect of the DFTS extends farther distally than its palmar aspect. The proximal digital annular ligament is adhered closely to the palmar aspect of the SDFT in the proximal pastern.1,3-5,16 The distal digital annular ligament forms a sling over the distal part of the DDFT. These two structures are thin in normal horses. The palmar ligaments of the proximal interphalangeal joint originate in pairs from the medial and lateral aspects of the proximal phalanx, medial or lateral (respectively) to the SDFT branches, and insert on the scutum medium between the straight distal sesamoidean ligament and the branches of the SDFT. These are large, round to oval ligaments that extend in a diagonal direction from the origin to the insertion. The collateral ligaments of the proximal interphalangeal joint originate from a small eminence on the lateral and medial aspects of the proximal phalanx, distal to the origin of the palmar ligaments, and arc across the joint to insert on a small eminence on the lateral and medial aspects, respectively, of the proximal aspect of the middle phalanx.1,3,7,10 The proximal interphalangeal joint has a closely adhered joint capsule. The common digital extensor tendon is located on the dorsal aspect of the pastern.1 The extensor branch of the suspensory ligament (SL) joins the common digital extensor tendon in the distal part of the proximal phalanx. The main insertion of the common digital extensor tendon is on the extensor process of the distal phalanx, but there are also areas of insertion onto the proximal and middle phalanges. A bursa is present between the tendon and the proximal interphalangeal joint.

ULTRASONOGRAPHIC ANATOMY The pastern has been divided into five zones: three zones for the proximal phalanx and two zones for the shorter middle phalanx 1-6,11-14 (see Chapter16).

Superficial Digital Flexor Tendon In the proximal pastern (zone PlA) the SDFT is imaged from the palmar aspect and is homogeneously echogenic and has a

CHAPTER 83 thin, half-moon shape in the transverse plane.1-6,11-13 In longitudinal images the SDFT has a parallel fiber pattern and a triangular shape along the midline in zone PlA, because its thickness decreases distally. In normal horses, distinguishing the proximal digital annular ligament from the DFTS and the palmar border of the SDFT is difficult. The body of the SDFT ranges in thickness (palmar to dorsal) from 2 to 6 mm in PlA to 1 to 4 mm over the middle of the proximal phalanx.3 The teardrop-shaped branches in the proximal to mid-pastern region (at the junction of zones PlA and P1B) are imaged from the palmaromedial and palmarolateral aspects and are followed individually to their triangular-shaped insertions. The SDFT branches are similarly homogeneously echogenic, with a parallel fiber pattern throughout. The branches of the SDFT range in thickness from 4 to 7 mm in the proximal pastern to 7 to 12 mm distally.14 The CSA of the two SDFT branches ranges from 0.3 to 0.4 cm2 in the distal portion of zone PlA where the branch begins, increases to 0.4 to 0.6 cm2 in zone PlB, and further enlarges to 0.6 to 0.8 cm2 near the insertion.

Deep Digital Flexor Tendon The DDFT has an oval to bilobed appearance in the pastern and is imaged on the palmar midline of the pastern until the DDFT is lost from view distally.1-6,11-14 The two lobes are symmetrical. The fibers of the DDFT extend obliquely from a deeper to a more superficial position in the more distal portion of the pastern and are separated from the straight distal sesamoidean ligament by an anechogenic space. The dorsopalmar thickness and lateral to medial width of the DDFT decrease in the mid-pastern and increase again in the distal pastern. The DDFT measures 5 to 10 mm (palmar to dorsal) in the proximal pastern, slightly less in the midpastern, and 7 to 12 mm in the distal pastern region. The width of the DDFT in a lateral-to-medial direction ranges from 18 to 33 mm in the proximal pastern, decreasing to 15 to 23 mm in the mid-pastern, and increasing in the distal pastern to 23 to 32 mm.3 Along the dorsal aspect of the DDFT in the mid-pastern region is a synovial fold of the DFTS that is imaged readily, surrounded by a small amount of anechogenic synovial fluid. In the distal pastern region the palmar aspect of the DDFT adheres to the synovial membrane of the DFTS.

Oblique Distal Sesamoidean Ligaments The origin of the medial or lateral branch of the oblique distal sesamoidean ligament is best found by placing the ultrasound transducer over the medial or lateral PSB and scanning distally over the bone to its base.1-6,11,12 Alternatively, the origin of the oblique distal sesamoidean ligament can be found by following the SL branches distally over the respective PSBs to the base. Immediately distal to the base of the PSB is the origin of the oblique distal sesamoidean ligament, best located initially in its transverse section as a large, round to oval structure. The branches of the oblique distal sesamoidean ligament merge in the distal part of zone PlA into a broad, rectangular band dorsal to the DDFT. The oblique distal sesamoidean ligament then inserts on the palmar or plantar aspect of the proximal phalanx in zone P1B. The oblique distal sesamoidean ligament is the most difficult to follow to its insertion, because the ligament extends diagonally from its origin to its insertion. Following the medial or lateral branch from its origin to the main body of the oblique distal sesamoidean ligament requires a transducer angle of about 45º from the base of the PSBs to the palmar midline of the proximal phalanx. Properly aligning the transducer and eliminating off-normal incidence artifact is difficult. The oblique distal sesamoidean ligament branches may appear less echogenic because of an oblique orientation. The branches are thickest in the medial to lateral

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direction proximally. The oblique distal sesamoidean ligament branches measure 12 to 20 mm (lateral to medial) in proximal PlA, decreasing to 9 to 17 mm just before their convergence, and 0 to 9mm (one side only) at their insertion. The palmar to dorsal thickness of the oblique distal sesamoidean ligament branches is 5 to 12 mm in PlA, decreasing to 2 to 6 mm just proximal to the convergence, and decreasing again to 0 to 3 mm at the insertion.

Straight Distal Sesamoidean Ligament The origin of the straight distal sesamoidean ligament is found by angling the transducer in a proximal and dorsal direction from the proximal most aspect of the pastern, just underneath the ergot, to image the ligament and the base of the PSBs. The straight distal sesamoidean ligament becomes a more oval-shaped structure and is palmar to the oblique distal sesamoidean ligament in zone P1B. The straight distal sesamoidean ligament remains dorsal to the DDFT as it inserts on the scutum medium. The dorsal-to-palmar thickness of the straight distal sesamoidean ligament gradually increases as the medial to lateral width decreases. The straight distal sesamoidean ligament measures 5 to 9 mm (palmar to dorsal) proximally, increasing slightly over the distal aspect of the proximal phalanx to 6 to 12 mm, and increasing again to 8 to 14 mm at the scutum medium. The medial-to-lateral thickness of the straight distal sesamoidean ligament ranges from 17 to 30 mm in zone P1A, decreases to 10 to 15 mm, and then widens over the scutum medium to 45 to 65 mm.3 The straight distal sesamoidean ligament is echogenic with normal parallel fiber alignment throughout. Care must be taken to be sure that lesions are not created at the insertion of the straight distal sesamoidean ligament because of the difficulty in aligning the transducer perpendicular to the ligamentous fibers because of the horse’s heel. A hypoechoic area of dropout is detected at this location with most ultrasound transducers, because the shape of the heel bulbs precludes obtaining a 90º angle between the transducer and the ligament. If proper angulation of the transducer can be achieved, however, this off-incidence artifact is not imaged.

Cruciate Distal Sesamoidean Ligaments The cruciate distal sesamoidean ligaments are imaged only in the proximal most portion of the pastern and measure 2 to 4 mm in a palmar to dorsal direction.3

Collateral Ligaments The collateral ligaments of the proximal interphalangeal joint are easiest to examine by imaging them longitudinally and then evaluating them in the transverse plane. The collateral ligaments of the proximal interphalangeal joint are homogeneously echogenic structures, with a parallel fiber pattern from their origin on the distal aspect of the proximal phalanx to their insertion on the proximal half of the middle phalanx.1,2

Proximal Interphalangeal Joint The proximal interphalangeal joint is easiest to image initially in longitudinal plane by identifying the joint space, and then a transverse evaluation of the joint can be made.7 Fluid normally is not imaged in the proximal interphalangeal joint.

Palmar/Plantar Ligaments of the Proximal Interphalangeal Joint The palmar ligaments of the proximal interphalangeal joint can be imaged from the origin on the middle of the proximal phalanx to the insertion on the proximal palmar aspect of the middle phalanx. These ligaments are paired on the medial and lateral aspects of the pastern and are located by placing the

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transducer dorsal to the branch of the SDFT. The more abaxial branch originates first and is easier to follow than the more axial branch. Each branch has a round to oval shape, is homogeneously echogenic with a parallel fiber pattern, and must be followed individually from origin to insertion.

Digital Nerves The digital nerves are located dorsal to the lateral and medial aspects of the SDFT, adjacent to the lateral or medial palmar digital arteries.1 The nerves are found most easily by identifying the digital vein and artery, looking immediately adjacent to the digital vein and the adjacent SDFT. The nerves are tiny, homogeneously echogenic circular structures. The normal thickness of the palmar or plantar digital nerves is 2 to 3 mm, with a CSA of 0.5 to 1 mm2.1

TENDON AND LIGAMENT INJURIES In the fore pastern the SDFT is the most frequently injured tendon or ligament in all performance horses. The oblique distal sesamoidean ligament is the second most commonly injured structure in the fore pastern, followed by injuries to the DDFT and straight distal sesamoidean ligament.1-6 In the hind pastern, injuries to the DDFT are most common, with a low incidence of injuries to the other tendonous and ligamentous structures.1-5 Injuries to the DDFT are accompanied most often by tenosynovitis of the DFTS.1-6 Injuries to the collateral ligaments of the proximal interphalangeal joint occur infrequently and are more common in the forelimb.1,3,7 Injuries to the palmar/plantar ligaments of the proximal interphalangeal joint are also uncommon and occur in forelimbs (most common) and hindlimbs. The tendonous and ligamentous structures in the pastern have little covering, and thus they are vulnerable to injury with puncture wounds and lacerations. Ultrasonographic evaluation of the pastern in a horse with an acute laceration or puncture wound to the pastern should be performed aseptically and is an integral part of the evaluation of these soft tissue structures to determine if injury occurred and the severity of the injury.

Superficial Digital Flexor Tendonitis Injuries to the branches of the SDFT are more common in the forelimb.1-6 Injury in the pastern may occur in isolation, without an injury to the SDFT in the metacarpal or metatarsal region, or may be an extension of a more proximal tendon injury. Extension of the SDFT injury into the proximal pastern region, and less frequently into the mid- and distal pastern, is more common in the forelimb. Abnormal conformation such as a long pastern, an underrun heel, or an axially displaced heel may predispose the horse to injury of an SDFT branch. Lameness usually occurs at the onset of injury, is more common with SDFT injuries in the pastern than with those in the metacarpal or metatarsal region, and may persist longer, lasting for 1 to 4 weeks. Longitudinal swelling that extends in a proximal-to-distal direction along the lateral or medial aspect of the pastern throughout its length is often characteristic.1,2 Focal heat and sensitivity usually accompany this swelling. However, in horses with acute injuries, no localizing clinical signs may be apparent, but lameness is alleviated by palmar (abaxial sesamoid) nerve blocks. Generally, swelling develops within 3 to 4 days. Ultrasonographic examination in the absence of swelling may result in false-negative results. Subluxation of the proximal interphalangeal joint can occur in horses with severe injury to or complete rupture of the SDFT in the pastern. Severe dropping of the fetlock joint with weight bearing can occur in horses with severe SDFT injury. Core injuries are the most common detected by ultrasonography (Fig. 83-1), followed by diffuse injury to the

Fig. 83-1 Ultrasonographic images of the left fore lateral branch of the superficial digital flexor tendon obtained in the proximal part of zone P1B in a horse with acute injury. The anechoic to hypoechoic core lesion is apparent within the branch (arrows) in the transverse (left image) and longitudinal (right image) views. Fiber disruption and short linear fibers are imaged within the lesion in the longitudinal view, consistent with a recent injury and early healing. The horse was 1 out of 5 degrees lame, with focal swelling, heat, and sensitivity.

affected branch.1,2 Complete ruptures or near complete ruptures of the branches do occur, but they are less frequent. These injuries can be unilateral or bilateral and uniaxial or biaxial, although uniaxial injuries are most common. The medial SDFT branch appears to be more frequently injured than the lateral branch. Peritendonous soft tissue swelling is common. Avulsion fracture of the insertion of the SDFT branch occurs infrequently. Ultrasonographic evaluation of the more proximal SDFT in the metacarpal or metatarsal region is indicated to determine if the injury is an extension of a more proximal injury (see Chapter 70) (Fig. 83-2). Ultrasonographic evaluation of the contralateral fore- or hindpastern is recommended, because bilateral disease may be present, more frequently in the forelimb. Radiographic evaluation of the pastern is indicated for all horses with subluxation of the proximal interphalangeal joint, avulsion fractures at the insertion of the SDFT branch, or a ruptured SDFT branch. Treatment for horses with acute superficial digital flexor tendonitis in the pastern is similar to that in the metacarpal or metatarsal region.1,2 Horses with SDFT injuries in the pastern may have a poorer prognosis for returning to racing than those with injuries in the metacarpal region, with a more frequent recurrence of injury.1,2,17 However, successful return to performance does occur for horses with SDFT branch injuries. Rare horses are able to continue to compete with SDFT branch injuries, without a period of rest, but these are the exceptions rather than the rule. Healing of the SDFT occurs similarly to that in the metacarpal region, with an increase in the echogenicity of the lesion and the subsequent appearance of short, usually randomly aligned linear echoes. Rehabilitation of horses with injuries to the SDFT is similar to that described for bowed tendons and is based on the injury severity (see Chapter 70). A minimum of 6 months in a controlled exercise program is needed for horses with mild SDFT branch injury, whereas 12 months or more are indicated for those with severe injury to the SDFT branch to maximize the horse’s chance of returning to its previous level of competition. Ultrasonographic monitoring of tendon healing is an important part of the rehabilitation program. A central echogenic scar surrounded by a hypoechoic halo may be detected in the SDFT branch with a healed core lesion (Fig. 83-3). Peritendonous echogenic tissue representing immature and maturing fibrous tissue often is imaged adjacent to the injured SDFT branch and can result in adhesions between the branch and the surrounding tendonous and peri-

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Fig. 83-2 Ultrasonographic images of the right superficial digital flexor tendon in the metacarpal region (A) and pastern (B) obtained from a horse with an acute severe injury to that tendon. This horse was lame at the walk, with substantial swelling of the superficial digital flexor tendon in the metacarpal and pastern regions and heat and sensitivity of the tendon on palpation. The metacarpophalageal joint dropped on weight bearing, and mild subluxation of the proximal interphalangeal joint was apparent. The transverse images are on the left, and the longitudinal images are on the right. A, The superficial digital flexor tendon is enlarged and slightly hypoechoic and was injured from 5 to 32 cm distal to the accessory carpal bone. The superficial digital flexor tendon in zone 3A is surrounded by a thickened hypoechoic digital flexor tendon sheath at the proximal reflection of the sheath (arrows). Although the superficial digital flexor tendon still appears relatively echogenic in the transverse image, moderate fiber disruption is visible in the longitudinal image (arrows). B, The medial branch of the superficial digital flexor tendon in the distal portion of zone P1A is hypoechoic with an abaxially located anechoic lesion (arrow) in the branching portion of the tendon in the transverse view (on the left). The surrounding digital sheath and peritendonous tissues are greatly thickened and hypoechoic, and the distinction between the abaxial margin of the superficial digital flexor tendon branch and the peritendonous structures is difficult to discern, particularly in the longitudinal image (on the right). The medial branch of the superficial digital flexor tendon (outlined by arrows) has nearly complete fiber disruption in the longitudinal image.

Distal Sesamoidean Desmitis Oblique Distal Sesamoidean Desmitis

Ultrasonographic images of the left fore lateral branch of the superficial digital flexor tendon obtained in zone P1B of a horse with a chronic healed core injury. The horse had sustained the original injury more than 5 years earlier, and after a long, controlled exercise program the horse had raced successfully several times a year, although some small areas of re-injury were detected periodically, necessitating short periods of downtime from race training. The original central core lesion is still visible in this branch as an echogenic central area, with a thin hypoechoic rim (arrow) in the transverse view (left image) and longitudinal (right image) views. In the longitudinal view the central area of the tendon has a more random fiber pattern than the periphery.

Fig. 83-3

tendonous structures. New areas of fiber disruption often occur adjacent to the previously healed area (see Fig. 83-2) or are associated with adhesions to the surrounding tendonous or peri-tendonous structures.

Deep Digital Flexor Tendonitis Deep digital flexor tendonitis is discussed in Chapter 71.

Desmitis of the oblique distal sesamoidean ligament is most common and has been seen in all types of performance horses.1-6 Horses with a valgus or varus limb conformation or a long sloping pastern may be at increased risk for oblique distal sesamoidean ligament injuries. Swelling in the pastern region in horses with oblique distal sesamoidean ligament injuries is characteristic, because this ligament runs diagonally across the proximal to mid-pastern and swelling of the pastern usually occurs in this direction. Most horses have local swelling, heat, and pain detected on palpation of the affected ligament and lameness in the affected leg. Subluxation of the proximal interphalangeal joint can occur in horses with complete rupture of the oblique distal sesamoidean ligaments. Complete biaxial rupture of the oblique distal sesamoidean ligaments is more common in Thoroughbreds and can have catastrophic implications. Distal sesamoidean ligament injury involving the medial branch of the oblique distal sesamoidean ligament is more common than injury involving the lateral branch and is more common in the forelimb than in the hindlimb.3 Hindlimb oblique distal sesamoidean ligament injuries are more common in horses that are not used for racing. Horses with SL injury are also at increased risk of injuring the oblique distal sesamoidean ligaments. Therefore ultrasonographic evaluation of the SL is recommended for all horses with oblique distal sesamoidean desmitis. Discrete core lesions often are seen in the medial and lateral branches of the oblique distal sesamoidean ligament, although diffuse areas of fiber damage and splits also occur (Fig. 83-4). Injuries to the insertion of the oblique distal sesamoidean ligament are usually diffuse (Fig. 83-5). Periligamentous soft tissue thickening is often seen. Comparison of the ultrasonographic findings in the affected limb with the

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Fig. 83-4 Ultrasonographic images of the origin of the left fore medial branch of the oblique distal sesamoidean ligament obtained in zone PlA. The abaxial portion of the oblique distal sesamoidean ligament is diffusely hypoechoic (arrow) in the transverse (left image) and longitudinal (right image) views. Substantial fiber disruption is visible in the longitudinal view, beginning at the base of the proximal sesamoid bone (arrow). Some periligamentous echogenic soft tissue thickening surrounds the branch. The stallion was sound, but had local heat, swelling, and mild sensitivity of the medial oblique distal sesamoidean ligament.

Fig. 83-5 Transverse (on the right) and longitudinal (on the left) ultrasonographic images of the lateral branch of the right fore oblique distal sesamoidean ligament obtained where the two branches join. The lateral aspect of the transverse view is on the right side of the image. This horse had sustained an acute injury to the lateral branch of the oblique distal sesamoidean ligament from the base of the lateral proximal sesamoid bone to its insertion. A large anechoic to hypoechoic core lesion (arrows) is visible. The horse was lame at the walk, with mild subluxation of the proximal interphalangeal joint and local swelling, heat, and sensitivity along the entire lateral branch of the oblique distal sesamoidean ligament. DDFT, Deep digital flexor tendon; SSL, straight sesamoidean ligament; SDFT, superficial digital flexor tendon.

contralateral limb is recommended to be sure that subtle or early injuries are not missed. The origin and insertion of the oblique distal sesamoidean ligaments should be carefully evaluated for avulsion fractures.1,2 Avulsion fractures usually occur in association with fiber tearing in the distal sesamoidean ligaments and occur from the base of the PSBs (Fig. 83-6) and the insertion on the proximal phalanx. Avulsion fractures remain visible for years after the original injury, long after the associated desmitis in the distal sesamoidean ligament has resolved. Radiographs of the fetlock (particularly the PSBs) and the pastern regions should be obtained in all horses with oblique distal sesamoidean desmitis, paying careful attention to the base of the PSBs. However, it is important to recognize that entheseous new bone on the base of one or both of the

Ultrasonographic images of the lateral branch of the oblique distal sesamoidean ligament obtained in zone PlA of the left forelimb in a horse with chronic active desmitis of the oblique distal sesamoidean ligament and small basilar sesamoid fractures. The hyperechoic bony fragments (arrows) are distracted away from the base of the proximal sesamoid bone in the transverse view (left image) and the longitudinal view (right image). Hypoechoic to anechoic areas are visible in the transverse view, abaxial to the fracture fragments, and areas of amorphous and random fiber pattern are imaged in the longitudinal view, distal to the fracture fragments (to the left of the image). The basilar surface of the lateral proximal sesamoid bone is irregular (open arrows). The horse was 1 out of 5 degrees lame, with thickening of the base of the lateral proximal sesamoid bone, but no heat or local sensitivity.

Fig. 83-6

PSBs or on the mid-palmar aspect of the proximal phalanx can be seen as incidental radiographic abnormalities, unassociated with lameness or active desmitis. Homogeneously radiopaque mineralized bodies are also sometimes seen distal to the PSBs as incidental findings. Horses with acute injuries to the oblique distal sesamoidean ligament should be managed in the same way as those with other tendon and ligament injuries, with initial anti-inflammatory therapy and exercise restriction.1,2 A controlled exercise program with incremental increases in the exercise level should be based on ultrasonographic monitoring. As the injury heals, the CSA of the ligament usually decreases, the echogenicity of the lesion increases, and linear echoes are imaged in the area of previous fiber tearing (Fig. 83-7). A long recuperative period usually is indicated for horses with oblique distal sesamoidean desmitis to maximize the chance of return to athletic function. Prognosis for horses with oblique distal sesamoidean ligament injury is guarded to grave for returning successfully to racing and other competitive athletic activities and depends on the severity of the injury. Horses with coexisting suspensory desmitis, basilar fractures of the PSBs, or subchondral palmar third metacarpal or plantar third metatarsal bone disease have a poorer prognosis for return to athletic function. The incidence of recurrence of oblique distal sesamoidean ligament injury is high. Prognosis is grave for athletic horses with subluxation of the proximal interphalangeal joint associated with distal sesamoidean desmitis.

Straight Distal Sesamoidean Desmitis Injuries to the straight distal sesamoidean ligament occur infrequently and may occur alone or with other soft tissue injuries.1-6 These injuries usually are associated with lameness, but focal heat, swelling, and sensitivity are not always detected. Lameness is usually acute in onset and may be severe. Some horses, especially those with proximal lesions, never develop localizing soft tissue swelling, and diagnosis depends on localizing pain to the pastern region by diagnostic analgesia and subsequent ultrasonographic identification of a

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T

DDF

Ultrasonographic images of the right fore pastern obtained in zone P1B from a horse with an acute injury to the straight distal sesamoidean ligament. The horse was lame at the walk, with swelling of the palmar aspect of the pastern and local heat and sensitivity. The large anechoic core lesion (arrows) in the palmar aspect of the straight distal sesamoidean ligament is visible in the transverse view (left image), with complete fiber disruption in this region that is best imaged on the longitudinal view (right image). The straight distal sesamoidean ligament is enlarged in dorsal to palmar and medial to lateral directions. Note also the thickened subcutaneous tissues. DDFT, Deep digital flexor tendon.

Fig. 83-7

lesion. The ease with which the most proximal aspect of the ligament can be seen depends on the conformation of the horse and the position of the ergot. Ultrasonographic viewing of the straight distal sesamoidean ligament is most difficult in horse with short pasterns and easiest in those with relatively long, upright pasterns. Small splits or core lesions may be seen in the straight distal sesamoidean ligament.1-6 Large areas of fiber disruption in the straight distal sesamoidean ligament are uncommon (Fig. 83-7). Areas of periosteal proliferative change or avulsion fractures at the insertion of the straight distal sesamoidean ligament on the proximal aspect of the middle phalanx may be seen (Fig. 83-8). Avulsion fractures of the origin of the straight distal sesamoidean ligament are less common than with oblique distal sesamoidean ligament desmitis, but the base of the PSBs should be evaluated carefully. Treatment for horses with desmitis of the straight distal sesamoidean desmitis is similar to that recommended for horses with oblique distal sesamoidean desmitis.1-6 Horses with mild injuries have returned successfully to racing, but the prognosis for horses with more severe lesions is guarded for any form of competitive athletic function, because recurrent injury is common. Horses with multiple tendonous or ligamentous injuries in the pastern have a guarded to grave prognosis for returning to full athletic function.

DDFT

Ultrasonographic images of the left fore straight distal sesamoidean ligament obtained in zone PlC-P2A from a horse with an acute severe injury to the straight distal sesamoidean ligament and an avulsion of its insertion onto the scutum medium. The horse was lame at the walk, with subluxation of the proximal interphalangeal joint and substantial soft tissue swelling of the palmar pastern, with local heat and pain on palpation of the oblique distal sesamoidean ligament and straight distal sesamoidean ligament. The hypoechoic lesion (small arrows) in the distal most portion of the oblique distal sesamoidean ligament and the hyperechoic fragment distracted away from the middle phalanx (large arrows) are visible in the transverse (right image) and longitudinal (left image) views. There is anechogenic effusion (open arrows) in the digital flexor tendon sheath. DDFT, Deep digital flexor tendon.

Fig. 83-8

SOFT TISSUE SWELLING Soft tissue swelling in the pastern, without tendonous or ligamentous injury, can result from skin irritation caused by liniments, blisters, local therapeutic ultrasound or cold laser treatment, local trauma from a blow, bandaging, or bell boots, or from a skin infection. Ultrasonographic findings of thickened anechogenic to echogenic subcutaneous tissues, with normal tendonous and ligamentous structures, are typical for injury or inflammation to the skin and subcutaneous tissues. Thickening of the skin also may be seen in horses with skin irritation or infection. These horses usually respond well to local or systemic anti-inflammatory therapy.

TENOSYNOVITIS OF THE DIGITAL FLEXOR TENDON SHEATH Tenosynovitis of the digital flexor tendon sheath is discussed in Chapter 75.

ABNORMALITIES OF THE PASTERN JOINT

Cruciate Distal Sesamoidean Desmitis Desmitis of the cruciate distal sesamoidean ligament is rare and difficult to diagnose by ultrasonography because of the location of these ligaments.1,2

Proximal Digital Annular Desmitis Desmitis of the proximal digital annular ligament or proximal digital annular ligament constriction occurs infrequently.1,3 Affected horses usually have chronic moderate to severe lameness. Distention of the palmar pouch of the DFTS is usually present, in addition to subtle distention proximal to the palmar annular ligament of the fetlock. Thickening of the proximal digital annular ligament and skin usually is substantial, with a combined thickness of 4 to 5 mm (normal thickness is 1 to 2 mm) and distention of the DFTS.17

Lameness and local swelling are two common findings in horses with injuries of the collateral or palmar ligaments of the proximal interphalangeal joint.1,3-5,7-9 Swelling is usually primarily medial and lateral, although it can be circumferential. Acute desmitis of the collateral ligaments may be confirmed by ultrasonography, with decreased echogenicity and loss of fiber pattern, with or without an associated avulsion fracture (Fig. 83-9).1,3-5,7 In horses with more chronic injuries enthesophyte formation at the origin and the insertion of the collateral ligaments usually is detected. A smoothing of these areas of insertional injury occurs as the desmitis becomes inactive. Similar ultrasonographic findings may be detected in horses with acute (Fig. 83-10) and chronic injury (Fig. 83-11) to the palmar ligaments of the pastern. These

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Fig. 83-9

Ultrasonographic images of the lateral collateral ligament of the proximal interphalangeal joint of the right forelimb of horse with moderate lameness and localized swelling. The thickening of the lateral collateral ligament (arrows) and the short random fiber pattern seen in the longitudinal view (left image) are consistent with desmitis. The distal portion of the proximal phalanx is on the right side of the longitudinal view. The small anechoic slit between the proximal and middle phalanges represents the joint space (small arrow). Some echogenic subcutaneous thickening is viewed best superficial to the collateral ligament in the transverse view (right image).

Fig. 83-11 Ultrasonographic images of the lateral palmar ligament of the proximal interphalangeal joint in a horse with chronic severe desmitis and severe enthesopathy. The bony proliferative changes of the proximal phalanx in the transverse (left image) and longitudinal views (right image) make imaging the ligament in its entirety in the longitudinal plane impossible. The visible portion of the ligament appears homogeneously echogenic in the transverse image (arrows), but there is a hypoechoic area within the ligament adjacent to the bony proliferative change in the longitudinal view (arrow). The mare was 2 out of 5 degrees lame, with thickening over the lateral and medial aspects of the proximal phalanx, but no heat or local sensitivity was detected.

Fig. 83-10 Ultrasonographic images of the left abaxial plantar ligament of the proximal interphalangeal joint in a horse with severe desmitis associated with mild lameness and localized swelling. There is enlargement of the ligament. It is hypoechoic and circular to oval in the transverse view (left image), and has a random fiber pattern in the longitudinal view (right image). The arrows outline the margins of the ligament. A small amount of echogenic peritendonous subcutaneous tissue is visible.

Fig. 83-12 Ultrasonographic images of the left hind lateral plantar digital nerve obtained from a horse with neuritis resulting in acute onset of moderate lameness with local swelling, heat, and exquisite sensitivity to palpation. The enlarged nerve (arrows), oval to circular shape, is located plantar to the digital artery in the transverse view (left image). The cross-sectional area of the nerve is increased to 0.17 cm2. A hypoechoic area disrupts part of the nerve (arrows) in the longitudinal view (right image).

horses have a guarded prognosis for return to full athletic function.

injury. A large amount of perineural echogenic tissue may be present in horses with chronic neuromas.

NEURITIS/NEUROMA Neuritis of the palmar (plantar) digital nerves results in acute lameness associated with exquisite pain on palpation of the nerves and localized heat and swelling. Ultrasonography shows swelling and decreased echogenicity of the nerve (Fig. 83-12). Neuromas following palmar digital neurectomy initially appear as focal painful swellings over the stump of the digital nerve. With ultrasonography the nerve appears enlarged and hypoechoic, with perineural soft tissue swelling in horses with an acute neuroma. The neuroma becomes more echogenic and heterogeneous with increasing chronicity of

REFERENCES 1. Reef VB: Musculoskeletal ultrasonography. In Reef VB, editor: Equine diagnostic ultrasound, Philadelphia, 1998, WB Saunders. 2. Reef VB: Ultrasonic diagnosis of tendon and ligament disease. In White NA, Moore JN, editors: Current practice in equine surgery, Philadelphia, 1990, JB Lippincott. 3. Denoix J, Crevier N, Azevedo C: Ultrasound examination of the pastern in horses, Proc Am Assoc Equine Pract 37:363, 1991. 4. Dyson S: Ultrasonographic examination of the pastern region, Equine Vet Educ 4:254, 1992.

CHAPTER 84 5. Dyson S, Denoix J: Tendon, tendon sheath, and ligament injuries in the pastern, Vet Clin North Am Equine Pract 11:217, 1995. 6. Redding NW: Sonographic exam of the digital flexor tendon sheath, distal flexor tendons, and soft tissues of the palmar pastern region, Proc Am Assoc Equine Pract 39:11, 1993. 7. Denoix JM, Audigie F: Ultrasonographic examination of joints in horses, Proc Am Assoc Equine Pract 46:366, 2001. 8. Wright IM: Ligaments associated with joints, Vet Clin North Am Equine Pract 11:249, 1995. 9. Wright IM: Ligaments associated with joints, Proc First Dubai Int Equine Symp 1:241, 1996. 10. Denoix J: Functional anatomy of tendons and ligaments in the distal limbs (manus and pes), Vet Clin North Am Equine Pract 10:273, 1994. 11. Denoix J: Diagnostic techniques for identification and documentation of tendon and ligament injuries, Vet Clin North Am Equine Pract 10:365, 1994.

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723

12. McClellan PD, Colby J: Ultrasonic structure of the pastern, J Equine Vet Sci 6:99, 1986. 13. Redding WR: Ultrasonic imaging of the structures of the digital sheath, Comp Cont Educ Pract Vet 13:1824, 1991. 14. Redding WR: Evaluation of the equine digital flexor tendon sheath using diagnostic ultrasound and contrast radiography, Vet Radiol Ultrasound 34:42, 1993. 15. Dik KJ, Dyson SJ, Vail TB: Aseptic tenosynovitis of the digital flexor tendon sheath, fetlock and pastern annular ligament constriction, Vet Clin North Am Equine Pract 11:l51, 1995. 16. Dik KJ, Boroffka S, Stolk P: Ultrasonographic assessment of the proximal digital annular ligament in the equine forelimb, Equine Vet J 26:59, 1994. 17. Reimer JM: Ultrasonography of the pastern. 1. Anatomy and pathology. 2. Outcome of selected injuries in racehorses, Proc Am Assoc Equine Pract 43:123, 1997.

84

Skeletal Muscle and Lameness Stephanie J. Valberg and Sue J. Dyson

DIAGNOSIS OF SPECIFIC MUSCLE DISORDERS Diagnosis of a particular muscle disorder is accomplished best with a thorough neuromuscular examination. The key components of the examination include the items mentioned in this section.

History A history of stiffness, muscle cramping, pain, muscle fasciculations, exercise intolerance, weakness, or muscle atrophy may indicate a muscle disorder. Further characterization requires a detailed account of the horse’s exercise schedule; diet; vaccination history; signs of respiratory disease; duration, severity, and frequency of muscle problems; any factors that initiate the muscle problem; and all medications with which the horse is being treated.

Physical Examination A detailed evaluation of the muscular system includes inspection of the horse while standing with the forelimbs and hindlimbs exactly square to assess symmetry of muscle mass. Any evidence of fine tremors or fasciculations should be noted before palpating the horse. The entire muscle mass of the horse should be palpated for heat, pain, swelling, or atrophy, comparing contralateral muscle groups. Firm, deep palpation of the lumbar, gluteal, and semimembranosus and semitendinosus muscles may reveal pain, cramps, or fibrosis. The triceps, pectoral, gluteal, and semitendinosus muscles should be tapped with a fist or percussion hammer and observed for a prolonged contracture suggestive of myotonia. Running a blunt instrument, such as artery forceps, a needle cap, or a pen, over the lumbar and gluteal muscles should illicit extension (swayback), followed by flexion (hogback), in healthy animals.

Guarding against movement may reflect abnormalities in the pelvic or thoracolumbar muscles or pain associated with the thoracolumbar spine (see Chapter 54) or sacroiliac joints (see Chapters 52 and 53). The horse should be observed at a walk or trot for any gait abnormalities and some horses should be ridden.

Ancillary Diagnostic Tests Muscle Enzymes Skeletal muscle necrosis may be identified by determining the activity in blood of serum enzymes or proteins that are normally present in high concentration within intact muscle cells but leak out into the blood stream following cell damage.1,2 Three enzymes are used routinely to assess muscle necrosis: creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). Carbonic anhydrase III and serum myoglobin also have been suggested as markers of equine muscle necrosis.3,4 The permeability of the muscle cell membrane, rate of enzyme production, alternate tissue sources of the enzyme, and rate of enzyme excretion and degradation also may influence serum enzyme activities.1 Serum creatine kinase. Isoforms of CK are found in skeletal muscle, cardiac muscle, and nervous tissue. CK is a relatively low molecular weight protein (80,000 d) that is involved intimately in energy production within the cell cytoplasm. CK is liberated within hours of muscle damage or increased cell membrane permeability into the extracellular fluid and usually peaks at 4 to 6 hours after muscle injury (half-life [t1⁄ 2] is 108 minutes).5 A threefold to fivefold increase in serum CK from normal values is believed to represent necrosis of about 20 g of muscle tissue.6 Rhabdomyolysis results in a proportionately greater increase in the skeletal muscle isoform than the cardiac muscle isoform, although some studies disagree with the tissue

CHAPTER 84 5. Dyson S, Denoix J: Tendon, tendon sheath, and ligament injuries in the pastern, Vet Clin North Am Equine Pract 11:217, 1995. 6. Redding NW: Sonographic exam of the digital flexor tendon sheath, distal flexor tendons, and soft tissues of the palmar pastern region, Proc Am Assoc Equine Pract 39:11, 1993. 7. Denoix JM, Audigie F: Ultrasonographic examination of joints in horses, Proc Am Assoc Equine Pract 46:366, 2001. 8. Wright IM: Ligaments associated with joints, Vet Clin North Am Equine Pract 11:249, 1995. 9. Wright IM: Ligaments associated with joints, Proc First Dubai Int Equine Symp 1:241, 1996. 10. Denoix J: Functional anatomy of tendons and ligaments in the distal limbs (manus and pes), Vet Clin North Am Equine Pract 10:273, 1994. 11. Denoix J: Diagnostic techniques for identification and documentation of tendon and ligament injuries, Vet Clin North Am Equine Pract 10:365, 1994.

CHAPTER •

• Skeletal Muscle and Lameness

723

12. McClellan PD, Colby J: Ultrasonic structure of the pastern, J Equine Vet Sci 6:99, 1986. 13. Redding WR: Ultrasonic imaging of the structures of the digital sheath, Comp Cont Educ Pract Vet 13:1824, 1991. 14. Redding WR: Evaluation of the equine digital flexor tendon sheath using diagnostic ultrasound and contrast radiography, Vet Radiol Ultrasound 34:42, 1993. 15. Dik KJ, Dyson SJ, Vail TB: Aseptic tenosynovitis of the digital flexor tendon sheath, fetlock and pastern annular ligament constriction, Vet Clin North Am Equine Pract 11:l51, 1995. 16. Dik KJ, Boroffka S, Stolk P: Ultrasonographic assessment of the proximal digital annular ligament in the equine forelimb, Equine Vet J 26:59, 1994. 17. Reimer JM: Ultrasonography of the pastern. 1. Anatomy and pathology. 2. Outcome of selected injuries in racehorses, Proc Am Assoc Equine Pract 43:123, 1997.

84

Skeletal Muscle and Lameness Stephanie J. Valberg and Sue J. Dyson

DIAGNOSIS OF SPECIFIC MUSCLE DISORDERS Diagnosis of a particular muscle disorder is accomplished best with a thorough neuromuscular examination. The key components of the examination include the items mentioned in this section.

History A history of stiffness, muscle cramping, pain, muscle fasciculations, exercise intolerance, weakness, or muscle atrophy may indicate a muscle disorder. Further characterization requires a detailed account of the horse’s exercise schedule; diet; vaccination history; signs of respiratory disease; duration, severity, and frequency of muscle problems; any factors that initiate the muscle problem; and all medications with which the horse is being treated.

Physical Examination A detailed evaluation of the muscular system includes inspection of the horse while standing with the forelimbs and hindlimbs exactly square to assess symmetry of muscle mass. Any evidence of fine tremors or fasciculations should be noted before palpating the horse. The entire muscle mass of the horse should be palpated for heat, pain, swelling, or atrophy, comparing contralateral muscle groups. Firm, deep palpation of the lumbar, gluteal, and semimembranosus and semitendinosus muscles may reveal pain, cramps, or fibrosis. The triceps, pectoral, gluteal, and semitendinosus muscles should be tapped with a fist or percussion hammer and observed for a prolonged contracture suggestive of myotonia. Running a blunt instrument, such as artery forceps, a needle cap, or a pen, over the lumbar and gluteal muscles should illicit extension (swayback), followed by flexion (hogback), in healthy animals.

Guarding against movement may reflect abnormalities in the pelvic or thoracolumbar muscles or pain associated with the thoracolumbar spine (see Chapter 54) or sacroiliac joints (see Chapters 52 and 53). The horse should be observed at a walk or trot for any gait abnormalities and some horses should be ridden.

Ancillary Diagnostic Tests Muscle Enzymes Skeletal muscle necrosis may be identified by determining the activity in blood of serum enzymes or proteins that are normally present in high concentration within intact muscle cells but leak out into the blood stream following cell damage.1,2 Three enzymes are used routinely to assess muscle necrosis: creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). Carbonic anhydrase III and serum myoglobin also have been suggested as markers of equine muscle necrosis.3,4 The permeability of the muscle cell membrane, rate of enzyme production, alternate tissue sources of the enzyme, and rate of enzyme excretion and degradation also may influence serum enzyme activities.1 Serum creatine kinase. Isoforms of CK are found in skeletal muscle, cardiac muscle, and nervous tissue. CK is a relatively low molecular weight protein (80,000 d) that is involved intimately in energy production within the cell cytoplasm. CK is liberated within hours of muscle damage or increased cell membrane permeability into the extracellular fluid and usually peaks at 4 to 6 hours after muscle injury (half-life [t1⁄ 2] is 108 minutes).5 A threefold to fivefold increase in serum CK from normal values is believed to represent necrosis of about 20 g of muscle tissue.6 Rhabdomyolysis results in a proportionately greater increase in the skeletal muscle isoform than the cardiac muscle isoform, although some studies disagree with the tissue

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specificity of serum CK isoforms in the horse.7 Limited elevations in CK (1-KM RACETRACKS (NO.)

1 0 4 5 1 0 0 0

Data from UET (European Trotting Union), update December 2000. *The total number includes all racetracks in which at least 1 day of racing is held, but less important, occasional, and fair-like tracks (which are especially popular in France) are not considered in the subsequent columns.

APPROACHING LAMENESS PROBLEMS Only STB trotters are allowed to race in Europe, and this makes the trainer’s work more challenging. Any possibility to switch gaits or to move an unnaturally fast gaited trotter to a potentially good pacer is precluded. When the fast gait is compromised by biomechanical problems and significant interference between limbs (unlike in the pacer), corrections aimed at avoiding interference are attempted. Finding a solution for mechanical problems is not always possible, and corrective shoeing that alters the natural gait may cause compensatory lameness in different locations. A series of mechanical limitations may be present at the beginning of training, and relatively soon they are followed by pain-related problems, usually affecting joints and less frequently digital flexor tendons and the suspensory ligament. A less than 100% natural trotting athlete is more likely than a natural trotter to have its gait totally compromised, even by a mild subclinical lameness problem, and consequently gait limitations increase. However, anything that is attempted by the trainer to improve gait (corrective shoeing, special equipment that prevents turning the head and neck toward one side, or shifting the hindlimbs toward one shaft) forces the horse to a non-natural fast gait and often results in lameness. In fact, when a non-natural gait is forced, the end result is usually that a single limb (or a biped) is overloaded, and the uneven loading is exacerbated by the progression of training. When young horses start training, they frequently have been subjected to basic lameness and radiographic evaluations. This allows trainers the opportunity to treat conditions such as osteochondrosis or to be aware of other abnormalities. Prepurchase radiographic examinations and, when needed, preventative arthroscopic surgery (mostly for osteochondrosis of the tarsocrural joint and osteochondral fragments in the fetlock joints) are now practices that have received general acceptance. The reason to operate early is to have the horse rested before any training program is started. In yearlings eligible for autumn sales, it is important to perform surgery early to have presale radiographs without osteochondral fragments and to decrease effusion before the sale. When moderate gait anomalies are present, experienced trainers usually give the horse time and keep going with a light exercise program instead of making radical changes. This allows, in many horses, a complete maturation of the equine athlete and, when the growth is complete and the muscular function well conditioned, the gait in many horses automatically improves without injuring the immature skeleton.

Shoeing is also central in early training. Light plastic shoes are ideal to allow foot growth and expansion and to minimize trauma in the early phases of fast training.

TEN MOST COMMON LAMENESS CONDITIONS The following are the 10 most common lameness conditions: 1. Hoof or foot pain 2. Osteoarthritis of the distal interphalangeal joint 3. Osteoarthritis of the metacarpophalangeal joint 4. Lameness of the middle carpal joint 5. Proximal palmar metacarpal pain including proximal suspensory desmitis (PSD) 6. Sesamoiditis 7. Suspensory branch desmitis 8. Lameness of the metatarsophalangeal joint 9. Superficial digital flexor tendonitis 10. Osteochondrosis of the tarsocrural joint

LAMENESS EXAMINATION Horses with acute, severe lameness should be allowed to rest. Radiographs are frequently diagnostic, revealing the most common severe musculoskeletal injuries affecting trained STBs, such as incomplete sagittal fractures of the proximal phalanx, fractures of the proximal sesamoid bones, splint bone fractures, fractures of the third or radial carpal bones, fractures of a palmar process of the distal phalanx, fractures of the lateral condyle of the third metacarpal bone (McIII), slab fractures of the third tarsal bone, and stress fractures of the palmar aspect of McIII or the plantar aspect of the third metatarsal bone (MtIII). Apical fractures of the proximal sesamoid bones (PSBs) are a common injury in young STBs, and the lateral sesamoid in the hindlimbs is the most common location.1 The conditions mentioned previously represent injuries of the racing STB requiring rest or surgical repair. More commonly the veterinarian is consulted for mild or obscure lameness, gait disturbances, or poor performance. In any case a thorough history is mandatory before the lameness examination is initiated. A basic lameness history must include the following: • What is the trainer’s complaint? • What is the horse’s gait (naturally born versus artificial trotter)?

CHAPTER 110

• The European and Australasian Standardbreds

• Describe shoeing management: recent changes, difficulties in combining appropriate shoeing and fast gait, ideal shoeing for the horse, and attempts at correcting the problem • What is the horse’s recent performance? • When was the onset of the problem and correlation with previous lameness, if any? • When does the problem arise during the race? Does the horse worsen in the turns or on the straight? Is the horse better at the beginning of the race and does it worsen at the end? • Is the horse lame after the race? • What about the day after the race? • How is the horse during daily jogging, a question best addressed to the groom or assistant trainer? • How does the horse behave when trained clockwise (though races are counterclockwise)? • Is the horse better when trained on a straight track, when available? • Does the problem worsen on a particular racetrack and specifically on hard tracks? • Is the horse on a line? • Is the horse on a shaft? • Does the horse break stride? If so, when? At the start, approaching turns, in turns, coming out of turns, or in the straightaway? • Does the horse deviate left in the turns and right on the straight lines? Does the tendency worsen at the end of the race? • Has the horse been submitted to any previous lameness examination? • Was the horse subjected to any previous treatment with paints, ointments, or local injections? • Did previous therapy lead to any improvement? • Was any other problem diagnosed or suspected (exerciseinduced pulmonary hemorrhage, rhabdomyolysis)? Concerning conformation, the clinician should check the following: • Foot conformation (club foot or low heels, toed in, toed out, hoof wall angle, correction of the lateral-tomedial balance, quality of the horn, characteristics of the sole and quarters, type of shoeing). Club feet may indicate osteoarthritis of the distal interphalangeal joint. Toed-out horses have the most frequent gait disturbances because they tend to hit the contralateral carpus or the ipsilateral metatarsal region. Toed-in horses have less significant gait problems, but the uneven distribution of the weight is likely to produce lameness of the middle carpal joint or suspensory desmitis. • Torsional defects proximal to the hoof (fetlock and carpus and, more rarely, the tarsus), uncorrected angular limb deformities, offset (bench) knees, tied in behind the knees, straight conformation of the hindlimbs. Any of these abnormalities invariably produce secondary injuries such as suspensory desmitis, superficial digital flexor tendonitis, and middle carpal joint lameness. • Conformation of the foot is important. Asymmetrical foot size is often a consequence of reduced weight bearing and lameness on one side and the smallest foot is generally on the lame side.

Palpation Many clinicians spend little time palpating a lame horse, a practice that I feel is a mistake. Areas of warmth (heat), especially in the hoof wall, must be detected, and regions of special interest include the fetlock joints, the metacarpal and metatarsal regions, carpus, hock, stifle, and back.

915

In the forelimb the distal interphalangeal joint capsule just above the coronary band is palpated to detect effusion. The digital arteries are located abaxially at the base of the PSBs, and the character of the pulse is evaluated and compared between limbs. Hoof tester examination can be considered part of palpation. When possible, feet are first tested without removing the shoes, and ideally the horse should be kept shod until any examination in movement is completed. When diagnostic analgesia is needed, hoof testing must precede palmar digital analgesia, and shoes may be removed temporarily if bar shoes or pads prevent accurate testing. These six points are tested in each horse: lateral and medial quarters, lateral and medial middle sole, and lateral and medial toe. Testing the frog rarely produces useful information, and squeezing the quarters from lateral to medial with hoof testers may cause pain unrelated to the primary lameness.2 Pain arising from quarters, especially mild pain medially, should not be overevaluated because this region is frequently sensitive to hoof testers in normal horses. The contralateral foot may serve as a reference. In my experience the right medial quarter is the most common area where clinically important pain is elicited by hoof tester examination in STBs, and this is probably secondary to the counterclockwise direction of racing. Generally speaking, a painful response is considered more important when it arises from the toe or from the lateral side of the sole. When shoes are removed, a further evaluation of the lateral-to-medial balance is performed. The sole itself is observed, and when it appears flat and painful, this may correlate with type of shoes and padding that are used. Overzealous padding may add to, rather than relieve, pressure on the sole. A leather or rubber layer may allow sand to pack quickly under the pad and create pressure and secondary bruises. These horses are better managed with shoes in which the contact is limited to hoof wall and no contact is made with the sole. In the forelimb the fetlock joint is examined for effusion, alteration of the dorsal outline, and enlargement of the suspensory branches. The latter are palpated carefully with the joint flexed. Each branch is pressed gently axially, and alterations in consistency and pain response are noted. Range of motion of the fetlock joint is assessed. In a normal STB the fetlock joint can be flexed up to 90º (angle between the metacarpophalangeal region and the proximal phalanx) without eliciting a painful response. With one hand holding the dorsal pastern region, the dorsal aspect of the fetlock joint can be palpated further by using the other hand to compress the dorsal joint capsule against the bony prominences of the sagittal ridge and condyles of McIII. Horses with osteochondritis dissecans or a hypertrophic synovial pad exhibit a response. The bony profile of McIII must be followed with fingers to detect painful areas in the dorsal, lateral, and medial aspects. Palmar soft tissues are evaluated with the limb in a weightbearing position and while being held off the ground. Each structure is palpated accurately to detect heat, pain, and edema in horses with acute lesions or fibrotic consistency and adhesions in those with chronic conditions. Fingers must be pressed firmly, deep in the proximal palmar metacarpal region, where pain originating from the proximal suspensory ligament (SL) is hard to detect. The carpus is better evaluated by holding the leg in a moderate degree of flexion. Careful digital palpation along the dorsal aspect should be performed. Of particular importance is the dorsomedial aspect where a thickened joint capsule and painful response corresponds to the common finding of osteoarthritis of the middle carpal joint. Palpation of the forelimb proximal to the carpus is rarely helpful. Elbow and shoulder lameness are rare, and bicipital bursitis has seldom been reported. In the distal hindlimb, palpation is similar to that described for the forelimb with the exception that foot lameness is less

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Lameness in the Sport Horse

important. The metatarsophalangeal joint region is best evaluated while holding the limb in a semi-flexed position. When the regions of proximal metatarsal region and distal tarsus are palpated, some painful reactions frequently are elicited, especially on the medial aspect. This pain frequently is overemphasized in horses with back pain, especially when the trainer thinks the horse has primary lameness in the tarsus. Effusion of the tarsocrural joint often indicates osteochondrosis. The stifle must be palpated deeply and carefully, because the joint is complex and palpation is limited. The femorotibial joints seldom appear distended, but increased pressure in the medial femorotibial joint is an important sign. More frequently, joint effusion is limited to the femoropatellar joint. Distention of the latter must lead to specific examination of both femorotibial joints, because inflammatory processes involving the femorotibial joints may cause distention of the femoropatellar joint. With the exception of acute trauma, painful responses to palpation are rare in this area, even from the patellar ligaments that are identified easily. On the medial side, scar tissue and irregularities or enlargement of the medial patellar ligament may suggest previous desmotomy. When associated with femoropatellar effusion, the latter sign may suggest apical patellar fragmentation, and radiographic examination is indicated. The stifle can be flexed only in unison with most other hindlimb joints, so a painful response is not specific. With moderate flexion the medial collateral ligament can be stressed by the veterinarian pulling the tibia in a lateral direction with both hands and pressing the shoulder against the femur. Palpation of the back is aimed at evaluating pain arising from joints (intervertebral, lumbosacral, sacroiliac, and sacrococcygeal), nerve roots, and muscles. The latter are the most likely origin of pain elicited by palpation, but other problems must be ruled out if associated clinical signs (atrophy, asymmetry) are present. Pain in the gluteal area may be secondary to many problems, including straight hindlimb conformation, hock or stifle pain, sore feet, gait imbalance, and stiff corrective harness equipment. So pain in this area should not be treated as a primary problem unless a thorough clinical examination has ruled out other sources of pain.

Movement After palpation, the horse is examined during movement. I commonly tranquilize each horse I examine for lameness. Tranquilization (10 mg acetylpromazine maleate intravenously) improves the possibilities of handling the horse and lowers the risk of injuries to the veterinarian. Furthermore, the horse appears less stiff, mild lameness becomes somewhat more obvious, and the horse stands better for radiographic or ultrasonographic examination. The trainer must be consulted before injecting a tranquilizer, because this practice may preclude racing because of doping (the term used in Europe for a positive blood or urine drug test of a prohibited substance). Lameness is rarely detectable at the walk, but it is important to observe the way the horse lands with each foot to identify lateral-to-medial hoof imbalance. The horse is then trotted in a straight line on a firm surface, and the character of movements is observed. Abduction or circumduction of forelimbs is considered characteristic of carpal lameness, because the horse appears to attempt to avoid flexion. In the hindlimb, stiffness has been related anecdotally to distal tarsitis but in fact is not a specific sign. In horses with pain arising from the distal part of a hindlimb (frequently the metatarsophalangeal joint) the horse tends to moderately overflex the hock and stifle to shorten the weight-bearing phase of the stride.3 In horses with more severe lameness, drifting forward of the sound limb is observed and a drop of the fetlock joint is easily seen. Abduction of the hindlimb is thought to be related to stifle lameness.

Flexion tests are used to supplement findings during movement and are similar to those used in other sport horses. Flexion of the carpus is accomplished by pulling the metacarpal region laterally, and the clinician’s elbow may act as a lever against the horse’s radius to stress the medial aspect. In young horses affected by carpitis, this maneuver frequently elicits pain.

DIAGNOSTIC ANALGESIA Diagnostic analgesia can be performed in sequence from distal to proximal, or to save time, selective analgesic techniques can be used. For example, European trotters with a positive response to forelimb lower limb flexion inconsistently respond to palmar digital analgesia, so analgesia of the metacarpophalangeal or distal interphalangeal joints may be the first option. Perineural analgesia is preferred, however, to avoid minor risks of joint infections or to save the opportunity to provide intraarticular therapy immediately (when working in stables, trainers frequently are interested more in treatment than in diagnosis). I frequently start with low plantar analgesia in the hindlimbs, because lameness of the digit is rare. In young STBs with forelimb lameness and a positive response to carpal flexion, I block the middle carpal joint first. In horses with obscure lameness or when lameness is only apparent during fast exercise, examining the horse on the track may be useful. The horse is rigged in full harness and first examined trotting in a clockwise direction. Speed then is increased, and the horse is turned to train in a counterclockwise direction, the same as racing. Clinicians can drive the horse themselves, sit in a two-seat wagon, or observe the horse from a car or from a distance. In my opinion, watching the horse during exercise is important, especially when routine training and racing can be simulated, and I prefer the horse to be driven by its usual trainer. Having the horse fully equipped, mimicking the stress of racing, and observing the horse in turns are important advantages to this form of lameness examination. Diagnostic analgesia is useful, but the clinician must be aware of related risks and make the trainer and owner aware as well. Diagnostic blocks should be avoided in horses suspected of having incomplete fractures. Radiographic examination should precede diagnostic analgesia in these horses. When examining a horse on the track after local analgesia, the trainer should be told to limit the speed as much as possible, avoiding any sudden stop or sharp turn. An experienced trainer normally is able to appreciate the benefits of a block quickly and without stressing the horse. Examination at speed is needed to make a diagnosis in horses with plantar process osteochondrosis fragmentation of the proximal phalanx and fragmentation of the distal border of the distal phalanx.

DIAGNOSTIC IMAGING Sophisticated equipment for diagnostic imaging is now available in most European equine clinics. Scintigraphy is available in Europe but is limited to large referral hospitals. Radiography remains the mainstay of equine diagnostic imaging, and the availability of excellent portable units has improved the radiographic examination under field conditions. Ultrasonographic examination commonly is performed. Common pathological findings in the distal limb of European trotters include osteophyte formation on the distal aspect of the middle phalanx, sometimes associated with remodeling of the extensor process of the distal phalanx, as seen on a lateromedial view of the foot (Fig. 110-1). This radiographic pattern often is associated with heel growth proceeding faster than toe growth (club foot). When associated

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917

Fig. 110-1 Lateromedial radiographic view of the distal interphalangeal joint of a Standardbred trotter. Osteophyte formation on the distal border of the middle phalanx associated with moderate remodeling of the extensor process of the distal phalanx (arrows) is a common finding in European trotters. Dorsoproximal 45° medial-plantarodistolateral oblique radiographic view of a hind fetlock of a 2-year-old Standardbred. There is plantar fragmentation (arrow) of the proximal medial aspect of the proximal phalanx.

Fig. 110-2 with a positive lower limb flexion test and lameness abolished using analgesia of the distal interphalangeal joint, this radiographic finding is important and indicates osteoarthritis. Fragmentation of the extensor process of the distal phalanx has controversial clinical significance, but in my experience these fragments cause synovitis of the distal interphalangeal joint and are removed best by arthroscopy. The solar radiographic view of the foot, unlike scintigraphy, rarely helps in diagnosing pain arising from stress remodeling of the distal phalanx, so the diagnosis of pedal osteitis is limited to horses with chronic lameness characterized by substantial radiolucency.4 Fragmentation of the lateral and medial palmar processes of the distal phalanx, although controversial as a cause of acute lameness, may be an important source of pain best managed by shoeing. The flexed lateromedial view of the metacarpophalangeal or metatarsophalangeal joints is useful in evaluating lesions of the distal aspect of McIII or MtIII. In the hindlimb the oblique views must be taken in a proximal to distal direction (downangled) to see better the area between the proximal phalanx and the base of the PSBs. Fragmentation of the proximal plantar aspect of the proximal phalanx represents a major cause of subtle hindlimb lameness (Fig. 110-2). A dorsopalmar view of the carpus helps to evaluate the proximal suspensory attachment, and focal or diffuse palmar cortical sclerosis may be found (Fig. 110-3). In yearlings and young horses, this view allows examination of the distal radius, and pathological modifications of the growth plate on the medial side (physitis) are a frequent cause of early lameness. The most common lesions of the carpus are seen with the dorsolateral-palmaromedial oblique view and the dorsal 33º proximal-dorsal distal oblique (skyline) view of the flexed carpus to highlight the distal row of carpal bones. The latter must be of excellent quality, and the appropriate projection must be performed, because false-negative radiographs are frequent. Abnormal findings include areas of radiolucency in the dorsoproximal articular border of the radial fossa of the third carpal bone, radiolucent lines suggestive of fractures, and sclerosis of the third carpal bone.5 A moderate degree of sclerosis in the radial fossa of the third carpal bone is considered normal in racing horses, but more severe scle-

Dorsopalmar radiographic view of the proximal metacarpal region of a Standardbred trotter. Sclerosis of the palmar cortex of the proximal aspect of the third metacarpal bone (arrows) is a common finding in trotters with chronic proximal suspensory desmitis.

Fig. 110-3

rosis associated with radiolucent areas represents a pathological finding.6,7 In the hindlimb the centrodistal and tarsometatarsal joints frequently appear normal radiographically even when distal tarsitis is diagnosed clinically as the source of pain. Scintigraphy is an excellent tool for diagnosing osteoarthritis of these joints.8

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The tarsocrural joint is a predilection site for osteochondosis in STBs, and fragments associated with effusion may represent an indication for arthroscopic surgery. Lesions affecting the lateral trochlear ridge of the talus and medial malleolus of the distal tibia more frequently cause lameness and effusion than do those of the cranial intermediate ridge of the distal tibia. In horses with effusion but without obvious fragmentation a specific dorsal 20° lateral-plantaromedial oblique projection is indicated to evaluate the axial aspect of the medial malleolus. Subtle osteochondral fragmentation or radiolucency easily can be overlooked (Fig. 110-4). Curb is not seen frequently but can develop in the early stages of training in young horses. Curbs represent thickening of the plantar aspect of the hock and must be differentiated from the soft swelling caused by distention of a tarsal sheath. Abnormal stress to the plantar soft tissue structures can be predisposed by sickle-hocked or cow-hocked conformation. Accurate palpation differentiates curb from tarsal tenosynovitis. Ultrasonographic evaluation helps characterize the soft tissue structures involved in curb and assess severity (see Chapter 79). In the European STB, curb nearly invariably represents inflammation and thickening of the plantar ligament, but ultrasonographic evaluation is necessary to differentiate plantar desmitis from other soft tissue injury. Trainers frequently ask for radiography or ultrasonography of the stifle because they seem to incriminate this joint as the source of pain in horses with obscure hindlimb lameness. Radiography of the stifle is important in foals and yearlings when femoropatellar effusion is present. Lateromedial and caudocranial views must be obtained. Osteochondritis dissecans of the lateral trochlear ridge and, less frequently, subchondral bone cysts of the medial femoral condyle can cause effusion and lameness in young STBs. Ultrasonographic evaluation of the stifle is useful in detecting soft tissue injuries, but these lesions are rare in STBs. Mild dimples or cartilaginous defects on the articular surface of the medial femoral condyle can be detected using ultrasonographic examination by holding the stifle in a semiflexed (90º) position.

Dorsal 20° lateral-plantaromedial oblique radiographic view of the hock of a 2-year-old Standard bred colt. There is axial fragmentation of the medial malleolus (arrows), which is difficult to detect unless oblique views are obtained. The condition can cause effusion of the tarsocrural joint and lameness.

FINAL DIAGNOSIS, PROGNOSIS, AND TREATMENT OPTIONS A final diagnosis is made easily when the horse has obvious severe lameness, as is the case in horses with the more common fractures and tendon or ligament injuries (incomplete sagittal fracture of the proximal phalanx, proximal sesamoid bone fracture, carpal chip or slab fractures, superficial digital flexor tendonitis, and acute suspensory desmitis). Surgery or rest most often is recommended for these horses. In some horses, rest is the best option, and accurate monitoring of the healing process must follow (fracture of the distal phalanx, stress fractures of the proximal aspect of the third metacarpal bone, and proximal suspensory desmitis). Osteoarthritis of the distal interphalangeal, metacarpophalangeal/metatarsophalangeal, and middle carpal joints (particularly in young horses) can cause chronic lameness. Racetrack clinicians frequently inject the tarsometatarsal, centrodistal, and tarsocrural joints, but the true incidence of problems arising from these joints has not been substantiated using diagnostic analgesia. Problems affecting the proximal hindlimb, in the absence of visible lameness, frequently are diagnosed, but definitive diagnosis is difficult to substantiate. Intra-articular therapy includes steroids or non-steroidal antiinflammatory drugs (NSAIDs). A series of four intra-articular injections of polysulfated glycosaminoglycans (PSGAGs), 250 mg every fourth day and then at weekly intervals, is helpful in treating STBs with juvenile osteoarthritis, especially in the carpus. PSGAGs also have been useful parenterally (500 mg every 4 days for seven treatments).9 High molecular weight hyaluronan (20 to 40 mg) may be used alone or with corticosteroids. Hyaluronan (20 to 40 mg) may be used intravenously.10 The most popular corticosteroids for intra-articular therapy in horses include methylprednisolone acetate (40 to 60 mg), betamethasone disodium phosphate or betamethasone acetate (3 to 9 mg), and triamcinolone acetonide (6 mg). A basic treatment includes three intra-articular injections, using 60 mg methylprednisolone acetate for the first injection, followed by two injections of 40 mg at 2-week intervals. A similar protocol may be applied to betamethasone disodium phosphate and betamethasone acetate (6 to 9 mg the first time followed by two injections of 6 mg each). This treatment is usually helpful in horses with chronic osteoarthritis of the distal interphalangeal, metacarpophalangeal/metatarsophalangeal, and distal tarsal joints and sometimes resolves acute synovitis in young horses. When using triamcinolone acetonide (6 mg), clinicians must be aware of systemic effects and problems (laminitis and rhabdomyolysis) if several joints are injected at the same time. Although the cause is unsubstantiated, these complications may develop because of iatrogenic hyperadrenocorticism. Liniments, paints, and blisters are still popular, and despite lack of scientific support, they appear strongly tested by time. Iodide-based light paints diluted in dimethylsulfoxide may be helpful in improving circulation to the distal limbs and help to remove edema. Stronger blisters (with iodide mercury, cantharids, cedar oil, or turpentine) may play a role in improving circulation in some areas, but trainers must be made aware of possible secondary effects of the chemical induced inflammation (scars, adhesions, cellulitis, and excessive joint inflammation) and that using most irritant blisters is not justified anymore. Thermocautery (pin firing) is now less popular in Europe but is still used to treat STBS with curbs and proximal splint exostoses. Paints and blisters are used more frequently in France and Italy than in northern Europe.

Fig. 110-4

CORRECTIVE SHOEING Corrective shoeing is important for many forelimb lameness conditions. Generally speaking, a good lateral to medial

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balance and an ideal dorsal hoof wall angle must be provided before any shoe is applied. Then a large-based (wide web) shoe is ideal but not always possible because of gait characteristics. Many trainers prefer thinner and lighter shoes, because they are associated with increased speed. In horses with a flat sole the shoe must be in contact only with the wall border, and any rubber, leather, or silicon pad must be avoided. In these horses a rigid (aluminum) sole may prove helpful, but frequent cleaning is required to avoid sand accumulation under the sole. In horses with osteoarthritis of the metacarpophalangeal or metatarsophalangeal joints, bar shoes must be avoided because the bar prevents the natural slipping of the foot when landing and increases stress on these joints. A bar shoe may prove helpful in horses with superficial digital flexor tendonitis, but I prefer to leave this shoe on only during the recovery phase and during light training, whereas an open shoe is preferred for fast training and racing.

TRAINING PROGRAMS Alternative training programs can be a valuable adjunct therapy, especially when dealing with unnatural fast gaited trotters. Clockwise jogging and training, training on straight tracks (using interval training schedules), and swimming are preferred. Training programs aimed at reducing speed and stress on the large upper limb muscles, such as fast trotting in a circle in deep sand, use of heavy wagons or wagons with preselected brake sets (power carts) have been used, but scientific studies and objective data to support use of these alternatives are lacking.

PROCEEDING WITHOUT A DIAGNOSIS Progress in diagnostic imaging has made the situation rare in which an clinician cannot determine a diagnosis. When available, whole body scintigraphic examination in horses with occult lameness is useful. Results of scintigraphy must not be overinterpreted, and clinicians must be aware that conditions may be subtle or difficult to detect. Bone remodeling around osteochondritis dissecans or osseous cyst-like lesions may be subtle. When detailed clinical examination has failed to reveal a diagnosis, I suggest the following options: 1. The horse should be re-assessed 10 to 15 days later. This may help in horses with acute lesions without initial radiographic signs and when scintigraphy is not available. 2. A second opinion can be considered, especially if the horse can be referred to a center that is equipped with advanced imaging equipment. 3. The horse should be treated with NSAIDs (phenylbutazone, 2.2 mg/kg a day orally for 5 days and then every second day for 10 days) and then re-evaluated. 4. The clinician should treat the most likely site or sites of pain with short-acting corticosteroids. Some trainers prefer this approach because they feel the horse does not lose time and often feel something has been done. In some horses, experienced horsemen may help the clinician effectively by asking for a specific therapy that may help the situation. 5. The clinician should give the horse a period of controlled exercise or rest. This decision is particularly helpful when dealing with young horses, in which early training may have promoted bone and soft tissue adaptation and remodeling that requires time to heal. Before resting the horse, a complete radiographic examination is a good idea because horses with advanced disease may have a poor prognosis or may require additional rest.

919

LAMENESS IN THE EUROPEAN TROTTER Hoof Pain This non-specific definition refers to a number of conditions, including what most clinicians and trainers call foot pain. Lameness varies and the response to flexion may be equivocal. Negative flexion tests in a lame horse may suggest nonarticular hoof pain, and the same applies to horses in which the trainer’s complaint is pain (with compromised gait) at the end of the race. Horses may break stride on the last turn or may get on a line in the straightaway. Physical examination includes visual inspection of the feet (club foot, lateral-to-medial hoof imbalance, or toed-in or toed-out conformation), accurate palpation of the coronary band, appreciation of alterations in the digital pulse, and hoof temperature. A complete hoof tester examination is essential. A series of selective diagnostic analgesic procedures follows. Palmar digital analgesia commonly improves lameness by 75% to 90%. If a less than 50% response is obtained, an abaxial sesamoid block is performed. I avoid analgesia of the distal interphalangeal joint, because I may choose to medicate the joint. Recent evidence suggests analgesia of the distal interphalangeal joint is not specific, and pain originating from the sole may be abolished.11 Diagnostic imaging includes radiography and scintigraphy. Stress remodeling of the distal phalanx is a common finding in trained STBs. Radiographs are usually negative, although occasionally marginal changes of the distal phalanx suggestive of pedal osteitis are present. Management includes corrective shoeing, controlled exercise, distal interphalangeal joint injections, and local application of iodide ointments or blisters. Temporary pain relief has been reported anecdotally after perineural injection of cobratoxin, alcohol, or other preparations and after percutaneous cryotherapy. Horses with mild lameness respond to corrective shoeing: rubber or leather soles may be added to wide web shoes, or different types of rubber flaps may be used temporarily. Light training for 2 to 3 weeks is suggested, and the horse is best trained on a soft track or on a straight track if available. Swimming is a good alternative method of training.

Osteoarthritis of the Distal Interphalangeal Joint History, character of the lameness, response to flexion tests, and shape of the hoof are points to consider when osteoarthritis of the distal interphalangeal joint is suspected. Horses can be lame or reported to be intermittently lame. The tendency is for horses to develop osteoarthritis of the distal interphalangeal joint and club foot because the hoof growth in the heel region is faster than in the toe region. Evaluation and trimming of the hoof wall to lower the dorsal angle may help prevent this conformational change. Palpation of the area over the coronary band may elicit pain, especially medially where the condition must be distinguished from chronic, distal interphalangeal collateral ligament strain. Mild pain also may be detected by palpation of the proximal SL in the forelimb and muscles of the back, two common compensatory lameness conditions. Diagnosis can be frustrating because horses are not always improved with distal interphalangeal analgesia (this may suggest pain originating in the subchondral bone), and the gait may be abnormal because of other problems frequently secondary to pain originating from the distal interphalangeal joint. An 80% to 90% positive response to the perineural analgesia must be considered clinically relevant. Lateromedial radiographs of the distal limb frequently show a prominent osteophyte on the distal aspect of the middle phalanx, sometimes associated with secondary remodeling of the proximal aspect of the distal phalanx (see Fig. 110-1). Fragmentation of the extensor process of the distal phalanx may also be observed, in which case the hoof wall frequently has a grossly triangular shape. Osteoarthritis of the

920

Fig. 110-5

PART X

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Lameness in the Sport Horse

A flap or flip-flop shoe can be useful in trotters with

foot pain.

distal interphalangeal joint may be bilateral but is most commonly unilateral. Suggested therapy includes intra-articular therapy with corticosteroids, PSGAGs, high molecular weight hyaluronan, or a combination of these drugs 3 times, at 7-day intervals (14 days when using corticosteroids). Corrective trimming to decrease excessive heel growth and maintaining the hoof angle at about 50º appear important. Wide-web shoes distribute load on a large surface area, and when possible, a rubber or leather pad is needed. The shoe should have a rolled toe to ease breakover. A thick rubber pad (flap or flip-flop) is used sometimes to replace the classic shoe (Fig. 110-5).

Osteoarthritis of the Metacarpophalangeal Joint Osteoarthritis of the metacarpophalangeal joint may be acute or chronic. Acute synovitis is seen in young horses when training is intensified or when the track surface changes. Clinical signs include mild to moderate lameness, pain on palpation, and lameness after flexion. Radiographs are usually negative in young horses, but flattening or more severe changes of the sagittal ridge of McIII in older horses with chronic osteoarthritis often are seen. Contrast radiography reveals a filling defect corresponding to the hypertrophic synovial pad in the dorsal aspect of the distal, dorsal aspect of McIII. Ultrasonographic examination reveals various degrees of dorsal joint capsule thickening and increase in echogenicity of the synovial pad. Intra-articular analgesia abolishes the lameness in most horses. In horses with acute synovitis, training program modulation (2 to 3 weeks of light jogging), corrective shoeing (widebased shoes and pads), and intra-articular corticosteroids (a series of three injections at 2-week intervals) may resolve the problem. In these horses, concurrent pathological conditions of the articular cartilage, subchondral bone, and the synovial pad usually are lacking or mild. Horses with hypertrophic synovial pads benefit from arthroscopic surgery to remove the thickened tissues, because response to medical management is poor. This is frequently the case in older horses, in which advanced osteoarthritis is often present. Prognosis after surgery is only fair to guarded, however.

Middle Carpal Joint The middle carpal joint is the most common site of lameness in young STBs. Typically, affected horses tend to trot with a wide gait, abducting the affected limb or limbs in an attempt

to minimize carpal flexion.12 Visual inspection from a dorsolateral perspective reveals abnormal contour of the dorsomedial aspect of the carpus. Palpation often elicits a painful response over the dorsal aspect of the radial and third carpal bones. Usually the response to carpal flexion is positive, and intra-articular analgesia abolishes lameness in most horses. A negative result from intra-articular analgesia does not rule out the middle carpal joint as the source of lameness, because subchondral bone damage under a relatively normal cartilage layer may cause pain that may not be desensitized completely. Radiographs are usually diagnostic, especially the skyline view of the distal row of carpal bones. Radiographic findings range from complete slab fracture of the third carpal bone to more subtle signs of radiolucency of the radial fossa of the third carpal bone. Scintigraphy is a sensitive and excellent tool in the early diagnosis of middle carpal joint lameness.8 Training program modulation and intra-articular injections of PSGAGs, hyaluronan, or small amounts of corticosteroids are the first steps in the treatment program. Arthroscopy is suggested when evidence of more severe bone damage exists. Chip fractures in STBs most frequently involve the third and radial carpal bones. Counterclockwise racing, especially in the turns, concentrates forces along the medial aspect of the right forelimb, and this makes the right middle carpal joint more predisposed to injuries.13-15 The proximal border of the third carpal bone is involved more frequently than the distal border of the radial carpal bone in the STB, unlike in the Thoroughbred (TB) and in the pacer.13,15,16 Arthroscopic surgery and rest generally yield a fair to good prognosis.15 Incomplete slab fractures of the third carpal bone may heal with rest, possibly preceded by diagnostic arthroscopy and curettage of the lesion. Horses with complete slab fractures are best treated by internal fixation. Thin fragments are removed. When arthroscopy shows substantial loss of articular cartilage, the micropick technique may augment the possibilities of cartilage repair.17 Arthroscopic findings in young STBs have been shown to correlate poorly with radiographic findings, and lesions appear frequently more severe than expected.16 In horses without radiographic changes, I frequently find depressions and discoloration of articular cartilage (especially in the radial fossa of the third carpal bone), loss of articular cartilage in focal areas of the third and radial carpal bones, and partial or complete tearing of the medial palmar intercarpal ligament. Ligament injuries, especially affecting the medial palmar intercarpal ligament must be suspected in the absence of radiographic findings.18 However, medial palmar intercarpal ligament injuries are rare. These horses are treated using arthroscopic trimming and are given 4 to 6 weeks of stall rest followed by 4 weeks of stall rest with hand walking exercise, and joints are injected with short-acting corticosteroids.

Proximal Palmar Metacarpal Pain Including Proximal Suspensory Desmitis Proximal palmar metacarpal pain affects many more horses than we once thought. Mild pain in the proximal palmar aspect of the metacarpal region may be secondary to other gait disturbances and may reflect attempts to maintain balance when trotting fast. In this case the lesion rarely is substantiated by ultrasonography, but pain may be detected with accurate palpation (racetrack clinicians used to diagnose and treat blind splints in this area). PSD is usually acute in onset, and direct palpation of the SL elicits pain. A carpal flexion test is often positive. Intra-articular analgesia of the middle carpal joint produces a variable amount of improvement, but some degree of lameness still is elicited by flexion. Subcarpal analgesia (4 mg of local anesthetic solution placed axial to each of the second and fourth metacarpal bones or direct infiltration of 2% mepivacaine over the proximal suspensory ligament) usually abolishes lameness.

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Diagnostic imaging includes radiography, scintigraphy, and ultrasonography. Scintigraphy is useful in identifying horses with bony injury, including horses with an avulsion fracture at the attachment on McIII or those with a longitudinal fracture of McIII, or with enthesopathy. Horses with PSD without bony involvement may have positive pool-phase images, but delayed images are usually negative. Radiography (dorsopalmar and flexed lateromedial views) may reveal associated longitudinal or avulsion fractures of the palmar aspect of McIII or, in horses with chronic lameness, sclerosis of McIII at the SL origin (Fig. 110-3). Ultrasonography is useful in identifying patterns of ligamentous injury, palmar cortical bone damage, and monitoring the healing process. The prognosis is fair to good, provided the affected horse is subjected to walking exercise and controlled training with concurrent monitoring of the healing process. STBs may tolerate an acceptable level of training with chronic injuries of the SL compared with TBs, possibly because of the increased percentage of muscle fibers present in the SL.19 The prognosis in horses with PSD is better than those affected with lesions in the body of the ligament. Therapy includes 6 to 8 weeks of rest followed by 4 to 6 weeks of 20 to 60 minutes of walking exercise or swimming. Local application of blisters and injections of corticosteroids or PSGAGs have been suggested, but they rarely are able to shorten the healing period. Cryotherapy has gained some popularity in treating STBs with PSD in racetrack practice, but its usefulness has not been substantiated scientifically. Intralesional injection of liquid bone marrow is a new, promising therapy that can be combined with fasciotomy.20 More recently, shock wave therapy has been used to treat horses with PSD (see Chapter 99).

Sesamoiditis Sesamoiditis may be defined as enthesopathy at the attachment of the branches of the SL to the abaxial surface of the PSBs. The condition also may affect the base of PSBs, but this form is rare and is best defined as distal sesamoidean desmitis. Two types of sesamoiditis are recognized. Type 1, or juvenile sesamoiditis, is characterized by radiolucent lines (vascular channels) in the proximal third of the PSB, radially oriented as seen in lateromedial or oblique radiographic views, and is a frequent feature in young (2- and 3-year-old) STBs (Fig. 110-6). This radiographic pattern is not associated constantly with lameness, and no link has been observed between the presence of these lines and PSB fractures.21 Affected horses tend to be lame after training, but pain subsides with rest. Intra-articular analgesia does not abolish lameness. Lameness disappears after perineural analgesia of the medial and lateral plantar (palmar) nerves. The condition usually involves one or both hindlimbs, and the lateral PSB is affected more frequently. Scintigraphic findings indicate increased bone metabolism, but radiographic changes are seen in only 50% of STBs showing increased radioisotope uptake.8 The lateral PSB represents one of the most frequent locations for abnormal scintigraphic findings in racing STBs.8,22 Type 2 sesamoiditis is chronic, frequently affects a single PSB, and is found more commonly in the forelimbs of older horses. Radiographic signs of type 2 sesamoiditis (evidence of radiolucent lines in the proximal half of the bone, irregular palmar/plantar and abaxial outline of the bone, enthesophytes, and mineralization of the adjacent intersesamoidean ligament) are associated with ultrasonographic evidence of suspensory insertion desmitis. One or both suspensory branches often are involved. Focal loss of echogenicity in horses with acute disease and increased echogenicity in horses with chronic lameness are common ultrasonographic findings. The insertion on the PSB (enthesis) becomes grossly irregular.

921

Fig. 110-6 Dorsolateral-plantaromedial oblique radiographic view of a metatarsophalangeal joint of a lame 2-year-old Standardbred colt with juvenile sesamoiditis. Note the radiolucent lines on the abaxial aspect of the lateral proximal sesamoid bone. In horses with type 1 sesamoiditis, treatment involves rest, slow training, or turnout for 30 to 90 days, depending on the degree of lameness present. Radiographic monitoring of the lesion is probably not helpful, because lameness may improve substantially despite the persistence of radiolucent lines. More information is provided by scintigraphy initially and during follow-up examination. Medical treatment includes local application of paints or mild blisters, corrective shoeing (bars must be avoided, the quarters must be lowered moderately, and shoes must provide a wide base in the hindlimbs). Medical treatment is aimed at improving local blood flow, and isoxsuprine hydrochloride (0.6 to 1.2 mg/kg per os bid) and sodium acetylsalicylate (10 mg/kg PO bid) are recommended for 45 to 60 days. The efficacy of this therapy, however, is questionable. The prognosis is fair if lameness is not severe and if the horse tends to warm out of lameness. If severe lameness is observed and associated radiographic changes are pronounced, the prognosis is guarded. These horses are best given long periods of rest and paddock turnout (6 to 8 months). Treatment of horses with type 2 sesamoiditis includes rest, corrective shoeing (wide web aluminum shoes, leather pad, with particular attention to lateral-to-medial hoof balance), local application of dimethylsulfoxide, and paints and blisters. Pin firing is no longer justified. Cryotherapy has become popular in recent years, but in my opinion its clinical efficacy is poor. The prognosis is fair, but hoof balance must be monitored to prevent recurrence. Low-level or alternative (swimming) training is indicated.

Suspensory Branch Desmitis Suspensory branch desmitis can be acute or chronic and is caused by lateral-to-medial hoof imbalance, exercise over uneven track surfaces, strains, and chronic fractures of the second and fourth metacarpal/metatarsal (splint) bones. Acute desmitis can be associated with metacarpophalangeal/metatarsophalangeal joint effusion. Shoeing changes, particularly when the hoof angle is modified (usually increased), frequently precede the condition, and when treating the condition, hoof

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Lameness in the Sport Horse

imbalances must be identified and corrected. Ideally the dorsal hoof angle in the forelimb should be kept between 48º and 52º, with a shoe providing good support to the heels. The routine training regimen, track conditions, and the counterclockwise direction of racing may affect the distribution of suspensory branch desmitis. In my experience the right forelimb and right hindlimb are most commonly affected, and lesions of the medial branch are twice as common as those of the lateral branch. Radiography and ultrasonography are performed to assess ligament damage and bone involvement. Enlargement and loss of definition of the margins of the branch, focal hypoechoic areas, or diffuse loss of echogenicity and hyperechoic foci in horses with chronic desmitis are the most frequent ultrasonographic findings.23 Radiographically the ipsilateral splint bone may appear deviated abaxially, and in horses with chronic lameness, adhesions may develop between the splint bone and suspensory branch, causing fracture during fast exercise. For the latter reason, radiographic monitoring of the splint bones is suggested in horses with chronic desmitis. The insertion of the branch on the PSB must be assessed by ultrasonography for lesions affecting the branch insertion on the bone. The treatment in horses with acute desmitis includes rest, anti-inflammatory drugs (phenylbutazone 2.2 mg/kg), or local application of dimethylsulfoxide and poultices. Intra-articular injection of corticosteroids may be beneficial when the condition is associated with metacarpophalangeal/metatarsophalangeal joint effusion. In horses with chronic or severe desmitis, rest and local application of mild blisters may help. Fast training must be avoided when possible, and corrective shoeing must be provided. Alternative training programs, especially swimming physiotherapy, are indicated and can allow an acceptable level of exercise without worsening the lesion.

Metatarsophalangeal Joint The metatarsophalangeal joint represents a major source of hindlimb lameness in STBs.24 Lameness of the metatarsophalangeal joint and specifically the plantar aspect is frequently subtle, and diagnosis can be challenging. Stress or non-adaptive remodeling of the plantar aspect of the metatarsophalangeal joint, proximal plantar fragmentation of the proximal phalanx, and non-union of the lateral eminence of the proximal phalanx represent the most common conditions. Traumatic osteochondrosis of the distal plantar metatarsal condyles and mineralization of the distal sesamoidean ligaments are observed rarely. Subchondral stress remodeling of MtIII has been described recently and represents a scintigraphic finding, with a corresponding radiographic pattern not easily identifiable (Fig. 109-7).22 Proximal plantar fragmentation of the proximal phalanx has been reported by several authors in radiographic surveys of young STBs and is commonly seen (see Fig. 110-2).25,26 Plantar fragments from the proximal phalanx rarely are associated with lameness at a trot in hand. Trainers’ complaints include gait disturbances during fast exercise, especially in turns, and the tendency for the horse to be on one shaft. Intraarticular analgesia of the metatarsophalangeal joint can alleviate lameness, but a fast exercise test is required and owners must be aware of the potential consequences of this procedure. For this reason, when the clinical pattern indicates pain arising from the metatarsophalangeal joint, a radiographic examination including the oblique projections (dorsoproximolateral-plantarodistomedial oblique and dorsoproximomedial-plantarodistolateral oblique) is required. In horses with plantar process osteochondritis dissecans fragments, arthroscopic surgical removal of fragments is indicated. The prognosis after surgical treatment is good. In horses with stress remodeling of the distal MtIII, rest or reduced training, intra-articular injections of PSGAGs, or low doses of corticosteroids and hyaluronan, are recommended.

Fig. 110-7 Radiolucent defect in the distal, plantarolateral aspect of the third metatarsal bone is visible on the dorsal 45° lateral 45° proximal-palmarodistal oblique radiographic view, the result of stress or non-adaptive remodeling.

Superficial Digital Flexor Tendonitis The incidence and morbidity of tendonitis in STBs is lower compared with TBs, but tendonitis of the superficial digital flexor tendon (SDFT) represents the main indication for ultrasonographic examination of the distal limbs in STB racehorses in Europe. In my experience, most of the lesions are located in the middle and distal thirds of the tendon. A core lesion located in the palmarolateral border of the tendon during ultrasonography characterizes more than 30% of the lesions. More rarely central core lesions are seen. Horses with chronic lesions have the typical pattern of diffuse tendonitis. Therapy includes rest, corrective shoeing, local application of anti-inflammatory ointments, poultices, dimethylsulfoxide, paints, or blisters, tendon splitting, desmotomy of the accessory ligament of the SDFT, and desmotomy of the palmar annular ligament. Intralesional injections of hyaluronan or PSGAGs have been reported. My treatment of choice in horses with acute lameness includes corrective shoeing (moderate lowering of the heels, correcting lateral-to-medial balance, and using widebased shoes without pads, especially rubber pads), local application of dimethylsulfoxide, cold water therapy twice a day, poultice application, and walking exercise for 2 to 4 weeks. The initial treatment is followed by the local application of an iodide blister, and the horse is given an additional 4 to 8 weeks of walking exercise. The horse usually is able then to resume jogging unless lameness is present. Ultrasonographic examination is performed 12 weeks later. In horses with recurrent tendonitis, our treatment of choice includes desmotomy of the accessory ligament of the SDFT (superior check desmotomy). Desmotomy of the palmar annular ligament also is performed when substantial tendonitis involving the distal aspect of the tendon or digital flexor tendon sheath effusion is present. After surgery, horses are given 2 weeks of box stall rest, followed by 8 weeks of walking exercise. Tendonitis of the SDFT within the pastern region is less common but more difficult to manage than tendonitis in the metacarpal region. Lameness is more pronounced, and recurrence of clinical signs is common. With ultrasonography lesions can be detected at the tendon insertion over the lateral or medial aspect of the middle phalanx. Treatment includes

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rest, local and systemic anti-inflammatory drugs, blisters, corrective shoeing, and alternative training, particularly swimming. Monitoring of the healing process is important to prevent recurrence.

Osteochondrosis of the Tarsocrural Joint Joint effusion represents the most common feature of tarsocrural osteochondrosis, a condition that has been reported with a prevalence ranging between 4% and 20% in several surveys.25-33 Tarsocrural osteochondrosis frequently is diagnosed in yearlings, and breeders are particularly concerned because the condition may lower the yearling’s price at the autumn sales. For this reason, tarsocrural effusion in yearlings now represents a frequent indication for radiographic examination and preventative arthroscopy. Lameness associated with osteochondrosis is rare, but selected lesions may cause gait disturbances. In horses with effusion and osteochondral fragmentation, it is important to rule out other causes of lameness. Lesions affecting the lateral trochlear ridge of the talus and medial malleolus of the tibia are more likely to cause lameness and synovial effusion than are lesions of the cranial aspect of the distal intermediate ridge of the tibia. Focal areas of radiolucency or loss of radiopacity on the medial malleolus may be associated with osteochondral fragmentation and may represent an indication for diagnostic arthroscopy.34 In young horses with effusion, arthroscopic removal of fragment(s) represents the best option. Prognosis after arthroscopic treatment of tarsocrural osteochondrosis is good, but synovial effusion may persist especially when osteochondrosis involves the lateral trochlear ridge of the talus and the medial malleolus.35,36 Recent studies performed in Europe found no significant differences in the racing performance and longevity of STB trotters with or without tarsocrural osteochondrosis dissecans.1,32,37

REFERENCES 1. Torre F, Motta M: Incidence and distribution of 369 proximal sesamoid bone fractures in 354 standardbred horses (1984-1995), Equine Pract 21:6, 1999. 2. Trotter GW: Aspects of palmar heel pain, Proc Am Assoc Equine Pract 45:195, 1999. 3. Buchner HHF: Gait adaptation in lameness. In Back W, Clayton H, editors: Equine locomotion, Philadelphia, 2001, WB Saunders. 4. Moyer W, O’Brien TR, Walker M: Nonseptic pedal osteitis: a cause of lameness and a diagnosis? Proc Am Assoc Equine Pract 45:178, 1999. 5. Ross MW, Richardson DW, Beroza GA: Subchondral lucency of the third carpal bone in standardbred racehorses: 13 cases (1982-1988), J Am Vet Med Assoc 195:789, 1989. 6. De Haan CE, O’Brien TR, Koblik PD: A radiographic investigation of third carpal bone injury in 42 racing thoroughbreds, Vet Radiol 28:88, 1987. 7. Pool RR, Meagher DM: Pathologic findings and pathogenesis of racetrack injuries, Vet Clin North Am Equine Pract 6:1, 1990. 8. Ehrlich PJ, Dohoo IR, O’Callaghan MW: Results of bone scintigraphy in racing standardbred horses: 64 cases (1992-1994), J Am Vet Med Assoc 215:982, 1999. 9. Trotter GW: Intra-articular corticosteroids. In McIlwraith CW, Trotter GW, editors: Joint disease in the horse, Philadelphia, 1996, WB Saunders. 10. Kawcak CE, Frisbie DD, Trotter GW, et al: Effects of intravenous administration of sodium hyaluronate on carpal joints in exercising horses after arthroscopic surgery and osteochondral fragmentation, Am J Vet Res 58:1132, 1997.

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11. Schumacher J, Steiger R, Schumacher J, et al: Effects of analgesia of the distal interphalangeal joint or palmar digital nerves on lameness caused by solar pain in horses, Vet Surg 29:54, 2000. 12. Bramlage LR, Schneider RK, Gabel AA: A clinical perspective on the lameness originating in the carpus, Equine Vet J Suppl 6:12, 1988. 13. Palmer SE: Prevalence of carpal fractures in thoroughbred and standardbred racehorses, J Am Vet Med Assoc 188:1171, 1986. 14. Schneider RK, Bramlage LR, Gabel AA: The incidence and location of 371 third carpal bone fractures in 313 horses, Equine Vet J Suppl 6:33, 1988. 15. Lucas JM, Ross MW, Richardson DW: Post operative performance of racing standardbreds treated arthroscopically for carpal chip fractures: 176 cases (1986-1993), Equine Vet J 31:48, 1999. 16. Torre F: A comparison of the radiographic and arthroscopic findings in the third carpal bone in the young standardbred horse, Equine Pract 19:14, 1997. 17. McIlwraith CW, Frisbie DD, Trotter GW, et al: Use of subchondral bone plate micropick technique to augment healing of articular cartilage defects, Proc Am Assoc Equine Pract 44:233, 1998. 18. McIlwraith CW: Tearing of the medial palmar intercarpal ligament in the equine midcarpal joint, Equine Vet J 24:367, 1992. 19. Palmer SE: Splints, fractures of the second and fourth metacarpal/metatarsal bones, and associated suspensory ligament desmitis. In Robinson N, Wilson MR, editors: Current therapy in equine medicine, ed 4, Philadelphia, 1997, WB Saunders. 20. Ross MW: Personal communication, 2001. 21. Hardy J, Marcoux M, Breton L: Clinical relevance of radiographic findings in proximal sesamoid bones of twoyear-old standardbreds in their first year of race training, J Am Vet Med Assoc 198:2089, 1991. 22. Ross MW: Scintigraphic and clinical findings in the standardbred metatarsophalangeal joint: 114 cases (19931995), Equine Vet J 30:131, 1998. 23. Dyson SJ: Diagnosis and prognosis of suspensory desmitis. Proceedings of the Dubai International Equine Symposium, March 1996. 24. Ross MW, Nolan PM, Palmer JA, et al: The importance of the metatarsophalangeal joint in standardbred lameness, Proc Am Assoc Equine Pract 37:741, 1991. 25. Sandgren B: Bony fragments in the tarsocrural and metacarpo- or metatarsophalangeal joints in the standardbred horse: a radiographic survey, Equine Vet J Suppl 6:66, 1988. 26. Sandgren B, Dalin G, Carlsten J: Osteochondrosis in the tarsocrural joint and osteochondral fragments in the fetlock joints in standardbred trotters. I. Epidemiology, Equine Vet J Suppl 16:31, 1993. 27. Haakenstad LH, Birkeland R: Osteochondritis dissecans i haseleddet hos hest. Proceedings of the twelfth Nordic Veterinary Congress, 1974. 28. Hartung K, Keller H, Munster B: Ein beitrag zur Roentgendiagnostik des Spat der Trabrennpferde, Der Prakt Tierarzt 59:177, 1978. 29. Alvarado AF, Marcoux M, Breton L: The incidence of osteochondrosis in a standardbred breeding farm in Québec, Proc Am Assoc Equine Pract 35:293, 1989. 30. Schougaard H, Falk-Ronne J, Phillipson J: A radiographic survey of tibiotarsal osteochondrosis in a selected population of trotting horses in Denmark and its possible genetic significance, Equine Vet J 22:288, 1990.

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31. Grondahl AM: The incidence of osteochondrosis in the tibiotarsal joint of Norwegian standardbred trotters: a radiographic study, J Equine Vet Sci 11:997, 1991. 32. Storgaard Jorgensen H, Proschowsky H, Falk-Ronne J, et al: The significance of routine radiographic findings with respect to subsequent racing performance and longevity in standardbred trotters, Equine Vet J 29:55, 1997. 33. Torre F, Motta M: Osteochondrosis of the tarsocrural joint and osteochondral fragments in the fetlock joints: incidence and influence on racing performance in a selected group of standardbred trotters, Proc Am Assoc Equine Pract 46:287, 2000. 34. Torre F, Toniato M: Osteochondral fragments from the medial malleolus in horses: a comparison between radiographic and arthroscopic findings, Proc Am Assoc Equine Pract 45:167, 1999. 35. Laws EG, Richardson DW, Ross MW, et al: Racing performance of standardbreds after conservative and surgical treatment for tarsocrural osteochondrosis, Equine Vet J 25:199, 1993. 36. McIlwraith CW, Foerner JJ, Davis DM: Osteochondritis dissecans of the tarsocrural joint: results of treatment with arthroscopic surgery, Equine Vet J 23:155, 1991. 37. Brehm W, Staecker W: Osteochondrosis (OCD) in the tarsocrural joint of standardbred trotters: correlation between radiographic findings and racing performance, Proc Am Assoc Equine Pract 45:164, 1999.

THE AUSTRALASIAN STANDARDBRED • Chris Whitton

DESCRIPTION OF THE SPORT STB horses have been racing in Australia and New Zealand for more than 130 years. In both countries the sport does not enjoy the same high profile as TB racing, and prize money is generally lower, which attracts fewer professional trainers than TB racing. Owner/trainers are common, with most stables having fewer than 10 horses. Horses can begin racing at 2 years of age and generally race until 8 or 9 years of age. Most races are for pacers, with trotting races being much less common. In Australia races range in distance from 1600 to 2400 m, and most pacing races are from a mobile start, with an occasional standing start. All trotting races are from a standing start. In New Zealand, races tend to be longer, up to 3200 m, and standing starts are more common. Regional meetings carry prize money of $A2000 (Australian dollars) to $A4000 per race, whereas metropolitan meetings offer $A15,000 per race. The 15 most valuable pacing races in Australia and New Zealand make up what is called the Grand Circuit. Prize money for Grand Circuit races ranges from $A100,000 to $A500,000 for the Interdominion Pacing Championship Final. Prize money for trotting races is substantially less than that for pacers. The Interdominion trotter’s Championship Final carries a $A200,000 prize. An increased number of stakes programs for young horses have become available in recent years. The Australasian Breeders Crown is held over all states of Australia and both islands of New Zealand for 2-, 3-, and 4-year-old pacers and trotters. Australian Pacing Gold is a program for yearlings sold at the sales of the same name and also has feature races for 2-, 3-, and 4-year-olds. The value of these programs puts great pressure on trainers and clinicians to persist with young horses that may benefit from rest.

Race speeds generally are expressed as mile rates, which is the time taken to travel 1 mile averaged over the whole race. Tight tracks result in slightly slower rates than large tracks. Typical mile rates for pacers in 1600-m races are 1:56 to 1:58. For 2400-m races mile rates of 2 minutes are typical.

TRACK SURFACE OR TRAINING SURFACE AND LAMENESS Most of the racetracks are 700 to 1000 m in circumference, and races are run in a counterclockwise direction, except for the north island of New Zealand where races are run clockwise. Track surfaces vary but usually consist of sand or fine gravel. Banking of turns tends to be modest, although a trend to greater degrees of banking and reduced injury rates has been demonstrated. Many trainers have their own homemade training track that is often just graded dirt or sand and not always well maintained, and recurrent foot bruising can be a major problem. Banking on these tracks tends to be minimal. In coastal areas, training on the beach is popular and considered beneficial for horses with injuries.

TRAINING METHODS A typical training program involves a period of jogging exercise, generally of about 6 weeks, and these sessions generally last 35 to 40 minutes. Higher-speed work in hobbles (pace work) is introduced 2 to 3 times a week. A typical workout is two intervals of half to three-quarter pace over 11⁄2 miles. The speed of these workouts is steadily increased over 4 to 6 weeks until speeds approaching those of race speed are achieved. A horse that is racing generally is hobbled twice a week and jogged on the other days. Training in New Zealand is similar, with the major difference being the tendency to house horses in paddocks rather than in stables.

THE TEN MOST COMMON LAMENESS CONDITIONS The following are the 10 most common lameness conditions: 1. Subsolar bruising 2. Foot abscess 3. Osteoarthritis of the metacarpophalangeal or metatarsophalangeal joint 4. Suspensory desmitis 5. Osteoarthritis of the distal tarsal joints 6. Superficial digital flexor tendonitis 7. Fracture of the distal phalanx 8. Sagittal fracture of the proximal phalanx 9. Carpal joint disease 10. Osteochondrosis of the tarsocrural joint

LAMENESS EXAMINATION Experience in examining STBs for lameness is essential because of their awkward gait, even when trotting. An extremely high incidence of lameness occurs in horses in full work, and often several limbs are affected.

Examination at Rest (Preferably in a Stable) The clinician should observe the horse standing for any obvious swelling, abnormal weight bearing, and areas of hair loss on the proximal limbs associated with the position of the hobbles. The clinician should palpate the neck and back to detect any areas of pain; palpate the supraspinous ligament,

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dorsal spinous processes, and dorsal sacroiliac ligament, along with the longissimus dorsi muscles; and then examine each limb in turn. Palpation is performed with the limb bearing weight and not bearing weight. The veterinarian should palpate the digital pulses on the distal pastern or over the abaxial surface of the proximal sesamoid bones; observe each joint and palpate for swelling or effusion. Palpate the tendons and ligaments for heat, pain, and swelling. Particular attention should be paid to all levels of the SLs of the forelimbs and hindlimbs. The clinician should take time to examine the hind fetlock joints for effusion; flex the joints firmly to detect pain and apply hoof testers to each foot.

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Ultrasonographic examination of the flexor tendons and SLs commonly is required. SDFT lesions are often peripheral rather than core lesions. Lesions also may involve the distal third of the metacarpal region or the proximal metatarsal region, areas that are examined less commonly by ultrasonography and may be more difficult to assess. Cross-sectional area measurements comparing affected and non-affected limbs are essential when assessing subtle lesions. When examining the SLs, it is important to assess the full length, because lesions can affect the origin, body, and branches.

PROCEEDING WITHOUT A DIAGNOSIS Trotting in a Straight Line The horse should be trotted on a firm flat surface. Many horses pace initially, which makes the diagnosis of subtle lameness difficult. Persistence is important, because most horses will trot after 2 or 3 runs up and down. The horse should be observed trotting away from and toward the observer and should be observed from the side.

Flexion Tests Flexion tests have limitations but are a useful addition to the lameness examination. It is important to perform hindlimb fetlock flexion tests separately from proximal limb flexion tests because hindlimb fetlock problems are common.

Intra-articular corticosteroids often are used to assist in diagnosing subtle hindlimb lameness. Bilateral intra-articular injection of the tarsometatarsal and centrodistal joints may be used in horses in which hindlimb lameness is too subtle for accurate assessment by nerve blocks. Triamcinolone acetonide is the most commonly used intra-articular corticosteroid because of its relatively short and predictable detection time, combined with a long duration of action. Treatment of metatarsophalangeal joints also is often performed, because lameness can be subtle. The clinical relevance of plantar proximal fragments of the proximal phalanx is often questionable, and intra-articular therapy may be the only method of confirming that metatarsophalangeal joint pain exists.

DIAGNOSTIC ANALGESIA SHOEING CONSIDERATIONS Nerve blocks generally are required where no cause of lameness is obvious or the significance of a clinical finding is not clear. Where no localizing clinical signs are apparent, the clinician uses a standard approach: in the forelimb a pastern ring block is performed. The veterinarian should avoid nerve blocks at the level of the PSBs, because distinguishing between PSB pain and foot pain is difficult. This is followed by a low four-point block and then a subcarpal block and intra-articular blocks of the middle carpal and then the antebrachiocarpal joints. Should the horse fail to respond to these blocks, median and ulnar nerve blocks are performed to rule out the lower limb as a source of pain. Rarely are blocks of the elbow joint, intertubercular (bicipital) bursa, or shoulder joint required. A similar sequence of blocks is used in the hindlimb. A single lateral plantar metatarsal nerve block may be performed if plantar condylar subchondral bone pain is suspected. A subtarsal block is followed by an intra-articular block of the tarsometatarsal joint and then the centrodistal joint. The tarsocrural joint is seldom blocked because swelling generally is associated with intra-articular pathological conditions. Tibial and fibular blocks are performed to rule out the lower limb as the source of pain. Occasionally an intra-articular stifle block is required, in which case all compartments should be blocked at one time.

IMAGING CONSIDERATIONS Radiography remains an important imaging technique. Oblique views of the distal phalanx are important when a fracture is suspected, because some may be missed on dorsopalmar views. A flexed lateromedial view of the metacarpophalangeal joint should be obtained to highlight the sagittal ridge of the distal aspect of McIII and the dorsal surfaces of the PSBs. Proximodistal oblique views of the hind fetlocks are obtained to demonstrate proximal plantar fragments of the proximal phalanx and the lateral condyle of MtIII. Carpal views should always include a skyline of the third carpal bone.

Most horses are shod and trimmed by the trainer or owner. The quality therefore varies extremely. Steel rim shoes generally are used, with trailers on the hind feet being universal. These shoes are thin and provide little protection for the sole. An occasional horse is trained and raced barefoot. Wider web aluminum shoes, similar to those used on TB racehorses, are available, but the use of these shoes is less common. These shoes generally have steel inserts to improve grip. Glue-on shoes rarely are used. In an attempt to promote increased length of stride, toes are often left overlong. The combination of overlong toes and the lack of sole protection predisposes horses to subsolar bruising.

DIAGNOSIS AND MANAGEMENT OF LAMENESS Subsolar Bruising The diagnosis of subsolar bruising is based on pain with the application of hoof testers over the sole, either localized or generalized, and increased lameness after concussion of the foot. Lameness is localized to the foot with a pastern ring block, and radiography is performed to rule out a fracture of the distal phalanx. Chronic bruising may result in lysis and modeling of the margins of the distal phalanx, but these changes do not necessarily mean that the bruising is active. Hemorrhage within the horn of the sole may or may not be evident. Horses with acute lameness are treated with rest and NSAIDs. Careful attention should be paid to foot balance and wide web aluminum shoes should be fitted.

Fracture of the Distal Phalanx STBs with a sudden onset of forelimb lameness after racing or fast work but with no localizing signs should be suspected of having a fracture of the distal phalanx. Application of hoof testers usually elicits pain, but this is not always consistent. Oblique radiographic views of the foot often are required to assess the fracture properly. It is important to determine whether the fracture enters the distal interphalangeal joint.

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Most fractures are intra-articular. In horses that race counterclockwise, left forelimb fractures are generally of the lateral palmar process and right forelimb fractures are generally of the medial palmar process. Horses with non-articular fractures are treated with a bar shoe with quarter clips or a rim shoe and 12 months of rest. Horses with articular fractures may be treated in the same manner or by internal fixation with a single 4.5-mm lag screw along with a bar shoe with quarter clips. Evidence on the success of these treatments is limited, with the choice depending on individual preference.

of not running straight. Lameness is generally mild or not present at low speeds. Osteochondral fragments of the proximal plantar aspect of the proximal phalanx are most common on the medial aspect but can occur laterally or biaxially. These fragments are present by 1 year of age and are thought by some to be traumatic in origin. Treatment involves arthroscopic removal, and treated horses can be returned to training within 6 weeks. Intra-articularly administered corticosteroids are sometimes used to determine the significance of these lesions, because not all are associated with poor performance.

Sagittal Fracture of the Proximal Phalanx

Superficial Digital Flexor Tendonitis

The clinical presentation of horses with sagittal fractures of the proximal phalanx depends on fracture configuration. Short, incomplete fractures may be associated with chronic lameness that is localized to the fetlock joint with nerve blocks. Longer fractures often cause acute onset of lameness. Swelling may be present, and the horse often has pain on palpation of the dorsal aspect of the proximal phalanx. Nerve blocks are contraindicated because of the risk of progression of the fracture. Radiography confirms the diagnosis. Horses with non-displaced fractures may be treated with external coaptation. Internal fixation with lag screws is recommended for horses with complete and displaced fractures. Horses with short, incomplete fractures may heal with rest. Lag screw fixation has been recommended for fractures that fail to heal.

Tendon injuries are easy to diagnose when the midmetacarpal or mid-metatarsal area is involved. Swelling and pain on palpation are indications for ultrasonographic examination to confirm the diagnosis and differentiate from peritendonous inflammation. Horses with moderate to severe injuries are treated with rest and anti-inflammatory therapy until the swelling is reduced, followed by a controlled exercise program. Full work should not be re-introduced until 12 months after injury. Less severely injured horses may be kept in work, provided the exercise level is reduced and the tendon is monitored by ultrasonography. Such management is more successful with hindlimb injuries. Tendon injuries at the level of the digital flexor tendon sheath may result in secondary palmar annular ligament (PAL) constriction and tenosynovitis. Lameness and tendon sheath effusion are observed when the horse is returned to training. Provided healing of the tendon injury is adequate, the PAL can be sectioned and the horse rapidly returned to training to prevent the formation of adhesions.

Osteoarthritis of the Fetlock Joint Osteoarthritis of the metacarpophalangeal or metatarsophalangeal (fetlock) joint may or may not be associated with joint effusion and swelling. Usually the horse shows pain on passive flexion and a positive response to a fetlock flexion test. Lameness should be improved with a low four-point block or intra-articular analgesia. If lameness is recent, no radiographic abnormalities will be apparent, but more chronic lameness is associated with modeling changes on the dorsal aspects of the proximal phalanx and McIII/MtIII. Modeling also may be observed on the articular margins of the PSBs and the palmar/plantar aspect of the proximal phalanx. In advanced osteoarthritis, subchondral lysis or cystic lesions may be observed in the palmar/plantar aspect of the condyle of McIII/MtIII. This is most common in the lateral condyle of MtIII and is best observed on a proximodistal oblique view. Scintigraphy may be required for horses with few radiographic changes and demonstrates increased radiopharmaceutical uptake in the subchondral bone.

Proliferative Synovitis Proliferative synovitis occasionally causes lameness in STBs. Lameness generally is localized to the metacarpophalangeal joint by either perineural or intra-articular analgesia. Abnormal concavity proximal to the sagittal ridge of McIII is observed on the dorsal and occasionally the palmar aspects on lateromedial radiographs. Ultrasonography demonstrates enlargement of the synovial pad medial or lateral to the sagittal ridge on the dorsal aspect, which must be differentiated from the joint capsule. Intra-articular corticosteroids may be used, but the results often are disappointing. Surgical excision of the synovial pad via arthroscopy is usually effective in resolving the lameness. The prognosis is poorer in horses with modeling of the palmar aspect of McIII, because this usually reflects a more advanced, chronic condition.

Axial, Articular (Type 1) Osteochondral Fragments of the Proximal Plantar Aspect of the Proximal Phalanx Proximal plantar fragments of the proximal phalanx are best observed on proximodistal oblique radiographs of the metatarsophalangeal joints. These views should be included in the workup of horses with low-grade hindlimb lameness or a history

Suspensory Desmitis In most horses with suspensory desmitis, swelling and pain on palpation of the affected area of the SL is obvious, but lesions confined to the origin may be more difficult to diagnose, and subcarpal/subtarsal nerve blocks are required for diagnosis. Ultrasonographic examination confirms desmitis based on increased cross-sectional area and areas of decreased echogenicity. Radiography is used to assess the palmar/plantar aspect of McIII/MtIII and the PSBs at the proximal and distal attachments of the SL. The ideal treatment involves an initial period of rest and anti-inflammatory treatment to allow the inflammation to resolve, followed by a period of controlled exercise. Horses should not return to full work for 12 months. In practice this is not always possible, and many horses can be managed by reducing the work load for shorter periods, treating with anti-inflammatory drugs, and monitoring the response with ultrasonography.

Carpal Joint Disease Intra-articular fractures of the carpal bones generally involve the middle carpal joint. Fractures involving the antebrachiocarpal joint are less common. The horse may be performing poorly or have mild lameness. More severe lameness is associated with slab fractures or severe joint injury. Joint swelling and pain on flexion are common. Radiographs should always include a skyline view of the third carpal bone. Often lameness may be localized to the middle carpal joint with intraarticular analgesia, and only sclerosis with or without focal lytic areas of the third carpal bone are observed. Treatment options include arthroscopic surgery to remove diseased bone and cartilage, intra-articularly administered corticosteroids, and rest.

Osteoarthritis of the Distal Tarsal Joints Confirmation of the distal tarsal joints as the source of lameness involves using intra-articular analgesia or intra-articular medication in horses with more subtle lameness. Although

CHAPTER 111 radiographs are useful for determining the extent of bony changes, they are not always diagnostic. Treatment involves intra-articular injection of long-acting corticosteroids. Triamcinolone acetonide is the most commonly used because of its reliable excretion times and relatively long duration of action.

Tarsocrural Osteochondrosis The most common osteochondrosis lesion affecting the tarsocrural joint of STB horses involves the distal intermediate ridge of the tibia. Most horses have effusion of the tarsocrural joint, and lameness is absent or subtle. Radiographs demon-

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strate fragmentation of the intermediate ridge. The fragments are removed arthroscopically.

Stifle Disease Lameness localized to the stifle is rare in the STB racehorse. These horses appear to be able to race successfully with radiographic evidence of osteoarthritis of the femorotibial joints. Direct trauma to the stifle may result in soft tissue and bony injuries as in other types of horses. Trainers often are concerned that a horse may be locking its stifles, but this generally resolves with increased fitness, and sectioning of the medial patellar ligament is rarely necessary.

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The Racing Quarter Horse Robert D. Lewis

HISTORY AND DESCRIPTION OF THE SPORT In the early 1600s, horses imported to Virginia from England were crossed with local horses of Spanish ancestry to produce a compact and heavily muscled horse that could run short distances at incredible speeds. Colonists referred to these horses as Quarter Pathers, and they were the forerunner of what are now known as American Quarter Horses. Early races were generally match races between two horses running no more than a quarter of a mile. These sprint races were the earliest known examples of Quarter Horse (QH) racing in the United States. The first QH races were recorded in Enrico County, Virginia, in 1674. Racing popularity grew as the breed grew, and racing spread west as pioneers and early settlers moved in that direction. Organized QH racing started in Tucson, Arizona, with the first track devoted to QH racing being Rillito Park, built in Tucson in 1943. Today QH racing is conducted at more than 100 racetracks throughout North America, with total purses reaching $53 million. The goal of many in this industry is to own, saddle, or ride the winner of the $2 million All American Futurity, run each year on Labor Day at Ruidoso Downs in New Mexico. The racing QH today is faster than ever, some having been clocked at speeds exceeding 50 mph, earning them the title America’s Fastest Athlete. Racing QHs traditionally are broken to ride as yearlings in the fall, and breaking commonly is not delayed beyond the year end, with the exception of delays from previous injury or illness. Training a racing QH is quicker than training a Thoroughbred (TB), and most race as early as 2-year- olds, and although some jurisdictions prohibit racing of 2-year-olds before a certain date (e.g., March 1 or actual second birthday of the horse), many regions commence racing early in the year. In general, QHs are raced younger than TBs. Futurities are races for 2-year-olds for which a horse must be nominated, with regular payments. Scheduling of these races largely dictates the planning of races for 2-year-old QHs. Derbies are managed similarly for 3-year-old horses. Similar races also exist for older horses. Preliminary trial races usually

are held to determine qualifiers for the final race, which is run about 2 weeks later. Purses for futurities and derbies vary, but they are usually attractive and drive the racing QH industry. Owners strive to acquire horses that are talented enough to be competitive in these races.

TRAINING THE RACING QUARTER HORSE Actual training methods vary widely, but the number of gallops and amount of work performed before the first race and subsequently between races is substantially less than for TBs. Many older racing QHs exercise daily on a mechanical walker and may have one or two easy gallops per week between races.

LAMENESS RELATED TO TRACK SURFACE QHs race at many racetracks throughout the United States, with some racing conducted on track surfaces devoted primarily to QHs and other racing being conducted on track surfaces also used for TB racing. Some tracks conduct separate racing meets for TBs and QHs, whereas others conduct mixed race meets. Characteristics of track surfaces vary. In my experience, QH trainers prefer a firmer, faster surface than do TB trainers. Racetrack management often requests that maintenance crews produce a firm surface during QH race meets. Uniformity across the entire width of the racing surface is paramount. Most racing QH trainers agree that deeper, more yielding surfaces result in more soft tissue injuries, such as suspensory desmitis and flexor tendonitis, and a higher incidence of hindlimb lameness and what is typically described as muscle soreness in the hindquarters and loin muscles. Harder surfaces are considered to produce more lameness attributed to bones and joints of the forelimb, and these reflect most of the lamenesses diagnosed in racing QHs.

CHAPTER 111 radiographs are useful for determining the extent of bony changes, they are not always diagnostic. Treatment involves intra-articular injection of long-acting corticosteroids. Triamcinolone acetonide is the most commonly used because of its reliable excretion times and relatively long duration of action.

Tarsocrural Osteochondrosis The most common osteochondrosis lesion affecting the tarsocrural joint of STB horses involves the distal intermediate ridge of the tibia. Most horses have effusion of the tarsocrural joint, and lameness is absent or subtle. Radiographs demon-

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strate fragmentation of the intermediate ridge. The fragments are removed arthroscopically.

Stifle Disease Lameness localized to the stifle is rare in the STB racehorse. These horses appear to be able to race successfully with radiographic evidence of osteoarthritis of the femorotibial joints. Direct trauma to the stifle may result in soft tissue and bony injuries as in other types of horses. Trainers often are concerned that a horse may be locking its stifles, but this generally resolves with increased fitness, and sectioning of the medial patellar ligament is rarely necessary.

111

The Racing Quarter Horse Robert D. Lewis

HISTORY AND DESCRIPTION OF THE SPORT In the early 1600s, horses imported to Virginia from England were crossed with local horses of Spanish ancestry to produce a compact and heavily muscled horse that could run short distances at incredible speeds. Colonists referred to these horses as Quarter Pathers, and they were the forerunner of what are now known as American Quarter Horses. Early races were generally match races between two horses running no more than a quarter of a mile. These sprint races were the earliest known examples of Quarter Horse (QH) racing in the United States. The first QH races were recorded in Enrico County, Virginia, in 1674. Racing popularity grew as the breed grew, and racing spread west as pioneers and early settlers moved in that direction. Organized QH racing started in Tucson, Arizona, with the first track devoted to QH racing being Rillito Park, built in Tucson in 1943. Today QH racing is conducted at more than 100 racetracks throughout North America, with total purses reaching $53 million. The goal of many in this industry is to own, saddle, or ride the winner of the $2 million All American Futurity, run each year on Labor Day at Ruidoso Downs in New Mexico. The racing QH today is faster than ever, some having been clocked at speeds exceeding 50 mph, earning them the title America’s Fastest Athlete. Racing QHs traditionally are broken to ride as yearlings in the fall, and breaking commonly is not delayed beyond the year end, with the exception of delays from previous injury or illness. Training a racing QH is quicker than training a Thoroughbred (TB), and most race as early as 2-year- olds, and although some jurisdictions prohibit racing of 2-year-olds before a certain date (e.g., March 1 or actual second birthday of the horse), many regions commence racing early in the year. In general, QHs are raced younger than TBs. Futurities are races for 2-year-olds for which a horse must be nominated, with regular payments. Scheduling of these races largely dictates the planning of races for 2-year-old QHs. Derbies are managed similarly for 3-year-old horses. Similar races also exist for older horses. Preliminary trial races usually

are held to determine qualifiers for the final race, which is run about 2 weeks later. Purses for futurities and derbies vary, but they are usually attractive and drive the racing QH industry. Owners strive to acquire horses that are talented enough to be competitive in these races.

TRAINING THE RACING QUARTER HORSE Actual training methods vary widely, but the number of gallops and amount of work performed before the first race and subsequently between races is substantially less than for TBs. Many older racing QHs exercise daily on a mechanical walker and may have one or two easy gallops per week between races.

LAMENESS RELATED TO TRACK SURFACE QHs race at many racetracks throughout the United States, with some racing conducted on track surfaces devoted primarily to QHs and other racing being conducted on track surfaces also used for TB racing. Some tracks conduct separate racing meets for TBs and QHs, whereas others conduct mixed race meets. Characteristics of track surfaces vary. In my experience, QH trainers prefer a firmer, faster surface than do TB trainers. Racetrack management often requests that maintenance crews produce a firm surface during QH race meets. Uniformity across the entire width of the racing surface is paramount. Most racing QH trainers agree that deeper, more yielding surfaces result in more soft tissue injuries, such as suspensory desmitis and flexor tendonitis, and a higher incidence of hindlimb lameness and what is typically described as muscle soreness in the hindquarters and loin muscles. Harder surfaces are considered to produce more lameness attributed to bones and joints of the forelimb, and these reflect most of the lamenesses diagnosed in racing QHs.

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CONFORMATION RELATING TO LAMENESS Many successful racing QHs have obvious flaws in conformation, but good conformation is at least as important, if not more so, than in other breeds of racehorses. Racing QHs do not have the option of being shipped to Europe to race on grass courses, which is a common practice with TBs with less than desirable conformation. Undesirable conformation flaws in forelimbs include calf knees, upright pasterns, and unusually small front feet, especially because of the hard racing surfaces. Excessively straight stifles and sickle-hocked or excessively cow-hocked conformations should be avoided. It is critical that horses break sharply from the starting gate, and horses with hindlimb pain for any reason are likely to fail to break competitively.

valuable information. I assess the stifle joint by holding the hindlimb partially flexed with one hand, and exerting deep pressure over the medial femorotibial joint with the thumb, followed by similar pressure over the lateral femorotibial and femoropatellar joints. In my experience, effusion usually is associated with femoropatellar joint pain, but that is not necessarily the case with femorotibial joint pain. The medial femorotibial joint most often is affected in the racing QH. Soreness in the loin and gluteal muscles occurs as in other racehorses, and palpation of these muscle groups is routine. At times it is necessary to use perineural and or intraarticular analgesia to localize the source of pain causing lameness. Assessing the horse jogging under tack with a rider up can be helpful. Extended examinations at the racetrack are the exception rather than the rule, and horses with more difficult lameness are referred for further investigation.

LAMENESS EXAMINATION Examination of racing QHs is done largely in the same fashion as for other breeds of racehorses. Although not always entirely achievable at many racetracks, observing the horse at a trot on a hard surface is the most productive means of detecting lameness. Jogging the horse in a circle, in both directions, is useful for evaluating hindlimb pain. Variations do exist in interpreting results of an examination. Normal TB racehorses often show some pain on fetlock flexion (lower limb flexion), but pain on fetlock flexion in a QH is of greater clinical significance. Many TBs exhibit positive responses to the Churchill test and to flexion of the hocks for 90 to 120 seconds. This may be viewed as normal, but in a racing QH this response is important. If obvious lameness is noted at a trot in hand, the affected limb is evaluated for heat or swelling, and the character and intensity of digital pulses are assessed. In a forelimb the fetlock and the carpus are flexed separately to detect pain, and comparison is made with the contralateral limb. Firm digital palpation of the lower limb is performed to detect pain, including deep palpation of the fetlock, suspensory ligaments (SLs), flexor tendons, and both carpal joints. Palpation of the dorsum of the third metacarpal bone (McIII) is routine, especially in 2-year-olds, to detect pain. With the forelimb pulled craniad, resting on the clinician’s thigh, deep digital pressure is applied just proximal to the dorsal aspect of the coronary band, to detect pain caused by synovitis of the distal interphalangeal joint. Hoof tester examination is performed routinely on any horse observed to be lame, but results must be assessed with care, because many horses respond to pressure with hoof testers, especially those training and racing on firm surfaces. Horses with significant hoof pain usually have a prominent increase in the digital pulse amplitude. I look elsewhere if the digital pulse amplitude is not increased after exercise. If no abnormalities are detected from the carpus down, the elbow is assessed by maximal forced flexion. This quick test yields a positive response in some but not all horses with elbow pain. I detect pain in the shoulder joint by picking up the lower limb and allowing the horse to relax with the carpus partially flexed, applying deep digital pressure in the depression between the cranial and caudal eminences of the greater tubercle of the humerus, and then comparing the response in the contralateral limb. Horses with pain in the shoulder joint often try to withdraw from this pressure. For hindlimb lameness, palpation for heat and character of the digital pulse is done as for the forelimb. Fetlock flexion, hoof tester examination, and the Churchill test for pain in the distal joints of the tarsus are performed routinely. If pain in the tarsus is suspected, flexion of the limb for 90 to 120 seconds, followed by observing the horse at a trot often yields

THE TEN MOST COMMON LAMENESS CONDITIONS The following are the 10 most commonly diagnosed lamenesses: 1. Bucked shins 2. Desmitis of the interosseous ligaments (splints) 3. Synovitis of the metacarpophalangeal and distal interphalangeal joints 4. Carpal synovitis 5. Distal hock joint pain 6. Stifle pain 7. Foot soreness 8. Osteochondral fractures of the carpus 9. Osteochondral fractures of the metacarpophalangeal joint 10. Osteochondrosis

IMAGING CONSIDERATIONS Radiography is the most common imaging modality and is particularly invaluable for assessing carpal and fetlock lameness. The incidence of flexor tendonitis and suspensory desmitis is low, but diagnostic ultrasonography is useful in selected horses. I identify pain in the proximal SL in young horses in training that have just begun speed work. In most horses structural abnormalities cannot be detected with ultrasonography, and the problem resolves with 30 days of rest and slow resumption of training. Nuclear scintigraphy is used less than in TB racehorses because the incidence of stress fractures is considerably less.

SHOEING The two most commonly observed errors in shoeing are the long toe, low, underrun heel configuration, and improper medial to lateral hoof balance. QHs do not race on turf. Many trainers break horses with flat plates, and later horses train in a level grip type of shoe, but by the time they begin racing, nearly all horses have toe grabs. Aluminum shoes are the norm. Full pads and rim pads are used commonly to try to avoid foot soreness. In my opinion, training or racing a QH with chronic soreness anywhere in the limb inherently results in increased trauma to the carpus. Although many of the orthopedic conditions that create soreness (such as bucked shins and metacarpophalangeal or distal interphalangeal joint synovitis) cannot be avoided totally, many conditions of the foot can be avoided with careful attention to good shoeing.

CHAPTER 111 DIAGNOSIS AND MANAGEMENT OF SPECIFIC LAMENESS Although nothing is unique about the methodology in treating lameness in the racing QH, close attention must be paid to minor sources of pain. For horses to perform competitively, they need to be sound. QHs race at tremendous speeds for short distances and must break sharply and competitively to race successfully. One of the earliest indications of developing lameness is refusing to break from the starting gates properly. Rules of racing in most jurisdictions make no distinction between breeds relative to permitted therapeutic medications, doses, and times of administration. The use of intraarticular medication is more prevalent in the day-to-day management of the racing QH than in other racehorses. The incidence of synovitis is high, and several joints often are treated simultaneously. In my experience, lameness and soreness in the forelimbs are identified easily, but detecting subtle lameness in the hindlimb often is more challenging. Yet given the nature of the way these horses race and the tremendous speed required at the start of a race, hindlimb pain can be an insidious cause of poor performance.

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tant, and if evidence of healing does not occur within 60 days, then surgical cortical fenestration with lag screw compression is recommended. If the fracture is unusually large or shows evidence of an exit line dorsally, surgery usually is recommended initially. Surgery also is recommended for horses with acute fractures if they are older than 2 years of age.

Exostoses of the Second and Fourth Metacarpal Bones Exostoses of the second (McII) and fourth (McIV) metacarpal bones (splints) are common, and although they rarely produce profound lameness, they do cause acute discomfort. Exostoses usually involve the proximal 50% of McII. A firm bony swelling develops rapidly, with heat and pain on palpation. Swelling usually persists, although once the acute soreness dissipates, performance is unaffected. Distally located splints or those involving McIV are more troublesome. Radiography should be performed to eliminate the presence of a fracture. Most horses respond to rest for 3 to 4 weeks. Treatment with counterirritant paints and mild blisters and therapeutic thermocautery is popular. If McII or McIV is fractured, surgical removal of the distal portion of the bone is necessary, and post-operative prognosis is excellent.

Bucked Shins

Acute Synovitis of the Metacarpophalangeal Joint

Bucked shins are common, and they usually occur in 2-yearolds. In some horses clinical signs develop as speed work begins, before the first official race, but more often signs appear after racing, usually by the third official race. Occasionally, bucked shins occur later in a horse’s racing career. Lameness varies in degree, and if severe, radiographic examination of McIII is recommended. Focal or widespread loss of bone opacity in the outer 50% of the dorsal cortex of McIII may occur with multiple parallel cortical stress fractures in more lame horses. Vertical fractures also occur; these appear as a vertical shear line between original cortical bone and newly developed bone. Stress fractures are common and are best managed if detected early. Treatment of QHs with bucked shins varies. Managing horses with early bucked shins with continued but reduced training regimens has gained acceptance. With more severe signs, using counterirritants and mild blistering agents is popular. Other treatments include injections of corticosteroids (often diluted in saline or a local anesthetic solution), flooding the subcutaneous tissues over the dorsal aspect of McIII, thermocautery, and a percutaneous technique that produces vertical transection of the periosteum over the dorsal aspect of McIII using a 14-gauge needle (periosteal scratching). Periosteal scratching is used in horses with no radiographically apparent abnormalities that have experienced recurrent lameness, despite rest and a period of reduced training. The technique is performed in a standing horse, using appropriate sedation and local analgesia, flooding the dorsal metacarpal region with local anesthetic solution and 2 mg of dexamethasone. Lacerations in the periosteum from proximal McIII to the origin of the metacarpophalangeal joint capsule are created in three locations, dorsomedially, dorsally, and lateral to the common digital extensor tendon. This provides rapid relief from periosteal pain and in my experience allows a more rapid return to reduced training. The short-term relief of pain likely can be attributed to the corticosteroid used, but similar short-acting corticosteroids used in the past by simple subcutaneous injection did not give extended relief. Full-thickness dorsal cortical stress fractures usually are detected after a race. Two-year-olds with acute injuries heal without surgical intervention if given immediate, sufficient rest for 90 to 120 days, followed by extended and slow return to full training. Follow-up radiographic examination is impor-

Acute synovitis of the metacarpophalangeal joint, characterized by heat, effusion, and pain on flexion, is fairly common in young QHs. Acute synovitis is distinguished from chronic fetlock disease (osteoarthritis) by the ability to reduce swelling in the joint to a clinically normal appearance by cessation of work, ice or cold therapy, non-steroidal anti-inflammatory drugs (NSAIDs), poultices, or a combination of these treatments. Usually no detectable radiographic abnormalities are apparent. The condition is usually bilateral and often is referred to as green osselets. Although rest is desirable, racing schedules often create pressure on the trainer and veterinarian to manage these horses medically while the horse continues to train. Intra-articular therapy with hyaluronan, with or without corticosteroids, is common. The use of intravenously administered hyaluronan or intramuscularly administered polysulfated glycosaminoglycans (PSGAGs) is widespread.

Acute Synovitis of the Distal Interphalangeal Joint in the Forelimb Acute synovitis of the distal interphalangeal joint in a forelimb is common, particularly when horses are training or racing on firm surfaces. The condition is usually bilateral, and affected horses move like horses with sore feet. Increased amplitude of digital pulses in both forelimbs often is detected, so a diagnosis of bruised soles often is made initially. Fetlock flexion often produces pain, but careful examination reveals that this pain is not originating in the metacarpophalangeal joint. Digital pressure just proximal to the dorsal aspect of the coronary band often elicits a painful response, and effusion may be detected by soft swelling in this area. Radiographic examination usually reveals no abnormality, although enthesophyte formation on the extensor process of the distal phalanx often is seen in horses that have been racing with recurrent synovitis. Treatment of this condition varies, with systemic NSAIDs; intra-articularly administered hyaluronan, with or without corticosteroids; intravenously administered hyaluronan; and intramuscularly administered PSGAGs all being used widely. Ice or cold therapy is routine, and most trainers tend to treat horses like those with bruised soles, using foot soaks and packing the bottom of the foot with various poultices or other medicaments. Prognosis is favorable.

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Synovitis of the Carpus

Foot Soreness

Acute synovitis of the carpus is seen commonly and is often unilateral. Clinical signs may develop during training but more often develop after a horse commences racing. If the condition persists despite medical management, it often becomes bilateral. The horse tends to travel wide with the forelimbs slightly abducted and somewhat stiff legged at the trot, especially on a hard surface. Localized heat and effusion are often present in both the antebrachiocarpal and middle carpal joints. Maximal flexion of the carpus sometimes elicits a painful response, but I rely more heavily on pain elicited by deep digital palpation with the joints flexed. Medical therapy as described for synovitis of the metacarpophalangeal and distal interphalangeal joints is usually successful. In my experience, horses that are refractory to treatment or have recurrent clinical signs often develop osteoarthritis, and bone failure may result in osteochondral fragmentation (see later discussion). Extended rest always should be considered as a management option in horses with acute synovitis of the carpus.

The incidence of sore feet varies from track to track, depending on the track surface, and is usually from bruising. Most trainers pack the soles with products such as ichthammol under a foot bandage and walk the horse for several days. If lameness persists, radiographic examination is warranted to determine the presence of pre-existing disease or a fracture of the distal phalanx. Solar margin fractures sometimes occur. A fracture of a palmar process of the distal phalanx usually causes a more severe, acute lameness. Subsolar abscesses are common, and routine extensive hydrotherapy resulting in soft soles may be a predisposing factor. Navicular disease occurs uncommonly.

Distal Hock Joint Pain Pain in the centrodistal and tarsometatarsal joints is common and can have a profound effect on performance, resulting in failure to break sharply from the starting gates. The Churchill test and hock flexion test are useful diagnostic aids. The condition is often bilateral, and affected horses often travel narrow behind, with the limbs adducted slightly. Many horses with painful hocks begin to interfere, striking the opposite limb from the pastern up to the tarsus. The condition may develop at any point during a horse’s career and, if chronic, radiographic evidence of osteoarthritis is often apparent. Treatment comprises intra-articularly administered hyaluronan or corticosteroids, with or without NSAIDs, intravenously administered hyaluronan, or intramuscularly administered PSGAG. In the absence of obvious radiographic evidence of osteoarthritis, most horses can be managed successfully, although repeated treatment often is required.

Osteochondral Fractures of the Carpus Chip fractures are common especially in the faster horses, particularly in 2-year-old horses that compete in futurities. Extent of injuries varies widely from microfractures of the subchondral bone to failure of bone integrity resulting in fragmentation. Major fractures, particularly of the third carpal bone, occur more commonly than in TB racehorses. Osteochondral fragmentation is usually bilateral and often involves the antebrachiocarpal and middle carpal joints. The horse usually has a history of previous carpal pain, and the radiographic changes suggest accumulated trauma over time resulting in bone failure, emphasizing the need for careful management of acute carpal synovitis. Arthroscopic surgery for removal of osteochondral fragments is common, particularly for more successful racehorses. Some good horses undergo arthroscopic surgery several times during a career. Lesser horses often are managed conservatively, with extensive intra-articular medication.

Osteochondral Fractures of the Metacarpophalangeal Joint Fracture of the dorsomedial aspect of the proximal phalanx occurs most commonly; fracture of the dorsolateral aspect is less common. Fractures of the proximal sesamoid bones most commonly affect the medial sesamoid bone, but the incidence is less than in TBs. In my experience, condylar fractures of McIII do not occur. Subchondral bone trauma in the palmarodistal aspect of McIII is seen in older horses that have raced extensively.

Stifle Pain Lameness originating in the stifle is not uncommon and may cause signs similar to distal hock joint pain. In some horses performance is reduced without overt lameness. I find deep digital palpation of a partially flexed joint useful for identifying pain, but intra-articular analgesia is often required to confirm the source. The medial femorotibial joint is affected most often. In a young horse radiographic examination should be performed to rule out osteochondrosis; in older horses radiographic examination is useful to identify evidence of previous injury. I prefer intra-articular treatment with hyaluronan and methylprednisolone acetate and consider that any horse showing pain on deep palpation should be treated. If lameness is more severe or a horse fails to respond to treatment, arthroscopic evaluation of the joint is indicated.

Osteochondrosis Osteochondrosis occurs in many joints in QHs and is usually clinically evident before a horse starts training. Osteochondrosis can be career limiting, but some horses are treated surgically and are suitable for racing. Mild lesions may not cause obvious lameness until a horse is racing, and some affected horses race successfully without apparent clinical problems. Osteochondrosis of the stifle and hock usually is diagnosed before training begins. In my practice, osteochondrosis of the fetlock is the most common form in racing QHs. Osteochondral fragmentation involving the sagittal ridge of McIII or the third metatarsal bone is most common. Fragmentation of the proximopalmar (plantar) aspect of the proximal phalanx also occurs, especially in hindlimbs. Osseous cyst-like lesions occur occasionally in the distal aspect of McIII.

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112

Lameness of the Arabian Racehorse Mark C. Rick

HISTORY OF RACING The Arabian racehorse originates directly from the Thoroughbred (TB) foundation sires of all light- or hot-blooded horses. In the seventeenth century, these TB sires—the Darley Arabian, Godolphin Barb, and Byerly Turk—were imported to England and bred to the Queen’s mares. The Arabian was used originally as a war horse, and although the true beginnings of the Arabian horse are under a shroud of mystery and legend, the consensus is that the Middle Eastern desert Bedouin tribes played a large role in the breeding and early development of the breed. Arabian racing in North America and around the globe is less popular, and the number of races is fewer and the amount of prize money is less compared with TB, Standardbred, and Quarter Horse racing. Throughout the Middle East and Europe, Arabian racing and performance are more deeply rooted than in North America. The popularity of Arabian racing has grown enormously in the United Kingdom in the last 15 to 20 years, with a growing number of professional trainers and jockeys and a progressive increase in prize money, in part because of the high Middle Eastern sponsorship. The Arabian Horse Registry of America, founded in 1908, includes many types and uses. Known for stamina, speed, and elegance, Arabian horses often were bred and raised for showing in halter and performance classes. In the latter part of the twentieth century Arabian horse popularity and breeding selection shifted to criteria based more on aesthetics than athleticism. The Arabian racehorse lineage reflects more athleticism than is found in Arabian show horses. Consistent winners often are more heavily muscled and have stronger hindquarters with a more sloping croup and a lower head and neck carriage than a typical Arabian show horse. Recent influx of new breeding lines has given rise to concern and controversy over the purity of the lineage and the possible infusion of impure Arabian blood. Certain new stallions appear to be much taller and longer, with a body type similar to the modern day TB racehorse. Constant vigilance and careful documentation of lineage is required to preserve the pure Arabian racehorse breed. Arabian racehorses race on the same surfaces, dirt and turf, as TB racehorses. In North America selected meets are held from California to Delaware, Florida to Michigan, Colorado, Texas, and Washington and a few other tracks. Arabian racehorses perform in fair meets, allowance races, claiming races, and futurity nominated stakes races. Racing Arabian horses also compete in the United Kingdom, Poland, France, Russia, and South America and in many Middle Eastern countries. In North America, racing begins on March 1 of the 3-year-old year. Race distances are similar to those for TB races, but the length and configuration of the racecourses vary. Shorter sprint distances, 41⁄2 to 6 furlongs, often are run on the small tracks, whereas the longest race (2 miles) is usually run on a large track. Typically, races are 41⁄2 furlongs to 13⁄4 miles. A sound racehorse may compete as often as every 7 to 10 days, but most are given 2 weeks between races. Because relatively few Arabian racehorses

are raced, lack of entries may mandate racing whenever enough horses are entered to meet race conditions rather than when trainers and owners prefer. Racing in the United Kingdom starts in late April. Until 2001, horses did not race until 4 years of age, but in 2001 a restricted number of races for horses 3 years of age were introduced. These are high-value races and also attract horses trained in France and other European countries. Races range from 5 furlongs to 3 miles.

TEN MOST COMMON RACING-RELATED LAMENESS CONDITIONS The following are the 10 most common racing-related lameness conditions in the Arabian racehorse: 1. Dorsal third metacarpal bone (McIII) disease 2. Superficial digital flexor tendonitis 3. Suspensory desmitis 4. Stifle lameness 5. Tarsocrural osteochondrosis and distal hock joint pain 6. Back pain 7. Proximal sesamoid bone (PSB) fractures 8. Metacarpophalangeal joint lameness 9. Carpal osteochondral fragmentation 10. Lameness of the foot

Dorsal Third Metacarpal Bone Disease Many racehorses trained intensely at speed at a young age experience the sore-shin or bucked-shin complex. Although intense training may not begin until the 3-year-old year and the Arabian racehorse is smaller in stature and weight than its TB counterpart, bucked shins remain a major cause of lameness requiring reduction in training intensity. Trainers are well aware of this problem and often can diagnose it accurately based on clinical findings and the observation of a sore horse, traveling short. A veterinarian usually confirms the diagnosis clinically, but in some horses radiography and occasionally scintigraphy are necessary. With advanced dorsal cortical pain. typical dorsal cortical periostitis or a dorsal cortical fracture is seen radiographically (see Chapter 104). With periostitis comes intense, diffuse increased radiopharmaceutical uptake (IRU), whereas focal IRU is seen in horses with a dorsal cortical fracture (see Chapter 19). However, scintigraphy is used more commonly to diagnose stress-related bone injury and stress fracture of other long bones in Arabian racehorses. Conservative management is preferred with rest, reduction in strenuous training, or return to the layup farm. Pin firing and blistering are not used routinely. Dorsal cortical fractures are rare, but if present, I prefer surgical management using osteostixis (dorsal cortical drilling) or insertion of a bone screw placed in lag fashion in the dorsal cortex. The prognosis is good.

Superficial Digital Flexor Tendonitis Superficial digital flexor tendonitis (bowed tendon) is common and occurs from a combination of training overload and fatigue. Occasionally, horses run uphill at the end of a

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race, and superficial digital flexor tendonitis occurs commonly under this condition. Sudden changes in track surfaces or training conditions are associated with an increased incidence of tendonitis. Severe tendonitis usually is recognized by the trainer, because swelling and pain are present during palpation. More subtle swelling and pain are detected during careful palpation by a veterinarian. Thorough ultrasonographic examination is imperative to confirm the diagnosis. Careful assessment requires proper patient preparation, sedation, clipping and cleaning the leg, and use of a high-quality ultrasound machine and a 7.5 (or greater) MHz linear transducer. Cross-sectional area (CSA) of the tendon and lesion, fiber alignment, and echogenicity of the lesion are evaluated, and any associated pathological conditions such as palmar annular ligament constriction, carpal tenosynovitis, or other soft tissue damage are assessed. Swelling is often mild if horses have been given local and systemic anti-inflammatory therapy and rest. A slight increase in CSA measurement may be the only indication of superficial digital flexor tendonitis, and comparison with the contralateral superficial digital flexor tendon (SDFT) is mandatory. Initial management includes rest, local ice and bandage application, and administration of systemic non-steroidal anti-inflammatory drugs (NSAIDs). Horses with mild or moderate superficial digital flexor tendonitis often are sent to a layup or rehabilitation farm for 3 to 6 months. Follow-up examinations are performed at 2-month intervals to determine quality of the healing and the appropriate time to return the horse to race training. A slow return to training includes progressive walking, jogging, cantering, speed work (breeze), and then racing. Time span and progression depend on maintaining an acceptable ultrasonographic appearance during each incremental increase in stress or exercise level. Tendon splitting and desmotomy of the accessory ligament of the SDFT used separately or concomitantly are successful in horses with with moderate or severe tendonitis. Intra-lesional injections of β-aminoproprionitrile fumarate (Bapten; no longer commercially available) have been used successfully. Prognosis varies with the severity of the injury and the stage of racing when the injury occurred. Because many Arabian horses race as older horses, even stallions and mares, providing up to a year or more of rest is not uncommon, assuming the lesion heals, before returning the horse to race training.

Suspensory Desmitis Forelimb suspensory desmitis is an intermittent problem of many Arabian racehorses early in training. Suspensory desmitis is not considered to be as debilitating or career limiting as it is for TB racehorses. A trainer often complains that the horse is sore, but overt lameness is not present. The differential diagnosis includes bucked shins, superficial digital flexor tendonitis, and metacarpophalangeal joint and carpal lameness. Careful palpation reveals pain and enlargement of the suspensory ligament. Although ultrasonographic examination should be performed to confirm and grade desmitis, this pattern of subtle inflammation and soreness often precedes lesions detectable by ultrasonography. Scintigraphy may be useful but is seldom recommended. Suspensory desmitis is not severe, and most often the finding of body soreness in response to increased training intensity is the only apparent clinical sign. Traumatic disruption of the suspensory apparatus is rare. Horses with suspensory desmitis usually are kept at the track because they do not require or benefit from extensive time off. I recommend 1 to 2 weeks of rest or simply a decrease in training intensity to allow for tissue adaptation. The prognosis for horses with early suspensory desmitis is good if the condition is recognized early and horses are given a period of much reduced work intensity and slow rehabilitation.

Stifle Lameness The most common source of hindlimb soreness is the stifle region. Early in training a horse may become sore and stiff, usually bilaterally. Intermittent upward fixation of the patella is common as in other young sport horses. Stifle soreness is common in young horses shod with flat shoes and training on a soft track. Soft tissues around the stifle become inflamed. Clinical signs include a shortened stride and an unwillingness to extend the stride behind, or actual upward fixation of the patella, with characteristic stifle and hock extension and toe drag. With early detection, horses with stifle region lameness are assumed to have a soft tissue problem and are treated with decreased training and NSAIDs. Occasionally, an internal blister is injected around the patellar ligaments, especially if evidence of upward fixation of the patella exists. If effusion of the femoropatellar joint accompanies the upward fixation of the patella, radiographs should be obtained. Results are usually negative, but some horses have underlying osteochondritis dissecans of the lateral trochlear ridge of the femur. Surgical debridement is recommended, especially if a flap-like lesion exists. Osteochondritic lesions usually are detected early in race training if they are clinically important. Rarely, subchondral bone cysts of the medial femoral condyle are seen. Horses with subchondral bone cysts are treated by rest, injection with corticosteroids, or surgery. If radiographs reveal evidence of osteoarthritis, such as enlargement of the medial tibial plateau, or if ultrasonographic examination reveals flattening, wrinkling, or other change of the medial meniscus, then the prognosis for racing is diminished. If discovered early in training, horses with osteochondrosis and subchondral bone cysts are best managed with arthroscopic surgery. The prognosis for a horse with a sore stifle, ligament laxity, and intermittent upward fixation of the patella is good, assuming a favorable response to alterations in training regimen. Lameness in Arabian racehorses with sore stifles appears similar to that seen in young TBs with tibial stress fractures, but the origin of pain is different. The prognosis for horses with osteochondrosis varies but is poorer if evidence of osteoarthritis exists.

Tarsocrural Osteochondrosis and Distal Hock Joint Pain Tarsocrural osteochondrosis is an occasional cause of hindlimb lameness. If bog spavin is recognized when the horse is a weanling or yearling, arthroscopic surgical removal of osteochondritic fragments usually is performed then. However, horses may arrive at the racetrack or training stable with mild tarsocrural effusion. If lameness is observed, if a horse has a positive response to upper limb flexion, or if moderate effusion is persistent, then radiographs should be obtained. If osteochondritic fragments are found, I recommend arthroscopic surgery and a short (2- to 3-month) period of rest before training resumes. Distal hock joint pain occurs in the Arabian racehorse and is seen most commonly after changes in track surfaces. These horses often do not push off or propel themselves well behind, may refuse to grab the bit or bow the neck, and use the front end to pull ahead, a gait that may lead to secondary forelimb lameness. Clinical signs often are lacking, and an upper limb flexion test may be only mildly positive. Radiographs are often negative, but scintigraphic examination reveals IRU in the distal hock bones.

Back Pain Primary hindlimb lameness causes secondary back pain in most Arabian horses, particularly those with primary lameness of the stifle and hock joints. Often back pain resolves after management of the primary hindlimb lameness. However, treatment of back pain concomitantly allows earlier resolution of both problems. Exercise riders or jockeys may suspect back pain and

CHAPTER 112 often report a sensitivity or soreness over the top line. Horses usually show pain on palpation or when pressure is applied along the back. The back is palpated carefully, and pressure should be applied uniformly and gently. Thermography has been of some value in horses with back pain resulting from a poorly fitting saddle. The saddle can be evaluated thermographically and compared with any warm spots on the horse’s back. Nuclear scintigraphy may reveal IRU in the summits of the dorsal spinous processes. Radiographic examination may confirm overriding of the dorsal spinous processes. However, radiography and scintigraphy are often negative, and back pain is assumed to originate from soft tissues. Nonetheless, if back pain is severe, I suspect a bony source of pain. The back can be evaluated by ultrasonography, dorsally or rectally, for myositis, nerve root impingement or enlargement, and osteophytes associated with the vertebral articulations.

Proximal Sesamoid Bone Fractures PSB fractures do occur in Arabian racehorses but are less common than in TBs. Clinical signs, management, and prognosis are similar to the TB racehorse (see Chapter 37). Other fractures, such as mid-sagittal fractures of the proximal phalanx and condylar fractures of the distal aspect of McIII, are rare in North America. However, in the Middle East both medial and lateral condylar fractures of McIII occur.

Metacarpophalangeal Joint Lameness and Carpal Osteochondral Fragmentation Osteochondral fragmentation or chip fractures of the carpal and metacarpophalangeal joints occur in Arabian racehorses but less frequently than in TBs and Quarter Horses. Smaller body size, a more gradual training regimen, and racing older horses likely account for the difference in incidence. Early signs of arthrosis without chip fracture resolve quickly, with minor interruption in race training. The diagnosis of fetlock or carpal osteochondral fragments is straightforward. Arthroscopic surgery to remove osteochondral fragments is well accepted and successful. The prognosis depends on location, size, duration, previous treatment, and amount of associated cartilage damage. Horses with acute osteochondral fragments with only mild cartilage damage have a good prognosis. The decision for surgery often is based on economic factors. Proliferative synovitis (villonodular synovitis) and associated fragmentation of the dorsal, proximal aspect of the proximal phalanx occurs in the young Arabian racehorse. Horses have characteristic signs of effusion and a noticeable dorsal swelling. Dorsal swelling can be insidious and go unrecognized early in the disease process. Plain radiographs often reveal soft tissue swelling on the dorsal, distal aspect of McIII and osteochondral fragments of the proximal phalanx. Radiolucent

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changes of McIII are seen in horses with severe proliferation. Ultrasonographic examination usually reveals enlargement of the dorsal synovial pad. I recommend arthroscopic evaluation, removal of osteochondral fragments, and debridement of the synovial pad with a 5.2- or 3.4-mm suction punch (Dyonics; Andover, MA). In older Arabian racehorses, chronic osteoarthritis of the metacarpophalangeal joint is recognized. The trainer complains of poor performance or racing below previous levels. The metacarpophalangeal joint is enlarged from effusion or fibrosis and is warm. Horses usually respond positively to lower limb or fetlock flexion tests. Comprehensive radiographic examination should be performed. Radiographic evidence of osteoarthritis, such as marginal osteophytes of the PSBs and joint space narrowing, enthesophytes at capsular attachments, and soft tissue thickening often are seen. Osteoarthritis of the metacarpophalangeal joint is seen frequently without osteochondral fragments and appears to be related to chronic wear and tear. In some horses osteoarthritis can be managed by judicious use of intra-articular medication, but the prognosis for return to previous performance levels is guarded.

Lameness of the Foot Although Arabian horses are alleged to have solid foot structure, they do get sore feet. Long-toe, low-heel conformation is not common. Arabian horses are protected from some of the lameness conditions of the feet simply because of small body size and weight. Sore feet develop after a fast workout or race on a hard, packed racetrack. Trainers often recognize signs, and the condition is managed using ice baths, NSAIDs, and 3 to 4 days of rest.

PROCEEDING WITHOUT A DIAGNOSIS Occasionally, lameness is suspected but cannot be pinpointed. Horses with such lameness are characterized by a drop in performance, increase in race times, a subtle gait change, refusing to switch leads, a drop in class, or acting sore, but no clinical signs are observable. In this situation, I usually recommend a whole body scintigraphic examination, but correlating findings with clinical signs is often difficult. Comprehensive evaluation for poor performance considers not only a musculoskeletal problem but also cardiovascular and muscle abnormalities. Arabian horses may be more fragile and highly strung than other racehorses, and some trainers attribute poor performance to this portion of the horse’s personality. Under certain circumstances the Arabian racehorse may not endure hard training or racing.

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National Hunt Racehorse, Point to Point Horse, and Timber Racing Horse Sue J. Dyson, Rob van Pelt, Kevin Keane, Alastair Nelson, James Wood, and Anthony Stirk

DESCRIPTION OF THE SPORT For as long as horses have been domesticated and ridden, they have been raced. The oldest record of racing in Britain shows that the Romans used to race their horses in Chester. Subsequently, little is known about any organized horse racing during the Middle Ages, but by about 1150 racing had become established at Smithfield, a horse market, where horses were tried and sometimes raced before sale. By the early part of the sixteenth century, racing had returned to Chester, where the prize for the winner in 1511 was a silver bell. All of these races were on turf with no obstacles to negotiate. At about the same time that horses were competing for the Chester bell, fox hunting (rather than hunting deer or wild boar) started to become established and rapidly increased in popularity. One reason for this may have been the changing agricultural landscape as more and more land was enclosed, providing natural obstacles for those following the hunt to jump. Inevitably, rivalry developed between those who regularly followed fox hunts across country as to who had the fastest horse, and a new sport was born, known as steeplechasing. The origin of the name is simple. Because no courses were defined over which the races could take place, the participants had to race from one church to another, using the high church steeple toward which they were heading as a landmark. The riders could choose their own route and had to jump a variety of fences such as hedges, banks, walls, timber fences, and brooks during the course of the race. The first steeplechase of this type was held in Buttevant in Ireland in 1752, when two neighbors raced between Buttevant church and the St. Leger church, a distance of 41⁄2 miles (7.2 km). After a time this new sport was formalized, with specially constructed courses, which allowed more participants to take part and more spectators to watch. The first such organized race meeting in Britain was held at St. Albans in 1830. The Grand National was first staged in 1839, the National Hunt Steeplechase followed at Market Harborough in 1859, and the first meeting at Cheltenham (Prestbury Park), arguably the best known modern jump racing venue, was in 1898. As the sport developed, regulating it became important, but the Jockey Club, which had been regulating flat racing since the mid-eighteenth century, regarded the new sport with suspicion. Accordingly, a separate National Hunt Committee was established in 1866 and continued to run jump racing until 1969, when it and the Jockey Club merged to bring all racing, on the flat and over jumps, in Britain under one governing body. The National Steeplechase Association oversees racing over fences in the United States. Modern National Hunt racing now consists of several categories, all run on turf on clockwise and counterclockwise courses. Horses run under similar rules in the United Kingdom, Ireland, and France. Elsewhere in Europe, racing over fences takes place but on a much lower scale. Most races

are hurdle races or steeplechases, but some races run over more natural obstacles remain, some over exclusively timber fences and some, called National Hunt flat races, that are run without obstacles. Apart from the fences, three major differences exist between National Hunt and flat racing, which are important in the epidemiology of the injuries that may occur in the different sports. These differences are the race distance, the age of the horses, and the weights of the riders. All National Hunt races are more than a minimum of 2 miles (3.2 km) compared with the minimum distance of 5 furlongs (1 km) on the flat, and the horses are at least 3 years old. Forty percent of National Hunt Flat races involve horses of 4 years of age, a slightly higher percentage are 5 years of age, and less than 20% are 6 years of age or older. Most horses competing in flat races are 2 or 3 years old, although for horses over the age of 10 to race in National Hunt races is not unusual, especially in steeplechases. Finally, National Hunt horses carry between 133 and 175 lb (60 to 79 kg), considerably more weight than flat horses. Hurdle races are held over fences smaller than those encountered in steeplechasing. In Britain, most hurdles are based on the simple portable fences used to create temporary pens for sheep. They are usually 72 inches (1.83 m) wide and must be not less than 42 inches (107 cm) from top to bottom bar and constructed of ash or occasionally oak. Several hurdle sections are placed end to end to produce an obstacle that must be at least 30 feet (9 m) wide. Each hurdle section consists of two uprights with pointed legs that are driven into the ground and five horizontal rails, between which is interwoven birch or another suitable material. Gorse, which is durable but has sharp thorns, is not permitted. The hurdles must be driven into the ground at an angle of 62º so that the top bar is set back 20 inches (51 cm) from the vertical, and the effective height of the hurdle is 37 inches (94 cm). All of the exposed timber parts must be padded with a minimum of 1⁄2 inch (1.3 cm) of highdensity polyethylene or closed cell foam rubber (Fig. 113-1). Timber hurdles have the advantage that if a horse misjudges the fence and does not jump it cleanly, the hurdle gives way on impact. Old style hurdles were not padded as well as the modern versions and occasionally led to lacerations on the dorsal aspects of the hindlimbs, which could be extensive with degloving injuries of much of the metatarsal region. These injuries have been virtually abolished by the new padding. In countries other than Britain and Ireland, timber hurdles are replaced by fences that look like small versions of steeplechase fences. Such fences also are seen on a small number of racecourses in Britain, and proponents of these types of fences argue that they provide a better introduction to racing over obstacles for horses that ultimately are intended to be steeplechasers. This may be true, but only 35% of horses that run over hurdles convert to steeplechasing, indicating that hurdle

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A hurdle race. The jump of the leading horse, which has almost run through the hurdle, is awkward, the hindlimbs are positioned asymmetrically, and the horse’s back is hollow.

Fig. 113-1

racing has become a specialty sport that draws many of its participants from horses that have raced previously on the flat. Steeplechases are run from 2 to 41⁄2 miles (3 to 7 km) over fences which, with the exception of those at Aintree over which the Grand National is held, have a standard construction. The course must have at least six fences per mile, one of which must be an open ditch, with the other plain fences. The plain fences must be a minimum of 54 inches high (1.37 m) and constructed of birch, or birch and spruce, in a frame. The use of gorse is not permitted. The base of the fence must be 72 inches (1.83 m) from front to back, with the thickness of the fence at its top not less than 18 inches (46 cm) (Fig. 113-2, A). Plain fences usually have a guard rail on the face of the fence that usually is padded with the same material as the hurdles. An open ditch has similar overall dimensions, but the ditch in front of the fence, which may or may not be dug out, must be at least 72 inches (183 cm) from front to back and be delineated by a takeoff board that is up to 24 inches high (146 cm). Designers of racecourses also, if they wish, may include a water jump in steeplechases. These consist of a smaller fence, up to 36 inches (91 cm) high with a 108-inch (2.74-m) wide water ditch, that must be 3 inches (7.6 cm) deep, on the landing side of the fence. Point to point races (Fig. 113-2, B), named because originally they were run from one point to another, represent the amateur branch of steeplechasing and are restricted to horses that have qualified to race by hunting with a registered pack of hounds. Races for such horses also take place on licensed racecourses and are known as Hunters’ Steeplechases. Some races, notably in France, at Punchestown in Ireland, and at Cheltenham in Britain, are run over more natural obstacles, including banks and growing hedges. Timber races are held over upright (United States) or sloping (Britain) post and rail fences (Fig. 113-3). To make the obstacles less dangerous, the top rails may be sawn through so that they will knock down if they are hit hard. Finally, National Hunt flat races are staged for horses that have not run previously on the flat and are at least 4 years old.

The races are intended to teach horses to acclimatize to the environment of a racecourse and the rigors of a race, without the additional hazard of obstacles. They also provide a way of demonstrating a horse’s ability, so that it can be sold. Colloquially, National Hunt flat races are known as bumpers, because originally they were restricted to amateur riders, and the combination of inexperienced riders and horses led to their pejorative nickname.

NATIONAL HUNT HORSES British and Irish National Hunt horses may be Thoroughbreds, which are registered in the General Stud Book, or nonThoroughbreds that are in the Non-Thoroughbred register. Many top-quality French jumping horses are of the Selle Français breed. Horses are started in jump racing by one of two routes. They are raced on the flat at 2 or 3 years of age before moving on to hurdling and possibly to steeplechasing, or they are bred specifically for National Hunt racing. Red Rum, who won the Grand National on three occasions, is an example of a horse that started racing in flat races as a 2-year-old. In general, however, horses that graduate from the flat tend to be restricted to hurdle races, and this is why only 35% of horses that race over hurdles go on to race in steeplechases. Steeplechasers, however, tend to be bred for that particular type of racing and are usually bigger framed Thoroughbreds compared with flat racehorses. Breeding steeplechasers is less straightforward than breeding for flat races, because most steeplechasers are geldings, meaning that it is unlikely that males can be chosen based on racecourse performance. Finding performance-tested mares also is difficult, because the average age of steeplechasers is the oldest of all racing categories, and by the time a mare has proved her ability, she may be past her breeding prime. Therefore most stallions that are popular as sires of steeplechasers are horses that have shown stamina on the flat and then prove to sire successful progeny. Many mares

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A

B

A, A steeplechase race in France. B, A Point to Point race. The fences are smaller than in steeplechase races, and the amateur jockeys tend to be less well positioned.

Fig. 113-2

that are used to breed steeplechasers are chosen because of pedigree rather than performance. Once foaled, many horses destined for steeplechasing are left unbroken until 3 or 4 years of age, when they are often sold as National Hunt stores intended to start a racing career at 4 or 5 years of age. This traditional system has been used for many years and could be said to have stood the test of time. However, recent preliminary research suggests that horses benefit from an early introduction to regular exercise and from early racecourse experience, and this may reduce the risks of injury.

TRAINING NATIONAL HUNT HORSES At its simplest, training involves conditioning the cardiovascular, respiratory, and musculoskeletal systems of horses to

tolerate maximal exercise. The skill of the trainer is to exert the horse sufficiently to achieve this while avoiding physical injury and without inducing an aversion to hard work. Human athletes, being motivated to succeed, tolerate extreme discomfort during training to achieve their goals. Horses have to be encouraged to exercise and never to anticipate that the result of exercise will be discomfort or pain. Horses that move to National Hunt racing from flat racing receive the basic conditioning as yearlings and young 2-yearolds. Store horses (horses bred specifically for National Hunt racing), however, may do little regular exercise until they are virtually skeletally mature at 4 years. Because they are older, thinking that they require less time to adapt to exercise is tempting, whereas the reverse may be true. It is therefore essential that early preparation is graduated gently and that early signs of failure to adapt, such as sore shins or joint effu-

CHAPTER 113

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Fig. 113-3

937

A timber race. The horse is jumping well, and the rider is in good balance.

sions, are noted and training intensity adjusted. If clinical signs go unrecognized or ignored, more serious skeletal defects may develop, such as stress fractures of the tibia, humerus, or pelvis, which may precede catastrophic fractures on the gallops or racecourse. Traditionally, store horses spent at least 6 weeks walking and trotting on quiet roads and tracks before they commenced any faster work. This initial slow preparation has now been abandoned by many trainers, partly because of the difficulty of finding a suitable safe, quiet environment and partly because of the economic pressure to see the horse on the racecourse. Most trainers of National Hunt horses now use a simple adaptation of interval training over distances of about 1000 m, almost invariably up an incline that may be steep. An average morning workout would be an initial slow warm-up, followed by two brisk canters up the incline on an easy morning, alternating with three faster ascents on a work morning. One of the most important aspects of training National Hunt horses is teaching them to jump appropriately. Hurdle races are conducted at a fast pace, and some trainers believe that horses that jump the obstacles without touching them and with the same action as a show jumper, use energy unnecessarily and concede ground to rivals who jump low and flat. This is possible because the timber hurdles give way if the horse hits them, although the ease with which they do this depends on the ground into which the legs of the hurdles are driven. Once horses have acquired this style of jumping, some trainers argue that the horse finds it difficult to jump the larger, more solid, steeplechase fences. This accounts for the relatively low number of horses that make the transition from hurdling to steeplechasing and the demand in Britain by some trainers for a brush hurdle that, although relatively small, has to be jumped with care. Specialist steeplechasers are encouraged to jump much as horses intended for other disciplines that involve jumping, and they jump low poles and logs, with and without a rider, before progressing to larger obstacles. However, the amount of training carried out over fences by steeplechasers is proportionately much less in the United Kingdom and Ireland than for event horses or show jumpers.

RACING NATIONAL HUNT HORSES Jump racing developed as a winter sport, probably originally because of the connection with fox hunting, which also is conducted during the winter months. However, jump racing is now held in Britain throughout the year, although those courses that hold summer jump meetings are required to ensure by artificial irrigation that the ground conditions are kept no worse than good to firm. This is because epidemiological studies have shown that firm ground conditions are more likely to be associated with serious injuries. The reason for such a relationship is complex. It is probably related to the speed at which the horses travel, but other complex factors influence the interaction of the horse’s foot with the ground under various conditions, some of which are related to ground hardness, and these require further research and elucidation. Jump racing remains seasonal, however, because the major races take place between November and March, and many horses spend a few weeks turned out during the summer. Seasonal racing influences injury management, because if a horse sustains a significant injury in, for example, late February, the owner or trainer applies pressure for the horse to be ready for the next season, that is, to resume training by October of the same year. Horses are trained by individual trainers spread throughout the United Kingdom, Ireland, and France who may travel long distances to compete. Therefore any single veterinary surgeon usually does not deal with more than 4 or 5 trainers and their horses. At race meetings the horses are subjected to pre-race veterinary inspections, and each race is monitored carefully by veterinary surgeons driving on the outside of the track alongside the race and a veterinarian observing the entire race from an appropriate vantage point. Point to point races are held between January and June. Point to point racing is an amateur sport, raced over obstacles that are smaller and softer versions of the steeplechase fences on licensed racecourses. Some horses that perform well in Point to Points successfully graduate to steeplechasing, and this route to steeplechasing is chosen by some owners in preference to hurdle racing, possibly after one or more National

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Fig. 113-4

A faller at a Point to Point race. Note the extreme position of the hindlimbs.

Hunt flat races. While National Hunt horses run on average between four and five times per year, Point to Point horses may run more frequently during the season, because the race meetings are usually held at weekends. However, the average number of starts per Point to Point horse in 2000 was only three. Because of the two distinct sources of horses that enter National Hunt racing, a wide variety of injuries are seen, ranging from injuries related to beginning training to degenerative injuries associated with overuse. In addition to the injuries sustained while the horse is in training, a National Hunt horse is more prone to injury after a fall than is a flat racehorse (Fig. 113-4). It is also important to be aware that horses that are skeletally mature when they begin training (4- to 5-year-old store horses) still suffer from the same pathophysiological processes that lead to stress fractures, albeit in different sites from the 2- or 3-year-old Thoroughbred. Because National Hunt racing continues throughout the year, the going under foot (footing) can vary and both extremes of soft and firm going place the National Hunt horse under extra stress from injury. A substantially higher death rate occurs in National Hunt racing compared with flat racing. In a retrospective analysis of data from all starts between January 1990 and December 1999, 2015 deaths were recorded on racecourses from 719,099 starts.1 The death rate per 1000 starts was substantially higher in steeplechasers (6.7; 34.5% of the total) and hurdlers (4.0; 43.4% of the total) compared with flat racehorses (0.9; 18.8% of the total). Spinal injuries occur much more frequently in hurdlers (19% of all hurdle deaths) and steeplechasers (23% of steeplechase deaths) compared with flat racehorses (1% of flat racehorse deaths). Tendon breakdown injuries resulting in humane destruction at the racecourse were also substantially higher in hurdlers (20% of hurdler deaths) and steeplechasers (14% of all steeplechase deaths) compared with flat racehorses (8% of flat racehorse deaths). Risk of mortality was associated with a number of variables. With steeplechase horses a higher risk occurred in horses that started steeplechase racing at 8 years of age or older. The weight carried was also influential, with horses carrying more than 70 kg minimum weight being more at risk.

Races longer than 4 miles had a higher risk than shorter races. Heavy going, resulting generally in slower speeds, reduced the risk. Good to firm or hard going increased the risk of mortality in hurdlers and steeplechasers.

TIMBER RACING Timber racing is considerably more popular in the United States than in the United Kingdom and is more structured. Novice or stakes horses compete only against each other, with greater prize money for stakes races, the most valuable being the Maryland Hunt Cup. The most prestigious race in United Kingdom is the Marlborough Hunt Cup. Both of these races are open only to amateur jockeys. Timber racing horses often have raced previously on the flat or over hurdles, are usually 6 to 12 years of age, and may have injuries from earlier racing.

TRACK SURFACE OR TRAINING SURFACE AND LAMENESS The surfaces and terrain over which horses train vary extremely because the trainers are dispersed widely geographically. Much of the work is done on grass, but fast work often is done on all-weather purpose built gallops. Many horses hack up to a mile to and from the gallops, ensuring good warm-up and warm-down. However, the standard of maintenance of the gallops varies. Poor gallops with an inconsistent surface varying from soft to deep may increase the risk of tendon injuries or predispose horses to stumbling and accidents such as third carpal bone fractures. Many trainers are based in areas of chalk downland (natural rolling hills with a chalk subsoil), which drains well, but the large number of flints (sharp stones) in the soil may result in a high incidence of bruised soles or sole punctures unless the horses have wellconformed feet. The steepness of the terrain over which the horses do fast work may influence injury. An increased number of pelvic fractures was noted after a new gallop was laid, the last section of which was up a steep incline (R.v.P.).

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• National Hunt Racehorse, Point to Point Horse, and Timber Racing Horse

Fig. 113-5

939

Horse No. 12 is about to be brought down by a fallen horse and jockey.

The influence of falls on the nature of injuries is substantial. Most falls occur on landing over a fence. Falls may result from the horse or jockey making a jumping error, from interference by another horse still in the race, or from a loose horse that had previously unseated its rider. The fall of one horse may result in the fall of one or more other horses (Fig. 113-5). Thus injuries may result from the fall and impact with other horses. Falls may result in fatal fractures of the cervical or thoracolumbar vertebrae. Rib fractures usually result from a fall and may cause severe lameness and or respiratory signs. Other fractures seen commonly, usually resulting from a fall, include scapular, radial, and humeral fractures; fractures of the accessory carpal bone; and fractures of the lateral malleolus of the tibia. Major muscle ruptures, especially in the hindlimbs (e.g., semimembranosus, quadriceps, or adductor) also usually result from a fall. Rupture of fibularis tertius may occur if the horse falls with forced hyperextension of the hock. A significant statistical correlation exists between certain factors and the incidence of injury on racetracks: • Increased firmness of the going results in an increased injury rate in all forms of National Hunt racing. • Increased incidence of injury on firm ground is further increased by increasing the length of the race. • In hurdle races run over more than 21⁄2 miles with only a few obstacles (6 to 8), the casualty rate increases compared with the same distance with nine or more fences. • Races ridden by amateur riders carry a higher risk of serious injuries. Flexor tendon lacerations frequently are sustained as horses race over fences and generally occur on the palmar aspect of the metacarpal region, proximal to the proximal sesamoid bones (PSBs). It is important to recognize that the site of a skin laceration may not coincide with the site of a tendon laceration. Some important injuries occur more commonly during racing than training. Luxation of the superficial digital flexor tendon (SDFT) from the tuber calcanei sometimes occurs. Rupture of the musculotendonous junction of the superficial digital flexor muscle is an unusual injury, but is an important

injury in steeplechasers. Superficial digital flexor tendonitis is common in National Hunt horses, and recurrent injuries may result in complete rupture of the tendon.

CONFORMATION AND LAMENESS With an increasing proportion of National Hunt horses starting training earlier, and running first on the flat at 3 years of age and then over hurdles at 4 years of age, the trend has been toward using smaller, lighter-framed horses. Although such horses are not necessarily more prone to injury, they seem less able to cope with deep, holding going often encountered in the winter months compared with the more traditionally bred rangy National Hunt store horses, which are often rather late maturing. For a National Hunt steeplechaser or hurdler to race until 10 years of age is not uncommon, so the racing career is considerably longer than for a European flat racehorse. Horses should be well balanced and proportioned, with good feet and adequate bone for body size and weight. Horses with back-atthe-knee conformation, carpus valgus, offset knees, or substantial toed-in or toed-out conformation particularly maybe predisposed to forelimb problems. A long back may be associated with an increased risk of back problems. A horse with straight hocks or long, sloping hind pasterns may have an increased risk of hindlimb lameness.

THE TEN MOST COMMON CAUSES OF LAMENESS The following are the 10 most common lameness conditions of hurdlers, steeplechasers, and Point to Point horses: 1. SDFT injuries 2. Suspensory ligament (SL) injuries 3. Lameness associated with the carpus 4. Lameness localized to the hocks 5. Lameness associated with the pelvis

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6. Lameness localized to the feet 7. Fractures of the third metacarpal (McIII) and third metatarsal (MtIII) bones 8. Lameness localized to the metacarpophalangeal joints 9. Traumatic injuries, particularly of the back and neck, after falls 10. Back problems The following are the 10 most common lameness conditions of timber racing horses: 1. Superficial digital flexor tendonitis 2. SL desmitis 3. Osteoarthritis of the distal hock joints 4. Distal sesamoidean desmitis 5. Osteoarthritis of the metacarpophalangeal joint 6. Soft tissue trauma of the stifle 7. Interference injuries during racing 8. Timber shins 9. Fracture of the patella 10. Fracture of the accessory carpal bone

LAMENESS EXAMINATION Diagnosis of lameness starts with a full history, which should include stage of training, because, for example, a 6-year-old store horse starting training is as susceptible to stress fractures as an immature athlete. The clinician should establish whether the horse has run recently. Is the lameness of recent onset, or is it a chronic problem that has been getting progressively worse? Some trainers request advice as soon as lameness is recognized, whereas others may restrict the horse to light work and seek veterinary advice only if lameness persists. Some trainers treat a lame horse with phenylbutazone. Many trainers are happy for horses to come out rather short, shuffly, and stiff and warm up to move more freely; however, inevitably more overt lameness usually supervenes or a back problem develops secondarily.

Fig. 113-6 neck.

It is important to determine if the horse has had any time off recently with the present trainer or a previous trainer that may suggest a previous injury. There may be a history of warmth associated with the palmar metacarpal region which, if the horse has been subsequently rested, may not be obvious on clinical examination. Does the horse have any history of trauma? Jumping history is also important: did the injury occur while the horse was schooling over fences or in a race? Did the horse fall or collide with another horse (Fig. 113-6)? Does the lameness improve with rest or with work? If the horse had a history of a fall, it is important to establish how the horse fell. Did the horse turn a full somersault and land on its pelvis and develop lameness thereafter? A pelvic injury should be suspected. Did the horse fall at the end of a 3-mile race on heavy going and lay winded? Information from the racecourse veterinarian may be particularly useful. If a horse has a history of poor jumping performance, trying to establish if the horse has ever been a good jumper over hurdles or fences is worthwhile. Many of these horses are lame. The veterinarian needs to find out how the horse is jumping. Does the horse stand off the fences or jump flat? If a horse does not want to take off, it may have a hindlimb problem. If the horse jumps flat, it may have a back problem. If the horse is reluctant to land, it may have a forelimb problem. If a horse is presented for evaluation for poor performance, it is important to try to assess the orthopedic component. About 50% of horses with a complaint of poor performance are lame. When did the horse last race and over what ground conditions? Did the jockey make any comments when he dismounted? Has the horse coughed? Is rectal temperature routinely monitored? Routine hematological examination and measurement of fibrinogen, comparing results with a baseline for that horse, are useful for detecting systemic abnormalities. Endoscopic examination of the upper airways and trachea, combined with a tracheal wash, are useful screening tools to eliminate a respiratory component to the problem.

A fall at The Chair at the Grand National. The horse pitches steeply and lands on its

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The clinical examination does not differ from a routine lameness evaluation of any other type of horse, but because many horses have chronic problems with which they have been living until more obvious lameness supervened, the entire horse should be assessed, not just the postulated lame limb. In view of the high incidence of superficial digital flexor tendonitis and suspensory desmitis, particular attention should be paid to the palmar metacarpal soft tissues. If the horse has a history of a fall while jumping, particular attention should be paid to the neck, back, and pelvic regions. A thorough clinical examination may reveal palpable abnormalities in the palmar metacarpal region, evidence of effusion, or pain on flexion of a particular joint. Skeletal pelvic asymmetry or muscle wastage over the quarters also may be evident. Back and pelvic reflexes and the tone of the back and pelvic muscles should be assessed. Is any evidence of guarding apparent? Abnormal shoe wear may give clues about which limb or limbs are lame, which is otherwise not always easy to determine in a horse moving short because of pain in several limbs. Dynamic examination at the walk and trot in a straight line, followed by flexion tests, should be followed by examination on firm and soft going on the lunge at the trot and canter. The horse should be turned tightly to the left and to the right. If a history of a fall exists, a complete neurological examination should be performed. If a horse is lame after a recent fall, the investigative approach depends on the degree of lameness and the rate of improvement. A horse with a pelvic injury is usually very lame initially, although lameness associated with an ilial wing fracture usually improves substantially within 24 hours. Lameness associated with an ilial shaft fracture is usually persistent, and the horse remains extremely lame. These horses should be crosstied, assuming the horse’s temperament is suitable. Some ilial wing fractures can be detected with ultrasonography, but the diagnosis of others requires nuclear scintigraphy. Nuclear scintigraphy may give false-negative results if done before 5 to 7 days after injury. If a horse shows only mild to moderate lameness after a recent fall, the horse generally is allowed rest for 7 to 10 days and is then re-assessed, and only if lameness persists is further investigation carried out.

DIAGNOSTIC ANALGESIA If no obvious cause of lameness is apparent, then diagnostic analgesia is performed, but no particular differences in approach exist for this type of horse. However, if clinical signs suggest an intra-articular problem, such as synovial effusion and pain on passive manipulation of a joint, then intra-articular analgesia of the suspect joint may be performed first. If intra-articular analgesia is carried out, clipping a small area is preferred, but some trainers are reluctant to allow this, and provided that the hair coat is not excessively long, a timed 5-minute surgical scrub is performed before injection. If a fracture is suspected based on the history or clinical signs, nerve blocks are not performed. A horse that pulled up lame on the gallops or finished work and then became severely lame while walking home may have a stress fracture. Stress fractures of McIII and MtIII and the tibia are common. If a stress fracture is suspected, the horse is examined radiographically or scintigraphically. If soft tissue swelling is identified clinically, then ultrasonography is performed routinely as the next diagnostic step.

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examination. Some stress fractures are difficult to identify radiographically, and if a fracture is suspected on clinical grounds, radiographic examination is repeated 10 to 14 days later. If the clinician suspects an abnormality of the palmar metacarpal soft tissues, an ultrasonographic examination should be performed. In view of the high incidence of bilateral lesions, both limbs should be examined routinely. A systematic approach is essential, focusing on the SDFT, deep digital flexor tendon, and SL in turn. It is almost invariably necessary to clip the metacarpal and metatarsal regions to achieve satisfactory image quality, because most National Hunt horses have thick guard hairs. However, satisfactory images of the pelvis usually can be obtained after washing with chlorhexidine for about 10 minutes, soaking with alcohol, washing off (to avoid alcoholinduced damage to the transducer), and liberal application of coupling gel. Transverse and longitudinal images of the metacarpal and metatarsal regions are required to gain a full appreciation of the severity of injury. An injury index giving a quantitative assessment of damage can help in communication with trainers and may help to convince them of the significance of an injury associated with only mild clinical signs. Each structure should be evaluated sequentially from proximally to distally at predetermined measured intervals (4 or 5 cm) distal to the accessory carpal bone or examining each zone (see Chapter 17). Crosssectional area (CSA) or circumferential measurements are made at comparable sites in each limb. Measurement of the size of damaged fibers is also useful. One author (R.v.P.) describes the severity of a core lesion by multiplying the percentage of CSA of the tendon damaged by the length of the lesion and by the percentage of the fibers damaged within the injury (assessed visually). For example, a core lesion that occupies 10% of the CSA of the tendon and extends 10 cm proximodistally and is assessed visually as having 75% of the fibers within the core lesion damaged has an index of 10 × 10 × 0.75 = 75. A similar lesion occupying 30% of the CSA has an injury index of 30 × 10 × 0.75 = 225. All images should be recorded routinely for future comparisons. Nuclear scintigraphy is indicated as a screening tool when a lame horse is presented after a bad fall, particularly when a moderate to severe lameness has persisted for more than 3 or 4 days. Scintigraphy also may be indicated if severe, suddenonset lameness occurs with no localizing clinical signs to rule out fracture before a dynamic workup is contemplated. Scintigraphy often is more rewarding in horses with acute injuries than those with chronic lameness. Scintigraphy usually can be targeted to specific areas such as the pelvis or both hindlimbs unless the horse has lameness involving several limbs. During evaluation of the pelvis, radioactive urine in the bladder can confound interpretation. The use of furosemide may help, but this drug may make the horse fidgety, and catheterization of the bladder, followed by flushing with warm water, may be preferable.

PROCEEDING WITHOUT A DIAGNOSIS National Hunt horses have a longer career than flat racehorses, and less prize money is available to be won. Therefore the pressure to get a horse sound quickly often is less, and many trainers accept resting the horse if a diagnosis cannot be achieved by the techniques described previously. However, an attempt to reach a diagnosis always should be made.

IMAGING CONSIDERATIONS

SHOEING CONSIDERATIONS AND LAMENESS

Radiography is performed routinely using standard radiographic projections. Special views at different angles may be required for demonstrating specific lesions, based on the preliminary

Most National Hunt horses train and run in light steel shoes with one toe clip in front and two side clips on hind shoes. Some trainers change to a hind shoe with a single toe clip for

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racing. Good shoeing is essential. Given the high incidence of foot problems causing lameness, a good relationship with a skilled farrier is invaluable. Poor foot conformation, especially low collapsed heels, may predispose the horse to superficial digital flexor tendonitis. Bar shoes combined with a rolled toe often are used for horses with collapsed heels. If a foot is conformed poorly, the risk exists of shoes being pulled off repeatedly in training, particularly if the branches of the shoe are set too far medially or laterally.

DIAGNOSIS AND MANAGEMENT OF LAMENESS IN STEEPLECHASERS, HURDLERS, AND POINT TO POINT HORSES Superficial Digital Flexor Tendonitis An epidemiological study demonstrated an 86 % incidence of SDFT injuries in National Hunt horses.2 Although most of the injuries occur in the forelimbs, hindlimb injuries also occur. Many trainers routinely assess forelimb SDFTs daily, and some are adept at detecting relatively subtle lesions. Veterinary involvement may enhance these skills. Many, but not all, trainers are keen to have ultrasonographic assessment of suspected tendon injuries. Some trainers tend to ignore suspicious injuries at the end of a season, contrary to veterinary advice. This may be one reason why a peak incidence of tendon injury tends to occur at the beginning of the season when horses start galloping after a short summer break. Other horses may have been kept in training late in the season to get an extra race and may have suffered injury, which may or may not have been manifest clinically. A second peak incidence of injuries tends to occur at the end of the season, perhaps related to races run on faster going. Superficial digital flexor tendonitis is more common in steeplechasers than in hurdlers, but this may reflect the older population of the horses rather than the type of racing itself. The degree of lameness at the time of acute injury may reflect the severity of tendon damage. Horses with acute lesions are managed with aggressive anti-inflammatory treatment for 5 days, including systemic non-steroidal anti-inflammatory drugs (e.g., phenylbutazone and eltenac), with or without a single dose of corticosteroids (e.g., dexamethasone), and cold hosing several times daily. Cold water bandages or cold kaolin is applied to the limbs. Some thin-skinned horses are prone to blistering, so any bandaging must be done with care. Other popular proprietary poultices, such as Animalintex (Robinson Animal Health Care, Chesterfield, UK) and a variety of clay-based preparations, may irritate small unnoticed wounds and are therefore avoided. A first ultrasonographic examination is performed about 7 days after the injury is first recognized. Horses with central core lesions may be treated by decompression, using needle fenestration or a fixed blade. This is performed with the horse sedated and using regional analgesia. Follow-up ultrasonographic examinations frequently are performed 3 to 4 weeks after injury, because the preliminary examination may underestimate the degree of damage because of ongoing enzymatic degradation. This gives a baseline scan for the injury. Many differing views are given on the best management of superficial digital flexor tendonitis in National Hunt horses. Adequately rehabilitating a tendon that was injured late in a season so that the horse can race the following season, without a disproportionately high risk of re-injury, is difficult. Firing remains a popular treatment, and because many owners and trainers are prepared to rest a horse for 12 months after firing, when they would not give such a long convalescent period if rest alone was recommended, this treatment still is carried out widely. Nonetheless, the re-injury rate remains high, so many alternatives have been tried with various

success. These alternatives range from at least 9 months of field rest, intralesional injection of hyaluronan, polysulfated glycosaminoglycan, a phenol derivative, β-aminoproprionitrile fumarate or growth factors, combined with a variety of exercise regimens. Intralesional β-aminoproprionitrile fumarate combined with a strictly controlled exercise program has produced good results in selected horses (R.v.P. and S.J.D.); however, the time for return to racing often is prolonged, in part dictated by the time of injury and the seasonal nature of racing. The average time to return to racing was 17 months. The owner or trainer must be committed to at least 3 to 4 months of walking exercise after treatment, and some horses are unsuited to this temperamentally, unless a horse walker is available. Regardless of the methods of management, a slow, gradual rehabilitation before resuming ridden work seems beneficial. Ideally the horse should be walking on a horse walker daily for 3 months before resuming ridden exercise. The horse can be turned out during this 3 month period. A cage horse walker in which the horse is free and in which the speed can be set manually to encourage the horse to walk briskly is best. Serial ultrasonographic examinations are particularly useful as exercise is resumed, about 1 month after resuming walking, then again before cantering commences, and a third time before fast work commences. Commonly as work intensity increases, small hypoechoic areas develop, especially in areas in which the fiber pattern is not parallel. In some horses these lesions disappear, provided the horse is maintained at the same exercise level, whereas in others a core lesion redevelops, and the trainer should be warned accordingly. The prognosis is related partly to the severity of injury.3 In a follow-up study of 73 National Hunt and Point to Point racehorses, lesions were graded by ultrasonography as mild (160 mm in length). All mildly affected horses returned to training and 63% raced. Fifty percent of horses with a moderate lesion resumed training and 23% raced, but only 30% of horses with severe lesions resumed training, despite up to 6 months longer convalescence, and 23% raced. The mean reinjury rate of those resuming work was 40% in the period of follow-up (9 to 30 months). The type of racing in which the horse is involved may influence the prognosis for return to racing after superficial digital flexor tendonitis. Fifty-one (73%) of 70 hurdlers raced five or more times after desmotomy of the accessory ligament of the SDFT for treatment of tendonitis compared with 39 (58%) of 67 of steeplechasers.4 Cellulitis, skin necrosis, and necrosis of the underlying SDFT are poorly understood conditions that have been recognized in National Hunt horses (S.J.D.) and flat race horses that have run over long distances (>11⁄2 miles) (R.v.P.). Many horses run in boots or exercise bandages, which are removed after racing. Whether exercise bandages would be on long enough to cause pressure necrosis is debatable. The typical history is that a proprietary clay-like substance (Kaolin, IceTite) or commercial poultice (e.g,. Animalintex) is applied to the metacarpal regions after racing, with or without overlying bandages. The applied substance is removed the following day. Clinical signs may be apparent within 24 to 72 hours, with the development of peritendonous edema and serum ooze, progressing to skin slough and slough of deeper tissues, which may take several weeks. The degree of damage varies between horses, and one or both limbs may be affected. One author (S.J.D.) has seen this unassociated with superficial digital flexor tendonitis, whereas another (R.v.P.) often has seen concurrent superficial digital flexor tendonitis. The prognosis depends on the depth of the lesions. One author (R.v.P.) recommends that horses should be thoroughly cooled after

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racing before anything is applied topically to the limbs to minimize the risks of these complications. If a SDFT injury is suspected, then the advice of the course veterinarian should be sought.

Suspensory Desmitis Suspensory desmitis is a major problem in National Hunt horses, especially steeplechasers and Point to Point racehorses. Injuries of the body or branches occur in forelimbs and hindlimbs, sometimes with a fracture of the distal third of the second (McII/MtII) or fourth (McIV/MtIV) metacarpal or metatarsal bones, apical or abaxial sesamoid fractures, or sesamoiditis. Proximal suspensory desmitis does occur in forelimbs and hindlimbs and is recognized more commonly in hindlimbs, but the true incidence may be underestimated. Body and branch injuries of the SL often go unrecognized until the ligament is grossly enlarged; possibly some of these are cumulative injuries rather than single-event injuries. More careful monitoring of the SLs by regular palpation with the limb not bearing weight may lead to earlier detection of important lesions. The degree of swelling sometimes makes it difficult to palpate accurately the distal end of McII and McIV. Assessment of structural damage is done by ultrasonography in a way similar to that described for SDFT lesions. Lesions are assessed acutely (up to 7 days after injury and 4 to 6 weeks later) to determine the baseline degree of injury. Some of the swelling contributing to the apparent swelling of a SL branch is often a periligamentous reaction. Radiographic examination is necessary to evaluate McII/MtII or McIV/MtIV and the PSBs. Body and branch injuries are associated with a prolonged convalescence irrespective of the way in which they are managed, and returning to racing often takes longer than for a horse with superficial digital flexor tendonitis. The rate of recurrent injury is high. Surgical removal of fractures of McII or McIV (MtII or MtIV) has little bearing on the horse’s final outcome. Conservative management of rest alone, splitting the SL, intralesional injections of β-aminoproprionitrile fumarate, and pin firing have been used with no significant differences in outcome.

Fractures of the Third Metacarpal and Metatarsal Bones The most common long bone fractures in National Hunt horses are condylar fractures of the McIII or MtIII bones. Such fractures often are recognized in hindlimbs and frequently involve the medial condyle and may spiral proximally. Full evaluation of the fracture may require multiple oblique radiographic views of MtIII. Such fractures are more common in hurdlers than in steeplechasers. With prompt surgical treatment by internal fixation the prognosis is good. Compound, comminuted fractures of the distal aspect of McIII and MtIII may occur during racing and may be associated with luxation of the fetlock. These horses have a guarded prognosis for return to racing. Incomplete palmar cortical fatigue fractures of McIII occur commonly, especially in horses older than 4 years of age entering National Hunt or Point to Point training for the first time. Pre-existing sclerosis in the proximomedial aspect of McIII detected when lameness is first recognized in some horses suggests that abnormal bone modeling has existed for some time, subclinically or without clinical signs being recognized. Lesions are often bilateral. Lameness is characterized by the horse becoming lamer the further it trots and then improving if walked a few steps. Usually no localizing clinical signs are apparent, and diagnosis depends on localizing pain to the proximal palmar metacarpal region, and identifying radiographic lesions or scintigraphic evidence of increased bone

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turnover, in the absence of ultrasonographic abnormalities of the proximal aspect of the SL. Treatment of 3 months of rest with a graduated return to work is usually successful, and recurrent injury is unusual. Less commonly transverse stress fractures of the distal metaphyseal region of McIII cause acute-onset lameness. No localizing signs may be apparent, but lameness is alleviated by a four-point nerve block of the palmar and palmar metacarpal nerves. Usually pre-existing callus formation is evident on the distal metaphyseal region of McIII on the dorsal or palmar aspects.

Lameness Associated with the Hock The degree of lameness caused by hock pain varies, and lameness is more commonly unilateral, unlike bilateral lameness usually seen in the flat racehorse. The most common cause is osteoarthritis of the distal hock joints, although traumatic injuries also occur. The horse may adduct the lower limb as the leg is brought forward at the walk and trot. The lameness often worsens after flexion and when the lame limb is on the inside on the lunge. More subtle signs of poor jumping or back pain may herald a problem originating in the hocks. Lameness most often is alleviated by intra-articular analgesia of the tarsometatarsal joint. It is rare to have to inject the centrodistal joint as well, despite the variable communication between the joints and the fact that osteoarthritic changes seen radiographically often affect both joints. Radiography of the hocks should include four standard views, because radiographic changes may be visible only on one projection. Abnormalities range from mild peri-articular osteophyte formation to osteolysis, with narrowing of the joint spaces, with or without peri-articular new bone. Occasionally, young horses in the first year in training have significant radiographic changes in one limb. The damage was probably present before onset of training and may be associated with collapse of the distal tarsal bones or a traumatic incident earlier in the horse’s life. Care should be taken when interpreting scintigraphic images of the hocks in National Hunt horses. Often areas of increased radiopharmaceutical uptake (IRU) are seen but do not appear to correlate with clinical signs of lameness (A.N.). Treatment of horses with osteoarthritis of the distal tarsal joints usually consists of intra-articular medication of the tarsometatarsal joint with combinations of hyaluronan and corticosteroids. Consideration should be given to chemical fusion of painful distal hock joints in young National Hunt horses. Traumatic injuries involving the hock are common. Injuries frequently sustained after a fall include fracture of the lateral malleolus of the tibia and tearing of the attachments of the collateral ligaments. The lameness associated with lateral malleolar fractures can be mild, and lesions may be missed if radiography is not carried out. Ultrasonography may be more useful than radiography for the early diagnosis of collateral ligament injury. Follow-up radiography some weeks later may reveal some entheseous new bone formation. Horses with these injuries have a good prognosis for a return to racing, although improvement in lameness may be slow. Some debate exists about the optimal management of horses with lateral malleolar fractures: conservative or surgical. Both treatments carry favorable prognoses. Surgical removal is usually easiest by making an incision directly over the fracture fragment(s) rather than by attempting arthroscopic removal.

Lameness Associated with the Pelvis Lameness associated with the pelvis in the National Hunt horse is more likely to result from a traumatic incident than a stress fracture. Falls or poor landings while jumping (see Fig. 113-4) may lead to subluxation of the sacroiliac joint or pelvic fractures. However, ilial stress fractures also occur, especially

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in horses entering training at 5 years of age or older. A strong correlation between pelvic lameness and working horses on loose all-weather surfaces, especially an unmanaged wood chip surfaces and particularly uphill, has been noted (A.S. and R.v.P.). Clinical signs can vary from severe lameness with obvious crepitus to mild stiffness. It is important to examine the pelvis per rectum when pelvic damage is suspected. A horse with an ilial fracture sustained during a fall may be lame initially and improve rapidly within 48 hours. If an ilial wing fracture is non-displaced, the horse could return to cantering exercise before lameness recurs. Muscle spasm may result in significant asymmetry of the tubera coxae in the acute stage, but this usually also resolves within 24 hours. Severe lameness associated with an ilial shaft or acetabular fracture is invariably persistent. Ilial stress fractures may cause only mild clinical signs, and sometimes the most important abnormality is shortening of the contralateral forelimb stride as the horse moves off from standing still. This gait abnormality rapidly resolves. Fractures of the ilial wing involving the dorsal surface often can be diagnosed by ultrasonography, but incomplete stress fractures involving the ventral aspect cannot be seen. Nuclear scintigraphy is invaluable for assessing pelvic pain. With sacroiliac disease IRU in the sacroiliac joint contralateral to the lame limb occurs, in one contributor’s (A.N.) experience. Assessment of pelvic fractures should be delayed for at least 5 to 7 days after injury to avoid falsenegative results. If scintigraphy indicates IRU in the region of the coxofemoral joint, obtaining multiple oblique scintigraphic views is worthwhile to try to assess whether the fracture involves the joint. Other scintigraphic changes seen include IRU at the greater and third trochanters of the femur associated with damage to the insertions of the deep and middle gluteal tendons and the superficial gluteal insertion, respectively. Horses with non-displaced ilial wing fractures have a good prognosis, whereas the prognosis for those with fractures of the ilial shaft or ilial fractures involving the acetabulum is poor.

Back Pain Back pain in the National Hunt horse may be primary or may develop secondary to chronic lameness in one or more limbs and is being recognized with increasing frequency. Nuisance problems include the development of seromas underneath the saddle, which are probably attributable to an ill-fitting saddle and poor riding. Most trainers regularly use a physiotherapist, who may be the first person asked to look at a horse that is not right. Only if the horse fails to respond to one or two treatments, or if the physiotherapist recognizes obvious lameness, is veterinary advice sought. A good working relationship with the physiotherapist is valuable, because without a doubt the rehabilitation and long-term management of horses with chronic back pain can be helped by regular physiotherapy treatment. However, the veterinarian should have responsibility for both the diagnosis and the development of the treatment program. Knowledge of back problems in National Hunt horses has increased greatly with more routine use of nuclear scintigraphy. Thorough investigation of the back is warranted in horses with chronic back pain, a history of jumping awkwardly (see Fig. 113-1), or after bad falls. Physical examination of the back often can be unrewarding concerning specific diagnosis, because the examination may only reveal stiffness and pain on palpation. Underlying problems such as active kissing spines or osteoarthritis of the dorsal articular facets of the vertebrae are common in the National Hunt horse and can be ruled in or out using scintigraphy and radiography. In a horse with an acutely sore back after a fall, scintigraphy can be used to determine if

any bony damage occurred. The clinician should bear in mind that falls may involve more than one horse, and a fallen horse may get shunted (pushed) by one behind. Serious vertebral fractures can produce nothing more than severe stiffness and guarding in some horses after a fall, if the spinal cord itself is not compromised. For example, scintigraphy may reveal intense focal IRU suggesting a fracture in the region of the second or third lumbar vertebra. Radiography may demonstrate an obvious change in orientation of the spinous processes at this level, without being able to demonstrate a fracture. Lateral and dorsal scintigraphic images are useful to identify fractures of the transverse processes of the lumbar vertebrae. Ultrasonographic examination is also useful for identifying some soft tissue injuries such as desmitis of the supraspinous or dorsal sacroiliac ligaments. Horses with traumatic injuries often respond well to prolonged rest combined with physiotherapy. Horses with kissing spines often improve after local infiltration with corticosteroids. Successful management of chronic back pain needs a broader approach. Many National Hunt horses have an inadequate jumping education and poor technique (see Fig. 113-1). Traditionally in the United Kingdom and Ireland, horses learn to jump by loose schooling over small fences; horses are schooled ridden over two or three small fences, once or twice when they are fresh. In France horses often are trained to jump out of deep going, when they are tired, providing a better grounding for racing conditions. The standard of riding of the work riders is often only moderate, and employing some staff with a background of working with event horses or show jumpers may be beneficial. Time should be spent teaching the horse to jump properly. Often more time is available in the summer break period to devote to such problems. Additional work from the field, or keeping the horse in work, or bringing the horse in early should be advised. The horse should be encouraged to work in a round outline by exercising in draw reins to improve the development of the epaxial muscles. The horse can be given a warm-up period on a horse walker before being ridden. Use of a well-fitting hunting saddle rather than a racing saddle should be encouraged. After exercise the horse may benefit from being led home from the gallops rather than ridden.

Neck Lesions Neck trauma usually results from a fall (see Fig. 113-6) and is more common in steeplechasers and Point to Point racehorses than in hurdlers. Neck trauma may result in ataxia or a stiff neck, with or without forelimb lameness, and can cause death. Ataxia may be transient or persistent. Radiographic examination should be performed if ataxia or neck pain and stiffness persist for more than a few days. Fractures in the cranial or mid-neck regions are most common, but occasionally fractures occur caudally, which may be difficult to assess without a fixed, high-output x-ray machine. Nuclear scintigraphy can be helpful in localizing such fractures, but false-negative results in the caudal cervical spine are possible. Horses with persistent ataxia have a guarded prognosis. Most horses with a fracture unassociated with ataxia can return to racing despite residual neck stiffness.

Lameness Associated with the Front Feet Lameness associated with the front feet may vary from a shortened gait to an obvious lameness. The most common causes of foot lameness include solar bruising, corns, and subsolar abscesses. Other commonly recognized causes of foot lameness in the National Hunt horse include pedal osteitis, palmar heel pain, and fractures of the distal phalanx. Palmar heel pain may be caused by bruising of the heel bulbs or may be caused by deeper pain associated with the deep digital flexor tendon or navicular bone, with a much poorer progno-

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• National Hunt Racehorse, Point to Point Horse, and Timber Racing Horse

sis. Horses that train on downland are particularly at risk to bruising the feet or penetrating injuries of the sole caused by flints. The latter may result in infectious osteitis of the distal phalanx. Protective aluminium pads may prevent solar penetrations but do not prevent bruising, because the pad is distorted and puts pressure on the sole if a horse stands on a flint. In horses with chronic lameness associated with foot pain, local analgesia, radiography, and ultrasonography sometimes can be unrewarding or give equivocal results. Nuclear scintigraphy using soft tissue and bone-phase images is sometimes helpful.

Lameness Associated with the Carpus Synovitis and osteoarthritis of the middle carpal joint are common and are treated by intra-articular injection with hyaluronan, with or without triamcinolone. A horse with synovitis may be treated more conservatively than a flat racehorse when the pressure is great to maintain the horse in training if at all possible. With a young National Hunt horse with a career of several years ahead, restricting the horse to walking exercise until clinical signs have resolved fully often is more prudent. Chip fractures of the dorsal border of any of the carpal bones are common and often are associated with pre-existing osteoarthritis. Treatment is by surgical removal of the fragment(s), and prognosis depends on the degree of osteoarthritis; most horses are able to return successfully to racing. Slab fractures of the third carpal bone are also common but are not always associated with obvious clinical signs. Lameness is often mild and associated with only slight effusion of the middle carpal joint. Accessory carpal bone fractures usually result from a fall and are common in National Hunt horses. Most fractures are longitudinal and occur midway between the dorsal and palmar borders of the bone, but less commonly articular chip fractures occur on the proximal or distal dorsal articular margin. The latter must be removed surgically or otherwise severe osteoarthritis ensues. Horses with the more common longitudinal fractures do not require treatment other than prolonged rest. Some fractures heal only by fibrous union, but the prognosis for return to racing is good. Some horses have effusion in the carpal sheath when work is resumed, which responds well to the intrathecal administration of triamcinolone and for which retinacular release is seldom necessary.

Lameness Associated with the Metacarpophalangeal Joint Most lameness associated with the metacarpophalangeal (fetlock) joint is degenerative. Fetlock lameness is often present bilaterally with a shortened forelimb gait, warmth around the joint, and reduction of range of motion. Flexion often exacerbates lameness. Lameness often is improved by intra-articular analgesia of the metacarpophalangeal joint. Radiography may reveal peri-articular osteophytes or a small fragment on the dorsoproximal border of the proximal phalanx. If the proximal sesamoid bones and SL attachments are involved in sesamoiditis, a low palmar or four-point nerve block is required to alleviate lameness. New bone formation and osteolysis may occur on the abaxial surface of the PSBs at the attachments of the SL. This form of sesamoiditis more commonly is associated with damage to the attachments of the SL onto the PSB rather than a primary sesamoid bone disease and is seen much more frequently in National Hunt horses than other types of horses. The condition is related to the stress to which the palmar metacarpal soft tissues are subjected during jumping and galloping. Treatment options include the following: 1. Injection of the fetlock joint with hyaluronan, with or without corticosteroids

945

2. Arthroscopy and removal of any free fragments 3. Blistering the palmar aspect of the fetlock to treat sesamoiditis The prognosis for lameness affecting the fetlock is more guarded in the National Hunt horse than in the flat racing horse but occurs much less frequently.

Other Injuries National Hunt horses seem particularly to lacerations involving the distal palmar (plantar) aspect of the metacarpal (metatarsal) region, which may involve the SDFT or the digital flexor tendon sheath (DFTS), usually resulting from the horse being struck or from penetration by a sharp stone. Such injuries should be treated early and aggressively, especially if the DFTS is involved. With early lavage of the DFTS using an arthroscope, combined with intravenous broad-spectrum antimicrobial treatment for 5 to 7 days, the prognosis is usually excellent unless significant damage of the SDFT has occurred. A high number of complex injuries to the palmar (plantar) soft tissues of the pastern have been seen in National Hunt horses as sequels to previous superficial digital flexor tendonitis in the metacarpal region or as primary injuries. Although injury to one or both branches of the SDFT may occur alone, simultaneous injuries of the oblique and straight sesamoidean ligaments are not uncommon. The prognosis for such injuries generally is guarded.

DIAGNOSIS AND MANAGEMENT OF LAMENESS IN TIMBER RACING HORSES Lameness falls into three groups: acute injury or breakdown after racing, chronic wear injury caused by the horse’s age and length of competitive career, and traumatic injuries caused by interference from another horse or hitting a fence. Eighty-five percent of acute injuries after racing are caused by superficial digital flexor tendonitis and SL desmitis. Many timber horses have had previous SDFT injuries from earlier flat racing. The long courses (up to 4 miles), variable turf quality and terrain, fatigue, and weather conditions predispose horses to injury. Injuries range from small tears to catastrophic breakdowns that may necessitate humane destruction. Regular clinical and ultrasonographic monitoring is useful for detecting subtle changes and for making recommendations about running on specific footing (ground) conditions (K.K.). Once recognized, osteoarthritis of the metacarpophalangeal and the distal hock joints requires management, because increased lameness may be induced by the increased work leading up to a race. Keeping horses as comfortable as possible throughout training is preferable, which may necessitate intraarticular medication 2 to 3 times during a season, using hyaluronan for the metacarpophalangeal joints and hyaluronan and corticosteroids for the distal hock joints (K.K.). Orally administered glucosamine and chondroitin sulfate are used commonly. It is important to keep the horse well shod and to use cold hydrotherapy after strenuous exercise. Traumatic injuries sustained during racing are common, with the hindlimbs particularly vulnerable because of the horse hitting fences at speed. Damage to the quadriceps muscles, peri-articular soft tissues of the stifle, and stifle joint are common, although determination of the severity of injury is usually easiest several hours after a race rather than immediately. Radiographic examination is indicated to rule out a patellar fracture, which requires surgical management. Bruising of the patellar ligaments is common, with or without effusion of the femoropatellar joint, and is treated by drainage of excess synovial fluid and injection of hyaluronan (4 to 6 ml) combined with controlled exercise and non-steroidal antiinflammatory drugs.

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Lameness in the Sport Horse

Timber shin describes firm enlargement of the dorsal aspect of the metatarsal region because of chronic bruising of the long digital extensor tendon, with fibrosis of the tendon and peritendonous soft tissues. Timber shin is unsightly and is not associated with long-term lameness, but recent trauma results in lameness from severe swelling of the leg, with pain on protraction. Injuries sustained by interference from another horse, for example, traumatic heel bulb laceration or strike injuries on the palmar or plantar aspect of the fetlock, are common (see page 939). Injuries also can result from falls, for example, fracture of the accessory carpal bone, or from a galloping horse treading on a faller.

CHAPTER •

REFERENCES 1. Wood J: Unpublished data, 2001. 2. Pickersgill C: Epidemiological studies into orthopedic conditions of the equine athlete, MVM thesis, 2000, University of Glasgow (Scotland). 3. Marr C, Love S, Boyd J, et al: Factors affecting the clinical outcome of injuries to the superficial digital flexor tendon in National Hunt and point to point racehorses, Vet Rec 132:476, 1993. 4. Ordidge R: Comparison of three methods of treating superficial digital flexor tendonitis in the racing thoroughbred by transection of its accessory ligament alone (proximal check ligament desmotomy), or in combination with either intra-lesional injection of hyaluronidase or tendon splitting, Proc Am Assoc Equine Pract 42:164, 1996.

114

The Finnish Horse and Other Scandinavian Cold-Blooded Trotters Kristiina Ertola and Jukka Houttu

HISTORY OF THE BREEDS The Finnhorse is the only original horse breed in Finland. Sweden and Norway also have similar cold-blooded breeds. The Finnhorse has been known for about 1000 years and originally was used for farm and forest work and in the army. The Stud Book of the Finnhorse was founded in 1907 for Draft and carriage horses but is now divided into four parts for racing trotters, riding horses, draft horses, and small pony-type horses. Seventy-five percent of the registered Finnhorses are trotters. The Finnhorse is heavy and well muscled, with a short neck and usually a heavy head. The average height is 155 to 160 cm, but pony-sized Finnhorses exist. Swedish and Norwegian coldblooded horses are slightly lighter and smaller than Finnhorses, with an average height of 150 to 160 cm. Trotting competitions are the main use of Finnhorses. In Scandinavia all harness races are for trotters; there are no pacing races. The first records of trotting races are from 1817, when races were arranged on the ice of the river Aura in Turku. The first races with official timing took place 1862 in Viipuri. In the early years the trotting races were arranged by the state to support and develop horse breeding in Finland. In the first races the distance was 2138 m, and they were on a straight track. The horses raced individually, and prizes were given according to the times. The first official Finnish record was from 1865 by the mare Brita. The average time for 1000 m and was 1.51.3 (1 minute 51.3 seconds, equivalent to a mile in 2 minutes 59 seconds). Today the record is held by Viesker and is 1.19.9 (2:08.5). Betting was first introduced 1928 but developed slowly until the 1960s, after which rapid growth has followed. In Sweden, racing also was started in the early nineteenth century on roads and icetracks. The first permanent tracks were built in the early twentieth century. The first official record in Sweden was in 1829, 1.37.6 (2:37), held by a

Norwegian horse, Sleipner Varg. Today the record is 18.6 (2:07) by a Norwegian stallion, Spikeld. When racing became more popular, Swedish and Norwegian horsemen started trading horses across the border, and the Swedish and Norwegian breeds began to merge together. Today the breeds are genetically alike, and they now are considered to be the same breed. Sweden and Norway have a close collaboration in breeding and racing, and their horses race in the same races. Today the races are held at modern dirt tracks, and in the same events there are separate races for Finnhorses and Standardbreds (STBs). The Finnhorses are allowed to race first at the age of 3 years, but not uncommonly they start racing as late as 5 or 6 years old. They are allowed to race until 16 years of age, and a Finnhorse usually is considered to be best between 7 and 10 years of age. Some stakes races are held for 4- and 5-year-olds, but the main events are for older horses. The biggest event for Finnhorses is the Kuninkuusravit, The Royal Trot, which is held annually in July and August at a different track in Finland each year. The race is one of the major sporting events in Finland, attracting about 50,000 people. Separate races are held for mares and stallions; geldings are excluded. To be allowed to race in the Kuninkuusravit, the horse has to be approved for public breeding and has to be entered in the Stud Book, which requires inspection and approval by a special board. The horses race 3 times in 2 days over distances of 1609 m, 2100 m, and 3100 m, and the final result is based on the total time for all three races. To win the royal title is the biggest honor a Finnhorse can ever get, and the best stallions have won the title 5 times (Vieteri, Vekseli, and Viesker), and the best mares, 4 times (Suhina and Valomerkki). This is a good proof of stamina and endurance, which are typical for the Finnhorse at its best. In Sweden and Norway horses usually start racing at 3 years of age and are allowed to race until the age of 16. Stakes

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PART X

•

Lameness in the Sport Horse

Timber shin describes firm enlargement of the dorsal aspect of the metatarsal region because of chronic bruising of the long digital extensor tendon, with fibrosis of the tendon and peritendonous soft tissues. Timber shin is unsightly and is not associated with long-term lameness, but recent trauma results in lameness from severe swelling of the leg, with pain on protraction. Injuries sustained by interference from another horse, for example, traumatic heel bulb laceration or strike injuries on the palmar or plantar aspect of the fetlock, are common (see page 939). Injuries also can result from falls, for example, fracture of the accessory carpal bone, or from a galloping horse treading on a faller.

CHAPTER •

REFERENCES 1. Wood J: Unpublished data, 2001. 2. Pickersgill C: Epidemiological studies into orthopedic conditions of the equine athlete, MVM thesis, 2000, University of Glasgow (Scotland). 3. Marr C, Love S, Boyd J, et al: Factors affecting the clinical outcome of injuries to the superficial digital flexor tendon in National Hunt and point to point racehorses, Vet Rec 132:476, 1993. 4. Ordidge R: Comparison of three methods of treating superficial digital flexor tendonitis in the racing thoroughbred by transection of its accessory ligament alone (proximal check ligament desmotomy), or in combination with either intra-lesional injection of hyaluronidase or tendon splitting, Proc Am Assoc Equine Pract 42:164, 1996.

114

The Finnish Horse and Other Scandinavian Cold-Blooded Trotters Kristiina Ertola and Jukka Houttu

HISTORY OF THE BREEDS The Finnhorse is the only original horse breed in Finland. Sweden and Norway also have similar cold-blooded breeds. The Finnhorse has been known for about 1000 years and originally was used for farm and forest work and in the army. The Stud Book of the Finnhorse was founded in 1907 for Draft and carriage horses but is now divided into four parts for racing trotters, riding horses, draft horses, and small pony-type horses. Seventy-five percent of the registered Finnhorses are trotters. The Finnhorse is heavy and well muscled, with a short neck and usually a heavy head. The average height is 155 to 160 cm, but pony-sized Finnhorses exist. Swedish and Norwegian coldblooded horses are slightly lighter and smaller than Finnhorses, with an average height of 150 to 160 cm. Trotting competitions are the main use of Finnhorses. In Scandinavia all harness races are for trotters; there are no pacing races. The first records of trotting races are from 1817, when races were arranged on the ice of the river Aura in Turku. The first races with official timing took place 1862 in Viipuri. In the early years the trotting races were arranged by the state to support and develop horse breeding in Finland. In the first races the distance was 2138 m, and they were on a straight track. The horses raced individually, and prizes were given according to the times. The first official Finnish record was from 1865 by the mare Brita. The average time for 1000 m and was 1.51.3 (1 minute 51.3 seconds, equivalent to a mile in 2 minutes 59 seconds). Today the record is held by Viesker and is 1.19.9 (2:08.5). Betting was first introduced 1928 but developed slowly until the 1960s, after which rapid growth has followed. In Sweden, racing also was started in the early nineteenth century on roads and icetracks. The first permanent tracks were built in the early twentieth century. The first official record in Sweden was in 1829, 1.37.6 (2:37), held by a

Norwegian horse, Sleipner Varg. Today the record is 18.6 (2:07) by a Norwegian stallion, Spikeld. When racing became more popular, Swedish and Norwegian horsemen started trading horses across the border, and the Swedish and Norwegian breeds began to merge together. Today the breeds are genetically alike, and they now are considered to be the same breed. Sweden and Norway have a close collaboration in breeding and racing, and their horses race in the same races. Today the races are held at modern dirt tracks, and in the same events there are separate races for Finnhorses and Standardbreds (STBs). The Finnhorses are allowed to race first at the age of 3 years, but not uncommonly they start racing as late as 5 or 6 years old. They are allowed to race until 16 years of age, and a Finnhorse usually is considered to be best between 7 and 10 years of age. Some stakes races are held for 4- and 5-year-olds, but the main events are for older horses. The biggest event for Finnhorses is the Kuninkuusravit, The Royal Trot, which is held annually in July and August at a different track in Finland each year. The race is one of the major sporting events in Finland, attracting about 50,000 people. Separate races are held for mares and stallions; geldings are excluded. To be allowed to race in the Kuninkuusravit, the horse has to be approved for public breeding and has to be entered in the Stud Book, which requires inspection and approval by a special board. The horses race 3 times in 2 days over distances of 1609 m, 2100 m, and 3100 m, and the final result is based on the total time for all three races. To win the royal title is the biggest honor a Finnhorse can ever get, and the best stallions have won the title 5 times (Vieteri, Vekseli, and Viesker), and the best mares, 4 times (Suhina and Valomerkki). This is a good proof of stamina and endurance, which are typical for the Finnhorse at its best. In Sweden and Norway horses usually start racing at 3 years of age and are allowed to race until the age of 16. Stakes

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• The Finnish Horse and Other Scandinavian Cold-Blooded Trotters

races are open to Swedish and Norwegian horses, and big races are held for 3- and 4-year-olds and for older horses. Finnish horses are not allowed in these races, and only a few races are held in which all Scandinavian horses race together.

TRAINING A COLD-BLOODED TROTTER Traditionally the horses have been bred and trained by farmers, and many remain home bred and trained. There are no sales for Finnhorses, Swedish, or Norwegian trotters. Most horses are broken at 2 years of age, spend the next summer at pasture, and then start more serious training in the winter at 3 years of age, often with a summer break. Farm and forest work has been part of the training to build up strength. Speed work is not done at all at this stage, and traditionally some trainers have never used speed work. Horses started racing at 5 to 6 years of age and raced themselves to condition. However, many professional trainers now train cold-blooded horses, and the horses are better prepared for the races and start racing younger. The race times for the beginners are faster, which has caused problems for many old-school trainers. Many Finnhorses are not natural trotters, and building them up to speed takes time and training. If fast speeds are demanded too early, gait abnormalities develop at higher speeds, and horses lose complete control of the trotting action while appearing sound at a slower trot. Training cold-blooded trotters takes much more time than for STBs, making training more expensive and leading to problems in getting new owners and trainers. In all Scandinavian countries, fewer cold-blood races are held than STB races, and they are concentrated in the north. Nonetheless, cold-blood racing is supported by the central racing organizations of each country and continues to thrive.

RACETRACKS AND WEATHER CONDITIONS The racetracks in Scandinavia are 1000-m oval dirt tracks, and the horses race counterclockwise. The climate is cold in the

Fig. 114-1

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winter, and the tracks freeze and get covered by snow (Fig. 114-1). In winter temporary tracks also are made on ice for smaller races with no betting. The variable climate causes track problems. In late autumn when the track is frozen but not yet covered by snow, the surface can be treacherous. Snowfall makes the tracks smooth but not hard, and provided the horse is shod properly, the track is not slippery. In the springtime, when the snow begins to melt, the track conditions vary throughout the day, being hard in the morning after a night frost, becoming good for a few hours when the frost melts, and then becoming wet and soft the rest of the day. Keeping the track in good condition requires much skill. Because of the long winter, much of the training has to be done on snowy or icy surfaces. Snow is a good surface on which to train a horse, but special shoeing with studs is essential so that the horses do not slip. In the winter many trainers do much of the speed work in snow, which can be deep. The training speeds can be lower because of the resistance, but the training effect is equal or even better than when the training is done on the track. Snow provides a soft and smooth surface, acting as a shock absorber. Many horses with lameness problems race better in winter because of the training in snow. Horses also are trained on the ice of lakes, which is also a good surface. The surface of the ice gives slightly, and shoes with studs can get a good grip. The worst training surface is ground frozen hard like asphalt, creating many lameness problems.

SHOEING CONSIDERATIONS In the winter (November to April) special requirements for shoeing are needed to prevent the horses from slipping on ice. Studs, 5- to 15-mm in length with sharp tips that offer a good grip of the ice or snow, are screwed into the shoes. Four to 15 studs are used per shoe; more studs usually are used in the hind shoes. It is important to have enough studs to avoid slipping slightly at every step, causing joint and muscle soreness. A risk of interference injuries exists, and some horses with poor action cannot race in the winter. Forelimb heel

Winter racing. (Courtesy Olavi Ilmonen, Lahti, Finland.)

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Lameness in the Sport Horse

injuries are common if a horse breaks stride. Elbow boots may be necessary to protect the elbows from stud-induced trauma. Some lameness problems get worse during the winter, because traction by the studs stops the feet abruptly. Hock-related lameness is often worse during the winter, and tendon and suspensory ligament (SL) problems increase. The shoeing of racing Finnhorses is otherwise much like that in STBs, but many Finnhorses are not natural trotters and tend to gallop or pace, so many trainers use special shoeing to help the horse to balance. Young horses often need heavy front shoes with toe weights and bell (overreach) boots when they are learning to trot. The total weight per foot can be up to 500 to 800 g, and this predisposes the horses to lameness, particularly tendon and SL injuries. On the hind feet Finnhorses usually wear normal STB shoes. The lateral branch of the shoe is often longer and bent slightly outward to make the hind action wider and therefore avoid interference between the forelimbs and hindlimbs. Although many STBs race unshod, this is rare in Finnhorses.

CONFORMATION AND LAMENESS The Finnhorse is a heavy, draft-type horse compared with other racehorses. The forehand is heavier than the rear of the horse and is combined with a heavy head and a thick and short neck, causing much stress to the forelimbs. Finnhorses often stand back at the knee, and this sometimes is combined with lateral deviation of the carpus (offset knees). Forelimb tendon, SL, and carpal injuries are not uncommon. The rear end usually is conformed better in Finnhorses than the front end. The most common faults are sickle hocks and cow hocks, which can cause curbs or other lameness problems in the tarsal area. Fetlock conformation is often good, and most Finnhorses have big hooves with good-quality horn.

lameness are usually worse in the turns. Horses with left hindlimb lameness are worse in the straightaways and usually are worst in the turns in a clockwise direction. 4. Is the horse better on soft or hard surfaces? Sidebones often cause lameness on hard surfaces, as do many other foot problems. 5. Is the horse worst when it starts to trot? Does the horse warm into or out of the lameness problem? In young horses (4- to 5-year-olds) bilateral hind fetlock pain is a common cause of lameness, resulting in a short hindlimb stride when first trotting. The lameness usually improves if the horse is jogged for about 1000 to 3000 m. 6. Do the studs in the shoes affect the lameness in the winter? Many horses with carpal or tarsal lameness are worse with studs. The veterinarian should assess the type and use of the horse, its conformation, muscular development, and general condition and should systematically palpate all the limbs, because concurrent lameness in several limbs often occurs. Many horses are trained with sleighs in the winter and are harnessed with collars. If the collar is not fitted properly, it can cause shoulder musculature soreness. Soreness of the shoulder or scapular musculature also can point to other problems in the forelimbs, especially when the lameness is bilateral. Inflammation of the carpal sheath is common because of the heavy front of Finnhorses and the conformation of the carpi and invariably is associated with palpable distention. Proximal suspensory desmitis (PSD) sometimes occurs, and pain may be induced by palpation of the proximal metacarpal region. The second (McII) and fourth (McIV) metacarpal bones in Finnhorses are sometimes thick and prominent, but this is not usually significant (Fig. 114-2), although thick metacarpal bones are sometimes seen in horses with PSD or tenosynovitis of the carpal sheath. Ossification of the cartilages of the foot

LAMENESS EXAMINATION Many Finnhorses complete a racing career without serious lameness problems and require substantially less veterinary treatment than STBs, perhaps because of slower racing speeds. The lameness examination for a Finnish horse is similar to that for a STB racehorse, and similar problems occur. Clinical history is particularly important, and the following questions should be asked: 1. How long has the horse been in training, and how has it been trained? What is the duration of lameness, and has the horse ever trotted sound at high speed? A Finnhorse often develops slowly and has to be taught to trot. Therefore many action problems in young horses are not caused by lameness but by lack of coordination. Lack of strength or condition may predispose horses to lameness. 2. Does the horse trot straight? Is the horse hanging on a line? Is the horse hanging on a shaft? Does the horse need sidepoles or headpoles? A great many lameness problems only show at higher speeds, especially in the early stages of the problem. This is particularly true with hindlimb lameness. Usually in right hindlimb lameness the horse’s rear end turns to the left shaft, and the horse hangs on the right line. Correspondingly problems in the left hindlimb cause hanging on the left line and turning the rear end to the right shaft. In forelimb lameness this is less obvious. A horse with bilateral lameness may move straight. 3. Does the horse trot better in turns or straightaways? In which direction are the turns better? In a counterclockwise direction horses with right hindlimb

Dorsomedial-plantarolateral oblique radiographic view of the metacarpal region. The splint bone is enlarged, which usually has no clinical significance.

Fig. 114-2

CHAPTER 114

• The Finnish Horse and Other Scandinavian Cold-Blooded Trotters

usually can be felt by thickening and loss of elasticity in the region of the coronet, but pain is seldom evident in palpation. In the hindlimbs special emphasis needs to be given to palpation of the tarsus. Tarsal pain is common in Finnhorses with poor conformation. Curbs are common in younger horses (3 to 6 years of age), and distal hock joint pain is common in older horses. The Churchill test works well in Finnhorses. Stifle lameness is not common in Finnhorses, and upward fixation of the patella is rare. Osteochondrosis of the lateral trochlear ridge of the femur occurs occasionally in foals and young horses, sometimes with large defects that respond poorly to arthroscopic debridement. The gait and response to flexion tests can be evaluated properly only when the horse is calm and well controlled by the handler. It is essential that the horse trots straight and not too fast. Most horses are too eager and excited and need to be sedated or tranquilized mildly for flexion tests. Acepromazine (0.01 to 0.025 mg/kg) or romifidine (0.01 to 0.03 mg/kg) are suitable. Sedation is especially important for Finnhorse stallions, which are often difficult to handle, and sometimes two leaders are necessary to control the horse and keep it trotting straight. Horses used for riding can be examined in a circle on the lunge, but trotters are seldom taught to lunge. When doing flexion tests, it is essential for the veterinarian always to examine all limbs and not only those that are suspected to be lame. The tests always should be done in a similar manner and order. When doing flexion tests, the clinician should note all reactions. We do not think false-positive reactions exist, only reactions of different grades. The clinician needs to collect all the information and decide which reactions are significant. Proximal and distal limb flexion tests are done separately in the forelimbs and hindlimbs, using a force of approximately 40 kPa for 60 seconds. In general, all the trotting Finnhorses also are examined at the track at high speeds. Many action problems, especially in the young horses, show only at high speeds. The horse is harnessed in a higher sulky than normal, so the driver of the vehicle does not obscure the horse. The veterinarian drives a car behind or beside the horse at the racetrack. Examining the horse from the car is more helpful than driving the horse, because the clinician can be some distance away from the horse to see the action more clearly, and abnormalities can be assessed more easily. Diagnostic analgesia is used as in STBs. The clinician must keep in mind that high-speed lameness seldom can be resolved totally by analgesic techniques. Every block changes the horse’s action, and when the veterinarian does several blocks on the same horse, assessing the meaning of each block is difficult. When examining a horse with high-speed lameness, the clinician must believe what vision, touch, and experience indicate.

IMAGING CONSIDERATIONS In Finnhorse trotters, radiographic changes are found much less commonly than in STBs. Carpal chip fractures are rare in Finnhorses, and sclerosis of the third carpal bone is unusual. Osteochondrosis is also rare in the Finnhorse, though the prevalence has been increasing slightly in the past decade. Because osteochondrosis is unusual, young Finnhorses are not radiographed routinely if clinical signs are absent. Controlling osteochondrosis in Finnhorses is attempted by radiographing all stallions that are proposed for public breeding. Stallions with osteochondrosis generally are not accepted. Ossification of the cartilages of the foot is a common radiographic finding in Finnhorses. Navicular disease is a rare diagnosis. Enlargement of McII and McIV is common and often does not cause clinical signs. Flake-like fragments adjacent to McII usually result from interference.

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Ultrasonography is invaluable for assessing soft tissue injuries and may be more useful than radiography in examining the splint bones, because splint-bone problems often are associated with carpal canal syndrome or PSD.

UNDIAGNOSED LAMENESS Some young trotting Finnhorses trot soundly at slow speeds and show no signs of lameness during a lameness examination, but when asked for speed, the horses lose the action completely. Loss of rhythm causes this; the horse simply cannot trot at higher speeds. This often happens to talented horses that have early speed with little training but do not have the strength to maintain it. The training regimen must be aimed at building strength, especially in the hindlimbs. Horses are trotted in 1- to 3-minute intervals with resistance with a special resistance cart, in deep snow, or uphill. Training takes a long time, sometimes up to a year, until these horses learn to trot again, and some horses never recover. Because the main racing events are for aged horses, time is not as big a factor for Finnhorses as for STBs. It is quite possible for a horse to recover completely and become a top-class racehorse at an older age.

THE TEN MOST COMMON CAUSES OF LAMENESS The following are the 10 most common causes of lameness: 1. Carpal lameness 2. Tarsal lameness 3. Superficial digital flexor tendonitis 4. Suspensory desmitis 5. Curb 6. Ossification of the cartilages of the foot 7. Splints 8. Metatarsophalangeal joint pain 9. Tenosynovitis of the digital flexor tendon sheath 10. Loss of rhythm

LAMENESS CONDITIONS TYPICAL OF FINNHORSES Carpal synovitis is common in Finnhorses, and signs are similar to those seen in STBs. In the early stages a horse warms out of lameness quickly. Often horses with carpal problems begin to roll over and may try to pace or gallop instead of trotting. The horse may trot if the shoes are weighted more, but this may accentuate the primary problem. Without treatment the lameness deteriorates, and the horse begins to hang on a line and gradually becomes overtly lame. Radiographic changes rarely are seen, probably because of the slower racing speeds compared with those of Thoroughbreds and STBs. Treatment consists of intra-articular medication with hyaluronan, polysulfated glycosaminoglycans or corticosteroids, alone or in combination, together with rest for several weeks. Carpal canal syndrome is also common in Finnhorses, sometimes simultaneously with carpitis, sometimes on its own. Ultrasonography is useful for confirming the diagnosis. The treatment is usually rest, combined with intrathecal administration of hyaluronan or corticosteroids. Some horses do not respond to conservative therapy, and surgical treatment using tenoscopy may be necessary. Tarsal lameness is common in Finnhorses and is the most frequent cause of hindlimb lameness, usually because of distal hock joint pain. Mild lameness in horses is not noticed easily at slow speeds, but with increasing speed the horse begins to

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PART X

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Lameness in the Sport Horse

drag the affected limb, and the rear end moves to the opposite shaft. The horse usually hangs on the line on the side of the affected limb. Radiographic evidence of osteoarthritis may or may not be apparent. Intra-articular treatments with corticosteroids, hyaluronan, or polysulfated glycosaminoglycans are used widely. In some horses cunean tenectomy can be useful. Superficial digital flexor tendonitis and suspensory desmitis are common. Superficial digital flexor tendonitis usually occurs in forelimbs, and poor conformation or overweighting the shoes may be predisposing factors. In the hindlimb, tendon injuries are usually traumatic. Suspensory desmitis occurs more frequently in forelimbs than hindlimbs, probably because of the heavy front conformation. Suspensory branch injuries are most common. Finnhorses cope better with chronic suspensory desmitis than do STBs because of the lower racing speeds, longer rest periods, the horses being able to race at an older age, and thus better opportunities to heal. Suspensory desmitis is sometimes associated with splint bone fractures or exostoses. Treatment of Finnhorses with superficial digital flexor tendonitis and suspensory desmitis is most often conservative, with long rest periods. Tendon splitting or desmotomy of the accessory ligament of the superficial digital flexor tendon sometimes is used for tendonitis. Hot firing has been a traditional treatment for tendonitis and desmitis for many decades, and some veterinarians still use it in some horses, though with mixed success. Curbs (soft tissue enlargement in the proximal plantar metatarsal region) often are seen in young horses (3 to 5 years old) in early training, especially those with sickle hocks (see Chapter 79). Curbs seldom cause spontaneous lameness. Usually the signs show first at higher speeds, when the cranial phase of the stride in the affected limb is shortened, and the horse begins to drag the limb. Most veterinarians treat curbs symptomatically, without ultrasonographic examination to determine the structure involved. Treatments include rest, corticosteroid or dimethylsulfoxide injections, or pin firing. Cryotherapy is not used as widely as pin firing. The prognosis with all treatments is very good. Ossification of the cartilages of the foot (sidebones) is a common finding in the front feet of heavy horses, occurring in 80% of Finnhorses. The condition is more common in females than in males and positively correlates with the size of the horse. The grade of the ossification is usually mild, but extensive ossification sometimes occurs. The cause is unclear, but a heritable component exists. The cartilages start ossifying at an early age, unassociated with training of the horse. Other contributory factors may include hoof conformation, shoeing, and concussion. The clinical significance of sidebones is questionable. Most horses with mild or moderate ossification show no clinical signs. Ossification is detected only by radiography. With extensive ossification the cartilages are palpable proximal to the coronary band. Palpation does not induce pain. In general, horses with large sidebones show some clinical signs, especially on hard ground. Lameness at slow speeds is rare, but at

high speeds with increased concussion the forelimb stride is shortened and the horse breaks to pace or gallop. The diagnosis is confirmed radiographically, using dorsopalmar views. Osteoarthritis of the distal interphalangeal joint and navicular disease may cause similar clinical signs and may be present concurrently with sidebones. The treatment options are limited, because the condition persists. Shoeing with egg bar shoes, often combined with thick pads, is helpful in some horses. Most horses with sidebones can race with moderate to good success when shod properly and raced only on good surfaces. Because of the hereditary background all Finnhorse stallions that are used for public breeding have to be radiographed for sidebones before being accepted. Splints are fairly common in the forelimbs of young, growing horses and horses are usually treated conservatively with rest. Most splints resolve spontaneously, but local corticosteroid injections or cryotherapy sometimes is used. Interference injury may result in a flake of bone detached from McII. These fragments do not heal with rest and respond poorly to corticosteroid injections or cryotherapy. Surgical removal is usually necessary. Chronic tenosynovitis of the digital flexor tendon sheath is a common cause of lameness in aged cold-blooded trotters and usually develops gradually, with mild or moderate swelling and no lameness for long periods. In time the sheath becomes fibrotic, and masses and adhesions develop. At this stage constriction by the palmar annular ligament may occur. Many horses can perform well despite chronic tenosynovitis, especially in hindlimbs. Intrathecal administration of hyaluronan, with or without corticosteroids, is used for horses with acute tenosynovitis. Frequent corticosteroid injections often seem to increase tenosynovial masses. Tenoscopy and transection of the palmar annular ligament is used if the condition is advanced. Cold-blooded horses with chronic tenosynovitis seem to respond poorer to treatment than do STBs with similar lesions. This may be because Finnhorses are often older and of greater weight. In young Finnhorses, bilateral hindlimb fetlock pain is fairly common and causes a short and stiff hindlimb stride when they start to trot, which improves with exercise early in the condition. When both hind fetlocks are blocked simultaneously, the action changes completely. Pain is considered to be associated with subchondral bone remodeling of the distal aspect of the third metatarsal bone. A variety of treatments have been used, including joint lavage and intra-articular treatment with hyaluronan or corticosteroids, often combined with NSAIDs. If lameness is severe, surgical drilling of the subchondral bone is performed. Horses remain lame for several months, but the long-term prognosis is reasonable. Osteochondrosis is rare in Finnhorses, but when it does occur, osteochondrosis most often is seen in the distal intermediate ridge of the tibia and causes effusion of the tarsocrural joint. Treatment is removal of the fragment(s) by arthroscopy.

SECTION • 3 Non-Racing Sport Horses CHAPTER •

115

Prepurchase Examination of the Performance Horse Richard D. Mitchell and Sue J. Dyson

he purchase or prepurchase examination is a much discussed and sometimes feared subject for equine practitioners. Careless conduct and poor documentation can leave veterinarians wishing they had not agreed to perform the examination, whereas forethought and good planning can lead to a rewarding experience for the practitioner and the client. In the United States the examination is referred to as the purchase examination, because in many cases the deal already has been completed, whereas in Europe the examination usually is referred to as the prepurchase examination, because generally the purchaser has agreed to buy the horse subject to a satisfactory veterinary examination. However, in some countries (e.g., Holland), where many horses are sold through professional dealers, a horse may be purchased by the dealer and then examined by a veterinarian on behalf of the dealer before resale within a few days.

T

GOALS OF THE EXAMINATION When requested to evaluate a horse for purchase, the veterinarian should keep several goals in mind. First, the examination should be an objective assessment of the horse’s physical condition. Second, the examination should be a fact-finding mission to aid the purchaser in his or her decision to make a purchase. This may involve the veterinarian in making some predictions based on experience and probability, but care must be taken to be factual and objective. Last, the prepurchase examination can serve as a formal introduction to a horse for which the practitioner may provide long-term care. Such relationships may affect the veterinarian’s decisionmaking process relative to a client’s needs. It is helpful to have knowledge of the disciplines in which the horse has been and will be involved. Various equine sports place differing demands on the horse, and the clinician should be aware of sometimes subtle, yet important, differences. Some physical characteristics or conditions may be acceptable for certain levels of performance but not acceptable for others. For example, a previous strain of a superficial digital flexor tendon (SDFT) may be an acceptable risk for a show hunter but may carry a high risk for a racehorse. Veterinarians should avoid performing prepurchase examinations on horses that will be involved in disciplines with which they are not familiar. The veterinarian needs to discuss the goals of the examination and horse ownership with the prospective purchaser. Understanding the client, the trainer, and what is expected of the horse will help the veterinarian in assessing the horse’s potential suitability. Passing or failing the horse is not the veterinarian’s job, but it is his or her role to advise on how existing conditions may affect the future use of the horse. It is therefore self-evident that prepurchase examinations should

not be performed by recent graduates, who may be fully competent in performing clinical examinations, but generally do not have the experience of how to interpret the findings of the examinations and are not in a position to evaluate risk. The prospective purchaser requires advice about the risks of proceeding with the purchase. Prior knowledge of clients, their expectations of the horse, and their attitude toward risk make offering such advice easier, compared with clients about whom clinicians know little. A veterinarian must be open-minded and should consider themselves as a facilitator for the sales contract: the vendor wishes to sell the horse, the purchaser may have searched for a long time to find a suitable horse, and the veterinarian’s role is to enable the transaction to take place if such is reasonable. Nonetheless, the veterinarian must be streetwise and recognize that a minority of unscrupulous vendors may try to misrepresent a horse. Caveat emptor. Veterinarians also should be aware that prospective purchasers often are keen to buy horses and in their enthusiasm may wish to overlook any problems that are identified during the prepurchase examination. A veterinarian who believes that the risks of buying a horse are too high is responsible for trying to dissuade the purchaser from proceeding further. If the purchaser ignores the advice, it is essential that the veterinarian has documented adequately his or her observations and advice. Purchasers can have remarkably selective memories when things start to go wrong. The scope of the examination can range from a comprehensive clinical examination of the horse, using basic powers of observation, to a complex investigation using advanced techniques such as radiography, ultrasonography, endoscopy, thermography, and scintigraphy. The wishes of the buyer are important in determining the extent and depth of the examination, which also must be dictated to some extent by the value of the horse and its future athletic expectations. Some consideration to cost should be given, however, but not at the cost of the quality of the examination. The veterinarian should allow some latitude for deciding what is needed to answer questions posed by the clinical examination.

CONTRACT A veterinarian enters a business arrangement with a purchaser when he or she agrees to perform a prepurchase examination. It is imperative for the veterinarian to understand the buyer’s intentions for the horse and the expectations of the proposed examination. The terms, details, and costs of the examination should be discussed at the time of the initial request. The extent and depth of the examination and its limitations should be emphasized. This is straightforward when the veterinarian is dealing directly with the purchaser, assuming that the purchaser has knowledge of horses. The terms of

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agreement become more difficult when a veterinarian is speaking to an agent for the owner or to the prospective rider of the horse, when the actual purchaser has no knowledge of horses. Such persons may have expectations of the horse as if it was a mechanical object like a car.

Purchaser’s Reservations The veterinarian is responsible for the following: 1. Establishing if the purchaser has any reservations about the horse 2. Determining whether the horse has been in regular work up until the examination 3. Warning the client of the hazards of performing an examination on a horse that has not been in regular work; previous lameness or back problems may be inapparent until the horse is in regular work. It may be helpful to suggest that the purchaser check the horse’s official competition record to determine whether any unexpected breaks from competition have occurred.

Purchase for Resale If the horse is to be purchased for resale, this should be noted. The purchaser should be warned that the clinician’s interpretation of the findings may not be identical to that of another veterinary surgeon. The examining veterinarian may regard the horse as a reasonable risk for purchase, but this is not a guarantee that others have the same opinion. All observations should be well documented so that comparisons can be made should questions arise at a subsequent resale examination. Such notes may well help save a sale in the future and save face for the initial veterinarian.

Insuring the Horse It is important to establish if the horse will be insured for loss of use for a specific athletic activity or for veterinary fees. The purchaser should be advised that the examining veterinarian may consider the horse a reasonable risk for purchase but that does not necessarily equate with the horse being a normal insurance risk. The veterinarian may consider that a small, well-rounded osseous opacity on the dorsal aspect of the distal interphalangeal joint is unlikely to be of clinical significance, but for an insurance company to place an exclusion on problems related to the joint would not be unreasonable. The veterinarian should advise the purchaser that if such problems arise, the purchaser should communicate with the insurance company before completing the purchase transaction.

Blood Tests and Limitations The client should be informed clearly that the results presented are good for the day of examination, but predictions about future soundness and suitability are impossible. The limitations of analysis of blood for drugs must be detailed, bearing in mind the difficulties of detection of many drugs administered by the intra-articular route. The client should be warned that several days may elapse before the results of blood tests are known and that the purchase transaction should not be completed until the results are known. The veterinarian should discuss with the client how the findings will be transmitted and what kind of report will be issued.

Conflicts of Interest Any potential conflicts of interest for the veterinarian must be disclosed to the buyer. Previous dealings with the vendor, although the vendor may not be a current client, could be perceived as a conflict of interest. In the horse world today, not to have such conflicts arise is difficult, but such conflicts should be acknowledged, and the buyer should be given the option of having someone else perform the examination.

COMMUNICATION WITH THE VENDOR The vendor must understand clearly what facilities are required for the examination and should be advised that the horse should be stabled before the examination and not worked earlier in the day. If the vendor is unable to be present at the examination, the veterinarian should establish the answers to a number of important questions in advance: 1. How long has the horse been in the owner’s possession? 2. Is the horse in regular work? 3. Has the horse had any previous lameness? 4. Has the horse had any previous medical problem? 5. Is the horse receiving any medication, or has it done so in the last 8 weeks? 6. Does the horse have any vices (crib-biting, wind sucking, box walking), or does it bite or kick? 7. Has the horse been seen to shake its head? 8. Has the horse had previous surgery? 9. Does the horse normally live in or out? 10. Does the horse have dry or soaked hay or a haylage preparation? 11. When was the horse last trimmed or shod? Ideally vendors should sign a copy of their responses to these questions (Fig. 115-1). When the examination actually is performed, ideally all involved parties or their agents should be present. This provides an environment in which the veterinarian can ask pertinent questions of the buyer and seller regarding the horse’s history and future use and can assure the buyer a complete examination was performed. Problems that arise during the examination can be discussed with the purchaser. The veterinarian should not compromise the standard of the examination because of physical conditions. If modifying the procedure of the usual examination technique is necessary, such should be noted in the subsequent report, and the purchaser should be advised accordingly. The limitations of the conclusions drawn from the examination should be documented. If an uncooperative vendor or agent makes conducting the usual examination difficult, the veterinarian may choose not to continue the examination to protect the interests of the buyer and personal interests.

EXAMINATION AT A DISTANCE A client may request the veterinarian to examine a valuable competition horse that is a long distance away or possibly in a foreign country. A number of alternative strategies can be applied. It may be prudent to first have the horse undergo radiographic examination and proceed with visiting the horse only if these radiographs are considered acceptable. The veterinarian is of course relying on the honesty of everyone concerned that the radiographs provided are current images of the horse in question. It is critical that the veterinarian provide clear guidelines of the views required and be prepared not to compromise on quality. Alternatively, the veterinarian can travel and examine the horse and be present for the radiographic assessment. However, this may mean that the clinical examination is compromised by inadequate riding facilities at a veterinary clinic or that substantial time is spent traveling between the site where the horse is examined and the veterinary clinic where ancillary tests are performed. However, clinic facilities may be required anyway for ultrasonography or endoscopy. A client may inform the veterinarian of an intended purchase of a horse from a foreign country and that he or she has been recommended to employ a specific clinician from that country to carry out the prepurchase examination. The client Text continued on page 958

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953

BEVA Prepurchase Examination Worksheet Purchaser's name and address

............................................................................................................. ..............................................................................................................

Telephone no.

.............................................................................................................

Agent's name and address

............................................................................................................. ..............................................................................................................

Telephone no.

.............................................................................................................

Vendor's name and address

............................................................................................................. .............................................................................................................. ............................................................................................................

Telephone no.

Intended use of horse ............................................................ Stated age .................................. Stated height ............................................ Purchaser's reservations .................................................................................................................................................................................... Is horse to be insured? Name

YES Permanent incapacity/All risks of mortality

NO

......................................................................................... Breed

....................................................................................................

Gelding

Sex Colour

Mare

Entire

...................................................................................................

Size ...................... Estimate app./Measurement/By documentation Duration of current ownership?

....................................................................................................................................................................

In current work?

YES

NO

..........................................................................................

Was horse stabled prior to examination?

YES

NO

..........................................................................................

YES

NO

.........................................................................................

Previous lameness?

YES

NO

.........................................................................................

Previous medical problems?

YES

NO

.........................................................................................

Previous surgery?

YES

NO

.........................................................................................

Vices?

YES

NO

Behavioural abnormalities?

Head shaking

Bedding?

Straw

Shavings

Food?

Dry hay

Soaked hay

Receiving medication or received medication in last 4 weeks?

Husbandry? When was horse last shod?

Cribbing

Windsucking

Box walking

Biting

Paper

Weaving Other

Other

Lives out

............................ ............................ ............................

Haylage/silage ...........................................................

........................................................... Stabled At grass In & out ............................................................................................................................

Vendor's declaration: To the best of my knowledge the answers to the above questions are correct. Signature of vendor/vendor's agent:

..................................................................................................... Continued

Fig. 115-1 British Equine Veterinary Association (BEVA) prepurchase examination worksheet. (Courtesy British Equine Veterinary Association.)

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Examined at .....................................................

INSTRUCTIONS 1. Written description should be typed or written in block capitals.

2. Written description and diagram should agree. 3. All white markings should be hatched in red. 4. Whorls must be shown; thus "X" and describe below in detail.

........................................................................... On ..................................................................... At ........................................................... AM/PM Present ..............................................................

Right side

Left side

............................................................................ ............................................................................ ............................................................................ Weather ...........................................................

Fore (rear view)

............................................................................

Hind (rear view)

............................................................................ ............................................................................ Identification

Head and neck (ventral view)

Muzzle

Left Right

Left

Right

Head ................................................................................................................................................................................................................ ........................................................................................................................................................................................................................... Neck ................................................................................................................................................................................................................. ........................................................................................................................................................................................................................... Limbs: LF ...................................................................................................................................................................................................... RF ...................................................................................................................................................................................................... LH ....................................................................................................................................................................................................... RH ....................................................................................................................................................................................................... Body ................................................................................................................................................................................................................ ........................................................................................................................................................................................................................... Acquired marks/Brands/Freeze brands ref loss of use Microchip scanned

Not scanned

.......................................................................................................................... Present? Yes/No

No. ...................................................................

Stage 1–Preliminary Examination (tick if normal; note abnormalities) Bodily condition:

Overweight

Good

Lean

Poor

Stance, attitude, and demeanour .................................................................................................................................................................... Head

Ears ................................................................................................................................................................................ Eyes (including opthalmoscopic examination) ................................................................................................................. Nose ............................................................................................................................................................................... Gums .............................................................................................................................................................................. Mandible ......................................................................................................................................................................... Other ................................................................................................................................................................................

Age and teeth Incisor

Wolf teeth Permanent

Yes/No Infundibulum

Location ........................................................................................ Dental Star

Enamel Spot

1 2 3

Fig. 115-1—cont’d British Equine Veterinary Association prepurchase examination worksheet. LF, Left forelimb; RF, right forelimb; LH, left hindlimb; RF, right hindlimb. (Courtesy British Equine Veterinary Association.)

Shape

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• Prepurchase Examination of the Performance Horse

Hook incisor 3—Left

Hook incisor 3—Right

Galvayne’s groove Left

Galvayne’s groove Right

955

Angle Abnormal wear Molars Approximate age

Range

Documented age

Integument Ventriculectomy

Laryngoplasty

Surgical scar

Laparotomy

Medial patellar desmotomy

Neurectomy

Other Other acquired scars Sarcoids

Yes/No (note location)

Melanomata

Yes/No (note location)

Other Faeces, urination Respiratory system

Spontaneous cough

Yes/No

Cough reflex

Yes/No

Auscultation of thorax Cardiovascular system Urogenital system Nervous system Conformation LF RF LH RH Body Hindquarters Symmetrically muscled Yes/No

Tubera sacrale symmetrical Yes/No

Musculoskeletal system LF RF LH RH Back Bulb of heel sensation Feet

Horn quality

Good

Poor

Foot pastern axis

Straight

Broken back

Broken forward

Hoof testers Trimming & shoeing Symmetry

Continued

Fig. 115-1—cont’d British Equine Veterinary Association prepurchase examination worksheet. LF, Left forelimb; RF, right forelimb; LH, left hindlimb; RF, right hindlimb. (Courtesy British Equine Veterinary Association.)

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Stage 2–Trotting up (tick if normal/note abnormalities) Walk Trot Circle Reverse

Flexion test

Yes/No LF RF LH RH

Lunged on soft

– – – –

+ + + +

Yes/No

Left rein Right rein

Lunged on hard

Yes/No

Left rein Right rein

Stage 3–Strenuous Exercise (tick if normal/note abnormalities) Inside/outside

Ridden/lunged

State going

Trot Canter Gallop Respiratory noise

Inspiratory

Nasal discharge

Yes/No

Expiratory

Cough

Yes/No

No/Yes

Auscultation Recovery Stage 4–Rest Observations Crib biting

Yes/No

Stage 5–Second Trot and Foot Examination (tick if normal/note abnormalities) Walk Trot Circle Reverse Flexion test

Yes/No

Lunged on firm surface

Yes/No

LF RF LH RH Shoes removed

Yes/No

Fig. 115-1—cont’d British Equine Veterinary Association prepurchase examination worksheet. LF, Left forelimb; RF, right forelimb; LH, left hindlimb; RF, right hindlimb. (Courtesy British Equine Veterinary Association.)

• Prepurchase Examination of the Performance Horse

CHAPTER 115

General observations Blood collected

Yes/No

NSAID only

Analysed/stored

Full screen

Health profile

Specialised Techniques Radiography Area Examined

Views (circle which used)

Comments

LF Foot

LM, DPr-PaDiO, PaPr-PaDiO

RF Foot

LM, DPr-PaDiO, PaPr-PaDiO

L Mc/P Joint

LM, DL-PaMO, DM-PaLO, DPa

R Mc/P Joint

LM, DL-PaMO, DM-PaLO, DPa

L Carpus

LM, DL-PaMO, DM-PaLO, DPa

R Carpus

LM, DL-PaMO, DM-PaLO, DPa

L Hock

LM, DL-PIMO, PIL-DMO, DPL

R Hock

LM, DL-PIMO, PIL-DMO, DPL

Other

Ultrasonography Yes/No

Area examined & comments

Yes

Endoscopic examination of URT

No

Other special techniques

Signed

Date

Record of discussion

Suitable for purchase Certificate issued (Date)

In person

Yes

Time

Telephone

No

Date

Time

Deferred: reason

Signed

Fig. 115-1—cont’d British Equine Veterinary Association prepurchase examination worksheet. LF, Left forelimb; RF, right forelimb; LH, left hindlimb; RF, right hindlimb; L, lateral; M, medial; D, dorsal; P, proximal; Pa, palmar; Di, distal; O, oblique; Pl, plantar; URT, upper respiratory tract. (Courtesy British Equine Veterinary Association.)

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should be warned that the method of carrying out and reporting the examination may differ from what he or she is used to seeing and may have limitations of which he or she is unaware. For example, in some countries in Europe the examination is much more limited and does not encompass assessment of conformation. It is not usual practice to examine the horse being ridden. It is worthwhile developing a group of professional colleagues whose clinical expertise and trustworthiness the veterinarian respects, one of whom can be recommended to the purchaser. The veterinary surgeon performing the examination should be requested to communicate with the client’s own veterinarian and to send radiographs for assessment. Discussion between two colleagues, one of whom has examined the horse and the other who knows the client, can result in a highly satisfactory outcome.

CLINICAL EXAMINATION AT REST Various national bodies have established guidelines for the way in which a prepurchase examination should be carried out and reported, to which the veterinarian obviously should adhere. The legal responsibilities for the veterinary surgeon and the vendor may vary in different countries. For example, in Holland the expectations of the veterinary examination performed on behalf of an amateur purchaser are higher than that for a professional purchaser. In Denmark, if clinically significant radiological abnormalities are discovered soon after purchase, which obviously predate the purchase, the vendor is liable. The clinical examination should evaluate all organ systems as comprehensively as possible. The examination should be methodical and repeatable. Using a checklist may help. The principle aims of this chapter are to focus on the examination of the musculoskeletal and neurological systems1,2 and to discuss the interpretation of abnormal findings. The veterinarian should identify the horse, including name, breed, sex, age, markings, tattoos, freeze marks, brands, and height. In Europe a freeze brand L signifies that the horse has previously been a loss of use insurance case. The horse’s identity should be compared with its passport or vaccination certificate. The horse first should be examined in the stable, with assessment of demeanor, attitude, stance, conformation, and thorough observation and palpation of the head, neck, back, and limbs as described in Chapters 4 to 6. Collection of blood samples may be performed at this stage or when the examination is completed and the veterinarian deems that purchase will probably be recommended. More comprehensive evaluation of the feet, overall conformation, and evaluation of muscle symmetry is best performed outside, where the horse can be viewed better from all angles. If the horse will be used for show purposes, when the cosmetic appearance of the horse is important, the veterinarian should draw the purchaser’s attention to all possible abnormalities, such as a prominent head to the fourth metatarsal bone, that a lay judge may misconstrue as a curb. If the purchaser has expressed reservations about a swelling such as a splint, the veterinarian should be sure to document its size and possible significance. If the purchaser is concerned about the horse’s hock conformation, recommending radiographic examination of the hocks is worthwhile, even if the veterinarian considers the conformation to be acceptable and the horse appears sound.

Conformation Although assessment of conformation as far as it may influence future lameness is considered an important part of the examination in the United States and Great Britain, this is not usual practice, and in Holland, for example, is not included. It is important to recognize that breed differences in conformation exist and that what might be acceptable in one breed does not

necessarily apply to others. The significance of conformational abnormalities in part is dictated by the discipline in which the horse is involved.1 Most Arabian horses have a short-coupled and slightly lordotic back; thus they are likely to have some degree of impingement of dorsal spinous processes. However, this is unlikely to compromise the horse’s show performance. However, a dressage horse with a short back may well develop a clinical problem associated with impinging dorsal spinous processes when working at an advanced level. In such a horse the flexibility of the back at rest and when the horse is moving in hand and ridden must be assessed with great care, paying great attention to the freedom and elasticity of the gaits. Even if the horse is symptom free currently, the purchaser should be advised that problems may occur in the future. Young Warmblood breeds have a relatively high propensity for intermittent upward fixation or delayed release of the patella, especially those with a straight hindlimb conformation. Although the condition may be manageable in some, in others it can become a chronic problem, albeit a subtle one, resulting in low-grade discomfort and unwillingness to work. The veterinarian should observe the horse carefully as it moves over in the stable, to assess smooth or jerky movement of the patella on the left and right sides, and should check carefully for a surgical scar and the size of the medial patellar ligament, which if enlarged is likely to reflect a previous desmotomy. Very straight conformation of the hocks or abnormal extension of the hind fetlock joints are predisposing factors for proximal suspensory desmitis and suspensory branch injury. A purchaser should be advised not to proceed with purchase for any form of athletic activity except light pleasure riding. The examination should be terminated at this stage rather than the veterinarian running up a large bill and antagonizing the vendor by wasting more time. The clinician should pay particular attention to the conformation of the feet and relate this to the type of ground surface on which the horse will have to work. A horse with flat feet and thin soles is not a good candidate for endurance riding. A horse with crumbly hoof walls is predisposed to losing shoes, and this can be disastrous for three-day event horses. Although changing the horse’s nutrition and foot management may result in some improvement, accurate prediction of the degree of improvement that may be achieved is difficult. Sheared heels and underrun heels in the forelimbs or hindlimbs may be primary problems or predispose horses to altered ways of moving, causing soreness in the more proximal parts of the limbs. These findings are particularly important in jumping and dressage horses and those used for cutting and reining. The veterinarian should assess the forelimb conformation carefully from the front and ensure that the foot is positioned symmetrically under the central limb axis of the more proximal parts of the limb. A disproportionately high incidence of distal limb joint problems occurs in horses in which the pastern and foot are set more to the outside, with a tendency for the medial wall to become more upright and the lateral wall flared (Fig. 115-2). Many Warmblood breeds naturally have much narrower and upright foot conformation than other breeds. This predisposes the horses to develop thrush, and careful stable hygiene and foot cleanliness are necessary to control this problem. Asymmetry of front foot shape and size always should be documented and may reflect previous lameness in the limb with the more contracted foot but also may reflect development of a mild flexural deformity of the distal interphalangeal joint when the horse was a foal, which may be of no long-term significance. The veterinarian should beware if the feet are long and misshapen; this finding may mask underlying conformational problems or asymmetry in foot shape and size. Postponing further assessment of the horse until the feet have been trimmed and shod properly is preferable.

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Tendons and Ligaments Particular attention should be paid to the size, shape, and stiffness of the tendonous and ligamentous structures of the metacarpal and pastern regions, bearing in mind that if the horse has sustained a bilateral tendon injury, both tendons may be enlarged slightly, and the clue to previous damage may be rounding of the margins of the tendons or abnormal stiffness. The significance of a previous injury to the SDFT or suspensory ligament must be assessed in the light of the horse’s previous and future career. These injuries carry a high risk of recurrence in racehorses, event horses, high-level show jumpers, and endurance horses. However, the horse may perform satisfactorily as a hunter, a dressage horse, or a pleasure horse or at a low level in more demanding sports. The purchaser should be advised that further information about the repair of the injury may be obtained by ultrasonographic examination. Further information about when the injury was sustained and what the horse has done since then may be helpful. Decision making must be based on the athletic expectations of the horse, all other aspects of the horse’s suitability, and whether the horse is being bought for resale. If the horse is a perfect schoolmaster for a junior rider and the price is reasonable, the risk/benefit ratio may be acceptable.

Assessment of Joints

Dorsal view of a forelimb with significant conformational abnormalities. Note the position of the foot and pastern relative to the central axis of the metacarpal region (dotted line). The hoof capsule is distorted, and the foot shape is asymmetrical.

Fig. 115-2

Some conformational abnormalities, such as over at the knee, do not appear to influence a horse’s future soundness greatly but must be described. Failure to document observations leaves the veterinarian open to litigation if future problems arise.

Muscle Symmetry Muscle asymmetry of the hindquarters may reflect previous or current hindlimb lameness, although it is not necessarily associated with future chronic lameness. Muscle asymmetry should alert the veterinarian to pay particular attention to the hindlimb gait in hand, on the lunge, and ridden and to the response to flexion tests. Asymmetry is an indication for flexion tests before and after ridden exercise. The potential significance of muscle asymmetry must be discussed with the purchaser. Slight asymmetry of the tubera sacrale is a common finding and frequently is not of clinical significance. Nonetheless, the purchaser should be informed.

Many horses have mild fetlock joint capsule distention or thickening. The significance of distention must be assessed based on the environmental temperature: if it is cold joint capsules are more likely to be tight than if it is warm. Asymmetry between left and right is of greater significance than bilateral symmetry. The joints should be assessed carefully for any evidence of restricted range of motion or pain on manipulation. The range of motion varies between horses and is in part a reflection of age and work history, but asymmetry between left and right should be viewed with caution. The response to distal limb flexion and the horse’s action on the lunge on a hard surface must be assessed carefully. Distention of the antebrachiocarpal or middle carpal joint capsules is rarely an insignificant finding and even if unassociated with detectable lameness should prompt radiographic examination. During hindlimb assessment, care should be taken to differentiate between pain on flexion of the proximal limb joints and reluctance to stand on the contralateral hindlimb, perhaps associated with sacroiliac pain. Abnormal limb flexion may be present if the horse is a shiverer. A high incidence of this condition occurs among high-performance Warmblood breeds and does not appear to compromise performance. However, an intending purchaser must be warned that the condition may be progressive and may make the horse difficult to trim and shoe. Flexibility of the neck and back should be assessed, and the presence of any abnormal muscle tension or abnormal reaction to palpation of acupuncture trigger points should be noted. The veterinarian also should pay attention to the presence of sarcoids in a position where they may be abraded by tack. If a sarcoid is identified, the client always must be warned that such lesions may increase in number, but assuming that the client is aware of the risks, a small number of lesions at sites removed from the tack should not mitigate against purchase. The mouth should be examined carefully. Large hooks on the rostral aspect of the first upper cheek teeth are usually an indicator that large hooks also may be present on the caudal aspect of the lower caudal cheek teeth, which may be difficult to manage. Sensation in the heel region of the forelimbs and the reaction to vigorous application of hoof testers should be assessed carefully to determine if a previous neurectomy may have been performed. The absence of a visible or palpable scar does not preclude previous surgery.

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ASSESSMENT OF GAIT The horse should be examined moving freely at a walk and trot on a firm surface, with particular attention directed to the stride length and lift to the stride relative to the horse’s type. The veterinarian should bear in mind that a horse with a bilateral forelimb or hindlimb lameness may not appear overtly lame but merely may have a slightly restricted gait. The veterinarian should beware of the situation encountered particularly in a professional’s yard when the horse is encouraged by an assistant to trot excessively quickly, is unduly restrained, or is excessively fresh and trots crookedly. The horse must trot in a regular, relaxed rhythm with freedom of the head and neck; otherwise, lameness may be missed. The veterinarian should pay particular attention to how easily the horse turns when changing direction and the flexibility of the neck and back. If the horse trots in a particularly loose and extravagant way, the veterinarian should bear in mind that the horse may be mildly ataxic. Ataxia may not jeopardize a dressage horse when competing at lower levels, but when finer degrees of muscular strength and coordination are required in advanced dressage, performance may be compromised. The safety of a mildly ataxic horse jumping must be questioned. The veterinarian should watch the horse carefully as it decelerates, when signs of mild ataxia or jerky movement of the patella associated with its delayed release may be apparent. Watch the horse turning in small circles and moving backward, assessing flexibility of the neck and back, limb coordination and placement, and any quivering movement of the tail suggestive of shivering.

Flexion Tests The interpretation of flexion and extension tests is controversial.3,4 The force applied, the duration of flexion, the way in which the joints are flexed, and the work history of the horse may all influence the response. Positive results of flexion tests in a horse that does not demonstrate lameness before flexion may not be a cause for termination of the examination, unless other suspicious clinical signs have been identified already. The horse should be evaluated on the lunge and ridden for evidence of lameness. Many positive results on flexion tests are found to change during the course of the exercise examination (perhaps as the horse warms up or loosens up), and these may not have clinical significance. A difference in response between distal limb flexion of the left and right forelimbs may be more important than a symmetrical response. A positive response to carpal flexion or to proximal limb flexion of a hindlimb must be viewed with caution. A veterinarian should aim to perform flexion tests as consistently as possible so that they know the ranges of response anticipated in clinically normal horses.

Lunging and Ridden Exercise The requirements for lunging and ridden or driven exercise vary between the guidelines for prepurchase examinations in different countries and also are dictated by the type of horse under examination. The methods used for a 3-year-old Thoroughbred racehorse differ from those for a 6-year-old destined for horse trials. Seeing the horse lunged on soft and hard surfaces and ridden is helpful to gain maximum information about any potential lameness problems. The vendor should be encouraged to use any protective boots or bandages that might be used normally. Subtle lameness or restriction in gait because of thoracolumbar or sacroiliac discomfort may not be evident until the horse performs specific movements when it is ridden.5,6 Small figures of eight may be particularly revealing. Watching the horse do what it specifically is intended to do is good practice. The veterinarian should watch the horse being tacked up and mounted to learn about any cold back behavior or evidence of back pain or other behavioral abnormalities. The horse should be worked reasonably hard relative to its fitness. In many European countries, evaluating a ridden horse is not standard

practice, and if an examination is being performed on behalf of the client by a foreign veterinarian, the client should be advised accordingly. Clinicians who have the prerequisite skill and experience may wish to evaluate horses further by riding or driving them themselves. Feeling the horse in this fashion may answer questions regarding a peculiar gait or way of going and may aid the evaluation of subtle lameness or respiratory noises. Such practice should be done with caution, because legal problems could arise from an unfortunate accident. A signed disclaimer may be helpful in this situation. After strenuous exercise the horse should be allowed to stand for 15 to 20 minutes before being re-evaluated in hand at the walk and the trot. This is a mandatory part of the examination in Great Britain but is not practiced widely in the rest of Europe. Previously inapparent lameness now may become evident. Any previously questionable response to flexion tests may be re-assessed.

EVALUATION OF IDENTIFIED PROBLEMS The veterinarian should now have gained enough information either to discontinue the examination after consultation with the purchaser or to make recommendations for further special examinations. If the horse is lame and a potential cause that may resolve is obvious (e.g., nail bind), re-evaluating the horse on a subsequent occasion may be worthwhile, but the veterinarian should try to ensure that the horse has been worked properly for several days before the re-examination. The veterinarian should always bear in mind that in a mature competition horse, it is relatively unusual not to identify some problems. Taking no risks and advising against purchasing the horse is easy, but that actually may be doing the purchaser, the vendor, and the veterinary profession a disservice. It is important to weigh the risks and describe them to the purchaser as objectively as possible, based on previous experience. At this point having in-depth knowledge of the purchaser, his or her aspirations for the horse, and the attitude to risk and financial ability to take the consequences of risk is most valuable. Further information obtained from radiographic and ultrasonographic examinations may help provide further objective information on which decisions can be based. Decisions also must be related to the horse’s recent competition record, its age, and the future expectations for athletic performance. Low-grade hindlimb lameness associated with mild radiographic changes of the distal hock joints might be an acceptable risk for a horse as a schoolmaster for a young rider, but similar abnormalities identified in a 6-yearold about to step up a level in competition must be regarded as potentially more serious. A veterinarian always must bear in mind that minor problems may become major problems with a change of rider, work pattern, and environment.

RECTAL EXAMINATION Rectal examination is not a routine part of a prepurchase examination and should be performed only with the vendor’s consent if indicated clinically or if a mare is to be used later for breeding.

RADIOGRAPHIC EXAMINATION Radiographic examination is not a standard part of a prepurchase examination. The extent of routine radiographic examination in the United States and some European countries is probably higher than elsewhere. In Holland a strict grading system for evaluation of radiographs is used. The purchaser

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must be made aware that the presence of some radiological abnormalities is not necessarily synonymous with future lameness and the absence of radiographic changes does not preclude future lameness.7 If radiographs are to be obtained for a specific area, then a comprehensive set of radiographs should be ordered to avoid missing lesions apparent on only one view. In many European countries, obtaining only three views in evaluation of the hocks and omitting a dorsomedialplantarolateral oblique view is common. This action may risk the veterinarian missing lesions such as peri-articular osteophytes, which are present only on the dorsolateral aspect of the joints (Fig. 115-3). The regions to be examined and the interpretation of findings are dictated by the previous and intended career of the horse and the results of the clinical examination. Examination of the front feet, fetlock, and hock joints is considered routine in many countries. Evaluation of the carpi, hind fetlock and pastern joints, stifles, and dorsal spinous processes of the thoracic region may be considered. It is, however, important not to overinterpret the significance of some radiographic abnormalities, bearing in mind the variability between breeds and the knowledge that even some obvious changes may be clinically insignificant. For example, Warmblood breeds have a tendency to have a greater number of lucent zones along the distal border of the navicular bone than do Thoroughbreds (Fig. 115-4). A relatively high incidence of spur formation on the dorsoproximal aspect of the middle phalanx occurs in Warmbloods (Fig. 115-5), but this rarely is associated with lameness. However,

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one of the authors (R.D.M.) recognizes a higher incidence of clinically significant osteoarthritis of the proximal interphalangeal joint in Warmblood horses compared with other breeds. Evidence of abnormal lucent zones in the proximal sesamoid bones (sesamoiditis) (Fig. 115-6) should alert the veterinarian to re-evaluate the branches of the suspensory ligament. An ex-racehorse may have periosteal new bone on the dorsal aspect of one or more carpal bones, but this is unlikely to influence the horse’s career as an event horse. A small osteochondral fragment on the dorsal aspect of the distal interphalangeal or metacarpophalangeal joint is often asymptomatic. A small spur on the dorsoproximal aspect of the third metatarsal bone (MtIII) is a frequent incidental finding. However, such findings also must be described to the purchaser, and the potential future significance must be discussed. Small spurs on the dorsoproximal aspect of MtIII do not necessarily reflect osteoarthritis but may reflect entheseous new bone at the attachment of the fibularis tertius or cranialis tibialis. Despite the fact that these spurs are a common finding, accurately predicting the future behavior is impossible. Some spurs may reflect osteoarthritis and may be progressive (see Fig. 115-3). Small osteochondral fragments at the distal intermediate ridge of the tibia in a 3-year-old that has done little work may be asymptomatic, but if they became unstable with increased work, it might result in distention of the tarsocrural joint capsule, and surgical removal may be indicated. Such a finding in a mature competition horse is usually of no consequence. Complete fusion of the centrodistal joint may be identified

A

B

C

D

Fig. 115-3 Plantarolateral-dorsomedial oblique radiographic views of the left (A) and right (B) hocks of 9-a year-old Grand Prix show jumper. There is a small osteophyte on the proximal aspect of the third metatarsal bone (arrow), and subtle modeling of the articular margins of the centrodistal joint in each hock. The horse was clinically sound. C and D, The same horse 24 months later. At this stage the horse showed right hindlimb lameness that was alleviated by intra-articular analgesia of the tarsometatarsal joint. Considerable peri-articular osteophyte formation (arrows in D) involves the centrodistal and tarsometatarsal joints of the right hock (D). The spur on the dorsoproximal aspect of the left third metatarsal bone was changed little (arrow).

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Dorsolateral-palmaromedial oblique view of a 6-yearold Thoroughbred that had raced previously on the flat and was used now for eventing. Note the large lucent zones in the lateral proximal sesamoid bone. The horse had no history of lameness.

Fig. 115-6

A, Dorsoproximal-palmarodistal oblique view of the right front foot of a clinically normal 6-year-old Dutch Warmblood horse with good foot conformation. Note the large size and number of the radiolucent zones along the distal border of the navicular bone. The horse competed successfully for many years with no evidence of foot pain. B, Palmaroproximal-palmarodistal oblique view of the same foot. Note the large, oval-shaped lucent zones in the medulla of the navicular bone.

Fig. 115-4

Lateromedial radiographic view of the left hock of a 9-year-old clinically normal Thoroughbred advanced event horse. The centrodistal joint is fused completely. The horse competed successfully for another 8 years before being retired because of a tendon injury.

Fig. 115-7

ligaments may be indicated. Evidence of osteochondrosis of the trochleas of the femur is of concern in a 3-year-old, even if the condition is asymptomatic, whereas mild flattening of the lateral trochlear ridge of the femur in a 10-year-old jumper free from lameness would be of no concern. Lateromedial radiographic view of the left front pastern of a clinically normal 7-year-old Belgian Warmblood show jumper. Note the modeling of the dorsoproximal aspect of the middle phalanx (arrow). Such spurs are a common finding in Warmblood breeds and usually are not associated with lameness.

Fig. 115-5

unassociated with any other radiological change of the hock (Fig. 115-7). Some horses may compete successfully with such changes for many years, but occasionally lameness subsequently develops because of pain associated with the talocalcaneal-centroquatral (proximal intertarsal) or tarsometatarsal joints. Wellrounded osseous opacities frequently are identified distal to a proximal sesamoid bone (Fig. 115-8). These are often innocuous, but ultrasonographic evaluation of the distal sesamoidean

NUCLEAR SCINTIGRAPHIC EXAMINATION Nuclear scintigraphic examination is not a routine part of a prepurchase examination. If the horse is clinically normal, the interpretation of results of whole body screening is difficult. This practice should be discouraged. In selected horses when interpretation of the significance of specific radiological abnormalities may be in dispute, focused nuclear scintigraphic examination may be helpful.

ULTRASONOGRAPHIC EXAMINATION Ultrasonographic examination of the limbs requires three important pre-requisites: high-class image quality, experience of

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the future significance of which depends on the intended use of the horse, chronicity of the lesion, severity of the lesion, and degree of healing. If ultrasonographic examination is recommended but is refused by the vendor or the purchaser, this should be noted on the prepurchase examination certificate.

THERMOGRAPHIC EXAMINATION Thermography also may provide a useful indicator of low-grade inflammation and help to identify signs of early tendonitis, suspensory desmitis, and splint development. However, a normal thermographic appearance does not preclude the presence of a subclinical tendon lesion.

BLOOD TESTS

Fig. 115-8 Lateromedial radiographic view of the left forelimb of a clinically normal 7-year-old Thoroughbred. There are two well-rounded osseous opacities distal to the proximal sesamoid bones. Such opacities are usually clinically innocuous. interpretation (knowledge of normal anatomy and its variations and the ability to detect abnormality and to interpret its potential significance) and client compliance. A number of clinical situations occur in a prepurchase examination when ultrasonographic examination provides invaluable clinical information not otherwise available. These situations include the following: • An event horse that has competed in a three-day event within the last 6 months but has not competed since or a racehorse that has run recently but has not done fast work since. Strain of the SDFT, unilaterally or bilaterally, is a common injury in event horses and racehorses. Clinical signs of localized heat and swelling may resolve quickly or even pass unnoticed by the vendor (see Chapter 70). Clinical signs of tendonitis may be inapparent at the prepurchase examination but may become evident when fast work is resumed. If the left and right SDFTs are slightly enlarged with rounded margins but are symmetrical, this may pass unnoticed during the clinical evaluation. • An event or racehorse that has not competed or raced in the last several months during the season. The purchaser may have given a plausible explanation for this, but the clinician should be suspicious that the absence from competition may reflect injury. • Known previous tendon or ligament injury. Ultrasonographic examination gives more objective information than can be obtained from palpation alone but does not give information about strength of the structure. • Suspected enlargement of one or more tendonous or ligamentous structures, detection of localized heat, or pain on palpation. • Moderate enlargement of a digital flexor tendon sheath, especially if unilateral, particularly in a forelimb. • Enlargement on the palmar (plantar) aspect of the pastern. It can be difficult to determine by palpation alone if thickening reflects localized fibrosis or swelling of a tendon or ligament. Interpretation of findings in a horse with no identifiable clinical abnormality may not be straightforward, but enlargement of a tendon or ligament usually does reflect previous injury,

The use of blood tests is controversial, and limitations should be discussed with the prospective purchaser. Screening for non-steroidal anti-inflammatory drugs, mood-altering drugs, sedatives, and possibly also corticosteroids is advisable, but the purchaser must be aware that blood tests are less sensitive for these drugs and metabolites than is urine analysis. If the vendor knows in advance that the horse will be tested, this knowledge may provide a deterrent to the unscrupulous. Alternatively, blood may be collected and stored suitably and be analyzed only if a problem arises within the first few weeks of purchase. In Great Britain the Veterinary Defence Society and the Horse Race Forensic Laboratory run a scheme jointly. The vendor signs a form to permit collection of the sample in a specialized container provided by the Horse Race Forensic Laboratory, to which is applied a bar-coded label. The purchaser can elect to have the sample analyzed immediately for a fee or it can be stored at the Horse Race Forensic Laboratory at no charge with the potential for analysis at a later date. This system has proved to be legally robust. The purchaser must be aware that drugs administered intraarticularly may not be detectable, depending on the nature of the drug and the time of administration relative to the time of examination. In professional dealers’ yards in Europe, a high incidence of joint medication to mask lameness occurs. If the horse is being purchased in one country for export to another, testing for evidence of specific diseases may be necessary. For example, horses entering the United States should be tested for equine infectious anemia, dourine, glanders, and piroplasmosis. A horse from an area where African horse sickness has occurred should be tested. Screening for contagious equine metritis may be indicated. Use of hematological and serum biochemical screening and other assays, such as measurement of cortisol and insulin, as an aid to detect equine Cushing’s syndrome in older horses is controversial. Serum testing for equine protozoal myelitis potentially is misleading and should be actively discouraged.

NERVE BLOCKS In some circumstances, nerve blocks may aid interpretation of clinical findings. A horse may appear completely sound under all circumstances but have an unusually short forelimb stride. Does this reflect bilateral foot pain, or is this gait completely normal and natural for this horse? With the vendor’s permission this question could be answered by bilateral perineural analgesia of the palmar nerves at the level of the proximal sesamoid bones. If a horse is lame, but the vendor claims that the horse has never been lame previously, the situation should be discussed with the purchaser. Re-examining the horse on a subsequent occasion may be best, but the vendor should be advised that

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after resolution of the lameness the horse must be worked for at least a week before re-assessment. The veterinarian should ask the vendor to sign a form declaring that the horse has been worked properly and has not received medication, and the veterinarian should collect blood for medication testing when the horse is re-examined. The examining veterinarian’s role is not to perform a lameness investigation; this would be unethical. A lameness investigation is a job for the vendor’s own veterinarian.

SUMMARY OF OBSERVATIONS The veterinarian should summarize the basic assessment of the horse’s physical condition for the buyer. Abnormalities of conformation, insignificant swellings, and any clinical abnormality should be discussed and documented. The initial report should be made verbally to the client or the client’s agent. When dealing with an agent, informing the agent that the client also will be receiving a complete written report is wise. Comments should be as factual as possible, with minimal personal bias, but findings must be interpreted and the risk assessed and documented. Although the veterinarian is working for the buyer, the veterinarian does have an obligation to the seller. The findings should not be discussed with anyone other than those involved in the sale. With permission of the buyer, the veterinarian can divulge any and all information to the seller. A written report reviewing the findings of the examination should be provided to the buyer. The American Association of Equine Practitioners has an excellent set of guidelines for reporting the prepurchase examination. This report can serve as documentation of significant findings for future reference. The veterinarian should advise the buyer about the risks of purchase, without making the decision for the buyer. The veterinarian is not responsible for assessment of the suitability of the horse for a rider or for determining an appropriate value for the horse. However, if the horse is clearly likely to be unsuitable for the purchaser because of temperament or ease of management or riding, the purchaser should be advised accordingly.

GUIDELINES FOR REPORTING PREPURCHASE EXAMINATIONS The American Association of Equine Practitioners has approved the following guidelines for reporting equine prepurchase examinations. The spirit of these guidelines is to provide a framework that aids the veterinarian in reporting a purchase examination and to define that the buyer is responsible to determine if the horse is suitable. These guidelines are neither designed for nor intended to cover any examinations other than prepurchase examinations (e.g., limited examinations at auction sales and other special purpose examinations such as lameness, endoscopic, ophthalmic, radiographic, and reproductive examinations). Although compliance with all of the following guidelines helps to ensure a properly reported prepurchase examination, the veterinarian has the sole responsibility to determine the extent and depth of each examination. The American Association of Equine Practitioners recognizes that for practical reasons not all examinations permit or require veterinarians to adhere to each of the following guidelines. 1. All reports should be included in the medical record. 2. The report should contain the following: a. A description of the horse with sufficient specificity to identify it fully. b. The time, date, and place of the examination.

3. The veterinarian should list abnormal or undesirable findings discovered during the examination and give his or her qualified opinions as to the functional effect of these findings. 4. The veterinarian should make no determination and express no opinion as to the suitability of the animal for the purpose intended. This issue is a business judgment that is solely the responsibility of the buyer that he or she should make on the basis of a variety of factors, only one of which is the report provided by the veterinarian. 5. The veterinarian should record and retain in the medical record a description of all the procedures performed in connection with the prepurchase examination, but the examination procedures need not be listed in detail in the report. 6. The veterinarian should qualify any finding and opinions expressed to the buyer with specific references to tests that were recommended but not performed on the horse (x-rays, endoscopy, blood and drug tests, EKG, rectal examination, nerve blocks, laboratory studies, and so on) at the request of the person for whom the examination was performed. 7. The veterinarian should record and retain the name and address of parties involved with the examination (buyer, seller, agent, witness, and so on). 8. A copy of the report and copies of all documents relevant to the examination should be retained by the veterinarian for a period of years not less than the statute of limitations applicable for the state in which the service was rendered. Local legal counsel can provide advice as to the appropriate period of retention.

REFERENCES 1. Dyson S: Evaluation of the musculoskeletal system. II. The limbs. In Mair T, editor: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal. 2. Dyson S: Evaluation of the musculoskeletal system. III. The feet and hooves. In Mair T, editor: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal. 3. Dyson S: Evaluation of the musculoskeletal system. IV. The use of flexion tests and small diameter lungeing. In Mair T, editor: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal. 4. Chandler N: Evaluation of the musculoskeletal system. V. The use of flexion tests and small diameter lungeing: an alternative view. In Mair T, editor: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal. 5. Cauvin E: Evaluation of the musculoskeletal system. I. The neck and back. In Mair T: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal. 6. Dyson S: Evaluation of the musculoskeletal system. VI. The role of ridden exercise in identifying lameness. In Mair T, editor: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal. 7. Phillips T: The use of radiography in the prepurchase examination. In Mair T: British Equine Veterinary Association manual: the prepurchase examination, Newmarket, 1998, Equine Veterinary Journal.

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Lameness in the Show Hunter and Show Jumper Robert P. Boswell. Richard D. Mitchell, and Sue J. Dyson

HISTORICAL PERSPECTIVE Show jumping and related competitions have origins in hunting sport and military tradition. The show hunter, most popular in North America, has evolved from the traditions of fox and stag hunting. These horses were expected to provide fast, safe, and athletic passage for the rider, and considerable pride was taken in being well mounted and having the horse admired. Today in the showring these horses are judged for beauty, athletic ability, manners, and way of going. Jumping style is important and must be coupled with consistent performance. Some competitions encourage the development of a young horse to a higher level of training, others award a mature horse for outstanding performance, and others separate amateur and professional riders. Horses often are selected based on suitability for a particular division of competition. The modern show jumper has many of its origins with military traditions. Many cavalry officers were by necessity highly skilled and accomplished horsemen. Thus when the era of the modern Olympics began, the equestrian competitors were military men. With the mechanization of the military and the replacement of the cavalry with motorized transport, the private sector became more involved in Olympic show jumping. Many of the early civilian competitors were retired military men. Show jumping has become increasingly more popular, and many talented riders have emerged on the national and international scenes. Since the 1960s many women have entered the sport once dominated by men.

STRUCTURE OF THE SPORT Show jumping combines athletic effort of the horse and rider. The scoring process is objective, with the winner jumping the course with the fewest rails knocked down and, in the jump off, in the fastest time. Heights of fences range from 1 m at novice level to 1.7 m for advanced competitions. As the jumps get bigger, the potential for injury increases, and many conditions develop from repetitive strain. Many of the fences are set at distances to each other so that the horse must adjust stride length to fit in the appropriate number of strides. A good horse must have explosive power and great athleticism, combined with carefulness—a desire not to hit fences. Contrary to many equine sports, similar numbers of mares and geldings or stallions compete. Some older horses compete at levels of competition lower than they have reached to be schoolmasters for less experienced riders. These older horses may experience unique problems related to age and use. Today show jumping is a highly diverse and competitive sport enjoyed all over the world from beginners to the level of the Olympic Games. At the top level the sport is entirely professional, with horses changing hands for huge prices and with large amounts of prize money available, putting pressure on the veterinarian to keep horses sound. Competition continues throughout the year with

outdoor shows during the summer months and indoor shows during the winter, so horses potentially get little break.

CHARACTERISTICS OF THE JUMPING SPORT HORSE Many breeds are capable of show jumping and related activities and include Thoroughbred, European Warmbloods, Thoroughbred/Warmblood crosses, and American Quarter Horses and related crosses. The European Warmbloods most often are represented by the Hanoverian, Holsteiner, Trakhener, Dutch Warmblood, Selle Français, Swedish Warmblood, and Irish crossbred breeds. Breeding in continental Europe has become highly specialized and has developed in part through financial support from state governments. Most modern day top-level show jumpers are naturally well-balanced, goodmoving athletes. Various pony breeds, such as the Welsh crosses, are used for children (see Chapter 127). Current preferences are for lighter and taller horses than previously, with moderate muscling. This body type is associated with greater speed and agility, which are assets to a modern show jumper. This body type also benefits hunters because they have graceful movement, with good extension and natural balance. Larger horses, if not excessively heavy, are at an advantage for show jumping because of greater stride length and overall strength and explosive power. The Thoroughbred long has been preferred by American trainers for the hunter ring; however, in recent years Warmblood breeds and American Quarter Horses have gained favor because of a calmer nature and better manners. Horses often start competing at 4 years of age, reach peak ability at 9 to 12 years of age, and may continue to compete until 18 to 20 years of age, therefore the competition career is exceptionally long.

TRAINING Training of the hunter/jumper emphasizes using the hindquarters for engagement and collection, which places more weight and stress on the hindlimbs as they are brought forward and under the rider during locomotion. Such a posture is somewhat unnatural for the horse, whose normal inclination is to distribute weight over the forehand. These stresses may contribute to or accelerate the development of problems of the thoracolumbar and pelvic regions and joints of the hindlimbs. Early in the training of a young horse, lameness often reflects musculotendonous problems and relates to lack of accommodation to work. When training over fences begins, new loads on the hindlimbs occur that place more stress on soft tissues and joints. Stresses on the forelimbs also are increased because they are involved in takeoff and landing. The forelimbs are involved in setting up the jump and aiding in the directional change from horizontal to vertical. On landing the forelimbs

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receive considerable impact loads and absorb the entire weight of the horse. Increased load places stress on the foot, joints, and the soft tissues. Horses must learn to adjust stride length by shortening or lengthening the stride, to jump from a line perpendicular to a fence or at an angle, to turn quickly, to change leading legs in canter, and to jump from variable speeds of approach. Unwillingness to change leads or always favoring one lead when landing after a fence may indicate a problem (see Chapter 100). Much of the basic flat work training is similar to dressage. Many lameness conditions encountered early in a horse’s training begin as subtle performance-limiting problems, progress relatively slowly, and may disappear with further conditioning. However, excessive training leads to the development of important problems such as chronic muscle soreness, fatigue, and behavioral changes. Slow, steady work with a gradual buildup in exercise intensity and duration results in fewer joint and soft tissue problems later.

TRAINING AND COMPETITION SURFACES Training, warm-up, and competition surfaces may play a substantial role in the development of lameness in a jumper. Soft, deep footing requires much more effort by the horse and is responsible for early fatigue of muscles, tendons, and ligaments. Injuries include gluteal muscle strain and spasm, suspensory desmitis, desmitis of the accessory ligament of the deep digital flexor tendon (ALDDFT), and superficial digital flexor tendonitis. Sandy soils contribute to the development of hoof wall problems. Hard surfaces may result in bone- and joint-related injuries, including foot problems such as subsolar bruising, distal interphalangeal joint synovitis, and osteoarthritis of the proximal interphalangeal and distal interphalangeal joints. Most outdoor competitions in Europe take place on grass, with a few of the higher-level competitions taking place on all-weather surfaces. The nature of the footing depends highly on the weather and can vary extremely. To enhance traction, screw-in studs often are used in the front and hind shoes. Studs may be used in the medial and lateral branches of the shoe or just the lateral branch to reduce risk of interference injuries. If studs are used in only one branch of the shoe, this immediately creates mediolateral imbalance and the potential for abnormal torque. Studs also alter the dorsopalmar balance, especially if the ground is firm. Horses that flex the carpi excessively during jumping may have to wear a girth guard to protect the sternal region from self-inflicted injuries. If a horse is jumping on firm going, studs concentrate the forces of impact and can predispose the horse to deep-seated bruising of the foot. There is a tendency in horses with poor quality horn for the hoof wall to break in the region where studs are placed. Excessive work, such as long period of lunging a hunter to calm it down, prolonged competitive efforts, and long show schedules of repeated competitions play a role in the development of many injuries in hunters and jumpers.

Toe-in or toe-out forelimb conformation may predispose horses to proximal interphalangeal and metacarpophalangeal joint problems. Short, more upright pasterns predispose horses to navicular disease and distal interphalangeal joint and proximal interphalangeal joint synovitis or osteoarthritis. These horses are often straight through the shoulder as well and lack the stride and extension necessary for jumping. Long, more sloping pasterns sometimes are associated with sesamoiditis and soft tissue injuries to the distal limb. Over-at-the-knee conformation may predispose horses to SL strain and should be avoided in selecting a jumper. Offsetknee conformation predisposes a jumper to medial splint problems. However, attention always should be paid to subclinical contralateral hindlimb lameness in a mature horse that develops an acutely painful medial splint bone. Subtle angular limb deformities are rarely a problem, provided proper attention is paid to shoeing and hoof balance. Extremely sickle-hocked conformation is associated with weak hindlimbs and places more stress on the plantar ligaments and the centrodistal and tarsometatarsal joints. A straighter hock is actually more desirable, but an overly straight hock may predispose to SL strain and distal hock joint pain. Horses that are extremely straight through the stifle are poor jumping prospects and have a high incidence of instability and upward fixation of the patella. A more angular stifle gives the horse a longer, more powerful stride and is thought to provide more strength for jumping. A long, sloping hip and croup are desirable characteristics in a jumping horse, providing strength and power. Horses with a flat croup often suffer from thoracolumbar and sacroiliac pain. Asymmetry of the tubera sacrale and tubera coxae can be seen in the absence of lameness and may reflect previous trauma. An experienced rider usually can manage these horses. Horses with excessively base-wide or base-narrow hindlimb conformation place abnormal stress on the feet and joints. Base-wide horses may have an increased incidence of hock problems, whereas base-narrow animals may suffer more from stifle problems.

SHOEING CONSIDERATIONS Many lameness problems are a direct result of trimming and shoeing. Neglected feet are frequently a source of lameness, and a poorly shod foot also may contribute to lameness by forcing the horse to transfer abnormal and excessive stresses to other parts of the limb or to other limbs. Many of the Warmblood breeds have relatively tall, narrow upright feet, which are predisposed to the development of thrush and sheared heels. Studs in the shoes may create foot imbalance and may increase the severity of interference injuries. A good cooperative relationship with an experienced farrier is an essential element in lameness prevention and management. This can be a problem for top-level competition horses that are constantly moving from show to show and are being trimmed and re-shod by different people with varying talent.

TEN MOST COMMON LAMENESS PROBLEMS Conformation and Lameness Conformational abnormalities of the foot predispose horses to lameness. Underrun heels, long toe, and a broken hoofpastern axis frequently contribute to palmar heel pain and distal interphalangeal joint synovitis. Horses with improper medial-to-lateral hoof balance may develop sheared heels, crushed bars, and chronic foot pain. Base-wide or base-narrow forelimb conformation may contribute to injuries to the suspensory ligament (SL), its branches, and the distal sesamoidean ligaments.

The following are the 10 most common lameness problems of show hunters and show jumpers: 1. Palmar foot pain 2. Distal hock joint pain 3. Osteoarthritis of the distal interphalangeal joint 4. Proximal suspensory desmitis 5. Thoracolumbar and sacroiliac pain 6. Osteoarthritis or trauma of the metacarpophalangeal joint

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7. Stifle pain 8. Osteoarthritis or trauma of the proximal interphalangeal joint 9. Gluteal myositis 10. Superficial digital flexor tendonitis and desmitis of the ALDDFT Many of these problems are interrelated, and more than one problem may occur simultaneously. We have attempted to list these in relative order of frequency; however, this is not intended to imply that one is more serious than another.

LAMENESS EXAMINATION Before examining a horse for a suspected lameness problem, several factors should be considered. If the horse is currently competing, will any diagnostic tests or treatment have an effect on the horse’s ability to continue competition? Knowledge of the competition rules and drug use guidelines are essential. Has the horse recently competed? Has a change in exercise intensity or duration been made? Does the horse have a new trainer? When was the horse last shod? If the horse has been competing away from home, it is important to determine if another veterinary surgeon already has examined and treated the horse, and if so with what. The lameness examination should begin as the horse is walked from the stall or paddock, because movements such as a small circle to reverse its direction may offer clues as to which limb or limbs may be affected. The horse should be examined at the trot in hand on a firm, level surface; lunging in small circles in both directions on firm footing may exacerbate subtle lameness. It is sometimes necessary to see the horse ridden to determine which limb is lame. Proximal and distal limb flexion tests are performed on all limbs. The method and duration of flexion is a personal preference but should be consistent and interpreted with care, bearing in mind that joints and soft tissue structures may be stressed simultaneously. It has become common practice for top-level competition horses to be examined periodically throughout the year to try to detect early warning signs of impending problems. A positive response to flexion is often followed by treating the stressed joint(s). The true value of this practice is difficult to determine objectively. The response to hoof testers is assessed, and each limb is palpated systematically. An obvious source of pain may be identified, but perineural or intra-articular analgesia often is required to determine the sources of pain. Results are sometimes confusing and always should be related to the clinical examination. Aseptic preparation is essential for intrasynovial injections to minimize the risk of infection. One author (R.P.B.) also administers gentamicin intravenously before entering any synovial space. The conditions of the work area and the temperament of the horse being examined influence which local analgesic technique to use. Intrasynovial analgesia may be delayed or not performed if no clean, dry place is available for safe injection. Although intra-articular analgesia is considered to be more specific than perineural analgesia, it may influence peri-articular pain. In some instances the response to medication may be helpful in localizing pain to a joint. In situations where subtle lameness makes interpretation of nerve blocks difficult, in horses with multiple-limb lameness, for animals that are difficult or dangerous, or when comprehensive blocking fails to localize the lameness, other techniques such as nuclear scintigraphy should be considered. When horses are competing regularly, especially away from home, owners, riders, trainers, and peers often put pressure on the veterinarian to treat the horse based on an index of clinical suspicion, rather than a complete lameness evaluation,

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including local analgesia. Although this can be successful and a positive response to treatment clearly indicates a correct diagnosis, one must bear in mind that some injuries do require rest for the best long-term outcome. A transient response only to treatment or lack of response warrants further investigation of the lameness, and this routinely should include local analgesic techniques.

IMAGING CONSIDERATIONS Only after successfully localizing the source of pain causing lameness or after an extensive physical examination has provided the veterinarian with a reasonable indication of the problem should the examination progress to diagnostic imaging, including radiography, ultrasonography, and if indicated, nuclear scintigraphy, computed tomography, or magnetic resonance imaging. Routine techniques are used, with no special views. High-quality diagnostic imaging is related directly to the veterinarian’s success as a diagnostician.

FAILURE TO MAKE A DIAGNOSIS Every veterinarian, no matter how astute as a lameness diagnostician, eventually will be confused, unsure, or simply have no idea as to why a horse is lame, and consultation with associates or referral to other experts should be considered. Just as a good relationship with a farrier is paramount to the successful management of many foot-related problems, good relationships with other veterinarians are necessary. The veterinarian must be honest and open about the horse with the owners and trainers. Re-examination at a later date also may be beneficial. Some bone lesions may take a few weeks to become visible on plain radiographs, so the veterinarian should consider reimaging if the lameness has been localized.

TREATMENT In recent years the trend has been toward much more aggressive treatment, with many different treatment modalities often being combined to manage a single condition. Although in some circumstances this can be justified, it does mean that the veterinarian is often not sure which treatment really is effective. More targeted treatment actually may be equally effective.

DIAGNOSIS AND MANAGEMENT OF COMMON CAUSES OF LAMENESS Palmar Foot Pain Foot Soreness The most common site of forelimb lameness in a hunter/ jumper is the foot. The horse naturally supports 60% to 65% of its body weight over the forelimbs, and impact forces when jumping dramatically increase load and structural stresses in tissues within the hoof capsule. The manner in which a horse is shod has a tremendous significance in the development of hoof- and foot-related problems. Long toe and underrun heels are common hoof conformational defects and frequently contribute to heel pain because of hoof wall separation or bruising in the heel, quarter, and bar areas. The heels themselves may be excessively long and collapsed inward, and the horse actually may be bearing weight on the outer wall. This often results in sensitivity to hoof tester pressure applied to each heel and when the heels are squeezed together. Lameness is often improved by analgesia of the palmar digital nerves.

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Lateromedial radiographic views of the foot may reveal that the distal phalanx is abnormally oriented, so that the palmar most aspect of the bone is lower (more distal) than the toe. A flattened and chronically bruised heel and bar area (corns) may be seen after removal of the shoe. In horses with chronic lameness deep digital flexor tendonitis and distal sesamoidean impar desmitis may contribute to pain associated with underrun heels. Clinically relevant lesions recently have been documented using magnetic resonance imaging in show jumpers with poor and good foot conformation (S.J.D.). Some horses with underrun heels do not respond well to shoeing. Removing the shoes, trimming back the abnormal heel wall, and placing the foot in a support bandage is recommended. One author’s (R.P.B.) preference is to fashion a cushion support for the palmar hoof using a two-part putty elastomer material (EDSS, Equine Distal Support System, Inc., Penrose, CO). Using the sulci of the frog for support is believed to suspend the heels and promote the new growth to be more vertical in its orientation. This process, however, requires a long-term commitment by the owner and trainer, because new heel growth may take up to 6 months to be sufficient for the reapplication of shoes.

Subsolar Bruising Horses with subsolar bruising often respond well initially to Epsom salt poultices and non-steroidal anti-inflammatory drugs (NSAIDs), for example, phenylbutazone, followed by corrective shoeing. Rasping excessive toe from the solar surface proximally up the dorsal wall to create a 45º angle with the ground surface and application of a shoe fitted full in the heels may be of benefit by removing resistance to breakover. Ideal breakover is located between two points; the first is located by extending a line distally along the dorsal surface of the distal phalanx to the bearing surface, and the other by drawing a perpendicular line from the toe of the distal phalanx to the bearing surface. Egg bar shoes may be required to gain adequate heel support. Shoes such as the EDSS natural balance shoe (Equine Digital Support System, Inc.), with the web behind and squared off at the toe, also improve breakover and reduce stress in the palmar portion of the foot. We do not recommend the application of plastic wedge pads because they actually may contribute to further crushing of the heel and promote the heel bulbs to slide forward and grow horizontally. Leather pads may be helpful in some horses if sole pain is present and sole protection is desired. In horses with a chronic problem, long-term use of aspirin (60 g every other day) may be helpful. Hoof growth supplements containing biotin and methionine also may be of benefit, and we recommend feeding of biotin (100 mg daily) to promote hoof wall growth. Careful attention should be paid to the condition of the gastric mucosa with long-term NSAID use in show horses, because gastric ulceration may occur. Concurrent administration of acid pump inhibitors such as omeprazole should be considered. Extreme sensitivity to hoof testers may be evident along the periphery of the sole at the level of the distal phalanx. Such pain may be associated with bruising, solar margin fractures or inflammation of the distal phalanx caused by chronic concussion from hard ground, or excessive sole pressure from the shoe. These conditions may be more common in North America than in Europe. Radiography is necessary for diagnosis of solar margin fractures of the distal phalanx. Shoeing should be directed at reducing local pressure on the affected areas and improving the overall hoof balance. Egg bar shoes and rim pads are often effective, but soft sole pours that provide extra cushion and shock absorption also help. Twopart putty elastomer is thought to benefit by providing support and lift from the sulci of the frog. Care should be taken with a pour or putty elastomer to avoid overfilling, causing excessive sole pressure.

Subsolar Abscess Subsolar abscesses occur commonly and result from shoe nails improperly applied, poor environmental conditions, a shoe moving slightly, and poor hoof structure. Onset of clinical signs may be rapid, such as immediately following an event, or within the first several days following shoeing. The additional trauma of jumping exacerbates the condition, leading the rider or trainer to suspect trauma or serious injury. Warmth in the hoof wall, increased digital pulse amplitudes, and focal, extreme sensitivity to hoof testers are usually diagnostic, provided that the hoof horn is not excessively hard. Perineural analgesia is rarely necessary to confirm the suspected diagnosis and also may be confusing, because not all horses respond positively. After blocking and trotting the horse to reassess lameness, re-examination of the solar surface of the foot may reveal purulent drainage from the area of suspicion. Treatment is directed toward liberal opening of the solar surface of the foot at the point of maximum sensitivity to establish adequate drainage. If drainage is not established, bandaging the foot with hyperosmotic agents such as products containing magnesium sulfate (Epsom salts) is recommended. Twice daily soaking of the foot with a hot, supersaturated solution of Epsom salts with the bandage left on is also recommended for 3 to 5 days. Once drainage has been established, the foot is bandaged in a similar fashion, and NSAIDs also may be administered to reduce the inflammation. Antibiotics rarely are indicated but are sometimes used if soft tissue swelling occurs above the coronary band.

Navicular Disease Initially to think that a horse is suffering from inflammation of the distal interphalangeal joint when the problem is navicular disease is not uncommon, but navicular disease is also overdiagnosed as a cause of heel pain. The diagnosis of navicular disease carries the stigma of a permanent and disabling lameness and is upsetting to the horse owner and trainer. Therefore the veterinarian should make an exhaustive effort to rule out all other possible sources for the pain causing lameness before making the diagnosis. Navicular disease lameness usually is characterized by a slow, insidious onset. Early signs include shortening of the stride length, tripping, toe stabbing, and an intermittent unilateral lameness, although the lameness is almost always bilateral. Show horses are often more lame the day after a competition. Some horses with no previous lameness history become suddenly lame and are often refractory to standard therapies. Recent experience using magnetic resonance imaging suggests that a proportion of horses that were previously thought to have navicular disease have primary lesions of the deep digital flexor tendon within the hoof capsule (S.J.D.). The response to hoof testers varies, and often the horse shows only resentment when the heels are squeezed together. The wedge test may accentuate lameness. Lameness may be increased after distal limb flexion, but the response is non-specific. Lameness usually is eliminated by palmar digital nerve blocks, and a previously undetected lameness often appears in the contralateral limb. Analgesia of the distal interphalangeal joint or the navicular bursa often improves lameness. Interpretation of the radiographic appearance of the navicular bone is not easy; many horses with navicular bone pain have no detectable radiological abnormality. We consider that radiolucent cyst-like lesions in the body of the bone, large lollypop-shaped radiolucent areas on the distal border of the bone, and enthesophyte formation on the proximal and distal borders of the bone should be considered significant. Nuclear scintigraphy is useful in those horses that appear normal radiographically. The solar view is most useful and may reveal increased radiopharmaceutical uptake in the

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navicular bone, reflecting abnormal bone metabolism. Lateral pool-phase images are also useful for highlighting horses that may have deep digital flexor tendonitis within the hoof capsule or navicular bursitis. Ultrasonographic examination of the navicular bone via the frog may demonstrate roughening of the flexor surface, but subtle changes easily are missed, and only a limited portion of the flexor surface can be examined. Therapy for navicular disease includes pain management and corrective shoeing. Clients should be advised that this disease rarely is cured and requires a long-term commitment to its management. Horses with chronic, refractory lameness may require neurectomy. Trimming and shoeing should be directed toward facilitating breakover, providing support to the palmar aspect of the foot, and in some horses elevating the heels to reduce tension in the deep digital flexor tendon (DDFT). A swelled heel egg bar shoe or the EDSS natural balance shoe is useful. The forward edge of the shoe should be set back from the toe and the branches fitted full at the heel. Leather wedge pads have been used to elevate the heels; however, the foot should be monitored closely to prevent crushed heels. A commercially available aluminum wedge-shaped shoe also may be used to provide heel elevation. Medical management includes the use of NSAIDs, isoxsuprine, pentoxifylline, and aspirin; intra-articular injection of the distal interphalangeal joint and intrathecal injection of the navicular bursa with corticosteroids and hyaluronan; and rest. Many of these therapies, usually in combination, have proved successful in managing this condition, and we generally would recommend the least invasive therapies first. The degenerative nature of this disease, however, ultimately may result in the failure of any treatment, and palmar digital neurectomy may be considered. Surgical case selection is important, and consideration should be given to the overall condition of the horse and its level of performance. Horses with evidence of deep digital flexor tendonitis and proximal or distal distal interphalangeal osteoarthritis are not considered good candidates because of the possibility of tendon rupture or exacerbation of osteoarthritis. Some horses may experience temporary pain relief from the application of a chemical nerve block using a mixture of corticosteroids, ammonium sulfate, and Sarapin locally injected at the level of the palmar digital nerves. This procedure may work well initially only gradually to lose its effectiveness. Shock wave therapy recently has been introduced as a non-invasive therapeutic option for pain management in navicular disease. Several investigators have reported good results, but differences in equipment and protocols require further investigation.

Sheared Heels Sheared heels are a serious problem in hunters/jumpers. Lameness is often insidious in onset, or a critical point of instability may be reached, producing a more acute lameness. Subtle conformational abnormalities and poor hoof balance likely contribute to this condition. The medial heel often is displaced proximally, with the remainder of the foot splayed laterally. When viewed from the solar surface of the foot, the lateral half of the foot is larger and flared compared with the medial half. The medial heel may be painful to hoof testers, and the heel bulbs may be manipulated independently. Analgesia of the medial palmar digital nerve frequently improves lameness, but usually it is necessary to desensitize both heel bulbs before the horse appears sound. Many horses have radiographic lesions of the medial palmar process of the distal phalanx, such as roughening or demineralization of the margin of the bone, presumably because of chronic trauma and inflammation. The therapeutic goal is to stabilize the

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heel bulbs and reduce pressure on the driven up or proximally displaced bulb. Stabilization most often is accomplished best by improving balance and breakover so that the foot lands flatly and relieving the affected heel from excessive loading during weight bearing. In a jumper, an egg bar shoe is usually satisfactory. Horses with more severely affected feet may benefit from a heart bar, diagonal bar or G-bar shoe. A rim pad with the portion to lie beneath the affected heel cut away may float the heel enough to allow that side to descend into a more normal position. Six to 9 months of persistent treatment are required before a more stable heel structure is established.

Distal Hock Joint Pain Distal hock joint pain is the second most common reason for lameness in a hunter/jumper and is the most common hindlimb lameness. Conformational defects, developmental abnormalities, and the incredible torsional stresses placed on the distal hock joints during jumping are thought to contribute to lameness. A variety of subtle signs becomes manifest before the onset of clinical lameness. Often the trainer or rider complains of a loss in the horse’s stride length, poor impulsion, and a change in the horse’s jumping style. Many horses may develop a tendency to switch leads in front of a jump or may have difficulty jumping from a particular lead. The horse consistently may develop the tendency to jump to one corner of the obstacle, and wider jumps appear to require more effort than usual or even necessary. Clinical examination reveals sensitivity to palpation of the muscles of the lumbar area and shortened cranial phase of the stride. The upper limb flexion test may or may not be positive, and some horses are reluctant to move forward immediately into a trot after flexion and may canter away from the veterinarian. The Churchill test is often positive in horses with tarsometatarsal joint pain but may be negative with centrodistal joint pain. Some horses with proximal suspensory desmitis also respond positively to the Churchill test (R.D.M.). Tarsocrural effusion may or may not be present. We (R.P.B. and R.D.M.) rarely perform regional analgesia of the fibular and tibial nerves, because we consider the procedure difficult to interpret and somewhat dangerous to perform. Intra-articular analgesia of the centrodistal and the tarsometatarsal joints is preferred. However, a negative response to intra-articular analgesia does not preclude centrodistal and tarsometatarsal joint pain, and using fibular and tibial nerve blocks to identify some horses with distal hock joint pain may be essential. With practice this is a highly reliable and safe technique (S.J.D.). With subtle hindlimb lameness or complaint of poor performance and no apparent lameness, it may be necessary for the horse to be ridden and for the rider to interpret the results of the block. The veterinarian should allow this with only the most experienced and talented riders. Radiographic changes vary from none to severe, with what may appear as total radiographic evidence of fusion. Radiographic changes do not necessarily correlate to the degree of lameness. Osteochondral fragments on the distal intermediate ridge of the tibia, or at the distal aspect of the medial trochlea of the talus in a mature athlete in the absence of lameness, are an incidental finding of little if any clinical significance. The severity of the degenerative changes may be similar in the centrodistal and the tarsometatarsal joints; however, the tarsometatarsal joint often has less severe abnormalities. The reason for this is unclear. Nuclear scintigraphy can be helpful and reveals increased radiopharmaceutical uptake (IRU) in the distal aspect of the tarsus. Occasionally, small, focal, moderate to intense areas of IRU may reflect focal areas of loss of joint space, bone trauma, or tearing of ligamentous attachments.

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It has been generally accepted that radiographic evidence of distal joint(s) fusion is desirable, because the suggestion is that once joint fusion has occurred, the inflammation and therefore the pain should disappear. This is an unfortunate myth. Surgical arthrodesis is a currently accepted treatment for horses with osteoarthritis of the centrodistal or tarsometatarsal joints that have become refractory to routine therapies. We challenge this belief and have observed evidence to the contrary. Once arthrodesis has occurred, the normal function of the joint is lost. The distal joints are responsible for the dissipation of the twisting or torsional forces in that area. With this capability gone, these forces are concentrated, and stress fracture of the central or the third tarsal bones may occur or osteoarthritis of the talocalcaneal-centroquatral (proximal intertarsal) joint may develop. Treatment of horses with distal hock joint pain varies. Intra-articular injections of corticosteroids (20 to 40 mg methylprednisolone acetate or 5 to 7.5 mg betamethasone in each joint) and hyaluronan (2 ml per joint) is usually the first treatment, combined with NSAIDs, and is usually the best and most expeditious means of treatment. With radiographic evidence of severe osteoarthritis we use a long-acting corticosteroids alone. Treating horses with more mildly affected joints with a low corticosteroid dose in combination with hyaluronan may be chondroprotective and extend the useful life span of the joint. Combined therapies have grown popular because of the perception that they work better and the effects last longer. Most horses respond favorably, and the riders comment on how much better the horse performs. Many horses, especially those with demanding show schedules, have the hocks (and perhaps other joints also) routinely injected at intervals predetermined by the history of when the horse has previously become unsound following previous injections. Maintenance treatment is performed about 1 month earlier. This reduces the risks of loss of performance, recurrent lameness, or development of a secondary problem. Many horses also are treated with the oral nutraceuticals, parenterally administered polysulfated glycosaminoglycans (PSGAGs), and intravenously administered hyaluronan. These products are incorporated into a maintenance program designed to keep the horse comfortable and prolong the interval between intra-articular joint injections. Frequently the large size of these horses means that they are treated with twice the normal dose of PSGAGs. Horses often are treated with intramuscularly administered PSGAGs and intravenously administered hyaluronan the evening before competition. This is thought to enhance the horse’s ability by making the joints more comfortable. Occasionally, horses with joints unresponsive to corticosteroids and hyaluronan do respond to intra-articularly administered PSGAGs, with or without corticosteroids. Once the horse is made more comfortable, an exercise program consistent in intensity and duration, emphasizing strengthening the hindquarters and abdominal muscles, improves performance. Recent reports describe shock wave therapy being used to control pain. Shoeing is aimed at encouraging breakover in the center of the hoof by squaring the toe. Some veterinarians prescribe a lateral trailer in an effort to decrease the twisting motion of the limb. Alternative therapies such as muscle massage and acupuncture are used commonly with traditional therapies.

Distal Interphalangeal Joint Synovitis and Early Osteoarthritis Inflammation of the distal interphalangeal joint is common in jumping horses and usually results in subtle lameness that is frequently bilateral. Palpable joint effusion may or may not be present. Many horses, but not all, respond positively to the distal limb flexion test. Forelimbs are most commonly affected, but the hindlimbs also may be involved. The horse

may have a reduction in stride length, and lameness is most obvious when the horse circles on firm footing. The rider or trainer may complain of a reduction in jumping performance, such as a reluctance to leave the ground and landing in a heap. Very hard surfaces for training or competition and surfaces that are too soft, irregular, and unstable may be predisposing factors. Soft footing, although not seemingly likely to contribute to excessive concussion, produces torsion forces on the distal interphalangeal joint that strain the peri-articular soft tissues. An underrun heel, long-toe conformation is probably the single most important contributing factor. The horse often shows a painful response to hoof testers with pressure applied from either heel to the opposite frog and from the center of the frog to the dorsal hoof wall. Lameness usually is improved with analgesia of the palmar digital nerves and eliminated with palmar (abaxial sesamoid) nerve blocks or intra-articular analgesia of the distal interphalangeal joint. Lameness in the contralateral limb may become apparent. Radiographic changes may be absent or subtle; however, in horses with more chronic or severe disease, reactive periosteal bone may be present on the dorsal aspect of the middle phalanx, and remodeling of the extensor process of the distal phalanx may occur. With chronic, severe osteoarthritis of the distal interphalangeal joint there may be subchondral radiolucent areas in the distal phalanx consistent with collapse of the joint. Prominent radiolucent areas representing synovial invaginations may be present on the distal border of the navicular bone. Nuclear scintigraphy is useful to rule out bone involvement. An area of IRU in the synovial structures of the joint may be visible in pool-phase studies. Differentiating the palmar pouch of the distal interphalangeal joint from the navicular bursa is difficult, and both structures may be involved in horses with severe lameness. Therapy for distal interphalangeal joint synovitis depends on the severity of the lameness and the horse’s competition schedule. Proper trimming and shoeing as for palmar heel pain is essential. The use of NSAIDs is common. Peripheral vasodilating agents such as isoxsuprine are of questionable value, although higher than standard doses are sometimes effective. Intra-articular injection of high molecular weight hyaluronan and corticosteroids (triamcinolone or betamethasone) with proper shoeing and an appropriate amount of rest usually yields the best results. Occasionally, repeated injections are necessary after 4 to 6 weeks; however, injections repeated more frequently than once every 3 months should be avoided. Nutraceuticals and parenterally administered chondroprotective agents (PSGAGs) may be beneficial.

Collateral Ligament Injury of the Distal Interphalangeal Joint Some horses with synovitis of the distal interphalangeal joint that are unresponsive to therapy should be evaluated for possible collateral ligament injury of the distal interphalangeal joint. In a few horses, we (R.D.M. and S.J.D.) have identified thickening and tearing of the collateral ligament ultrasonographically, and unusually, focal increased radiopharmaceutical uptake of the palmar aspect of the distal phalanx, scintigraphically. Differentiating this injury from other more common conditions of the distal phalanx may be difficult. Horses with this injury should be managed with corrective shoeing and rest. Work level is reduced substantially. Extracorporeal shock wave or therapeutic ultrasound therapy combined with a 2- to 3-month period of rest appears to be effective.

Suspensory Desmitis Injury to the SL is the most common soft tissue injury and certainly one of the most serious injuries of the jumping horse. Early lesions may go unnoticed by even the most skilled horseman, because the rider or trainer is aware of only a vague

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problem, from which the horse warms out of fairly quickly. Exercise continues and the injury eventually worsens to the point of causing enough damage to produce an obvious lameness. The lameness usually is more pronounced when the horse is trotted in a circle with the affected limb on the outside and also may be exacerbated in soft footing. Mid-body and branch lesions are diagnosed easily by palpation; however, diagnosis of injury to the proximal aspect of the SL is more challenging. The distal limb flexion test may increase the lameness with mid-body and branch lesions, whereas carpal flexion and upper hindlimb flexion frequently accentuate lameness associated with proximal suspensory desmitis, which can cause confusion with hock pain. A high palmar metacarpal nerve block, direct infiltration of the SL origin, or analgesia of the lateral palmar nerve eliminates lameness in the forelimb. Analgesia of the proximal aspect of the hindlimb SL requires caution, because injury to the veterinarian and patient can occur. Analgesia is best performed with the horse restrained with a twitch and the leg positioned in the veterinarian’s lap as if the horse’s foot were being examined. Displacing the flexor tendons medially and isolating the SL for injection is thus easier. The SL is infiltrated with local anesthetic solution from the axial aspect of the lateral splint bone, fanning across the SL from lateral to medial. During injection, the local anesthetic solution should go in with considerable resistance if it is being deposited within the SL itself. Alternatively, perineural analgesia of the deep branch of the lateral plantar nerve can easily and safely be performed with the limb bearing weight (S.J.D.). With direct infiltration of the ligament, soundness should be almost immediate. Some risk exists of entering the palmar outpouching of the carpometacarpal joint capsule using direct infiltration in the forelimb, causing potential diagnostic confusion; however, infiltration in the hindlimb inadvertently entering the tarsometatarsal joint is less likely. Ultrasonographic examination of the SL may reveal obvious lesions; however, finding minimal evidence of damage in horses with acute injuries is not uncommon. Recent nerve blocks may confuse interpretation, so ultrasonographic examination is best delayed for 1 to 2 days. Alternatively, ultrasonographic examination may precede nerve blocks. In our opinion, ultrasonographic imaging of the proximal SL in the hindlimb is difficult. The transducer should be placed on the plantaromedial aspect of the limb to get the best-quality images. A cross-sectional area of greater than 1.5 cm2 suggests proximal suspensory desmitis, even in the absence of a focal or diffuse loss of echogenicity. Radiographic examination of the proximal aspect of the third metacarpal or metatarsal bone may demonstrate sclerosis with or without lysis in a dorsopalmar (dorsoplantar) view or subcortical sclerosis in lateromedial views. Incidental radiographic changes can be seen in hindlimbs. Nuclear scintigraphy has proved useful in characterization and prognosis of horses with proximal suspensory desmitis. The pool phase may reveal increased radiopharmaceutical uptake in the ligament. A unique pattern of uptake is present in the forelimbs and hindlimbs in the bone phase. The lateral view is most important in the forelimb because focal IRU is present on the proximopalmar aspect of the third metacarpal bone (McIII) if bone injury accompanies proximal suspensory desmitis. Proximal suspensory desmitis occurs often without chronic changes in the palmar/plantar cortex of the third metacarpal or metatarsal bone. Dorsal views of the forelimb are less sensitive than lateral views. In the hindlimb the lateral view is equally important. The veterinarian should not confuse as a lesion IRU in the proximolateral aspect of the metatarsal region in plantar views, which is a normal finding. Ultrasonographic abnormalities of the SL and abnormal scintigraphic images confirm injury to the bone at the origin of the SL, indicating a complex injury involving two tissue types and adversely affecting the prognosis.

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Therapy for horses with proximal suspensory desmitis varies. NSAIDs, combined with rest and physical therapy, are the most popular and yield the most consistent results. Clients should be advised that treatment may take 6 to 12 months. We recommend stall rest for 10 to 14 days after the injury, with twice daily hand walks. Phenylbutazone is administered (2 g BID for 4 days and then 1 g BID for 10 days). Walking under saddle then is commenced for 20 to 30 minutes once or twice daily for the next 30 days. Follow-up ultrasonographic examinations are performed after 44 days and every 30 to 60 days thereafter. The duration and intensity of exercise gradually are increased based on the ultrasonographic appearance of the SL and the clinical appearance of the horse. Trotting begins once the horse is sound. Many veterinarians in North America recommend an internal blister, using 2% iodine in almond oil infiltrated into the SL. Light exercise is continued immediately following this therapy, with a gradual return to full work. Shoeing should be improved if necessary. In horses with acute proximal suspensory desmitis with no significant ultrasonographic changes, local injection of corticosteroids may decrease inflammation and eliminate pain. We use triamcinolone (12 to 18 mg), betamethasone (30 mg), or isoflupredone acetate. Sarapin (4 ml) also may be added. Recently a surgical procedure has been reported in which the tight fascia overlying the proximal SL is transected or released so as to reduce any increased pressures or compression created by this apparent compartmental syndrome. Bone marrow aspirate taken from the sternum then is injected in the area of the injury in an effort to stimulate healing. Early results from this technique appear promising; however, further investigation and long-term follow-ups are needed. Neurectomy of the deep branch of the lateral plantar nerve has been used successfully for management of hindlimb PSD (S.J.D.). Shock wave therapy has been reported to aid healing of proximal suspensory desmitis, especially in horses with bone involvement. This technique provides profound analgesia and therefore a decrease or elimination of lameness. Further investigation is warranted. Horses with larger lesions within the body of the SL or its branches may benefit from splitting. This appears to allow a more complete healing of core lesions, which otherwise may be slow to resolve. Following surgery, therapeutic ultrasound or infrared laser therapy may aid and reportedly speed healing, although evidence is mainly anecdotal.

Back Pain Back pain is common in jumpers, and although signs are recognized easily, the etiological diagnosis may be elusive and complex. The trainer or owner may perceive that a horse has back pain from many clinical signs including sensitivity to grooming and saddling, resistance to rider weight, overall body stiffness, poor performance, and pain on palpation of the muscles over the back. Many of these signs are also common to other diseases or injuries and may be secondary to clinical or subclinical hindlimb lameness resulting in an altered gait. Primary back pain may be caused by severe muscle strain, impingement or overriding of the spinous processes, diskospondylosis, sacroiliac desmitis, supraspinous desmitis, osteoarthritis of the facet joints, and sacroiliac joint pain. The veterinarian should first attempt to rule out any lameness. Horses with distal hock joint or stifle pain may swing the hindlimb outward away from the body or inward toward the midline in an attempt to reduce the degree of joint flexion required to advance the limb. Hindlimb lameness should be suspected in horses with simultaneous gluteal and back pain. Chronic forelimb soreness, particularly involving the foot, also may contribute to back pain because of an inverted way of jumping that somewhat protects the foot on landing. Teeth problems or neck pain also should be considered.

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Severe back pain suggests a primary back problem. The horse may move with a shortened, stiff gait and appear to be flat or hollowed out in the back when ridden but appear much more comfortable when moving free in a paddock. Injection of local anesthetic solution into the painful areas of the back frequently changes the horse’s movement.

Impinging Spinous Processes Radiography of the thoracolumbar spinous processes may reveal impingement with sclerosis and bone proliferation and bone lysis. Nuclear scintigraphy can be used to diagnose and support the diagnosis of spinous process impingement and osteitis, although false-negative results are sometimes obtained. Occasionally, areas of IRU are visible in the spinous processes without any radiographic changes, and supraspinous ligament desmitis should be considered. The treatment for impingement of the spinous processes or supraspinous desmitis is similar. NSAIDs and methocarbamol are prescribed routinely for a prolonged period. Sarapin and corticosteroids frequently are injected between and around the impinging spinous processes. The locations for injection are determined best by placing a radiodense marker on the top of the back during radiography and then identifying the affected vertebrae by clipping the hair.

Muscle Injury Acute muscle strain may be accompanied by spasm, which is evident as a firm, painful swelling. Immediate application of ice and administration of NSAIDs such as phenylbutazone or naproxen are beneficial One author (R.P.B.) also administers between 20 and 40 mg of dexamethasone once daily for 2 days in horses with acute pain. Later, moist heat and therapeutic ultrasound reduce pain and inflammation. Acupuncture has proved useful in managing back pain no matter what the cause. Chiropractic manipulation may be of some benefit in relieving pain and muscle spasm in an injured back. Pulsating magnetic field therapy is used routinely in show jumpers for the longterm management of back pain. We believe that many owners feel pressure to do everything possible for their horses, and because of anecdotal reports of benefit in people, certainly no harm will come from using such therapy. Saddle fit always should be evaluated critically in a horse with chronic or recurrent back pain, and thermography may be helpful, together with advice available through most good saddle manufacturers.

Fracture of the Withers Fracture of the withers is not uncommon if a horse flips over backward. The withers area may appear flat and is extremely painful to palpation. The horse plaits in front and holds the neck stiffly. Radiographs are diagnostic. Treatment is directed toward reducing pain and inflammation by applying ice and administering NSAIDs immediately following the injury. Bone sequestrae occasionally develop, and purulent drainage may appear weeks after the injury. However, most fractures are uncomplicated and horses usually may be able to return to work after 6 to 12 months of rest.

Sacroiliac Joint Pain Sacroiliac strain is common in show jumpers. Many horses suffer from chronic low-grade pain that never seems adversely to affect the ability to perform. With severe pain a horse may stand parked out (the hindlimbs are extended unusually) and rest one hindlimb. Unilateral lameness may develop, and the horse’s performance then is affected severely. The horse may experience pain on palpation around the lumbosacral region and directly over the tubera sacrale, but this is not specific. Exerting pressure on one of the tubera sacrale may reveal slight motion and even may be resented by the horse. The horse may offer considerable resistance when one of the hind feet is picked up and the limb is flexed high. Rocking the pelvis may cause the horse to grunt. A hunter’s bump is not associated necessarily with this condition, although it may be. Injection of local anesthetic solution deep into the muscles

directed toward the sacroiliac articulations should be performed with caution because the horse may lose its ability to stand, which causes severe distress. Nuclear scintigraphy may reveal little if any IRU in this region and is therefore unreliable, but with modern motion-correction software program and improved image quality, useful information is acquired in some horses (S.J.D.). Rest and time are the most important factors influencing the outcome. These horses require at least 6 months to heal. Severely affected horses should be given stall rest for 30 days, followed by 2 to 3 months of controlled paddock rest. Light exercise then may begin, gradually increasing the intensity and duration of the work. In our experience, acupuncture has been extremely useful for pain management and the treatment of muscle spasm. Horses with less severe injuries may be managed successfully by local injections of corticosteroids and Sarapin deep into the painful areas. These horses are able to continue to exercise and compete successfully. The procedure involves directing a 9-cm needle from a point just medial to one of the tubera sacrale along the inner surface of the ilium deep toward the sacroiliac articulation. Injection of the acupuncture points on either side of or parallel to the sacrum with the same solution also may be performed. Chiropractic manipulation often is attempted in horses with sacroiliac injury. Although chiropractic has proved useful as a diagnostic tool and may be of benefit with mild sacroiliac strain, manipulation of the sacrum in more severe injuries never replaces the need for prolonged rest. Pulsating magnetic field therapy, cold laser, and therapeutic ultrasound may be used for the long-term management of chronic sacroiliac problems.

Fetlock Joint Synovitis and Osteoarthritis Metacarpophalangeal joint synovitis and osteoarthritis are common in older horses with lengthy careers. Chronic capsulitis results in a thickened, prominent joint capsule with a dramatic decrease in the flexibility of the joint. At least a moderate amount of joint effusion occurs, but many sound horses may have chronic effusion, thickening of the joint capsule, and reduced range of motion. The source of pain is confirmed by a low four-point palmar/plantar nerve block or intra-articular analgesia. Radiographic examination may reveal osteophyte formation on the proximal aspects of the proximal phalanx and the proximal sesamoid bones, and flattening of the sagittal ridge of McIII. McIII may have a scalloped appearance on the dorsal or palmar aspect in horses with advanced disease. Subchondral lucent areas may develop in McIII or the proximal phalanx and result from severe, focal trauma or end-stage osteoarthritis. The prognosis for horses to return to athletic competition following the development of these lesions is considered poor. Acute fractures and small chips are uncommon in the hunter/ jumper. Small, round, smooth fragments on the proximodorsal aspect of the proximal phalanx are seen in forelimbs and hindlimbs and likely are related to osteochondrosis. These fragments rarely are associated with lameness but occasionally may become unstable and require removal. Nuclear scintigraphy may reveal mild to moderate IRU in the distal aspect of McIII, the proximodorsal aspect of the proximal phalanx, or both. In some horses flexed lateral views are required to separate the bones, especially if radiopharmaceutical uptake in one area is so intense that identifying the adjacent structures is impossible. In the absence of substantial radiographic abnormalities medical therapy should include NSAIDs, intra-articularly administered corticosteroids and hyaluronan, and orally and parenterally administered PSGAGs. Physical therapies such as

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icing, cool water therapy, poultices, sweats, cold laser, therapeutic ultrasound, support wraps, and rest are also beneficial. Arthroscopic exploration of the metacarpophalangeal joint is indicated if the response to medical treatment is transient or poor. Clients should be advised that although the causal problem may be revealed, treatment may not be possible. Debridement of damaged cartilage and subsequent replacement with fibrocartilage may be curative; however, excessive erosion of the articular cartilage warrants a poor prognosis for continued jumping. Therapeutic shoeing targeted at providing support to the palmar aspect of the foot, such as a wide-web egg bar shoe, may be of benefit (R.D.M. and R.P.B.). Proper medial to lateral hoof balance is also important in reducing torque on the metacarpophalangeal joint.

Ultrasonographic examination of the patellar ligaments may reveal desmitis characterized by thickening and a focal or diffuse hypoechoic region. Horses with transient upward fixation of the patella benefit from NSAIDs and an increased exercise program designed to increase muscle tone in the quadriceps group, which stabilizes the patella. Failure to respond to these measures may justify a more aggressive procedure, such as local injection of 2% iodine in almond oil at the proximal aspect, middle portion, and insertions of all three patellar ligaments and into the muscle just proximal to the stifle. This procedure has proved effective in treating transient upward fixation of the patella and subtle soreness in the adjacent muscles. Anecdotal reports describe benefit from estrone sulfate, estradiol, and calcium channel blockers.

Sesamoiditis

Trauma to the cranial cruciate ligament produces profound lameness. Intra-articular analgesia of the femorotibial joints may or may not abolish the lameness, and radiographs of the stifle may be normal in horses with an acute injury. With chronic injury new bone may be seen cranial to the intercondylar eminences, most obvious in a flexed lateromedial view. Injury to the medial meniscus is most common. Intraarticular analgesia of the femorotibial joint on the affected side usually produces improvement in the lameness. Radiographs may reveal osteophyte formation on the proximomedial aspect of the tibial plateau indicative of osteoarthritis and a subjective decrease in the joint space width on the affected side.

Sesamoiditis frequently is associated with chronic suspensory branch desmitis. Horses are variably lame and may warm out of the lameness. Distal limb flexion test usually is resented and results in increased lameness. The suspensory branches may be palpably thickened and painful. Intra-articular analgesia of the metacarpophalangeal joint may improve lameness but does not alleviate it. Lameness is abolished by a low four-point palmar nerve block. Radiographic findings include linear lucent zones or lytic areas within the body of the proximal sesamoid bone (PSB). A generalized loss of bone opacity or proliferative, reactive bone also may be present on the abaxial margins in association with suspensory branch desmitis and insertional lesions of the SL and palmar annular ligament. We find proximodistal oblique views of the PSBs useful. Nuclear scintigraphy is sensitive to inflammation in the PSBs, and IRU in the PSBs often is intense. A flexed lateral view helps to separate the PSBs from McIII. Dorsal or plantar views are required to distinguish between the medial and lateral PSBs. Treatment for horses with sesamoiditis includes rest, NSAIDs, and supportive shoeing similar to that prescribed for fetlock joint problems. Shock wave therapy may be helpful.

Stifle Joint Pain Problems involving the stifle joint are common in show jumpers and frequently accompany problems in the tarsus. Femoropatellar effusion is present variably. Stifle pain may be primary and related to trauma, mechanical problems, developmental diseases, and osteoarthritis, or it may be secondary to other lameness. Primary problems include osteoarthritis, osteochondrosis, meniscal and cruciate ligament trauma, upward fixation or delayed release of the patella, and patellar desmitis. Signs may be subtle at first, with mild shortening of the stride or switching leads at the canter or gallop. Caudal back pain also may be present. The proximal limb flexion test may or may not be positive, and the veterinarian should look closely for subtle gait changes such as a shortening of the cranial phase of the stride. Separation of stifle and tarsal pain may be accomplished by flexing the stifle with the hock slightly extended so that the metatarsal region is held behind the tail and perpendicular to the ground, with the tibia held parallel to the ground. The Churchill test also may help to separate hock from stifle pain. Cranial to caudal motion of the tibia relative to the femur during weight bearing (cruciate test) may produce a change in stride (R.D.M.). However, intra-articular analgesia always is required to confirm the source of pain. Horses with straight stifle conformation are predisposed to upward fixation and instability of the patella. Pain results from subsequent patellar ligament strain and synovitis. Although the limb may be observed to lock in extension, more frequently a slight hesitation in the advancement of the limb is noted. Femoropatellar effusion may be present.

Cranial Cruciate Ligament and Meniscal Injury

Osteochondrosis and Subchondral Bone Cysts Osteochondrosis and subchondral bone cysts should be considered in a young Warmblood that has recently started training or increased its training intensity and has developed lameness localized to the stifle. Intra-articular analgesia usually at least partially eliminates the lameness. We recommend blocking all three joint spaces. Radiographs are usually diagnostic. Arthroscopy may be indicated. Horses with subchondral bone cysts and other lesions on the medial femoral condyle usually have a poorer prognosis than those with osteochondritic lesions of the lateral trochlear ridge of the femur. We recommend radiography of the stifles as part of the routine radiographic study when examining a young Warmblood for purchase. Nuclear scintigraphy of the stifle with osteochondrosis may reveal little if any IRU. The caudal view is important and should always accompany the lateral views. Visible uptake (to any degree) in the distal medial femoral condyle in the caudal view almost always is associated with a pathological condition (R.P.B.).

Synovitis and Osteoarthritis Mature horses may develop synovitis and osteoarthritis of any one or a combination of the stifle joints. Often the femoropatellar and medial femorotibial joints are involved; however, lateral femorotibial osteoarthritis may occur alone. Intraarticular analgesia of all three joints should be performed. The diagnosis may or may not be confirmed radiographically. Osteophyte formation on the proximal medial aspect of the tibia is not uncommon. Nuclear scintigraphy may reveal mild to moderate IRU in the femoral condyle and the opposing surface of the tibia on the affected side in a caudal view. Intra-articular injection of corticosteroids and hyaluronan usually has favorable results. Each joint should be injected separately with double doses of a high molecular weight hyaluronan combined with methylprednisolone acetate (40 to 80 mg) or betamethasone (5 to 10 mg). NSAIDs, parenterally administered PSGAGs, and intravenously administered hyaluronan are also beneficial and may be used routinely with nutraceuticals as part of a maintenance program. Adequate rest also should be prescribed; however, strict stall confinement is not necessary.

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Walking these horses under saddle for 30 minutes once or twice daily is preferred. Alternative therapies such as those described for distal tarsitis are also beneficial. Acupuncture commonly is used for managing horses with stifle pain.

Pastern The pastern region is subject to considerable stress in the jumping horse. Osteoarthritis of the proximal interphalangeal joint is not uncommon and often is associated with distal interphalangeal osteoarthritis. Horses with base-narrow or toe-in conformational defects are affected most frequently. Distal sesamoidean desmitis is also a common problem. Trainers complain that many horses with osteoarthritis of the proximal interphalangeal joint start out stiff when training and feel much better after warming up, but eventually the lameness becomes persistent. With chronic injury comes obvious thickening in the distal aspect of the pastern. Palmar (abaxial sesamoid) nerve blocks normally eliminate the lameness, although a low palmar (four-point) block sometimes is required. Intra-articular analgesia of the proximal interphalangeal joint also usually produces soundness. The veterinarian must beware that a palmar digital nerve block may alleviate lameness associated with osteoarthritis of the proximal interphalangeal joint because of proximal diffusion of the local anesthetic solution.

Osteoarthritis IRU usually occurs in the proximal interphalangeal joints of sound jumping horses relative to other joints. With osteoarthritis the intensity of the IRU usually increases. We (R.P.B. and R.D.M.) therefore believe that subclinical osteoarthritis of the proximal interphalangeal joint is common. Radiographic changes of osteoarthritis of the proximal interphalangeal joint include osteophyte formation on the proximodorsal aspect of the middle phalanx. Subchondral osseous cyst-like lesions in the proximal aspect of the middle phalanx may be associated with severe trauma or end-stage osteoarthritis. Acquired osseous cystlike lesions usually are associated with focal, intense IRU. Management of osteoarthritis of the proximal interphalangeal joint includes using NSAIDs, intra-articularly administered corticosteroids and hyaluronan, and orally and parenterally administered PSGAGs. The horse should be trimmed and shod to reduce resistance to breakover at the toe and to balance the foot to land as flat as possible. Occasionally, wedge pads provide comfort by opening up the dorsal aspect of the joint space. Recently, shock wave therapy has been suggested to be of benefit to horses with advanced ringbone, but this requires validation. Horses with severe osteoarthritis of the proximal interphalangeal joint may respond poorly to medical management, and arthrodesis may be required. Arthrodesis is often successful in the hindlimbs of jumping horses, but results are often unsatisfactory in forelimbs. Tibial neurectomy also has been used successfully.

Soft Tissue Injury Injury to the distal sesamoidean ligaments may or may not be accompanied by obvious swelling or pain on palpation. Analgesia of the palmar (abaxial sesamoid) nerves usually eliminates the lameness. Ultrasonographic examination reveals focal or diffuse hypoechoic regions in the affected ligament. Palmar or plantar displacement of the DDFT medially or laterally may be secondary to distal sesamoidean ligament injury. The veterinarian should image all structures carefully in the pastern, because several structures may be injured simultaneously. DDFT injuries are more common in the pastern than in the metacarpal region. Chronic strain at the insertion of the middle distal sesamoidean ligaments may be evident radiographically as enthesophyte formation on the palmar or plantar lateral and medial borders of the proximal phalanx. Horses with strains and tears of the distal sesamoidean ligaments usually respond to supportive shoeing, NSAIDs, and

rest. Horses with acutely torn ligaments may benefit from cast or splint application for about 1 month. Physical therapy such as therapeutic ultrasound may speed recovery. Injury to these ligaments usually requires from 6 to 12 months for convalescence. Returning the horse to work too soon results in thickening and fibrosis of the pastern and prolonged lameness.

Gluteal Myositis Strain and inflammation of the gluteal muscles is common in jumping horses and usually results from an altered gait secondary to lameness elsewhere in the ipsilateral or contralateral hindlimb. Primary strain may occur in a horse during jumping, when a horse refuses a jump, or after a fall. Palpation of the gluteal muscles at the insertion on the greater trochanter of the femur and over the middle gluteal region reveals milder reactivity in horses with secondary strains and a much more severe response or resentment after a primary muscle injury. Upper limb flexion tests may be positive, especially if the gluteal soreness is secondary to lameness involving the hock or stifle. Treatment depends on the severity of the muscle injury or inflammation. Identification and appropriate treatment of the primary lower limb lameness, if present, may do much to reduce mild soreness in just a few days. Most horses with mild injury also respond well to NSAIDs, local application of moist heat, dimethylsulfoxide, and therapeutic ultrasound. Methocarbamol (20 mg/kg PO BID) may be of benefit. Acupuncture treatments, and in horses with severe injuries local injection of corticosteroids mixed with Sarapin (mix Sarapin, prednisolone, and betamethasone in equal parts in a 12-ml syringe and inject 3 ml per site), provide pain relief. Injections are performed on either side of the spine into the sorest portions of the muscle at 5- to 8-cm intervals or at specific acupuncture sites. Rest and a reduction in the intensity and duration of exercise also may help. Some horses may require total rest with exercise limited to hand walking for several weeks.

Superficial Digital Flexor Tendonitis, Tenosynovitis of the Digital Flexor Tendon Sheath, and Desmitis of the Accessory Ligament of the Deep Digital Flexor Tendon Superficial Digital Flexor Tendonitis Injury to the superficial digital flexor tendon (SDFT) in a hunter/jumper is far less common and severe than in a racehorse, probably because the horse is not trained at high speeds. Injuries are more likely to result from a misstep in deep footing rather than from muscle or tendon fatigue proceeding to failure, but low-grade injuries occur frequently in top-level horses from about 10 years of age. Spontaneous rupture of the SDFT also is seen in old (mid-teens) jumpers. Often no indication of any tendonitis is apparent before rupture. We also have seen several aged horses no longer in competition with spontaneous SDFT rupture. Geldings are overrepresented and there may be an association between this severe trauma and hormonal imbalance. The diagnosis of superficial digital flexor tendonitis is not difficult, and unlike injury to the DDFT usually is not accompanied by substantial lameness, unless an acute injury occurs in the proximal metacarpal region. Ultrasonographic evaluation is recommended to assess the severity, location, and extent of the injury. Several re-examinations are important to determine the rate of healing and predict the time to return the horse safely to competition. The therapeutic goals for management of a hunter/jumper with an acutely injured tendon are rapid reduction of the inflammatory response and elimination of edema. This is achieved with the administration of NSAIDs, low doses of corticosteroids, and diuretics. Ice, hydrotherapy, and support bandages also are used and applied as soon as possible, and in

CHAPTER 117 many horses the trainer does these before the veterinary examination. For horses with strains or injury without actual fiber tearing (type 1 to 2 lesions), peritendonous injection of corticosteroids or intralesional injection of hyaluronan may dramatically decrease the size of the tendon and produce favorable cosmetic results. The trainer must be advised not to exercise the horse and that total healing actually may be delayed slightly. Following the injection, the limb should be supported with a firm, modified Robert Jones bandage to prevent the return of any swelling. Tendon splitting is indicated in horses with substantial core lesions (type 3 or 4 with a diameter greater than 0.5 cm). In horses with smaller lesions, injection of hyaluronan intralesionally may reduce inflammation. Therapeutic ultrasound after the initial phase of healing (3 to 4 weeks after injury) encourages resolution of inflammation and promotes healing. Overall, the time required for tendons to heal sufficiently so the horse may return to jumping depends on the severity of the injury and to some degree the location of the injury. Routine superficial digital flexor tendonitis takes less time to heal than an injury to the SL at the same location. A mild injury takes 3 to 4 months and a severe injury takes about 12 months to heal. Monthly ultrasonographic examinations are used to determine the physical therapy schedule and the optimum time for the horse to return to jumping. Horses often can continue to compete despite active SDFT injuries, although the lesions may progress slowly.

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test is usually positive. Moderate effusion is usually present in horses with an acute injury, but those with chronic injuries may have a thickened, fibrotic DFTS and much less fluid. The proximal aspect of the sheath may show effusion, yet none may occur distally in the pastern. Lack of effusion likely results from a compartment syndrome with thickening of the DFTS synovium, the SDFT, and possibly the palmar annular ligament, thus preventing the flow of fluid distally past the PSBs. Lameness may vary and may only be evident following flexion of the distal limb. Intrathecal analgesia of the DFTS usually improves lameness. Ultrasonographic examination should include the fetlock and pastern regions and reveals increased fluid, allowing the tendons and a thickened synovium to be evaluated easily. The flexor tendons may appear to be normal. Therapy for horses with tenosynovitis of the DFTS varies depending on the severity of the problem and the structures involved. Anti-inflammatory therapy consisting of ice, cool water therapy, poultices, NSAIDs, and corticosteroids is effective in the mild injuries. In horses with more severe injuries, intrathecal injection of corticosteroids and hyaluronan is beneficial. Rest is essential. Horses with mild injuries may return to work in 1 to 2 weeks, but those with more severe injuries require more time. Good trimming and shoeing are beneficial. Horses with chronic, unresponsive tenosynovitis may require endoscopic examination or desmotomy of the palmar annular ligament.

Tenosynovitis of the Digital Flexor Tendon Sheath

Desmitis of the Accessory Ligament of the Deep Digital Flexor Tendons

SDFT injury within the DFTS frequently is seen in jumpers at any age or level of competition. Tenosynovitis also occurs without tendon injury. Superficial digital flexor tendonitis may result in a chronic tenosynovitis and often plagues older horses. Tenosynovitis is slightly more prevalent in the hindlimb, presumably because of the strain caused by the push off in jumping. The DFTS may be warm and swollen. Digital pressure at the proximal and distal aspects of the DFTS usually is resented. Pressure applied directly over the palmar/plantar aspect of the fetlock also may cause pain. The distal limb flexion

Desmitis of the ALDDFT is a common problem, especially in older show jumpers, and often results in sudden onset of lameness after landing over a fence, with rapid development of localized swelling. These clinical signs are typical, but ultrasonography is required to determine the location, severity, and extent of the injury and subsequently to monitor healing. Treatment is similar to that for superficial digital flexor tendonitis. A premature return to work may result in recurrent injury and ultimately adhesion formation between the ALDDFT and the SDFT.

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Lameness in the Dressage Horse Svend E. Kold and Sue J. Dyson

THE SPORT Dressage is the ultimate athletic challenge in equestrian sports because it combines balance, suppleness, and power in a unique gravity-defying manner. A good horse gives the impression of athletic elegance and expressive animation. The gaits are described using terms such as balance, suppleness, and hindlimb activity. The first demand is that the horse is completely obedient and has to go wherever the rider wants and carry out movements at his or her request. In doing so the horse has to rely on its rider, to trust and to accept the rider as its superior. The key to the training and development of a dressage horse from the lowest levels to International Grand Prix is gymnastic exercises, with the aim of strengthening the muscles and thereby avoid-

ing injury to joints and tendons associated with an increased workload. The Federation Equestre Internationale dressage rules state that the object of dressage is the “harmonious development of the physique and ability of the horse.” Through the levels of dressage training, the center of gravity of the horse and rider is placed further caudally, obtained by increasing the degree of flexion and loading of the hindlimbs, while at the same time freeing the front end of the horse to create a more airborne, uphill set of movements. This can be obtained only by increasing the power of the hindlimbs, by synchrony in movement between the forelimbs and the hindlimbs, and through the freedom of movement of the back.

CHAPTER 117 many horses the trainer does these before the veterinary examination. For horses with strains or injury without actual fiber tearing (type 1 to 2 lesions), peritendonous injection of corticosteroids or intralesional injection of hyaluronan may dramatically decrease the size of the tendon and produce favorable cosmetic results. The trainer must be advised not to exercise the horse and that total healing actually may be delayed slightly. Following the injection, the limb should be supported with a firm, modified Robert Jones bandage to prevent the return of any swelling. Tendon splitting is indicated in horses with substantial core lesions (type 3 or 4 with a diameter greater than 0.5 cm). In horses with smaller lesions, injection of hyaluronan intralesionally may reduce inflammation. Therapeutic ultrasound after the initial phase of healing (3 to 4 weeks after injury) encourages resolution of inflammation and promotes healing. Overall, the time required for tendons to heal sufficiently so the horse may return to jumping depends on the severity of the injury and to some degree the location of the injury. Routine superficial digital flexor tendonitis takes less time to heal than an injury to the SL at the same location. A mild injury takes 3 to 4 months and a severe injury takes about 12 months to heal. Monthly ultrasonographic examinations are used to determine the physical therapy schedule and the optimum time for the horse to return to jumping. Horses often can continue to compete despite active SDFT injuries, although the lesions may progress slowly.

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test is usually positive. Moderate effusion is usually present in horses with an acute injury, but those with chronic injuries may have a thickened, fibrotic DFTS and much less fluid. The proximal aspect of the sheath may show effusion, yet none may occur distally in the pastern. Lack of effusion likely results from a compartment syndrome with thickening of the DFTS synovium, the SDFT, and possibly the palmar annular ligament, thus preventing the flow of fluid distally past the PSBs. Lameness may vary and may only be evident following flexion of the distal limb. Intrathecal analgesia of the DFTS usually improves lameness. Ultrasonographic examination should include the fetlock and pastern regions and reveals increased fluid, allowing the tendons and a thickened synovium to be evaluated easily. The flexor tendons may appear to be normal. Therapy for horses with tenosynovitis of the DFTS varies depending on the severity of the problem and the structures involved. Anti-inflammatory therapy consisting of ice, cool water therapy, poultices, NSAIDs, and corticosteroids is effective in the mild injuries. In horses with more severe injuries, intrathecal injection of corticosteroids and hyaluronan is beneficial. Rest is essential. Horses with mild injuries may return to work in 1 to 2 weeks, but those with more severe injuries require more time. Good trimming and shoeing are beneficial. Horses with chronic, unresponsive tenosynovitis may require endoscopic examination or desmotomy of the palmar annular ligament.

Tenosynovitis of the Digital Flexor Tendon Sheath

Desmitis of the Accessory Ligament of the Deep Digital Flexor Tendons

SDFT injury within the DFTS frequently is seen in jumpers at any age or level of competition. Tenosynovitis also occurs without tendon injury. Superficial digital flexor tendonitis may result in a chronic tenosynovitis and often plagues older horses. Tenosynovitis is slightly more prevalent in the hindlimb, presumably because of the strain caused by the push off in jumping. The DFTS may be warm and swollen. Digital pressure at the proximal and distal aspects of the DFTS usually is resented. Pressure applied directly over the palmar/plantar aspect of the fetlock also may cause pain. The distal limb flexion

Desmitis of the ALDDFT is a common problem, especially in older show jumpers, and often results in sudden onset of lameness after landing over a fence, with rapid development of localized swelling. These clinical signs are typical, but ultrasonography is required to determine the location, severity, and extent of the injury and subsequently to monitor healing. Treatment is similar to that for superficial digital flexor tendonitis. A premature return to work may result in recurrent injury and ultimately adhesion formation between the ALDDFT and the SDFT.

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Lameness in the Dressage Horse Svend E. Kold and Sue J. Dyson

THE SPORT Dressage is the ultimate athletic challenge in equestrian sports because it combines balance, suppleness, and power in a unique gravity-defying manner. A good horse gives the impression of athletic elegance and expressive animation. The gaits are described using terms such as balance, suppleness, and hindlimb activity. The first demand is that the horse is completely obedient and has to go wherever the rider wants and carry out movements at his or her request. In doing so the horse has to rely on its rider, to trust and to accept the rider as its superior. The key to the training and development of a dressage horse from the lowest levels to International Grand Prix is gymnastic exercises, with the aim of strengthening the muscles and thereby avoid-

ing injury to joints and tendons associated with an increased workload. The Federation Equestre Internationale dressage rules state that the object of dressage is the “harmonious development of the physique and ability of the horse.” Through the levels of dressage training, the center of gravity of the horse and rider is placed further caudally, obtained by increasing the degree of flexion and loading of the hindlimbs, while at the same time freeing the front end of the horse to create a more airborne, uphill set of movements. This can be obtained only by increasing the power of the hindlimbs, by synchrony in movement between the forelimbs and the hindlimbs, and through the freedom of movement of the back.

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Fig. 117-1

Passage. Note the severe extension of the left metatarsophalangeal joint (inset).

In the German equestrian literature the following terms describe the aims of the correctly trained dressage horse: • Takt (i.e., rhythm) • Lossgelassenheit (looseness and suppleness) • Anlehnung (contact with the bit) • Schwung (energy and swing) • Geraderichten (straightness) • Versammlung (collection) Dressage is an international sport, although it always has had its main center of excellence in Northern Europe, most particularly Germany, but in later years also in Holland, Denmark, and Sweden. Dressage developed from the military institutes and only in the twentieth century became a truly civilian sport. Even up to the time of the Second World War military officers participated at all the major dressage games. In Europe the competitive sport has been divided into three levels: L, M, and S. L covers novice level (novice and elementary); M covers medium and advanced medium; and S covers Prix St. Georges, Intermediare I and II, Grand Prix, and Grand Prix Special. The movements required at each of these levels reflects the horse’s degree of collection, with the L classes expressing balance and freedom of movement, M classes requiring more collection and lateral movements, and S classes demanding ultimate collection to enable movements of maximum collection and suspension, such as piaffe, passage (Fig. 117-1), and canter pirouettes (Fig. 117-2). However, even the most skilled rider or trainer has difficulty selecting the right horses, because many promising young horses with excellent gaits fail to learn passage and piaffe, probably because of our insufficient knowledge of the biokinematics of collection.1 Lateral movements apply specific, unique strains to different structures within the skeleton. In shoulder-in, half pass, renvers, and travers the horse is bent evenly in its neck and body but moves on more than two tracks. In shoulder-in, the horse moves on three tracks (1, outside hindleg; 2, inside hindleg and outside foreleg; and 3, inside foreleg) with the body at an ideal angle of 30º to the direction of movement. In

Canter pirouette to the left. The horse intermittently takes all weight on the hindlimbs, resulting in extension of the metatarsophalangeal joints and great strain on the suspensory apparatus.

Fig. 117-2

travers (quarters in) and renvers (head to the wall) the horse moves on four tracks. These movements create an unusual strain on the horse’s back and an additional twisting movement on the appendicular joints. The increased engagement of the hindlimbs developed through collected work allows for greater storage of elastic

CHAPTER 117 strain energy in the hock joints and pelvis which, via the increased lifting of the forehand, allows for high-energy movements such as medium and extended trot. The term cadence is associated closely with working through the back and selfcarriage. Self-carriage reflects a level of training in which the horse has learned to balance itself and its rider and additionally has developed its musculature to allow movement with greater range of freedom. Anlehnung (contact with the bit) is an important concept to understand, requiring the horse to move freely forward with impulsion, to take the bit, and to accept it and react to it without resistance. The Federation Equestre Internationale rules require the horse to work on the bit, that is, with the front of the head positioned in the vertical plane. In recent years the tendency has been toward training dressage horses in an over-bent fashion, with the horse’s forehead behind the vertical plane. This is said to be a requirement for developing the trapezius, rhomboidius, and other muscles of the shoulder/withers region and thus enabling a greater lift of the forehand via the shoulder girdle. Although this method of training contradicts the Federation Equestre Internationale requirement for the horse’s forehead to be in a vertical plane, top riders are able to place the horse’s head in virtually any position according to what is required. Contact with the bit and on the bit frequently are misunderstood terms. The horse must move with energy and impulsion, working through the back for correct contact with the bit. Misinterpretation leads to restriction of the horse by the hands, sometimes resulting in loss of action and gait irregularities.

THE DRESSAGE HORSE Most dressage horses competing internationally are Warmbloods (WBLs) with a high proportion of Thoroughbred (TB) breeding. Dressage horses today combine the elegance and athleticism of the TBs with the power and trainable mind of the WBLs, which have been selected for many generations for these traits. Few pure TBs reach international standard. The TB has been bred to run fast or show courage jumping obstacles crosscountry, which are not of great value when the rider requires complete obedience to perform movements that go as much upward and sideways as forward. Most TBs also lack the strength in all three paces compared with the WBLs, in particular the walk and the trot. Most TBs do not show the same degree of natural engagement of the hindlimbs typical of many WBLs. Many of the greatest TB sires in post-war European dressage breeding (Der Löwe, Velten, and Pik As) have been neither particularly physically impressive nor equipped with more than an average trot. Theoretically, TB stallions in WBL breeding have required a minimum general handicap to ensure that they had been physically and mentally strong enough to stand up to training and race reasonably successfully. The dressage horse must be naturally well balanced. The head and neck must be set sufficiently high to facilitate working up hill and making easy contact with the bit. The shape of the withers region is important, so that the saddle sits easily in the correct position. The dressage rider spends a lot of time sitting in the saddle in sitting trot; therefore correct weight distribution is critical. Most dressage horses are broken at 3 or 4 years of age and begin competing in young horse classes at 5 years of age. Medium classes are reached by the age of 7 and many future Grand Prix dressage horses do a small tour at the age of 8 and 9. Once a dressage horse has reached Grand Prix level, the training predominantly involves repetition of movements, maintaining suppleness, and increasing physical power. Thus dressage horses obviously rarely succumb to acute stressinduced traumatic injuries but more likely succumb to repet-

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itive, accumulative subclinical injuries that may surface at irregular intervals. This means that, with the correct training and management, dressage horses can continue to compete at the highest level at an advanced age, often as old as 15 to 20 years. Many of the Lipizzaner stallions at the Spanish Riding School in Vienna are touring and performing adequately well after 20 years of age. A true link between conformation and soundness is difficult to establish, because what creates an outstanding dressage horse in terms of conformation does not necessarily create a particularly sound dressage horse, and vice versa. However, in a study of 4-year-old Swedish WBL horses, highly significant correlations were found between conformation and movement and between conformation and orthopedic health, whereas no correlation was found between the overall conformation score and competition performance.2 A series of elite dressage horses had larger hock joint angles and more sloping shoulders than more average horses, whereas good forelimb movements were characterized by a large range of flexion of the elbow and carpal joints during the second half of the swing phase. This is what previously has been referred to incorrectly as shoulder freedom. It is important that a young horse naturally places the hindlimbs well underneath itself, because the approach angle does not seem to be influenced by training.1 Wear and tear lesions frequently occur because of a less than ideal joint and limb angulation, but many other factors influence the durability of the horse, including genetic predisposition and less than ideal management conditions before skeletal maturity. The main requirement must be the ability of the horse to balance itself at all paces, because imbalance and asynchrony in movement apply unusual strains on many structures. Holmström1 found that a large positive diagonal advanced placement (the spatial difference between the contralateral forelimb and hindlimb contacting the ground) correlates with high trot scores and suggests this as an important indicator of the horse’s natural balance. The positive diagonal advanced placement does not change with more collection and therefore may become a useful selection criterion. Holmström also found that a group of selected elite horses with high gait scores had significantly larger stride duration, increased hind stance phase duration, and greater diagonal advanced placement than a group of horses with low gait scores.

TRAINING SURFACES Dressage horses are trained predominantly on artificial surfaces with a high degree of cushion, providing a consistency in the training surface not paralleled in other equestrian sports. All dressage competitions in mainland Europe take place on artificial surfaces, and only in England does dressage at the lower levels (L) still take place on grass. A multitude of artificial surfaces have been developed over the last 20 years. Most are based on silica sand mixed with a variety of rubber and polyvinyl chloride material, together with a binding and dust-limiting agent such as vaseline, which ensures that such surfaces remain frost-free down to –10º C. This standardization of working and competition surfaces unquestionably plays a huge role in the low occurrence of many acute orthopedic problems in the dressage horse. Some trainers, however, consider constant working on ideal surfaces likely to soften the limb structures and recommend that the horses occasionally are jumped or hacked on less ideal surfaces to provide a stimulus for joint, tendon, and ligament adaptation. Arena maintenance is paramount; drainage is an essential key to a good surface. An adequate drainage system through central and perimeter drains is absolutely essential to maintain

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a good arena. Dead corners of deep sand predispose horses to momentary loss of balance and may predispose to the development of lameness. Any sudden change of surface integrity predisposes horses to lameness. Young horses in particular work more easily and confidentially on firmer artificial surfaces, where they can obtain a more confident grip and are less likely to fatigue.

TACK The horse must be comfortable in its tack if it is going to work optimally. Dressage saddles are designed to position the rider with a deeper seat and with an extended leg position. The surface area over which the weight is distributed must be as large as possible, to avoid focal pressure points. The use of gel pads and layers of numnahs (saddle pads) is not a substitute for good saddle fit. The saddle must fit the horse and the rider and must position the rider appropriately in balance. The fit must be assessed with and without a rider. The shape of the horse’s back musculature may change as the horse develops muscular strength and power; therefore a previously wellfitting saddle may become constricting. Acceptance of the bit is crucial in the dressage horse. Horses vary considerably in the shape of the mouth and the sensitivity of the corners of the lips, bars, and tongue. Great variation also exists in the thickness of the tongue between horses. A slight crack in the corner of the mouth, caused by an inappropriate bit, can cause major problems with proper acceptance of the bit and the horse’s willingness to work straight. At S level, horses have to compete wearing a double bridle, that is, the mouth has to accommodate both bradoon (snaffle) and curb bits. These vary greatly in shape and design, and selection of the most appropriate can be critical.

LAMENESS EXAMINATION Examining the lame dressage horse does not differ in any great detail from examining any other equine athlete. However, examination frequently requires more time being spent observing the horse ridden, because many dressage horses only reproduce the perceived problem, often no more than a resistance, when ridden through certain movements. This, however, does not mean that the horse should not be examined in hand, including walking and trotting on a straight line and lunging on hard, non-slip surfaces (such as gravel) and on softer artificial surfaces. Not only does lunging on tarmac or concrete carry the risk of the horse slipping, with potentially disastrous consequences, but also in most horses such lunging alters the gait so much that it has little value in a lameness examination of an extravagant moving dressage horse. Leading the horse on a circle at a trot also tends to alter the horse’s stride. The horse does not have the freedom to move its neck and instead will set its head on the leader’s hand. In many horses the usual rider has to be available to reproduce the described problem, if lameness is not overt. However, one should remember that just as bad riders create lameness, so good riders may hide lameness. The latter may take place completely unintentionally and may involve no more than a corrective change of point of balance of the rider through a corner, but enough that for a long time the problem may not be observable from the ground. Most veterinarians who are not competent riders are not experienced fully to appreciate the subtle differences in high-quality dressage horses and by attempting to ride the horse to better appreciate the problem may create an embarrassing situation. They are better advised to spend more time observing the horse from the ground.

The veterinarian should not just focus on the limbs when watching the horse ridden. It is important to observe changes such as an increased lathering of the mouth, audible change in the rhythm of the stride, or even absence of teeth grinding or grunting after a particular diagnostic test. For many horses the veterinarian relies heavily on the conceived observations of the rider during the lameness examination; this may involve the appreciation of subtle change of gait, or even just an impression of a stronger rhythm or less heavy contact on the bit after a peripheral nerve block. Many riders feel through their own body that the horse is working crookedly, that is, not straight and is not in complete balance, and will be able to tell the clinician if this feeling has been altered by any of the diagnostic tests. In many horses, alternating between lunging and ridden work is useful, often going back to lunging with full tack after the horse has been ridden to see a possible difference in the gait from being ridden. A useful test is to ask the rider to ride deliberately on the wrong diagonal, that is, to sit to the trot in the saddle when the inside forelimb is bearing weight. Horses with forelimb or hindlimb lamenesses and horses suffering from back pain may alter the gait when the weight-bearing diagonal (of the horse) is changed. The difference between the horse’s outline and attitude when changing between sitting and rising trot also may add valuable information. In some horses lameness is created by the rider. This most commonly occurs with amateur riders who misunderstand the principles of creating an outline and working the horse forward to the bit. Over-restriction by the hands, with inadequate impulsion, can create gait irregularities. Lower-level trainers are sometimes unable to appreciate these problems and may themselves be unable to work the horse better. Using a good professional rider who is not the trainer to work the horse is therefore preferable. Determining definitively whether the problem is one of riding or of training or a reflection of a genuine lameness may require several days. A rider who sits consistently crookedly can create back pain and loss of hindlimb rhythm and symmetry. Some dressage horses are exuberant and expressive movers and also strong-willed characters that may refuse to go forward properly if ridden by an enthusiastic but less competent amateur rider, especially if the rider is somewhat apprehensive and inclined to be overrestrictive. Nappy (resistant) behavior and unwillingness to work may reflect a pain-related problem, but not necessarily so. One should remember that not all horses are athletes. Many owners tend to think that all horses can learn to do dressage. Veterinarians must in certain situations be prepared to offer the opinion that the particular horse has too many shortcomings physically or psychologically to be able to perform advanced dressage. A veterinarian may be able to help a horse overcome a specific problem but cannot provide missing athleticism. The veterinarian should not forget to check the obvious. Dressage horses physically alter during a training lesson. As the muscles over the withers and shoulders expand, a particular saddle that may appear to fit correctly before working the horse may be restricting an hour later, when the horse begins piaffe and passage movements. It is also important to check that the bit is the correct size and is placed correctly in the horse’s mouth. Horses’ tongues vary greatly in size and when using two bits some adjustments may be required. The corners of the mouth are easily cracked and can become sore. The horse may be apprehensive about taking the bit, may take irregular steps, or may be reluctant to bend properly. Wolf teeth frequently are blamed for reluctance to accept the bit properly and for irregularities in gait. Provided that a wolf tooth is immediately in front of the first upper cheek tooth and is not mobile, the tooth rarely is associated with pain.

CHAPTER 117 Horses with a short poll and a relatively large mandible have difficulty in acquiring the correct degree of neck flexion. In these horses it is also important to check that air flow is not impaired. Restricted airflow is not necessarily accompanied by an audibly abnormal inspiratory and/or expiratory noise. If a diagnosis cannot be made because clinical signs are too subtle, or if it is difficult to determine whether the presenting clinical problem is pain related, working the horse while treating it with anti-inflammatory medication (2 to 4 g phenylbutazone/day PO) for 2 to 3 weeks may be useful. If lameness returns once the medication is withdrawn, the performance problem can be attributed to pain. The lameness also may be worse, making further investigation easier. If the horse appears to have a low-grade bilateral problem, starting by blocking one limb (front or hind) to see if a contralateral limb lameness subsequently becomes obvious can be useful. This is sometimes misleading, however, and blocking both limbs simultaneously and then re-assessing the overall freedom of movement and balance may be more valuable.

DIAGNOSTIC ANALGESIA Technically no differences exist between dressage horses and other equine athletes concerning diagnostic analgesia. However, the horse’s response should be assessed when ridden and when trotted in hand. Because only minor irregularities in gait are often the point of investigation in lame dressage horses, it is particularly important that the conditions, including the surface, remain consistent throughout the lameness investigation. Starting the investigation on one surface only to find that halfway through the nerve blocks the horse has to be assessed on a different surface is not possible. Indoor arenas obviously are of great assistance in severe winter conditions. Although the sequence of the nerve blocks in theory should be the same in all equine athletes, known common lameness sites in dressage horses often make focusing on these areas possible to save time and to avoid an unnecessary number of injection sites and undesirable number of clipped sites. If clipping is essential, many riders prefer the entire limb (and contralateral limb) clipped symmetrically rather than many small clipped sites in one limb.

IMAGING CONSIDERATIONS Imaging of the lame dressage horse is no different from imaging any other equine athlete. However, the frequent lack of overt lameness in a sub-maximally performing dressage horse often makes including every possible diagnostic modality necessary. This is particularly true for evaluation of the neck and the back, both of which are important structures for balance and coordination. These are areas where diagnostic analgesia is less applicable than in the limbs. Radiographic evaluation of the thoracolumbar region requires fixed or semi-mobile radiographic equipment. Use of a Dodger-T aluminum wedge filter to attenuate the primary x-ray beam facilitates acquisition of high-quality images of the dorsal spinous processes.3 Diagnostic ultrasonography of the thoracolumbar and pelvic regions is also useful, used transcutaneously or per rectum to image the supraspinous ligament and epaxial musculature, the synovial articulations (facet joints), and the ventral aspect of the lumbosacral junction.4 Nuclear scintigraphic evaluation can be particularly helpful in evaluating the thoracolumbar and pelvic regions. However, no studies have been done on the variation in radiopharmaceutical uptake in a population of normal dressage horses. Such a study may throw light on subclinical orthope-

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dic problems in dressage horses. However, as with all imaging techniques great scientific integrity is demanded to distinguish between normal variations and pathological lesions, and results must be correlated carefully with clinical observations and with other imaging modalities. Computerized thermographic image analysis may be helpful. Thermography is a non-invasive physiological imaging technique that may detect pathological changes before structural changes are apparent. Thermography is also capable of identifying more than one area of altered tissue metabolism, which may reflect a secondary area of pain. Thermographic data does not lie, but interpretation of data is challenging.

TEN MOST COMMON LAMENESS CONDITIONS The 10 most common lameness conditions in dressage horses are listed not necessarily in strictly decreasing order of importance or frequency, but they represent a selection of the most commonly encountered lameness problems. 1. Proximal suspensory desmitis (PSD) a. Hindlimbs b. Forelimbs 2. Suspensory branch lesions 3. Synovitis or osteoarthritis of the forelimb distal interphalangeal joints 4. Desmitis of the forelimb accessory ligament of the deep digital flexor tendon (ALDDFT) 5. Osteoarthritis of the centrodistal or tarsometatarsal joints 6. Synovitis of the middle carpal joint (possibly with palmar intercarpal desmitis) 7. Synovitis or osteoarthritis of the metacarpophalangeal and metatarsophalangeal joints 8. a. Palmar/plantar annular desmitis b. Tenosynovitis of the digital flexor tendon sheath: forelimbs and hindlimbs 9 Palmar cortical stress fracture of the third metacarpal bone 10. Thoracolumbar and sacroiliac pain

Proximal Suspensory Desmitis: Hindlimbs Probably the most important cause of lameness in dressage horses working at medium and advanced levels is PSD. The carrying capacity of the hindlimbs is increased with increased collection required for more advanced work, and movements such as piaffe, passage, and canter pirouettes (see Fig. 117-2) place great strain on the hindlimb suspensory apparatus. Suspensory desmitis is believed to be caused by an accumulation of repetitive strains within the suspensory ligament (SL) and its proximal origin. Detection of PSD is often delayed because of its bilateral nature, which often means that overt hindlimb lameness is not present or noticed by the rider. Accurate diagnostic nerve blocks therefore are required to reveal lameness. When no obvious lameness is present, lameness often is created subsequently in the contralateral hindlimb by diagnostic analgesia of either of the (non-lame) hindlimbs. A negative response can be misleading, and it is sometimes necessary to block both hindlimbs simultaneously, after which there may be a substantial improvement in gait. Direct palpation of the region often fails to indicate a problem because of the deep location of the proximal SL. The clinical diagnosis is confirmed by positive subtarsal analgesia, together with negative intra-articular analgesia of the tarsometatarsal joint. Extensive ultrasonographic and radiographic changes often reflect a chronic and long-standing problem. Ultrasonographic images reveal enlargement of the proximal SL in the lateromedial and dorsoplantar planes, with areas of reduced echogenicity, often involving one or both of the dorsal quadrants of the

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ligament. Radiographic diagnosis requires high-quality radiographs of the proximal metatarsal region; dorsoplantar and lateromedial views are the most useful. Irregularity of the proximal plantar cortex may occur in the region of insertion of the SL origin, with a varying degree of endosteal new bone resulting in trabecular sclerosis over a distance of up to 5 cm. On dorsoplantar radiographs this may be seen as a centrally positioned, triangular-shaped area of sclerosis within the trabecular metaphysis of the third metatarsal bone (MtIII). One should remember, however, that such radiographic changes may be present in an asymptomatic horse because of previous problems, leading to the risk of a false-positive diagnosis. Diagnosis should never be based only on radiographic examination. Occasionally, nuclear scintigraphy can be useful in horses with early desmitis where no radiographic changes are present and subtle, equivocal abnormalities are detected with ultrasonography. Increased radiopharmaceutical uptake may occur in the proximoplantar aspect of MtIII in bone-phase (delayed) images. Pool-phase (soft tissue) images are rather insensitive, and not all horses have associated increased radiopharmaceutical uptake in MtIII. Thus a negative bone scan does not preclude PSD. Treatment of this condition often is frustrating because of the chronic nature of the problem at the time of detection. Corrective shoeing using egg bar shoes provides some support in horses with severe hyperextension of the fetlock joint. Prolonged rest (3 to 6 months) often provides a disappointing response, and a controlled exercise program may be more successful. Periligamentous injection of 2 ml of hyaluronan (Hyonate, Bayer AG, Leverkusen, WG) plus a corticosteroid (e.g., 10 to 20 mg of methylprednisolone [Depo-Medron, Upjohn, Crawley, UK] or 10 mg of triamcinolone acetonide [Adcortyl, Squibb & Son, Hounslow, UK]) are now used frequently and are believed to provide an initial reduction in inflammation to enable a reasonably pain-free walking program to be initiated. This frequently is continued for as long as 12 weeks before slow, balanced trotting on a good surface is initiated. The ultrasonographic appearance of the SL often changes little, even in horses that are returned successfully to full training. Egg bar shoes often are removed when normal training is initiated, because many riders believe that they provide too much breaking action on ground impact of the hindlimbs. The likelihood of recurrence of PSD is high, and special care should be taken not to over-work the horse on deep or holding surfaces. Modification of the training program often is required, particularly in terms of avoiding fatiguing training session in deep or loose surfaces. Some horses have chronic lameness that fails to respond to therapy. Recently some encouraging results have been achieved by treatment of horses with acute and chronic desmitis with shock wave therapy, using three treatments at 2-week intervals, with substantial improvement in lameness and ultrasonographic appearance of the ligament. Neurectomy has a role in horses that fail to respond to medical management.

Proximal Suspensory Desmitis: Forelimbs Forelimb PSD is seen more often than hindlimb PSD in younger horses and may result from hyperextension of the carpus in extravagantly moving horses, in particular horses volunteering extended trot. PSD often results from the horse working on less than ideal surfaces. Lameness is often unilateral and acute in onset but is sometimes bilateral. Most sound horses resent firm manual squeezing of the body of the SL, and the proximal region of the SL is difficult to access by palpation; therefore local analgesic techniques are required to verify the source of pain. In horses with peracute PSD, slight filling in the proximal metacarpal region may occur, but this often resolves within

24 hours. Lameness may be transient unless the horse is worked again. In these horses, the veterinarian relies on a history of acute-onset lameness that is worse with the affected limb on the outside of a circle for diagnosis. Lameness is often easier to feel (by a rider) than to see. Some improvement is often seen after perineural analgesia of the palmar and palmar metacarpal nerves at mid-cannon level. Lameness is substantially improved or resolved by blocking the lateral palmar nerve or the palmar metacarpal nerves at the subcarpal level. Because of the close proximity of the middle carpal joint capsule, positive subcarpal analgesia should be followed by intra-articular analgesia of the middle carpal joint to exclude articular pain. Radiography is frequently of little or no value in dressage horses with forelimb PSD. Ultrasonography is required to confirm the diagnosis. Because subtle lesions may be present and may be a reflection of a previous pathological condition (possibly subclinical), high-quality ultrasonographic images of both limbs are required for comparison, together with knowledge of normal variations. Lesions vary from subtle enlargement of the proximal aspect of the SL with normal echogenicity to large areas of reduced echogenicity. Rest, often for 12 to 16 weeks, together with a controlled, ascending walking program, in hand using a horse walker or ridden, is the treatment of choice. Intralesional injection using 2 ml of a polysulfated glycosaminoglycan (PSGAG [Adequan, Janssen Pharmaceutical, High Wycombe, UK]) may be tried. The prognosis is good in horses with early PSD, provided that the horse is managed carefully subsequently, avoiding the medium or extended trot in training. In horses with chronic PSD the risk of recurrence is moderately high. Shock wave therapy has been useful in treating some of these horses. In some horses, ultrasonographic appearance may not change substantially, despite a favorable clinical response to treatment, leading to a risk later of false-positive diagnosis in an asymptomatic horse.

Desmitis of the Suspensory Ligament Branches: Forelimbs and Hindlimbs Desmitis of a branch of the SL is often acute in onset and results in palpable enlargement of the suspensory branch and often moderate lameness. Occasionally, both medial and lateral branches are involved in a hindlimb. The branch is painful to palpation. Diagnosis is confirmed by ultrasonography. Enlargement of the branch is often accompanied by some subcutaneous echogenic material, often with a central (sometimes eccentric) hypoechogenic or anechogenic core lesion. The interface between the ligament branch and the proximal sesamoid bone may be disrupted. This is best seen on longitudinal images and merits a more guarded prognosis. If both branches in a hindlimb are involved, echogenic material may be visible between the branches. The PSBs may or may not show radiographic evidence of enthesopathy, with linear opacities extending from the palmar/abaxial margin. Ectopic mineralization within the SL branch is occasionally seen with ultrasonography and radiography. Treatment is prolonged rest (4 to 6 months) with a slow return to exercise. Intralesional injections using 1 ml of a PSGAG may be tried but generally have met with disappointing results. Counterirritation (pin firing) has been tried on old, indurated lesions and chronic lameness, but again with disappointing results. Some horses have responded to intralesional treatment with β-aminoproprionitrile fumarate. Encouraging results also have been obtained recently with shock wave therapy (three treatments at 2-week intervals), combined with a controlled walking exercise program for 3 to 4 months. The risk of recurrence is high. Any predisposing causes such as limb deviations or lateromedial imbalance of the feet should be corrected or at least adjusted.

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Synovitis or Osteoarthritis of the Distal Interphalangeal Joint

Desmitis of the Accessory Ligament of the Deep Digital Flexor Tendon: Forelimbs

Pain arising from the distal interphalangeal joint is a frequent diagnosis in all equine sports. The unique anatomical position of the distal interphalangeal joint, with the forces distributed on it through the rigidity of the hoof capsule and the forward thrust of the deep digital flexor tendon and the navicular bone during weight bearing and limb protraction, are likely to be contributory factors. Lateromedial imbalance of the foot contributes to the joint trauma in many horses. The diagnosis is made from comparing the response to intra-articular analgesia with perineural analgesia of the palmar digital and palmar (abaxial sesamoid) nerves and occasionally intrasynovial analgesia of the navicular bursa. The interpretation of the response to intra-articular analgesia is not black or white. Recent studies have confirmed that intra-articular analgesia of the distal interphalangeal joint is not specific and can influence pain associated with the navicular bone, distal phalanx, and subsolar tissues. A rapid (within 5 minutes), positive response to a small volume (maximum of 6 ml) of local anesthetic solution may be a good indicator of the possible response to subsequent intraarticular medication. A good response to subsequent treatment requires at least 75% clinical improvement after intra-articular analgesia, together with absence of significant radiographic changes involving the distal interphalangeal joint or the navicular bone. Radiographic changes usually involve the extensor process of the distal phalanx and the dorsoproximal margin of the navicular bone. One should remember that a considerable shape variation exists in the extensor process within sound horses. Minor modeling changes may not be of clinical significance. Small, mineralized fragments proximal to the extensor process may be seen incidentally. Large fragments may require surgical removal to prevent secondary osteoarthritis. Intra-articular medication using a number of individual drugs or combination of drugs has given encouraging results, although results vary between clinicians and populations of horses. Horses with recent onset of lameness with palpable distention of the distal interphalangeal joint capsule may respond favorably to 10 mg of triamcinolone acetonide or 10 to 20 mg of methylprednisolone acetate, combined with a short period of controlled walking exercise (e.g., 2 weeks of ridden walk or on a horse walker). Injection with hyaluronan probably will provide a similar response in such horses. The most successful long-term results have been seen after a triple series of intra-articular injections of a PSGAG. PSGAGs received some negative press after a research study in North America in 1989 that suggested that PSGAGs have a potentiating effect on a subinfectious dose of Staphylococcus aureus in a joint. Subsequently, this preparation has been used sparingly intra-articularly and in many horses only in combination with intra-articular amikacin. We have not seen any negative reaction (inflammatory or infectious) to multiple intra-articular joint injections of PSGAGs and do not use systemic or intra-articular antibiotics. Strict asepsis and a skillful technique are essential. Because of its distal location in the limb, distal interphalangeal joint should always be bandaged for at least 24 hours after injection. Eighty-two percent of dressage horses returned to soundness after PSGAG medication of the distal interphalangeal joint, whereas only 65% of a similar size group of horses competing in cross-country jumping returned to soundness.5 In most horses the initial triple injection proved adequate, and remedicating the joint in successfully treated horses was rare. Corrective shoeing by improving the foot-pastern axis and re-establishment of correct hoof balance should be performed with intra-articular medication. Egg bar shoes often are used for an initial 3- to 6-month period.

Desmitis of the ALDDFT frequently occurs as an acute injury associated with sudden onset of lameness and palpable inflammation (heat and swelling) in the proximal metacarpal region. Over-extension of the carpus, because of imbalance in young horses or resulting from imperfect working surfaces, often is believed to be a contributory cause. The diagnosis is confirmed by ultrasonography in both transverse and longitudinal planes. There is enlargement of the ALDDFT, together with loss of definition of the margins and areas of reduced echogenicity. A definite, hypoechoic core lesion is recognized infrequently. Horses with desmitis of the ALDDFT respond better to a controlled walking exercise program than to complete box rest. Three to 6 months of controlled walking often is required in horses with severe desmitis. The risk of recurrence is moderately high. Local invasive treatment of desmitis of the ALDDFT seldom has been rewarding, although some horses have responded favorably to treatment with β-aminoproprionitrile fumarate.

Osteoarthritis of the Centrodistal and Tarsometatarsal Joints Lameness or poor performance (e.g., inability to perform piaffe or passage) associated with pain arising from the centrodistal or tarsometatarsal joints occurs frequently in dressage horses. Likewise, a horse with an outstanding freedom of movement in the trot may have an unexplainably poor canter associated with distal distal joint pain. A poor correlation exists between the clinical signs, including response to intraarticular analgesia of the tarsometatarsal and centrodistal joints, and the radiographic appearance of these joints. Many dressage horses have confirmed pain from the joints but have fairly equivocal radiographic changes. One should remember that the degree of joint collapse and osseous ankylosis always is underestimated from conventional radiographs because of the curvilinear nature of the joints and the low radiodensity of immature bone bridging the joint centrally. Nuclear scintigraphy may be a sensitive indicator of increased bone modeling in the absence of radiological abnormalities or in horses with equivocal changes and also can be helpful in horses with subtle lameness, when the response to local analgesic techniques is difficult to interpret. Alternatively, diagnostic medication with intra-articular corticosteroids may be helpful. Pain is often bilateral, and often the presenting problem is shortening of the hindlimb stride and an inability to collect. Clinical signs mimicking back pain, rather than overt lameness, may be present. Most horses respond to intra-articular analgesia of the tarsometatarsal and centrodistal joints, although occasionally a better response is seen after fibular or tibial nerve blocks or after treatment of the joints. Intra-articular analgesia of the tarsometatarsal joint and the response to subtarsal analgesia should be compared. In horses with advanced radiological changes, false-negative responses to intra-articular analgesia may occur. Horses with few or no radiographic changes may respond satisfactorily to intra-articular medication with a corticosteroid (e.g., 10 to 20 mg of methylprednisolone acetate or 10 mg of triamcinolone acetonide), and/or 1 ml of a PSGAG if lameness is of longer duration. Medical treatment often is combined with a program of controlled walking exercise for 4 to 6 weeks (pending response to treatment), together with alterations of the shoeing. Horses that tend to plait or swing the affected limb axially during protraction may benefit from a lateral extension shoe, which may help to normalize posture and hindlimb gait pattern with an additional effect on secondary back pain.

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Repeated medication of the joint(s) may be required at monthly or quarterly intervals. A longer response may be achieved by combined use of corticosteroids and hyaluronan. Additional PSGAG medication given intramuscularly on a weekly basis (500 mg/ml, 7 × 5 ml) may be beneficial. Glucosamines and chondroitin sulfate given orally on a daily basis often are administered, but clinical efficacy is unproven. If substantial radiographic changes are present and the joint is changed irreversibly and the horse fails to respond to repeated intra-articular medication, fusion of the joints by surgery or by intra-articular injection of sodium monoiodoacetate can be considered, but the prognosis for high-level dressage is guarded.

Synovitis of the Middle Carpal Joint Lameness associated with pain in the middle carpal joint has been seen in many dressage horses, in particular young horses that still may be struggling to establish balance and synchronicity in all paces with the additional weight of the rider. Lameness is often mild and most frequently unilateral, being most noticeable when the limb is on the outside of a 10-m diameter circle. Momentary hyperextension of the carpus, often on a tight circle, is believed to be involved. If the response to analgesia of the middle carpal joint is positive, the proximal SL should be examined by ultrasonography to preclude injury. Usually no radiographic or ultrasonographic changes involve the middle carpal joint. Arthroscopy of the middle carpal joint sometimes reveals damage to one or both (most frequently the medial) of the palmar intercarpal ligaments, which show edema, petechial hemorrhage, and fraying of superficial fibers. Most horses respond well to intra-articular medication using a triple series of 1 to 2 ml of a PSGAG given 8 days apart, or treatment with short-acting corticosteroids combined with hyaluronan. Six to 8 weeks of ridden walk or on a horse walker should be followed by a modified training program for at least another 3 months.

Synovitis or Osteoarthritis of the Metatarsophalangeal and Metacarpophalangeal (Fetlock) Joints Fetlock joint disease is not a common problem in dressage horses and certainly does not seem to be as common in this type of equestrian sport as in others. The absence of galloping across often firm and irregular surfaces associated with crosscountry jumping is a likely explanation. The diagnosis is confirmed by palpation and intra-articular analgesia. In the absence of radiographic changes, intra-articular medication using a corticosteroid (e.g., 10 mg of triamcinolone acetonide), together with 2 ml hyaluronan in horses with synovitis, or 1 ml of PSGAG in horses with more long-standing osteoarthritis, frequently has proved successful. Generally the response to medication is good and the likelihood of recurrence is low in the forelimbs. The response is poorer in hindlimbs. Horses with radiographic abnormalities consistent with osteoarthritis warrant a more guarded prognosis.

Palmar/Plantar Annular Desmitis Desmitis of the palmar (plantar) annular ligament (PAL) occurs more commonly in forelimbs than in hindlimbs and usually results in acute-onset lameness. The PAL has localized heat and is palpably enlarged, with pain elicited by firm pressure. Mild distention of the digital flexor tendon sheath (DFTS) may occur. Diagnosis is confirmed by ultrasonography. The PAL is thickened, with a diffuse reduction in echogenicity or focal hypoechoic areas. Horses with acute desmitis usually respond well to box rest and controlled walking exercise for 3 months. In the acute phase, non-steroidal anti-

inflammatory drugs (e.g., phenylbutazone 2 g bid PO for 5 days) are beneficial.

Tenosynovitis of the Digital Flexor Tendon Sheath Tenosynovitis of the DFTS often results in sudden-onset lameness associated with distention. Some horses have long-standing distention of the DFTS without lameness (windgalls), especially in the hindlimbs, but subsequently develop clinically important tenosynovitis. Constriction of the DFTS by the PAL may be apparent. Lameness may vary from mild to severe and usually is accentuated by distal limb flexion. If distention of the DFTS is acute in onset, then local analgesia is usually unnecessary. However, if distention of the DFTS has been present for some time, then the source of pain should be confirmed by local analgesia. Intrathecal analgesia of the DFTS usually results in substantial improvement in lameness but often does not alleviate it fully. Perineural analgesia of the palmar (plantar) (midcannon) and palmar metacarpal (metatarsal) nerves usually eliminates lameness. Improvement sometimes is seen after perineural analgesia of the palmar nerves at the level of the PSBs. Excluding the metacarpophalangeal joint as a potential source of pain by intra-articular analgesia may be necessary. Ultrasonographic examination should be performed in the metacarpal and pastern regions. Usually an abnormal amount of fluid within the DFTS allows better visibility of synovial plicae extending from the medial and lateral margins of the deep digital flexor tendon (DDFT) in the distal metacarpal region and the synovial fold on the palmar aspect of the DDFT in the pastern region. These should not be confused as adhesions or tears of the DDFT. In horses with chronic tenosynovitis, the DFTS wall may be thickened, with echogenic bands within the DFTS representing adhesions. Ultrasonography frequently underestimates adhesion formation. The SDFT and DDFT should be inspected carefully, because tenosynovitis may be secondary to a primary pathological tendon condition. Lesions of the DDFT occur more commonly, either as core lesions or marginal tears. The latter can be difficult to detect by ultrasonography. Enlargement of the cross-sectional area of the tendon compared with the contralateral limb suggests a lesion, which may be confirmed only by tensocopic evaluation of the sheath contents. Mineralization within the DDFT warrants a guarded prognosis. Horses with early tenosynovitis without adhesions respond well to intrasynovial administration of a corticosteroid (e.g., 10 mg of triamcinolone acetonide) or 2 ml of hyaluronan, together with a pressure bandage and box rest with hand walking for 4 to 6 weeks. If the horse fails to respond adequately to medical therapy, then surgical exploration is warranted. Tenoscopic evaluation should be performed to evaluate the extent of adhesion formation and to detect longitudinal tears in the medial or lateral margins of the DDFT, which may extend proximally under the manica flexoria. Resection of intrasynovial adhesions and lavage, with or without resection of the palmar/plantar annular ligament, may resolve the problem. Horses with lesions of the DDFT that may be debrided and possibly sutured warrant a more guarded prognosis. Surgery is frequently followed by intrasynovial injection of 2 ml of hyaluronan, repeated 4 to 6 weeks later to reduce inflammation and to try to prevent adhesions reforming. The response to surgery depends on the chronicity of the problem, the number of intrasynovial adhesions, and the presence of lesions of the DDFT. Horses with lesions involving the forelimbs appear to have a better prognosis than those involving the hindlimbs. Surgery is accompanied by 8 to 12 weeks of absence from training, although controlled walking in hand or on a horse walker is essential to try to stretch any adhesions that reform.

CHAPTER 117 Proximal Palmar Cortical Stress Fracture of the Third Metacarpal Bone Proximal palmar cortical stress fracture of the third metacarpal bone occasionally is seen in dressage horses with an acute onset of moderate to severe lameness. Hyperextension of the carpus and imbalance of limb synchrony in immature horses are believed to be contributing factors. The diagnosis sometimes can be suspected by inducing pain by digital pressure on the palmaroproximal aspect of the third metacarpal bone. When the horse trots on a firm surface, the lameness tends to increase the farther the horse trots. If the horse turns and then trots again, lameness appears to be improved and then increases again. Lameness usually is improved substantially by perineural analgesia of the palmar metacarpal nerves. If the fracture extends into the carpometacarpal joint, improvement also may be seen after intraarticular analgesia of the middle carpal joint. On radiographs a fracture may be recognized on a dorsopalmar projection as a linear radiolucent line, usually in the medial aspect of the third metacarpal bone and extending up to 8 cm, possibly with surrounding sclerosis. In some horses a fracture line cannot be seen, although sclerosis is present. In some horses no radiographic abnormality is identified. In these horses diagnosis is confirmed by nuclear scintigraphy. Treatment is complete box rest for 6 weeks, followed by 6 weeks of controlled walking exercise. The prognosis is good, and the likelihood of recurrence low.

Thoracolumbar and Sacroiliac Pain Thoracolumbar and sacroiliac region pain are frequent causes of reduced performance in the dressage horse. Although caudal thoracic back muscle soreness may be secondary to primary hindlimb lameness, primary back pain does occur and usually is not associated with overt lameness. The horse may have a history of unwillingness to perform certain movements, stiffness, loss of impulsion and cadence, loss of action or being less easy to work in a correct outline, and sometimes bucking or other nappy (resistant) behavior. The horse usually moves better on the lunge than when being ridden. The most common causes of back pain include the following: 1. An ill-fitting saddle 2. The rider sitting crookedly 3. Primary muscle spasm 4. Impingement of dorsal spinous processes in the mid-thoracic to cranial lumbar regions 5. Osteoarthritic changes involving the synovial articulations (facet joints) in the region of the thoracolumbar junction 6. Sacroiliac disease 7. A combination of lesions in the thoracolumbar and sacroiliac regions

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Definitive diagnosis of the cause of back pain can be a diagnostic challenge. Obvious causes such as ill-fitting saddle or the position of the rider should be eliminated first before proceeding with more sophisticated diagnostic tests such as nuclear scintigraphy, radiography, thermography, and ultrasonography. If back muscle tension or spasm is obvious, assessing the response to treatment using physiotherapy (e.g., manipulation and therapeutic ultrasound) or anti-inflammatory medication may be worthwhile before further investigation. Thermography provides pictorial images of the surface temperature of the body, which gives a physiological identification of changes in tissue perfusion or sympathetic neuromuscular dysfunction. Thermography is a useful tool to demonstrate to an owner the effect of a poorly fitting saddle or the rider sitting crookedly and also may be useful in identifying acute superficial ligamentous or muscle injuries. Nuclear scintigraphy is much more sensitive than radiography for detecting lesions in the thoracolumbar or sacroiliac regions, but radiography potentially gives more structural information, such as the proximity of the dorsal spinous processes. It is important to verify the clinical significance of any lesions identified by infiltration of local anesthetic solution whenever possible. If dorsal spinous processes are extremely crowded, injecting between them may not be possible, but injecting around them (20 to 50 ml of mepivacaine) usually results in substantial improvement within 15 minutes of injection. Ultrasound guidance is necessary for infiltration around synovial articulations. Treatment is aimed at removing any predisposing factor and control of pain. Local infiltration with corticosteroids (e.g., methylprednisolone acetate combined with mepivacaine) or Sarapin is successful in some horses. If pain associated with impinging dorsal spinous processes fails to be controlled by medical management, then surgical treatment should be considered. Infiltration of a sclerosing agent, P2G (Martindale Pharmaceuticals, Ramford, Exxes, UK), around the sacroiliac joints produces clinical improvement in some horses with pain associated with these joints.

REFERENCES 1. Holmström M: Quantitative studies on conformation and trotting traits in the Swedish warmblood riding horse, dissertation, Uppsala, 1994, Swedish University of Agricultural Sciences. 2. Lundquist K: Kvalitetsbedömming av unge ridhäster, samband mellam bedönningsresultat och fremtida brukbarhet. Examensarbeta i husdjursförädling, Uppsala, 1983, Swedish University of Agricultural Sciences (in Swedish). 3. Butler J, Dyson SJ, Colles CM, et al: Clinical radiology in the horse, ed 2, Oxford, 2000, Blackwell Scientific. 4. Denoix JM: Ultrasonographic evaluation of back lesions, Vet Clin North Am Equine Pract 15:131, 1999. 5. Kold S: Unpublished data, 2000.

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Lameness in the Three Day Event Horse Andrew P. Bathe

SPORT OF EVENTING The sport of eventing generally is considered the most allround test of a horse’s athletic ability, and as such the horses tend to be jacks of all trades rather than excelling in any one particular area. The competition consists of three disciplines, namely dressage, show jumping, and cross-country, with the latter being the most influential phase. The Three Day Event or Concours Complet is the pinnacle of the sport (Fig. 118-1) and is run over 4 days: 2 days of dressage, followed by a day for the speed and endurance phases and a day of show jumping. The speed and endurance test consists of roads and tracks at trotting speed, a steeplechase, and the actual crosscountry phase over fixed obstacles. This is a severe athletic test, and horses normally only compete in two or maximally three such competitions in a year.

One Day Events, or Horse Trials, compress the same disciplines into a shorter time frame, but without the roads and tracks and steeplechase phases. The distance and thus time for the cross-country are also much shorter, so that many such competitions may be completed in a season. For most advanced horses One Day Events are used as training for the Three Day Events, although a large number of recreational competitors only aspire to compete in One Day Events. The emphasis of this chapter is the Three Day Event horse, because the extreme demands placed on this horse give characteristic patterns of lameness; whereas the novice One Day Event horse can be considered a standard riding club or recreational horse from a veterinary point of view. Eventing is an established Olympic sport and a substantial equine industry. The highest grade of competition is the fourstar event (CCI****). Traditionally these have been the English events of Badminton and Burghley, although events of this level now have been established in Lexington, Kentucky, in the United States and in Adelaide, Australia. The sport has a high-risk element for rider and horse and a noticeable recent trend has been to try to make courses safer. The sport includes substantial veterinary involvement. During a Three Day Event, the horse is examined by the official veterinarians on arrival, the day before commencing the dressage, before and after the cross country, and in the morning before show jumping. The horse must be deemed fit to compete—that is, the horse must be sound—throughout the competition, and thus any orthopedic disorders are of great significance. A mild degree of hindlimb gait asymmetry may be acceptable to the Inspection Panel, but any noticeable forelimb lameness normally is not permitted.

HORSE TYPES

Fig. 118-1 Example of a cross-country fence at CCI**** level. (Courtesy Kit Houghton Photography, Bridgewater, Somerset, UK.)

Because the Three Day Event places great emphasis on the horse’s speed and stamina, there is a preference toward the Thoroughbred (TB) or predominantly TB-cross breeds. A substantial proportion of horses are of uncertain or unknown breeding. Exceptions have been notable, but Warmbloods and classic Irish hunter types normally do not have the endurance required at the top level. Such horses often may do extremely well at the lower levels, however, because they move and jump better than the pure TB. Figure 118-2 demonstrates what could be considered the ideal modern eventing stamp, a highly successful New Zealand TB. A horse’s ability and mental aptitude are the most important determinants, and other body types are successful (Fig, 118-3). An average ideal size would be 16.2 hands, but the rules are not hard and fast. The financial value of event horses is considerably lower than that for racehorses, show jumpers, or dressage horses, so any horse with outstanding ability in one of these phases is likely to be used in that sport first. If the horses do not succeed, then they may be tried as potential event horses. These horses bring with them any injuries they may have accumulated, but because of the different stresses imposed

CHAPTER 118 during eventing, this may not be a problem. For example, event horses tolerate low-grade carpal pathological conditions from previous race training. A small number of horses are bred specifically for eventing. Stallions generally are considered to lack the courage required to compete at the top level, and because the horse takes a number of years to reach its peak, choosing proven sires is a problem. The predominantly TB Irish sport horse and the relatively larger-boned New Zealand and Australian TBs are sought after. Event horses normally commence dressage and show jumping training at 4 years of age and start competing in prenovice and novice One-Day Events from the age of 5.

Fig. 118-2 An ideal modern eventing stamp. This 16.1-hand high New Zealand Thoroughbred gelding was an individual Olympic and World Championship gold medalist. (Courtesy Badminton Speciality Feeds, Oakham, Rutland, UK.)

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Depending on the horse’s ability and rider’s skill and patience, a horse usually competes in its first (graded as a CCI* or CCI**) Three Day Event at 6 to 7 years of age. A significant proportion of horses do not have the ability, courage, or physical durability to proceed beyond the CCI** or CCI*** level to the top grade of CCI****.

INFLUENCE OF THE SPORT ON LAMENESS Event horses are generally skeletally mature when they commence training and are not trained at the same speed or intensity as racehorses. They therefore have different patterns of injury, although most of the problems are still related to training. Primary long bone pathological conditions are rare. Soft tissue injuries such as tendonitis are common and often career limiting. The amount of endurance training necessary produces repeated cyclic loading, and problems such as osteoarthritis are common. The other subset of event horse injuries is acute traumatic injuries sustained during competition. Because the horses are jumping large fixed obstacles at speed, they are prone to falls and to direct traumatic fractures. Fence design has changed in recent years. Square-shaped fences are avoided and rounded top contours are now more common. These fences give horses more leeway to correct mistakes and cause less severe direct impact trauma. The fences may be 1.2 to 1.4 m high, with a 2-m spread and a 2-m drop, so substantial strain can be placed on the supporting structures of the limbs on landing. The quality of the terrain also appears to have an important impact on the incidence of lameness problems. The competitions are run predominantly on turf, the nature of which depends on the soil type, local weather, and management factors. At the lower level, financial constraints generally preclude much improvement on the quality of the ground, but some of the top events try to maintain a permanent track that is tended carefully. The prolonged period and intensity of training required for horses to reach an elite level means that those horses not metabolically or physically suited to the sport are selected out. For instance, few elite horses have recurrent exertional rhabdomyolysis or navicular syndrome. Three Day Events are regulated by the Federation Equestre Internationale. A strict medication control program is enforced, which permits only emergency medication at the competition after official veterinary approval or the use of a small number of permitted forms of medication, including antibiotics, rehydration fluids, and preparations for treating gastric ulcers.

TRAINING METHODS

Example of a successful but tall and hunter-bred horse. This 17-hand high gelding Thoroughbred-cross Irish Draft horse was a Badminton CCI**** winner and Open European Championship Team gold medalist. (Courtesy Kit Houghton Photography, Bridgewater, Somerset, UK.)

Fig. 118-3

Event horses train in all three disciplines, with the actual methods varying greatly between riders. A complete description of training methods is available elsewhere.1 Most competing horses have natural cross country ability, so little time generally is spent on training for this, because the progression of competitions provides sufficient experience. Event horses normally are selected for natural jumping action, but jumping technique during the cross country phase is different than that needed for show jumping. Therefore event horses may not be as careful when show jumping and can have a tendency to touch poles. Most event horses are show jumped regularly, especially during the off season. The event horse’s weakest link is usually the dressage phase. The movements required are no more than a medium level of pure dressage, but the different breeding and level of fitness of these horses means that the major challenge can be to control the horse’s temperament. Most of the skills training revolves around this discipline, and a high standard now is required to be competitive at the top level.

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Fitness training is a major component of the preparation for a Three Day Event and is where most orthopedic damage is incurred. The horse is likely to undergo a 3- to 4-month training period for the target Three Day Event. Training methods vary greatly between riders and often depend on local factors such as the availability of hills for trotting or allweather gallops. Restricting the horse to training solely on an artificial surface is not advisable, because this seems to predispose the horse to injury when the horse actually competes on a natural surface. Event horses normally receive a 6-week initial period of walking and trotting on the roads, and then commence cantering exercise. Different riders vary in their use of conventional or interval training, but usually peak the quantity of work at around three canters of 8 minutes, or shorter if a hill is available. The quality of the work usually is increased closer to the Three Day Event to include faster work. One Day Events are used to monitor the horse’s fitness and as additional training. The dressage and jumping training also substantially contributes to the fitness regimen.

CONFORMATION AND LAMENESS Although the horse’s stamp may vary, as discussed previously, the basic conformation must be correct. Eventing is unforgiving to conformational defects compared with show jumping and dressage. The general principles are the same as for any equine athlete. Serious conformational defects include being back at the knee, having upright pasterns and hocks, and a moderate or severe toed-out conformation. Of slightly lesser significance are a long or short back, being over at the knee, or having long, sloping pasterns. Defects such as offset knees and a slight to moderate toed-in conformation seem to be less important. A good foot conformation is always desirable, but many event horses have the TB trait of weak feet with collapsed heels. The prepurchase examination for a young event prospect, with hopes of a Three Day Eventing career, is likely to be strict. The conformation should be assessed critically at this stage. Although the horse may have sufficient talent, defects in conformation may not allow it to stand up to the 5 or so years of training necessary to reach the top level of the sport. Conversely, it is possible to be more lenient in the interpretation of subtle problems when performing a prepurchase examination on an older, experienced horse. The horse’s competitive record should be assessed carefully, because advanced horses are likely to have accumulated wear and tear changes during an extended career. Any conformational or subtle soundness queries can be addressed in the light of the horse’s proven ability to perform its task.

TEN MOST COMMON LAMENESS CONDITIONS Some conditions are more common during training and others are more common at competitions. The overall prevalence is as follows: 1. Thoracolumbar and cervical soreness and restriction 2. Foot soreness (bruising, imbalance, and nail bind) 3. Traumatic osteoarthritis a. Distal interphalangeal joint b. Metacarpophalangeal and metatarsophalangeal joints c. Tarsometatarsal and centrodistal joints d. Proximal interphalangeal joint 4. Superficial digital flexor tendonitis 5. Suspensory desmitis a. Branch desmitis b. Proximal suspensory desmitis

6. External trauma a. Lacerations including overreaching injury b. Penetrations c. Stifle bruising 7. Pain in the sacroiliac region 8. Fractures of the stifle region 9. Other fractures 10. Rhabdomyolysis

CLINICAL HISTORY A routine lameness history should be obtained, emphasizing and obtaining the following information: • Horse’s competitive level • Competition targets and timing, ahead or behind in its fitness schedule • Previous problems • Recent competitive/training program • Current medications • Prodromal signs • Onset acute or insidious • Exact nature of problem (limb swelling, lameness, or poor performance) • Progression of problem • Response to treatment

LAMENESS EXAMINATION My standard approach to the lameness examination is found in the following discussion. The regions requiring particular attention and the most rewarding procedures are outlined for horses with subacute or chronic lameness problems. Care should be taken to palpate all limbs and the back thoroughly, because many concurrent or compensatory injuries can be found that way. Because many problems are subtle, the horse should be examined on a variety of surfaces and at different gaits. Particular attention should be paid to the feet. The size, shape, and conformation should be assessed in relation to the size and breed of horse. The suitability of the shoe type for that horse should be determined, because farrier preference may have been influenced by fashion. The fit of the shoe should be correlated with stage in the shoeing cycle. Fortunately, the trend is to move away from the traditional problem of shoeing the horse short and tight at the heels. The hoof should be palpated for heat and any cracks or defects. The sole should be pared and hoof testers carefully applied over the entire solar surface, assessing the solar compliance and any painful response. Horses with recurrent bruising associated with soft soles may not have demonstrable pain at examination, but the lack of solar rigidity is clearly evident. Percussion may be helpful in a small proportion of horses. An increased digital pulse amplitude can be helpful in determining any inflammation in the foot and is especially important if the amplitude is asymmetrical in the limb or between feet. A subtle increase in digital pulse amplitude is best evaluated after trotting the horse in hand on a hard surface. The horse should be palpated carefully for distention of the distal interphalangeal and metacarpophalangeal/metatarsophalangeal (fetlock) joint capsules. The range of joint flexion and any resentment to flexion should be assessed carefully. Particular attention should be given to the palmar metacarpal structures for presence of subtle, diffuse filling and any discrete swelling, heat, or pain in the tendonous or ligamentous structures. Owners and riders of event horses tend to be thorough in their own palpation of this region and often know the normal contours of their horse well. However, they

CHAPTER 118 often are misled by distention of the medial palmar vein or diffuse swelling from a more distal inflammatory lesion. In the hindlimbs, pain on palpation over the cunean bursa and in response to the Churchill test should be determined. The medial femorotibial and femoropatellar joint capsules should be palpated to detect distention. The muscle tension in the back and hindquarters should be assessed carefully. Trigger points and painful foci should be determined, and the range of spinal flexibility in response to running a blunt object along the back should be assessed. During the static examination the horse should be assessed for symmetry. The horse’s condition and degree of muscling should be assessed in relation to its level of fitness. The freeness of stride, dynamic foot placement, and foot flight arcs should be assessed at the walk. At the trot any head nod and the range of gluteal excursion should be assessed to determine any lameness. Lunging in a circle on a hard surface frequently is used to exacerbate subtle lameness. However, it is also critical to see the horse lunged on a soft surface, a portion of the lameness examination that often is omitted. Different lameness conditions may be evident on different surfaces, and this comparison is valuable. For instance, a horse may have a lowgrade concussive distal limb lameness evident when lunged on the hard surface. However, the primary problem may be proximal suspensory desmitis, pain from which is evident only when the horse is lunged on a soft surface. Although not decrying the value of evaluating all the lameness problems present, many of these horses have multiple, low-grade sites of pathological conditions to which they have adapted. Evaluating these can be a frustrating business, and it is important to determine the current problem noticed by a knowledgeable owner or rider. Evaluation of the horse while the horse is being ridden can be more difficult, but this form of movement can exacerbate low-grade lameness. Riding may be the only way of observing problems evident during certain movements, such as lack of hindlimb impulsion during a change of gait or when jumping. Seeing the horse ridden by a different, preferably more experienced rider can be helpful in some horses suspected of having back pain or when schooling or behavioral problems are present. Determining the normal range of soundness is a difficult and contentious issue. Because of age and level of work, most top-level event horses have some degree of orthopedic pathological condition. I prefer to score lameness on a scale of 0 to 10, with 0 being sound and 10 being non-weight bearing. An advanced horse should be sound in the forelimbs when trotted in a straight line, but a large proportion demonstrate a 1 of 10 bilateral forelimb lameness when trotted in a circle on a hard surface. Some horses that are competing satisfactorily may show a greater degree of symmetrical lameness, but asymmetry in lameness may indicate that an important problem exists. Advanced horses can demonstrate up to a 2 of 10 hindlimb lameness when trotted in a straight line, without being penalized for this in a trot-up at a Three Day Event. Many have a 2 to 3 of 10 bilateral hindlimb lameness while circling on a hard surface. Hindlimb lameness evident on soft surfaces is likely to produce lower dressage scores, because the horse will exhibit poor and asymmetrical action. Flexion tests are useful to exacerbate any subtle lameness problems, but these tests are not specific. Flexion tests can be particularly helpful in evaluating horses with lameness evident only immediately after they have completed an event. These horses can be frustrating, because they are often clinically sound when evaluated subsequently. A persistent positive response to flexion that can be alleviated by diagnostic analgesic techniques is important. Limb protraction, retraction, adduction, and abduction can be helpful in exacerbating upper-limb pain. Turning the horse in a tight circle can be

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used to assess coordination and flexibility. The range of cervical movement is assessed by observing the horse reach for food (voluntary movement) and by manual manipulation (forced movement). Many horses can cheat and reach the flank by rotation of the upper cervical region, rather than by full lateral flexion of the entire neck. Different considerations apply when examining the horse with a history of an acute, severe lameness, usually after the cross country phase of a competition. A comprehensive approach of evaluating the acutely lame horse must be performed (see Chapter 13).2 Unfortunately, localizing signs may be minimal, the horse may be in cardiovascular shock, and initial efforts must be directed at providing support to the horse and the suspected region of injury. Fractures are caused most commonly by external trauma. Particular attention should be paid to the shoulder region for signs of fracture of the supraglenoid tubercle of the scapula and to the stifle for effusion or peri-articular swelling associated with patellar or other fractures. Soft tissue injuries such as severe suspensory desmitis or superficial digital flexor tendonitis may cause acute, severe lameness.

DIAGNOSTIC ANALGESIA Diagnostic analgesia is an important tool in lameness diagnosis in event horses. Because the horse may have many palpable abnormalities, differential diagnosis is important. However, no localizing clinical signs may be apparent, and diagnostic analgesia is critical to identifying the painful region. Specific treatment can be given if a problem is identified accurately. A positive response to intra-articular analgesia usually means a horse is likely to respond to intra-articular medication, leading to a quicker return to work. In horses with lameness problems too subtle for accurate interpretation of diagnostic blocks, intra-articular administration of corticosteroids may be useful to assess the long-term response to treatment. Even with experienced riders this method of management can have a placebo effect, because the rider may desire for the problem to be veterinary rather than from schooling. Perineural and intrasynovial analgesic techniques are used commonly. Intra-articular analgesia is particularly helpful because many problems are joint-related, and a quick and definitive diagnosis can be achieved. Owners greatly resist clipping of the hair during the competition season, and clipping is not necessary in fine-coated animals if a thorough scrub is performed. The preferred techniques for the most commonly performed blocks are described subsequently. The palmar digital nerve block should be performed as far distal as possible, angling the needle axially and distally to the cartilages of the foot. Separate medial and lateral blocks may be helpful to localize the pain to a specific heel. Blocking the palmar nerves at the level of the fetlock is less likely to desensitize the fetlock joint with a block performed just below the base of the proximal sesamoid bones, rather than at the abaxial sesamoid level. The palmar portion of the low fourpoint block should be performed just proximal to the digital sheath to decrease the risk of proximal migration of local anesthetic solution, taking care to go above or below the communicating branch of the palmar nerves. The lateral palmar nerve block is a satisfactory method of achieving proximal palmar metacarpal analgesia. Because the middle carpal joint is not a likely source of pain in event horses, the risk of confusing pain from this site with that from the origin of the proximal suspensory ligament is minimal. The distal interphalangeal joint is injected most easily at a site on the dorsal midline, using a vertically directed needle. Six milliliters or less of local anesthetic solution should be used to decrease the risk of diffusion from the joint. For the

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fetlock joints I prefer the lateral sesamoidean ligament approach because most horses do not have gross joint distention and the fixed anatomy of this approach is reliable. In the hindlimbs the distal interphalangeal, proximal interphalangeal, and metatarsophalangeal joints often are overlooked sources of pain. Perineural analgesia normally starts with a basisesamoid block, followed by a low six-point block if necessary. Analgesia of the proximal plantar metatarsal region can be performed most easily by blocking the lateral plantar nerve 1 cm distal to the tarsometatarsal joint. This blocks the nerve before it branches into the plantar metatarsal nerves and carries a minimal risk of inadvertent penetration of the distoplantar outpouchings of the tarsometatarsal joint capsule.

IMAGING CONSIDERATIONS Radiography Radiography is the mainstay of imaging, but a few special considerations are necessary in event horses. Lateromedial and dorsopalmar radiographs of the distal extremity can be helpful in assessing foot balance. The palmaroproximalpalmarodistal oblique projection often is under-used in assessing subtle pathological conditions of the navicular bone and the palmar processes of the distal phalanx. The flexed cranioproximal-craniodistal projection of the stifle is especially valuable for assessing the medial aspect of the patella for fractures. It is important to angle the x-ray beam so that the trochlear ridges are not superimposed over the patella, because some fractures or evidence of comminution may otherwise be obscured. A relatively underexposed and undercollimated lateromedial projection is also beneficial to detect small, displaced fragments, which otherwise may be missed.

Ultrasonography Ultrasonographic evaluation of the palmar metacarpal structures is a vital part of the lameness evaluation of an event horse. Superficial digital flexor tendonitis is a common and career-threatening injury, and if the veterinarian has any doubt about even a subtle problem, an ultrasonographic examination should be performed. Even when primary forelimb lameness is located at a distal site, the most important lesion may be a compensatory tendonitis in the contralateral limb. It is usually not necessary to clip the coat, particularly if the hair is fine, and diagnostic images can be obtained after thorough scrubbing and the liberal application of alcohol and gel. The coat may be clipped to obtain maximal detail if subtle tendonitis needs to be investigated. Clients are often reluctant to have the coat clipped for a precautionary scan during the competitive season, because they perceive that the horse will be flagged as having a problem when it next competes. In my experience, sufficient detail is visible in fine-coated horses without clipping, although the clients are warned that greater image quality can be obtained with clipping, and if the image quality is non-diagnostic, the coat needs to be clipped. Often the difficulty is not in identifying abnormalities within the tendon but in determining the significance of any changes that are present. Many advanced horses have changes in fiber pattern of the superficial digital flexor tendon. Transverse and longitudinal views should be obtained in a systematic fashion. Different focus, gain, and frequency settings optimize evaluation of different structures. The cross-sectional area of the superficial digital flexor tendon should be obtained routinely, because sequential monitoring of this may allow the early detection of tendonitis. Determining the cross-sectional area also assists in assessing the current significance of chronic lesions, which is an important and helpful part of the ultrasonographic examination and should not be omitted.

Ultrasonography also can be helpful in assessing articular and peri-articular pathological conditions in structures such as the patellar ligaments. Examination of the ventral sacroiliac ligaments per rectum also can be valuable when pain in this region is suspected.

Scintigraphy Nuclear scintigraphy is a useful technique for evaluating some lame event horses. Scintigraphy commonly is used in horses with hindlimb lameness, back problems, multiple limb lameness, and forelimb lameness with an equivocal or negative response to diagnostic analgesia. Image quality can be a concern, because event horses are skeletally mature and the degree of pathological bone conditions is low. Normal bone uptake can be limited, except in horses with acute trauma. Good technique is therefore essential to obtain diagnostic images, and postprocessing techniques, such as using motioncorrection software can be helpful. Case selection is also important, because the more chronic and low-grade the problem, the lower the likelihood of finding an obvious focal region of increased radiopharmaceutical uptake (IRU). Examples of conditions for which scintigraphy can be rewarding include nonlocalized foot pain (pedal osteitis and insertion injury of the deep digital flexor tendon attachment), stress fractures (although these are rare overall), and osteoarthritis of the thoracolumbar facet joints. Normal scintigraphic patterns are described poorly in the literature, especially for non-racehorses. Regions that commonly have IRU in event horses, but without associated pathological conditions, include the distal phalanx, the proximal interphalangeal, fifth and sixth cervical and sixth and seventh cervical articulations, and the distal tarsal bones. The distal tarsus appears to have active bone remodeling when evaluated scintigraphically, but many event horses do not show lameness or a positive response to either flexion tests or local analgesia. In a study evaluating the accuracy of scintigraphy in horses with confirmed distal hock joint pain, we found a positive predictive value of 0.70 and a negative predictive value of 0.91 for focal IRU.3 Because of this high false-positive rate, scintigraphy should be used with thorough clinical examination. Although relying on scintigraphy in fractious horses may be tempting, authenticating the diagnosis using diagnostic analgesia is important.

Thermography Thermography has been used for more than 25 years but is still a developing diagnostic modality. The technology has improved recently, and thermography units are now affordable. The handheld infrared imaging cameras are particularly attractive. Thermographic imaging provides a sensitive representation of skin surface temperature, but many confounding variables make interpretation of these images difficult. To develop expertise involves a steep learning curve, and a considerable amount of time and experience are necessary to make consistently useful interpretations. Major advantages include that the technique is non-invasive and is quick to perform. Thermography is similar to scintigraphy because it is a physiological rather than an anatomical imaging technique. Given the high prevalence and importance of soft tissue injuries in event horses, thermography has applications in detection and in monitoring response to therapy. Because of low specificity, however, thermography should be used with other imaging techniques. Thermographic imaging is useful in evaluating foot balance and in differentiating various types of inflammation of the foot (Fig. 118-4; Color Plate 10). Examinations before and after exercise are particularly useful for this purpose. Similarly, pre-exercise and post-exercise thermograms are helpful in identifying specific muscle injuries. Accurate

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Fig. 118-4 Examples of different thermographic foot patterns (solar views). A, This hoof has a medial corn, manifested as a focal hot spot (white) within an area of increased temperature. B, This hoof has subacute laminitis, with a pattern of increased heat in the region of the tip of the distal phalanx. identification of local muscle strain permits treatment to be focused on the affected area, with a consequently shortened convalescent period. Thermography is also a useful tool in evaluating neck and back problems, although interpretation is more complex in these regions. Thermography can be particularly useful in monitoring superficial digital flexor tendonitis and can be used as part of a routine screening procedure, with regular examinations in the run up to a Three Day Event. Thermography can detect small lesions before clinical signs are evident, or it can be helpful in determining if a chronic lesion is active (Fig. 118-5; Color Plate 11). If thermography suggests a lesion is present, then ultrasonographic examination is indicated. During the convalescent phase after injury, regular thermographic screening allows detection of any signs of inflammation in the affected region, as the plane of exercise is increased. Care must be taken to avoid artifacts from bandaging, previous clipping, and topical medication.

SADDLE PRESSURE ANALYSIS Computerized saddle pressure analysis using a force-sensing array system allows an objective assessment of pressure distribution beneath the saddle (Fig. 118-6; Color Plate 12). Poor saddle fit is an important problem in event horses and is discussed in greater detail (see pages 991 and 992). Computerized saddle pressure analysis is straightforward to perform and is complementary to conventional saddle fitting. By allowing an objective assessment, computerized saddle pressure analysis can be useful to confirm a problem to a rider, owner, or saddler. The better systems allow dynamic assessment of saddle fit at exercise, which is not otherwise possible.

PROCEEDING WITHOUT A DIAGNOSIS Although in general a diagnosis can be made in most lame event horses, factors such as the experience level of the veterinarian, the thoroughness of the lameness workup, the number of imaging modalities available, and the nature, severity, and stage of the disease process affect diagnostic ability. If a horse is seen repeatedly on a first-opinion basis, stepping back and re-assessing the horse as if from the start is some-

times necessary. It may be necessary to refer the horse for a second opinion or for advanced imaging techniques, such as scintigraphy, if these have not been performed. In some horses the precise diagnosis continues to remain elusive. In horses with obscure forelimb lameness, I routinely perform an ultrasonographic examination of the palmar metacarpal soft tissue structures, because tendonitis and desmitis are important and highly prevalent. Serial cross-sectional area measurements of the superficial digital flexor tendons should be obtained, because the most significant problem with an undiagnosed low-grade lameness may be a compensatory tendonitis in another limb. Any evidence of tendonitis indicates that exercise level should be decreased. Similarly, any persistent clinical signs of swelling in the palmar metacarpal structures should prompt a cautious approach. Even in the absence of ultrasonographic changes, mild swelling should alert the veterinarian to the possibility of a subclinical problem with tendonitis or desmitis. It is important not to rely too much on ultrasonography for diagnosis of soft tissue injuries, because early lesions may not be apparent. Generally in horses with low-grade, undiagnosed lameness the response to a period (few days to weeks) of rest should be assessed. If the response is poor, then most horses with an undiagnosed, low-grade hindlimb lameness can be continued in work, with or without the use of a systemic non-steroidal anti-inflammatory drug (NSAID) such as phenylbutazone. Greater caution normally is advised in horses with undiagnosed forelimb lameness, because the risk of developing a career-limiting injury with continued exercise is greater compared with similar injuries in the hindlimbs. If a subtle problem persists, then it may be necessary to increase exercise intensity to exacerbate the problem to a point where diagnostic local analgesia can be performed. If a competition is imminent, the owner or rider may apply considerable pressure to treat the most likely problem in the hope of rendering the horse sufficiently sound to compete. If lameness is severe without initial diagnosis, then the horse should be given box rest, and the workup should be repeated until a diagnosis is achieved. If an upper limb soft tissue problem or a back problem is suspected, then a physiotherapeutic or chiropractic/osteopathic opinion can be helpful. Although veterinary opinion is divided on the validity and value of these techniques, an owner frustrated by the lack of a veterinary diagnosis is likely to turn to these. Horses with

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Palmar thermographic image and subsequent transverse (on the left) and longitudinal ultrasonographic images of an advanced event horse 10 days after successfully completing a Three Day Event. The horse was having a routine examination, and no clinical localizing signs were evident in the tendon. The thermogram (top) demonstrates a focal hot spot over the left distal superficial digital flexor tendon (arrow), and the ultrasonographic images reveal a hypoechoic core lesion in the same region.

Fig. 118-5

poor performance may have schooling or behavioral problems. Assessment by an experienced and different rider can be helpful.

SHOEING CONSIDERATIONS Foot problems are vitally significant in event horses, and the importance of high-quality farriery in minimizing the incidence of lameness cannot be over-emphasized. Regular and good farriery is important in maintaining good medial to lateral and dorsal to palmar (plantar) hoof balance. Types of shoes vary between the traditional fullered hunter-type shoes, continental flat shoes, four-point style shoes, and various types

of bar shoes. For routine shoeing the conventional fullered shoe offers the advantage of superior grip. Many farriers prefer the extra width of the flat section shoe, because this shoe is easier to fit, has sufficient width at the heels, and gives extra sole cover. If not applied correctly, flat-section shoes may cause excessive sole pressure in horses with flat feet. Traction devices are necessary if flat section shoes are put on horses working on tarmac. Natural balance shoeing has become popular recently in event horses, but although the technique suits some horses, others may actually develop lameness because of improper shoeing technique. However, the natural balance concept of a more palmar location for the breakover point has been well accepted. Seeing horses shod with the shoe set well back is now common, and quarter clips rather

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Computerized saddle pressure analysis images. Cranial is to the left, and left is to the bottom. A, This image shows a poorly fitting saddle, with a focal pressure point in the left wither region. B, This image demonstrates failure of a gel pad to alleviate the pressure point and the development of an additional pressure point caudally.

Fig. 118-6

than toe clips are most common. This is helpful in horses with long-toe conformation, osteoarthritis of the distal interphalangeal joint, or navicular syndrome. A rolled-toe shoe may give a similar effect, although bringing the breakover point back to the same degree is difficult, and care must be taken to set the shoe back sufficiently. The most common therapeutic shoe used in event horses is the bar shoe. The egg bar shoe is used commonly to manage horses with navicular syndrome and other causes of palmar heel pain and to provide support in horses with collapsed heels. Egg bar shoes are heavy if they protrude beyond the heel bulbs and may be pulled off. Shoe loss is an important issue in event horses, more so than in other sport horses. As a compromise the straight bar shoe may provide additional foot stability

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while reducing the risk of shoe loss. In those horses requiring egg bar shoes, overreach boots can be used to reduce the risk of shoe loss, and by using a more palmar point of breakover, the front feet may leave the ground more quickly compared with horses with conventional shoes. In horses with weak heels or quarters, laminar separation, or focal osteitis of the distal phalanx, an egg bar shoe may provide inadequate support and a heart bar shoe can be beneficial. This shoe is heavy, does not project as far beyond the heels as does the egg bar shoe, and transfers some portion of weight-bearing load to the frog. In horses with pain localized to one heel or quarter, a half bar shoe can provide sufficient support and is lighter than a full heart bar shoe. Pads and cushions are used infrequently in event horses. Although pads may provide short-term benefit in horses with solar pain, they promote excess movement of the clenches and premature shoe loosening. Full pads cause a poor solar microenvironment. Modern synthetic hoof repair materials can be beneficial in horses that have lost portions of the hoof wall, because the defect can be filled and shoe nails can be placed subsequently. However, routine use of hoof repair materials to augment hoof wall in horses with poor-quality, cracking, and flaking feet should be discouraged and may even cause the problem to persist. If used, repair material should be removed at the end of the season, and the horse should be turned out without shoes. The foot may break up initially but will grow back stronger without the repair materials. Steel shoes are used routinely, but some riders switch to aluminium shoes at a Three Day Event. The foot must be of sufficient quality to cope with the lower degree of support offered by the more flexible aluminium shoe, and switching is not recommended if the horse has any history of foot-related lameness. Any speed and recovery benefits of the lighter shoes do not appear to be obvious in event horses. Synthetic shoes rarely are used. Road nails or studs often are used, especially in broad section shoes, to decrease the risk of slipping on the roads during walking and trotting exercise. Improper use of road nails or studs may cause hoof imbalance. If the grip point is positioned near the middle of the foot (rather than near the heel), the foot may rock over this point during weight bearing. Event horses commonly wear studs for competition. Some advocate that a single stud be worn simply on the basis that if the stud is on the outside, the risk of the horse treading on itself is less. With a single stud, the foot can still twist, causing less jarring to the limb overall. Conversely, a single stud severely imbalances the foot, and because the roads and tracks phase of a Three Day Event often includes sections of metaled road or tracks, this could induce excessive strain on the joints (Fig. 118-7). Studs should be avoided for the roads and tracks phase if logistically possible. However, some horses will only jump with confidence if two or more studs per foot are applied. The studs always should be chosen based on ground conditions, and a blunt inside stud decreases problems from tread injury. Care should be taken to avoid positioning a stud hole over an area of defective hoof wall. Horses are normally re-shod one week before a Three Day Event, because if a horse is pricked or any foot soreness occurs after shoeing, the horse has time for recovery.

TACK CONSIDERATIONS Saddle fit is of great importance in event horses. Injuries to the withers and back may manifest as poor performance in the dressage or show jumping phases of competition. Different saddles are required for the different disciplines of eventing, predisposing the horse to fitting problems. The fit of the saddle to the horse is sometimes a secondary consideration

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Fig. 118-7 Palmar view of horse with single studs, showing the degree of mediolateral imbalance induced when the horse is on a hard surface.

to riders who may have a particular saddle in which they feel secure. Event horses often have high withers and fitting a saddle is often difficult. Saddle fit can be affected adversely by the tendency of event horses to lose weight dramatically in the run up to a Three Day Event. Therefore a saddle that is fitted 2 weeks before an event can sit too low by competition time. Unfortunately, the use of pads and numnahs to correct poor saddle fit is not effective. Computerized saddle pressure analysis has shown that even gel pads are ineffective in alleviating focal pressure points, and that numnahs and pads placed beneath well-fitting saddles can be detrimental (see Fig. 118-4).4 Thick or multiple pads elevate the saddle and put pressure on the midline and over the dorsal spinous processes, a situation that impedes spinal flexibility. Opinions vary on the benefits of protective leg wear. Tendon boots are used almost universally for the cross country phase, because the risk of direct traumatic injury to the distal limb is high. However, the additional insulation increases the temperature of the distal limb. There are theoretical concerns that elevation in temperature could damage tenocytes and predispose the horse to tendonitis, although no clinical evidence indicates that this occurs. Some boots have reinforced sections to give additional protection against speedy cut injuries to the palmar aspect of the tendons, but the large rigid section may rub against the tendons at exercise and cause abrasions. Conversely some of the flimsy boots do not give sufficient protection against this kind of laceration. Bandages give a greater degree of conformity, but they are more difficult to apply correctly and require inclusion of a reinforcing layer if they are to provide substantial protection. Neither bandages nor boots reduce risk of tendon strain but simply protect against direct trauma.

DIAGNOSIS AND MANAGEMENT OF LAMENESS Thoracolumbar and Cervical Soreness and Restriction Neck and back soreness are common clinical findings in event horses, although they do not always limit performance. Soreness may be secondary to lameness as occurs, for example, when pain on palpation of the brachiocephalicus muscle is found in horses with distally located forelimb lameness. Primary problems may be subtle, and determining the importance of clinical findings can be difficult. To know an

individual horse’s normal degree of sensitivity and flexibility can be extremely helpful, because any changes can be correlated with the onset of a performance problem. Questioning a knowledgeable owner, groom, or physiotherapist can be helpful. Sometimes the significance of any soreness can be assessed only by the horse’s response to treatment. Event horses are particularly prone to muscle soreness when exercise intensity is varied or increased. Intense dressage training initially causes a transient period of lumbar muscle soreness, especially during the sitting trot. Areas of focal pain and muscle spasm may be easily palpable, but assessing flexibility and range of movement is also important. Radiographs are not helpful in diagnosing the significance of dorsal spinous process impingement, and clinical signs, scintigraphic examination, and positive response to local analgesia are necessary to confirm if a lesion is active. Ultrasonographic examination can be helpful in diagnosing supraspinous ligament injury. Thermography is helpful in detecting acute soft tissue injuries in the thoracolumbar region (see Chapter 25). Many horses with neck and back pain respond well to physiotherapy. If range of movement is decreased, then mobilization of the affected region is beneficial (see Chapters 94, 96, and 98), which then can be followed by continued stretching exercises, performed by the owner or rider. Massage is beneficial but yields only temporary improvement. Various modalities such as laser, therapeutic ultrasound, and neuromuscular stimulation can be helpful. Initial results with extracorporeal shockwave therapy have been encouraging. In some horses, chiropractic manipulation is beneficial. Acupuncture also can be effective in the right hands. Given the range of physiotherapeutic treatment options available, the degree of experience necessary for optimal treatment results, and the nature of these therapeutic modalities, I suggest that veterinarians should work with an experienced and qualified therapist. It behooves the veterinarian to be familiar with these techniques, because case selection and palpation skills can improve. Horses with lower cervical restriction caused by osteoarthritis of the dorsal cervical articular facets may show a positive response to intra-articular or peri-articular medication with methylprednisolone acetate (80 mg) injected under ultrasonographic guidance. Each affected facet joint is injected, and the horse is rested for 2 weeks, after which time improvement is normally dramatic. Horses with mild to moderate impingement of the thoracic dorsal spinous processes

CHAPTER 118 can be treated successfully using local injection of methylprednisolone acetate (80 mg) and Sarapin (4 ml). The horse is lunged or long reined for 2 weeks and then returned to exercise. The duration of effect can be as short as 6 weeks, but in a large proportion of horses, the problem resolves without repeat medication. Marks provides a review of the various veterinary options in treating back pain.5 The importance of management and riding factors in treating these conditions cannot be overemphasized. Rehabilitation and reschooling of horses with moderate to severe pain are necessary to build up the local musculature and to develop flexibility.

Foot Soreness (Bruising, Imbalance, and Nail Bind) Foot soreness is a common clinical problem in event horses. Temporary solar bruising is frequent, especially in flat- and thinsoled horses. Foot imbalances predispose horses to soreness, and medial to lateral hoof imbalance is commonly present. In horses with collapsed heels, pain to hoof testers and corns are commonly found. Horses with persistent foot lameness may have laminar separation or focal osteitis of the distal phalanx, and scintigraphy is helpful in differential diagnosis. Poor foot conformation in many horses can predispose them to nail bind or pricking when shod. Shoes often are pulled off, which can lead to breakup of the wall and further problems with shoe security. Regular, high-quality farriery is more import in maintaining good hoof quality than is the feeding of supplements or applying topical applications. Good stable hygiene is also important. Shoeing aspects have been discussed (see page 990).

Osteoarthritis Distal limb joints are especially prone to traumatic joint disease, especially in the forelimb. Osteoarthritis of the distal interphalangeal joint is most common, followed by that of the metacarpophalangeal joint. Osteoarthritis of the proximal interphalangeal joint is rare. Diagnosis is confirmed by observing a positive response to intra-articular analgesia, effusion or fibrosis, a positive response to flexion, and low-viscosity synovial fluid. Radiographs are often unremarkable in horses with early or low-grade osteoarthritis. Response to intra-articular medication is normally excellent. Combining hyaluronan with a low dose of corticosteroid, such as triamcinolone acetonide (5 mg) produces the greatest therapeutic effect. Hyaluronan alone produces an inconsistent response, and low doses of triamcinolone have been shown to be chondroprotective. Medium viscosity hyaluronan usually is used initially based on economic factors, but high molecular weight products may give a greater effect in some horses. Systemic administration of hyaluronan (intravenously) or polysulfated glycosaminoglycan (intramuscularly) is not nearly as effective as is specific intraarticular medication. Systemic medication does not carry the same risk of iatrogenic infection and is easier to administer and so is used frequently as an adjunct therapy. Prophylactic use of systemic therapy frequently is used in horses in the run up to a Three Day Event or to manage those with pathological conditions of multiple joints or generalized stiffness. Feeding of nutraceuticals such as chondroitin sulfate and glucosamine is also common practice. Although in vitro evidence of efficacy is substantial, no convincing clinical studies demonstrate efficacy in vivo. In fact, studies have demonstrated a lack of oral absorption of chondroitin sulfate in horses.6,7 In horses with osteoarthritis of the distal interphalangeal and metacarpophalangeal joints that has been non-responsive to medication, and especially with radiographic evidence of osteochondral fragmentation, arthroscopic evaluation can be beneficial. Focal areas of pathological conditions of cartilage and subchondral bone may be identified, and the horse often responds positively to debridement. Access is limited in the distal interphalangeal joint, but lesions often are found on the extensor process.

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Osteoarthritis of the tarsometatarsal and centrodistal joints is not infrequent, but the distal tarsal joints show scintigraphic evidence of remodeling even in normal event horses. Horses with authentic osteoarthritis of these joints usually respond well to medication with low doses of long-acting corticosteroids (40 mg of methylprednisolone acetate). The condition rarely seems to progress sufficiently to necessitate chemical or surgical arthrodesis.

Superficial Digital Flexor Tendonitis Although not the commonest lameness problem in event horses, tendonitis is the most substantial cause of wastage because of prolonged convalescence and high recurrence rates. Although tendonitis can occur as a single-event injury, especially if the horse falls, stumbles, or trips badly, the condition most commonly results from repetitive cyclic loading. Unlike the suspensory ligament, tendons in adult horses do not strengthen in response to exercise and therefore are prone to develop accumulated microdamage during intense training. This damage can give the prodromal signs of slight filling or heat in the palmar metacarpal structures. The clinical signs of a tendon strain then may develop acutely after a training canter or competition. For horses to develop subclinical tendonitis after a Three Day Event is not uncommon. The condition may not be apparent during the rest period after the competition but develops into clinical tendonitis when the horse resumes training or competitive work, even after 3 to 6 months. Close monitoring is thus essential, and I recommend routine ultrasonography after each Three Day Event. Ultrasonographic evaluation is important to assess the severity of injury and to determine a prognosis and an appropriate treatment plan. Lesion length and percentage of cross-sectional area involvement should be determined. Tendons may increase in crosssectional area up to 10% normally with intense training, but this tends to return to baseline at the end of the season. If ultrasonographic examination is performed soon after injury, the extent of the lesion may not be apparent and severity may be underestimated. Severity of tendon damage is assessed most accurately between 1 and 4 weeks after injury. Initial treatment of event horses with tendonitis is aimed at limiting inflammation and preventing any further tendon damage. The horse should be given box rest for 2 to 4 weeks, and anti-inflammatory therapy should be commenced. Systemic NSAIDs appear to decrease swelling and pain, and no evidence indicates that they impede healing. Conversely, prolonged corticosteroid administration may interfere with fibroplasia, although a single systemic dose helps decrease inflammation without any apparent detrimental effects. Support bandages or firm stable bandages should be applied for the first few weeks to reduce swelling. Topical dimethylsulfoxide can be useful to decrease inflammation early after injury but should not be used for more than 5 days, because it can weaken collagen fibers and blister the skin. Local treatment with cold water hosing and ice application is beneficial while the signs of acute inflammation persist. For horses with mild to moderate injuries, the benefits of being able to perform local therapy seem to outweigh the greater external support that can be provided by application of a Robert Jones bandage. In horses with severe tendonitis in which loss of support (sinking) of the metacarpophalangeal joint has occurred, external support using a Robert Jones bandage is recommended. A heel wedge should be applied if the animal is severely lame. Heel elevation theoretically does not decrease load on the superficial digital flexor tendon but appears to provide analgesia to horses that stand with the heel off the ground. In horses with severe breakdown injury, support with a proprietary splint, such as a Kimzey LegSaver, (Kimzey, Woodland, CA) is recommended.

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Controlled exercise, to encourage development of a longitudinal fiber pattern but without placing excessive load on the tendon to damage the healing fibers, is the mainstay of recuperation. Serial ultrasonographic examinations are helpful to determine the appropriate rate of progress and the response to increasing exercise. After the period of box rest, walking in hand normally is commenced. Mechanical horse walkers appear detrimental in the early stages of healing, because constant turning places excessive load on the weak tendon. However, such walkers are extremely helpful after the initial 4 to 6 weeks of walking in hand, when duration of walking is increased. A major problem during this stage is degree of tolerance shown by the horse to this restricted level of exercise. Many horses are too excitable to be walked safely in hand, but they behave appropriately on a horse walker or if ridden under saddle. Exercise programs must be tailored to account for rider competence and the horse’s behavior. Once trotting has been commenced, the horse normally settles down into the exercise regimen. A large number of treatment options exist for managing event horses with tendonitis. Tendon splitting, usually performed percutaneously in the standing horse, appears beneficial in horses with acute core lesions. Tendon splitting may decompress the core lesion and allow neovascularization but is most effective when performed in the first 10 days after injury. Intralesional injection of hyaluronan or a polysulfated glycosaminoglycan has not proved beneficial. Initial clinical studies investigating intralesionally administered β-aminoproprionitrile fumarate unfortunately lacked representative control groups. The drug has received a mixed reception since becoming licensed and is not the panacea that some initially promoted it to be. The drug has been used in a limited number of event horses that returned to compete at the top level. Use of intralesional growth factors is an area of current research interest. Insulin-like growth factor 1 and equine growth hormone, which induces the production of insulin-like growth factor 1, have been studied. I have had success in a small number of horses using transforming growth factor β (TGF-β) in horses with tendonitis. The drug appears to promote fibroplasia. Although this gives a quicker healing rate and horses have returned to work successfully, whether the expected increase in strength and decrease in elasticity are desirable is theoretically debatable. I have had rewarding results using TGF-β in horses with chronic tendonitis. When ultrasonographic evidence of poor infilling exists, intralesional injection of TGF-β improves fiber pattern, and horses are able to withstand increased exercise intensity. After treatment, some horses have returned to CCI**** level and have completed successfully in up to three events. Desmotomy of the accessory ligament of the superficial digital flexor tendon (superior check desmotomy) also can be beneficial in selected horses. Because of the risk of general anesthesia, I reserve its use for horses with recurrent tendonitis or those in which the ultrasonographic appearance of the tendon deteriorates inappropriately during the controlled exercise regimen. In a small number of horses in trotting exercise after tendonitis, increased cross-sectional area and decreased echogenicity are observed. Even after the plane of exercise is reduced to walking for another 6 to 8 weeks or even longer, the ultrasonographic appearance of the tendon does not change. After desmotomy, however, these horses tolerate an increased plane of exercise without ultrasonographic deterioration or subsequent recurrence of tendonitis. Because the procedure may increase the risk of suspensory desmitis after surgery, desmotomy should not be used in horses with a concurrent pathological condition of the suspensory apparatus. Systemic medication with a polysulfated glycosaminoglycan is used as an adjunct treatment in horses with tendonitis. Ease of administration and lack of potential complications make such treatment popular, but no evidence indicates that

any systemic medication, or feed supplements for that matter, has beneficial effects in tendon healing. The total convalescent period depends on severity of initial injury, how well the injury appears to heal as viewed by ultrasonography, and the degree of compliance with the controlled exercise regimen. In horses with mild tendonitis (subtle loss of fiber pattern and ≤10% increase in cross-sectional area) as few as 6 weeks of walking exercise is sufficient. Horses with loss of fibers and frank tendonitis require a convalescent period of 9 to 15 months. Recurrence rate is less in horses that are given at least a year to recuperate before commencing full work. After tendonitis, many horses can be managed successfully to complete one Three Day Event, but sustaining the horse through a number of Three Day Events without recurrence is more difficult. A small number of horses seem to suffer recurrent clinical signs regardless of management protocol and these are best restricted to One Day Events in which they will often then compete successfully for many years.

Suspensory Desmitis The two main levels of suspensory injury in Three Day Event horse are branch desmitis and proximal suspensory desmitis. Mid-body desmitis is rare. Suspensory branch desmitis can be considered an occupational disease of event horses. Advanced horses commonly develop inflammation and enlargement of the branches after a Three Day Event, and the condition is often transient with no associated lameness. Viewed by ultrasonography, the branches have periligamentous fibrosis with no areas of obvious hypoechogenicity, although some loss of longitudinal fiber pattern may occur. In many horses this pathological condition is missed or ignored, and the horse is just turned out. Even a short period of controlled exercise often decreases the risk of recurrence, however. Some degree of synovitis of the metacarpophalangeal joint commonly occurs and usually responds favorably to intra-articular medication. Proximal suspensory desmitis is a common cause of forelimb lameness. Lameness may be acute in onset and inflammation obvious after exercise, or the disease can be insidious without any localizing signs. Diagnostic analgesia is mandatory, and ultrasonographic examination is valuable. Radiographic and scintigraphic examinations are useful adjunct tools. Most horses have true desmitis, although a small number have enthesopathy and associated bone remodeling, with significant IRU and minimal ultrasonographic abnormalities. Most horses respond well to 4 to 9 months of controlled exercise, and no convincing evidence exists that any intralesional medications are beneficial. Extracorporeal shock wave therapy has been used to treat horses with suspensory desmitis and may provide quick analgesic effect. However, this may encourage a premature return to full exercise, thus increasing the risk of recurrence. Shock wave therapy may well have a role in horses with chronic, active desmitis, especially those with bone involvement that does not respond appropriately to controlled exercise. I feel that proximal suspensory desmitis in the hindlimb is a most important but underdiagnosed condition. Similar to that seen in the forelimb, hindlimb proximal suspensory desmitis may cause acute or chronic lameness. The prognosis is generally much poorer in the hindlimb, however, because of the development of a local compartment syndrome and associated pressure on the plantar metatarsal nerves. Thus most horses remain chronically lame, even after the ligament appears healed on ultrasonographs. I have had success in treating chronic lameness resulting from hindlimb proximal suspensory desmitis using local infiltration of triamcinolone (10 mg) in horses with static or healed ligaments but with persistent lameness. Although lameness abates, treatment needs to be repeated at 6-month intervals and may be detrimental to the ligament in the long term. Thus a surgical technique has been developed for use in

CHAPTER 118 horses with chronic desmitis that has yielded extremely good results.8 The surgical technique involves the resection of a 3-cm segment of the common branch of the plantar metatarsal nerve, distal to its origin from the lateral plantar nerve. This is combined with incision of the fascia (fasciotomy) overlying the origin of the suspensory ligament. This technique combines decompression with analgesia, and has allowed horses to return to a normal level of work within 3 months. The horses are restricted to walking only for the first month, after which time turnout and ascending exercise are permitted. I have long-term follow-up data on 20 horses, and all returned to the previous level of work (including CCI****). Recurrence of proximal suspensory desmitis was seen in only two horses.

External Trauma Event horses are prone to traumatic lacerations during competition, the most common being overreach injuries to the heel bulbs. Standard principles of treatment apply, although owners often apply pressure to minimize healing time during the competition season. Aggressive early treatment is advised, and horses with deep foot or pastern wounds should be managed with a fiberglass cast for 10 to 14 days, a treatment that may shorten the convalescent period. Wounds should be assessed carefully for synovial penetrations. Thorn penetrations from brush or hedge fences can lead to infectious arthritis of the carpal or stifle joints, with only minimal clinical signs evident initially. Direct trauma from jumping solid fences is common. Trauma directly over bone can lead to a severe, transient lameness. Acute lameness from this type of bone bruising can be difficult to differentiate from a fracture on an initial clinical examination. Trauma over the soft tissues may lead to the development of a considerable hematoma or edema, so local cold and pressure are indicated in the early stages.

Pain in the Sacroiliac Region A low-grade form of sacroiliac disease is common in event horses and is manifest as a loss of impulsion and scope when jumping, with a reduced hindfoot flight arc. Most advanced event horses have bony pelvic asymmetry when critically assessed. Clinical signs include pain on palpation around the tubera sacrale and resentment of gentle lateral rocking action when the horse is in a weight-bearing position, with the opposite hindlimb held up. Often associated muscle soreness and spasm are present in the surrounding musculature, notably the middle gluteal muscle. Most of these horses appear to have sacroiliac joint instability, but minimal evidence of IRU is seen on scintigraphic examination. Clinical signs can be localized by assessing the response to infiltration of local anesthetic solution around the dorsal aspect of the sacroiliac joint, using a spinal needle angled ventrocraniolaterad from just caudal to the opposite tuber sacrale. Ultrasonographic evaluation of the ventral sacroiliac ligaments per rectum also can be helpful to localize any pathological condition. The condition usually occurs when the horse is unfit and being brought into work or when the plane of exercise is increased. Sacroiliac pain often is self-limiting because the musculature increases as the plane of exercise increases and stabilizes the sacroiliac joint. Administering a systemic NSAID such as phenylbutazone helps the horse work through the period of lameness. Physiotherapy can assist in treating the local muscle spasm, and some horses improve with chiropractic or osteopathic manipulation. Horses with refractory pain sometimes improve after the local infiltration of methylprednisolone (120 mg) or a sclerosing agent (50 ml; e.g., P2G Solution, Martindale Pharmaceuticals, Romford, UK) using the same approach as for local analgesia. Horses are continued in the same plane of work, and improvement normally is reported within a week. The duration of response varies, and some horses do not require repeat treatments.

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Stifle Fracture Fractures of the patella are common in event horses,9 and the imaging aspects have already been discussed. For medial fractures, surgical removal offers the best prognosis. The original surgical description is for an incision 15 to 25 cm in length, but I prefer to use arthroscopic guidance, enabling me to create a minimal surgical incision (5 to 7 cm) centered directly over the fragment. This is satisfactory for small fragments and also allows for thorough evaluation of the femoropatellar joint and easy removal of any loose fragments.

Other Fractures Fractures caused by direct trauma of the distal phalanx and second and fourth metacarpal bones are not uncommon. Occasionally, condylar fractures of the third metacarpal or metatarsal bones or sagittal fractures of the proximal phalanx occur during training or competition, although they are rare. The standard considerations apply for evaluation and treatment. Vertebral or upper limb fractures can occur after a fall, and the initial evaluation can be complicated by adrenaline dominance.

Rhabdomyolysis Recurrent rhabdomyolysis is rare in advanced-level horses, because horses prone to this disease are selected out at the lower levels. Sporadic episodes are common at Three Day Events, however. Many potential trigger factors exists, including the stress of travel, stabling away from home, the competition itself, dehydration, climate changes, electrolyte imbalance, and dietary changes. I have noted a particularly high incidence in horses that were switched to haylage products immediately before a competition. This practice is done frequently because of the greater convenience of the small, packaged bales. A period of at least 4 to 6 weeks is recommended to allow adaptation to the new diet. The clinical manifestations at a Three Day Event can vary between collapse and recumbency on the roads and tracks phase to slight stiffness developing many hours after the completion of the crosscountry phase. To reduce the risk of rhabdomyolysis, attention should be paid to avoiding the trigger factors. Vitamin E levels are frequently low in event horse diets. Many commercial electrolytes do not contain sufficient quantities of salt, and horses may be at risk if owners follow manufacturers’ recommendations. Routine blood sampling to monitor the muscle-derived enzymes aspartate aminotransferase and creatine kinase is performed frequently, but considerable fluctuation in asymptomatic event horses can occur,10 making interpretation difficult. This variation tends to decrease as horses become fitter, as the muscle cells appear less leaky. With the recognition of polysaccharide storage myopathy as a cause of rhabdomyolysis, some event horses have been successfully managed on a diet high in fat and low in soluble carbohydrates, although actual diagnosis is difficult to confirm.

PREVENTION OF LAMENESS When considering the time involved to train a horse to the top level and the potential for a long athletic career, preventing lameness is especially desirable in event horses. However, many important factors are beyond the veterinarian’s influence. The number and frequency of competitions, having the opportunity to choose events with good going and an appropriate riding surface, and a high standard of riding ability are factors difficult to control. The veterinarian may be able to assist with other factors such as a high standard of farriery and optimizing training programs. Regular veterinary monitoring can be valuable by allowing the early detection and treatment of any

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lameness problems. Monitoring for incipient tendonitis can be useful by performing periodic clinical examinations, using thermographic and ultrasonographic examinations, and by monitoring serum markers of tendonitis. Serial determination of markers such as cartilage oligomeric matrix protein holds promise. Initial studies have shown that cartilage oligomeric matrix protein increases as training intensity increases, and higher cartilage oligomeric matrix protein levels are found in horses that subsequently developed tendonitis.11 The concurrent use of all of these maximizes the veterinarian’s ability to detect subclinical tendonitis. Many medications and supplements are sold with the aim of decreasing the risk of orthopedic disease. In racehorses, intramuscularly administered polysulfated glycosaminoglycan and intravenously administered hyaluronan have been shown to decrease the number of races missed, although the incidence of injuries was not decreased. Thus these drugs seem to be acting as anti-inflammatory rather than as disease-modifying agents. Glucosamine has disease-modifying properties in vitro, has been shown to be efficacious in human studies, and is a sufficiently small molecule that absorption would be expected. A role for oral glucosamine supplementation in horses may be found, but further studies are required. Many commercial products are available with unproven efficacy and variable and uncertain composition. The future of lameness prevention may be the modulation of skeletal development by early training. Waiting until the horse is skeletally mature before breaking it in means that the different loads of carrying a rider and performing athletic exercises are imposed on a skeleton with little adaptive capacity. Conversely, overworking an immature skeleton can lead to a high incidence of orthopedic injury, such as is seen in young racehorses. A compromise position may be found that theoretically could lead to the early development of a skeleton adapted for the loads that will be placed on it and with the development of a higher-quality extracellular matrix that will better withstand the work that it has to perform.

CHAPTER •

REFERENCES 1. Dyson SJ: Training the event horse. In Hodgson DR, Rose RJ, editors: The athletic horse, Philadelphia, 1994, WB Saunders. 2. Dyson S: Assessment of an acutely lame horse. In Dyson S, editor: A guide to the management of emergencies at equine competitions, Newmarket, England, 1996, Equine Veterinary Journal. 3. Lambiase M, Henson FMD, Bathe AP: The use of scintigraphy as an indicator of osteoarthrosis of the distal tarsal bones of the hock. In British Equine Veterinary Association Congress handbook, vol 38, London, British Equine Veterinary Association, 1999 (abstract). 4. Lambiase M, Henson FMD, Jeffcott LB, et al: Use of dynamic force sensing array measurements to assess the benefits of various numnahs and therapeutic pads beneath the saddle. In British Equine Veterinary Association Congress handbook, vol 38, London, British Equine Veterinary Association, 1999 (abstract). 5. Marks D: Back pain. In Robinson NE, Wilson MR, editors: Current therapy in equine medicine, ed 4, Philadelphia, 1997, WB Saunders. 6. Bathe AP, Humphrey DJ, Henson FMD: The oral bioavailability of chondroitin sulphate in horses: a pilot study. In Lindner A, editor: The elite showjumper. Proceedings of the Conference on Equine Sports Medicine and Science, Sicily, Italy, 2000. 7. Ramey R: Personal communication, 2001. 8. Bathe AP: Plantar metatarsal neurectomy and fasciotomy in the surgical treatment of hindlimb proximal suspensory desmitis: technique and preliminary results, Vet Surg 30:298, 2001 (abstract). 9. Dyson S, Wright I, Kold S, et al: Clinical and radiographic features, treatment and outcome in 15 horses with fracture of the medial pole of the patella, Equine Vet J 24:264, 1992. 10. Bathe AP: Resting haematological and biochemical parameters in a group of event horses, Pferdeheilkunde 12:712, 1996 (abstract). 11. Bathe A, Smith R: Unpublished observations, 1998.

119

Lameness in Endurance Horses Martha M. Misheff

DESCRIPTION OF THE SPORT The ancient Bedouin raced their horses long distances across the desert, British and American cavalry units used endurance tests as part of their military training, and nineteenth-century Austrians had a Vienna to Budapest ride, but organized endurance riding is a young sport. The first modern endurance ride, the 100-mile (160-km) Tevis Cup from Nevada to California has been run every year since 1955. The Tom Quilty Gold Cup, a prestigious 160-km endurance race named for its founder, was established in 1966 and is held every year in a dif-

ferent part of Australia. The oldest endurance organization, the American Endurance Ride Conference, has been in existence only since 1972. The American Endurance Ride Conference International was established in 1991. The first Federation Equestre Internationale (FEI) European Championship was held in Florac, France, in 1984, and the first Endurance World Championship in Rome, Italy, in 1986. Since then many recognized international competitions have been held under the auspices of the FEI, including the Endurance World Championship, held every 2 years in a different country. Many countries have endurance or long-

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lameness problems. Monitoring for incipient tendonitis can be useful by performing periodic clinical examinations, using thermographic and ultrasonographic examinations, and by monitoring serum markers of tendonitis. Serial determination of markers such as cartilage oligomeric matrix protein holds promise. Initial studies have shown that cartilage oligomeric matrix protein increases as training intensity increases, and higher cartilage oligomeric matrix protein levels are found in horses that subsequently developed tendonitis.11 The concurrent use of all of these maximizes the veterinarian’s ability to detect subclinical tendonitis. Many medications and supplements are sold with the aim of decreasing the risk of orthopedic disease. In racehorses, intramuscularly administered polysulfated glycosaminoglycan and intravenously administered hyaluronan have been shown to decrease the number of races missed, although the incidence of injuries was not decreased. Thus these drugs seem to be acting as anti-inflammatory rather than as disease-modifying agents. Glucosamine has disease-modifying properties in vitro, has been shown to be efficacious in human studies, and is a sufficiently small molecule that absorption would be expected. A role for oral glucosamine supplementation in horses may be found, but further studies are required. Many commercial products are available with unproven efficacy and variable and uncertain composition. The future of lameness prevention may be the modulation of skeletal development by early training. Waiting until the horse is skeletally mature before breaking it in means that the different loads of carrying a rider and performing athletic exercises are imposed on a skeleton with little adaptive capacity. Conversely, overworking an immature skeleton can lead to a high incidence of orthopedic injury, such as is seen in young racehorses. A compromise position may be found that theoretically could lead to the early development of a skeleton adapted for the loads that will be placed on it and with the development of a higher-quality extracellular matrix that will better withstand the work that it has to perform.

CHAPTER •

REFERENCES 1. Dyson SJ: Training the event horse. In Hodgson DR, Rose RJ, editors: The athletic horse, Philadelphia, 1994, WB Saunders. 2. Dyson S: Assessment of an acutely lame horse. In Dyson S, editor: A guide to the management of emergencies at equine competitions, Newmarket, England, 1996, Equine Veterinary Journal. 3. Lambiase M, Henson FMD, Bathe AP: The use of scintigraphy as an indicator of osteoarthrosis of the distal tarsal bones of the hock. In British Equine Veterinary Association Congress handbook, vol 38, London, British Equine Veterinary Association, 1999 (abstract). 4. Lambiase M, Henson FMD, Jeffcott LB, et al: Use of dynamic force sensing array measurements to assess the benefits of various numnahs and therapeutic pads beneath the saddle. In British Equine Veterinary Association Congress handbook, vol 38, London, British Equine Veterinary Association, 1999 (abstract). 5. Marks D: Back pain. In Robinson NE, Wilson MR, editors: Current therapy in equine medicine, ed 4, Philadelphia, 1997, WB Saunders. 6. Bathe AP, Humphrey DJ, Henson FMD: The oral bioavailability of chondroitin sulphate in horses: a pilot study. In Lindner A, editor: The elite showjumper. Proceedings of the Conference on Equine Sports Medicine and Science, Sicily, Italy, 2000. 7. Ramey R: Personal communication, 2001. 8. Bathe AP: Plantar metatarsal neurectomy and fasciotomy in the surgical treatment of hindlimb proximal suspensory desmitis: technique and preliminary results, Vet Surg 30:298, 2001 (abstract). 9. Dyson S, Wright I, Kold S, et al: Clinical and radiographic features, treatment and outcome in 15 horses with fracture of the medial pole of the patella, Equine Vet J 24:264, 1992. 10. Bathe AP: Resting haematological and biochemical parameters in a group of event horses, Pferdeheilkunde 12:712, 1996 (abstract). 11. Bathe A, Smith R: Unpublished observations, 1998.

119

Lameness in Endurance Horses Martha M. Misheff

DESCRIPTION OF THE SPORT The ancient Bedouin raced their horses long distances across the desert, British and American cavalry units used endurance tests as part of their military training, and nineteenth-century Austrians had a Vienna to Budapest ride, but organized endurance riding is a young sport. The first modern endurance ride, the 100-mile (160-km) Tevis Cup from Nevada to California has been run every year since 1955. The Tom Quilty Gold Cup, a prestigious 160-km endurance race named for its founder, was established in 1966 and is held every year in a dif-

ferent part of Australia. The oldest endurance organization, the American Endurance Ride Conference, has been in existence only since 1972. The American Endurance Ride Conference International was established in 1991. The first Federation Equestre Internationale (FEI) European Championship was held in Florac, France, in 1984, and the first Endurance World Championship in Rome, Italy, in 1986. Since then many recognized international competitions have been held under the auspices of the FEI, including the Endurance World Championship, held every 2 years in a different country. Many countries have endurance or long-

CHAPTER 119 distance riding associations, all of which have been established only in the last 30 years.1 All of the organizations require that horses be at least 5 years of age to compete at distances of 80 km (50 miles) or more, and all of the organizations have stringent veterinary controls. Competitors undergo an initial veterinary inspection. The total distance of the ride is divided into segments. After riding each section the competitor must pass a vet gate or veterinary checkpoint where a panel of veterinarians evaluates the horse for lameness and metabolic criteria. The heart rate must be at or under a maximum criterion (usually 64 beats per minute) set before the ride by the veterinary commission. A cardiac recovery index often is used, in which a second heart rate is measured 1 minute after the commencement of an approximate 80-m trot, during which time the horse is evaluated for lameness. Although not a criterion for elimination in and of itself, a positive cardiac recovery index, in which the second heart rate is elevated more than a few beats above the first one, is an indication that the horse merits further evaluation. Other metabolic parameters, such as mucous membrane color, capillary refill time, skin turgor, and auscultable intestinal motility are checked and recorded. Any saddle sores, girth rubs, or bit-related lesions also are noted. A heart rate above the maximum allowed, lameness, injury, and synchronous diaphragmatic flutter are grounds for elimination. Endurance horses are not permitted to compete on medication, and regulatory bodies conduct random testing for those substances that are not permitted. Some jurisdictions routinely test the first several finishers. Although smaller competitions often use the same veterinarians for control and treatment, many of the larger competitions now have separate veterinarians dedicated to treatment. Typically a horse that is eliminated by a control veterinarian for a lameness or metabolic problem is referred to the treatment veterinarian for further evaluation. If the treatment veterinarian deems that treatment is prudent, treatment may be provided at a field clinic at the ride site, or the horse may be transported to a local veterinary clinic with which prior arrangements have been made. Ride site treatment clinics at the larger venues are able to offer relatively sophisticated care, and only those horses that require continued care or further investigation are referred.

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Some endurance organizations require a horse to complete a qualifying ride at a lesser distance before being permitted to compete at the next distance level. Overtraining of endurance horses tends to be more of a problem than under-training, particularly by novice trainers. In some countries endurance competition is rapidly evolving from an amateur sport in which the same person owns, trains, and rides the same horse for many years, competing for pleasure with little financial reward, to large multiple-horse stables run by professional trainers with riders that may never have ridden their horses before, competing for high-value prizes. Even if the prize money is a paltry sum, compared with other sports, the value of a horse winning or running successfully in a prestigious international competition may increase exponentially. This amateur to professional shift has meant that the speed required to win international competitions over flat terrain has increased dramatically. Speeds at high profile rides over mountainous terrain have not changed substantially. Essentially the sport has changed at some venues from endurance riding to endurance racing. The winner of the 1998 World Championship in the United Arab Emirates averaged 17.77 km/hr for 160 km. The winner of the 2000 World Championship in France averaged 16.96 km/hr over 161.7 km, and at some competitions the winning speed has increased to greater than 25 km/hr. This is the equivalent of a continuous fast canter or gallop. Years ago this would have been unheard of, and opinions differ as to whether this is desirable progress. From a veterinary standpoint, at rides where speeds are increasing we are beginning to see injuries more like those seen in flat racing horses, as well as serious metabolic abnormalities, because horses tend to be pushed harder when high prize money is at stake.

COURSE TERRAIN Endurance horses compete and train over some of the most highly variable terrain of any sport horses. They go up rocky mountains, through creeks, across sandy deserts, along tarmac and gravel or dirt roads, across grassy fields, and on other surfaces depending on where the ride is held. Course terrain has a bearing on the types of injury in a predictable way. On rocky ground more horses have stone bruises and painful joint injuries, whereas on soft or sandy ground more horses have ligament and tendon injuries.

TYPE OF HORSE Most endurance rides are open to horses of any breed, but horses of Arabian extraction are most popular for endurance riding because of their light build and stamina over long distances. Larger, heavier framed horses are less able to sustain the speed required over the distances traveled. A few Middle Eastern endurance rides are restricted to purebred Arabians or Arabian crossbreeds.

TRAINING METHODS Methods differ considerably among trainers, but most would agree that horses take 2 to 3 years of training to make good endurance racers. Training distance and frequency depend largely on individual circumstances (terrain, weather, and availability of pasture or turnout paddocks), but in general endurance horses are ridden at least several times a week. A typical program might include rides of 10 to 20 km with 40- to 50-km rides at weekly or 10-day intervals. Horses are ridden at a walk, trot, and canter with the proportion of the time spent at each gait varying considerably among trainers. Horses aiming for a 100- to 160-km ride usually complete 60 km or more in a training ride on at least two occasions before the competition.

CONFORMATION AND LAMENESS Lameness in endurance horses essentially can be divided into ligament and tendon injuries, muscle problems, injuries to joints and feet, and miscellaneous less common causes. Lameness also can be separated into two categories: first, transient problems that may be cause for elimination on the day of competition but then resolve, and second, more persistent problems that are likely to be recurrent. Endurance horses, compared with other athletic horses, tend to be scrawny, scraggy-looking beasts. Like human marathon runners, the good ones are ectomorphs. Because endurance horses often compete over an 8- to 10-year period, most horses with glaring conformation defects tend to weed themselves out by attrition. Plenty of moderately toed-in, toedout, sickle-hocked, post-legged (straight-legged), calf-kneed, bench-kneed, or club footed endurance horses are used. Provided the conformational abnormality is not extreme, the overall function of the horse may not be compromised. A toed-in horse may develop splint exostoses that impinge on the suspensory ligament (SL), causing desmitis that may be recurrent; such horses ultimately may be unsuitable for endurance use.

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LAMENESS EXAMINATION AND PROCEEDING WITHOUT A DIAGNOSIS A lameness examination in any horse is performed most easily and efficiently when the lameness is visible, and the endurance horse is no exception. Making a specific diagnosis concerning the cause of a horse’s lameness is not possible if the horse is not lame at the time of examination. Watching the horse trot while lame, applying hoof testers, and noting any palpable abnormalities and response to flexion or other manipulative tests usually help to narrow the possible causes. Adhering to the principle of starting at the bottom and working upward during diagnostic analgesia is a particularly useful means of localizing the source of pain. Sometimes, despite a careful and complete lameness examination, diagnostic analgesia, and ancillary diagnostic aids such as radiography, ultrasonography, and scintigraphy, a specific diagnosis cannot be reached. In some horses lameness can never be eliminated by local analgesia. In others pain can be localized to a specific region, but no lesion can be found. A horse with lameness localized to a specific region by local analgesia—with no identifiable radiographic, scintigraphic, or ultrasonographic abnormalities—should be re-examined by the most appropriate imaging modality after 2 to 4 weeks. Stress fractures are particularly notorious for not being visible on the first examination and being readily visible later. If the lameness has resolved and no abnormality is identified when the horse is re-examined, returning the horse to light training is reasonable. If lameness recurs, the lameness examination should be repeated. Horses with a lameness that cannot be localized to a specific area should be evaluated for neurological disease, because this can be a cause of or mimic lameness. Generally, horses that have a lameness that cannot be localized are subjected to full body

scintigraphy. If lameness resolves, scintigraphy can be repeated before training is resumed. This is probably less important in endurance horses than in Thoroughbreds, because of less risk of stress fractures turning into catastrophic fractures. Not all owners want to pursue a diagnosis to this degree, and sometimes despite every attempt at imaging and re-imaging the veterinarian is still left with a lame horse and no diagnosis. When this point is reached, benign neglect and a prolonged rest period (8 to 12 months) sometimes work miracles.

TEN MOST COMMON CAUSES OF LAMENESS The following sections deal with the 10 most common causes of lameness in endurance horses (Box 119-1).

Suspensory Desmitis The leading cause of chronic or recurrent lameness in endurance horses, regardless of terrain, is suspensory desmitis, most commonly proximal suspensory desmitis.1-3 Suspensory desmitis may occur in a forelimb or hindlimb but is more common in front. Lameness typically develops in the later stages of a race, when the horse becomes fatigued, but is more likely to occur in the earlier stages in an unfit horse. Lameness from proximal suspensory desmitis may be sudden in onset and severe or more insidious. Often little swelling occurs, but careful palpation may elicit pain. Lameness associated with forelimb proximal suspensory desmitis often is accentuated by distal limb flexion. The diagnosis is confirmed by local analgesia. The origin of the SL may be blocked by the following methods: 1. Blocking the deep branch of the lateral palmar nerve at the level of the accessory carpal bone (proximal to its bifurcation into the medial and lateral palmar metacarpal nerves) and the lateral palmar nerve

Box • 119-1 Ten Most Common Causes of Lameness in Endurance Horses Lameness 1. Suspensory desmitis 2. Foot problems

3. Myositis

4. Superficial digital flexor tendonitis

5. Osteoarthritis of the fetlocks 6. Distal hock joint pain 7. Paravertebral myalgia 8. Splints 9. Gluteal myalgia 10. Lumbosacral or sacroiliac pain

Comments Suspensory desmitis is a common cause of chronic or recurrent lameness. More frequently localized to the origin than to the body or branches. Bruising of the foot is a common cause of elimination during competitions. Laminitis is seen with increasing frequency as a sequela to serious metabolic abnormalities. Navicular problems are uncommon. Myositis may be a nuisance disease causing generalized shortening of the stride, bilateral forelimb or hindlimb lameness, and elimination from competition. In its more serious forms, coupled with metabolic abnormalities, myositis may be life-threatening. Tendonitis may be acute or chronic, low grade or severe. In general, endurance horses have a better prognosis for return to competition than do Thoroughbreds or horses that race faster over shorter distances. Osteoarthritis can be present without causing lameness. Diagnostic analgesia helps in determining whether treatment is necessary. Radiographic changes do not always correlate with clinical signs. Pain often is treated empirically and frequently occurs with sore feet and sore back (the terrible triad). Paravertebral myalgia is related to rider fatigue, occurring as the horse experiences muscle fatigue, and also is caused by sore feet and hocks causing gait alteration. Splints are a common, often nuisance problem necessitating a short break from training. Gluteal myalgia is related to strenuous work over long distances and may occur with primary forelimb lameness. Severe inflammation may occur with rhabdomyolysis. Pain also is related to rider fatigue and repetitive stress over long distances.

CHAPTER 119 2. Direct infiltration 3. A high palmar and palmar metacarpal nerve block (high four-point) Inadvertent desensitization of the carpometacarpal and middle carpal joints is rarely a problem with the latter blocks, because lameness in endurance horses seldom is localized to the carpus. If a high index of suspicion of proximal suspensory desmitis exists, but a horse does not improve with one of the three blocks, the block should be repeated or one of the other two should be tried, because some variability in response occurs. Ultrasonography is used to confirm diagnosis of proximal suspensory desmitis. Abnormalities include loss of echogenicity of the most dorsal fibers close to the third metacarpal bone immediately distal to the carpometacarpal joint, seen best in longitudinal images (Fig. 119-1). The farther distally the fiber loss extends (from zone 1 into zone 2), the worse the injury. The key to determining whether acute injury has occurred is symmetry. Both suspensory origins should be compared. Bilateral change often is present, but the clinically affected side appears less echogenic. If the SL appears normal with ultrasonography, inflammation of the ligament may exist but without accompanying detectable structural change. Horses in such condition have a better prognosis than those in which lesions are identified by ultrasonography. It is important to recognize that a horse that has undergone any strenuous work may have some degree of structural change in the proximal SL,4 such as reduced echogenicity or fiber malalignment. Therefore diagnosis of proximal suspensory desmitis depends on response to local analgesia and comparison of the ultrasonographic appearance of the SL in each forelimb. Proximal suspensory desmitis is particularly treacherous to a horse’s career because the initial lameness often responds to a short period of rest. The horse’s caretakers are lulled into a false sense of security, and the horse is returned to work. Most of the time lameness recurs, which is why ultrasonographic evaluation is critical to management success. If substantial structural change is present, strenuous work should be avoided for at least 8 months. Radiography and scintigraphy are useful ancillary diagnostic aids, particularly in horses with avulsion of the origin of the SL (Fig. 119-2). Initial management of horses with proximal suspensory desmitis should be aimed at reducing inflammation. Systemic

Fig. 119-1 Longitudinal ultrasonographic images of the palmar metacarpal soft tissues. The left forelimb is on the left. Proximal is to the right. There is marked loss of echogenicity and fiber pattern in the proximal aspect of the right forelimb suspensory ligament (arrows). Some loss of echogenicity is also seen in the proximal aspect of the suspensory ligament of the non-lame left forelimb.

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corticosteroids (a single injection of triamcinolone acetonide, 0.03 mg/kg) along with 2 to 3 weeks of non-steroidal antiinflammatory drugs (NSAIDs) and local therapy (ice, poulticing, and bandaging) are beneficial. The horse should be restricted to hand walking until no lameness is apparent trotting in hand on a hard surface without the influence of NSAIDs. If no structural change has been identified, the horse may walk under tack for an additional 2 weeks. The horse should be re-examined ultrasonographically to confirm that no substantial structural change is present, because lesions visible by ultrasonography can lag behind clinical signs. Assuming the ligament is structurally normal, training then may progress to gradually increasing periods of trotting for 1 month, and then normal training may be resumed. A horse with structural abnormalities of the SL should have the same initial local and anti-inflammatory therapy and 6 weeks of hand walking and then be re-evaluated with ultrasonography. If healing is satisfactory and the horse is quiet, turnout into a small paddock is recommended. Ultrasonographic examinations are repeated at 6-week intervals until 30 weeks, at which time trotting may be resumed if healing is satisfactory. Time for rehabilitation depends on the horse’s temperament, the amount of help available, and the facilities available, but the best success is achieved with a controlled and gradual increase in exercise over 8 to 12 months. The bottom line has never changed: horses that sustain substantial damage to the SL or superficial digital flexor tendon (SDFT) need a long time off (8 months to 1 year) and will always be at higher risk of reinjury. The reason that conventional wisdom becomes conventional is that it has withstood the test of time.

Foot Problems Problems with the feet are a common cause of elimination from endurance competition and are a common cause of chronic or recurrent pain. Foot problems may occur in the forelimb or hindlimb but are more common in front. Many

Fig. 119-2 Lateral bone-phase scintigraphic images of the left and right forelimbs. There is intense focal increased radiopharmaceutical uptake in the proximopalmar aspect of the right third metacarpal bone (arrow) at the site of attachment of the suspensory ligament.

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problems are transient in nature, from bruising or a dislodged shoe. The importance of a properly trimmed, well-balanced, well-shod foot cannot be overemphasized. Because endurance horses go farther in a 24-hour period than any other horses, all of these things have a great impact, particularly on the support structures of the limb. Incredibly, the long-toe, lowheel syndrome still exists, even in endurance horses. This type of trimming and shoeing can lead to direct heel trauma and can increased strain on the SL and flexor tendons. Farriers who are accustomed to working with horses that wear keg shoes may be impatient with the requirements of endurance horses, which can sometimes require a more innovative approach aimed at providing the foot with increased protection and support. Inflammation of the solar structures occurs frequently in horses moving on hard ground. Lameness is manifest as a shortened, choppy gait, and hoof tester examination reveals a painful response around the solar margins. Lameness often is more pronounced in one foot. Diagnostic analgesia (abaxial sesamoid block) in the limb in which the lameness is most noticeable may result in a switch in lameness to the other side. Inflammation of the solar structures may or may not be accompanied by remodeling of the distal phalanx (pedal osteitis). Radiographic changes associated with remodeling of the distal phalanx include decreased radiopacity at the solar margin and increased size and number of vascular channels, resulting in a ragged appearance. Management is aimed at protecting the solar margins and reducing concussion. Wide webbed shoes, orthotic shoes, full pads, or rim pads can be used to accomplish these goals. Inflammation of the distal interphalangeal joints also may occur and can be treated with intra-articular medication. Sore feet often occur in horses with hock and back pain (the terrible triad), and each area must be addressed separately, but the horse must be considered as a whole. Navicular syndrome is uncommon in Arabian and Arabian crossbreeds but should be ruled out using diagnostic analgesia and imaging. Endurance horses are subject to traumatic laminitis, which often becomes apparent in the first 24 to 72 hours after a competition, and may range from mild but frightening to disastrous. Separation of the hoof wall from the coronary band may occur, serum often oozes from the coronary band, and a bounding digital pulse is present. These clinical signs are alarming but do not always correlate with the final outcome. In some horses the outer layer of hoof wall peels away from the coronary band, but the horse is not lame and no rotation or sinking of the distal phalanx occurs. The episode is marked by a distinct defect in the hoof wall that must grow out. Horses without rotation or sinking usually are able to return to endurance competition. Sometimes horses with the worst outcome (death) do not show much in the way of early warning signs. Any horse that begins to shift its weight or act uncomfortably after competition should be scrutinized carefully. Predicting which horses will have a satisfactory outcome and those which will not is not possible, therefore aggressive treatment aimed at halting the progression of laminitis should always be instituted (flunixin meglumine [0.25 mg/kg intravenously tid], acepromazine [0.025 mg/kg intramuscularly qid], pentoxyfylline [8.5 mg/kg PO tid], and dimethylsulfoxide [1 g/kg intravenously diluted to 10% to 20% solution sid to bid]). However, the horse should receive fluid therapy before administration of NSAIDs or acepromazine.

in the earliest or latest stages of a competitive ride. Horses with severe exertional myopathy often have pronounced swelling and hardening of the gluteal muscles. Asymmetry of the gluteal muscles may be present. Fluid therapy (0.9% sodium chloride) is the mainstay of treatment. Horses with severe exertional myopathy require large volumes (50 to 80 L) of fluids. Horses with myoglobinuria should urinate normal colored urine before flunixin meglumine (0.55 to 1.1 mg/kg or 250 to 500 mg/450 kg) is administered. When in doubt as to the status of renal function, it is better to give a lower dose and repeat as necessary. Blood urea nitrogen and creatinine should be monitored if possible. Highly portable, relatively inexpensive, user-friendly blood analyzers now make it possible to monitor kidney and muscle enzymes, and electrolytes and packed cell volume conveniently in the field. Dimethylsulfoxide (l g/kg intravenously in a 10% to 20% solution) also may be beneficial. Dantrolene may be useful but is not available in an intravenous form and is expensive to use orally at recommended dosages (15 to 25 mg/kg). Horses that have suffered an episode of exertional myopathy or myositis should not be returned to training until muscle enzymes return to normal.

Superficial Digital Flexor Tendonitis Tendonitis of the SDFT may be acute or chronic, low-grade or severe. Acute ruptures or partial ruptures do occur occasionally during competition. Initial management is directed at trying to reduce swelling and inflammation and to relieve pain. Ice, bandaging, and NSAIDs are used. Dehydrated horses should not be treated with NSAIDs until they are rehydrated. A horse that sustains a rupture or partial rupture of the SDFT has a poor prognosis for return to endurance competition. Horses with less severe damage of the SDFT can be more challenging to diagnose and treat. Training injuries occur frequently. The SDFT may be warm and tender on palpation, but lameness is usually not apparent. Ultrasonography should be performed to determine if fiber damage exists. The ultrasonographic appearance does not change initial management, but it determines whether the horse may continue training after a short rest period or whether a more prolonged rest period is required. Those horses with transient heat and tenderness, but no swelling or fiber damage, usually can be safely returned to training within 2 to 4 weeks after the resolution of clinical signs. If the tendon is enlarged or if fiber separation has occurred, a substantially longer absence from training and competition is required. Horses that sustain tendon fiber injuries in training or competition are managed similarly to flat racing horses. Management with one injection of triamcinolone acetonide (0.03 mg/kg), local application of ice for the first few days, bandaging, poulticing, and NSAIDs for 2 to 3 weeks is beneficial in reducing inflammation. Surgical splitting of those tendons with central core lesions, autogenous bone marrow grafting of split SDFT5 and desmotomy of the accessory ligament of the SDFT may be beneficial, but whether these therapies are more beneficial than rest alone is unproven. Because the career of endurance horses tends to span many years, time is on the veterinarian’s side, and the tendency is to treat endurance horses with superficial digital flexor tendonitis conservatively rather than surgically. Endurance horses with tendonitis of the SDFT have a better prognosis for return to competition than horses that race over short distances at higher speeds.

Exertional Myopathy Exertional myopathy, rhabdomyolysis, or myositis in endurance horses is not so much a lameness problem per se as a part of a larger picture of fatigue and metabolic abnormalities. Exertional myopathy is manifest as stiffening and shortening of the stride in all limbs and may be accompanied by trembling and profuse sweating. The condition usually occurs

Osteoarthritis of the Metacarpophalangeal Joint Osteoarthritis of the metacarpophalangeal joints and the distal joints of the hock occurs with similar frequency. This is hardly surprising, given the ongoing nature of the degenerative process and the fact that endurance horses may compete until they are 18 to 20 years old. Osteoarthritis of

CHAPTER 119 the metacarpophalangeal or metatarsophalangeal joints may occur with or without joint effusion and may be unilateral or bilateral. Osteoarthritis is far more common in the forelimbs but also occurs in the hindlimbs. Flexion of the joint produces pain, and the joint often has a decreased range of motion and thickening of the joint capsule. Radiographic changes may be subtle, such as narrowing of the joint space, or may consist of more severe peri-articular osteophyte or enthesophyte formation and joint remodeling. Radiographic changes do not always correlate with clinical significance, so diagnostic intra-articular or perineural (low palmar and palmar metacarpal blocks) analgesia is used to confirm the site of pain. Acute, traumatic synovitis or capsulitis of the metacarpophalangeal joint may occur occasionally, but in general, long-term management of chronic osteoarthritis is the more common scenario, and management is no different from that in any other athletic horse. Local therapy (ice, poultice, and sweats), intramuscularly administered glycosaminoglycans, intravenously administered hyaluronan, and judicious use of an intra-articularly administered hyaluronan and corticosteroid combinations are beneficial. Intra-articular corticosteroid injections should be low dose (20 to 40 mg methylprednisolone acetate with 20 mg sodium hyaluronan per joint), used with a rest period of 3 to 10 days, and should be spaced as far apart as possible, no more than 2 to 3 times a year, because the idea is to prolong the horse’s career. Competitions should be selected carefully and spaced appropriately.

Distal Hock Joint Pain Distal hock joint pain is common in the endurance horse. Osteoarthritis of the tarsus usually affects the tarsometatarsal and centrodistal joints and is often bilateral, with one limb being more affected than the other. Joint effusion is not palpable, but occasionally during intra-articular injection of the tarsometatarsal joint one gets the impression that the pressure and volume of synovial fluid is increased. Affected horses respond positively to hindlimb flexion and are sensitive to the Churchill test (see page 56). Radiographic abnormalities include joint space narrowing and peri-articular osteophyte formation. Radiographic changes do not always correlate with clinical signs, but intra-articular analgesia is used less frequently in the hindlimb compared with the forelimb. If the clinical picture suggests distal hock joint pain, intra-articular medication is administered. A positive response is empirical evidence of a correct diagnosis. Distal hock joint pain frequently occurs concurrently with paravertebral muscle pain and sore front feet, the terrible triad mentioned previously. This probably results from a horse with sore front feet altering its gait in such a way as to cause strain in the paravertebral muscles and hocks. The best results are obtained when all three problems are treated simultaneously; otherwise, the pain in one area and gait alteration and soreness in another become a never-ending cycle.

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extending the spine normally when palpated, tends to squat or crouch. Paravertebral myalgia also occurs in horses that alter the gait from sore feet or sore hocks. Treatment consists of removing the inciting cause and reducing inflammation. Most horses respond to a 2-week rest period with NSAIDs and injection of the paravertebral muscles with an antiinflammatory agent. The longissimus dorsi muscles are injected bilaterally about 3 cm lateral to the spine at 5 or 6 sites about 5 cm apart, from the mid-thoracic area moving caudally, with methylprednisolone acetate (200 mg) or estrone sulfate (50 mg), mixed with an aqueous solution of soluble salts of the volatile bases from Sarraceniaceae (Sarapin, 10 ml). Complementary therapies (acupuncture, chiropractic manipulation, and physical therapy) may be beneficial in certain horses but require well-trained and experienced therapists under veterinary referral.

Splints Periosteitis and exostosis of the second and fourth metacarpal and metatarsal bones (splints) are usually nuisance problems that may necessitate a 4- to 6-week break from training. Radiographs of horses with splint enlargements should be obtained to rule out fractures. Ice, NSAIDs, and bandaging can be used to reduce inflammation. Cryotherapy also can be used to reduce inflammation and sometimes enables horses to train after several days. Most splints resolve with time and treatment, although a non-painful enlargement remains. If the exostosis continues to enlarge, training should be discontinued to avoid impingement on and damage to the SL. Sometimes suspensory involvement occurs before the problem is recognized. These horses require a longer rest period. Exostoses that enlarge to the point that they impinge on the SL and are far enough distal to allow removal should be removed surgically before the rest period.

Gluteal Myalgia Inflammation of the gluteal muscles occurs with relative frequency in horses subjected to strenuous work over long distances. The superficial and middle gluteal muscles are painful on palpation and the horse may crouch down or move away during palpation. Swelling or asymmetry may be apparent in the acute stages, with elevation of serum muscle enzyme concentrations. Severe inflammation of the gluteal muscles and accompanying rhabdomyolysis is a serious problem that is discussed with metabolic abnormalities (see page 1002). NSAIDs must never be administered in the acute stages of gluteal muscle inflammation unless it can be ascertained that hydration and renal function are not compromised. Horses with less severe gluteal muscle inflammation usually respond to NSAID therapy and a short (2- to 3-week) rest period. Soreness in the gluteal muscles often occurs with forelimb lameness, because horses alter hindlimb gait to protect themselves. It is important to identify and treat the primary source of pain. Once that is accomplished, the gluteal muscle inflammation will resolve.

Paravertebral Myalgia Paravertebral myalgia is caused by a fatigued, unbalanced rider. Unfortunately, diminished rider capability usually is occurring at the same time that the horse is experiencing its own muscle fatigue. Horses ridden by fit, experienced riders are less subject to battering of the paravertebral muscles than those ridden by novices. Similarly, those horses carrying live weight are less likely to be battered by flopping lead pads than those carrying dead weight, because a fit, competent rider is able to adjust his or her weight distribution to help a tiring horse. Horses competing in FEI rides often have to carry a minimum weight of 70 to 75 kg. A horse that has strained or injured the paravertebral muscles appears stiff or rigid, and instead of flexing and

Lumbosacral and Sacroiliac Pain Lumbosacral and sacroiliac pain occur in endurance horses from repetitive stress over long distances. Rider fatigue and diminished rider capability are again likely to be important components in the development of pain in the surrounding musculature. Muscle spasm is likely to exacerbate any existing instability in the sacroiliac region. Horses exhibit stiffening and shortening of stride, and pressure over the tubera sacrale produces a painful response. Scintigraphic examination shows increased radiopharmaceutical uptake. Manipulation and deep muscle massage to alleviate muscle spasm, performed soon after injury, may be helpful. NSAIDs in conjunction with rest help resolve inflammation.

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METABOLIC PROBLEMS Avoidance, diagnosis, and management of metabolic problems are the most controversial topics currently facing the sport of endurance. The pressures alluded to earlier are manifest in an increasing number of horses that require treatment for metabolic abnormalities. On one hand, veterinarians are becoming more adept at recognizing subtle signs of exhaustion and are becoming more willing to treat horses aggressively before they get into serious trouble. On the other hand, more horses are getting into serious trouble. The exhausted horse syndrome was described many years ago6 and unfortunately is still evident today. Exhausted horses undergo massive but poorly understood fluid and electrolyte shifts that lead to multiple organ system compromise. Most commonly the first signs are a persistently elevated heart rate and a profound ileus that do not respond to fluid therapy, electrolyte supplementation, or analgesics. Synchronous diaphragmatic flutter may be present. Horses with ileus should be checked for the presence of gastric reflux. It cannot be stressed enough or overemphasized that exhausted horses, or those with severe myositis, must not be treated with NSAIDs until they are adequately rehydrated. To do so risks renal failure, and these horses are already in a high-risk category. If lameness or myositis is present, the temptation always is to treat the horse immediately with phenylbutazone or flunixin meglumine. This temptation must be resisted. Lame horses, even those without evidence of metabolic compromise, should be rehydrated before administration of NSAIDs. Horses with acute tendon or ligament injuries should have the affected limb placed in ice while they are undergoing rehydration before NSAID administration. Exhausted horses or those with severe myositis should receive at least 10 L, and preferably 15 to 20 L of intravenous 0.9% sodium chloride (or other available isotonic fluid), before NSAID administration. Collapsed horses or those on the verge of collapse may be given prednisolone sodium succinate (0.22 to 1.1 mg/kg or 100 to 500 mg/450 kg ). Two intravenous catheters, one of which is 10 or 12 gauge, should be placed. Catheters should be 140 mm (5.5 inches) long and should be sutured in place to prevent dislodgment and extravasation of fluid. Time is always available to do a sterile skin preparation before catheter placement; most of these horses recover, but infectious phlebitis is an unwelcome complication. Sterile skin preparation materials should be handy in a catheter kit. Exhausted, dehydrated horses are also at risk of pleuropneumonia and laminitis. Some horses already have been stressed before competition by being shipped long distances. Profound leukopenia may precede the onset of pleuropneumonia. Laminitis may strike several days after the initial episode of post-race exhaustion. Treatment for laminitis, discussed elsewhere (see page 1000), should be instituted in horses that are depressed, inappetant, leukopenic, or febrile.

Prevention of Metabolic Problems Most metabolic problems could be avoided by common sense, but in the heat of competition, common sense is often lost. Both horse and rider inevitably get tired, but a shrewd rider who knows his horse should know when the horse has had enough. If a horse is not eating and drinking at rest stops or is

reluctant to move forward, the horse should be stopped. Horses must be allowed to drink at rest stops. Hay fed to a well-hydrated horse acts like a sponge or water reservoir in the large intestine. Endurance horses should be encouraged to eat hay and should have free access to water before competition so that they will have a fluid reserve available for absorption from the large intestine. Providing oral electrolyte replacement is helpful if the horse is drinking, and using electrolyte preparations may encourage a horse to drink. Concentrated electrolyte preparations that are force-fed, however, may actually be detrimental if the horse does not drink, because by raising the tonicity of the gastrointestinal lumen, more fluid is drawn into the lumen from the circulation, contributing to dehydration. Synchronous diaphragmatic flutter, or thumps, a condition in which the phrenic nerve is stimulated by atrial depolarization, causing contraction of the diaphragm and consequent thumping of the flank in time with the heartbeat, is a sign of serious electrolyte imbalance, most commonly hypochloremic metabolic alkalosis. Sometimes, a low total or ionized calcium level can be demonstrated. Rest, food, and water may be all that is required for the condition to resolve. If treatment is required, however, horses with synchronous diaphragmatic flutter invariably respond to intravenous calcium supplementation (100 to 300 ml 20% to 23% calcium borogluconate diluted in 2 to 3 L of saline solution or 5% dextrose solution given over 15 to 20 minutes to effect). It has been proposed that horses subject to synchronous diaphragmatic flutter be fed a diet that is low in calcium before competition, which may enable more efficient mobilization of calcium from bone reserves during periods of stress.7 Recently an additional examination has been added at selected veterinary checkpoints on some rides. The purpose of the additional examination is to try to identify those horses that, because of aggressive cooling and perhaps high circulating catecholamines, pass the initial veterinary examination but then deteriorate during the mandatory hold period. Without this second look these deteriorating horses return to the trail and may deteriorate further until treatment is required. Although identifying all those horses that are going to have metabolic problems is probably not possible, an additional examination appears promising in at least identifying some of them. Therefore implementing the second look should be supported and encouraged by riders, trainers, ride organizers, and veterinarians.

REFERENCES 1. 2. 3. 4. 5. 6.

Bryant JC: Personal communication, 2001. Misheff MM: Unpublished data, 2000. Randall RW: Personal communication, 2000. Rantanen NW: Personal communication, 2000. Herthel DJ: Personal communication, 2000. Mackay-Smith M, Cohen M: Exercise physiology and diseases of exertion. In Mansmann RA, McAlalister ES, Pratt PW, editors: Equine medicine and surgery, ed 3, Santa Barbara, Calif, 1982, American Veterinary Publications. 7. Carlson G: Synchronous diaphragmatic flutter. In Robinson NE, editor: Current therapy in equine medicine, ed 2, Philadelphia, 1987, WB Saunders.

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Lameness in the Polo Pony Paul Wollenman, P.J. McMahon, Simon Knapp, and Mike W. Ross

HISTORY OF THE SPORT Polo was the first equestrian sport in recorded history. With strong ties to military traditions, the game originated in China in AD 272 and was often substituted for war games in preparation for military battle. Polo evolved into an organized sport and spread into Greece, India, and China, where the British colonies adopted the game. During the nineteenth century, the game became more refined in Great Britain and eventually found its way into the northeastern United States in 1876. Today polo continues to be one of the fastest and most dangerous equine sports in the world. Polo is no longer a sport for only the wealthy, but an increasing number of small clubs start up each year that attract people of moderate incomes to take lessons, buy horses, and begin to play. The sport has become more complex, with international professional players competing year-round on different teams around the globe. Professional polo coaches, umpires, trainers, and breeders have thus emerged, solidifying polo as a genuine equine sport industry. Playing seasons in the northern and southern hemispheres are followed by nomadic players, grooms, horses, and spectators. During the winter months in the United States, thousands of horses enter Florida and California, where the tropical climate is inducive to world-class polo tournaments. During the spring, summer, and fall seasons these horses travel across the Midwest, up the northeast coast and into Canada. The high-goal season begins in the summer in England and Spain, but the season in Argentina commences in the fall.

over 11⁄2 hours. The number of horses that are required to mount a polo team make each owner’s total investment much larger than that for other equine disciplines. Polo requires the speed and stamina of a Thoroughbred or a Thoroughbred-cross horse, the ability to stop and turn quickly, and the boldness to meet and collide with other horses at high speed. Although called ponies, polo horses stand 15 to 16 hands tall, and mares are preferred to geldings at a ratio of 10:1. Most trainers look for a fine neck and throatlatch, a good strong shoulder, powerful hip, quiet disposition, and a responsive, light mouth. Many horses have not raced, so few racetrack-related injuries are found in polo ponies. Argentina, New Zealand, and Australia are the only countries that specifically breed large numbers of horses for polo competition. Horses indigenous to these countries tend to have more bone than those in the United States and Europe, rendering them slightly more durable. Argentina has historically produced the most horses used solely for polo. Since 1970

POLO AS AN INDUSTRY Today three types of polo are played: outdoor, indoor (arena), and snow polo. Outdoor polo is by far the most popular and is played on a large, finely manicured grass field measuring 274 m (300 yards) by 137 m (150 yards) (Fig. 120-1). Injuries are related to fatigue (because of the distances covered), stopping, turning, and speed. Arena polo is played in much smaller arenas and is more common in collegiate settings. Injuries tend to be less frequent and are usually impact related. Snow polo is regarded as a novel exhibition sport played on the surface of a frozen lake and produces surprisingly few injuries. Obviously, footing and surface conditions often can be responsible for the type of lameness seen. Heavy, soft, grass polo fields and deep, sandy, uneven exercise tracks are frequently responsible for proximal suspensory desmitis, suspensory branch desmitis, and metacarpophalangeal joint sprains. Hard fields, exercise tracks, and polo field sideboards may cause hoof and pastern region injuries and hard, fast ground predisposes horses to superficial digital flexor tendonitis. In outdoor polo each team is composed of four players, and each member brings an average of seven to eight horses to the field. A game normally runs for six chukkers (a chukker is 7 minutes), and a different horse is used for each chukker. Therefore a single match may have 50 to 55 horses playing

Fig. 120-1 Outdoor polo is the most popular format for the game today. Close proximity of horses and riders explains why polo ponies often develop injuries related to direct trauma. Polo is only played right-handed.

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thousands of Argentine horses have been imported into the United States and Europe, primarily because such a large selection was available at low cost. During the 1970s, inexpensive American ex-racehorses were sold as polo prospects, but many had numerous orthopedic problems. Today the price of high-goal Argentinian polo ponies continues to rise, and as the cost of importing horses into the United States increases, economic demands necessitate a greater influx of American Thoroughbreds into polo. Most horses are 3 to 4 years old when introduced to the game, and 2 years of training and playing generally are required before a pony becomes seasoned. Exceptionally talented horses are playing high-goal polo at 6 years of age. By the age of 12 to 14 years, speed usually has begun to diminish, and horses are sold to less demanding players. By the age of 15 to 16 years, depending on temperament, polo ponies may be sold to beginners before being retired. Neck reining is paramount in training a polo prospect, because the rider uses only one hand for control. Wide range of movement, the ability to stop and turn quickly, and the ability to exhibit rapid bursts of speed are required. How well and smoothly the horse performs these maneuvers often determines the number of years the horse stays sound and competes successfully. In addition to schooling, fitness training consists of daily galloping (legging up). Ponies often are tied together in sets of four to five. This time-saving practice teaches the horses to travel more calmly together in close contact but can result in traumatic injuries to the lower limbs (Fig. 120-2). Polo ponies are shod with special rim shoes in front that allow for traction and pivoting without applying excessive torque to the lower limb. Medial and lateral heel calks on the hind shoes are helpful for stopping abruptly but often result in coronary band and pastern region lacerations to other horses during competition. For safety reasons, the Great Britain Polo Association only permits a lateral calk on each hind shoe, whereas the United States Polo Association allows medial and lateral heel calks. The size limit for calks is regulated but seldom enforced. Therapeutic corrective shoeing is problematic in playing horses (those being used in polo competition), because they may lose traction and maneuverability. Some common

shoeing modifications include squared, rolled, and rocker toes; elevated and full-shod heels; and padded soles. The standard support and protection afforded the horse during exercise are leg wraps and coronet boots. All legs are wrapped with doublelayer rolled cotton bandages. Impact-resistant European racing boots may be added to cover the metacarpal regions to protect against mallet and hoof trauma. More recently, especially on previously injured limbs, cotton leg bandages have been replaced with neoprene fabric wraps that extend below the fetlock joint and provide additional support. Despite these additional protective barriers, horses may still injure tendons and receive skin laceration during a game or practice. Drug testing of polo ponies is not yet compulsory in the United States, and no mention of prohibitive medication is addressed in the United States Polo Association rulebook; however, limited testing is done in Great Britain and France. Attending veterinarians often work for many competing teams within the same tournament and prompt assessment of injuries is important. Low doses of non-steroidal antiinflammatory drugs (NSAIDs) commonly are used, especially in horses with wounds and solar bruising. The general aim is to have as many sound horses as possible sharing the workload during a match to avoid the practice of double-chukkering (same horse used for two chukkers). Minor conformation abnormalities in polo ponies often can be overlooked, but some faults predispose ponies to specific injuries. Long toes and underrun heels may result in tendonitis of the deep digital flexor tendon (DDFT) and palmar heel pain. Toed-in horses are prone to develop lateral suspensory branch desmitis, whereas toed-out horses are more likely to injure the medial branch. Horses with long pasterns and long third metacarpal bones (McIII) are at increased risk of tendonitis of the superficial digital flexor tendon (SDFT). The most common sources of lameness in polo ponies are similar to those seen in most other equine sports. Polo ponies are at higher risk for traumatic injury because of the highimpact play and the practice of tethering of horses in close proximity to other horses during shipping, exercise, and polo tournaments. Causes of lameness often seen concurrently include palmar heel pain and proximal suspensory desmitis

Daily legging up is an important part of training polo ponies. Ponies often are tied together in sets of four to five, and although this practice saves time, horses in close contact are at risk of traumatic injury.

Fig. 120-2

CHAPTER 120 and osteoarthritis of the fetlock joint with chronic suspensory branch desmitis.

TEN MOST COMMON LAMENESS PROBLEMS The following are the 10 most common lameness problems in polo ponies: 1. Tendonitis of the superficial digital flexor tendon 2. Osteoarthritis of the metacarpophalangeal joint 3. Proximal palmar metacarpal pain and suspensory desmitis a. Proximal suspensory desmitis and third metacarpal bone disease b. Body suspensory desmitis and splint bone disease c. Suspensory branch desmitis and sesamoiditis 4. Injury to the hoof and distal phalanx 5. Palmar heel pain including navicular disease 6. Osteoarthritis of the distal interphalangeal joint 7. Desmitis of the accessory ligament of the deep digital flexor tendon 8. Splint bone disease 9. Distal hock joint pain 10. Gluteal myositis and back pain

LAMENESS EXAMINATION Horses should be stabled overnight so that they cannot warm out of subtle lameness. The horse is first examined in the stall and then as it walks from the stall. The horse is observed at a trot in a straight line on a hard surface and is circled in both directions. Most polo ponies are reluctant to lunge. If necessary, the horse may be observed under saddle, but Argentine ponies generally resist trotting when ridden. A systematic examination at rest is begun with the hoof and hoof tester evaluation and then continued proximally in the limb, noting evidence of pain, swelling, or obvious injury. Findings always should be compared with the contralateral limb, especially when palpating the body of the suspensory ligament (SL). Joints are assessed for range of motion and a painful response to flexion. Lower limb flexion is followed by carpal or tarsal flexion. Walking the horse briefly between flexion tests to allow an aggravated response to wear off is wise. One of us (P.J.M.) attends to many older polo ponies that have effusion of the metacarpophalangeal joints, manifest a positive response to flexion, and even may have visible and radiographic evidence of osteoarthritis, but lameness often is abolished using low palmar digital analgesia. Palpation may reveal one or more fractured splint bones with callus, but the rest of the limb should be examined, because the cause of lameness may be elsewhere. If a definitive diagnosis cannot be made, diagnostic analgesia is performed. Because drug tests are not performed, local anesthetic solutions can be used for diagnostic purposes in actively competing horses. When performing a nerve block, it is important to remember that the block may affect a larger area than intended, primarily related to diffusion of local anesthetic solution to surrounding tissue. High palmar analgesia can mask middle carpal joint pain, and an abaxial sesamoid nerve block can eliminate pain associated with the fetlock joint. For this reason the horse should be observed at the trot shortly after injection of local anesthetic solution and then again after an appropriate wait. To reduce time and money spent on lameness diagnosis one author (P.W.) prefers to block large areas during the initial examination. Specific blocks then are performed, if necessary, the following day. For example, a horse that shows neither sensitivity to hoof tester examination nor an increased digital

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pulse may go sound after an abaxial sesamoid nerve block. The following day the same horse may show slight improvement after palmar digital analgesia and a 100% improvement with intra-articular analgesia of the distal interphalangeal joint. However, two authors (P.J.M. and M.W.R.) prefer to start distally and work proximally in systematic fashion. Intra-articular analgesia is used extensively in polo ponies because it is more specific than perineural analgesia. Although intra-articular analgesia requires aseptic preparation and carries a small risk of infection, clients are generally receptive. If lameness is localized to a specific joint on clinical examination, therapeutic agents such as corticosteroids and hyaluronan can be added to local anesthetic solution to confirm diagnosis and initiate treatment simultaneously. One author (P.W.) uses combination diagnostic and therapeutic arthrocentesis typically in the distal interphalangeal and proximal interphalangeal joints. The horse’s immediate response to local analgesia is noted, and response to therapy is usually evident 2 to 3 days later. Another author (P.J.M.) frequently uses combination diagnostic and therapeutic injections in the distal interphalangeal and distal hock joints. If treatment is not combined with intra-articular analgesia, injection of the joint with therapeutic medication should be delayed for 2 to 3 days. Combination injections can also be used simultaneously to diagnose and treat back pain. The dorsal aspect of the dorsal spinous process and the interspinous space can be infiltrated with a combination of local anesthetic solution, Sarapin, and a corticosteroid. Response to infiltration is evaluated immediately by riding the horse after injection, and response to medication is evaluated over the next several days. Because metacarpophalangeal joint disease and splint bone injury are common sources of pain in the polo pony, one author (P.J.M.) prefers specifically to differentiate these sources of pain by first performing intra-articular analgesia of the metacarpophalangeal joint and then later performing a low palmar block. If low palmar analgesia is performed first, both potential sources of pain are eliminated. If pain is detected on palpation of bony exostoses of the splint bones, these areas can be blocked first, before a systematic blocking strategy is followed. One author (P.J.M.) refers to this as the splint block. This block is performed by first blocking the palmar metacarpal nerve distal to the exostoses. If improvement is not seen, the palmar metacarpal nerve just proximal to the exostoses is then blocked (2 ml of local anesthetic solution). A biaxial splint block can be performed if exostoses are found medially and laterally. This block should be done well below the origin of the SL to clearly differentiate proximal suspensory desmitis from splint bone disease. Splint disease, mainly from direct trauma from mallets and calk trauma, is common in the hindlimb. Diagnostic analgesia is performed as described in the forelimb. Hindlimb proximal suspensory desmitis has become a common diagnosis because we are now more aware of it. In the United Kingdom a variation of the high plantar nerve block is commonly used to diagnose proximal suspensory desmitis. Three ml of local anesthetic solution is injected deep to the proximal aspect of the lateral splint bone and 2 ml each is placed over the medial and lateral plantar nerves. If this block is unsuccessful in abolishing pain, each hock joint compartment is blocked subsequently. This procedure then is followed by fibular and tibial nerve blocks. In Argentina chemical neurolysis (long-term nerve block) of the fibular and tibial nerves frequently is performed for horses with distal hock joint pain or proximal suspensory desmitis (P.J.M.).

UNDIAGNOSED LAMENESS In some horses the lameness is inconsistent and/or subtle, and diagnostic analgesia cannot be performed. Nerve trauma on

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the medial aspect of a proximal sesamoid bone (PSB) may cause episodic, transient severe lameness. An option in a horse with mild inconsistent lameness is to treat with phenylbutazone (2 g PO bid) for 5 days and then reassess the horse. If lameness resolves and does not return after treatment is discontinued, the horse gradually is put back into work. In horses with inconsistent lameness that fail to respond to rest or therapy, we recommend nuclear scintigraphic examination. Exercise intensity can be increased in horses with subtle lameness but is done so with caution. Lameness may become more apparent to the point which diagnostic analgesia can then be performed. In a horse with recurrent episodes of hindlimb lameness, the veterinarian should be aware of the possibility of an ilial stress fracture (S.K.). Occasionally a polo pony becomes acutely non-weight bearing, with lameness lasting only a few minutes and resolving before examination is possible. If this sort of episode becomes recurrent in the same limb and physical examination reveals no significant findings, we refer the pony for nuclear scintigraphic examination. Consultation with colleagues and seconds opinion are always options. It is also important to consider the option of extended turnout. Because the career of a polo pony can last 12 to 15 years, owners are often willing to give the horse 6 to 12 months of turnout to avoid any further injury. If subtle lameness resolves with phenylbutazone therapy, the polo pony can compete because there is no drug testing in polo competition. This option must be elected with caution, however. Several lameness problems may exist simultaneously in a polo pony, a fact that makes observing the primary or baseline lameness difficult. Subtle signs such as the failure of a horse to stop appropriately, a horse that jumps on after stopping, or a horse that turns one way or the other when stopping (which is probably from outside hindlimb pain; horses turn away from lameness) may reflect low-grade lameness. If these observations have been made, having the horse ridden to witness the problems firsthand is useful. In one author’s experience (P.J.M.) the most common source of pain in this type of situation is from the distal hock joints.

Diagnostic arthroscopy in horses with osteoarthritis of the metacarpophalangeal or carpal joints can be valuable in evaluating the condition of joint surfaces. Palmar intercarpal ligament injury has been diagnosed in ponies with lameness localized to the middle carpal joint but lacking radiographic and scintigraphic signs. Tenoscopy and bursoscopy also can be useful diagnostically and therapeutically.

SUPERFICIAL DIGITAL FLEXOR TENDONITIS Tendonitis of the SDFT is the most common soft tissue injury seen in polo ponies and is by far the most common reason for early retirement. Tendonitis can be divided into three categories by location on the limb—high (proximal), mid-metacarpal, and low (distal)—or by cause: trauma, speed, and fatigue. We believe that most peripheral injuries of the SDFT result from tendon trauma while the limb is bearing weight. However, peripheral injuries commonly are seen in other sport horses, such as Standardbred racehorses, in which direct trauma is usually not a factor (M.W.R.). These injuries occur much more frequently at the mid-metacarpal region on the lateral aspect and to a lesser extent on the palmar surface of the tendon (Fig. 120-3). Proximal tendonitis also can be caused by trauma (P.J.M.). These areas have a high degree of exposure to swinging mallets and flying hooves. Despite new protective boots the SDFT is still traumatized with surprising frequency. Traumatic tendon injuries are generally noticed 1 to 2 days after the incident and are characterized by a slight widening of the tendon (not a banana-shaped profile). Lameness is usually not present, but the area is warm and tender to palpation. Some horses have recurrent heat and swelling that resolves quickly with topical and systemic antiinflammatory therapy. Peripheral lesions may involve 20% or less of the cross-sectional area (CSA) of the tendon. However, careful ultrasonographic examination of the medial and lateral borders of the SDFT and critical evaluation of longitudinal images are necessary. Recurrent tendonitis leads to typical

IMAGING CONSIDERATIONS Conventional and computed radiography are the mainstays of imaging, with the front feet and front fetlock joints and hock joints being examined most frequently. The introduction of computed radiography has provided great advantages, because with the exception of faulty positioning, obtaining nondiagnostic radiographs is almost impossible. Exposure can be adjusted at the time of processing, and subtle details that would be difficult to see on conventional radiographs can be detected and scrutinized easily with computed radiography. Images can be enlarged, and the contrast and brightness can be improved, which are important factors in the diagnosis of incomplete fractures. Scintigraphic examination is particularly useful in polo ponies with undiagnosed lameness and in those with palmar heel pain, but it is not always helpful in horses with chronic lameness (S.K.). Motion-correction software has been an important innovation. Ultrasonography is extremely important in evaluating the damage and healing processes in tendons and the SL in the forelimb and hindlimb. Transverse views are used more frequently in identifying lesions, whereas longitudinal images aid in assessing healing. Ultrasonographic evaluation of the supraspinous ligament is often useful in horses with obscure hindlimb lameness. We have not found thermography particularly useful in our practices.

Transverse ultrasonographic image of the palmar metacarpal region of a polo pony with traumatic tendonitis of the lateral aspect of the superficial digital flexor tendon. Lateral is to the left. After initial diagnosis the horse continued to play, and the lesion progressed.

Fig. 120-3

CHAPTER 120 swelling and later lameness commonly found with moderate or severe tendonitis of the SDFT. Core lesions and lesions of the SDFT adjacent to the DDFT are thought to be injuries related to speed and fatigue. Hard, fast ground may a predisposing factor. Tendonitis of the SDFT may result in a banana-shaped profile of the metacarpal region (Fig. 120-4). Core lesions compromising between 20% and 25% of the CSA of the SDFT are serious, and the risk of recurrence is high. Horses with small CSA tears that extend more than 2.5 cm in length, or those with distally located tendonitis involving SDFT impingement by the palmar annular ligament, are at high risk of recurrence. Despite appropriate therapy these horses often have chronic and recurrent lameness, and ultrasonographic evaluation reveals a lesion that often fails to heal.

A

B

Fig. 120-4 A, Initial and B, 40-day follow-up transverse ultrasonographic images of the palmar metacarpal region of a polo pony with a typical core lesion of the superficial digital flexor tendon. Tendon splitting was done immediately after the initial image was obtained. The core lesion is more echogenic in the follow-up image but can still be seen.

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Initial treatment for any polo pony with tendonitis regardless of location or cause includes cold therapy (ice boots and cold-water hosing), application of sweats and compression wraps, and administration of NSAIDs. Peritendonous injections of corticosteroids and hyaluronan may help to reduce inflammation, but it is important that corticosteroids are not injected directly into a tendon. Peritendonous corticosteroid injection is frowned on in the United Kingdom (P.J.M.). A combination of injection and rest or surgical management has been successful (M.W.R.). Tendon splitting within a week after injury appears to be beneficial in decompressing the lesion. Tendon splitting must be done early, because granulation tissue forms quickly and cannot be decompressed. After appropriate sedation, perineural analgesia, and aseptic preparation, 30 to 40 incisions with a No. 11 scalpel blade in a stabbing manner (a fan-shaped pattern is avoided) are used to decompress only the affected tendon segment. One author prefers using a double-edged tenotomy in a fan-shaped pattern (M.W.R.). The procedure can be performed with the limb in a weight-bearing or flexed position, but a weight-bearing position is preferred. With experience the texture of diseased tendon can be differentiated from surrounding normal tendon structure. Bandages are applied, and horses are confined to a box stall and given controlled, increasing hand walking over the next 8 to 10 weeks. Application of a cast to support the fetlock and to provide pressure is preferred by one author (S.K.) to tendon splitting. Topical blisters may be beneficial in increasing local circulation or inducing fibrosis and may eventually improve cosmesis and can be used alone or with tendon splitting (P.W. and P.J.M.). Some veterinarians favor bar firing or an internal blister using ethanolamine (S.K.). Controlled exercise is recommended for a minimum of 4 to 6 months before any form of turnout exercise is given, but client compliance with this timetable is poor unless a horse walker is available. Unfortunately, most horses are turned out to pasture after blistering within 1 month of injury, a conventional practice we feel is harmful to tendon healing. Total time of turnout exercise (after controlled exercise) is 8 to 12 months. Follow-up ultrasonographic evaluation is important to monitor healing and to determine when exercise level can be stepped up. Other forms of therapy can be considered. Intra-lesional βaminoproprionitrile fumarate injections have not been used extensively in polo ponies, because of the difficulty in garnering owner compliance with the required extensive rehabilitation program. Intra-muscular administration of polysulfated glycosaminoglycans (PSGAGs) may be beneficial (S.K.). Desmotomy of the accessory ligament of the SDFT (superior check desmotomy) has been useful in horses with large CSA core lesions (≥25%) and those with small CSA tears that are >2.5 cm in length. Combining the surgical procedures of desmotomy and tendon splitting early after injury has been successful in returning horses with tendonitis of the SDFT to polo. After surgery, horses are given stall rest and hand walking for 4 to 6 weeks, with a total of 4 to 6 months of controlled exercise, before being turned out or conditioned for polo. Desmotomy of the palmar annular ligament occasionally is performed when the SDFT is injured and enlarged just above the ligament. This surgery interrupts a self-perpetuating cycle of injury that develops between the enlarged tendon and the thickened palmar annular ligament. One author (P.W.) believes that horses with distal tendonitis of the SDFT involving the palmar annular ligament should initially be treated with peritendonous injection of short-acting corticosteroids followed by compression wraps, not only to reduce the size and cosmetic appearance of the SDFT but also to prevent the need for desmotomy of the palmar annular ligament. The most common reasons for therapeutic failure in horses with tendonitis of the SDFT are lack of ultrasonographic follow-up after tendon splitting to determine if additional

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therapy is needed, poor owner compliance concerning walking the horse and stretching the injured tendon in the early stages of healing, not allowing for adequate rest before the horse is returned to work, and failure to perform ultrasonographic examination at the time of initial injury, resulting in an inability to evaluate maximal medical improvement before returning the horse to unsupervised work.

OSTEOARTHRITIS OF THE METACARPOPHALANGEAL (FETLOCK) JOINT Osteoarthritis of the fetlock joint is the most common articular problem in polo ponies and the most common articular problem necessitating early retirement. Ex-racehorses with mild osteoarthritis, osteochondrosis, or chip fractures may be sold for use as polo ponies and have a high risk of developing lameness. The fetlock region of any polo pony with forelimb lameness should be examined carefully. Lameness apparently originating from the fetlock joint based on the clinical observations of pain on palpation and a positive response to distal limb flexion must be differentiated from suspensory branch desmitis and splint bone disease. Intra-articular analgesia is important for differentiation. A full set of radiographs should be obtained. One author (P.J.M.) recommends using large cassettes to assess the fetlock joint and distal aspect of the splint

Fig. 120-5 Dorsolateral-palmaromedial oblique radiographic view of a metacarpophalangeal joint of a polo pony with osteoarthritis. Soft tissue swelling is apparent, a rounded osteochondral fragment is on the proximal dorsomedial aspect of the proximal phalanx, and proliferative changes involve the proximal aspect of the proximal phalanx and proximal sesamoid bones.

bones. Common radiographic findings include fragmentation of the dorsoproximal aspect of the proximal phalanx, radiolucent areas in the distal aspect of McIII (Fig. 120-5), proliferative new bone formation on the palmar aspect of the PSBs, and mineralization of the proximal and distal fetlock joint capsule attachments (Fig. 120-6). Intra-articular injections are the mainstay of treatment. One author (P.W.) injects both long- and short-acting corticosteroids and hyaluronan. Another author (P.J.M.) prefers PSGAG (Adequan) therapy or short-acting corticosteroids and hyaluronan or a combination of atropine, short-acting corticosteroid, and hyaluronan. Intra-muscular injections of PSGAGs at weekly intervals for 1 month, or possibly the entire season, are recommended. Horses that do not respond well to intra-articular injections are candidates for arthroscopic evaluation, because many of these horses have considerable cartilage damage. Daily icing, poulticing, and NSAID administration can help reduce inflammation in horses with chronic osteoarthritis. In horses with chronic osteoarthritis, radiographic changes may be extensive, but many horses are serviceably sound (Fig. 120-7). Chronic proliferative synovitis (villonodular synovitis) is common in polo ponies with chronic osteoarthritis of the fetlock joint and may be associated with capsular tearing (S.K.). The dorsal aspect of the fetlock joint develops an apple-shaped appearance, with only mild or moderate effusion. Chronic proliferative synovitis is most common in horses previously used as racehorses and becomes evident after several years of polo. Plain

Fig. 120-6 Lateromedial radiographic view. Mineralization at the insertion of the common digital extensor tendon and metacarpophalangeal joint capsule on the proximal aspect of the proximal phalanx is a common radiographic finding in polo ponies with osteoarthritis of the fetlock joint. Although the finding is important, it does not preclude successful playing.

CHAPTER 120 radiographs may reveal an abnormal contour of the distal dorsal aspect of McIII, and positive contrast radiographs may be diagnostic. We prefer ultrasonographic examination, because ultrasonography helps differentiate between horses that are surgical and non-surgical candidates. Chronic proliferative synovitis masses of 1 cm or larger should be removed arthroscopically to maximize long-term prognosis, whereas horses with smaller masses respond well to rest and intra-articular corticosteroid injections. Intra-articular atropine sulfate also has been used successfully (S.K.) to reduce effusion.

SUSPENSORY LIGAMENT Suspensory desmitis is seen at three levels: proximal suspensory desmitis, suspensory body desmitis, and suspensory branch desmitis.

Proximal Suspensory Desmitis Proximal suspensory desmitis occurs frequently and diagnosis is confirmed using high palmar or lateral palmar analgesia. Proximal suspensory desmitis results from polo ponies exercising on soft, uneven footing and is not related directly to playing polo. Lameness is usually only visible at a trot and varies in degree. The cranial phase of the stride is shortened, and lameness is usually most prominent with the affected limb on the outside of a circle. Palpation of the proximal palmar metacarpal region often reveals neither pain nor clinically appreciable enlargement of the SL. Polo ponies with proximal suspensory desmitis often fail to improve with rest

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and NSAID administration. Longitudinal ultrasonographic views are most useful in diagnosis of proximal suspensory desmitis. CSA measurements on transverse views are occasionally helpful if the same area is measured in the affected and contralateral limbs. One author (P.W.) has found that variation in CSA measurements leads to misdiagnosis, because even in normal polo ponies obtaining reliable repeat measurements is difficult. Hypoechogenic muscle tissue should not be confused as a lesion (S.K.). Proximal suspensory desmitis causes more subtle lameness and clinical signs in polo ponies than in other sport horses. Subtle injury and enlargement may cause the ligament to be pinched or compressed by overlying dense fascia, especially in hindlimbs. Horses with long-standing proximal suspensory desmitis often have sclerosis of McIII visible in lateromedial or dorsopalmar views. Absence of sclerosis does not rule out proximal suspensory desmitis, because horses with soft tissue injuries often lack bony involvement. Avulsion fractures of McIII associated at the origin of the SL, incomplete longitudinal fractures of McIII, and stress reaction can occur independently or concomitantly to proximal suspensory desmitis. Radiographic and ultrasonographic examination may reveal small or large fragments, or proliferative changes and radiolucency, associated with the palmar cortex of McIII. Computed radiography, xeroradiography, and nuclear scintigraphy are beneficial in diagnosing bony injury and differentiating it from proximal suspensory desmitis. Follow-up radiographs may be necessary, because avulsion or longitudinal fractures may not show up on initial radiographs. Even without treatment, almost all horses with proximal suspensory desmitis and bony causes of proximal palmar metacarpal pain recover within a 3-month rest period. In polo ponies with proximal suspensory desmitis in which a quick return to work is mandated, local injection into and around the origin of the SL of a combination of short-acting corticosteroids and PSGAGs hastens resolution of clinical signs. Ponies are walked for 1 week and then put in light work the second week. By the third week they may be galloped and are able to play shortly thereafter. Owners tend to keep polo ponies with proximal suspensory desmitis in work if the end of the season is near, because ponies are turned out routinely for 3 to 6 months after the season. Owners may gamble successfully by continuing to play the horse through the end of the season without permanently damaging the ligament. Proximal suspensory desmitis in a hindlimb, although rare, has a much more guarded prognosis, and one author elects neurectomy (S.K.). In the United Kingdom and Europe, injection of corticosteroids into the proximal SL is frowned on because this medication may slow healing and may mask the presence of fractures (S.K. and P.J.M.). This is especially true in horses with acute injuries. Shock wave therapy is popular and may prove beneficial once additional clinical studies are available. In horses with chronic proximal suspensory desmitis, once bony involvement has been ruled out, local injections of corticosteroid and Sarapin or internal blister may be warranted. Horses with known bony injury should be given rest. Recently fasciotomy and bone marrow injection has shown promise in polo ponies with chronic, recurrent desmitis.

Body Suspensory Desmitis

Lateromedial radiographic view of the distal forelimb of a serviceably sound polo pony. There is modeling of the proximal sesamoid bone and the dorsoproximal aspect of the proximal phalanx, and osteoarthritis and osteochondral fragmentation of the proximal and distal interphalangeal joints.

Fig. 120-7

Body suspensory desmitis is a serious and often career-ending injury. Diagnosis is straight forward if the SL is thickened and painful. Ultrasonographic examination is crucial in assessing SL damage, but radiography is important to evaluate the medial and lateral splint bones, because splint bone disease often is associated with suspensory desmitis in the polo pony. Radiographs should be obtained even if obvious areas of pain or bony and soft tissue swelling associated with the splint bones are absent. Treatment of polo ponies with acute desmitis

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includes immediate application of cold or ice therapy, alternating with topical sweats, and administration of NSAIDs. Periligamentous infiltration of short-acting corticosteroids early after injury improves cosmetic appearance and may minimize adhesion formation between the SL and splint bones. Injections are performed in polo ponies only if the owner agrees the horse is in need of long-term rest. The horse gradually is returned to hand walking in 5 to 7 days and can be turned out after 3 weeks. Sclerosing agents (e.g., ethanolamine) injected into the SL may be helpful (S.K.). Two authors (P.W. and P.J.M.) feel that long-term box stall rest may increase the chance of adhesion formation. One author (M.W.R.) prefers controlled exercise rather than turnout exercise. Ultrasonographic evaluation of ligament healing is important. One author (P.J.M.) has observed many polo ponies with distal body suspensory desmitis that involves the bifurcation and invariably at least one branch. If desmitis at the suspensory bifurcation is severe, the polo pony many never fully recover. The best results are seen with a combination of periligamentous injections of dimethylsulfoxide (DMSO) and corticosteroids and long-term rest. Performance level may need to be dropped to junior polo, and even at this level lameness may be persistent or recurrent.

Suspensory Branch Desmitis Suspensory branch desmitis is common in polo ponies. The lateral branch is injured more frequently than the medial branch, and occasionally both branches are injured simultaneously. Pivoting of the distal limb at high speeds is likely the cause of suspensory branch desmitis. Faulty conformation is another important predisposing factor. Horses that are toed in tend to develop lateral suspensory branch desmitis, whereas those that are toed out tend to develop medial suspensory branch desmitis. Palpation of the branches while the fetlock joint is in partial flexion is a preferred technique of one author (P.W.). Firm palpation and lower limb flexion followed by trotting exacerbates the degree of lameness. Ultrasonographic examination of the branches is accomplished easily and allows assessment of the degree of suspensory branch desmitis. Radiography should be performed to evaluate the distal aspects of the splint bones, because fracture and fracture displacement are common in ponies with suspensory branch desmitis. Mineralization in a branch close to attachment on a PSB may occur in horses with chronic injury (Fig. 120-8). Horses with acute injuries are treated identically to those with suspensory body desmitis. The appearance of the branch can be restored cosmetically to near normal over time with periligamentous injection of short-acting corticosteroids. The branch can be split 2 to 3 weeks after injury, although results in the United Kingdom have been disappointing (S.K.). Horses with suspensory branch desmitis need about 6 months of layup time before returning to polo training. One author (P.J.M.) feels that adhesions between the inflamed branch and surrounding tissue or the ipsilateral splint bone negatively influence prognosis, and corticosteroid injections may limit adhesion formation. Surgical adhesiolysis and distal ostectomy of the fractured splint bone may be useful in horses with chronic suspensory branch desmitis and splint bone fracture, but the cosmetic appearance is usually less than desirable. Counterirritants still are used in Europe with variable results. We feel that pin firing (hot firing) is not successful for horses with suspensory body desmitis, but it can be useful for horses with suspensory branch desmitis as a last resort. Shock wave therapy may be useful, but clinical studies are currently lacking.

INJURY TO THE HOOF AND DISTAL PHALANX Polo more than other types of equine sporting activity predisposes horses to direct hoof trauma. Direct trauma results from

Fig. 120-8 Dorsolateral-palmaromedial oblique radiographic view of metacarpophalangeal joint, with mineralization in the lateral branch of the suspensory ligament at the attachment to the proximal sesamoid bone. Note also the soft tissue swelling. swinging mallets; horses stepping directly on the hard polo balls used during playing; interference or direct impact from hooves of nearby horses; and from horses stepping on wooden sideboards at great speed. Calk or stud injuries to the hoof wall and pastern region are most common. Careful evaluation of wounds for involvement of deeper structures such as the proximal interphalangeal and distal interphalangeal joints is necessary. A common lameness that occurs during polo competition is called getting stung, referring to a sudden crippling lameness, lasting only a few minutes, generally resulting from a blow to the hoof or pastern by a mallet or hoof of another horse. The horse is usually sound within minutes of the incident with no clinical evidence of injury. Occasionally a fracture occurs that may not be evident radiographically for up to 14 days.

Fractures of the Distal Phalanx Acute fractures of the palmar processes of the distal phalanx often occur from mallet blows, and because polo is played right-handed, fractures usually are seen in the medial aspect of the left forelimb and lateral aspect of the right forelimb. Oblique fractures are sometimes difficult to see in conventional radiographic views and several proximodistal oblique views may be necessary. Rarely, fractures of the margin or of the extensor process of the distal phalanx are seen. Management of polo ponies with distal phalanx fractures is similar to that in other sport horses.

PALMAR HEEL PAIN INCLUDING NAVICULAR DISEASE Palmar heel pain in polo ponies with Thoroughbred and Thoroughbred-cross ancestry appears to be decreasing, primarily because of the successful efforts of farriers and owners. The problem may be worse in American Thoroughbreds than in Thoroughbreds originating from the United Kingdom,

CHAPTER 120 Australia, and New Zealand (P.J.M.). The long-toe and underrun heel complex and the tendency to shoe front feet with shoes with short branches that sit tight at the heel (to prevent front plates from being pulled off by hind feet) gradually have been corrected. Squared or rolled toe shoes, with or without elevated heels (world plates and natural balance plates), have reduced the number of polo ponies with broken pastern foot axes and have reduced DDFT tension due to prolonged breakover. Owners have allowed blacksmiths to reset polo plates more frequently during the playing season and to perform more frequent four-point trims during the off season than in previous years. Palmar heel pain is often difficult to differentiate from navicular disease. In both conditions the horse may show a painful response to hoof testers and lameness is abolished using palmar digital analgesia. Differentiation may be possible using distal interphalangeal analgesia, radiography, and scintigraphy. Many polo ponies with palmar heel pain have secondary pain at the origin of the SL, which is thought to be caused by alteration of gait. A common source of palmar heel pain is laminar tearing at the heels. Sudden stops force the horse to use the heels of the front feet as brakes. Corns or heel bruising can cause poor performance and lameness. Corns are diagnosed easily using hoof tests and by carefully inspecting the seat of the corn for hemorrhage or discoloration. One author (P.J.M.) has seen many polo ponies toward the end of the polo season with bilateral, biaxial horn staining resembling chronic corns that apparently did not result in overt lameness. Management of polo ponies with palmar heel pain resulting from corns is similar to that used for undiagnosed palmar heel pain, including the application of wedge pads to relieve heel pain for a few games, or by using the four-point trimming method with natural balance or straight bar shoes and acrylic rubber frog and heel support. One author (S.K.) has found that four-point shoeing provides poor grip and traction and considers it unsuitable for polo ponies. These shoeing techniques appear to decrease stress on the heels and the DDFT and navicular region. Hoof growth stimulants and NSAID administration may help horses with palmar heel pain.

Osteitis of the Distal Phalanx (Pedal Osteitis) Although definition and accurate diagnosis of osteitis of the distal phalanx remain obscure, many polo ponies with palmar heel pain have scintigraphic and radiographic evidence of disease in the margins of the distal phalanx. A lateromedial radiograph may show new bone projecting distally from the palmar aspect of the distal phalanx. This finding should be interpreted carefully on radiographs taken during purchase examinations.

Navicular Disease Navicular disease in a polo pony is characterized by chronic forelimb lameness, which is abolished using palmar digital analgesia, intra-articular analgesia of the distal interphalangeal joint, or analgesia of the navicular bursa, often with little radiographic abnormality. Nuclear scintigraphy may be helpful to differentiate navicular disease from other causes of palmar heel pain. Most horses with early navicular disease respond positively to intra-articular administration of hyaluronan and corticosteroids in the distal interphalangeal joint. Horses with advanced navicular disease or those unresponsive to therapy may be dropped from medium- or high-goal polo. The administration of NSAIDs and isoxsuprine and the application of corrective shoeing techniques (see “Palmar Heel Pain”) are valuable. Those ponies unresponsive to distal interphalangeal intra-articular injections may improve after injection of the navicular bursa, best performed under radiographic guidance. Palmar digital neurectomy is considered undesirable and rarely is performed today. Chemical neurolysis (long-term foot block) is of limited value. Cryoneurectomy can give

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limited relief but the palmar digital nerves regrow and lameness recurs. Concomitant or solitary injury of the DDFT does not appear to be as common in polo ponies as in other sport horses (P.J.M.). Shock wave therapy may offer a viable solution for these horses.

OSTEOARTHRITIS OF THE DISTAL INTERPHALANGEAL JOINT Early (synovitis) and chronic osteoarthritis of the distal interphalangeal joint can cause lameness in the polo pony, but diagnosis can be challenging due to the lack of specificity of analgesic techniques in the foot. For example if more than 6 ml of local anesthetic solution is injected into the distal interphalangeal joint, and lameness is evaluated after 3 to 5 minutes (S.K.) or 10 minutes (P.W.), pain from other areas of the foot including the sole can be blocked inadvertently. This effect can be avoided by using smaller amounts of local anesthetic solution. Horses with synovitis have distal interphalangeal effusion and manifest a painful response to lower limb flexion. However, this test may be positive in horses with many sources of pain, including either the navicular bone or the fetlock joint. Management of horses with osteoarthritis of the distal interphalangeal joint usually includes intra-articular medication. Short- or long-acting corticosteroids are preferred to injection with hyaluronan. One author (P.J.M.) combines corticosteroids and DMSO, because DMSO may improve distribution of corticosteroids to all parts of the joint and the navicular bursa. The distal interphalangeal joint is the only joint in which one author (P.W.) uses PSGAGs, combined with a single intravenous dose of gentamicin sulfate (6.6 mg/kg). Another author (P.J.M.) favors using PSGAGs in horses unresponsive to injections with corticosteroids. Most of these horses have clinical and radiographic evidence of advanced osteoarthritis. In some polo ponies lameness does not improve directly after intra-articular analgesia but inexplicably resolves 24 to 36 hours later, when presumably the effects of the corticosteroid begin. After intra-articular injection, horses are given 3 weeks of limited exercise and a tapered dose of NSAIDs. Weekly intramuscular administration of PSGAG for a minimum of 30 days and the application of corrective shoes to ease breakover are recommended.

DESMITIS OF THE ACCESSORY LIGAMENT OF THE DEEP DIGITAL FLEXOR TENDON Trainers and owners commonly confuse chronic desmitis or acute tears of the accessory ligament of the deep digital flexor tendon (ALDDFT) with bowed tendons. Desmitis of the ALDDFT occurs in polo ponies, especially older ponies (S.K.), but is less frequent than tendonitis of the SDFT. Mild desmitis is characterized by a meaty, non-tender swelling of the proximal palmar metacarpal region between the SL and DDFT. Horses with severe or complete tears can have prominent swelling at or near the junction of the ALDDFT with the DDFT, but neither lameness nor the response to palpation is commensurate with the degree of damage. Diagnosis must be confirmed and healing monitored using ultrasonographic examination. Initially, horses are managed with rest, cold therapy including ice, application of sweats, and administration of NSAIDs. Local infiltration of short-acting corticosteroids around (but not in) the ALDDFT can help cosmetic appearance. Stall rest for 2 weeks is recommended, and thereafter horses can be turned out for 3 to 4 months. Follow-up ultrasonographic examination reveals an enlarged, hyperechoic ALDDFT. Prognosis for future soundness and return to polo is usually excellent but swelling persists. Chance of recurrence is slim.

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SPLINT BONE DISEASE Traumatic exostoses (Fig. 120-9) caused by swinging mallets and fractures of the splint bones are common in polo ponies and are sometimes referred to as bamboo fever. Although trauma is usually the inciting cause of exostoses, injury of the SL may play a role (P.J.M.). Horses with splint exostoses resent direct palpation, but many do not manifest overt signs of lameness. If lameness is present but the exostosis is only mildly painful, a splint block (see page 1005) should be performed to confirm the diagnosis. Splint disease can make a veterinarian look foolish, because an acute injury may be confused with proximal suspensory desmitis, but subsequent development of a large golf ball-size swelling reveals the true diagnosis. Oblique radiographic views are most helpful for evaluating the splint bones. Local infiltration of corticosteroids and Sarapin is used to treat polo ponies with acute splint exostoses. Other injections include a combination of corticosteroids, Sarapin, calcitonin, and medroxyprogesterone acetate. Calcitonin (400 IU) and medroxyprogesterone acetate (200 mg) are used commonly in Europe (P.J.M.). Rest, compression wraps or sweats, and the administration of NSAIDs are useful. Polo ponies with chronic exostoses seem to benefit from pin freezing (cryotherapy), and this is the treatment of choice, with a quick return to work in 7 days. Cryotherapy appears to stimulate remodeling of chronic proliferative splint exostoses, and often a cosmetically acceptable limb profile is seen within 6 months. Despite the resulting white spots, clients seem to accept this form of therapy because of a high success rate. Thermocautery (hot firing) has merit, and early results of shock wave therapy appear promising (P.J.M.). Proximal splint bone fractures may require surgical fixation, and certainly horses need prolonged stall rest and a

Dorsolateral-plantaromedial oblique radiographic view of the metatarsal region. There is a comminuted fracture of the proximal aspect of the fourth metatarsal bone caused by mallet injury. This fracture usually does not require internal fixation, and prognosis for future soundness is good.

Fig. 120-9

slow return to work. If fractures are non-articular and fragments are not displaced or are displaced minimally, prognosis is favorable. Polo ponies with non-displaced diaphyseal splint bone fractures respond well to cryotherapy. Cryotherapy not only produces local analgesia, but also induces deep fibrous tissue formation that stabilizes fracture fragments. Probes are applied in firm contact with the skin covering the abnormal splint for 1 minute at each site at sites 1.5 cm apart. Ponies with non-displaced splint bone fractures are given rest for 4 to 6 weeks. Distal splint bone fractures can be diagnosed easily using longitudinal ultrasonographic evaluation or radiography. These fractures usually are associated with chronic suspensory branch desmitis, which is thought to cause bowing of the distal splint bone and subsequent displacement and proliferative changes (Fig. 120-10). Distal fracture fragments generally are removed surgically in the standing position, and concomitant splitting of the involved SL branch(s) often is performed, although results in United Kingdom have been disappointing (S.K.).

Dorsolateral-palmaromedial oblique radiographic view of the metacarpal region. A chronic displaced fracture of the fourth metacarpal bone is associated with suspensory branch desmitis. The second metacarpal bone is bowed away from third metacarpal bone; chronic proliferation has resulted from instability; sesamoiditis is apparent, and the suspensory branch shows mineralization.

Fig. 120-10

CHAPTER 120 DISTAL HOCK JOINT PAIN Polo ponies can play successfully with moderate to severe radiographic changes in the distal hock joints (Fig. 120-11). Most of the distal hock joint pain appears to be subclinical, meaning lameness is not the most noticeable clinical sign. Most polo ponies with distal hock joint pain are noticed by owners or riders to lack quick jump-out speed and the ability to stop abruptly and are noticed to be running through the bridle. These ponies generally improve if they are given ample warm-up time before playing. Distal hock joint pain appears to be one source of lameness with which a polo pony can live, but such pain is a major cause of poor performance and may induce compensatory lameness such as proximal suspensory desmitis in the forelimbs. Proximal limb flexion tests may elicit little response, and detecting pain or effusion using careful palpation is difficult in some horses. Because lameness is not necessarily proportional to radiographic changes, scintigraphic examination is helpful, especially in polo ponies with subtle hindlimb lameness. Diagnostic analgesia is an important tool if lameness is perceptible, and in horses with bilaterally symmetrical lameness, analgesia of one side may induce obvious contralateral lameness. Combining diagnostic and therapeutic injections is commonplace, because the practice saves time and money. The tarsometatarsal and centrodistal (distal intertarsal) joints are injected most commonly with methylprednisolone acetate, but in some ponies the tarsocrural joint also is injected. Intramuscular administration of PSGAGs and intravenous injection of hyaluronan throughout

Dorsomedial-plantarolateral radiographic view of a left hock with radiographic evidence of advanced osteoarthritis. This polo pony was not lame.

Fig. 120-11

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the playing season appear to be helpful in allowing horses to play up to potential. Horses are kept in work and placed on low doses of NSAIDs throughout the season, and training is limited. Although rare, avulsion injury and dislocation of the SDFT from the tuber calcanei is seen nearly once each year in a busy polo pony practice, resulting in extreme panic by the pony, necessitating sedation. The SDFT usually dislocates laterally, but diagnosis may be difficult before swelling develops. In our experience, surgical techniques including primary repair, mesh augmentation, and laterally located screws combined with full-limb cast application are neither successful nor necessary. Most horses respond well to confinement in a small pen and subsequent turnout for 6 to 12 months. Turnout exercise is recommended as soon as possible, and manually forcing the SDFT completely laterally is helpful if luxation is incomplete (P.J.M. and S.K.). Despite the fact that the SDFT remains displaced, causing a slight mechanical lameness, horses tend to perform well at the canter and gallop, with a fair to good prognosis for medium- and low-goal polo. Some polo ponies with lateral dislocation of the SDFT in one limb develop the same condition in the opposite limb 1 or 2 years later (P.J.M.).

GLUTEAL MYOSITIS AND BACK PAIN Gluteal myositis often accompanies subclinical low hindlimb lameness and is often a compensatory problem. One or both hindlimbs shows a shortened cranial phase of the stride. Deep palpation of the gluteal muscles elicits pain, although the muscles never feel as hard as they do in ponies with rhabdomyolysis. If possible, it is important to determine if gluteal myositis is a primary or secondary problem. Guteal myositis can be differentiated easily from rhabdomyolysis, because serum creatine kinase and aspartate aminotransferase levels are invariably normal. Polo ponies with gluteal myositis can be treated with local injections directly into the gluteal muscles and between the biceps femoris and semitendinosus muscles. The horse is allowed light work and is placed on NSAIDs. One author (P.W.) has had modest success using a 5-day series of rubeola virus immunomodulator. If gluteal myositis is secondary, the primary source of pain must be identified and managed successfully. Back pain in polo ponies is often secondary to lameness or results from mismanagement, including use of ill-fitting saddles, overweight amateur riders, and mouth problems. Poor dentition from lack of, or inappropriate, tooth floating procedures causes sharp molars to come in contact with gag bits. Horses carry the head and neck high to avoid pain and tend to hollow the back. Back pain can become a permanent or chronic problem if horses are mismanaged continually. Back pain generally is characterized by a painful response to palpation along the lateral edges of the longissimus dorsi muscles. The horse exhibits a crouching gait when mounted and during initial walking under saddle. Intramuscular injections of corticosteroids combined with Sarapin (2:1 ratio) are performed along the length of the longissimus dorsi muscle, from the caudal border of the trapezius muscle to the level of the tuber coxae, 15 cm lateral to the dorsal midline. Injection sites are placed every 15 cm, and 5 ml of the mixture is administered at each site. Because back pain may be compensatory to primary distal hock joint pain or other lameness, it is important to evaluate the hindlimb and pelvis carefully. Primary management of the distal hock joint pain in horses with lameness in this region and local treatment of acupuncture points in the back is commonplace. Dorsal spinous process (dorsal spinous process) impingement can be a source of back pain, and one author (P.J.M.) feels this is a major cause of back pain in the polo pony.

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Diagnosis should be confirmed by assessing the effect of local analgesia and/or performing scintigraphy (S.K.). Treatment involves injection of the spaces between the dorsal spinous processes with corticosteroids and Sarapin. Shock wave therapy may be beneficial (P.J.M. and P.W.). Horses with back pain are given NSAIDs and are kept fit during a 4- to 6-week period using ponying (being led from another horse) exercise. In Europe a common management regimen includes paddock exercise as much as possible, lunging exercise with the horse’s head down and little warm-up before polo games. Internal blisters have been used with some success, but care must be taken when injecting these compounds, because deep muscle abscesses can develop. Faradism is useful for longissimus dorsi and gluteal muscle strain (S.K.).

OTHER CONDITIONS Fractures of the Cranial Thoracic Dorsal Spinous Processes (Fracture of the Withers) Fracture of the withers is fairly common. Polo ponies are often tied next to each other for long periods, and a frightened horse occasionally rears up and flips over (Fig. 120-12), resulting in fractures of the longest dorsal spinous processes at the withers. Often up to four dorsal spinous processes are fractured, with ventral displacement of the fragments resulting in a flattened appearance of the withers. Ponies are usually only mildly painful to palpation but are generally reluctant to lower the head when grazing. The affected horse may travel with a painful, stiff, extended head and neck carriage, and some horses grunt with every stride. The prognosis for return to polo is excellent after rest for 4 to 6 months, as long as secondary infection does not develop. Special consideration should be

given to saddle fit; a croup strap may be necessary to keep the saddle from sliding forward.

Osteoarthritis of the Proximal Interphalangeal Joint and Other Pastern Region Injuries Osteoarthritis of the proximal interphalangeal joint (high ringbone) occurs occasionally in polo ponies and is seen most frequently in green horses playing on rough terrain in the western United States and generally results from irregular footing. Pain originating from the proximal interphalangeal joint is difficult to diagnose in horses with acute disease without radiographic changes, but it can be identified scintigraphically. Osteoarthritis of the proximal interphalangeal joint is often difficult to manage, and although motion of this joint is limited, lameness can be inappropriately severe. Rest (60 to 90 days), NSAID therapy, and intra-articular longacting corticosteroid therapy are recommended. A common finding in oblique radiographic views of the pastern region is periosteal reaction on the medial aspect of left forelimb and the lateral aspect of the right forelimb proximal phalanges (Fig. 120-13). Because polo always is played right-handed, powerful neck shots always hit the right side of each forelimb. Lameness is usually insignificant and shortlived. These radiographic changes should not be confused with those resulting from enthesitis at the attachment sites of the distal sesamoidian ligaments. To differentiate osteoarthritis of the proximal interphalangeal joint from these proliferative changes, intra-articular analgesia or pinpoint perineural or local analgesic techniques should be performed.

Sesamoiditis Inflammation (sesamoiditis) of the PSBs can be caused by direct mallet or hoof trauma and by stress-related injury at the

Polo ponies commonly are tied to rigid bars and in close proximity to each other. Occasionally a polo pony flips over and fractures the thoracic dorsal spinous processes at the withers.

Fig. 120-12

CHAPTER 120 suspensory branch insertions. Traumatic sesamoiditis occurs in the medial PSB in the forelimbs from interference injury and in the lateral PSB in the forelimb and hindlimb from mallet trauma. Diagnosis of sesamoiditis is straightforward using radiography and scintigraphy, but ultrasonographic evaluation provides information about the suspensory attachment as well. One author (P.J.M.) feels that shock wave therapy is a promising treatment modality for sesamoiditis. Fractures of the PSBs are rare, and response to surgery is similar to that of other sport horses. Ponies with fractures of the base of the PSBs rarely return to athletic soundness with or without surgery. Polo ponies with basilar fractures and desmitis of the oblique distal sesamoidean ligament often can be helped by using shock wave therapy (P.J.M.). An apical fracture of the PSB may be mistaken for mineralization of the suspensory branch. Polo ponies with apical fractures of the PSBs have a good prognosis, provided that SL injury is not concurrent. Horses with apical fractures associated with sesamoiditis and insertional suspensory branch desmitis often have recurrent lameness. It is important to differentiate true fractures from sesamoiditis or a commonly seen radiographic abnormality in older polo ponies, one to three stress lines in the PSBs, which most often are considered incidental changes.

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Digital Flexor Tenosynovitis and Desmitis of the Palmar Annular Ligament Tenosynovitis of the digital flexor tendon sheath (DFTS) is common in polo ponies. Debate exists as to whether this syndrome is caused by desmitis of the palmar annular ligament or whether the palmar annular ligament is a passive structure causing only constriction of the inflamed tendon sheath. The terms tenosynovitis and desmitis of the palmar annular ligament are sometimes used synonymously, but tenosynovitis with mild thickening of the palmar annular ligament is more common than primary desmitis. A normal or slightly thickened palmar annular ligament can restrict SDFT movement in horses with tendonitis, but this is a separate entity (see page 1006). In polo ponies desmitis of the palmar annular ligament can be solitary, diagnosed in horses with healthy flexor tendons. It can lead to tenosynovitis or can accompany tenosynovitis. Primary desmitis of the palmar annular ligament occurs most frequently from interference injury, when the hind feet strike the forelimb palmar annular ligament, or from direct mallet trauma. Initial trauma may be minor, but continued trauma can lead to substantial injury (Fig. 120-14). Whether primary or secondary, tenosynovitis with thickening and compartmentalization of the DFTS can occur proximal and distal to the palmar annular ligament. Diagnosis can be made by combining the results of clinical examination and intrathecal analgesia. Ultrasonographic evaluation is crucial and should include dynamic studies in which the flexor tendons and DFTS are evaluated for possible adhesions between tendons, DFTS, and the palmar annular ligament. Concomitant conditions such as osteoarthritis of the fetlock joint, sesamoiditis, and demineralization of the PSBs at the medial and lateral attachments of the palmar annular ligament should be assessed radiographically. Initial management is to apply cold therapy and sweats and to

PAL

SDFT

DDFT

Dorsomedial palmarolateral oblique radiographic view. Proliferative changes (arrows) along the medial aspect of the left forelimb proximal phalanx are typical of those seen from mallet injuries. Polo is played right-handed, and trauma usually involves the medial aspect of left forelimb and lateral aspect of right forelimb proximal phalanges.

Fig. 120-13

Transverse ultrasonographic view of the distal palmar metacarpal region. An acute injury caused by direct trauma resulted in a chronically thickened palmar annular ligament. PAL, Palmar annular ligament; SDFT, superficial digital flexor tendon; DDFT, deep digital flexor tendon.

Fig. 120-14

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administer NSAIDs. Decompression of the DFTS and injection of hyaluronan and corticosteriods then is followed by 3 weeks of stall rest. Tenoscopy is valuable in identifying horses with tendon tears and to perform adhesiolysis. Desmotomy of the palmar annular ligament in horses with chronic desmitis or in those with chronic tenosynovitis may be helpful. Definitive therapy should be instituted early and aggressively to minimize adhesion formation.

brachium and in the carpal sheath. Conservative management is usually successful, including the periligamentous injection of hyaluronan and corticosteroids. Surgical resection of the accessory ligament of the SDFT may be indicated, particularly in polo ponies with considerable fibrosis and bony proliferation on the caudal distal radius, or those that stand over at the knee.

Upper Forelimb Lameness Desmitis of the Distal Sesamoidean Ligaments Desmitis of the distal sesamoidean ligaments (bowed pastern) is seen occasionally in polo ponies and usually involves the straight distal sesamoidean ligament. Diagnosis is made by detecting pain and swelling, by performing perineural analgesia (abaxial sesamoid block), and by using ultrasonographic examination. Polo ponies with recurrent injury may not resent palpation, and ultrasonographic examination is necessary to differentiate this from other injuries. Proliferative changes along the base of the PSBs and abaxial surface of the proximal phalanx are often seen. These injuries may be career ending and at best are performance limiting. Long-term rest is necessary. Some owners request pinfiring.

Carpal Region Lameness The carpus is an uncommon source of lameness in the polo pony. Pre-existing chronic radiographic changes are often incidental findings, even in horses with reduced range of carpal flexion and mild effusion. Carpal chip fractures can occur, but they are unusual. Tearing of the medial palmar intercarpal ligaments can cause lameness. Transient traumatic carpitis occasionally is seen after direct trauma from a mallet or ball. Rupture of the carpal sheath is a rare cause of lameness in the polo pony. One author (P.J.M.) has seen two horses with massive swelling in the distal antebrachium, and ultrasonographic evaluation revealed rupture of the carpal sheath. Prognosis is not known. Fractures of the proximal aspect of the splint bones can lead to osteoarthritis of the carpometacarpal joint. Fracture of the medial splint bone is most serious, but polo ponies usually respond well to conservative management. Horizontal fracture of the accessory carpal bone may occur after collapse or a fall. Ponies are occasionally hit on the forehead by a hard struck polo ball, rendering them unconscious and causing the hind hoof to hit the back of the carpal region. Fracture can also occur if a horse trips inadvertently on a loose polo wrap. Prognosis appears to be indirectly proportional to fracture displacement. Vertical (longitudinal) fracture of the accessory carpal bone occurs rarely in polo ponies that fall onto a flexed distal limb. Treatment is conservative. Physiotherapy, forcing full carpal flexion, is helpful to restore normal mobility (S.K.). Tenosynovitis of the carpal sheath can occur primarily or after fracture of the accessory carpal bone and in ponies with tendonitis of the SDFT and DDFT, and in horses with desmitis of the accessory ligament of the SDFT (ALSDFT), but this condition is rare.

Desmitis of the Accessory Ligament of the Superficial Digital Flexor Tendon In the United Kingdom, between 10 and 15 polo ponies each year are diagnosed with desmitis of the accessory ligament of the SDFT, which may occur because of the fast and aggressive play of modern polo (P.J.M.). Awareness of the condition and use of ultrasonography may have resulted in increased recognition. One high-goal player had five horses with this problem in a single year. Diagnosis is made by eliminating the distal limb and by palpating pain and swelling in the distal ante-

Lameness associated with the antebrachium, elbow, and shoulder regions is uncommon in polo ponies. Occasionally, fractures of the radius or olecranon and wounds with bony sequestration occur from kick trauma. Repair of fractures of the olecranon has been successful. Shoulder region soft tissue trauma, fracture of the supraglenoid tubercle of the scapula, or suprascapular nerve injury occurs occasionally from falls, dangerous play, or wrecks.

Other Hindlimb Lameness The distal hindlimb is subject to the same type of bony injuries as seen in the forelimb, with the exception of navicular disease. Fractures of the distal and proximal phalanges and PSBs occur with the same frequency as in the forelimb, but prognosis is better in the hindlimb. In the hindlimb, osteoarthritis of the fetlock joint, flexor tendonitis, suspensory desmitis, and desmitis of the ALDDFT are not nearly as common as in the forelimb. Two soft tissue problems occur specifically in the hindlimbs. A form of severe suspensory desmitis occurs in older polo ponies with exceedingly straight hock conformation. The hind fetlock joint drops and the pastern region is parallel to the ground. Lameness, however, is often minimal, and despite the abnormal angle of the fetlock joint these horses can continue to play for years with the help of support wraps. The second specific soft tissue injury of the hindlimb is spontaneous rupture of the common digital extensor tendon above the fetlock joint. This injury results in lameness and hyperflexion of the fetlock joint at the trot. These horses respond well to conservative management, with support wraps and rest, and prognosis is excellent. Lameness from stifle injuries is uncommon. Osteochondrosis occasionally causes effusion and lameness or poor performance if present bilaterally. Collateral ligament injury may occur from severe bumps. Kick wounds to the tibial crest can cause pronounced lameness and may result in a fracture. Polo ponies with a history of poor stopping or turning ability respond favorably to injection of counterirritants (blisters) around the patellar ligaments and the insertion of the vastus lateralis and rectus femoris muscles. Horses are kept in a working schedule following these injections and typically may be played successfully several days later. Pelvic injury in polo ponies is infrequent but may result from dangerous play, such as a high-angle ride off behind the saddle (S.K.), and is best diagnosed using scintigraphy. Stress fractures of the ilium and traumatic fracture of the acetabulum occur but are rare. Disparity in height of the tubera sacrale often is seen, but with no effect on performance.

Rhabdomyolysis Rhabdomyolysis, or tying up, is fairly common, especially in mares. Two types of horses are predisposed to this syndrome. Unfit horses placed into work too rapidly often develop a stiff gait at the trot and tenderness to palpation over the dorsal musculature. Muscle enzyme levels are only moderately elevated and horses respond well to rest and NSAIDs. The most common form of rhabdomyolysis is seen in fit polo mares after an extended layup period for illness, unrelated lameness, or foul weather that prevents horses from being played regularly. Rhabdomyolysis can also occur on cold, clear mornings

CHAPTER 121 or blustery days during which a drop in barometric pressure occurs. Horses generally become affected after exercise, when they return to the barn or trailer; are reluctant to move; and have firm, tight gluteal regions. Epaxial muscles rarely are involved. Clinical signs may be confused with colic because horses with rhabdomyolysis often paw, stretch out, and sweat profusely. Muscle enzyme levels are elevated greatly. Management is similar to that described for other sport horses (see Chapter 84). Nutritional management appears to be important in Europe where bran, which is high in phosphorus (reduces calcium), is fed to reduce recurrence.

Gracilis Muscle Tear Gracilis muscle tears are seen in several polo ponies each year and are characterized by lameness at the trot and dramatic swelling in the medial thigh region. Abduction of the flexed

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hindlimb elicits a painful response and a large hematoma generally develops soon after the injury. The administration of NSAIDs, administration of DMSO intravenously, and the topical application of cold water are beneficial. If necessary seroma fluid can be drained surgically 5 to 7 days after injury, and exercise is limited for a minimum of 2 weeks.

Equine Protozoal Myelitis Mild neurological signs typical of equine protozoal myelitis or lameness associated with the disease can be confused with other causes of musculoskeletal pain, in particular hindlimb lameness. Equine protozoal myelitis is prevalent in the United States but is rare in England (P.J.M.). Occasionally a polo pony in the United Kingdom that was imported from the United States develops clinical signs consistent with equine protozoal myelitis under the stress of the latter half of the season.

121

The Western Performance Horse THE CUTTING HORSE • Jerry B. Black

DESCRIPTION AND HISTORY OF THE SPORT The cutting horse was born of necessity long ago on the open grass plains of West Texas. This was the era of Western history that included big cattle drives from the open ranges of ranches such as Burnett and the 6666 Ranch, Waggoner Ranch, the Pitchfork Ranch, and the Matador Ranch to Dodge City, Kansas. Cutting horses enabled big country ranches, where no barbed wire fences existed, the only means of working vast herds of cattle. In those days the task of the horse was simple, at least by definition. Guided by the rider, the cutting horse entered a herd of cattle quietly and deliberately. A single cow was cut, or separated, from the herd. The natural instinct of the cow is to return to the safety of the rest of the herd. The cutting horse, through breeding and training, controlled the calf with a series of moves and countermoves. The speed, agility, balance, and quickness of the cutting horse kept the cow from the herd, where other cowboys would hold the cut. The horse and rider would re-enter the herd again and again, cutting cattle out until the work was done. Only the top hands earned the right to ride the best horses of the remuda, the cutting horses. The unique skills of the cutting horse were a great source of pride to the frontier cowboy. This often led to impromptu or jackpot cuttings on the open range or, from about 1900, in outdoor pens of the large ranches. From this love of the cutting horse and the subsequent competition to determine who had the best horse came the roots of cutting as we know it today. The first cutting horse contest for money was held at the 1898 Cowboy Reunion in Haskell, Texas. Twelve cutting horses competed for a purse of $150. From this start, regular events occurred on ranches of the Southwest and at the Fort Worth Stockyards. Rules and prizes varied greatly, but the

ability of the cutting horse to separate a single calf from the herd always was and continues to be the goal of the competition. From these roots the National Cutting Horse Association was formed in 1946 during the Fort Worth Exposition and Fat Stock Show. The stated purpose of the organization was to standardize the rules and judging of competition and to preserve the tradition and history of the cutting horse with the ranching and livestock industry. Today, competitions approved by the National Cutting Horse Association occur throughout the United States and Canada. In addition, many association members from other countries such as Australia are conducting competitions outside North America. The format of these competitions and other Western performance horse disciplines, such as reining, present a unique challenge to the equine veterinarian.

TRAINING Training of the cutting horse begins at 2 years of age. Usually 60 to 90 days are spent in basic training before the horse is introduced to cattle. This generally is accomplished by turning one cow into a round pen that is 38 to 54 m in diameter. The horse is taught to mirror the movements of the cow as the cow moves around the perimeter of the arena. This process of training a cutting horse is repetitive and is done several days a week for months. The object of training is for the horse to develop an ability to perform identical movements with the cow. Simply put, when the cow stops or stops and turns, the horse does the same maneuver. This type of training is accomplished by asking the horse to stop with the aid of the bridle and turning the horse to move with the cow. The key to training is a complete and balanced stop. With time, the stop ultimately is followed by the instinctive ability of the horse to read the movement of the cow and to turn in the direction the cow is going. Because this ability to watch the cow and respond to its movement is instinctive to the working stock horse, breeding is of the utmost importance. Without this

CHAPTER 121 or blustery days during which a drop in barometric pressure occurs. Horses generally become affected after exercise, when they return to the barn or trailer; are reluctant to move; and have firm, tight gluteal regions. Epaxial muscles rarely are involved. Clinical signs may be confused with colic because horses with rhabdomyolysis often paw, stretch out, and sweat profusely. Muscle enzyme levels are elevated greatly. Management is similar to that described for other sport horses (see Chapter 84). Nutritional management appears to be important in Europe where bran, which is high in phosphorus (reduces calcium), is fed to reduce recurrence.

Gracilis Muscle Tear Gracilis muscle tears are seen in several polo ponies each year and are characterized by lameness at the trot and dramatic swelling in the medial thigh region. Abduction of the flexed

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hindlimb elicits a painful response and a large hematoma generally develops soon after the injury. The administration of NSAIDs, administration of DMSO intravenously, and the topical application of cold water are beneficial. If necessary seroma fluid can be drained surgically 5 to 7 days after injury, and exercise is limited for a minimum of 2 weeks.

Equine Protozoal Myelitis Mild neurological signs typical of equine protozoal myelitis or lameness associated with the disease can be confused with other causes of musculoskeletal pain, in particular hindlimb lameness. Equine protozoal myelitis is prevalent in the United States but is rare in England (P.J.M.). Occasionally a polo pony in the United Kingdom that was imported from the United States develops clinical signs consistent with equine protozoal myelitis under the stress of the latter half of the season.

121

The Western Performance Horse THE CUTTING HORSE • Jerry B. Black

DESCRIPTION AND HISTORY OF THE SPORT The cutting horse was born of necessity long ago on the open grass plains of West Texas. This was the era of Western history that included big cattle drives from the open ranges of ranches such as Burnett and the 6666 Ranch, Waggoner Ranch, the Pitchfork Ranch, and the Matador Ranch to Dodge City, Kansas. Cutting horses enabled big country ranches, where no barbed wire fences existed, the only means of working vast herds of cattle. In those days the task of the horse was simple, at least by definition. Guided by the rider, the cutting horse entered a herd of cattle quietly and deliberately. A single cow was cut, or separated, from the herd. The natural instinct of the cow is to return to the safety of the rest of the herd. The cutting horse, through breeding and training, controlled the calf with a series of moves and countermoves. The speed, agility, balance, and quickness of the cutting horse kept the cow from the herd, where other cowboys would hold the cut. The horse and rider would re-enter the herd again and again, cutting cattle out until the work was done. Only the top hands earned the right to ride the best horses of the remuda, the cutting horses. The unique skills of the cutting horse were a great source of pride to the frontier cowboy. This often led to impromptu or jackpot cuttings on the open range or, from about 1900, in outdoor pens of the large ranches. From this love of the cutting horse and the subsequent competition to determine who had the best horse came the roots of cutting as we know it today. The first cutting horse contest for money was held at the 1898 Cowboy Reunion in Haskell, Texas. Twelve cutting horses competed for a purse of $150. From this start, regular events occurred on ranches of the Southwest and at the Fort Worth Stockyards. Rules and prizes varied greatly, but the

ability of the cutting horse to separate a single calf from the herd always was and continues to be the goal of the competition. From these roots the National Cutting Horse Association was formed in 1946 during the Fort Worth Exposition and Fat Stock Show. The stated purpose of the organization was to standardize the rules and judging of competition and to preserve the tradition and history of the cutting horse with the ranching and livestock industry. Today, competitions approved by the National Cutting Horse Association occur throughout the United States and Canada. In addition, many association members from other countries such as Australia are conducting competitions outside North America. The format of these competitions and other Western performance horse disciplines, such as reining, present a unique challenge to the equine veterinarian.

TRAINING Training of the cutting horse begins at 2 years of age. Usually 60 to 90 days are spent in basic training before the horse is introduced to cattle. This generally is accomplished by turning one cow into a round pen that is 38 to 54 m in diameter. The horse is taught to mirror the movements of the cow as the cow moves around the perimeter of the arena. This process of training a cutting horse is repetitive and is done several days a week for months. The object of training is for the horse to develop an ability to perform identical movements with the cow. Simply put, when the cow stops or stops and turns, the horse does the same maneuver. This type of training is accomplished by asking the horse to stop with the aid of the bridle and turning the horse to move with the cow. The key to training is a complete and balanced stop. With time, the stop ultimately is followed by the instinctive ability of the horse to read the movement of the cow and to turn in the direction the cow is going. Because this ability to watch the cow and respond to its movement is instinctive to the working stock horse, breeding is of the utmost importance. Without this

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genetic instinct the horse simply does not respond to the movement of the cow and does not initiate the stop or turn necessary to continue to track the animal. A good cutting horse trainer knows in a relatively short period if a young horse has the instinct and athletic ability to be a successful cutting horse. The finished cutting horse must perform the necessary moves to keep the cow in proper position away from the herd, without any hand cues from the rider, relying on instinct to read the movement of the cow alone. Reining the horse is permitted only to make the cut of a single cow out of the herd. After the cut is successfully made, the reins are placed in a relaxed position on the horse’s neck, and only leg cues are permitted from the rider during the actual working time. The ability of the working cow horses to contain the individual cow provides the excitement of competition in cutting. Training of a cutting horse prospect that has shown good potential continues when it is a 3-year-old, preparing it for the first major competitions, the futurities. The futurity is the first of the horse’s aged event competitions that continue for 4 years. No horse can compete in aged events beyond 6 years of age. Aged events consist of two elimination go-rounds, followed by semi-finals and the final competition. Substantial musculoskeletal stress is placed on these athletic performance horses, with multi-day competitions over a short period. In addition, the horses usually are practiced on cattle daily, including the day of competition, to sharpen performance skills. Competition in these aged events is heavy, with the major shows having more than 500 entries in a single age division. Purses in this type of event can exceed a total of $1 million. The nature of this aged event competition, with large purses in numerous events over a 4-year period, has caused the cutting horse economy to grow rapidly over the last several years. Select yearling and training sales are conducted annually that are beginning to parallel the racing industry in financial return on sales. This has contributed to the current popularity and resurgence of breeding of the cutting and Western stock horse, which in turn will ensure the preservation of the tradition and heritage that this horse played in the history of the great Old West.

LAMENESS EXAMINATION The increasing popularity of the cutting and reining horse for show and performance is occurring nationally and internationally. Sales of this type of horse have increased to Europe, South America, and other countries. In North America the revival of interest stems primarily from excellent programs instituted by associations such as the National Cutting Horse Association and the National Reining Horse Association. These associations encourage owner participation at the amateur level in cutting and reining events. This type of performance horse creates a new diagnostic and treatment challenge for attending veterinarians, partially because of the rigid training schedules necessary for the 3- to 6-year-old horse to compete in futurities and aged events. Hindlimb lameness presents one of the more interesting diagnostic challenges to the equine clinician. The lameness is often difficult to diagnose and even more difficult to manage. A systematic approach must be developed to achieve an accurate diagnosis consistently. The veterinarian must use a routine that is repeated with each horse and must allow sufficient time to complete a thorough examination. Western stock horses may be difficult to evaluate while being led. These horses usually are not taught to lunge and are often difficult to trot in hand. A 10- to 15-m round pen with firm footing has proved to be beneficial for evaluating lameness of this and other types of horses.

DIAGNOSIS AND MANAGEMENT OF SPECIFIC LAMENESS Hindlimb lameness is more common than forelimb lameness in cutting horses. Mixed lameness with swinging and supporting components is common in the hindlimb, especially in upper limb lamenesses such as those involving the hock, stifle, and hip or sacroiliac region. Hindlimb lameness may be associated with two sources of pain; for example, chronic hock lameness and secondary lumbar and gluteal myositis. This section focuses on selected hindlimb lamenesses of the hock, stifle, and thoracolumbar regions.

Selected Lameness of the Tarsus Osteoarthritis of the Distal Tarsus (Distal Hock Joint Pain) Osteoarthritis of the distal tarsal joints is seen most commonly in horses that have repeated, excessive compression and rotation of the hocks at high speed, and a high incidence occurs in the young working cow horse, and in cutting and reining futurity prospects, reflecting the demanding training schedules of 5 to 6 days a week at 2 and 3 years of age. Sickle hocks, cow hocks, and narrow hocks also may predispose horses to lameness. Osteoarthritis also may develop secondary to partial collapse of the central and third tarsal bones, and affected horses often develop lameness within the first year after birth. In our practice, routine survey radiography of the tarsus in 20, 2-year-old cutting horse prospects before training began revealed evidence of osteoarthritis in 11 (55%). Clinical signs include reduced height of the foot flight arc, resulting in abnormal toe wear, and a shortened cranial phase of stride. Hard work increases the degree of lameness, although most horses are lame and stiff when first taken out of the box stall and improve to some degree during the initial warm-up. Trotting in a circle increases the degree of lameness. Gait alteration or lameness may be observed with the affected limb on the inside or outside of the circle. Cutting, reining, and stock horses are reluctant to stop properly. Flexion of the hock often increases the degree of lameness. Palpation of the distal medial aspect of the hock may reveal exostosis and soft tissue thickening. Deep palpation of the area can cause a painful withdrawal response. Thoracolumbar pain is present in about 50% of horses. Diagnosis is based on a positive response to intra-articular analgesia and radiography. Radiographic abnormalities are often only seen in a dorsolateral-plantaromedial view in 2- to 4-yearold cutting horses, findings that differ from those seen in other young sport horses. Therapy varies depending on the degree of lameness. Rest is generally not helpful in horses with advanced osteoarthritis, and obtaining trainer compliance if the lameness is subtle is difficult. Training usually is continued with the help of non-steroidal anti-inflammatory drugs (NSAIDs), such as phenylbutazone (2 g sid or 1.5 g bid) and intra-articularly administered anti-inflammatory drugs. Shoeing changes include removing excessive toe, squaring the toe of the shoe and extending both branches of the shoe for more heel support. Half-round shoes help aid breakover in some horses with cow-hocked or sickle-hocked conformation. Changes in training schedules include more paddock or free-choice exercise and longer warm-up periods before training. Training in deep surfaces, overtraining, or conditioning in circles should be avoided. Varying the gait frequently during training and conditioning helps the horse to stay more comfortable. Intra-articular medication is used to keep chronically lame horses in competition. A combination of methylprednisolone acetate (Depo-Medrol; 50 mg) and hyaluronan (10 to 20 mg) is injected separately into the centrodistal (distal intertarsal) and tarsometatarsal joints in horses with advanced osteoarthritis.

CHAPTER 121 The veterinarian should not rely on communication between the two joints. If good results are achieved, these injections are repeated as necessary every 8 to 12 weeks. Horses with early osteoarthritis respond favorably to intra-articular treatment with hyaluronan (Hylartin-V; 20 mg) and triamcinolone (Vetalog; 3 to 6 mg). Intravenous injections of hyaluronan (Legend; 40 mg in 7-day intervals, series of three) or intramuscular injections of polysulfated glycosaminoglycan (Adequan IM; 500 mg in 5-day intervals, series of four to eight) are used frequently as concurrent therapy. Combinations of intermediate-acting corticosteroids and hyaluronan administered intraarticularly have been used in horses that are lame immediately before leaving for circuit shows or important multi-day competitions such as cutting horse, snaffle bit, and reining horse futurities. Therapeutic levels of NSAIDs may be necessary during competition if allowed by the breed, performance, or state drug regulations governing the event. Phenylbutazone (2 g sid or 1.5 g bid) is usually effective. However, many stock horse trainers feel that this drug tends to dull the mouth and sides of the horse, thus limiting bit and spur response. Other NSAIDs that are effective include flunixin meglumine (Banamine; 1 mg/kg sid) or ketoprofen (Ketofen; 2 mg/kg sid). Horses vary in response to the therapeutic effects of each NSAID. If one drug is not effective, a different one should be assessed. Surgery has been an important adjunct to osteoarthritis therapy in horses requiring repeated intra-articular injections or continual therapy with NSAIDs. Horses with mild to moderate radiographic changes but normal joint spaces respond favorably to cunean tenectomy. Horses with substantial intra-articular changes and joint space collapse are treated best surgically with a combination of cunean tenectomy and fenestration of the affected joint or joints using a 3.2-mm drill bit and creating three to four tracts. The horse is returned to work as soon as possible after surgery to encourage ankylosis. Hand walking is begun the day after surgery, and light riding at a walk may begin 2 to 3 weeks later. Light riding exercise continues for another 3 weeks, and full training begins 45 to 60 days post-operatively if the horse is reasonably comfortable. Phenylbutazone, 2 g once daily as needed, is used initially if obvious lameness persists. Most horses show almost immediate improvement after surgery. This improvement may be caused partially by the release of intraosseous pressure after the fenestration procedure, plus cessation of the rotational effect of the cunean tendon on the distal tarsus. Radiographic evidence of ankylosis occurs over a prolonged period. Soundness does not seem to be related to radiographic evidence of ankylosis. Prognosis varies depending on the degree of osteoarthritis, the number of joints involved, and the type of competition in which the horse is engaged. Surgery offers the best prognosis for horses with chronic lameness.

Arthrosis of the Tarsocrural Joint Distention of the tarsocrural joint capsule is usually from osteochondrosis or trauma. Osteochondrosis lesions occur on the intermediate ridge of the distal tibia, the trochlear ridges of the talus, and the lateral or medial malleolus of the distal tibia. Trauma is related to quick turns, hard stops, loss of balance, and poor footing. Faulty conformation, such as overly straight angulation of hock and stifle joints, may be a predisposing factor. Distention of the tarsocrural joint capsule is observed most easily on the dorsomedial aspect of the hock, but swelling also occurs in the plantar pouches, laterally or medially. The horse may have pain on palpation, and lameness may follow trauma. The hock flexion test may or may not be positive, depending on the degree of joint capsule distention and synovitis. Radiographic examination is essential to determine the cause and should be repeated in 10 to 14 days if initial radiographs are normal.

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Osteochondrosis is treated surgically. Traumatic distention of the tarsocrural joint is treated by intra-articular injection of intermediate-acting corticosteroids and hyaluronan, 2 or 3 times, 14 to 21 days apart. Intra-articular injections often are followed by hyaluronan (40 mg) administered intravenously weekly for 3 weeks. All injected hocks are bandaged concurrently to help reduce joint effusion. Pressage elastic contour bandages (Jupiter Veterinary Products, Harrisburg, PA) provide adequate pressure and are easy to maintain. The horse is given rest for 3 to 6 weeks. Exploratory or diagnostic arthroscopy is justified in any horse that does not respond to conservative therapy, permitting identification of subtle osteochondrosis lesions not detectable radiographically and soft tissue injuries, and providing joint lavage. The prognosis is good if treatment is initiated early, and in horses with osteochondrosis lesions or severe trauma, all fragments and debris are removed soon after the synovitis is recognized. If conformation is the predisposing cause, the prognosis is poor.

Selected Lameness of the Stifle The stifle is a large, complex joint composed of two articulations: the femorotibial and femoropatellar joints. My experience has been that during arthroscopy of the femorotibial joint, despite high intra-articular fluid pressure, obvious distention of the femoropatellar joint capsule does not occur. Thus little or no distention of the femoropatellar joint capsule occurs in association with disease of the femorotibial joint. When performing intra-articular analgesia of the stifle, all three compartments should be injected separately.

Osteochondrosis Osteochondrosis of the trochlear ridges of the femur is seen commonly in young horses. Clinical signs include distention of the femoropatellar joint capsule and varying degrees of lameness, depending on the amount of joint surface involved. Diagnosis is confirmed radiographically. Arthroscopic surgery is the treatment of choice to debride all diseased cartilage and bone and to remove all free-floating bone and cartilage. Aftercare consists of 45 to 60 days of stall rest, followed by an equal amount of stall and paddock confinement. Training generally resumes 3 to 6 months post-operatively. Intra-articularly administered hyaluronan (20 mg) followed by intramuscularly administered polysulfated glycosaminoglycans (PSGAGs; 500 mg in 5-day intervals, series of four to eight) 2 to 3 weeks after surgery has helped to reduce post-operative synovitis.

Subchondral Bone Cysts Subchondral bone cysts of the medial condyle of the femur are the most frequently recognized bony lesions of the stifle in my practice. All horses with clinically relevant signs are lame at the walk or trot in one or both limbs. The degree of lameness varies greatly among horses. Some horses are subtly lame, requiring riding or repeated flexion to produce a recognizable lameness. Others have acute, severe lameness and are unwilling to trot. Moderately lame horses tend to swing the toe medially during protraction. This phenomenon is unlike the horse that carries the stifle out or abducts the limb with femoropatellar joint or patellar ligament lamenesses. Lameness may be more obvious with the affected leg on the inside of a circle. Subtle distention of the femorotibial joint capsule may be palpated between the medial patellar and medial collateral ligaments. Some horses resent deep digital pressure over the medial femoral condylar region. Diagnosis of subchondral bone cysts is based on clinical signs, response to intra-articular analgesia using 30 ml of mepivacaine and radiography. Conservative treatment for the most part yields only temporary improvement in the lameness and is used in our practice only when a performance horse needs to compete for the remainder of the season or when

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finances prohibit surgical intervention. Conservative treatment consists of intra-articular injections of hyaluronan, with or without corticosteroids such as betamethasone or triamcinolone. An intramuscularly administered PSGAG given in a series of four to eight injections at 5-day intervals also is used. Many trainers report a pronounced effect about 24 hours after administration of PSGAGs. Therapeutic levels of systemic NSAIDs may be also necessary during multi-day competitions. Owners should be informed that continued training and competition over an extended period might lead to secondary osteoarthritis. The treatment of choice in my experience is curettage and fenestration of the subchondral bone cyst. Before 1988, this procedure was done through an arthrotomy incision. Although the surgery was successful in most horses, wound dehiscence and prolonged hospitalization were of great concern. Currently the surgery is performed by arthroscopy, with the horse placed in dorsal recumbency and the limb in flexion. This position provides adequate visibility and good access to the cystic lesion via the instrument portal. Postoperative hospitalization is minimal, and to date no post-operative complications have been seen. The patient is confined for 60 days after surgery. Hand walking for 10 minutes daily is allowed during confinement. Free-choice exercise for an additional 2 to 4 months is allowed. Training usually resumes 6 months post-operatively or earlier, if the horse is sound. The prognosis for horses with surgically debrided subchondral bone cysts has been good (60% to 70%) in my practice. Most of these horses return to a competitive level of performance, if given adequate rest.

Upward Fixation of the Patella Partial or complete upward fixation of the patella is a common cause of stifle pain, which can eventually produce articular changes of the patella. In my experience this condition can occur in any type of body conformation and hindlimb angulation and may be related to the anatomical formation and depth of the notch on the proximal medial trochlear ridge. Lack of condition and loss of condition are contributory factors. Poor coordination between extensor and flexor groups of the stifle and lack of quadriceps development may explain why upward fixation is seen in young animals at the beginning of training. I have examined two horses in which upward fixation of the patella was secondary to a subchondral bone cyst in the medial femoral condyle. Upward fixation may have been caused by alteration of gait and foot placement because of pain in the medial femorotibial joint. Upward fixation resolved after arthroscopic treatment of the subchondral bone cyst. The duration of locking varies from an almost instantaneous release, with only slight backward jerk evident, to a complete locking that can last for hours and may require surgical release. Diagnosis is based on clinical signs. Often, although no obvious upward fixation occurs in extension, the leg snaps with an audible click while in an extended position. Occasionally, pushing the patella over the top of the trochlear ridge when the leg is in extension can produce the locking. Clinical signs often are exacerbated if the horse can be walked down a steep slope. The diagnosis is sometimes based almost entirely on the owner’s or trainer’s description of the condition. Treatment should remain conservative when at all possible. If complete upward fixation has occurred for any period, the femoropatellar joint usually shows effusion. Treatment should be aimed initially toward reducing inflammation and resting the tissues involved. Systemic corticosteroids (20 mg dexamethasone [Azium] IM sid) for 1 to 3 days, followed by 3 to 5 days of NSAIDs (2 g phenylbutazone bid) is a usual treatment schedule. Hand walking for 5 to 10 minutes is allowed if no further upward fixation occurs, but no free-choice exercise is allowed. Excessive toe is removed, and wedged shoes or

wedge pad and flat shoes are used if the heel is low. Halfround shoes allow the horse to break over in its most comfortable and natural position. Once the initial inflammation has subsided, a conditioning program is started. Long warm-up periods are essential. Thirty minutes of walking and trotting, followed by an increasing amount of extended trotting on the straightaway is recommended. Once the horse is becoming conditioned, trotting in the hills is prescribed, where possible. The concept of conditioning is to improve quadriceps development and tone and to improve overall coordination. Horses that are underweight should be fed to gain weight and to improve the overall body condition and the condition of the muscles involved in movement of the stifle. Horses that do not respond to conservative treatment may require an internal blister or medial patellar desmotomy. Internal blister is accomplished by local infiltration of 2% iodine in peanut or almond oil injected directly into the body of the medial patellar ligament. Care must be taken to avoid the accidental penetration and injection of the femoropatellar joint with the counterirritant solution. Desmotomy should be reserved as a last form of therapy because the postoperative complications include fragmentation of the apex of the patella, soft tissue fibrosis, and mechanical alteration of gait.

Femorotibial Pain Subtle soft tissue injuries may occur in the femorotibial joint, resulting in low-grade lameness that is most evident when the horse trots in circles. Such injuries often occur as training is increased. A typical example is a young cutting horse that is being worked hard on cattle before a futurity. The horse has a shortened cranial phase of stride and lowered foot flight, causing toe drag. Results of hindlimb flexion tests are generally negative. Mild distention of the medial femorotibial joint capsule may be palpable. Diagnosis is based on clinical signs, response to intra-articular analgesia of the femorotibial joint, and the absence of radiographic abnormalities. Treatment comprises intra-articular medication with hyaluronan and corticosteroids such as triamcinolone (6 mg), plus intramuscularly administered PSGAGs. Systemic NSAIDs are given in decreasing doses over 10 to 14 days. All trailers and calks are removed from shoes. A wedge pad may be added with an egg bar shoe or extended branch shoe, depending on the amount of heel support needed. Training is resumed after 14 to 21 days of rest. Long warmup periods and extended straightaway trotting is recommended to condition the muscles of the upper hindlimb. Prognosis is good if a consistent training schedule is maintained. Horses with irregular training schedules and frequent periods of several days off between exercise sessions tend to have recurrent problems.

Thoracolumbar Injuries Thoracolumbar Myositis Soft tissue injuries of the thoracolumbar region produce back soreness and are the most common injuries in a working stock horse. Thoracolumbar myositis may coexist with hindlimb lameness, such as distal hock osteoarthritis, or may be a primary traumatic lesion, frequently caused by the extraordinary forces of rotation and propulsion placed on the hindlimbs. Other factors include rigid training and competition schedules such as the fall futurities for 3-year-olds that result in an overworked young horse. Local myositis involving the muscles of the thoracolumbar and pelvic region can have a profound effect on the performance of a stock horse. A cutting horse has three basic components to work: the stop, turn, and ability to track the cow in mirror image across the arena at high speed. Localized back pain results in decreased performance in all of these,

CHAPTER 121 without obvious lameness. The trainer perceives the horse as simply not trying. Consequently the horse with back pain is forced to try even harder and soon falls into the overworked category. Clinical signs of thoracolumbar myositis include pain to palpation of the affected muscle groups and associated spinous processes, obvious discomfort during saddling or mounting, subtle bilateral or unilateral hindlimb lameness, unwillingness to stop in form, and overall lack of performance. Flexion tests are seldom positive, unless the back problem coexists with distal tarsal disease. One may reasonably believe that arthrosis of vertebral articulations in the lumbar and lumbosacral region exists in some of horses. However, because of the depth and mass of the muscles involved, distinguishing the exact pathological condition or even the exact site of the injury is impossible. Therapy is aimed at reducing inflammation and controlling the associated muscle pain and spasms. Prolonged rest periods from training always are indicated but in reality are difficult to achieve because of the rigid schedule of preparation for competition. For example, an average futurity horse being prepared for the National Cutting Horse Association futurity in December of its 3-year-old year accumulates a $20,000 to $24,000 debt in training and entry fees alone before competition. Convincing an owner and trainer that the horse should be allowed to rest immediately before the futurity is difficult, if appropriate therapy has even a remote chance of being effective. The systemic use of skeletal muscle relaxants such as methocarbamol (Robaxin; 10 mg/kg PO bid for 5 to 10 days) has been effective in treating generalized back pain. Dexamethasone (10 mg PO bid for 3 to 4 days) is indicated in horses with acute pain. Chronic back pain may be treated successfully during competition with a single dose of triamcinolone acetonide (12 to 16 mg IM), while concurrently administering methocarbamol orally. NSAIDs generally have not been effective, unless the back pain is secondary or coexists with distal tarsal osteoarthritis. Care must be taken to comply with any medication rules. Specific localized pain may be treated successfully by local injection of methylprednisolone acetate (200 to 400 mg) and Sarapin (50 ml). Treatment is repeated every 10 to 14 days until pain subsides. Other management considerations are important for recovery. Horses with low, underslung heels of the hind feet should be shod using raised heels. Evaluation of the fit of the saddle, type of pad and specific pressure points when ridden should be considered. Other modalities of therapy, such as pulsed electromagnetic field and ultrasound, have been useful in keeping a horse in competition. Long warm-up periods without the rider for 30 to 45 minutes by ponying (leading from another horse) at a walk and trot always are indicated. The trainer must be cautioned that overwork and severe fatigue must be avoided at all times.

Sacroiliac Desmitis Strain and subluxation of the sacroiliac joint are not uncommon in the working stock horse because of twisting and rotation of the back and pelvis during work. This rotation is complicated by the weight of tack and rider, who is attempting to maintain balance and remain stationary on top of the horse during sudden hard stops, turns, and bursts of speed. Many of the clinical signs observed in horses with thoracolumbar myositis are also common in those with sacroiliac desmitis, because the epaxial muscles go into spasm to provide stability to the traumatized sacroiliac joint. However, bilateral or unilateral lameness with stiffness and alteration of gait usually is associated with sacroiliac desmitis. Protrusion of the tubera sacrale may be evident when the horse is walking away from the observer. Flexion of the contralateral limb for

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2 minutes may result in elevation of the tuber sacrale, hip hike, and stiffness of the affected limb. Digital palpation adjacent to the tuber sacrale and over the gluteal regions usually elicits pain. Local infiltration of local anesthetic solution may result in improvement, but rarely are clinical signs fully alleviated. Deep intramuscular injections of methylprednisolone (400 mg) and Sarapin (50 ml) into the region of the sacroiliac joint have been effective in treatment. Disposable needles at least 10 cm long are necessary to reach the affected area. Strict aseptic technique must be followed. Injections usually are repeated after 2 to 3 weeks. Concurrent systemic therapy with NSAIDs is beneficial. Horses must have rest, and 2 to 6 months out of training is often necessary, with strict stall confinement for the first 30 to 45 days. Proper therapy and management of injuries to the thoracolumbar and sacroiliac regions generally are rewarding if initiated early in the course of the disease. Horses with chronic recurrent problems usually can be managed to allow some level of competition.

THE ROPING HORSE • Robin M. Dabareiner, G. Kent Carter, and Richard Galley

TEAM ROPING HORSE Description of the Sport A unique handicapping system implemented in the early 1990s has contributed to team roping becoming a rapidly growing equestrian sport. Team roping began as a rodeo event many years ago, evolving from the everyday work of cowboys on ranches. If a cow needed to be treated on the open range, the only method of restraint was to secure the head and heel of the animal, or to team rope it. The cowboys soon began wagering among themselves to see which team of a header and heeler could accomplish this feat in the shortest time. Currently nearly 1 million people compete in team roping competitions in North America. Because of the large number of participants, team roping has become of great economic importance. Many team roping organizations exist nationally, but the most prestigious is the United States Team Roping Championships. The numbering or handicapping system of the team ropers was begun by the United States Team Roping Championships and has become standard. A number, from 1 to 9, with 9 being the highest level of ability, is assigned to each of the team ropers. This number is based on various factors, including ability, previous prize earnings, experience, age, and physical handicaps. The roping categories also are assigned a numerical value that cannot be exceeded by the total handicap numbers of the two participating ropers. The highest level of roping (11) is the open roping, which allows the world champions to compete together, and the lowest beginner level is 4. This method allows the lower-level ropers to compete as a team with the world champions and to level the playing field of competition at all levels. The entry fees of the participants usually generate the purse money in a jackpot fashion. A portion of the entry fee is held out by the producer of the roping to pay for the arena, the cattle, and advertising, and the rest of the fee is placed in the purse money to be divided among the winners. Dally team roping is a timed event involving five basic elements: the header, the heading horse, the heeler, the heeling horse, and the steer. The steers that are used for the team roping event are usually horned cattle called Corriente cattle,

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often from Mexico. Other types of cattle used are longhorns or other native homed breeds ranging in weight from 170 to 320 kg. A typical run in dally team roping begins with a steer contained in a chute at the end of an arena. The heading box is to the left of the chute and the heeling box to the right of the chute. When the header calls for the steer, or asks that the steer be released from the chute, the chute gate is opened and the steer is allowed a head start called the score. If the header leaves the heading box before the steer crosses the score line, or reaches the predetermined head start, then the team is issued a penalty of 10 seconds. The timing of the run is begun when the steer crosses the score line. When cued by the riders, the horses leave the roping box much as a racehorse leaves the starting gate to attain maximum speed as quickly as possible. As the header approaches the steer, now with the heading horse running at full speed, the horse is trained to rate off, or to slow up slightly, once the horse reaches the hip of the steer to position the steer properly so that the header may rope the steer. Team roping has three legal head catches: both horns (a clean horn catch), a half head (1 horn and the nose of the steer), or a neck. All other catches are considered illegal, and the team is given a no time. After the header successfully catches the head of the steer and dallies (wraps in a full circle) the rope around the saddle horn, the heading horse drops its hindquarters and slows somewhat as it sets the steer and brings the steer’s head around to the left. As the steer’s body progresses to the left, the heading horse also is turned to the left and is moved out in front of the steer to allow the header to pull it across the arena at about a 90º angle to the original direction of travel, maintaining a constant slower speed, thus allowing the heeler to get into position to rope the hindlegs of the steer. As the header sets and turns the steer, the heeler turns left following the steer and positions just behind and slightly to the left of the steer as it is taken across the arena. As the heeling horse follows the steer in this position, maintaining a constant speed equal to that of the header and steer, the heeler properly times his swing and then releases the heel rope, placing the loop under the steer and ropes the hindlegs of the steer. If only one hindleg is caught, then the team is issued a 5-second penalty. As the slack is taken out of the heel loop and as the dally is made on the saddle horn, the heeling horse is signaled to drop its hindquarters and come to an abrupt stop. As the heading horse progresses away from the heeler with the steer still in tow, the ropes come tight, and when tight, the heading horse is cued to spin around to the right while maintaining a tight rope to face the steer. When the facing is complete, the rope is tight and in a straight line from the saddle horn of the header to the head of the steer and is tight from the hindfeet of the steer to the saddle horn of the heeler, and then the flagman signals the end of the run and the time is taken. The roping can be accomplished by experts in 6 to 7 seconds but requires thousands of hours of practice to achieve this and to minimize the danger to all of the participants. Runs recorded in the range of 3.6 to 3.8 seconds have been made by the World Champion caliber team ropers.

Conformation The horses, predominately geldings, used in team roping are usually American Quarter Horses (QHs), preferred because of exceptional athletic ability, quick acceleration over short distances, and a good mind. Other breeds are rarely used. The head horse must be larger and faster than the heel horse. Head horses typically weigh 545 to 590 kg and are heavily muscled to tow the steer across the arena. The heel horse is smaller and quicker with more cow sense than the head horse. Horses that

are trained for cutting but no longer are competing often make good heel horses because of size and cow sense. Team ropers prefer a mature, experienced horse, and so horses are usually over the age of 10 years, and many top ropers have horses in the mid to late teens. Repetitive injuries are therefore common, but because horses often have had several owners, a complete medical history is rarely available.

Training The training of heading and heeling horses involves thousands of team roping runs and many thousands of miles of hauling. The horse must anticipate every variable of a team roping run, so that rider intervention is unnecessary. This allows the roper to focus on nothing but the speed of the run, which is an important factor contributing to injury. The current high demand for a finished team roping horse has greatly increased the value of these horses, and because replacement is difficult, veterinary advice is now sought more often.

Lameness Examination Team roping horses experience many of the same problems as any of the Western performance horses. The hocks and the right front suspensory ligament (SL) are placed under tremendous pressure as the heading horse sets the steer. The right front is placed cranially and laterally to decelerate and brace against its forward motion and the weight of the steer, thus placing tremendous strain on this limb (Fig. 121-1). The distal tarsal joints are loaded with the rider’s weight, the horse’s weight, the deceleration of the full-speed forward motion, and the weight of the steer as primarily rotational forces. This occurs as the horse is asked to set and get under the steer and pull the steer’s weight forward across the arena. After a successful catch by the heeler, the heading horse must face or spin around to the right while the hocks and distal hindlimbs are loaded as described, and do so with the addition of a backward motion to maintain tightness of the rope. When attempting to diagnose lameness, it is extremely important to remember that often in the early stages little or no lameness may be present. The complaint from the owner or trainer is often that the horse is coming untrained or is exhibiting increasing behavioral problems. It is imperative that the veterinarian is familiar with how the team roping horse works to arrive at a diagnosis. The history of a heading horse may include a reluctance to go willingly into the heading box, or reluctance to turn and face the front of the heading box and stand relaxed as the roper prepares to ask that the steer be released. As the problem worsens, many horses may rear up and spin around in the heading box, or lunge out of the box and refuse to re-enter. The horse may overrun the steer or even run past the steer, rather than rating off as it is supposed to do. The horse may duck or drop the left shoulder excessively as the header attempts to dally the rope and as they set the steer. The way the horse handles the steer may change, and the horse may tend to lunge across the arena with the steer in tow rather than taking the steer at an even, controlled gait. The horse may be reluctant to face at the end of a run. As the steer is followed to the end of the arena after the run, the horse may prance and jump around, rather than loping in a relaxed fashion as it follows the steer. These problems usually reflect pain, especially of the distal tarsal joints, but horses are seldom clinically lame at this stage. The heeling horse often has a similar history, with problems in the heeling box, not making the corner properly as the steer is set and turned, or of nickering and bouncing out of the stop at the completion of the run while maximal tension is on the ropes. A common complaint by the rider is that the horse is not stopping anymore after the heeler’s rope is thrown (Fig. 121-2). Horses are often unwilling to drop the head and relax after a run and tend to prance out of the arena.

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Fig. 121-1 A header roping the steer and making a 90º turn to set the steer for the heeler. The weight of horse and rider result in excessive loading of the right forelimb of the head horse (grey horse).

A heel horse stopping after the heeler throws his rope. Note the flexion of the hock joints during the stop and the extreme forward placement of both hindlimbs.

Fig. 121-2

Clinical examination often reveals pain on palpation of the caudal lumbar area, the gluteal muscles, and over the point of both hips. This pain often is accompanied by the complaint that the horse is sore in the kidneys. If only the distal tarsal joints are involved, effusion usually is not detectable, but the horse may be reluctant to allow palpation of the medial aspect of the tarsus, as if anticipating pain. The craniomedial aspect of the distal tarsus may be enlarged. High-quality radiographic examination of the hocks is essential; lesions may be missed unless the radiographs are examined under magnification. Intra-articular analgesia is often ineffective because the horse has developed performance problems in response to the

pain experienced during every run, and the pain is anticipated, even though the area has been blocked. Thus horses become intractable in the roping box because they dread the pain that they will experience during the run. However, horses often respond well to intra-articular therapy when they realize, after several runs, that the pain has been lessened or stopped.

Diagnosis and Management of Specific Lameness Suspensory apparatus injury in the right forelimb is common, especially in a heading horse, and involves the SL, the accessory ligament of the deep digital flexor tendon, the distal

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sesamoidean ligaments, or a combination of these. These injuries usually cause lameness of varying degrees, and diagnosis by clinical examination is straightforward. Ultrasonography should be used to confirm the diagnosis. Distal sesamoidean ligament injury may be more difficult to diagnose but often results in acute, moderate to severe lameness (grade 2 to 3 of 5) after a run, associated with pain on palpation of the palmar aspect of the pastern. Perineural analgesia of the palmar digital nerves may improve the lameness, but analgesia of the palmar (abaxial sesamoid) nerves is needed for complete soundness. Fractures of the middle phalanx are also common, so the horse should be examined by radiography and ultrasonography. Ultrasonographic evidence of enlargement or reduction in echogenicity in the straight or oblique distal sesamoidean ligaments is diagnostic (Fig. 121-3). Radiography is usually negative if lameness is acute; however, chronic injury is often associated with periosteal proliferation on the palmar aspect of the proximal phalanx associated with oblique distal sesamoidean ligament injury or entheseous new bone on the proximopalmar aspect of the middle phalanx associated with straight sesamoidean ligament injury. In hindlimbs deep digital flexor tendonitis, tenosynovitis of the digital flexor tendon sheath, and proximal suspensory desmitis are common, especially in the left hindlimb of head horses. When turning to face the steer, the head horse turns 180º at fast speeds, putting a rotational torque on the distal aspect of the left hindlimb (Fig. 121-4).

Management of these soft tissue injuries includes rest consisting of confinement and controlled exercise (Box 121-1), ranging from 4 to 6 months for horses with desmitis of either forelimb SL or the accessory ligament of the deep digital flexor tendon, to 8 to 12 months for horses with distal sesamoidean ligament injuries, deep digital flexor tendonitis, and hindlimb injuries (Box 121-2). Given the usual QH conformation of large body size and small feet or short, upright pastern conformation, navicular disease and injuries to structures within the palmar aspect of the foot (navicular syndrome) are common. Diagnosis is based on the response to perineural and intra-articular analgesia and high-quality radiographs. Navicular bone pain results in a slowly progressive lameness, often bilateral, that responds to intra-articular medication of the distal interphalangeal joint, NSAIDs, and corrective shoeing. Soft tissue injuries of the palmar aspect of the foot (e.g., impar or collateral ligament desmitis and injury to the deep digital flexor tendon in the region opposing the flexor surface of the navicular bone) are also common in head horses and usually are acute, occurring

Box • 121-1 Exercise Regimen after Mild Injuries to Forelimb Suspensory Ligament or Accessory Ligament of the Deep Digital Flexor Tendon Weeks 1-4

SDFT

SDFT DDFT SSL OSL

DDFT

Weeks 5-8

SSL

Weeks 9-12

OSL

Weeks 13-16

Transverse (left) and longitudinal (right) ultrasonographic images of the mid-pastern region of the right forelimb of a head horse. There is a hypoechoic lesion in the straight sesamoidean ligament (SSL). SDFT, Superficial digital flexor tendon; DDFT, deep digital flexor tendon; SDSL, straight distal sesamoidean ligament; OSL, oblique sesamoidean ligament.

Fig. 121-3

The horse is given stall rest or a small run (6 × 10 m) with support bandage on limb. Confinement is continued with 15 minutes of hand walking twice daily. Confinement is continued with 30 minutes of hand walking daily. If horse is sound at the trot, then confinement is continued, but the horse is walked under saddle or is ponied 15 minutes a day plus 5 minutes of trotting. Five minutes of walking and trotting are added every third day. The horse is re-examined by ultrasonography before returning to roping activity.

A head horse (on the right) turns to face the heeler at the end of the run. Note the strain placed on the left hindlimb.

Fig. 121-4

CHAPTER 121 during a roping event. Lameness is improved by perineural analgesia of the palmar digital nerves or intra-articular analgesia of the distal interphalangeal joint. Often no radiographic abnormality is apparent. Extended rest is required for full recovery. Osteoarthritis of the distal hock joints is common, and head horses seem especially at risk. Most respond well to intra-articular medication of the centrodistal and tarsometatarsal joints. Injury to the back and pelvic area is seen, especially in the heading horse. Strain or tearing of the sacroiliac ligaments can occur. Diagnosis can be augmented by the availability of a level surface near a level reference point. When examining a horse with only the horizon or surroundings as reference, noticing a subtle change in one side of the pelvic area may be difficult. A level surface near a door, especially one with horizontal lines or ridges, offers a grid effect that makes asymmetry more apparent if the horse faces the door and is viewed from behind. Radiographic evaluation is difficult and often unrewarding, but ultrasonographic examination may reveal longissimus lumborum and gluteal muscle tearing and can be used to evaluate the sacroiliac area. Lameness predisposing to back pain must be eliminated. Rest combined with topical heat (hot towels) and dimethylsulfoxide helps many horses, but often months of rest are needed before the pain is eliminated. Treating the painful areas with local injections hastens

Box • 121-2 Eight- to 12-Month Tendon Rehabilitation Program Weeks 1-12

Weeks 13-16

Weeks 17-24

Weeks 25-32

Weeks 32-36

The horse is given stall rest or is confined to a small run (6 × 10 m) with 15 minutes of daily hand walking. Support bandages are used for first 30 days. The horse is re-examined by ultrasonography. If the lesion is healing, confinement continues, but hand walking is increased to 15 minutes twice daily. Confinement is continued. The horse is hand walked 30 minutes a day or walked under saddle for 20 to 30 minutes a day. If the horse is sound at the trot and greater than 70% healing has taken place as visible by ultrasonography, the horse is walked under saddle or ponied for 20 minutes and trotted for 5 minutes. Walking and trotting are increased by 5 minutes every third ride until the horse is walking 45 minutes and trotting 30 minutes. If the horse remains sound, treatment proceeds to next level. If lameness develops, treatment reverts back 30 days in the schedule and the horse is re-examined by ultrasonography. Riding is increased to include loping for 30 days. If horse remains sound, the horse can return to roping activity. The horse can be turned out into a larger pasture.

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the recovery time. We prefer a combination of 5 ml methylprednisolone acetate, 5 ml Sarapin, and 5 ml prednisolone diluted with 30 ml mepivacaine and depositing 3 to 5 ml in several sites around the painful muscle or ligament. The horse is given 2 to 3 weeks of light riding, with no roping activity, and then is re-evaluated by ultrasonography. Most horses return to roping activity within 4 weeks from the time of injury. Obviously all team roping horses are also susceptible to any of the same injury problems that other equine athletes experience. Most of these injuries produce overt lameness, and diagnosis is usually straightforward.

Shoeing Considerations Because rope horses are often middle-aged, are used frequently, and commonly have navicular problems, maintenance of proper hoof balance is critical in keeping these horses sound. Long toes and collapsed heels are common. From a solar view the heels grow too far forward and are left unsupported and thus are at risk of abnormal concussion. We recommend trimming the heels back to the widest part of the frog and setting the shoe further back on the foot, so the heels of the shoe end at the widest aspect of the frog. Care must be taken to fit the front shoes properly so that little of the medial side of the shoe is exposed, because head horses have a tendency to grab this portion of the shoe and pull a shoe off, especially the left front shoe. Easing the breakover of the limb can be accomplished by rockering the shoe. A rim shoe or steel natural balance shoe provides good traction and allows an easier breakover by the rounded and rockered toe region of the shoe construction. The natural balance shoe has a wider web than a normal shoe and is beneficial for horses with sore feet acquired from performing on harder ground. If trimming alone cannot establish a correct hoof-pastern angle, a 1º to 2º wedge pad is recommended. We prefer a cutout pad to a full pad that often traps moisture and can lead to thrush problems. Care must be taken to avoid pad pressure over the central region of the frog in horses with navicular pain. In horses with deep digital flexor tendonitis, we recommend applying a 2º to 3º wedge pad for the initial 4 to 5 months of rest to decrease tension on the tendon. The wedge is reduced gradually over three shoe resets, once the horse is sound. In horses with distal hock join pain, we try to ease breakover of the hindfeet by squaring the toes or by setting the shoe back under the toe 0.3 cm. Avoiding any type of trailer or extension on the rear shoes is also preferable, especially on the heading horse, because this can aggravate pain associated with distal hock osteoarthritis.

CALF ROPING HORSES Description of the Sport Calf roping originated on ranches of the Old West when sick calves were roped and tied down for medical treatment. Success in calf roping depends on the teamwork between a cowboy and horse. After the calf is given a head start (like a scoreline in team roping), horse and rider chase the calf, and as the rider ropes the calf, the rider dismounts and runs to the calf. As the rider dismounts, the horse must sit back on its hind end and come to a sudden stop, which takes the slack out of the rope and stops the running calf. This allows the cowboy to catch the calf and throw the calf to the ground, termed flanking the calf. Once on the ground the contestant ties three of the calf’s legs together with a pigging string. The horse is trained to work the rope as the cowboy ties the calf, meaning to back up if needed to keep the rope tight, thus keeping the calf still for the rider to tie. When the cowboy completes his tie, he throws his hands up in the air as a signal to the judge

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that his run is complete. The calf must stay tied for 6 seconds. A 10-second penalty is added if the calf roper breaks the barrier at the beginning of the run. An 8- to 9-second run is considered good, and Jeff Chapman of Athens, Texas, set the arena record in 1997 when he roped and tied a calf in 6.8 seconds.

Conformation American QHs are used for calf roping and must be athletic and well trained. Because the rider must dismount during the event, calf horses are usually not tall, often being 14.2 or 14.3 hands high. Calf horses also have wide-base and muscular frontquarters and hindquarters. Many ropers believe that the performance demands on a calf horse are greater than that of a team roping horse.

Diagnosis and Management of Specific Lameness Calf horses have lameness similar to that of team roping horses with a few exceptions. Hindlimb lameness is more common in horses used for calf roping. Osteoarthritis of the distal hock joints is the most common problem, but stifle lameness also occurs frequently. Collateral ligament damage or meniscus tearing occurs, but diagnosis is usually not apparent until after bony changes are seen radiographically, months after the initial injury. Bony reaction at the proximal medial aspect of the tibia is diagnostic. With rest, NSAIDs, and intraarticular medications, these horses often can return to roping, but at a lower level, perhaps as a calf roping horse for a child or beginner. Hindlimb proximal suspensory desmitis, traumatic fetlock osteoarthritis, and fractures of the proximal sesamoid bones and middle phalanx are common. The most common forelimb lameness is palmar heel pain, often resulting from improper shoeing.

Shoeing Considerations The same shoeing considerations are used for balance and protection of the navicular region in the forelimbs as described for team roping horses. In the hindlimbs if the toes of the feet are too short, so that the horse has a broken forward hoof-pastern axis, then the hind toe digs deep into the ground and the limb stops abruptly, causing sudden torque on the distal limb. Having more toe length and a shoe that fits full with the heel branches of the shoe extending to the heel bulbs is preferable, so that the horse slides as it stops. This not only protects the heel bulbs from the ground surface, but it also puts less strain on the distal limb. Horses used for calf roping often wear skid boots, protective leg gear aimed at minimizing friction between the ground surface and the plantar aspect of the hindlimb fetlock joints, because the horse skids to a stop. THE REINED COW HORSE • Van E. Snow The National Reined Cow Horse Association was initiated in 1949 as the California Reined Cow Horse Association and changed its name in 1970. The purpose of the association is to preserve the training traditions of the vaqueros, the horsemen of early California, who trained their horses for ranch work. As a result of selective breeding and refined training techniques, reined cow horses today are able to achieve more with livestock than was ever thought possible. The National Reined Cow Horse Association held its first Snaffle Bit Futurity in 1970 in Sacramento, California. Bobby Ingersoll, a renowned cow horse trainer, had the idea to showcase the best all-around cow horses in the world. The competition involves showing the horse in three different disciplines: herd work (cutting), rein work, and cow work (working a cow down a fence). In the Snaffle Bit Futurity the top 20 horses

from the first round of competition come back and do another round over 2 days, starting again with even scores. The sport of reined cow horse has evolved from 1970, when 27 horses competed for $3900, to 1999, when hundreds of horses competed at their annual futurity for nearly $1 million. The professionals compete on multiple horses in four divisions: snaffle bit, hackamore, two rein, and bridle. Competition consists of multiple levels, including professional, non-professional, amateur, and limited open. An auction is held each year at the reined cow horse futurity at which horses that range from 1 to 12 years of age and breeding stock horses are available for sale. Affiliate groups of the National Reined Cow Horse Association are organized in Canada, Germany, Belgium, and Australia, and a strong interest in the group exists in most of Europe and in South and Central America. No restrictions exist as to the breeds allowed to compete in the futurities. Numerically the American QH dominates, but Paint horses often compete successfully, and an Appaloosa has won. The competition requires that the horse be accomplished in its ability to run, stop, turn, and read and control a cow. These horses also must have a high level of endurance. These qualifications do not necessarily dictate a particular body type, but the reined cow horse tends to be a taller, leaner horse than the cutting horse. Stallions, mares, and geldings compete equally, as do all genders and age groups of riders. Reined cow horses are typically begun in training when they are less than 2 years old and start to compete at 3 years of age. They have about 20 months to learn all of the events and to become well enough conditioned to withstand the rigors of competition. This requires that the training surface, shoeing, and judgment of the trainer be optimal throughout the 20-month period. Most trainers have become knowledgeable in the prevention and the early detection of lameness. Musculoskeletal evaluations are done quarterly on the futurity prospects, beginning in the fall of the 2-year-old year. These evaluations include a complete lameness evaluation, including flexion tests. At this time good baseline information on each horse is established, and future insidious problems can be detected before they become unmanageable. In the past, it was commonplace for a trainer to blame himself or herself or the horse’s attitude for not being able to accomplish a certain task, when in fact low-grade lameness was developing. The trainer would continue to train the horse, and often a serious lameness would develop. For the trainer to suspect a subtle lameness and to have the horse evaluated is much more common now. Lameness detected at this point is usually manageable. The reined cow horse continues to compete beyond 3 years of age. As 4-year-olds they can continue in the snaffle bit or begin in the hackamore or bridle class. The 5-year-olds are shown in the hackamore or bridle class, and the 6-year-old in the bridle class. Hackamore and bridle horses compete in the reining and cow work divisions, but they do not do herd work. The intention is to finish the horse’s education by the time the horse is 6 years old.

TRAINING SURFACES The training surface has a strong influence on lameness in terms of incidence, degree of severity, and type of injury. In general the arena or round pen is best constructed as follows: The original ground is graded to a 1.5% grade from one corner to the other and is compacted to 95%. A 15-cm thickness of base material such as limestone rock dust is then added, watered, and compacted to 95%. The type of base used is dictated by what is available in the area, but it should be smaller-

CHAPTER 121 sized particles (not small rocks), which have interlocking edges. A 1.5% grade should be maintained. Sand is then added to the top of the base to a thickness of at least 5 cm and not more than 12 cm in the arena, and from 10 to 15 cm in a round pen. Adding the sand at the minimum levels first and adding more later if necessary is recommended. In general, less injury occurs with thinner layers of sand, but performance may be enhanced with thicker layers of sand. Fine beach sand is the best, because it has low abrasive characteristics and is light. These qualities are important because the sand gets between the skin and protective boots and also comes in direct contact with the back of the pasterns and fetlocks. If the sand is coarse and abrasive, it damages the skin and causes lameness. The density of the sand is important because the horse has to push the sand during sliding stops, and if the sand is too heavy, it causes injury and destroys the horse’s confidence. Water content of the training surface is also an important consideration. In general, applying the water a few hours before use is a good idea, so that the water is distributed evenly. If the training surface is too deep with sand or if the base is not consistent, I see more soft tissue injuries such as tendonitis, suspensory injuries, curbs, and sprained backs. If the training surface is too hard, I tend to see bone injuries such as osteitis of the distal phalanx, navicular syndrome, sesamoiditis, or fractured proximal sesamoid bones.

TRAINING AND ITS RELATIONSHIP TO LAMENESS The types of injuries commonly seen tend to vary as the training progresses. The young 2-year-olds have hoof and sole problems during the initial breaking process, before they are shod, associated with an increased digital pulse and sensitivity to hoof testers. Subchondral bone cysts in the medial femoral condyle and osteochondrosis of the fetlock may manifest at this time. Chip fractures, present but unnoticed when the horse was a foal or yearling, may become clinically apparent when ridden work starts. The work during the latter half of training for a 2-year-old involves more speed and collection, and low-grade lamenesses may develop that later become persistent problems. These lamenesses include suspensory desmitis, navicular syndrome, and hock and stifle pain. The 3-year-old year involves even more collection, cow work at speed, and harder stops. We generally see a continuation of the 2-year-old problems, if they are not managed well, and also more acute injuries to soft tissue and chip fractures of the fetlock and carpus.

CONFORMATION AND LAMENESS Conformation does have an effect on the development of lameness, but I feel that conformation often is overemphasized. The component of conformation that has the biggest effect on soundness is body conformation and the degree of balance in motion. I have seen many horses whose conformation was not impressive when viewed at a standstill but were impressive when evaluated in motion. Balance in motion is that somewhat immeasurable quality that gives one the impression that the horse could jump, stop, turn, or do almost anything on any given stride without effort. In my experience, these horses remain sound while performing to an exceptional level, whereas horses that have less balance suffer more frequent injury. Although static conformation related to lameness is important and should be evaluated, in my opinion, conformation in motion is equally important. The most common conformation problems that I see are toed in and toed out. These problems predispose the horse to

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lameness but are present to some degree in nearly all horses. Most often these conformational abnormalities are associated with injury to the SL and also can be associated with injury to the collateral ligaments of the digit. I try to manage these conformation faults before they cause injury to the horse by trimming and shoeing. A horse that toes out initially contacts the ground with the outside toe quarter with improper trimming. The hoof then slides along the ground and begins to rotate the toe out. The inside heel then makes contact with the ground, and the hoof rotation stops. However, this rotational force continues up the limb and places unnatural strain on the soft tissues below the carpus and eventually causes damage. I recommend removing more wall from the hoof at the point of contact and beveling the toe so that breakover is accomplished easily over a wide area. My goal is to get the entire hoof to contact the ground evenly and eliminate the rotational force. Horses that toe in generally contact the ground at the inside toe quarter. Horses with this problem need more hoof removed from the inside toe, the goal being to cause the foot to land flat.

TEN MOST COMMON LAMENESS CONDITONS The following are the 10 most common lameness conditions in the reined cow horse: 1. Suspensory desmitis 2. Osteoarthritis of the centrodistal and tarsometatarsal joints 3. Navicular syndrome 4. Hoof-related problems such as bruises, abscesses, and cracks 5. Superficial digital flexor tendonitis 6. Subchondral bone cysts, osteochondrosis, and traumatic injuries of the stifle 7. Fetlock arthrosis 8. Sesamoiditis 9. Distal interphalangeal joint synovitis or osteoarthritis 10. Osteitis of the distal phalanx

LAMENESS EVALUATION I begin the lameness examination by obtaining as complete a history as possible. I establish the duration of lameness; any change in lameness, if the horse has been rested or kept in work; any response to treatment; alteration in lameness with work; when the horse was last trimmed and shod; any changes in footing, type of work or shoeing; if lameness was associated with turnout or work; if the horse has received any intramuscular injections; if the horse kicks the paddock or stall; if the horse is turned out with others; if the horse stumbles; any known trauma; whether the lameness occurred insidiously or suddenly; and if the horse stands normally. Generally, the best history is obtained from the grooms and trainer, although some owners can provide information. I watch the horse at the walk, trot, and canter, loose in a 9-m round pen, and on firm footing on a 2% slope. The degree of lameness often is amplified when the horse is loose, on hard ground, and allowed to work on a slight slope. Some lameness characteristics are best seen at a slow trot and some at an extended trot. The round pen enables one to evaluate the horse’s ability to hold leads. Detecting low-grade ataxia is also easier when the horse works free, especially during downward transitions. Lameness may be manifest in how a horse does a sliding stop; lameness may be accentuated after several sliding stops from a canter. A horse may slide stronger on one hindlimb

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than the other. The complaint is often made that the horse is not stopping as well as previously, although lameness is not noticed. A horse may begin a sliding stop normally but then pick up the painful limb halfway through the stop and replace it. The stop is not held evenly. The stop becomes normal if pain is removed by local analgesia. Another common situation occurs when the horse is cutting a cow, the horse runs off at one end or does not come back with the cow as strongly at one end. The hindlimb farthest from the cow before the weak turn is generally the lame limb. If this horse is asked to do rollbacks in a round pen, the horse is much weaker when it reverses direction one way. Generally the hindlimb on the outside of the circle after the weak rollback is the lame limb. Competition is now so great that the difference between winning and losing is sometimes a matter of which horse feels the best. Performance diminishes before outright lameness is noted. Hindlimb lameness is particularly common in reined cow horses because of hock or stifle pain or proximal suspensory desmitis. Flexion tests include flexion of the digit in all limbs and carpal, hock, and stifle flexions. Notes are made on the results and whether the horse resented flexion. The digit is flexed in an oblique plane (applying medial and lateral torque), and any resentment or diminished elasticity is noted. All of the soft tissue structures are palpated, and any enlargements and sensitivity are noted. The hoof testers always are applied to the front feet, and to the hind feet of horses with hindlimb lameness. Any lameness or weakness is classified in degrees (grade 1 to 5); by the limb involved; by weight bearing or non-weight bearing or mixed status; by the effect of walking in a circle or on a straight line, on an incline or decline; by flexion tests; and by the effects of prolonged digital pressure over sensitive areas. If lameness is serious enough possibly to be caused by fracture, radiography is performed first; otherwise, diagnostic analgesia is used to establish the source of pain. Intra-articular analgesia is more specific than regional analgesia, which can be done at a later time if necessary, so I often start with intraarticular blocks, especially in forelimbs. I rely on the flexion tests to direct the start point. If flexion of the distal limb is normal but carpal flexion is positive, I usually use perineural analgesia of the proximal palmar metacarpal and palmar nerves (high four-point). If lameness persists, I perform intraarticular analgesia of the carpus. If flexion of the distal limb is positive, I perform intra-articular analgesia of the distal interphalangeal joint first and then proceed to the pastern and fetlock joints if necessary to eliminate the lameness. If intraarticular analgesia is not helpful and the flexion test is still positive, I perform perineural analgesia of the palmar digital nerves, followed by the digital nerves (abaxial sesamoid) and later a low four-point block. Knowing whether the problem is articular is useful, because horses with articular problems are often more amenable to treatment. For intra-articular analgesia I do a three-step povidoneidodine (Betadine) and alcohol skin preparation and use sterile gloves. I place a subcutaneous bleb of local anesthetic solution before injection and combine local anesthetic solution with gentamicin sulfate (40 mg). In a hindlimb I usually use perineural analgesia proximal to the fetlock, local infiltration around the region of the SL, intra-articular analgesia of the centrodistal and tarsometatarsal joints separately, and intra-articular analgesia of the femoropatellar and medial femorotibial joints. The lateral femorotibial compartment rarely is involved. If the response to a low four-point block is positive but the response to plantar (abaxial sesamoid) nerve blocks is negative, intraarticular analgesia of the metatarsophalangeal joint is performed the following day.

IMAGING CONSIDERATIONS Once the region of pain is localized, the area is examined using radiography and ultrasonography to identify the exact structure that has been damaged and to assess the degree of damage. The more specific I can be at this point, the more reliable the prognosis and treatment are. If the diagnosis is not specific, scintigraphy often is used. Generally a differential diagnostic list is generated based on the physical examination. Developing a therapeutic plan based on a tentative or vague diagnosis is a mistake. Nearly all diagnoses are tentative until the pain has been localized as specifically as possible through the use of diagnostic analgesia and appropriate imaging.

PROCEEDING WITHOUT A DIAGNOSIS Sometimes the cause of lameness cannot be discovered, even after all of the joints and nerves have been blocked and a complete scintigraphic examination has been performed. I then treat the horse for myofascial pain with drugs or chiropractic therapy. If the horse responds to these therapies, then this is indirect evidence of the cause. Another possible cause is equine protozoal myelitis. Horses with equine protozoal myelitis may show chronic lameness without other neurological signs.

LAMENESS AND SHOEING CONSIDERATIONS Proper foot balance is critical to resolving all lameness problems successfully. The foot should be trimmed to land evenly. Any medial-to-lateral imbalance should be removed by trimming. If the point of contact is the lateral toe quarter, then enough of the lateral wall should be removed so the foot lands flat. The foot should be trimmed or a wedge used to achieve a hoof angle that is the same as the pastern angle (about 55º in forelimbs and 57º in hindlimbs). A square-toed shoe that has a wide bevel, which extends from the medial to lateral toe nail holes, commonly is recommended and is useful. The shoe should be set back so the dorsopalmar axis is shortened. The heels are trimmed so the shoe comes in contact with the wall at the widest section of the frog. These specifications are designed to remove rotational forces up the limb that occur in horses with medial to lateral imbalances, to provide mechanical advantage to the palmar/plantar aspect of the limb that occurs in horses with with a long toe and low heels, and to reduce concussion to the digit that occurs in horses with the two-phase foot impact associated with foot imbalance. An egg bar shoe is used for horses with moderate to severe tendonitis, suspensory desmitis, or an apical sesamoid fracture. A reverse shoe is used sometimes for horses with navicular syndrome, ringbone, sesamoiditis, suspensory desmitis, tendonitis, constricted palmar/plantar annular ligament, carpitis, and tarsitis. Horses with bruising in the sole are shod with soft dental acrylic pads. Horses with heel and quarter cracks are managed with egg bar shoes.

TREATMENT OF LAMENESS Suspensory Desmitis For horses with suspensory desmitis, it is important to optimize foot balance as previously described. Corrective shoeing is designed to minimize any further physical damage and therefore prevent further pain and inflammation. Other treatments provide short-term results and are aimed at reducing the existing inflammation. Horses with minor to moderate fiber disruption are treated with perilesional injections of Sarapin and corticosteroids. If

CHAPTER 121 the lesion is proximal, a sterile skin preparation is recommended, with the addition of gentamicin sulfate (40 mg) in case the carpometacarpal joint is entered inadvertently. The drugs are injected under the loose tissue between the SL and the accessory ligament of the deep digital flexor tendon. Middle carpal joint pain may occur concurrently and is treated using intra-articularly administered corticosteroids, provided that no radiographic abnormalities are apparent. Physical therapy in the form of electrical stimulus modalities or low-level light laser therapy is started 3 days after injection and continued as needed through the intended competition. Magnets of 600 to 1200 G strength placed over the site have been used successfully and are kept in place for 60 days and then as needed for soundness. The lesion is monitored monthly using ultrasonography. If conservative treatment fails, extracorporeal shock wave treatment is used and administered with the horse under general anesthesia. Up to four treatments have been used, combined with rest for 60 to 90 days.

Centrodistal and Tarsometatarsal Joint Pain Intra-articular injection of corticosteroids is effective at relieving pain and inflammation in the centrodistal and tarsometatarsal joints. Horses are allowed to rest for at least 10 days after injection and then work gradually is increased as soundness dictates. The systemic use of hyaluronan and acetylglucosamine is helpful for maintenance. Orally administered chondroitin sulfate and glucosamine products also have been useful. If medication is ineffective, joint drilling or forage to induce joint ankylosis, or peri-articular extracorporeal shock wave treatment can be used effectively.

Navicular Syndrome Navicular syndrome is diagnosed based on a positive response to palmar digital analgesia and analgesia of the distal interphalangeal joint, radiography, and scintigraphy. Radiography can be misleading, and in my opinion scintigraphy is the most reliable method of diagnosis. Corrective shoeing is essential. Isoxsuprine hydrochloride (600 mg) is given orally once daily for 60 days. Aspirin (15 g) also is given orally once daily for 60 days. If this combination provides relief, it is continued for another 60 days or until the horse finishes the futurity season. Injection of the distal interphalangeal joint with corticosteroids, or a combination of corticosteroid and hyaluronan, often provides temporary relief (about 30 days). If the horse fails to respond to the corrective shoeing and medications, shock wave treatment is indicated and has been effective, except in horses with entheseous new bone at the attachment of the collateral ligaments of the navicular bone. Palmar digital neurectomy is used as a last resort.

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further damage. Possible causes for tendonitis include poor hoof balance, deep footing, fatigue, speed, overexertion from working a difficult cow, uncontrolled exercise (turnout), interference from hindlimbs, tight bandages, poorly fitting support boots, and hanging a leg on a hot walker, tie rope, or fence. Therapy for tendonitis involves depositing corticosteroids in the loose subcutaneous tissue in the proximity of the lesion. The leg is wrapped in a gelocast for 3 days and then is treated with ice and laser or electrical stimulus therapy. The horse is walked in hand or under saddle for 15 minutes twice daily for 7 days. Training then is resumed. The leg is maintained in a support wrap continuously. Shoeing, good footing, and conservative training are critical to the healing process.

Stifle Pain If no abnormalities are detected in the stifle radiographically, the affected joints are treated with intra-articularly administered corticosteroids and hyaluronan. The horse is prescribed weekly injections of systemic acetylglucosamine, which continue through the futurity. Subsequent intra-articular injections are not performed sooner than 6 months and preferably not at all. If radiographic evidence of osteochondrosis of the trochlear ridges of the femur exists, the same therapy is effective. The prognosis for horses with subchondral bone cysts of the medial femoral condyle is dismal, and I do not recommend that these horses continue training to be futurity horses.

Metatarsophalangeal Joint Pain Metatarsophalangeal joint pain may be caused by traumatic arthritis, fracture of a proximal sesamoid bone, sesamoiditis, fragments detached from the proximoplantar aspect of the proximal phalanx, or peri-articular soft tissue injury. If no radiographic lesions are present, the horse is treated with intra-articularly administered betamethasone and hyaluronan, followed by 10 days of rest. Systemic glucosamine is given every 2 weeks as maintenance therapy. Orally administered glucosamine and chondroitin sulfate also seem to be useful in managing metatarsophalangeal joint pain. Shoeing imbalances must be corrected concurrently.

Sesamoiditis The foot must be properly balanced to treat sesamoiditis. Egg bar shoes with a square toe and a wide roll or bevel are used. The shoe is set back to minimize the leverage on the palmar/ plantar aspects of the fetlock. The hoof angle is optimal when it matches the pastern angle. Isoxsuprine hydrochloride (600 mg) and aspirin (15 g) are given orally once daily for 60 to 90 days. Electromagnetic energy is applied to the affected region every other day for 3 months and thereafter as needed for soundness. The amount of training is dictated by the degree of soundness.

Traumatic Hoof Injuries Horses with bruises and cracks in the hooves respond well to egg bar shoes with soft dental acrylic pads or metal pads. A horse with a quarter crack is treated by trimming the wall palmar/plantar to the defect, so that no contact is made with the shoe, that is, floating the heel. The air gap is up to 6 mm deep and is reopened daily using a hacksaw blade to relieve pressure between the hoof wall and the shoe, until the defect has grown out. If the crack is moving and bleeding, a copper patch is attached to the wall with screws to span the defect and therefore stabilize it.

Superficial Digital Flexor Tendonitis Ultrasonography is used to characterize size and position of the lesion in horses with superficial digital flexor tendonitis. If a lesion is small, the owner or trainer usually decides to continue preparing for the futurity. It is important to try to determine the circumstances that caused the lesion to develop to eliminate

Distal Interphalangeal Joint Pain The foot must be properly balanced to treat distal interphalangeal joint pain. Soft dental acrylic pour-in type pads and shock-absorbing rim pads can be helpful. Intra-articular injection of a corticosteroid and hyaluronan is followed by the systemic use of acetylglucosamine and hyaluronan. It is imperative that training is continued on a soft surface.

Osteitis of the Distal Phalanx Soft dental acrylic pour-in type pads and shock-absorbing rim pads are used to treat horses with osteitis of the distal phalanx. The horse is treated with isoxsuprine hydrochloride (600 mg), aspirin (15 g), and phenylbutazone (2 g) given orally once daily for 60 days and then as needed for soundness. Training must be done in soft footing to reduce concussion to the foot. Extracorporeal shock wave therapy has recently been introduced to manage horses with osteitis of the distal phalanx.

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BARREL-RACING HORSES • Robin M. Dabareiner and G. Kent Carter Barrel racing began in 1948 when a group of Texas ranch women started riding horses around a cloverleaf pattern of barrels and the fastest horse around the course was the winner. Barrel racing has evolved into a multimillion-dollar industry called the Women’s Professional Rodeo Association. From this original organization many other barrel racing associations, which host numerous futurities for horses 4 or 5 years of age or younger and derbies for older horses, have arisen. In 2000, five futurity events were held nationwide, with each futurity paying out more than $800,000 in prize money from which the winner is guaranteed more than $100,000. The major competitions are divided into rodeo, futurities, derbies, open jackpots, and professional levels. Futurities and derbies are classified by age of the horse. Open competitions are open to any horse or rider and are highly competitive. Within the open jackpots, a new classification of barrel racing has developed, termed a 3D or 4D competition, which includes a handicapping system that allows less experienced horses or riders to compete with seasoned horses and riders. Barrel racing is a timed event with the clock beginning when a predetermined line is crossed. Three barrels (55-gallon steel drums) are positioned in a triangle or cloverleaf (Fig. 121-5). The contestant must turn the left or right barrel first (most

30 ft.

choose to turn the right-hand barrel first) in a manner that the path always crosses. The distance covered for the pattern varies with the size of the arena, but generally the distance from the starting line to the first barrel is 14 to 18 m. The distance between the first and second barrel is 21 to 27 m and between the second and third barrel is 27 to 32 m. The horses must start at the alleyway or entrance to the arena, run at full speed to the first barrel, slow down and complete a 360º turn around the barrel, speed up and run to the second barrel, turn 360º, head to the third barrel, turn 360º, and then sprint to the finish line. The fastest time to complete the pattern varies with distance of the pattern and arena size, but a good run for a large arena pattern is 15 to 16 seconds. An electric eye timing system usually is used, and times are recorded in hundredths of a second. If a rider hits a barrel and tips it over, a 5-second penalty is imposed. If the horse and rider fail to negotiate the pattern correctly, they are disqualified. The arena is often leveled after each horse.

CONFORMATION Horses are predominately American QHs and Appendix horses (QH and Thoroughbred crosses), but occasionally Thoroughbred, Paint, or Arabian horses are seen. Speed, quick acceleration, and agility to slow down quickly to turn the barrel are essential. Many barrel horses have QH racehorse pedigrees. Some prefer stockbred horses, which usually have a calmer personality. Geldings are preferred. Horses usually range from 14.3 to 15.1 hands. Barrel horses are not usually as muscular and wide based as calf roping horses. They usually have long, leaner muscle mass that provides the speed and flexibility needed to perform the 360º turns.4

TRAINING

90 ft.

15 ft.

90 ft.

15 ft.

70 ft.

40 ft.

40 ft.

Start/Finish line

30 ft.

40 ft. Arena back line

Fig. 121-5

Futurity competitions are popular because of the amount of prize money, and training usually starts at 2 years of age. Futurity horses often have short careers because of the pressure to perform at a high level of competition at only 4 to 5 years of age, resulting in advanced osteoarthritis, often in the distal tarsal joints. Successful futurity horses seldom have long-term careers because of behavioral problems or performance-limiting injuries.1 Horses that are 5 years of age or older, started slowly, and are allowed to mature before performing in serious competition may compete professionally for 5 years.2 The average age of a professional barrel horse is 10 to 15 years. Horses may compete in 50 to 100 rodeos per year and spend much time traveling. An experienced barrel horse is trained by practicing turns but rarely uses the barrels because the horse learns to anticipate the pattern and tires of it. Many professional horses are ponied (led from another horse), or are ridden just enough to keep them fit for competition, but they are never really worked unless competing.4,6 Older, semi-retired horses that are well trained to the barrel pattern, but not fast enough for upper-level competition, may be used for a child or beginner. These horses do make repetitive barrel pattern runs in a practice pen for the rider to learn and often have use-related injuries, requiring much maintenance to withstand the number of practice runs needed to teach a beginner.

Diagram of barrel racing cloverleaf.

LAMENESS EXAMINATION A barrel horse does not run at top speed over long distances like flat racehorses; therefore fatigue-type injuries like

CHAPTER 121 superficial digital flexor tendonitis or fetlock and carpal chip fractures are seen rarely. Some of the common injuries seen in barrel horses are attributed to the twisting and turning motion of the horse at high speeds (Fig. 121-6). Other musculoskeletal problems vary by the horse’s age and level of competition. A young futurity barrel horse may run up the fence, that is, the horse does not turn around the barrel but runs past it up the arena, or it may refuse to enter the arena. No lameness may be detectable, and the veterinarian has to determine whether the young horse is mentally stressed and showing behavioral problems or is responding to pain. Complaints about an older, experienced horse usually result from pain, but behavioral problems occur more often in young horses. Most barrel racers train their own horses, and the quality of training is inconsistent, and performance changes may be induced by the rider. The teeth are evaluated to eliminate bitting problems as a cause of performance changes. Radiographic examination of the hocks is performed because of the high incidence of distal hock joint pain. The stifles also are examined to eliminate osteochondrosis as a potential source of pain. If no radiographic abnormalities are detected, several options are presented to the owner to help determine if the horse is responding to pain or is overtraining. One option is to administer phenylbutazone (2.2 mg/kg daily for 2 weeks and then 1.1 mg/kg daily for 2 weeks) for 30 days and to keep the horse in barrel-race training. If the horse returns to normal performance, then we conclude that the horse is most likely experiencing pain. If the problem does not resolve, then we try to address any behavioral problems. If problems persist, we often suggest giving the horse a 3- to 6-month break from barrel racing and have the horse work cattle or perform other less intense activities. A second option is to increase the workload and try to establish lameness that can be identified and then located with diagnostic analgesia, but few owners select this option. Because of high incidence of distal hock joint pain

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and the poor correlation between clinical signs and radiographic abnormalities, the centrodistal and tarsometatarsal joints can be medicated with hyaluronan, with or without corticosteroids, and the response assessed. Nuclear scintigraphic examination can be performed but often is unrewarding; however, owners may be encouraged then to increase the horse’s work to see if overt lameness develops. An experienced horse may begin to have a change in behavior or performance rather than show an actual lameness. Behavioral problems occur more often than in other Western performance events, because the horse may experience pain at the same spot in relation to the barrel, regardless of arena size, and thus the horse begins to dread making the barrel turn.3 A common complaint is that the horse is coming up out of the turn on the first barrel, meaning that the horse heads into the turn normally, but as the horse comes into the backside of the barrel turn, it does not want to stay in the ground or push off aggressively to the next barrel. Instead the horse comes uncollected, bounces out of the barrel, and makes a wide turn around the barrel that adds time to the run. Such behavior often is associated with distal hock joint pain, especially involving the hindlimb on the inside of the turn. The horse may not run between the barrels as it should or is slower, 3 or 4 tenths of a second off its time. Trotting the horse in hand in a small circle (1.5- to 3-m radius), mimicking the barrel turn, is helpful. This may be the only time the horse shows lameness. Determining which barrel is the problem barrel is helpful. An owner may complain that the horse will not stay in the ground for the first barrel but works fine for the second and third barrels. The horse may perform fine for the first barrel but does not make a good turn around the second barrel. The first barrel (usually going to the right) is the hardest barrel and most often a problem, because the horse is running at full speed when it reaches the barrel and must slow quickly to make the 360º turn. When the horse is turning the barrel, the inside hindlimb appears to be under the greatest pressure (see Fig. 121-6). If the owner complains that the horse is swinging wide or pulling away from the first barrel, the horse does not want to turn to the right and is probably trying to avoid inside hindlimb pain. The outside forelimb is also under much stretching pressure as the horse goes into a barrel turn, but we also have seen horses that do not want to take the first barrel to the right and have right (inside) forelimb pain. Hindlimb lameness is more common than forelimb lameness, and less correlation exists between horses resisting a particular direction of the turn relative to a specific forelimb lameness.

DIAGNOSIS AND MANAGEMENT OF SPECIFIC LAMENESS

Fig. 121-6 A barrel horse turning a barrel. Note the pressure on the inside hindlimb. This horse is on the backside of the barrel coming out of the turn and is in correct position. At this point in the barrel turn a horse with hindlimb pain becomes uncollected and swings wide around the barrel.

Distal hock osteoarthritis is the most commonly diagnosed problem, causing reduced performance or lameness. Diagnosis is based on intra-articular analgesia, radiography, response to treatment, and sometimes nuclear scintigraphy. The centrodistal and tarsometatarsal joints are treated using methylprednisolone acetate (40 to 60 mg per joint) or triamcinolone acetonide (6 mg per joint) alone, or in combination with hyaluronan (20 mg per joint). Ideally the horse should have 7 to 10 days of turnout or light exercise before returning to barrel racing, but often the competition schedule does not allow this. Response to treatment may take up to 3 weeks. If the horse does not respond to treatment, we re-evaluate the horse for lameness. Hindlimb proximal suspensory desmitis is common in older, seasoned horses and can be a career-ending injury. Deep sand in arenas may contribute to the high incidence. Moderate lameness (grade 2 to 3 of 5) often is exacerbated by upper limb

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flexion. The horse usually has no swelling or minimal swelling and no heat and pain. Local analgesia is essential to verify the source of pain. Radiography of the proximal metatarsal area is often negative, although if the condition is chronic, sclerosis or entheseous new bone may be present. Ultrasonographic examination may reveal an enlarged and hypoechoic SL, but some horses have no detectable structural abnormalities. The latter are treated by local infiltration of triamcinolone acetonide (9 to 12 mg) and reduced work. With acute, mild proximal suspensory desmitis horses often return to work in 2 to 4 weeks. We also recommend confining the horse to a small area to avoid further damage from excessive uncontrolled exercise. If ultrasonographic abnormalities are detected, the horse is confined to a small area with no riding for 60 to 90 days before reexamination. Complete healing often takes 6 to 12 months, and some horses never return to full athletic function. Suspensory branch injuries are common in hindlimbs, especially the right, resulting in mild hindlimb lameness (grade 1 to 2 of 5), which is improved by a low plantar nerve block. Normally detectable ultrasonographic abnormalities are present, but radiographic abnormalities of the proximal sesamoid bones are unusual. Horses respond well to 60 to 90 days of small area confinement, followed by a gradual return to conditioning and resumption of competition after 4 months. We recommend the use of boots to protect the hindlimb soft tissues. If lameness is improved by a low plantar block but ultrasonographic and radiographic examinations are negative, intra-articular analgesia of the metatarsophalangeal joint and intrathecal analgesia of the digital flexor tendon sheath are performed. If the response is positive, the joint or digital flexor tendon sheath is treated with hyaluronan (20 mg) and triamcinolone acetonide (9 mg). These horses usually can continue competing but may have recurrent lameness. QH and Appendix QHs make up most of the barrel horses. Sore feet, navicular disease, and palmar foot pain are the most frequent causes of forelimb lameness, with poor hoof conformation and farriery and hard arena surfaces being predisposing factors. Diagnosis and management are similar to those described for the team roping horse. Proximal suspensory desmitis is also common in forelimbs. Deep arenas and long toes and low heels are predisposing factors. The prognosis for barrel racing horses with forelimb proximal suspensory desmitis is good, with most horses responding well to rest and controlled exercise for 3 to 4 months. Tendon protection boots are recommended. Metacarpophalangeal joint synovitis results in mild lameness (grade 1 to 2 of 5) that is exacerbated by fetlock flexion. The horse often strongly resists fetlock flexion. Lameness and response to fetlock flexion are eliminated by intra-articular analgesia. Radiographic examination is usually negative. The horse is treated with intra-articularly administered triamcinolone acetonide (6 mg) and hyaluronan (20 mg). The problem may or may not recur. If recurrence is frequent, diagnostic arthroscopy is recommended. Many times horses have undergone several types of alternative therapies (e.g., equipment changes, acupuncture, chiropractic, and herbal therapy) in an attempt to correct the perceived problems before being checked by a veterinarian. Often, for some inexplicable reason, an accurate diagnosis and conventional medical therapy is sought only after failure of these other treatments. Many owners rely on diagnosis from a fellow competitor, and request treatment that was successful in another horse. This makes client communication difficult.

SHOEING CONSIDERATIONS Traction, especially in the deep and often muddy arenas in which horses compete, is critical. A rim shoe is used most com-

monly on all feet, with one rim higher than the other to provide added traction. The rounded toe provides easier breakover than a normal flat steel shoe. Hind shoes may have square toes. Recently the natural balance shoe has gained popularity as owners are becoming more aware of good farriery principles and are trying to correct long-toe, low-heel problems. The natural balance shoe is available in steel or aluminum. The steel construction is preferred because of the added weight, which provides better traction than the aluminum shoe. The natural balance shoe has a rockered toe that eases breakover of the forelimb and is built with a wider web than a normal shoe, which benefits a sore-footed horse competing on hard surfaces.

OTHER CONSIDERATIONS Exercise-induced pulmonary hemorrhage is common in barrel horses. The owner may complain that the horse has lost a step or has become slower. If a musculoskeletal reason for the performance change cannot be determined, a respiratory evaluation is indicated. Obvious bleeding from the nostrils rarely is seen, but endoscopic examination within 30 minutes of the barrel race often reveals tracheal hemorrhage. Presently no drug testing or rules prevent drug administration for competition. Most horses receive phenylbutazone or flunixin meglumine 4 to 6 hours before competition and furosemide (4 to 8 ml per horse).

REFERENCES 1. Stricklin JB: Barrel racing, Proc Am Assoc Equine Pract 43:37, l997. 2. Cox J-B: Personal communication, 2002. 3. Galley RH: Personal communication, 2002. 4. Pearce G: Personal communication, 2002. 5. Women’s Professional Rodeo Association, 1235 Lake Plaza Drive, Suite 13, Colorado Springs, CO. 6. Hanover D: Personal communication, 2002. THE EUROPEAN WESTERN PERFORMANCE HORSE • Franco Ferrero The Western performance sport horse has developed in Europe since the mid-1980s. Most horses are American QHs and are used for reining, a sport most popular in Germany and Italy. The Italian reining and cutting futurities for 3-year-olds offer the highest prize money. The rules governing competition usually are based on the American rules, with a few notable exceptions in Germany. Horses entered in the Reining Breeder’s futurity must be 4 years of age. Strict rules govern which bits and harness are acceptable. Excessive use of force, spurs, or the whip may result in suspension of the rider. Reining QHs usually are broken at 18 months of age and may undergo intense training in preparation for the snaffle-bit futurity at 3 years of age, but these horses rarely compete at high levels when older. Only a limited number of horses compete after 6 years of age.

TEN MOST COMMON LAMENESS CONDITIONS The 10 most common causes of lameness in reining QHs 2 to 4 years of age are as follows: 1. Foot pain 2. Hock pain 3. Carpal pain

CHAPTER 122 4. 5. 6. 7. 8.

Fetlock pain Stifle pain Splints Superficial digital flexor tendonitis Desmitis of the accessory ligament of the deep digital flexor tendon 9. Suspensory ligament desmitis 10. Shoulder injury Causes of foot pain include subsolar abscessation, solar bruising, osteoarthritis of the distal interphalangeal joint, fracture of the palmar process of the distal phalanx, osteitis of the palmar processes of the distal phalanx, and navicular syndrome. Hoof tester examination is an essential diagnostic tool. Oblique radiographic views of the distal phalanx are invaluable for assessing the palmar processes. Poor foot conformation is often an important predisposing factor for the development of foot pain. The foot is often upright with overgrown angles of the walls and heels, flattening or convexity of

CHAPTER •

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the sole at the toe, and an underdeveloped frog. The shoes are often too small. Bar shoes also may prevent the heels from digging into the ground. Osteoarthritis of the distal hock joints is common. Horses of 2 years of age have a high incidence of partial collapse of the central and third tarsal bones with secondary osteoarthritis. Carpal problems occur more commonly than in North America and include synovitis of the antebrachiocarpal and middle carpal joints, osteoarthritis, sagittal fracture of the third carpal bone, and chip fractures of the distal aspect of the radial carpal bone. Conformational abnormalities such as carpus valgus, calf knees (palmar deviation of the carpal joints), tied-in knees, and offset knees may be important predisposing factors. The limited number of blood lines available for breeding may influence the incidence of these conformational abnormalities. Bench or offset knees also may predispose horses to the high incidence of splints causing lameness, especially in 2-year-old horses.

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The Tennessee Walking Horse James T. Blackford and James C. Sternberg

DESCRIPTION OF THE SPORT The Tennessee Walking Horse, commonly called the Walking Horse, is a light horse breed developed in middle Tennessee for use on southern plantations during the eighteenth century. The average Walking Horse is 15 to 16 hands tall and weighs 500 to 600 kg. The Tennessee Walking Horse is a composite breed, created by crossbreeding Canadian and Narrangansett Pacers, Morgan, Standardbred, and Thoroughbred horses. The Tennessee Walking Horse Breeders’ and Exhibitors’ Association was formed in 1935. Because of the versatility of the Walking Horse, along with a characteristic racking gait within the breed, a second breed association was recognized in 1971, the Racking Horse Breeders’ Association. This group of horses is commonly referred to as the Racking Horse. The Walking Horse performs three gaits: the flat-foot walk, running walk, and canter. Both walks are four-beat gaits, with one foot up and three feet in various phases of striking the ground. The footfall sequence is left hind, left front, right hind, and right front. High-stepping forelimbs with an extended reach characterize the flat-foot walk. The hind foot overreaches the imprint of the front foot by 15 to 55 cm in a straight, smooth, gliding motion. This over-stride is unique to the breed and is referred to as the big lick. The horse’s head and neck nod, and the ears flick forward and backward in rhythmical fashion with the rise and fall of the front feet. The appearance is that of pulling with the forelimbs and driving or pushing with the hindlimbs. The speed of the flat-foot walk is from 4 to 8 miles per hour. At the running walk, the gait is basically the same but faster (10 to 20 mph). The canter is a threebeat gait, with a left or right lead. In the canter the horse lifts the forehand, giving an easy rise and fall, in a rolling motion. The gait is referred to commonly as the rocking-chair canter because of the high, rolling movement of the horse’s body.

The Racking Horse gait is a bilateral four-beat gait, with one foot striking the ground with the other three limbs in various phases of elevation. The gait often is referred to as the single-foot gait. When shown, the Racking Horse performs the show walk, slow rack, and fast rack. The show walk is a smooth, collected, slow and easy four-beat gait. At the slow rack the horse’s head is held with the neck arched and ears erect. The fast rack is similar in form to the slow rack, but the horse displays speed and leg action. The natural head nod must not be exaggerated at the slow or fast rack. In both breeds the collected gaits of the show horse shift the center of gravity caudally, compared with most other light breeds, with increased loads on the hindlimbs resulting in a high incidence of hindlimb lameness. Both breeds are used for show, trail, and pleasure riding. Horses are shown at halter, harness, and under tack, with English or Western saddles. Horses that are shown wear a light shoe similar to a standard keg shoe, a plantation shoe, or a performance shoe, depending on the class. The plantation shoe cannot exceed 3.8 cm in width and 1.3 cm in thickness, and the heel calk cannot exceed 2.5 cm in height. The performance shoe, or stack, is a shoeing technique used to accentuate the show horse gaits. The shoe is constructed of several layers of flat or wedge pads, stacked one on top of another, placed between a nail pad at the solar margin and a metal shoe on the contact surface. Pads are made of leather, plastic, or hard rubber. The amount of height or extension the shoe provides must not exceed 50% of the natural hoof wall length, measured from the coronary band to the tip of the toe. Pleasure horses are commonly flat shod. Although the highest population of Walking and Racking horses is presently in the southeast United States, they are becoming more popular across North America, especially for trail and pleasure riding, because of the physical endurance and

CHAPTER 122 4. 5. 6. 7. 8.

Fetlock pain Stifle pain Splints Superficial digital flexor tendonitis Desmitis of the accessory ligament of the deep digital flexor tendon 9. Suspensory ligament desmitis 10. Shoulder injury Causes of foot pain include subsolar abscessation, solar bruising, osteoarthritis of the distal interphalangeal joint, fracture of the palmar process of the distal phalanx, osteitis of the palmar processes of the distal phalanx, and navicular syndrome. Hoof tester examination is an essential diagnostic tool. Oblique radiographic views of the distal phalanx are invaluable for assessing the palmar processes. Poor foot conformation is often an important predisposing factor for the development of foot pain. The foot is often upright with overgrown angles of the walls and heels, flattening or convexity of

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the sole at the toe, and an underdeveloped frog. The shoes are often too small. Bar shoes also may prevent the heels from digging into the ground. Osteoarthritis of the distal hock joints is common. Horses of 2 years of age have a high incidence of partial collapse of the central and third tarsal bones with secondary osteoarthritis. Carpal problems occur more commonly than in North America and include synovitis of the antebrachiocarpal and middle carpal joints, osteoarthritis, sagittal fracture of the third carpal bone, and chip fractures of the distal aspect of the radial carpal bone. Conformational abnormalities such as carpus valgus, calf knees (palmar deviation of the carpal joints), tied-in knees, and offset knees may be important predisposing factors. The limited number of blood lines available for breeding may influence the incidence of these conformational abnormalities. Bench or offset knees also may predispose horses to the high incidence of splints causing lameness, especially in 2-year-old horses.

122

The Tennessee Walking Horse James T. Blackford and James C. Sternberg

DESCRIPTION OF THE SPORT The Tennessee Walking Horse, commonly called the Walking Horse, is a light horse breed developed in middle Tennessee for use on southern plantations during the eighteenth century. The average Walking Horse is 15 to 16 hands tall and weighs 500 to 600 kg. The Tennessee Walking Horse is a composite breed, created by crossbreeding Canadian and Narrangansett Pacers, Morgan, Standardbred, and Thoroughbred horses. The Tennessee Walking Horse Breeders’ and Exhibitors’ Association was formed in 1935. Because of the versatility of the Walking Horse, along with a characteristic racking gait within the breed, a second breed association was recognized in 1971, the Racking Horse Breeders’ Association. This group of horses is commonly referred to as the Racking Horse. The Walking Horse performs three gaits: the flat-foot walk, running walk, and canter. Both walks are four-beat gaits, with one foot up and three feet in various phases of striking the ground. The footfall sequence is left hind, left front, right hind, and right front. High-stepping forelimbs with an extended reach characterize the flat-foot walk. The hind foot overreaches the imprint of the front foot by 15 to 55 cm in a straight, smooth, gliding motion. This over-stride is unique to the breed and is referred to as the big lick. The horse’s head and neck nod, and the ears flick forward and backward in rhythmical fashion with the rise and fall of the front feet. The appearance is that of pulling with the forelimbs and driving or pushing with the hindlimbs. The speed of the flat-foot walk is from 4 to 8 miles per hour. At the running walk, the gait is basically the same but faster (10 to 20 mph). The canter is a threebeat gait, with a left or right lead. In the canter the horse lifts the forehand, giving an easy rise and fall, in a rolling motion. The gait is referred to commonly as the rocking-chair canter because of the high, rolling movement of the horse’s body.

The Racking Horse gait is a bilateral four-beat gait, with one foot striking the ground with the other three limbs in various phases of elevation. The gait often is referred to as the single-foot gait. When shown, the Racking Horse performs the show walk, slow rack, and fast rack. The show walk is a smooth, collected, slow and easy four-beat gait. At the slow rack the horse’s head is held with the neck arched and ears erect. The fast rack is similar in form to the slow rack, but the horse displays speed and leg action. The natural head nod must not be exaggerated at the slow or fast rack. In both breeds the collected gaits of the show horse shift the center of gravity caudally, compared with most other light breeds, with increased loads on the hindlimbs resulting in a high incidence of hindlimb lameness. Both breeds are used for show, trail, and pleasure riding. Horses are shown at halter, harness, and under tack, with English or Western saddles. Horses that are shown wear a light shoe similar to a standard keg shoe, a plantation shoe, or a performance shoe, depending on the class. The plantation shoe cannot exceed 3.8 cm in width and 1.3 cm in thickness, and the heel calk cannot exceed 2.5 cm in height. The performance shoe, or stack, is a shoeing technique used to accentuate the show horse gaits. The shoe is constructed of several layers of flat or wedge pads, stacked one on top of another, placed between a nail pad at the solar margin and a metal shoe on the contact surface. Pads are made of leather, plastic, or hard rubber. The amount of height or extension the shoe provides must not exceed 50% of the natural hoof wall length, measured from the coronary band to the tip of the toe. Pleasure horses are commonly flat shod. Although the highest population of Walking and Racking horses is presently in the southeast United States, they are becoming more popular across North America, especially for trail and pleasure riding, because of the physical endurance and

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gentle disposition of the breeds. The show season generally is considered to be year-round, picking up in the spring and peaking in the fall with the national championships. The Tennessee Walking Horse National Celebration is held in Shelbyville, Tennessee, each year and is an 11-day event ending with the crowning of the national champions on the Saturday before Labor Day. The Racking Horse Celebration is held each year in Decatur, Alabama, during the last 2 weeks in September.

LAMENESS EXAMINATION Lameness evaluation of the gaited horse is best performed with the horse under complete tack with a rider. It is impossible to duplicate the head set, balance, and shifting of the horse’s center of gravity caudally without a rider. The horses generally exercise in a large, oval arena, and to perform a good evaluation, one needs to provide a place where the horse has room to work in all gaits. The ground surface in this area should be firm. A veterinarian’s impression when evaluating a show horse in performance shoes for the first time will be that the horse’s problem must be in the forelimb and more specifically the foot. In light of the negative publicity the stacked shoe receives, focusing one’s attention on this area is easy. Even as the horse is walked at halter, this impression may not change, because of the awkward nature of the horse handling the bulky shoe. In our experience, few problems are associated directly with the shoe, except hoof wall avulsions, when the shoe is accidentally pulled off in the show ring. Measures to control bleeding must be taken immediately, followed by good wound care. Hoof wall composites then can be used to restore hoof wall function. If an elevated shoe is removed completely and suddenly from an immature, developing horse early in training, removal causes a mechanical flexor contracture. The horse knuckles over at the fetlock joint because of the pain associated with pulling of the deep and superficial digital flexor tendons. Unfamiliarity with the standard gaits of Walking and Racking horses, especially when shod with a stacked shoe, may result in confusion with ataxia, particularly at faster speeds. Anecdotally, our impression is that a high incidence of cervical vertebral malformation occurs in Tennessee Walking Horses, so this should be kept in mind. Tennessee Walking Horses are stoical and seem to have a high pain tolerance. Problems encountered in the flat-shod Walkers or Rackers mirror the lameness problems seen in other light breeds; therefore the following discussion focuses on show horses in stacked shoes. The hoof tester evaluation is of limited value on the front feet of performance-shod horses. Careful palpation and manipulation of the limbs are performed routinely. Careful evaluation of the foot and shoe should not be overlooked. Pressure-shoeing techniques by unscrupulous owners and trainers, which causes soreness and increases the big lick, occasionally arise in a performance-shod horse and should not be overlooked. The technique is performed by over-trimming the hoof wall and thus increasing sole pressure. A carefully placed nail in the nail pad encroaching on the sole or the sensitive laminae may be noted. A foreign object, such as a stone inserted between the pad and

the sole inflict discomfort. Digital pulses, tapping on the hoof wall with hoof testers or a shoeing hammer, and response to nerve blocks may determine the problem. Problems seen in the forelimbs commonly are associated with imbalances in the shoeing, leading to an uneven height of the forelimb carriage. To evaluate the forelimb carriage, the observer should draw an imaginary line at the chest level, watching the carpal action to determine which leg is carried lower to the imaginary line as the limb advances, indicating the problem limb. When this problem is detected, careful evaluation of the shoeing technique and comparison between limbs are indicated. Correction of foot imbalance may resolve the problem. Osteoarthritis of the distal interphalangeal joint (low ringbone) frequently is seen in older horses but is not always correlated with lameness. Proximal suspensory desmitis usually is caused by slipping in an elevated shoe and may be associated with localized pain on palpation. Bicipital bursitis is seen occasionally. The horse may have asymmetry in shoulder motion and pain on palpation of the area, especially when the limb is raised. Abduction or adduction of the shoulder is performed. Like most breeds, sole abscesses are common in flat or performance-shod horses, as is laminitis. The highest percentage of lameness seen in our practice with Walking and Racking horses is associated with the hindlimbs, because of loading of the hindlimbs during exercise. As each hindlimb strikes the ground and the horse’s weight is carried through the stride, a rotational, twisting motion also is seen throughout the entire limb before the leg is advanced. This is especially noticeable in the Walking Horse at the faster gaits. The shifting weight and the twisting motion increase stress on the joints and surrounding support structures. Osteoarthritis of the distal hock joints and stifle is common. A positive response to the Churchill test is helpful in isolating pain to the distal hock joints. Careful palpation of the medial patellar ligament is particularly important in this type of sport horse, because at one time almost all of the show horses were subjected to medial patellar desmotomy with hopes of improving the over-reaching stride of the rear legs. Although the medial patellar desmotomy site only occasionally is found to be the origin of the lameness in these horses, the possibility should not be overlooked. The practice is not as common today as in the past; however, many trainers from the old school feel that having the desmotomy performed is important. Upper- and lower-limb flexion tests are performed. Local analgesia is used to define the source of pain. Trochanteric bursitis occurs in Walking and Racking horses and is related to the rotational, twisting motion of the hindlimbs. The horse has pain on deep palpation over the greater trochanter of the femur, during upper limb flexion tests, and when the hip is stretched forward or backward, abducted or adducted, and rotated. Other conditions are encountered in these horses. Some have muscular weakness in the hindlimbs, especially in young unconditioned horses. When weakness is combined with straight hindlimbs, instability of the patella is common. Chronic hip and stifle soreness caused by a trailer on the outside of the shoe may be an underlying cause of lameness. Osteochondrosis occurs in the forelimbs and hindlimbs. We see a substantial number of horses that are thought to be lame but have equine protozoal myelitis.

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Lameness in the American Saddlebred and Other Trotting Breeds with Collection Scott D. Bennett

DESCRIPTION OF THE SPORT The American Saddlebred, Morgan, Hackney Pony, National Show Horse, and Arabian (see Chapter 124) show horses are described as trotting breeds with collection. Lameness in disciplines such as dressage, road horses, and road ponies is similar. The American Saddlebred and National Show Horse have five gaits: walk, trot, canter, slow gait, and rack. The slow gait and rack are manmade gaits. These horses also perform in three gaited classes (walk, trot, and canter), fine harness classes, pleasure driving, pleasure-gaited classes, and equitation. Morgan and Arabian horses are shown similarly, but without the slow gait or rack. Hackney ponies are shown in harness, pleasure driving, and road pony classes. Show classes are further divided for professional, amateur, and juvenile riders. Equitation, hunt seat, Western, and numerous young horse and in-hand halter classes are available. In road horse classes, Standardbreds, Morgans, American Saddlebreds, or Standardbred-cross horses are shown at the walk, trot, and road gait pulling a bike similar to a sulky used for Standardbred racehorses. These horses usually are more animated in gait than Standardbred racehorses and go both ways around the ring when performing. The road gait is a high-speed performance gait. To understand lameness in the gaited show horse, the veterinarian must first understand the difference in locomotion between running and gaited horse disciplines. Concussion (impact) is a part of every gait. How the horse distributes concussion is related directly to athletic ability and the longevity of a horse’s career. Better equine athletes are more efficient in the distribution of concussion through the limbs and body. The superior equine athlete appears capable of using energy of concussion efficiently and distributing it for dispersion and recovery. Normally kinetic or stored energy from proper distribution of concussion causes recoil of the tissues receiving the energy of concussion. Tissue injury results in an inability to disperse concussive energy properly. Maintaining healthy hoof wall, bone, cartilage, tendons, ligaments, and muscles in a good conditioning and gait management program is essential. The veterinarian must be familiar with the gaits, because gait analysis is an important part of evaluating poor performance and subtle lameness. Gaits of the show horse are complex and must be synchronous to maintain distribution of concussion. Synchrony must be achieved in up to five gaits and is altered by the different gait specifications. The normal load distribution between forelimbs and hindlimbs in the show horse is about 35% and 65%, respectively (see Chapter 2). The show horse does not have to perform at speed. Compared with many sport horses, synchrony of concussion and weight distribution are totally different, and because much concussion is dispersed through the hindlimbs, hindlimb lameness is more important. In some other sports horses the head and neck are raised and lowered with the stride, a movement that assists in

balance, energy distribution, and propulsion. The show horse, like the dressage horse, maintains a fixed and flexed head and neck carriage. This further shifts the balance and energy of concussion to the hindlimbs. Show horses carry more body weight for a fleshier look than the greyhound-like racing counterparts. Riders of show horses, as a rule, also are heavier than racing jockeys. Longevity of show horses compared with racehorses is related directly to speed of performance, which is dramatically less. Racehorses must change energy distribution at high speed quickly, potentially leading to catastrophic breakdown, but such actions and injuries in show horses are rare. A show horse often can remain competitive into the late teens and early twenties, but chronic wear and tear may result in lameness. Although show horses do not perform at speed, high head carriage and high leg action and motion are strenuous. Show horses perform numerous gait changes and transitions going both directions of the ring, and for a high-level (stake class) five-gaited class to last from 30 to 40 minutes is not unusual. Because five-gaited movements and transitions are complex and arduous, compensatory lameness is common. A methodical approach to lameness diagnosis must be used to differentiate primary and compensatory lameness. A superior show horse distinctly separates its different gait movements, raising each carpus above the horizontal, with a high hock action. The horse drives off its hindlimbs with a flexed high head and neck carriage. Responsiveness to the bit, with an alert expression and attitude, and forward placement of the ears are desirable. Just as racehorses are bred for speed, show horses are bred for animated motion.

AMERICAN SADDLEBRED The American Saddlebred has a long history and aptitude for different gaits and is derived from many different lineages. The breed was developed by free men in a young free country where the best horses could be bred to the best. The American Saddlebred was developed as a horse of usefulness and beauty that could work in the field, pull a buggy or carriage, and have gaits that were smooth for travel under saddle. The ability of the American Saddlebred to perform lateral gaits (slow gait and rack) came from the Narragansett pacers, which were among the earliest known easy-riding pacers. The Narragansett pacers were derived from French Canadian pacers of Arabian and Andalusian descent that were bred 100 to 200 years before the American Revolutionary War and had a comfortable saddle gait. Early settlers brought these horses, known as saddlers, to Kentucky. During the late 1830s and 1840s, many of these easy-riding saddlers were bred to the Thoroughbred foundation sires, Denmark and Montrose. These crossbreeds were then bred to horses of trotting blood, from which the Standardbred breed was developed. Offspring of these crosses became favorite mounts of cavalry during the

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Civil War, because they had an easy gait, versatility, and an ability to withstand the pressures of war. On April 7, 1891, the American Saddlebred Breeders Association was founded in Louisville, Kentucky, and became the first all-American breed registry. In recent years the American Saddlebred has gained popularity in South Africa and has been crossed with European Warmblood and carriage bloodlines (e.g., Dutch Carriage Horse). During the 1980s, the National Show Horse was derived from American Saddlebred and Arabian lineage. The American Saddlebred ranges in height from 152 to 178 cm (15 to 17.2 hands; average 160 cm [15.3 hands]) and varies in weight from 455 to 545 kg. Colors include chestnut, bay, black, gray, golden (palomino), and spotted (chestnut, black, or bay mixed with white). As described in Modern Breeds of Livestock,1 the American Saddlebred has a strikingly long neck and considerable arch to the neck. The American Saddlebred is refined in appearance; has long, sloping pasterns that give spring to the stride; has a long, level croup; is strong and short-coupled; and has a back with high, well-defined withers above the level of the hips. The American Saddlebred is famous for refinement, smoothness, proportion, and a beautiful and handsome presentation and projects an alert, curious, expressive personality.

There are shows for American Saddlebreds throughout the United States and South Africa. The World Championship Horse Show is held each year in Louisville, Kentucky. Shows are run under the guidelines of USA Equestrian, which establishes rules, regulations, and drug-testing procedures. A veterinarian must be aware of current drug and medication rules, and failure to do so may result in fines and penalties to the horse, owner, and trainer.

SADDLEBRED GAITS The five gaits of the American Saddlebred and other gaited horses are as follows2: 1. Walk and flat walk—The flat walk is a relaxed, elastic, ground-covering, and collected four-beat gait, maintaining proper form and consistency in stride. The gait is required in pleasure classes. The animated walk is a highly collected gait, exhibiting much primp at a slow, regulated speed, with good action and animation. The gait can be a two- or four-beat gait and is performed with great style, elegance, and airiness of motion. 2. Trot—The trot is a natural, two-beat diagonal gait. A balanced trot features coordinated motion with straight, true shoulder motion of forelimbs, with flexing hocks carried close together. The gait is executed in a highly collected manner and should display the horse’s athletic ability. 3. Slow gait—The slow gait was developed from the pace to be a four-beat gait with each of the feet striking the ground separately. In the takeoff the ipsilateral front foot and hind foot start almost together, but the hind foot contacts the ground first. The slow gait is a highly collected gait with most of the propulsion coming from the hindquarters, whereas the forequarters assist in the pull of the final beats. The slow gait is not a medium rack. The slow gait is a restrained gait, executed slowly, but with true and distinct precision, and speed is penalized. The gait is high, lofty, brilliant, and restrained, denoting the style, grace, and polish of the horse. 4. Rack—The rack is a four-beat gait in which each foot meets the ground at equal, separate intervals. The gait is smooth and highly animated, performed with great action and speed in a slightly unrestrained manner.

Desired speed and collection are determined by the maximum rate at which a horse can rack in form. Racking in form should include the horse remaining with a good set head and should be performed by the horse in an effortless manner from the slow gait, at which point all strides become equally rapid and regular. Any tendency to become trotty, pacey, or hitchy-gaited is penalized. 5. Canter—The canter is slow, lofty, and fluid, with a definite three-beat cadence. High action, a good way of going, and proper collection are paramount. The propulsion is in the hindquarters, with the leading forelimb sustaining the concussion of the final third beat. A brief interval occurs when all feet are off the ground. The gait is an ambidextrous gait, executed on the lead that is toward the center of the ring to relieve stress and aid in balance.

TEN MOST COMMON LAMENESS CONDITIONS The 10 most common lameness conditions in show horses are the following: 1. Distal hock joint pain (tarsitis) 2. Gluteal myositis and back pain 3. Palmar heel pain, including contracted heels, sheared heels, quarter cracks, and navicular syndrome 4. Osteitis of the distal phalanx (pedal osteitis) 5. Osteoarthritis and osteochondrosis of the tarsocrural joint 6. Osteoarthritis and osteochondrosis of the fetlock joint 7. Osteoarthritis and osteochondrosis of the stifle joint 8. Suspensory desmitis 9. Tendonitis and desmitis, including deep digital flexor tendonitis, superficial digital flexor tendonitis, and desmitis of the accessory ligament of the deep digital flexor tendon 10. Splint exostosis

LAMENESS EXAMINATION The history of lameness and poor performance must be discussed with the trainer and rider to seek their perception. This should include noting any problems with the bridle and the way a horse pulls on the bit and bridle. Show horses with hindlimb lameness often fight the bit and try to lower the head, an observation known as diving in the bit. Horses that become one-sided in the bit may have contralateral hindlimb or ipsilateral forelimb lameness. Faulty bit and bridle placement may cause gait abnormalities particularly of the hindlimbs. Keeping the head up and fixed in position in a horse that dives in the bit is difficult. A horse with forelimb lameness is more likely to raise up out of the bridle. A horse cannot produce a gait properly or do proper gait transitions when being pushed into an uncomfortable bridle or if the rider is using the bit improperly. It is important to determine if the rider is using the bit to balance the horse or themselves. A rider using the bit poorly can induce a gait abnormality. Bit and bridle responsiveness is often a wild card that must be played during examination of the show horse for gait abnormalities and lameness. Problems with a particular gait may indicate the source of lameness. Back pain is seen in horses that have difficulty in the canter, a condition known as being broke in the middle. This occurs with asynchronous movement of the forelimbs and hindlimbs. Broke in the middle also can be caused by stifle pain that causes a reduction in the cranial phase of the stride. Most commonly, however, broke in the middle is caused by stringhalt. Stringhalt prevents the limb from moving forward

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at a time when the forelimbs are required to go faster, causing a mismatch in synchronization between the forelimbs and hindlimbs. Distal hock joint pain and back pain can cause a hitching motion of the hindlimbs, jerking the lame limb caudally and leaving the hocks behind the motion. Examination first begins in the stall before the horse is worked. Careful palpation with emphasis on the tendons, ligaments, joint capsules, and bulbs of the heels should be performed. Palpation of the back and gluteal muscles before working is important, because the horse can warm out of soreness in these areas. Digital pulse amplitudes should be assessed. The horse should be evaluated during movement under tack. Harness horses, road horses, and ponies should be examined while working with and without the over-check (checked up and without the check). Five- and three-gaited horses should be examined performing each gait going in both directions. Often horses are only lame while going in one direction or only in the turns. Horses with lameness from the hock distally are often worse with the lame limb on the inside, whereas those with pain located more proximally are lame with the lame limb on the outside of the turn. Forelimb lameness is usually worse with the affected limb on the inside. In most show horses flexion tests can be performed with a rider or in harness. The horse’s temperament may make this difficult, but I find that the horse being ridden or jogged in the cart after flexion is helpful.

DIAGNOSTIC ANALGESIA Diagnostic analgesia in show horses is similar to that described for other sport horses. I start distally and work proximally.

IMAGING CONSIDERATIONS Conventional and computed radiography are used extensively. Scintigraphy is most useful in horses with complex lameness, because primary and compensatory issues are difficult to differentiate. The solar scintigraphic view is mandatory to evaluate horses with palmar heel pain in which radiographs are negative, because modeling of the navicular bone and distal phalanx should be assessed carefully. Areas of increased radiopharmaceutical uptake in the distal phalanx may indicate excessive pressure that can be relieved by corrective shoeing. Thermography is of value in diagnosing tendonitis, sole pressure, muscle inflammation, and suspensory desmitis. Ultrasonographic examination is useful to confirm and assess damaged soft tissues and healing. Diagnostic arthroscopy is used occasionally.

SHOEING GAITED HORSES Shoeing gaited horses to assist with motion and gait transitions is an art form in itself. In general a long toe and high heel in front help to delay breakover and cause high knee action. In the past, weighted shoes and lead weights screwed into the bottom of shoe pads were used to induce animation. In recent years a transition to lighter is better has occurred, and now the focus is on fitness and training techniques to teach the horse to elevate its limbs to achieve animation. Shoeing depends to a great extent on the horse’s ability, conformation, and desired gait performance (e.g., five-gaited, three-gaited, or harness). For example, a three-gaited horse may have a long foot with long toe and heel length to delay breakover in the forefeet and hindfeet. This gives the extreme highly animated knee and hock action expected from a top three-gaited horse. In contrast, in a five-gaited horse a lower hind heel angle is used to assist with a longer hindlimb stride needed for the slow gait

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and rack. Compared with three-gaited horses, lighter and shorter front feet are maintained in five-gaited horses to promote speed at the trot and rack. Shoeing with high heels and long toes, with or without pads, predisposes the American Saddlebred to contracted heels, sheared heels, and quarter cracks. The recent use of cushion polymer compounds to maintain frog pressure is helpful, because frog pressure is lost with high heels and pads. Cushioned polymers placed in the collateral sulci (grooves) of the heel and over an atrophied frog have dramatically reduced hoof problems. Medial to lateral hoof balance is paramount.

SPECIFIC LAMENESS CONDITIONS Distal Hock Joint Pain and Distal Tarsitis There are two types of show horses, those that have distal hock joint pain and those that are getting it. Show horses with distal hock joint pain typically jerk the hindlimb caudally (hitching) and leave the hocks behind in motion. Many horses stab the toe, rather than landing normally with the heel first. Distal hock joint pain without radiographic abnormality is common in 2- and early 3-year-olds just starting to rack. As training and showing proceed, radiographic evidence of osteoarthritis, such as loss of joint space, can become apparent as early as 5 years of age and may be severe by 12 years of age. The tarsometatarsal joint is by far the most valuable point of intra-articular injection in show horses. Occasionally, injection of the centrodistal joint also is required. I prefer to use hyaluronan and a low-dose corticosteroid combination and recommend oral supplementation with glucosamine and chondroitin sulfate–containing products. Magnetic therapy appears beneficial. Horses with lameness that does not improve are considered candidates for shock wave therapy. Arthrodesis of the distal hock joints, using a drilling technique combined with laser ablation, is used in horses with severe pain. Although cunean tenectomy was once widely used, effects of the procedure are short-lived, and I do not recommend it. If the horse is hitching through the turns of a show ring, a 45º flat outside trailer is used on the hind shoe for support. The shoe is set back, and the toe is squared or rolled to improve breakover.

Gluteal Myositis and Back Pain Show horses are prone to gluteal myositis and back pain, which are often secondary to primary distal hock joint pain. A willing horse hyperflexes its back to compensate for lower hindlimb pain. The middle gluteal muscle passes over the greater trochanter of the femur and the trochanteric bursa. Gluteal myositis and tendonitis are common sequelae to distal limb pain, but they can cause primary lameness. Trochanteric bursitis (whorl bone disease) can accompany gluteal myositis. In horses with subacute gluteal myositis, upper limb flexion may stretch the gluteal muscles and produce a transient improvement in gait. Transient improvement may be seen by gently massaging the greater trochanter and gluteal muscles. However, in horses with chronic myositis with involvement of the trochanteric bursa, deep massage and pressure may make lameness worse. Horses with subacute primary gluteal myositis commonly have a tight-rope trot (plaiting). Plaiting is associated with distraction and rotation of the hindlimb, with subsequent lateral movement of the hip, motion that may cause gluteal muscle strain. Horses that plait usually have base-narrow conformation, and corrective trimming in the form of spreading the stance (lowering the outside hoof walls) may help. Back pain is identified easily using digital pressure along the thoracolumbar region, abaxial to the spinous processes. Many horses are so painful that one can almost put them on the ground with digital pressure. Diagnostic analgesia usually

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is not necessary. However, small amounts of local anesthetic solution injected at numerous sites along the affected muscles may give enough relief to allow evaluation for lameness that has been hidden by back or gluteal pain. Management of horses with gluteal myositis and back pain requires a multifaceted approach, including local injection of Sarapin and corticosteroids. In most horses non-steroidal antiinflammatory drugs (NSAIDs), methocarbamol, electrical stimulation, magnetic therapy, therapeutic ultrasound, and anti-concussion saddle pads are used in various combinations. Exercise regimens using stretching and flexing during the warm-up period are also beneficial. Acupuncture and chiropractic modalities often are used and can be of benefit if performed by skilled practitioners. Shock wave therapy may prove to be beneficial. Diagnosis and treatment of primary lameness problems, if present, are of utmost importance.

Palmar Heel Pain Because show horses are shod intentionally with a high heel and long toe to produce high motion, they are prone to contracted and sheared heels. Full or wedge pads are often applied to achieve the desired motion, and the lack of frog pressure can cause atrophy of the soft tissues of the heel. Without proper frog support, the bulbs of the heel contract and sheared heels often develop. As the heels contract or sheared heels develop, more stress is applied to the quarters, predisposing the hooves to quarter cracks. Differentiation of causes of palmar heel pain is critical but difficult, because palmar digital analgesia affects these conditions and navicular syndrome similarly. Recently more concern has arisen about maintaining frog pressure. Soft, acrylic polymers are now used for frog support in horses with frog atrophy. Turnout for several months, during which the horse is barefoot, may help. Expansion springs can be used to assist in re-establishing proper heel conformation. Severe quarter cracks are repaired using the techniques of lacing, applying screw compression plates, or nailing. Floating the heel and quarter located under the crack is important to reduce weight bearing, allowing showing to continue. Navicular disease is not uncommon, but in horses without abnormal radiological findings the diagnosis should be confirmed using scintigraphy. The aforementioned conditions of the hoof capsule and supporting soft tissues are much more common. Treatment of soft tissue causes of palmar heel pain involves maintaining comfort while proper anatomy is re-established. Corrective shoeing, NSAIDs, and long-term foot blocks often are used. If navicular disease is confirmed, intra-articular treatment of the distal interphalangeal joint using hyaluronan and corticosteroids is recommended. Drugs aimed at improving peripheral perfusion or decreasing intra-osseous pressure such as isoxsuprine may be useful with NSAIDs, long-term foot blocks, and corrective shoeing. Shock wave therapy appears promising in managing palmar heel pain.

Osteitis of the Distal Phalanx In horses with high stepping gaits the distal phalanx is prone to injury. Trauma to the solar margin such as bruising and fracture occurs. A careful evaluation for improper sole pressure or medial to lateral hoof imbalance should be performed. Wellexposed and well-positioned radiographs are essential. Digital venography may reveal compression of blood vessels within the hoof capsule and is useful to pinpoint a location of trauma. Fractures of the distal phalanx are rare. Palmar scintigraphic views are useful to diagnose fractures and other areas of distal phalanx trauma and can help to formulate a corrective shoeing plan. Thermography may be useful for diagnosis of distal phalanx trauma. For horses without distal phalanx fracture, management includes corrective balancing and shoeing to relieve improper

sole pressure and to provide support, NSAIDs, and isoxsuprine. If effusion of the distal interphalangeal joint is present, intraarticular treatment with hyaluronan and corticosteroids may help.

Osteoarthritis and Osteochondrosis of the Tarsocrural Joint Lameness of the tarsocrural joint is not as common as distal hock joint pain. Osteochondrosis of the tarsocrural joint in show horses is similar to that described for other sport horses. The most common location is the distal intermediate ridge of the tibia. Although show horses with osteochondrosis lesions may compete successfully without surgical intervention, effusion and capsulitis are indications that surgery should be performed. Prognosis after arthroscopic surgery is favorable. However, prognosis for for show horses with trochlear ridge lesions is guarded. Osteophytes and small fragments of the distal, medial trochlear ridge are not a major source of lameness. The diagnosis of osteoarthritis of the tarsocrural joint is derived from the results of physical examination, flexion tests, diagnostic analgesia, and radiography. Horses with early osteoarthritis of the tarsocrural joint are managed with intraarticular injections of hyaluronan, with or without corticosteroids. Oral supplementation with glucosamine and chondroitin sulfate-containing compounds appears beneficial. Intramuscular and intravenous administration of polysulfated glycosaminoglycans and hyaluronan, respectively, are helpful. NSAIDs may be necessary. Horses with chronically boggy hocks usually respond well to routine intra-articular medications, but if they are refractory, I add 0.5 ml atropine sulfate.

Osteoarthritis and Osteochondrosis of the Fetlock Joint Conditions of the fetlock joint in show horses are essentially the same as seen in other sport horses. The most common conditions are osteochondral fragments of the proximal dorsal aspect of the proximal phalanx and sesamoiditis. Plantar process osteochondritic fragments are uncommon but are recognized. During prepurchase examinations, I obtain lateromedial radiographic views of each metatarsophalangeal joint specifically to evaluate for plantar process fragments. Fractures of the proximal sesamoid bones occur infrequently. Osseous cyst-like lesions of the distal aspect of the third metacarpal bone and osteochondritis dissecans lesions of the sagittal ridge of the third metacarpal bone occur infrequently and are less devastating than in racing breeds. Mineralized proliferative synovitis lesions are often confused with osteochondral fragments, but show horses with this condition have a favorable prognosis. Primary osteoarthritis of the fetlock joint is seen commonly in show horses that wing the lower limb while moving, but radiographs are often negative. Diagnosis of lameness of the fetlock joint is routine. Nuclear scintigraphy is most useful in diagnosing sesamoiditis. Arthroscopic removal of osteochondral fragments of the proximal phalanx is not always necessary, because many show horses compete well and require little maintenance therapy when fragments involve the front fetlock joints. When fragments involve the hind fetlock joints, arthroscopic removal is recommended, because these horses have gait abnormalities characterized by a skipping motion that are accentuated at the rack and slow gait. Horses with sesamoiditis respond well to corrective shoeing (lowering the heel), NSAIDs, isoxsuprine, and injection of hyaluronan and corticosteroids into the fetlock joint. Shock wave therapy appears to be effective in managing horses with chronic sesamoiditis and collateral ligament damage.

Osteoarthritis and Osteochondrosis of the Stifle Joint Osteoarthritis of the stifle joints is a common lameness in young horses, particularly in horses being pushed to perform

CHAPTER 123

• Lameness in the American Saddlebred and Other Trotting Breeds with Collection

at a young age. Normal weight distribution favoring the hindlimbs, coupled with learning the slow gait and rack at a young age, predispose the horses to stifle pain. Horses with stifle lameness usually have a shortened cranial phase of the stride and are said to be humping up in the hip at the beginning of the caudal phase of the stride. Lameness often is pronounced with the limb on the outside of the ring and is worse in the turns. Diagnosis is made using gait analysis, diagnostic analgesia, radiography and, if necessary, nuclear scintigraphy. Subchondral bone cysts of the medial femoral condyles and osteochondritis dissecans of the trochlear ridges of the femur are commonly diagnosed in young show horses with stifle effusion. Arthroscopic surgery, debridement, and fragment removal are recommended in those horses with effusion and lameness. Prognosis for a five-gaited horse with osteochondritis dissecans of the stifle is guarded, even with surgery. Many of these horses can compete successfully in other divisions such as harness, pleasure driving, and equitation. Distal patellar fragmentation and cartilage damage is seen in older horses, and horses respond well to intra-articular injections of hyaluronan and corticosteroids. Arthroscopic surgery is recommended in horses refractory to this therapy. Lateral luxation of the patella occasionally is diagnosed in foals and has a guarded prognosis. Upward fixation of the patella is seen in young horses with under-developed quadriceps muscles. Most improve with training in a jog cart to build up the hindlimb musculature in lieu of intense riding and training. Trainers must be advised to be patient. Medial patellar desmotomy should be used as a last resort and should be done only if radiographs of the stifle are negative. Horses with early osteoarthritis and negative radiographs are managed by decreasing training intensity and implementing a jogging program to develop the hindlimb musculature. A weighted drag behind the cart is added later, before the normal riding program resumes. Internal blisters are used commonly. Intra-articular injection of hyaluronan and corticosteroids alleviates clinical signs, but without modification of exercise the results are short-lived. Horses with chronic osteoarthritis are maintained using intra-articular injections, oral supplements, intramuscularly and intravenously administered polysulfated glycosaminoglycans, and NSAIDs.

Suspensory Desmitis Show horses with long pasterns and high heels are prone to suspensory desmitis because the fetlock drops excessively and stretches the suspensory ligament. Show horses trained in deep footing (sand or mud) are at increased risk for suspensory desmitis. Avulsion fracture of the third metacarpal bone may occur in association with suspensory desmitis. Suspensory desmitis is more common in the forelimb than in the hindlimb. Treatment of show horses with suspensory desmitis involves rest, NSAIDs, periligamentous injection of corticosteroids, leg sweating, magnetic therapy, and support wraps. Rest includes hand walking, because horses with suspensory desmitis appear to respond better to limited, controlled exercise than to stall rest alone. The heels should be lowered and a palmar or plantar extension applied. Shock wave therapy has been extremely beneficial in show horses with suspensory desmitis, particularly those with proximal suspensory desmitis. I used to recommend bone marrow injection in horses with refractory suspensory desmitis, but the advent of shock wave therapy has decreased the need for surgery dramatically.

Tendonitis Performing in deep, muddy, outdoor show rings and a longtoe, high-heel hoof conformation predispose horses to tendonitis of the superficial digital flexor and deep digital flexor tendons and desmitis of the accessory ligament of the deep

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digital flexor tendon. As a rule the tendonitis is not nearly as devastating in show horses as in racehorses. Horses with tendonitis respond well to sweats, peritendonous injection of corticosteroids, NSAIDs, magnetic therapy, and shock wave therapy. Rarely, show horses require tendon splitting and desmotomy of the accessory ligament of the deep digital flexor tendon or the accessory ligament of the superficial digital flexor tendon. Serial ultrasonographic examinations are important to monitor healing.

Splint Exostoses Splint exostoses are caused by lunging young horses in tight circles too fast and too long. Direct trauma from interference can cause splint exostosis or fracture. Once splints become inactive, they rarely cause lameness, unless the mineralization impinges on the suspensory ligament or if the exostosis is so large it repeatedly becomes traumatized. Diagnosis is made by palpation and radiographic assessment for fracture. Treatment consists of leg sweats, subcutaneous injections of corticosteroids over the exostosis, and shock wave therapy in horses refractory to sweating and injections. Surgical removal of distal splint bone fracture fragments, large exostoses, or nonunions that impinge on the suspensory ligament should be performed.

OTHER LAMENESS CONDITIONS Stringhalt Stringhalt is common in the show horse and needs to be differentiated from other hindlimb lameness conditions. Local anesthetic solution (5 ml at each of three sites) is injected into the lateral digital extensor muscle, and the horse is observed while ridden 10 minutes later. If gait is improved, I recommend lateral digital myotenectomy. Previous trauma to the lateral or common digital extensor tendons can predispose horses to stringhalt (see Chapter 44).

Semimembranosus/Semitendinosus Myositis Myositis of semimembranosus or semitendinosus sometimes can mimic stringhalt and cause bizarre gait abnormalities. Horses and ponies (particularly road ponies) show restriction of the cranial phase of the stride. The hindlimb appears to hang up in a flexed position or the horse is short-strided. Typically a trainer says the horse cannot get underneath himself. This occurs particularly in gaited horses that cannot perform the slow gait or rack. This condition may be an early form of fibrotic myopathy. Diagnosis involves injecting 5 ml of local anesthetic solution in three to four sites each in the semimembranosus and semitendinosus muscles. The horse is evaluated ridden in 10 minutes, and often the change is dramatic. Short-lived benefit is seen by injecting the involved muscles with Sarapin and a corticosteroid and using electrotherapy. The best solution appears to be tenotomy of the medial branch of the semitendinosus muscle, the same procedure described for surgical management of horses with fibrotic myopathy.

Tibial Stress Fractures Young show horses, particularly young, talented five-gaited prospects, can become suddenly difficult to gait. Typically the trainer says, “The horse was one of the best young prospects I ever had and then suddenly I lost him,” or “Everything came undone.” Tibial stress fractures are the show horse counterpart to bucked shins in the Thoroughbred. Diagnosis is difficult and usually involves ruling out everything else first and proceeding to nuclear scintigraphy, the most consistent and best method of diagnosis. Horses are given 60 days of jogging and are re-assessed.

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Hindlimb Extensor Tenosynovitis

Cervical Myositis

The common digital extensor tendon sheath at the level of the hock can become inflamed and distended, a condition that is particularly prevalent in talented gaited horses. There is usually an indentation of the distended sheath just below the hock, caused by constriction by the retinaculum. Although lameness is unusual, severe distention of the sheath may cause a stiff gait, because the horse cannot flex the hock normally. Tenosynovitis may be confused with bog spavin. If left untreated, synovium becomes hypertrophic, and movement of synovium under constricting retinaculum causes a hitch in hindlimb gait. Treatment consists of draining synovial fluid and injecting a combination of hyaluronan, corticosteroids, and 0.5 ml of atropine sulfate. Massaging with dimethylsulfoxide and a corticosteroid is also beneficial.

The degree of neck flexion required in show horses often causes pain, particularly in young horses. Older horses may develop osteoarthritis of the facet joints. Horses with cervical myositis and pain often are observed to be fighting the bit. Diagnosis is made by palpation. Injection of Sarapin and corticosteroids in the affected muscles, methocarbamol, electrical stimulation, and NSAIDs are used. Acupuncture and chiropractic procedures also may be beneficial. Shock wave therapy may be beneficial in horses with osteoarthritis of the facet joints.

CHAPTER •

REFERENCES 1. Briggs HM: Modern breeds of livestock, ed 4, New York, 1980, MacMillan. 2. 2002 USA Equestrian rule book, Lexington, KY, 2002, USA Equestrian, Inc.

124

Lameness in the Arabian and Half-Arabian Show Horse Jeffrey A. Williams and Bradley S. Root

HISTORY OF THE ARABIAN

HISTORY OF THE SPORTING EVENT

The Arabian is one of the oldest breeds in the world. The horse originated in the deserts of the Middle East and was used by the Bedouins for transportation and in battle. The Arabian breed was noted for its speed and endurance. Three Arabian stallions (the Godolphin Barb, Byerley Turk, and Darley Arabian) imported to Europe during the late 1600s and early 1700s became the foundation of a new breed of horse, the Thoroughbred. Today, 93% of all modern Thoroughbreds can be traced to these three sires. In the 1800s many royal families of Europe established Arabian stud farms. Two of the most notable were the Polish National Arabian Stud in Poland and the Crabbet Arabian Stud in England. The Arabian is thought to have an influence on many of the light horse breeds that have developed throughout history. A typical Arabian ranges from 14.1 to 15.1 hands in height. The American Horse Show Association breed standards describe the Arabian as having a small, slightly dished face with large eyes set well apart, small ears, deep and wide jowls, a small muzzle, and large nostrils. The horse should have a long, arched neck; a long, sloping shoulder; wellsprung ribs; a short back with a relatively horizontal croup; and natural, high tail carriage. The limbs should have large, well-defined joints, short cannon bones, sloping pasterns of good length, and round feet of proportionate size.1 The Half-Arabian studbook originated with the U.S. Army Remount Service after World War II and was acquired by the International Arabian Horse Association in 1951. HalfArabians must have a registered purebred Arabian sire or dam. The Anglo-Arabian is a cross between an Arabian and a Thoroughbred, whereas the more recently developed National Show Horse is a cross between an Arabian and a Saddlebred. Many Half-Arabians are double registered.

The International Arabian Horse Association was created in 1950 to join the local and regional clubs across America into one united association. The International Arabian Horse Association promotes and coordinates all Arabian and HalfArabian horse show activities and develops horse show rules. The International Arabian Horse Association also maintains the Half-Arabian and Anglo-Arabian registries, whereas the Arabian Horse Registry of America maintains the registry and pedigree records for purebred Arabian horses in the United States and Mexico. The first U.S. National Arabian and Half-Arabian Show was held in 1966. The U.S. National Show is held in October and alternates yearly between Louisville, Kentucky, and Albuquerque, New Mexico. A separate Youth National show for riders under 18 years old is held in July of each year in Albuquerque. The Canadian National Horse Show is held in August in Regina, Saskatchewan. The United States and Canada are separated into 18 regions, each of which holds an annual show. Horses can qualify for the national show by placing in the top five at a regional show or by winning a championship or reserve championship at a Class A show. Some of the major shows other than the regionals and nationals are the Scottsdale Show (Arizona), the Buckeye Show (Ohio), the Pacific Slopes Show (California), the East Coast Championship (Pennsylvania), and the Pro-Am Challenge (Texas). Major international shows are held in England, France, South America, and Australia. Performance classes for Arabian and Half-Arabian horses cover a broad spectrum and are listed in Box 124-1. Each of these classes is held separately for Arabians and Half-Arabians. They may be divided further into sections for junior owner, adult amateur owner, amateur owner, junior exhibitor, and

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Lameness in the Sport Horse

Hindlimb Extensor Tenosynovitis

Cervical Myositis

The common digital extensor tendon sheath at the level of the hock can become inflamed and distended, a condition that is particularly prevalent in talented gaited horses. There is usually an indentation of the distended sheath just below the hock, caused by constriction by the retinaculum. Although lameness is unusual, severe distention of the sheath may cause a stiff gait, because the horse cannot flex the hock normally. Tenosynovitis may be confused with bog spavin. If left untreated, synovium becomes hypertrophic, and movement of synovium under constricting retinaculum causes a hitch in hindlimb gait. Treatment consists of draining synovial fluid and injecting a combination of hyaluronan, corticosteroids, and 0.5 ml of atropine sulfate. Massaging with dimethylsulfoxide and a corticosteroid is also beneficial.

The degree of neck flexion required in show horses often causes pain, particularly in young horses. Older horses may develop osteoarthritis of the facet joints. Horses with cervical myositis and pain often are observed to be fighting the bit. Diagnosis is made by palpation. Injection of Sarapin and corticosteroids in the affected muscles, methocarbamol, electrical stimulation, and NSAIDs are used. Acupuncture and chiropractic procedures also may be beneficial. Shock wave therapy may be beneficial in horses with osteoarthritis of the facet joints.

CHAPTER •

REFERENCES 1. Briggs HM: Modern breeds of livestock, ed 4, New York, 1980, MacMillan. 2. 2002 USA Equestrian rule book, Lexington, KY, 2002, USA Equestrian, Inc.

124

Lameness in the Arabian and Half-Arabian Show Horse Jeffrey A. Williams and Bradley S. Root

HISTORY OF THE ARABIAN

HISTORY OF THE SPORTING EVENT

The Arabian is one of the oldest breeds in the world. The horse originated in the deserts of the Middle East and was used by the Bedouins for transportation and in battle. The Arabian breed was noted for its speed and endurance. Three Arabian stallions (the Godolphin Barb, Byerley Turk, and Darley Arabian) imported to Europe during the late 1600s and early 1700s became the foundation of a new breed of horse, the Thoroughbred. Today, 93% of all modern Thoroughbreds can be traced to these three sires. In the 1800s many royal families of Europe established Arabian stud farms. Two of the most notable were the Polish National Arabian Stud in Poland and the Crabbet Arabian Stud in England. The Arabian is thought to have an influence on many of the light horse breeds that have developed throughout history. A typical Arabian ranges from 14.1 to 15.1 hands in height. The American Horse Show Association breed standards describe the Arabian as having a small, slightly dished face with large eyes set well apart, small ears, deep and wide jowls, a small muzzle, and large nostrils. The horse should have a long, arched neck; a long, sloping shoulder; wellsprung ribs; a short back with a relatively horizontal croup; and natural, high tail carriage. The limbs should have large, well-defined joints, short cannon bones, sloping pasterns of good length, and round feet of proportionate size.1 The Half-Arabian studbook originated with the U.S. Army Remount Service after World War II and was acquired by the International Arabian Horse Association in 1951. HalfArabians must have a registered purebred Arabian sire or dam. The Anglo-Arabian is a cross between an Arabian and a Thoroughbred, whereas the more recently developed National Show Horse is a cross between an Arabian and a Saddlebred. Many Half-Arabians are double registered.

The International Arabian Horse Association was created in 1950 to join the local and regional clubs across America into one united association. The International Arabian Horse Association promotes and coordinates all Arabian and HalfArabian horse show activities and develops horse show rules. The International Arabian Horse Association also maintains the Half-Arabian and Anglo-Arabian registries, whereas the Arabian Horse Registry of America maintains the registry and pedigree records for purebred Arabian horses in the United States and Mexico. The first U.S. National Arabian and Half-Arabian Show was held in 1966. The U.S. National Show is held in October and alternates yearly between Louisville, Kentucky, and Albuquerque, New Mexico. A separate Youth National show for riders under 18 years old is held in July of each year in Albuquerque. The Canadian National Horse Show is held in August in Regina, Saskatchewan. The United States and Canada are separated into 18 regions, each of which holds an annual show. Horses can qualify for the national show by placing in the top five at a regional show or by winning a championship or reserve championship at a Class A show. Some of the major shows other than the regionals and nationals are the Scottsdale Show (Arizona), the Buckeye Show (Ohio), the Pacific Slopes Show (California), the East Coast Championship (Pennsylvania), and the Pro-Am Challenge (Texas). Major international shows are held in England, France, South America, and Australia. Performance classes for Arabian and Half-Arabian horses cover a broad spectrum and are listed in Box 124-1. Each of these classes is held separately for Arabians and Half-Arabians. They may be divided further into sections for junior owner, adult amateur owner, amateur owner, junior exhibitor, and

CHAPTER 124

• Lameness in the Arabian and Half-Arabian Show Horse

Box • 124-1 Performance Classes for Arabian and Half-Arabian Horses Park Horse English Pleasure Country English Pleasure Hunter Pleasure English Show Hack Hunter Jumper Dressage Formal Driving Pleasure Driving Country Pleasure Driving Roadster Combination (Driving and Riding) Mounted Nature Costume Ladies Side Saddle Western Pleasure Reining Working Cow Horse Trail Cutting Equitation (Hunter Seat, Saddle Seat, and Stock Seat): youth classes only Western Horsemanship (youth only)

amateur. The Park horse has a strong animated trot, with the forearm horizontal and the leg extending fully forward. The hock has a well-raised driving action. The walk and canter are animated and collected. The English Pleasure horse is shown at a walk, trot, strong trot (faster and more animated than the normal trot), canter, and hand gallop. Its gaits are less animated than the Park horse although the forearm, at the trot, is horizontal. The same gaits are used in the Country English Pleasure class, but horses have lower leg action, and high action is penalized. The Country English Pleasure horse must also halt, stand quietly, back, and walk off on a loose rein. With all pleasure classes the horse must give the appearance of being a pleasure to ride. Park and English Pleasure horses are shown with the head carried high and considerable flexion at the poll. Saddle seat attire is required. In the English Show Hack class the horse must perform each gait (walk, trot, and canter) in a normal, collected, and extended manner. A transition between gaits should be noticeable and high knee action is not expected. Horses in the Hunter Pleasure division are shown under saddle at the walk, trot, canter, and hand gallop. The neck should be carried lower, the head should be carried with less bend at the poll and the horse should be in a generally longer frame than the English Pleasure or Show Hack horse. Working Hunters are shown over a course of fences set at levels of 0.6 to 1 m and are judged on performance, manners, and soundness. Jumpers are shown over courses of jumps that vary in height from 0.9 to 1.05 m. The maximum width (spread) is 1.5 m. Horses in driving classes are shown pulling a four-wheeled (Formal and Pleasure) or two-wheeled (Pleasure and Country Pleasure) vehicle. The gaits judged in the Formal, Pleasure, and Country Pleasure driving classes correspond to the Park, English Pleasure, and Country English Pleasure classes under saddle. The Roadster is a driving class, which focuses on the trot at three different speeds.

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The Western Pleasure horse is shown at the walk, jog (trot), lope (slow canter), and hand gallop. Ideally, contact with the reins is light, the head is carried low (approximately at the level of the withers), and the jog and lope are slow, easy gaits. The Working Western horse classes include reining, working cow horse, trail, cutting, and Western riding.

TRAINING: IMPACT OF INDUSTRY The Arabian and Half–Arabian are versatile breeds, as shown by the many sports in which they compete. When appropriate, differences between the two breeds are specified. These include halter, endurance (see Chapter 119), pleasure, jumping, dressage, reining, cutting, and racing (see Chapter 112). Young performance horses are not shown under saddle until they are 3 years old. They then compete in futurity classes for horses 3 years of age or junior horse classes for horses 5 years of age or younger. Because these horses do not compete in performance classes until 3 years of age, this allows more time for adequate skeletal development compared with racehorses and Quarter Horses that start training before 2 years of age. This and the lack of speed work help minimize injuries such as fractures, early osteoarthritis, and severe soft tissue injuries, which are common in the racehorse. The reason that training of Arabian show horses is started later than some other breeds may be partly because of smaller size and late maturation, but it is also related to the fact that no performance classes are available for 2-yearolds, and therefore no economic incentives exist to start intensive training early. Early training and conditioning typically involve a substantial amount of work in a round pen or by lunging. Excessive training in small circles causes increased torque on the distal interphalangeal joint, the navicular bone, and the distal phalanx. Seeing young horses trained in this manner and developing bilateral forelimb lameness localized to the distal interphalangeal joint is not uncommon. This type of training also causes increased stress on the other joints and support structures of the forelimbs and hindlimbs. These problems tend to be exacerbated by uneven and hard footing. Rules govern the shoeing of the Arabian and Half-Arabian show horses. A maximum shoe weight of 14 oz (392 g) excluding pads and nails is allowed. The maximum toe length including the shoe and any pads is 41⁄2 inches (11.43 cm). Pads are allowed, as are normal packing materials such as tar, oakum, and silicone. No weights are allowed under the pad. Foot length, shoe weight and shape, and pad usage are individualized for each horse to optimize the height and arc of flight of the forelimbs and hindlimbs. In English Pleasure horses, a common shoe is the toe-weighted shoe constructed by forging more steel in the toe of the shoe. The long foot and weighted shoes are used to enhance forelimb motion. Unfortunately this can contribute to strain on the suspensory ligament (SL) and joints of the lower limb. In all performance divisions horses are shown in a collected frame. In each division the type of work performed, the body position required, and the conformational defects of the individual horse contribute to the common lameness conditions. Differences are apparent in gaits, degrees of collection, and head and neck position in the various divisions. In the English Pleasure division, for example, the degree of collection, neck elevation, and poll flexion required shift weight to the hindlimbs and increases the work of the back and abdominal muscles. These positional factors can cause lameness of the hindlimbs (especially involving the stifle and SL) and back pain. In the Western Pleasure and Reining divisions, similar problems are seen because of the amount of collection required. These horses also incur a variety of lameness conditions because they commonly are worked for longer periods of

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time than English Pleasure horses. In the Western Pleasure and Reining classes, because any departure from a quiet, steady position is penalized, fatigue is part of the class preparation.

CONFORMATION AND LAMENESS Mild to moderate carpus valgus and toed-out conformation commonly are seen and do not appear to have a major impact on soundness (Fig. 124-1). One reason is that the carpus is not a common location for lameness. If these conformational faults are severe, horses are at risk of suspensory desmitis. Horses with long sloping pasterns, back-at-the-knee conformation, or offset knees are also predisposed to suspensory desmitis. These conformational faults are more common in the Half-Arabian and National Show Horse than in purebred Arabians and are more common in certain pedigrees. Horses with low, underrun heels certainly are prone to lameness from palmar heel pain. This fault can be difficult to correct, even with careful attention to shoeing and trimming. A small, upright, contracted foot (club foot) can be a source of lameness and appears to be increasing in incidence. Inflammation of the soft tissues such as the SL, accessory ligament of the deep digital flexor tendon, and distal sesamoidean ligaments tends to be more common in horses with club foot conformation.

A long, weak (sway) back and a short croup may predispose horses to soreness in the thoracolumbar, sacroiliac, and gluteal areas. Because problems in these areas are a common cause of poor performance, this type of conformation is a serious fault. Horses with cow-hocked conformation are the rule rather than the exception, but this conformation seems to have little effect on soundness.

TEN MOST COMMON LAMENESS CONDITIONS The 10 most common lameness conditions of the Arabian and Half-Arabian show horse are as follows: 1. Bruised and inflamed feet 2. Osteoarthritis of the distal interphalangeal joint and palmar heel pain 3. Suspensory desmitis 4. Osteoarthritis of the stifle joints 5. Thoracolumbar, sacroiliac, and gluteal pain 6. Osteoarthritis of the metacarpophalangeal and metatarsophalangeal joints 7. Distal hock joint pain 8. Splint bone injuries 9. Osteoarthritis of the proximal interphalangeal joint 10. Desmitis of the accessory ligament of the deep digital flexor tendon

LAMENESS EXAMINATION History When describing lameness, trainers often comment that problems occur or are more noticeable during the first direction or the second direction. This refers to the directional order in which rail classes are run. In the first direction horses enter the ring and travel counterclockwise, and in the second direction horses travel clockwise. Important questions regarding history include the division in which the horse competes, onset, degree and progression of the lameness, previous or current treatment and response to therapy. Additional information that can be helpful includes knowing which direction is harder for the horse at the trot (jog) and canter (lope), whether the horse pulls unevenly on the reins, whether the horse tracks straight in each direction, whether the horse falls out of leads behind (in the hindlimbs) in corners, and whether the rider rides the correct or incorrect diagonal in each direction. The age of the horse is important, because osteochondrosis is more likely to affect young horses recently started into training than older animals, but in older horses osteoarthritis is common. It is important to find out when the horse was last shod, and if any recent shoeing changes have been made. Altering medial to lateral hoof balance or hoof angle may increase pressure in certain areas and lead to bruising of the heel or sole. Increasing the hoof angle by raising the heel may increase load on the SL, which may lead to suspensory desmitis. The type and condition of the footing the horse has been working on is important to consider. Often footing at shows is less than ideal and in many cases is too hard, leading to the development of bruised feet. Conversely, if footing is too deep, it may lead to tendon and ligament injuries.

Visual Examination Fig. 124-1 A 4-year-old Half-Arabian with toed-out, carpus valgus, back-at-the-knee conformation. These are common conformation faults in the Arabian and Half-Arabian breeds and may predispose the horses to suspensory desmitis.

Stepping back and visually examining the horse for overall symmetry of the limbs and upper body is helpful. Asymmetry of upper limb muscle groups may be a sign of atrophy from denervation, chronic lameness, or neurological disease. Asymmetry in the height and position of the point of shoulder, the tubera sacrale, the tubera coxae, or the tubera ischii

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can indicate subluxations or fractures. The size, shape, and symmetry of the feet are important to note. Abnormalities such as club feet, underrun or sheared heels, growth rings, dished dorsal hoof walls, and contracted heels are some of the more common problems. Joint swelling, soft tissue swellings, poor conformation, scars, and abnormal structures such as splints are recognized quickly.

Palpation Thorough palpation of the lower limbs is performed with the horse in weight-bearing and non–weight-bearing positions. Degree of joint filling; abnormal contours of bones, tendons, and ligaments; and intensity of the digital pulses are best evaluated while the horse is bearing weight. With the limb elevated, painful response to palpation of tendons, ligaments (origins and insertions), and splints; pain on joint flexion; and range of motion of joints are assessed. In the Arabian and Half-Arabian show horses, in contrast to the racehorse, moderate filling of the metacarpophalangeal/metatarsophalangeal joint capsules is common and should not be over-interpreted. Effusion of the distal interphalangeal and stifle joints (especially the medial femorotibial joint) tends to be clinically relevant. To evaluate filling in the medial femorotibial joint, it is helpful to have the horse bearing weight with the limb being palpated slightly ahead of the opposite limb and perpendicular to the ground. Response of the Arabian and Half-Arabian to palpation of the SL varies greatly, depending on the horse. Differences between limbs should be considered important, and change in the response of an individual over time is noteworthy. Many horses have a painful response to palpation of the SL but have primary lameness localized to the foot. Possibly the SL is painful because of a compensatory gait caused by a primary foot problem. In contrast, absence of inducible pain, especially in the proximal suspensory region does not rule out this area as a source of pain causing lameness. Careful palpation of the thoracolumbar spine and upper body is useful in diagnosing the reason for poor performance and lameness. Asymmetry, abnormal contours, and painful response to palpation are important to assess. Particular attention should be given to the thoracolumbar musculature, the spinous process, and the sacral tuberosities, because these areas commonly are involved in horses that perform poorly.

Hoof Tester Examination Many Arabian and Half-Arabian show horses wear full pads in front during training and showing. Although sometimes inconvenient, especially at a competition, removing the shoe and pad for a complete hoof tester examination is helpful if the veterinarian suspects a foot problem. Some indication of painful areas may be obtained with the shoe and pad on, but many areas can be missed. Bruised heels and soles are common, especially at shows where footing may be too hard and horses are being worked longer than normal. Bruised heels and soles are two of the most common sources of lameness. Improvement in lameness can be dramatic if areas of bruising can be trimmed to reduce pressure or if the shoe is modified to eliminate weight bearing on a bruised area. Many horses are painful when the hoof testers are applied across both heels, but show no pain on the individual heel, soles, or bar of the hoof. These horses are just as painful with the shoe and pad on, and therefore this situation may relate to structures deeper in the heel of the foot, rather than simply bruising of the sole. Medial to lateral hoof imbalances may contribute to lameness and should be addressed whenever lower limb lameness exists and when sore feet have been identified with the hoof testers. In general, pain is associated with the high side of the foot or that area making ground contact first.

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Pain in the toe region occurs less commonly than in the heel, especially for horses in the English and Park divisions, and likely is related to the way the foot is trimmed. These horses usually have a long toe and thick sole that may protect sensitive structures from bruising and exaggerate heel first landing in the forelimbs. When pain over the middle of the frog is detected, bruising, palmar heel pain, or navicularrelated pain should be considered. Diagnostic analgesia should be performed to confirm the relevance of hoof tester examination, because false-positive reactions occur.

Flexion Tests Flexion tests are important, but responses should be interpreted carefully. A painful response to flexion of joints and the degree of lameness should be assessed. Many false-positive lower limb flexion tests occur in Arabian and Half-Arabian show horses. Many horses without lameness show pain to static flexion and a positive response when trotted. In a lame horse a lower limb flexion test is not specific. For example, in lame horses positive to a lower limb flexion test lameness may be localized anywhere from the foot to the distal metacarpal region. Carpal flexion usually is performed only in the static situation because we do not feel that substantial additional information is gained by trotting the horse. Horses that resent carpal flexion may have proximal suspensory desmitis, superficial digital flexor tendonitis, or carpal tenosynovitis, because bony injury of the carpus itself is unusual in Arabian and Half-Arabian show horses. Initially the entire hindlimb is held in flexion and then individual lower limb flexion and upper limb flexion tests are performed. We attempt to flex the stifle independently of the tarsus by holding the distal tibia upward and behind the horse for 60 seconds. These flexion tests are not specific, but they may increase the index of suspicion in a certain area. For example, horses with hindlimb proximal suspensory desmitis or distal tarsitis respond positively to upper limb flexion and must be differentiated based on the results of other tests. Mildly positive hindlimb flexion tests are seen in sound horses that are actively training and showing. These mildly positive flexion tests may be related to subtle lameness or could be a normal response. For horses that have been competing successfully to have a moderate to severe positive response to a lower limb flexion test after a lengthy show is not unusual. This fact needs to be taken into account when prepurchase examinations are performed directly after horses have competed.

Examination on the Lunge Line and Under Saddle If possible, examining the horse on the lunge line (or long line) and under saddle is helpful. Multiple-limb lameness, especially contralateral forelimb and hindlimb lameness and bilateral front foot lameness, is common and is important to keep in mind. The possibility of subtle neurological deficits should be considered during all phases of the lameness examination. In some horses lameness may not be apparent unless the horse is under saddle and working near the higher end of its performance capabilities. This type of lameness is more difficult to diagnose, and localization frequently requires diagnostic analgesia. Subtle lameness can be masked by a rider restricting free head movement or by controlling body position. The diagonal on which the rider sits can alter the appearance of lameness. When riding the left diagonal, the rider sits when the left forelimb and right hindlimb bear weight, and on the right diagonal the rider sits when the right forelimb and left hindlimb bear weight. The correct diagonal is the left when trotting clockwise and the right when trotting counterclockwise. In general a horse appears lamer behind when the rider sits when the lame limb is bearing weight, and the horse may try to throw the rider to the opposite diagonal. A horse with right hindlimb lameness appears lamer when the rider

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sits on the left diagonal, that is, the rider sits when the left forelimb and right hindlimb are bearing weight. In Park, English, or Country English Pleasure classes, where riders are not penalized for riding the incorrect diagonal, horses often are ridden on the diagonal that minimizes lameness. Often a lameness is involved when a horse is seen being ridden on the incorrect diagonal when traveling in one direction and on the correct diagonal going the other way. These horses are referred as right or left diagonal horses. An inconsistent relationship exists between the degree of forelimb lameness and the diagonal on which the rider sits, but lameness may be modified by switching diagonals. It is important to note whether the observed lameness is constant regardless of direction or pattern. It is important to note if lameness varies, whether the involved limb is on the inside or outside of a circle, whether the horse is on the straight or in a turn, and whether lameness is worse when the horse is on hard or soft ground. The only gait deficit visible in horses with subtle forelimb lameness may be a slight difference in the height or arc of flight of the involved limb. Often a head nod is absent, but the horse appears unsteady in the face (movement of the nose from a fixed position) because of the discomfort of the limb from landing or from pushing off the ground.

DIAGNOSTIC ANALGESIA If possible, it is important to perform diagnostic analgesia to confirm the source of pain. For example, many horses that appear to have foot pain because of sensitivity of hoof testers or pain on palpation of the SL actually have pain elsewhere. Under American Horse Show Association rules with a properly filed medication report, local anesthetic solution such as mepivacaine can be administered up to 24 hours before a class. If lameness is to be re-assessed with the horse under saddle or in a cart, intra-articular rather than perineural nerve blocks are preferred, because of possible loss of proprioception, which may lead to tripping or stumbling. After perineural blocks, horses may pull shoes or show an altered or awkward gait regardless of the lameness. If perineual blocks are performed in horses under saddle or in a cart, the rider or driver should be cautioned. Hindlimb nerve blocks can be difficult in uncooperative horses, and a tranquilizer (10 to 15 mg acepromazine intravenously) may be administered to fractious horses. Lameness also may be more obvious, but the risk of permanent penile prolapse with the use of acepromazine in stallions or geldings should be considered. In some horses, diagnostic analgesia of the hindlimbs may be impossible, and the response to intra-articular medication, administered under heavy sedation, must then be assessed.

ito-atlantoaxial malformation. Cerebellar abiotrophy is a congenital neurological abnormality that may have an inherited susceptibility and has been reported only in the Arabian horse and Gotland pony. Typical signs occur around 2 to 4 months of age and include head tremor, incoordination, hypermetria, and proprioceptive deficits. Horses may live into adulthood, and anecdotal evidence suggests that the condition may stabilize or improve, although for these horses to improve sufficiently to be useful performance horses is unlikely. Occipito-atlantoaxial malformation is an inherited congenital malformation that has been reported most frequently in Arabians. The severity of clinical signs varies greatly, from splinting of the neck to progressive ataxia and weakness to congenital tetraparesis. Reduced atlanto-occipital movement and abnormal head carriage with the neck extended are common findings.2 Diagnosis is confirmed radiographically (see Fig. 55-4, B). Developmental cervical vertebral anomalies also may cause ataxia.

UNDIAGNOSED LAMENESS When a diagnosis of the cause of lameness cannot be made, the veterinarian should consider the following: 1. Tack problems: A poorly fitting saddle may create abnormal pressure on the withers or lumbar region and cause poor performance or lameness. A poorly fitted bit or bridle that causes the horse to flip its head or lean into or away from the bit also can affect performance greatly. 2. Dental problems (causing behavior that may lead to poor performance): Sharp enamel points, wolf teeth, and fractured or infected tooth roots may all cause abnormal head carriage and poor performance. 3. Painful skin lesions in the area of the girth, saddle, or bridle may affect performance. 4. A poorly skilled rider pulling on the horse while posting, or with poor balance, or timing may affect the horse’s performance. 5. Recurrent exertional rhabdomyolysis affects performance. 6. Subtle neurological deficits may affect performance. If these problems are ruled out and a diagnosis still cannot be made, the veterinarian should try empirical treatment including a period of rest, a course of non-steroidal anti-inflammatory drugs (NSAIDs), systemic corticosteroids, intravenously administered hyaluronan, oral or systemic polysulfated glycosaminoglycans (PSGAGs), acupuncture, or chiropractic manipulation.

DIAGNOSIS AND MANAGEMENT OF LAMENESS NEUROLOGICAL EXAMINATION

Bruised and Inflamed Feet

An Arabian or Half-Arabian show horse with neurological disease may show subtle to overt clinical signs of weakness and ataxia, which may be mistaken easily for signs of musculoskeletal pain. Watching the horse pivot in tight circles, back up, and walk a figure of eight can be performed quickly and may pinpoint subtle deficits that were not noted or were less noticeable earlier in the examination. Traumatic injuries caused by fractious horses falling during handling and training, and equine protozoal myelitis, are the most common causes of neurological disease and dysfunction in the Arabian and Half-Arabian show horses in North America. Two rare neurological conditions that may be confused with lameness and are much more common in Arabians than in any other breed are cerebellar abiotrophy and occip-

Differential diagnoses for lameness in the foot of an Arabian or Half-Arabian show horse are sole bruising, osteitis of the distal phalanx, foot abscess, penetrating wounds, fractures, laminitis, navicular syndrome, osteoarthritis of the distal interphalangeal joint, and undiagnosed palmar heel pain. The most common foot problems are bruising, osteoarthritis of the distal interphalangeal joint, and palmar heel pain. Bruising is diagnosed by finding localized or generalized pain in the sole and by ruling out other lameness conditions. Digital pulse amplitudes are usually normal unless bruising is severe. Discoloration of the sole by hemorrhage usually occurs later and may not be seen with acute sole bruising. The most common causes of bruising are hard footing or poor medial to lateral hoof balance. The high side (longer when viewed from the palmar aspect) is usually the bruised side, and treatment

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may be as simple as balancing the hoof. If hoof balance is judged to be adequate, then a pad can be cut out or the shoe can be beveled to reduce pressure on the bruised area. A common problem is a low, underslung heel. One foot may be affected, while the other tends to be upright or club footed. Horses with low, underslung hoof conformation commonly develop bruised heels. Although raising the heel angle with a degree pad may appear desirable, this correction actually may cause further heel bruising by concentrating the force on the heel. We recommend the use of a heart bar shoe, frog pads, or an egg bar shoe and a pad cut out over both heels. Horses with club foot conformation also may develop contracted heels. Treatment involves the use of a heart bar shoe or a frog pad, or beveling the branches of the shoe. Some horses with the low, underslung heel or with club foot conformation may not be lame, and therefore attempts at correction should be tempered. In a flat-footed horse, sole bruising may occur in areas underlying the shoe, where the sole is not concave enough to prevent contact with the shoe or pad. In these horses a concave inner surface shoe should be used. Pads and packing material are important in treating and preventing bruised feet, but bruising can still be a problem. Silicone, tar, and oakum and newer products such as advanced cushion support are commonly used packing materials. However, if the packing is too firm, it may create rather than prevent sole bruising. Osteitis of the distal phalanx refers to a non-infectious inflammation of the distal phalanx, which in many horses appears to occur secondary to chronic sole bruising. The diagnosis is made radiographically by observing radiolucent changes and remodeling along the margins and proliferative new bone growth along the dorsal aspect of the distal phalanx. Horses that have these radiographic changes in the toe region also may have chronic bruising, laminitis, solar margin fractures, or club footed conformation. In the heel the margins of the distal phalanx are normally irregular and less well defined radiographically, and a distinction between bruising and osteitis is harder, if not impossible, to make. In most horses, however, the treatment is similar. Treatment of horses with acutely bruised feet also includes the administration of NSAIDs (phenylbutazone, 4.4 mg/kg bid for 3 days and then 2.2 mg/kg bid for 3 days) and physical therapy. If treatment is necessary during or close to a show in North America, NSAIDs must be given according to the American Horse Show Association rules for therapeutic medication under which the Arabian and Half-Arabian divisions operate. Currently (2001) the guidelines suggest horses can receive phenylbutazone at a dose of 4.4 mg/kg once daily for 5 days in a row no closer than 12 hours before a class. If 2.2 mg/kg phenylbutazone is given by mouth every 12 hours, then the drug can be dosed at any time before a class. Under American Horse Show Association rules, two NSAIDs from a list of five (flunixin meglumine, ketoprofen, naproxen, meclofenamic acid, and phenylbutazone) are allowed to be given at the same time, except that phenylbutazone and flunixin meglumine may not be given to the same horse within 7 days of a class. If bruising is severe and a second NSAID is required, intravenously administered ketoprofen (2.2 mg/kg sid) is helpful. This can be given up to 4 hours before a class. Isoxsuprine (400 mg PO bid) used to increase blood flow to the foot, although controversial, appears to be helpful in many horses. Physical therapy includes standing the horse in ice (15 minutes in and 15 minutes out for 3 repetitions, repeated several times a day) for the first 24 hours, followed by soaks in hot water and Epsom salts (15 to 20 minutes, 3 times daily). After soaking, the bottom and sides of the foot can be packed with a poultice and wrapped. Before the poultice is applied, dimethylsulfoxide painted on the affected areas is helpful. If

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areas of the sole are particularly soft, painting on a mixture of formaldehyde and tincture of iodine hardens the sole.

Osteoarthritis of the Distal Interphalangeal Joint and Palmar Heel Pain Synovitis or acute inflammation of the distal interphalangeal joint is common and likely represents an early form of osteoarthritis. Lameness is usually mild to moderate and frequently is bilateral. Lameness tends to be more obvious in circles or tight turns, frequently with the affected leg on the outside of a circle. When horses are affected bilaterally, the only signs may be a shortened cranial phase of the stride and reluctance to go forward. Effusion of the distal interphalangeal joint can be palpated just proximal to the coronary band on the dorsal aspect of the limb. Horses may show pain when hoof testers are applied across the heels, but examination of the sole of the foot is unremarkable, unless other problems such as bruising or navicular syndrome are present. Many young horses develop distal interphalangeal joint synovitis early in training and lameness improves with a short period (14 to 28 days) of rest and NSAIDs. Synovitis of the distal interphalangeal joint is also common in older show horses when it may be associated with poor foot conformation or a heavy show schedule. No radiographic abnormalities are detected unless the condition is chronic and advanced osteoarthritis develops. Lameness is abolished by analgesia of the distal interphalangeal joint or a basisesamoid nerve block. Three milliliters of mepivacaine deposited over the medial and lateral palmar digital nerves just above the bulbs of the heel also significantly alleviates pain originating from the distal interphalangeal joint.3 Analgesia of the distal interphalangeal joint is not specific, but use of a small volume (6 ml) of local anesthetic solution and evaluation of the response within 6 to 8 minutes may minimize the effects of diffusion into the digital nerves and inadvertent misdiagnosis. It is important to remember that several problems may coexist in the foot, and sorting out a single specific diagnosis can be difficult. Horses with low, underrun heels often have bruising, osteitis of the distal phalanx, and osteoarthritis of the distal interphalangeal joint. Horses with navicular syndrome may have bruising in the toe area related to decreased weight bearing on the heel. A bone scan may be useful in differentiating these potential causes of lameness. Horses with early, acute osteoarthritis of the distal interphalangeal joint should be evaluated clinically for abnormalities of hoof balance and hoof angle. Shortening and rolling the toe of the shoe to ease breakover can be helpful. Shortening the toe in English show horses may not be well accepted by trainers because they think it decreases the desired forelimb action. If the lameness is moderate or severe, the horse should be allowed to rest for 30 days or the workload should be reduced drastically. Intra-articular medication with hyaluronan (20 mg) and a corticosteroid (80 to 120 mg methylprednisolone acetate) and systemic phenylbutazone (2.2 mg/kg PO bid for 5 days) are recommended. If lameness is mild, training can resume 2 to 3 days after the injections. Treatment with systemic hyaluronan (40 mg intravenously once a week for 3 weeks) or PSGAGs (500 mg intramuscularly once every 5 days for 4 to 7 treatments) sometimes is used also, but it should not be a substitute for intra-articular therapy. These products frequently are used as maintenance medications (one dose every 2 to 4 weeks) and for pre-show medication (one dose 24 to 72 hours before a class) for joint-related lameness. Palmar heel pain is a frequent cause of lameness. Horses may or may not show pain on hoof tester examination, but lameness is eliminated by palmar digital analgesia. Causes include navicular syndrome, deep digital flexor tendonitis, impar desmitis, navicular suspensory desmitis, inflammation of the navicular bone, fragmentation of the distal border of the

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navicular bone, and congenital bipartate or tripartate navicular bones. Reaching a specific diagnosis in some horses may be difficult. Diagnosis and management of the navicular syndrome in the Arabian and Half-Arabian show horses are similar to that described for other horses, although this condition is less common than in Quarter Horses or Thoroughbreds. Although it is important to identify the source of lameness as specifically as possible, the treatment options in horses with palmar heel pain are somewhat limited and similar regardless of the cause. Rest, systemic steroidal and NSAID administration, therapeutic shoeing, medication of the distal interphalangeal joint or navicular bursa in horses with navicular involvement, and palmar digital neurectomy are the most common treatments. The natural balance shoes are not used routinely for English and Park horses because they decrease forelimb motion.

Suspensory Desmitis Proximal suspensory desmitis is one of the most common lameness conditions of the metacarpal and metatarsal regions. Although more prevalent in the forelimb, proximal suspensory desmitis is a common hindlimb problem and typically is an insidious lameness but may have an acute onset. Lameness is more obvious when the affected limb is on the outside of a circle and is worse on turns than in straight lines. Usually no swelling is detectable, and the response to palpation is unreliable. Definitive diagnosis is based on the response to diagnostic analgesia, combined with radiography and ultrasonography. Many treatments are available, including the use of systemic anti-inflammatory agents; local injections of antiinflammatory agents or counterirritants; topical agents with support wraps; shock wave, magnetic, laser, and ultrasound therapies; and various surgical procedures. The effectiveness of radial shock wave therapy currently is being investigated. A decision must be made whether the horse is sound enough to remain in work, as in horses with a chronic lowgrade proximal suspensory desmitis, or whether the horse should be allowed to rest. If the horse is to remain in work and local injections are to be part of the treatment regimen, the veterinarian has two options. An anti-inflammatory agent such as a short-acting corticosteroid, possibly mixed with hyaluronan or a PSGAG, may be used, followed by a few days of hand walking, before the horse resumes work. Alternatively, a counterirritant such as 1 to 2 ml of 2% iodine in almond oil is injected, followed by continued work. In both instances the work is limited to graduated periods of walking and low-speed trotting for several weeks. The walking and trotting generally are performed in escalating timed intervals. The canter or lope is not recommended initially, because the affected limb is the only limb on the ground for a portion of the gait sequence. The weight of the shoes and pads may be reduced during the initial portion of the recovery period. If the injury is too severe for the horse to remain in work, the horse is confined and hand walked until recovery is sufficient enough to begin a regimen of low-impact, controlled exercise. These horses are not turned out, because they tend to re-injure themselves with free exercise. Proximal suspensory desmitis tends to recur with prolonged intense exercise. Horses with bilateral club feet, low underrun heels, one club foot and one low heel, or substantial rotational and angular deformities are predisposed to proximal suspensory desmitis. Horses with a chronic lameness in the opposing limb or the diagonal limb also are predisposed to lameness because of compensatory loading. It is important to identify other problems, because resolution of lameness in another limb may be crucial to the long-term resolution of proximal suspensory desmitis. Suspensory branch desmitis also occurs frequently. With an acute injury there is pain, heat, and swelling over the affected

branch and a positive response to lower limb flexion. Usually some distention of the fetlock joint capsule occurs. Diagnosis is confirmed by ultrasonography, and the proximal sesamoid bones should be evaluated radiographically. Horses with acute injuries are treated symptomatically with ice, poultice, NSAIDs, and systemic corticosteroids. If sesamoiditis is present, isoxsuprine or pentoxifylline treatment may be helpful. The shoeing should be evaluated and imbalance (frequently a low heel on the affected side) corrected. If possible, the toe should be shortened, or a rolled toe shoe should be used to ease breakover. The branches of the shoe should be extended, or an egg bar shoe should be applied to support the SL. Horses with chronic active suspensory branch desmitis may benefit from injection of corticosteroids (methylprednisolone acetate and isoflupredone acetate) subcutaneously in the affected area. Most horses are managed with medical treatment, although surgical splitting of the branch or bone marrow injections are alternative treatment options. Suspensory branch desmitis tends to recur, can be difficult to manage successfully, and may be a career-ending injury.

Osteoarthritis of the Stifle Joints The stifle is a common source of lameness, and apart from occasional acute injuries most horses have chronic, often lowgrade lameness that may not be evident when examined in hand. Riders may complain that horses are hard on one side of the mouth, tracking with a shoulder or hip in or out, falling out of a hind lead in the corners, and bending poorly. Horses with stifle pain also have difficulties in downward transitions, because they cannot maintain a collected frame and tend to fall out behind. If forced to maintain collection, the head may be raised. Horses exhibit increased discomfort going downhill. If the work area has even a slight grade, an affected horse appears more comfortable going up the grade than down. Horses also fatigue easily in deep footing, with loss of collection, diving forward in the bridle (English divisions), raising out of the bridle (Western and Hunter divisions), and loss of hindlimb cadence at the trot. Lameness is worse in turns and improves in the straight portions of the arena. The medial femorotibial and femoropatellar joint capsules may be distended and fibrous thickening from a previous medial patellar desmotomy and other abnormalities from previous injuries may be apparent. Various flexion tests, such as pulling the limb caudally, may exacerbate lameness, but these tests are not reliable and may be dangerous to perform. Intraarticular analgesia usually is required. The medial femorotibial joint, the femoropatellar joint, and the lateral femorotibial joint are affected with decreasing frequency and generally are blocked individually in that order. Radiography should include caudocranial, lateromedial, and oblique views. Ultrasonographic examination, nuclear scintigraphy, and diagnostic arthroscopy are sometimes required. Most commonly lameness is improved by intra-articular analgesia of the medial femorotibial joint, but radiography is negative or equivocal. Affected horses are thought to have chronic inflammation of the soft tissues of the joint and synovitis. Some of these horses eventually develop an enthesophyte on the proximal medial aspect of the tibia. Lameness often recurs, because lameness reflects the type of work the horse performs, the collected frame required, and conformational weaknesses, such as lack of angulation in the hip, stifle, and hock, camped-out conformation, and weak hindquarters in general. The condition is managed by adapting the work level between shows and the show schedule of the horse to accommodate for lameness, by corrective shoeing, and by using systemic anti-inflammatory agents and intra-articular medication. Corrective shoeing is individualized but involves trimming the foot short and using a light shoe that assists breakover. Many horses break over the dorsomedial aspect of

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Thoracolumbar (Back), Sacroiliac, and Gluteal (Croup) Pain

A left hind shoe indicating natural breakover medial to the toe area (medial is right). Future shoes will be formed to allow breakover in this area rather than directly at the center of the toe.

Fig. 124-2

the toe, and that portion of the shoe can be rolled or shaped to ease breakover. A worn shoe can be examined for breakover location (Fig. 124-2). Some horses are more sound barefooted behind and compete that way. To maintain soundness at shows, horses are maintained at a work level between shows that does not require intra-articular treatment. Systemic administration of hyaluronan and a PSGAG may help. Systemic and intraarticular anti-inflammatory therapy is begun before competition to minimize lameness during the competition. If a horse requires frequent therapy between shows, it has a poor chance of enduring a competition in good form. Counterirritant therapy in the form of 2% iodine in oil commonly is injected in various patterns along the patellar and collateral ligaments of young horses and horses with loose stifles and in horses that have been rested as the intensity of training increases and the horse exhibits non-specific pain or weakness in the stifle area. Counterirritants are not used as a replacement for intra-articular therapy but may be used concurrently. Injections usually are limited to 5 to 10 ml to reduce postinjection inflammation and to decrease scarring from multiple injections. Work is continued, but the intensity is reduced for a short time as the horse recovers. Osteochondrosis is the second most common problem seen in the stifle. Osteochondral fragments from the femoral trochleas can be removed arthroscopically, usually with a favorable prognosis. Horses with lameness caused by subchondral bone cysts in the medial femoral condyle have a poorer prognosis. Some horses respond to intra-articular corticosteroids. Surgical treatment may fail to resolve the lameness.

Work-related back and croup pain is common in horses because of working in a collected frame frequently or for extended periods of time, compensatory altered carriage caused by lower limb injuries, poor saddle fit, poor balance and timing of a rider, injuries from falling and weakness from immaturity, lack of conditioning, or poor conformation (long, weak back). Back pain should be suspected when behavioral changes such as kicking out during lead changes and uncharacteristic bucking occur. The horse is observed for muscle asymmetry while it stands with the body straight and the limbs squared on a level surface. The back and croup are palpated for areas of pain, using gradual pressure with the flat surface of the digits. The lumbosacral junction should be evaluated by placing the heel of one hand on the left side of the loin and, with the other hand over the base of the tail, rocking the area back and forth. A normal horse allows this, but a horse with pain stiffens and steps away from the veterinarian. Unilateral abnormalities may indicate concurrent lower limb injuries. Unilateral lumbar pain often results from compensatory carriage of the hindlimbs to that side. Unilateral sacroiliac inflammation or dorsal ligamentous thickening often results from over-bearing on that side from a chronic contralateral or diagonal limb injury. For example, horses with a chronic left front or left hind lameness may have swelling and pain in the area of the right tuber sacrale. Rectal examination is used to evaluate pelvic symmetry and ventral lumbar muscular pain. Other diagnostic modalities include radiography, ultrasonography, nuclear scintigraphy, and thermography, but physical examination remains the most important and reliable method of diagnosis. Myositis also occurs commonly and is diagnosed by history, observation of altered gait, palpation, and serum enzyme assay. A variety of treatments is used, and these are discussed thoroughly elsewhere. Usually a period of rest is indicated, along with resolution of any associated lameness, followed by a period of reduced exercise. Systemic and local anti-inflammatory agents are administered. Other therapies include cold and heat therapy, acupuncture, chiropractic therapy, massage therapy, and magnetic, electromagnetic, laser, and ultrasound therapy. Successful treatment of horses with back and croup injuries depends on identification of initiating causes and making appropriate changes to alleviate these causes if possible. Educating the rider is also helpful, because changes in training routines or tack may be helpful in preventing recurrence.

Osteoarthritis of the Metacarpophalangeal and Metatarsophalangeal Joints Synovitis of the metacarpophalangeal and metatarsophalangeal joints, an early form of osteoarthritis, causes effusion, pain on fetlock flexion, and a positive response to a lower limb flexion test. The condition is frequently bilateral. Because mild effusion in sound Arabian and Half-Arabian show horses is seen commonly, it is important to perform intra-articular or perineural analgesia to confirm the source of pain when osteoarthritis of the metacarpophalangeal or metatarsophalangeal joint is suspected. Radiography is performed to determine the extent of osteoarthritic abnormalities. Many Arabian and Half-Arabian show horses perform well in spite of mild osteoarthritis of the fetlock (Fig. 124-3). Treatment is similar to that recommended for osteoarthritis of the distal interphalangeal joint, except that a shorter-acting corticosteroid such as triamcinolone or betamethasone is used for intra-articular medication.

Distal Hock Joint Pain Osteoarthritis of the centrodistal and tarsometatarsal joints or distal tarsitis is common. Tarsal lameness is often bilateral, although one limb usually is affected more severely. Affected

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Lateromedial radiographic view of a metacarpophalangeal joint of a sound Half-Arabian show horse. There is a moderately sized osteophyte (arrow) on the proximal dorsal aspect of the proximal phalanx, reflecting osteoarthritis.

Fig. 124-3

fractures of the second and fourth metatarsal bones are common, especially in young horses. Diagnosis of splintinduced lameness is made using palpation, diagnostic analgesia, and radiography. Associated suspensory desmitis should be considered and assessed by ultrasonographic examination. Predisposing causes include conformational defects such as offset knees or base narrow and toed out. Heavy shoes and pads can exacerbate a tendency to wing in and cause interference. Poor footing that is excessively deep or hard can contribute to the development of splints. Immature horses in excessive work, or wearing shoes and pads that are too heavy for their level of fitness, are predisposed to splints. Shoeing with improper medial to lateral balance, obesity, and dietary imbalances can be contributory causes. Proliferative periostitis originates from injury to the interosseous ligament, resulting in the development of proliferative fibrous connective tissue that subsequently mineralizes. Radiography is used to assess the injury and to determine the presence of fractures. Osteolysis of the third metacarpal or metatarsal bone and of the splint bone at the site of the injury is a sign of substantial inflammation and can indicate a prolonged recovery. Treatment includes rest (2 to 4 weeks), cold therapy, systemic and local administration of anti-inflammatory agents, topical agents with support wraps, and magnetic therapy. Large exostoses that interfere with surrounding soft tissue structures can be excised surgically. Work-related fractures are predominantly distal, closed fractures and are thought to result from over-excursion of the SL during fetlock hyperextension. These fractures frequently are displaced, heal by non-union, and tend to irritate surrounding soft tissues. For these reasons they commonly are removed surgically. Mid-splint bone non-displaced fractures often resolve with conservative therapy. Initial therapy is similar to the treatment of a true splint, except that local administration of corticosteroids is not performed. If conservative therapy fails, surgical excision of the exostosis and distal portion of the splint bone may be performed. Horses with proximal fractures are evaluated on an individual basis, because some respond to conservative therapy, whereas others require surgical intervention.

Osteoarthritis of the Proximal Interphalangeal Joint horses have reduced hock flexion at the trot and tend to travel with a hip off to one side, especially in the corners (drift away from the lame limb). Rider complaints are similar to horses with stifle lameness. Western horses may tend to rate poorly and lope (canter) with a four-beat rather than a three-beat action. Reining horses tend to raise up in spins to the affected direction, bend poorly, stop unevenly or on the forehand, and change leads late behind. Diagnosis is based on palpation, including the Churchill test, flexion tests, diagnostic analgesia, radiography, and occasionally ultrasonography and nuclear scintigraphy. Treatment comprises systemic administration of anti-inflammatory agents and intra-articular medication with corticosteroids, possibly with hyaluronan (60 to 80 mg of methylprednisolone acetate and 10 mg of hyaluronan per joint), repeated as necessary, often 2 to 3 times during a show season. If medical therapy fails, chemical, laser, and surgical fusion techniques are available. Cunean tenectomy usually is not performed because the procedure commonly does not resolve lameness. Corrective shoeing involves inspecting the old shoe and squaring the new shoe to accommodate the breakover, setting the shoe back, shortening the toe, reducing the weight of the hind shoe, and occasionally using asymmetrical trailers.

Splint Bone Injuries Proliferative periostitis, referred to as splints, and fractures of the second and fourth metacarpal bones and to a lesser extent

Incidental radiographic changes (lipping and spurring) indicating mild osteoarthritis of the proximal interphalangeal joint in Arabian and Half-Arabian show horses are not uncommon. Moderate to severe osteoarthritis, however, would be expected to cause chronic lameness. In most horses osteoarthritis of the proximal interphalangeal joint is caused by chronic repetitive trauma, although osteoarthritis secondary to a single severe injury is possible. In young horses osteochondrosis in the form of osseous cyst-like lesions and fragmentation may be involved. The importance of any radiographic changes should be validated using diagnostic analgesia. Lower limb flexion is usually positive, and lameness should improve with a basisesamoid or abaxial sesamoid block or analgesia of the proximal interphalangeal joint. Treatment is similar to that recommended for horses with osteoarthritis of the distal interphalangeal joint.

Desmitis of the Accessory Ligament of the Deep Digital Flexor Tendon Desmitis of the accessory ligament of the deep digital flexor tendon occurs less frequently than does proximal suspensory desmitis, primarily in limbs with club feet or low, underrun heels. Footing that accumulates under the shoe, creating a rocking motion of the foot during the weight-bearing phase of the stride, may predispose horses to desmitis. Lameness is usually acute in onset, and palpation often reveals a painful

CHAPTER 125 thickening along the length of the ligament that can be confused with the deep digital flexor tendon. If the condition is chronic and low grade, diagnostic analgesia may be required. Diagnosis is confirmed with ultrasonography. Treatment involves prolonged rest and systemic and local administration of anti-inflammatory agents. Adjuncts include cold therapy, topical agents with support wraps, and magnetic, laser, and ultrasound therapy. Because the predisposing conformational defect remains, the condition tends to recur.

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REFERENCES 1. General qualifications. 1998-1999 Arabian, Half-Arabian and Anglo Arabian division rule book, New York, 1997, American Horse Shows Association. 2. Hahn CN, Mayhew IG, Mackay RJ, et al: Diseases of the spinal cord. In Colahan PT, Merritt AM, Moore JN, et al, editors: Equine medicine and surgery, vol 1, ed 5, St Louis, 1999, Mosby. 3. Easter JL, Watkins J, Stephens S, et al: Effects of regional anesthesia on experimentally induced coffin joint synovitis, Proc Am Assoc Equine Pract 46:214, 2000.

125

Lameness in the Driving Horse Kevin Keane and Graham Munroe

DESCRIPTION OF THE SPORT This chapter deals with horses used for competitive driving purposes, those driven privately for pleasure, and those used as beasts of burden as a mode of transportation. The sport of driving horses in competition is relatively new and has many variations, requiring different types of horses performing different tasks. Certain breeds or breed types are perfectly suitable for one form of driving sport but not another, and variation in the size, type, and breed of horse used is considerable. Horses and ponies are used, and the term horse is used in this chapter to refer to both, except when specific reference to a pony is required. In the United Kingdom and Europe there is a much greater availability of a variety of driving competitions than currently exists in North America. Pleasure driving includes presentation classes in the show ring and general driving on roads and tracks. Presentation classes are grouped broadly into hackney and non-hackney types, the difference being based on the phenotype of the animal as opposed to a breed registry. The competitor pays close attention to the harness, attire of the driver, and an appropriate carriage to suit the horse, because judging is subjective and based on strict adherence to tradition, based on a suitable match of horses and carriage. The horses perform movements requested by the judges, and style and quality of the gaits are scored subjectively. These horses compete at the walk and trot (a park pace being roughly equal to a slow working trot). Pleasure driving events also can include drives at the walk or trot on roads and tracks of up to 5 to 10 miles. Competitive driving includes combined driving or horse driving trials and scurry driving. Scurry driving is seldom seen in North America but has a strong following in the United Kingdom and other parts of Europe. Scurry driving consists of a single pair, or more usually pairs, of mainly ponies competing over a tight, coned course in a show ring against the clock. The horses and carriages are often small to allow the narrow gates (the gap between a pair of cones) and corners to be negotiated at speed. Horse driving trials are a driven form of horse trials, or eventing, and like its ridden counterpart,

driving is a highly athletic, physically demanding sport for the horse and driver. Driving trials as an international equestrian sport started in 1968, when the Federation Equestre Internationale (FEI) international rules were drawn up under the instigation of HRH Prince Philip, who was then the President of the Federation. The first international horse driving trials event took place in 1971 in Hungary. Initially the competition was only for horse teams (four-in-hand). A team is four horses, two before two, and those in front are called leaders and those closer to the coach, wheelers. As the sport developed and individuals of more modest means entered the fray, competitions for singles (one horse), tandems (two horses harnessed one behind the other), and pairs (two horses harnessed side by side) rapidly blossomed. These classes were further divided into those for ponies (less than 148 cm or 14.2 hands high) and horses. The sport is now structured at various levels depending on the ability of the driver and horse(s). The FEI is responsible for the international rules that cover the world and European championships and selected international events such as the Royal Windsor International Driving Grand Prix. The national associations liaise with the FEI and are responsible for running the national events and championships and producing national rules. Local driving clubs (found in Europe, the United Kingdom, and the United States) also run local events that may differ substantially in standards and requirements of competitors, but they essentially mimic FEI rules. Important events include the following: Royal Windsor (United Kingdom), Aachen and Riesenbeck (Germany), Breda (Holland), Saumur (France), Waregem (Belgium), St. Gallen (Switzerland), and Fair Hill (United States). World championships are held every 2 years in singles, pairs, and teams in horses, and a European championship is held in pony teams. The first World Pony Championships (singles, pairs, and teams) will be held in Saumur in 2003. Competitions in Europe run from April to September, with championships held toward the end of this period. Horse driving trials consist of three phases—dressage, marathon, and cones—usually spread over 3 days, but in lower standard competition all three may take place over 1 to 2 days.

CHAPTER 125 thickening along the length of the ligament that can be confused with the deep digital flexor tendon. If the condition is chronic and low grade, diagnostic analgesia may be required. Diagnosis is confirmed with ultrasonography. Treatment involves prolonged rest and systemic and local administration of anti-inflammatory agents. Adjuncts include cold therapy, topical agents with support wraps, and magnetic, laser, and ultrasound therapy. Because the predisposing conformational defect remains, the condition tends to recur.

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REFERENCES 1. General qualifications. 1998-1999 Arabian, Half-Arabian and Anglo Arabian division rule book, New York, 1997, American Horse Shows Association. 2. Hahn CN, Mayhew IG, Mackay RJ, et al: Diseases of the spinal cord. In Colahan PT, Merritt AM, Moore JN, et al, editors: Equine medicine and surgery, vol 1, ed 5, St Louis, 1999, Mosby. 3. Easter JL, Watkins J, Stephens S, et al: Effects of regional anesthesia on experimentally induced coffin joint synovitis, Proc Am Assoc Equine Pract 46:214, 2000.

125

Lameness in the Driving Horse Kevin Keane and Graham Munroe

DESCRIPTION OF THE SPORT This chapter deals with horses used for competitive driving purposes, those driven privately for pleasure, and those used as beasts of burden as a mode of transportation. The sport of driving horses in competition is relatively new and has many variations, requiring different types of horses performing different tasks. Certain breeds or breed types are perfectly suitable for one form of driving sport but not another, and variation in the size, type, and breed of horse used is considerable. Horses and ponies are used, and the term horse is used in this chapter to refer to both, except when specific reference to a pony is required. In the United Kingdom and Europe there is a much greater availability of a variety of driving competitions than currently exists in North America. Pleasure driving includes presentation classes in the show ring and general driving on roads and tracks. Presentation classes are grouped broadly into hackney and non-hackney types, the difference being based on the phenotype of the animal as opposed to a breed registry. The competitor pays close attention to the harness, attire of the driver, and an appropriate carriage to suit the horse, because judging is subjective and based on strict adherence to tradition, based on a suitable match of horses and carriage. The horses perform movements requested by the judges, and style and quality of the gaits are scored subjectively. These horses compete at the walk and trot (a park pace being roughly equal to a slow working trot). Pleasure driving events also can include drives at the walk or trot on roads and tracks of up to 5 to 10 miles. Competitive driving includes combined driving or horse driving trials and scurry driving. Scurry driving is seldom seen in North America but has a strong following in the United Kingdom and other parts of Europe. Scurry driving consists of a single pair, or more usually pairs, of mainly ponies competing over a tight, coned course in a show ring against the clock. The horses and carriages are often small to allow the narrow gates (the gap between a pair of cones) and corners to be negotiated at speed. Horse driving trials are a driven form of horse trials, or eventing, and like its ridden counterpart,

driving is a highly athletic, physically demanding sport for the horse and driver. Driving trials as an international equestrian sport started in 1968, when the Federation Equestre Internationale (FEI) international rules were drawn up under the instigation of HRH Prince Philip, who was then the President of the Federation. The first international horse driving trials event took place in 1971 in Hungary. Initially the competition was only for horse teams (four-in-hand). A team is four horses, two before two, and those in front are called leaders and those closer to the coach, wheelers. As the sport developed and individuals of more modest means entered the fray, competitions for singles (one horse), tandems (two horses harnessed one behind the other), and pairs (two horses harnessed side by side) rapidly blossomed. These classes were further divided into those for ponies (less than 148 cm or 14.2 hands high) and horses. The sport is now structured at various levels depending on the ability of the driver and horse(s). The FEI is responsible for the international rules that cover the world and European championships and selected international events such as the Royal Windsor International Driving Grand Prix. The national associations liaise with the FEI and are responsible for running the national events and championships and producing national rules. Local driving clubs (found in Europe, the United Kingdom, and the United States) also run local events that may differ substantially in standards and requirements of competitors, but they essentially mimic FEI rules. Important events include the following: Royal Windsor (United Kingdom), Aachen and Riesenbeck (Germany), Breda (Holland), Saumur (France), Waregem (Belgium), St. Gallen (Switzerland), and Fair Hill (United States). World championships are held every 2 years in singles, pairs, and teams in horses, and a European championship is held in pony teams. The first World Pony Championships (singles, pairs, and teams) will be held in Saumur in 2003. Competitions in Europe run from April to September, with championships held toward the end of this period. Horse driving trials consist of three phases—dressage, marathon, and cones—usually spread over 3 days, but in lower standard competition all three may take place over 1 to 2 days.

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Table • 125-1 Basic Format of the Five-Stage Marathon Length

Gait

Section A

≈ 10 km

Section B Section C Section D Section E

1 km 4 km 1 km 10 km

Any type, usually trot Walk Fast trot Walk Trot/canter

Average Speed (kph)

15 7 19 7 14

The first phase is a driven dressage test, which consists of a set sequence of movements that are judged by a number of officials against a standard of absolute perfection. The test is designed to highlight the obedience, paces and suppleness of the horse(s), and the skill of the driver in handling of the reins. The second stage is the marathon, which tests the fitness and stamina of the horse(s) and the judgment of pace and horsemanship of the driver. The cross country marathon can be divided into three or five sections (depending on the level of competition) for which on each section a maximum and minimum time are allowed (Table 125-1). The speeds and time allowances are adjusted for different classes, especially ponies. At the end of sections B and D are mandatory 10-minute halts. During the second of these, the animals are subjected to veterinary checks for lameness, injuries, and fitness (respiratory rate, pulse rate, dehydration, temperature, and speed of recovery). Section E has eight obstacles. Each obstacle is made up of a number of lettered gates. The aim is to drive through these gates (between white and red markers) within each obstacle in the correct alphabetical sequence in the shortest possible time. Most injuries occur on the marathon, although lameness may not become apparent until later, just before the third phase, the cones competition. The object of the cones phase is to test the fitness and suppleness of the horse after the marathon phase by driving through a course of narrowly spaced pairs of cones within an allotted time. Each cone has a ball balanced on top of it that is dislodged easily if the horse or carriage strikes the cone. The winner of the competition is the competitor with the fewest penalty points. Veterinary inspections of horses taking part in an event also occur before the dressage day, at the end of the marathon, and at the beginning of the cones competition. Lameness at any of these inspections usually leads to elimination from the event, although considerable variation exists in the definition of working soundness among veternarians, particularly respecting hindlimb problems. Horses used by Amish and Mennonite sects (United States) as beasts of burden are nearly always American Standardbreds or Saddlebred horses and are driven as singles. The horses are driven when needed, with no structured fitness training, and lameness is common.

horse turnouts such as drays; Hackneys (including crosses), Thoroughbreds, and Warmbloods in smart town turnouts; Cobs, larger pony types such as Welsh Cobs, Welsh Section C, Dales, Fells, Fiordlanders, and Friesians in country turnouts; and smaller pony types such as Welsh Mountain Section A, Shetlands, New Forest, and Dartmoor in small carriage turnouts. These aforementioned breeds primarily cover the variety seen in the United Kingdom and Europe. In the United States Warmblood, Warmblood crosses, Welsh, Hackney, Morgan, and Friesans are used most often for pleasure and driving trials. Most presentation and pleasure driving is undertaken with a single horse turnout. The horses range from 4 to 20 years of age and many have been or are used for other equestrian disciplines. Scurry driving usually involves single or pairs of small ponies or pony-type horses such as Shetlands, Welsh Mountain, New Forest, and Dartmoor. These ponies are often younger than pleasure-driving animals and are less likely to be used for other equestrian sports, except perhaps combined driving trials. Driving trials horses must be older than 4 years before they can compete, and records show 19-year-old horses competing at world championship level. Many of the best driving trials horses are 12 to 19 years of age and have been used earlier for other purposes. This long working life and slow introduction to work at a young age, together with little high speed, more slow speed conditioning work, and regular winter breaks, has a considerable effect on the type of lameness seen in these animals. The types of horses and ponies used vary greatly. In continental Europe, Warmblood breeds are particularly popular; for example, Gelderlanders, Swedish Warmbloods, Dutch Warmbloods, Hanovarians, and Holsteiners, with a modern trait being an ever-increasing size. In the United Kingdom less uniformity occurs in the horses used; for example, Hackney crosses, Cobs, Welsh Cobs, Lipizzaners, Lusitanias, Orlovs, and some Warmbloods and Thoroughbred crosses. The most popular ponies used for driving trials in Europe are Welsh Sections A, B, and C, Haflingers, and New Forest crosses. In the practice radius of one of the authors (K.K.) is a unique opportunity to observe, evaluate, and diagnose lameness conditions in driving horses used by members of the Mennonite and Amish religious sects as a mode of transportation. Several regions throughout North America have populations large enough to provide a reasonable number of horse owners for which to provide veterinary services. The incidence of lameness is influenced by the necessity of driving reasonably long distances on asphalt surfaces (up to 30 miles in one day), with sometimes a single horse pulling a Meadowbrook cart containing up to seven family members. Electricity is not used by the Amish sect and is consequently not available, so a veterinarian must be guided by the ability to palpate precisely and interpret the findings often without the adjunct diagnostic procedures relied on daily, such as radiography and ultrasonography. The veterinarian also faces great pressure because a lame horse may strand an Amish owner.

TRAINING TYPES OF HORSES USED The type of horses used for driving varies considerably with the particular form of the sport or use to be undertaken. For pleasure and presentation driving the type of horse used is related mainly to the size and type of the carriage and the overall effect the driver is trying to convey to the judges (e.g., country or town turnout, meaning an informal or formal appearance of the coach, harness, and driver’s attire). Horses used include Shires, Clydesdales, and Percherons in heavy

The training regimen for driving horses varies considerably depending on the type of driving to be undertaken and the level of competition to be attempted. Top-class horse driving trials horses require a regimented fitness program of up to several hours daily, with techniques for such fitness varying from trainer to trainer. In addition, some time is spent practicing cones and hazard training through schooling obstacles set up to mimic what is seen in competition. In pleasure or presentation driving, animals normally are worked intermittently, mainly on roads and tracks at the walk and trot, usually

CHAPTER 125 in the summer months, with a rest or turnout to grass in the winter. In scurry driving the training required is more intense, with a combination of regular road work at the walk and trot to increase overall fitness, alongside school and field work concentrating on bending, suppleness, and turning at speed with accuracy. The scurry driving season can extend over longer periods of the year, when competition comes indoors. Amish horses attain a less quantitative level of fitness through irregular use and essentially no training. Conditioning exercise tends to start in February, aiming for the first events in late April. Competitions are then available almost every weekend (Thursday to Sunday) throughout the summer, culminating in the national and international championships in August to October. The type or breed of horse used in driving and the way the horse is trained have an important effect on the type and incidence of lameness. Differences in conformation, gait, and size have an influence. Generally, ponies are less likely to develop lameness, are easier to train to fitness, and are more agile. Pony conformation and foot shape are better and they carry less weight. Unfortunately, alongside this general toughness is all too frequently allied a cussed temperament. Cob types are similar to ponies in temperament and hardiness but are heavier and more powerful, often leading to low-grade osteoarthritis in later life. They often require considerable training to allow the necessary control and obedience to be obtained. Welsh Cobs and Hackney types and crosses have particularly exaggerated natural forelimb actions, which over long periods of use may increase wear and tear injuries in the forelimbs such as metacarpophalangeal joint problems. Some of the larger breeds, such as the Warmbloods, suffer from poor conformation, especially in the hindlimbs, such as straight in the stifle and hock, which has a major effect on the incidence of lameness. Most driving animals are not broken to harness until they are 3 to 4 years old and are not worked until they are 5 to 6 years old. Therefore conditions prominent at an earlier age, such as osteochondrosis of the tarsus and stifle, are uncommon. The incidence of lameness in driving horses is much influenced by a long working life; the training, which is mainly flat work at the walk and trot; the different stresses and strains placed on them by the carriage (increased pressure on the hindlimbs, especially distally); the regular rest periods during the driving career; slow start in life; and whether they have been used for other purposes, previously or concurrently. All of these factors contribute to a low incidence of lameness, especially from fractures or acute soft tissue injuries seen in racing animals, but an increased incidence of low-grade wear and tear injuries, particularly of the hindlimb joints. In recent years the increasing competition and prestige at the top end of the sport, particularly internationally, has led to increased demands on horses, less patience to wait for horses to mature or to become seasoned, and consequently more lameness.

GROUND CONDITIONS Training is usually carried out on roads or tracks of varying surfaces, depending on the region and country involved. In the United Kingdom this is mainly tarmacadam roads and firm tracks, whereas in the eastern United States, tarmacadam, dirt, and gravel roads and precut paths through agricultural fields predominate. Training for dressage and cones is usually in grass paddocks, although some drivers have access to all-weather areas. The variable, often hilly terrain in the United Kingdom and United States helps develop fitness. In Europe some of the competitions and areas for training are flat and have a sandy soil, which gives an even, absorbent, good surface for exercise. The firm surfaces on which many driving horses train and work tend to increase concussion to the feet and limbs, but

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they strengthen tendons and ligaments. Repeated concussion over many years may contribute to low-grade joint disease and does mean that good foot conformation and shoeing are imperative to help offset some of this constant trauma. The variable and unpredictable ground conditions present on marathon courses contributes to injuries to joints, such as the fetlock, and to ligaments and the digital flexor tendon sheath.

CONFORMATION The huge variety of breeds and types of animals used in driving means that no particular traits of conformation have been established as representative of this type of work. Many of the Warmbloods, which are the most common breeds on the continent of Europe and are now becoming so popular elsewhere in the world for riding and driving, have a conformation that appears to predispose them to an increasing incidence of osteoarthritis of the distal hock joints. The hindlimbs are often straight through the hock and stifle, with increased body weight on small-boned legs. Some are also sickle hocked and cow hocked. Many Warmblood breeds have a high incidence of osteochondrosis, especially of the tarsocrural and stifle joints, which may manifest itself later in the working life of the horse. The headlong dash in recent years for bigger and stronger Warmblood driving horses has in our opinion lead to a heavier, less agile animal, often with small feet and limited bone, which cannot help the animal cope with work over the many years that the horse is driven. Foot conformation in some of the carriage breeds, such as the Hackney, Orlov, Gelderlander, and Lipizzaner, can be upright and boxy, which may decrease concussion protection by the foot and increase trauma reflected up the limb. Many of the native breeds or crosses have good conformation and inherent limb soundness, which is reflected in their low level of lameness. The exception to this statement is the pleasure or presentation pony that is worked irregularly and kept at grass in the summer. The overweight (show condition) nature of these ponies and the access to large amounts of grass predisposes them to laminitis, which reflects more on owner management than inherent unsoundness.

TEN MOST COMMON LAMENESS CONDITIONS A 15-year retrospective study of the clinical practice of one of the authors (K.K.) led to the formation of the following list of common lameness conditions, in order of incidence. Some variation in incidence occurs from leaders to wheelers in fourin-hand teams and in other countries, such as the United Kingdom. 1. Suspensory desmitis 2. Foot lameness: palmar heel pain, corns, and navicular syndrome 3. Distal hock joint pain 4. Exertional rhabdomyolysis 5. Tenosynovitis of the digital flexor tendon sheath (DFTS) 6. Osteoarthritis of the proximal and distal interphalangeal and fetlock joints 7. Stifle lameness 8. Lesions associated with turnout: solar abscesses and bruising, mud fever, rain scald, cracked heels, and kick wounds 9. Interference and traumatic injuries of forelimbs and hindlimbs 10. Desmitis of the accessory ligament of the deep digital flexor tendon (ALDDFT) and superficial digital flexor tendonitis

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LAMENESS EXAMINATION Examination of lameness in the driving horse differs little from that of a standard approach. The major objectives are to decide if the animal is lame, which limb or limbs are affected, and which portion or portions of the limb(s) are affected and to determine a pathological process. This process is complicated in a driving horse, particularly as the horse ages, because of the possibility of old or insignificant lesions and the lowgrade and often bilateral nature of some causes of lameness. Further problems are related to intermittent or variable lameness. Identification of lameness is more difficult in a driving animal when being driven, especially in the hindlimb, than in a ridden horse. The history should consist of typical questions asked before any standard lameness evaluation: for example, how the lameness initially presented; what the duration of lameness is; whether lameness is worse on hard or soft ground; and whether the horse has responded to any treatments used. In addition, because driving horses are exercising between two poles that are parallel to the ground, straightness is generally fairly easy for the driver to observe. Is the horse resting one hip on the right or left shaft? Is the horse leaning more on one rein than the other? With pairs and four-in-hand is one horse taking more of the workload, indicating unwillingness of the other horse to pull an equal load? Have any changes in tack or harness been made? The veterinarian should observe the stance and attitude of the horse, areas of muscle atrophy, limb and foot conformation, and the presence of swellings before assessing the horse moving in hand at the walk and trot on a hard, flat surface. Examination in harness and carriage is rarely useful, because lameness is sometimes less evident while the horse is pulling, rather than moving freely and without restriction on a lunge line. When a driver or trainer feels that the demonstration of the lameness for which the horse is being presented is observed only when in work, that is, driven, seeing the horse in harness then may be necessary. Standard flexion tests of the forelimbs and hindlimbs are useful, but as a horse ages the likelihood of a positive result in an otherwise working, sound horse increases. Exercise on the lunge or in hand on a circle is helpful in bilateral or mild lameness. Exercise on different surfaces (hard and soft) and when possible on a slight incline up and down hill can be useful. Identification of the affected lame limb(s) should be followed by detailed palpation and manipulation of the limb(s), with the limb bearing weight and in a flexed position. Assessment of any swelling by digital palpation and manipulation of the limb(s) to determine whether pain can be elicited can help to differentiate old, clinically insignificant lesions. In older horses distention of fetlock and tarsocrural joint capsules and DFTSs is a common, insignificant finding. Skin scars and areas of fibrosis from previous trauma may further complicate the localization of the site of lameness. Careful examination of the foot with hoof testers is important. The use of diagnostic analgesia is considered vital to rule out incidental lesions or previously managed chronic problems.

of pain is initially undertaken by a sequence of perineural analgesic techniques beginning distally and moving proximally in a logical manner. In the forelimbs the sequence is palmar digital; abaxial sesamoid; low palmar and palmar metacarpal (four point); high palmar (subcarpal); and median/ulnar/musculocutaneous. In the hindlimb the sequence is abaxial sesamoid; low six point; and tibial/fibular. Nerve blocks of the antebrachium or crus are useful when the veterinarian is uncertain if the lesion is above or below mid-limb. Once that has been determined, more specific blocks may be planned proximally or distally as needed. If the veterinarian suspects a particular site, performing an intra-articular block at that site first may be more efficient. It may be necessary to perform intra-articular blocks after perineural analgesia. Sites for intrasynovial analgesia are prepared aseptically (with or with out clipping, at the discretion of the veterinarian), and fresh bottles of mepivacaine or bupivacaine, needles, and syringes are used. Gloves are mandatory for intrasynovial techniques. Assessment of response can be difficult in horses with mild or intermittent lameness or when several painful sites exist. The veterinarian should be as certain as possible of the degree of improvement in the lameness, but unfortunately this is sometimes equivocal. In a driving horse the most common intrasynovial structures injected are, in the forelimb, the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints and the DFTS; and, in the hindlimb, the proximal interphalangeal, metatarsophalangeal, tarsometatarsal, centrodistal, and tarsocrural joints and the DFTS. Local infiltration of local anesthetic solution around areas of possible damage, such as periosteal reactions and ligament insertions, may be helpful in horses with specific injuries.

IMAGING CONSIDERATIONS Many causes of lameness in the driving horse, especially in the older horses, are related to problems in the distal limb and the hock joints. Considerable variation in the radiological appearance of these structures can occur, representing normal anatomical variability, old injuries, incidental findings, or wear and tear. Only by localizing the site of pain to a particular joint by intra-articular analgesia is interpreting these findings possible. Standard radiographic views are obtained. Upper limb injuries are often induced by trauma, are not localized easily by diagnostic analgesia, and are difficult to examine with small x-ray machines. Ultrasonography is particularly useful in examining some of these injuries, not only to differentiate the soft tissue components (e.g., hematoma, muscle injury, edema, and wounds), but also to examine the cortical outline of the proximal limb bones in the shoulder and stifle regions for evidence of fractures or other damage. Comparison with the opposite limb is helpful in determining the normal in these areas. Ultrasonography is essential for examining the DFTS and associated structures and for definitive diagnosis and monitoring of desmitis of the suspensory ligament (SL) or ALDDFT.

DIAGNOSTIC ANALGESIA

DIFFICULTIES IN DIAGNOSIS

Many of the causes of lameness in driving horses are related to chronic wear and tear injuries in one or more joints. Distention of a joint capsule or DFTS can be an incidental finding. Localization of pain by a logical system of regional analgesia is central to our approach to lameness diagnosis and is particularly useful in horses with bilateral or multiple limb lameness, because such an approach allows the effect on the gait of one or more of the lame limbs to be removed, allowing identification of additional lame limb(s). In most horses localization

The most difficult problem in diagnosing lameness in a driving horse is an intermittent, often low-grade lameness that may flare up with increased exercise or competition. Many lamenesses are bilateral hindlimb problems, often with several sites of pain contributing to lameness. If making progress in these horses by standard examination techniques is impossible, scintigraphic examination may be useful. The advantages of scintigraphy include the ability to cover many areas of the body (forelimbs and hindlimbs, back and pelvis) at one session,

CHAPTER 125 the non-invasive nature of the technique, and its use to monitor healing. The disadvantages include cost, availability, and the lower sensitivity of the technique in localizing chronic sites of inflammation. Several sites may be detected as having increased radiopharmaceutical uptake, and other techniques, such as local analgesia, are necessary to assess clinical significance. Making a definitive diagnosis is not always possible, but it is important to treat what is diagnosable or visible and to monitor the horse’s progress carefully during convalescence. A re-assessment of the horse at regular stages may cast further light on the problem. Rest may be easy to accomplish in driving horses because they have a long working life, and in pairs and teams a spare horse may be available to take the lame horse’s place, allowing competition to be continued. A problem occasionally encountered in lameness from harness and carriage use is an abnormal gait, often intermittent, seen only while the horse is working in harness, usually with the carriage. Lameness often is manifested at the collected trot in the forelimb, and an extra lift in the shoulder movement during protraction is apparent. Usually only one limb is affected. The horse appears normal at the walk and extended trot, and the problem is not exacerbated by exercise. The actual diagnosis of this condition remains obscure, but one possible theory revolves around the effect of the neck collar on the action of the scapula while the animal is in harness: a mechanical interference. In some horses, changing from a neck collar to breast band harness appears to stop the problem.

SHOEING Most driving horses are shod conventionally, with few special techniques or shoes. Many are shod with flat, fullered shoes set rather short and tight at the heels to minimize interference injuries to the horse and other members in the pair or team. Other reasons for such shoeing given by farriers and owners include minimizing shoe loss in the varying surfaces of the competition and preventing inadvertent removal by the wearer or another horse by standing on the shoe. Shortshoeing a horse, with a tight fit in the heel, exacerbates poor foot conformation, whether the horse has upright, boxy feet or long-toed and low, weak-heeled feet. The use of studs and occasionally calks, especially in the hind feet, is common in an attempt to increase grip in the marathon phase of competition. In the teams, the wheelers, where the power is mainly delivered, often have studs or calks. If they have to be used, we prefer to see studs only put in for the marathon and, if possible, only for the obstacles. The extra grip studs can give may lead to ligament or joint damage, particularly in the lower limb. The use of studs or calks all the time, especially on hard tracks and roads, increases heel trauma and changes the forces transmitted up the limbs. Unilateral studs and calks are not acceptable and should be actively discouraged.

DIAGNOSIS AND MANAGEMENT OF LAMENESS Suspensory Desmitis Desmitis of the SL, both body and branches, is common, particularly in Amish and Mennonite carriage horses. Seventy percent of the Amish carriage horses are Standardbreds, nearly all of which have raced previously and have pre-existing chronic, healed, or healing desmitis. Forelimbs (80%) and hindlimbs (20%) are affected. Body and branch lesions occur with similar prevalence in forelimbs, but branch injuries predominate in hindlimbs. Suspensory desmitis may cause an acute onset, moderate lameness, but often a low-grade insidious lameness is reported

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by the owner or driver. There is often considerable swelling and inflammation associated with the SL. Horses with branch lesions especially are positive to a lower limb flexion test. Diagnosis usually is based on clinical examination and is confirmed by ultrasonography, but in some horses local analgesia is required to confirm that the SL is the source of pain. With branch lesions radiographic examination of the proximal sesamoid bones and splint bones is required to identify concurrent fractures or sesamoiditis, which influence prognosis. Proximal sesamoid bone fractures usually are seen in Standardbred horses that have raced previously and were retired with a fracture that becomes apparent after a second career as an Amish driving horse. Amish and Mennonite horses with a less than good prognosis may be culled. Rest is essential. The duration is determined by improvement in lameness, reduced sensitivity on palpation, and improvement in fiber pattern assessed by ultrasonography. In the initial, acute stages, cold hosing, icing for a few days, and support wrapping are recommended. The combined oral use of dexamethasone and a diuretic is helpful in decreasing inflammation and filling without masking pain. It is important to provide appropriate palmar support, and if necessary, an egg bar shoe is used to increase the weight-bearing surface. In horses with the most severe injuries, and in those where economics does not play a role in selection of treatment, intralesional β-aminoproprionitrile fumarate injections or percutaneous ligament splitting can be performed. We currently have insufficient data to determine whether intralesional β-aminoproprionitrile fumarate improves the prognosis over conventional therapies and surgery and the drug has been taken off the market. Very good results have been obtained with surgical treatment of horses with large core lesions in the body of the SL. After perineural analgesia and localization of the core lesion by ultrasonography, we use a sharpened teat bistoury to enter the core lesion with the limb bearing weight. Some clients prefer to turn out a horse with suspensory desmitis rather than adhere to a structured rehabilitation. Our impression is that lesions heal more slowly, often with less acceptable cosmetic results, compared with horses in which controlled exercise is used. Horses with branch injuries are treated conservatively with a long, slow progressive exercise schedule, with periodic ultrasonographic monitoring. Therapeutic ultrasound treatment also is recommended. Prevention of suspensory desmitis is primarily by selecting well-conformed horses with a good hoof-pastern axis and good feet with continual re-assessment of hoof balance, the adequacy of heel support, and the angle of the pastern relative to the limb conformation.

Foot Problems Foot lameness is common in driving horses and is traumatic, degenerative, or inflammatory. Lameness varies from simple trauma (puncture wounds and bruises) to infectious conditions such as thrush, degenerative conditions such as navicular syndrome, and a host of lesions caused or affected by quality of shoeing. Carriage horses receive a moderate amount of direct trauma resulting in wounds of the digit. The lack of available prepared and manicured training surfaces often necessitates fitness work on gravel roads and through streams and wooded areas, and solar punctures by stumps or sharp objects are not uncommon. Injuries to the coronary region of horses in pairs and four-in-hand occur when driving conditions are difficult, as in the hazards, when one or more horses may be stepped on by an adjacent horse. Although wounds of the coronary band are generally obvious, a puncture of the sole may not be readily apparent. A horse with a puncture may or may not be lame at the time

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of injury. The excitement of competition allows horses to continue without overt signs of discomfort, even with frank injury to the sole. Once back in the stable or sometimes the following day, lameness becomes apparent. Many wounds of the sole and frog are difficult to see, and they can be missed easily. Frog and sole tissue tends to close over the entry site, particularly if the offending object was sharp. If foreign material remains in the foot, severe lameness is usually present. Most horses respond well to curettage and soaking in antiseptic solutions, but protracted lameness is usually a sign of infection. Contrast radiography is useful to detect direction and depth of a tract. When a veterinarian cannot determine if vital structures are involved, surgical exploration may be indicated. Bruises and corns are diagnosed by localization of pain to the sole or heel, history, ruling out other causes of foot lameness, and identification of solar discoloration. Treatment for bruising is directed at protecting the sole. In the case of susceptible horses with a chronic tendency toward bruising, foot soaks or preferably packing gel with dimethylsulfoxide with an overwrap frequently are indicated for flare-ups. Horses with corns, in our experience, require changes in shoeing to relieve pressure on the heel and constant monitoring of the heel growth to discourage underrun, rolled in heels. Synovitis of the distal interphalangeal joint occurs as an acute or, less commonly, as a recurrent condition. Effusion of the distal interphalangeal joint and lameness generally are exacerbated by distal limb flexion. Diagnosis is confirmed by intra-articular analgesia. Treatment comprises phenylbutazone (2 g sid) or flunixin meglumine (500 mg sid) for several days, icing of the digit, and intramuscular administration of a polysulfated glycosaminoglycan (PSGAG), with or without intraarticular administration of hyaluronan or corticosteroids. Navicular syndrome may be more prevalent in carriage horses of certain breeds. The European Warmbloods, particularly the heavier horses, appear to be at risk. Navicular syndrome is nearly non-existent in driving ponies. Horses with navicular syndrome have an insidious lameness that usually resolves with palmar digital analgesia. Occasionally a horse has sudden onset of moderate to severe lameness without any history of a chronic problem. These horses may have dramatic lesions apparent radiographically without a reasonable explanation for why the lameness occurred suddenly rather than gradually. A critical evaluation of hoof balance is important, and we recommend using bar or egg bar shoes and oral isoxsuprine (400 mg bid). Horses with more pronounced lameness are also treated with phenylbutazone (1 to 2 gm PO sid). The greatest number of foot lamenesses seen in carriage horses fit into a broad category of palmar heel pain. Lengthy drives on hard surfaces result in chronic contusions to the hoof capsule and subsequent lameness. Palmar heel pain often is correlated with the degree of work the horse is undertaking currently and may occur seasonally in susceptible individuals. Lameness varies from slight to moderate and is exacerbated by circling on hard ground with the affected leg on the inside of the circle. Hoof tester examination may reveal pain from the medial or lateral sulcus across to that quarter, but a large number of horses have no reaction. Lameness is eliminated by perineural analgesia of the palmar digital nerves. Intraarticular analgesia of the distal interphalangeal joint and intrathecal analgesia of the navicular bursa ideally should be performed to rule out these structures as sources of pain. Radiographic examination usually is unrewarding. Assessment of hoof balance and shoeing is necessary, and until any imbalance has been corrected, recommending other therapies is pointless. We have had good results from increasing the length of support or ground surface in the dorsal/palmar direction of the hoof, without any other therapy. Many horse owners do not understand when instructed to move the weight bearing surface farther palmarly, and they simply raise the heel.

Talking directly with the farrier and providing explanatory diagrams to the client is worthwhile. If the heels are too weak or inadequate to allow for corrective trimming, using egg bar shoes until heel growth is adequate may be necessary.

Distal Hock Joint Pain Osteoarthritis of the distal tarsal joints is common, particularly in older and larger horses (>10 years old). Many of these horses are not presented by the owner or driver as overtly lame but with a history referring to lack of performance or action, stiffness, back problems, or poor bending. Some horses with osteoarthritis, especially from teams, are not identified until veterinary inspections at events. Many older driving horses, particularly those in horse driving trials at a high level, have an uneven hindlimb gait, especially when trotted in hand, and have positive upper limb flexion tests. The horse often is said to warm or work into its work (warm out of lameness), and owners do not request investigation. A high percentage of these horses have low-grade osteoarthritis of the distal tarsal joints. In some horses acute lameness or gradual worsening of lameness (often described as unilateral lameness by the driver) leads to lameness investigation. In the Warmblood breeds an earlier incidence of this problem has become apparent in recent years, with horses of 5 to 8 years old showing severe osteoarthritis and even ankylosis of affected joints. Many have poorly conformed and small hocks, and in some this osteoarthritis appears to be a sequel to developmental orthopedic disease in a young, growing animal. Diagnosis is based on clinical examination, intra-articular analgesia, and radiography. Many horses have bilateral lameness, with one side worse than the other, and evidence of gluteal muscle atrophy. Poor hock conformation (sicklehocked, straight, or cow-hocked) predisposes some horses to this condition. Shoe and hoof wear may indicate toe dragging or abnormal lateral breakover. Swelling may be palpable or visible at the seat of spavin. Tarsocrural joint distention is a common incidental finding, but it may indicate proximal intertarsal (talocalcaneal-centroquatral) joint involvement. The gait often is characterized by reduced foot flight arc and hock flexion, leading to toe dragging, and adduction of the limb medially underneath the body to land and then breakover laterally. On the lunge, lameness of the inside hindlimb may be worse, with shortening of the cranial phase of the stride and a tendency to fall toward the handler. Bilateral lameness is common, although one leg is often worse, leading to a choppy or stilted gait. Flexion tests of the upper hindlimb are often positive bilaterally, but the response varies enormously depending on the stage and extent of the disease and the individual horse. Positive flexion tests in the hindlimb of older driving horses are common, even in the absence of lameness. Initial localization of the lameness to the hock region can be accomplished by perineural analgesia, although intraarticular anesthesia is more specific Previously the centrodistal and tarsometatarsal joints were blocked separately, but more recently, only the tarsometatarsal is blocked, on the basis of recent research confirming the high rate of diffusion of mepivacaine between the two joints. A poor correlation exists between the degree of lameness and the extent of radiological abnormalities. Scintigraphic examination may be indicated in the absence of radiological abnormalities. Treatment depends on a variety of factors including the degree of lameness, other concurrent causes of lameness (e.g., back problems), the type and extent of radiological abnormalities, the age of the animal, the level of work, the competition undertaken, the time and cost constraints, and the response to previous treatment. Conservative treatments often are used when financial constraints exist, when lameness

CHAPTER 125 is mild, when radiographically the disease is advanced, or simply to assess the effects of treatment before considering more radical therapy. Surgical treatments involve the willingness of the owner to make the financial investment and subject the horse to the risk of general anesthesia. We usually assess all aspects on an individual basis before embarking on a standard treatment plan, involving three monthly clinical and radiographic examinations. In general, because of the low-grade and chronic nature of the complaint in driving horses, the horse initially is treated conservatively with corrective shoeing (graduated toe heel shoe, rolled at the toe, with or without lateral extension), a controlled graduated exercise program (up to 90 minutes) placing an emphasis on walking and trotting in a straight line (ridden or driven), and oral medication with variable levels of NSAIDs (usually phenylbutazone) to control pain and encourage a more normal action. Many driving horses make considerable clinical progress with this regimen, but few highlevel driving trial horses are able to return to competition quickly. Healing may take up to 18 months, and in some healing never happens using conservative treatments. Predicting the course of the disease and ultimate result in any one horse is difficult early on and requires consideration of all the clinical and radiographic findings. Many horses improve, but they do not become sound, and have minimal progression of radiological abnormalities over 6 to 12 months. Horses with more obvious lameness, or those that are unable to cope with exercise with orally administered phenylbutazone, may be candidates for intra-articular injections with long-acting corticosteroid preparations (40 mg methylprednisolone acetate per joint). This may result in improvement for 3 to 6 months, and repeated injection usually is required. The use of NSAIDs or corticosteroids is not allowed in official competitions, and drugs must be withdrawn according to the manufacturers’ recommendations before any competition. Arthrodesis is used in horses that fail to respond to conservative treatment, are too painful to achieve ankylosis by exercise, and where time to return to performance soundness is important. In horses with minimal radiographic changes, intraarticular injection of sodium monoiodoacetate is performed under general anesthesia. In horses with more advanced radiological abnormalities or those in which monoiodoacetate has failed to achieve ankylosis, surgical treatment using three drill holes is used in each joint. Controlled exercise postoperatively is essential for success with either treatment. Although many driving horses with osteoarthritis of the distal tarsal joints are useable with treatment, complete resolution of lameness is unusual.

Exertional Rhabdomyolysis Carriage horses have isolated episodes of tying up during competition or strenuous exercise, and this is a true exertional rhabdomyolysis. Competition horses may develop mild signs of muscle stiffness affecting the hindquarters, during or at the conclusion of an exertional session, such as the marathon. The condition may become apparent in the 10-minute box, during the formal veterinary examination section, or before the marathon course. Clinical signs are invariably subtle and may be interpreted as fatigue by an inexperienced competitor. Affected horses should be withdrawn from the competition to avoid further skeletal muscle damage. Treatment should include administration of anti-inflammatory drugs and low doses of acepromazine (5 to 25 mg total dose) and insuring adequate hydration. Horses should not be walked out of the stiffness and should be moved by trailer from the 10-minute box to a treatment stall. To prevent further episodes, the feeding up to and including the competition and the horse’s fitness program should be evaluated and amended as necessary. Teaching drivers how to

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assess the horse’s fitness by measurement of temperature and pulse and respiratory rates on the stress days of training sessions is particularly valuable. Acute, severe rhabdomyolysis (tying up) also occurs in horses driven by the Amish and Mennonites. These are frequently emergency situations. Horses have true, severe exertional rhabdomyolysis and are often in recumbency when examined. The clinical signs in non-recumbent horses are extreme muscle stiffness and swelling over the topline and gluteal muscle groups, increased heart rate, sweating, and colic-like symptoms. The history is consistent: the horse becomes stiff while being driven, but the driver needed to continue to a destination and may have been driven another 1 to 15 miles. The condition in colloquial Amish terminology is referred to as kidney shot. Rehydration and controlling pain and shock are imperative. Tranquilizers are particularly helpful, and measurement of packed cell volume and total protein concentration is useful for monitoring hydration. Measurement of creatine kinase may be useful prognostically in recumbent horses, although the initial response to treatment and the ability to get the animal on its feet are primary factors in determining whether the horse can be saved. Creatine kinase concentrations are often 400,000 to 800,000 IU/L (normal 130 to 400 IU/L), and we have treated horses successfully with levels up to 600,000 IU/L. Without prompt emergency attention, nearly all of the more severely affected horses die or are ultimately humanely destroyed. Most horses that remain recumbent after 24 hours are lost. Horses are viewed by Amish farmers as utilitarian and necessary for transportation, and prevention of fatal exertional rhabdomyolysis is not necessarily easy. Owners should be advised of the need to match exercise with the intake of concentrates. If possible, the horse’s entire body can be clipped if the onset of summer or warm weather is sudden or the winter coat is still present. Clipping can be done using a gas-powered generator for the clippers. Clipped horses have less risk of severe dehydration, and a clipped horse apparently is less prone to rhabdomyolysis than a hirsute horse.

Tenosynovitis of the Digital Flexor Tendon Sheath Tenosynovitis of the DFTS is a common cause of acute hindlimb lameness. Often extreme swelling of the DFTS occurs and is turgid and firm, which contrasts to chronic, benign distention of the DFTS in which fluid in an overly stretched sheath can be balloted from side to side. With horses with acute tenosynovitis there is a substantial response to lower limb flexion, and in some horses (5%) a non–weight-bearing lameness develops. Using local analgesia is unnecessary, but intrathecal analgesia using 6 to 10 ml of mepivacaine can be used to confirm the source of pain. Synoviocentesis is best performed distal to the fetlock and is facilitated by applying a disposable elastic bandage around the distal metatarsal region to push the fluid into the distal projections of the sheath on the plantar aspect of the pastern (Fig. 125-1). Once the sheath has been entered, an assistant cuts off the bandage, and local anesthetic solution is injected. Radiography is usually negative, but it is necessary to be certain that no unexpected lesion is missed. Ultrasonographic examination is essential to determine if tenosynovitis is associated with a lesion of the deep digital flexor tendon, which requires a longer convalescence and horses have a more guarded prognosis than those with primary tenosynovitis. Treatment is based on reducing inflammation and controlling exercise. Uncontrolled turnout results in prolonged healing, and stall rest followed by walking in hand is preferable. A horse with an acute injury is treated with icing for 40 minutes twice a day, for 2 to 3 days, and orally administered NSAIDs. Intrathecally administered hyaluronan is beneficial. Caution should

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A

B

A, Application of a pressure bandage isolates fluid in the distal outpouchings of the digital flexor tendon sheath, facilitating synoviocentesis. B, An assistant cuts the compression bandage during injection.

Fig. 125-1

be exercised in the use of corticosteroids, which may provide temporary relief and often give the client a false sense of security regarding the rate of healing. Isoflupredone acetate is recommended, is short-acting, and may control the acute flare-up without any long-term affect that makes monitoring progress difficult. Methylprednisolone acetate lasts at least twice as long and may predispose the horse to develop dystrophic mineralization in the sheath. We have had better long-term results with conservative medical management than with surgical treatment by desmotomy of the plantar annular ligament. Prevention of tenosynovitis and tears of the deep digital flexor tendon is difficult, because most injuries are acute and unforeseeable, occurring during strenuous exercise. A team horse previously used as a wheeler may be better placed as a leader. The foot should be kept well balanced, with a fullfitting shoe providing adequate plantar support.

Chronic Osteoarthritis of the Lower Limb Joints Many driving horses develop chronic osteoarthritis of the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints as a result of wear and tear because of the work they undertake, the length of time they are used, and other factors such as conformation, foot shape, and shoeing. Radiographic examination of these joints, especially in the hindlimbs and in larger animals, often reveals a variety of intra-articular and peri-articular abnormalities that may be

associated with lameness. Older driving horses often live with low-grade hindlimb gait abnormalities associated with lowgrade joint pain. This low-grade, chronic, and often multiple leg or multiple joint pain can be exacerbated by excessive or different exercise regimens, leading to acute flare-ups, increased lameness (often unilateral), joint flexion pain, periarticular heat, and joint swelling. Radiographs obtained at this time reveal little more than the pre-existing abnormalities. Intra-articular analgesia may be essential to localize lameness, but multiple limb and joint involvement can make localization difficult. Nuclear scintigraphy may be helpful, but it is expensive, and often is used only after early treatment has proved unsuccessful. Treatment of horses with acute flare-ups of osteoarthritis involves cold therapy such as cold hosing or ice packs, compression bandaging, systemic NSAIDs, topical applications of various anti-inflammatory substances and intra-articular or systemic medications such as corticosteroids, hyaluronan, and PSGAGs. Rest and a controlled, graduated return to exercise are important. Management of horses with chronic osteoarthritis involves a careful review and possible modification of the horse’s work program, judicious use of NSAIDs, physiotherapy techniques such as laser or ultrasound treatment, and systemic medication with hyaluronan or PSGAGs. The prognosis varies enormously depending on the severity and extent of the problem, the way in which the individual horse responds to

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pain and the level of work required to keep the horse sound and competing. In many horses, if the hindlimbs are affected and especially if the condition is bilateral and the horse is part of a pair or team, then the chronic low-level lameness is not observed, is undiagnosed, or is ignored. An acute flare-up may lead to recognition of the problem and diagnosis. Prognosis for horses with the first acute flare-up is reasonable, but those with further occurrences warrant a more guarded prognosis.

Stifle Lameness A definitive diagnosis of the cause of stifle pain in driving horses is often difficult to determine. Most horses with stifle lameness are wheelers of four-in-hand or one of a pair. It is generally accepted that wheelers supply 60% of the workload in pulling, which may affect the incidence of stifle lameness. Lameness is usually acute in onset and unilateral, with no stifle effusion or other localizing clinical signs. Stifle flexion may cause more obvious accentuation of lameness than other hindlimb flexion tests. Lameness is improved by intra-articular analgesia. Radiographs uniformly are negative. Ultrasonographic examination may sometimes reveal a lesion, but in more than 80% of horses no cause of pain can be identified. Arthroscopic exploration may be warranted, but this is expensive, and only a limited part of the stifle can be assessed. The prognosis generally is guarded for horses with a known meniscal or cruciate ligament injury and for those without a specific diagnosis. The best results have been achieved after intra-articular treatment with hyaluronan, combined with systemic administration of PSGAG and rest or rigidly controlled exercise, walking in hand. We recommend that horses should not resume work until 60 days after complete resolution of lameness and when they do not respond to flexion of the stifle.

Direct Trauma Traumatic injuries to the limbs and body of the driving animal are common.

Interference Injuries Distal limb lacerations of varying severity are common, especially in horses that are part of a team, particularly in combined driving, and are caused by over-reaching (forelimbs) or by interference from other horses. The most common lesions involve the heels and coronary band (Fig. 125-2), although wounds to the mid-pastern and distal palmar (plantar) aspect of the metacarpal (metatarsal) region occur frequently. Many wounds are superficial and consist only of contaminated skin, but it is essential to check for injury to the flexor tendons and the DFTSs, joint integrity, and damage to the coronary band. The horse should be restrained properly, the affected area clipped and vigorously cleaned, and the damage assessed before medical or surgical treatment is initiated. In some horses detailed examination using digital palpation with sterile gloves, radiography, ultrasonography, and even surgical exploration may be necessary. Early and aggressive treatment may improve the prognosis considerably in the short and long term.

Injuries to the Brisket, Lower Neck, Antebrachium, Stifle, and Crus Injuries usually occur during the marathon phase of driving trials, especially in the obstacles, or after runaways and accidents in any driven animal. The tendency of some drivers in combined driving in recent years to drive the carriage as a battering ram through the obstacles has increased the incidence of these injuries. Skin lesions occur, especially in the brisket and lower neck and upper forearm regions, and can range from full-thickness lacerations to mild hair loss and deeper bruising (Fig. 125-3). In some horses little is visible externally except mild swelling to suggest the site of impact. Stiffness or lameness often develops several hours later. Severe injuries, particularly involving broken shafts or obstacles, can lead to

Fig. 125-2 A severe heel bulb laceration sustained by a driving horse during a team competition, probably caused by interference from another horse.

life-threatening injuries to the chest, abdomen, or vital vascular structures. The injured area should be examined carefully, particularly when lacerations are present. In these, thorough lavage and cleaning, followed by digital exploration using sterile gloves to assess for additional deeper damage is essential. Surgical repair may be necessary. Horses with blunt soft tissue damage and bruising benefit from light walking in hand, cold therapy, topical and systemic anti-inflammatory medication, and physiotherapy techniques.

Desmitis of the Accessory Ligament of the Deep Digital Flexor Tendon Desmitis of the ALDDFT is a common cause of forelimb lameness. Older horses, including ponies, are more likely to be affected, and injury can occur at exercise or during turnout. Onset is usually acute, with unilateral forelimb lameness occurring during or immediately after exercise. Swelling of the ALDDFT occurs with edematous swelling of the surrounding soft tissues. In horses with severe desmitis, periligamentous hemorrhage can occur. Palpable pain is rare, but heat usually is apparent. Ultrasonographic examination is used to determine the extent of injury. Diffuse lesions are more common than focal core lesions. Damage to other tendon structures is uncommon, but adhesions to the SDFT or deep digital flexor tendon do occur, particularly in horses with chronic recurrent injuries.

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Lameness in the Sport Horse Treatment of horses with acute injuries includes cold therapy, compression bandaging, box rest, and topical or systemic anti-inflammatory medications. We regularly recommend the use of systemic PSGAG therapy and therapeutic ultrasound physiotherapy from 7 days after injury. Graduated walking in hand is encouraged from 7 days after injury, increasing in duration up until 12 weeks, when limited free exercise is allowed. Ultrasonography is essential to determine when healing is sufficient to allow exercise to begin. A total convalescent period of 6 to 15 months may be required. Some injuries, particularly in older horses, do not heal satisfactorily. Occasionally horses with chronic injuries with adhesions have been treated by desmotomy of the ALDDFT, but the prognosis for return to full soundness is guarded.

Superficial Digital Flexor Tendonitis Superficial digital flexor tendonitis is not common in the driving horse, although the condition is seen occasionally as a flare-up of a lesion sustained previously in another discipline, or in wheelers when the going during the marathon phase has been soft and deep. Most lesions are in the distal half of the metacarpal region and are generally mild. Diagnosis is based on clinical and ultrasonographic examinations. The prognosis for return to full work as a driving horse is generally good, because most of the injuries are mild and the type of work to be undertaken is usually slow.

A severe traumatic injury to the upper forelimb and brisket regions caused by a collision with an obstacle in the marathon.

Fig. 125-3

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126

Lameness in Draft Horses Dallas O. Goble

he Draft horse today enjoys a position in the world far different from when it was considered primarily a work animal. Draft horses supplied power for farming, transportation of commodities, lumbering, road building, and all such tasks until the 1930s, when the gasoline engine essentially replaced the horse. Isolated areas still continued to use the Draft horse for farming and some lumbering activities until the early 1940s. After this period, Draft horses were used primarily for specialty areas such as movie production, theme parks, parades, and frontier celebrations. But in some communities, religion and family tradition mandated the continual use of Draft horses as a power source for farming. During the 1950s and 1960s, Draft horses decreased in numbers in the United States and subsequently, the genetic pool was decreased. Draft horses started gaining popularity in the late 1970s and early 1980s and have once again become a popular member of the horse industry.

T

Draft horses today are different from those of the early 1900s. They perform different functions and are owned for a different purpose. A Draft horse is far more likely to be simply a hobby than an economic part of the family income. Many horses are used strictly for show purposes in classes such as halter, fine harness, and equitation, or for parades and advertising. Draft horses are used for trail riding, pleasure riding, fox hunting (often crossbred with Thoroughbreds), and other pleasure use. In some mountain areas, where selective lumbering of individual trees is undertaken, Draft horses are still used today. With a resurgence of interest in mules, Draft horse mares often are used in the breeding programs. Draft horses frequently are crossed with Thoroughbreds to change the genetic pool for the breeding of large hunter, jumper, and Three Day Event horses. Pulling contests are popular in certain areas and represent an additional use of the modernday Draft horse.

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Lameness in the Sport Horse Treatment of horses with acute injuries includes cold therapy, compression bandaging, box rest, and topical or systemic anti-inflammatory medications. We regularly recommend the use of systemic PSGAG therapy and therapeutic ultrasound physiotherapy from 7 days after injury. Graduated walking in hand is encouraged from 7 days after injury, increasing in duration up until 12 weeks, when limited free exercise is allowed. Ultrasonography is essential to determine when healing is sufficient to allow exercise to begin. A total convalescent period of 6 to 15 months may be required. Some injuries, particularly in older horses, do not heal satisfactorily. Occasionally horses with chronic injuries with adhesions have been treated by desmotomy of the ALDDFT, but the prognosis for return to full soundness is guarded.

Superficial Digital Flexor Tendonitis Superficial digital flexor tendonitis is not common in the driving horse, although the condition is seen occasionally as a flare-up of a lesion sustained previously in another discipline, or in wheelers when the going during the marathon phase has been soft and deep. Most lesions are in the distal half of the metacarpal region and are generally mild. Diagnosis is based on clinical and ultrasonographic examinations. The prognosis for return to full work as a driving horse is generally good, because most of the injuries are mild and the type of work to be undertaken is usually slow.

A severe traumatic injury to the upper forelimb and brisket regions caused by a collision with an obstacle in the marathon.

Fig. 125-3

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Lameness in Draft Horses Dallas O. Goble

he Draft horse today enjoys a position in the world far different from when it was considered primarily a work animal. Draft horses supplied power for farming, transportation of commodities, lumbering, road building, and all such tasks until the 1930s, when the gasoline engine essentially replaced the horse. Isolated areas still continued to use the Draft horse for farming and some lumbering activities until the early 1940s. After this period, Draft horses were used primarily for specialty areas such as movie production, theme parks, parades, and frontier celebrations. But in some communities, religion and family tradition mandated the continual use of Draft horses as a power source for farming. During the 1950s and 1960s, Draft horses decreased in numbers in the United States and subsequently, the genetic pool was decreased. Draft horses started gaining popularity in the late 1970s and early 1980s and have once again become a popular member of the horse industry.

T

Draft horses today are different from those of the early 1900s. They perform different functions and are owned for a different purpose. A Draft horse is far more likely to be simply a hobby than an economic part of the family income. Many horses are used strictly for show purposes in classes such as halter, fine harness, and equitation, or for parades and advertising. Draft horses are used for trail riding, pleasure riding, fox hunting (often crossbred with Thoroughbreds), and other pleasure use. In some mountain areas, where selective lumbering of individual trees is undertaken, Draft horses are still used today. With a resurgence of interest in mules, Draft horse mares often are used in the breeding programs. Draft horses frequently are crossed with Thoroughbreds to change the genetic pool for the breeding of large hunter, jumper, and Three Day Event horses. Pulling contests are popular in certain areas and represent an additional use of the modernday Draft horse.

CHAPTER 126 MODERN-DAY DRAFT HORSES The most important physical change of the modern-day Draft horse is its size. In many modern breeding operations, size is the main criterion used for selection. When Draft horses were used predominantly as working horses, the average weight was 680 to 775 kg (1500 to 1700 lb) and the average height was 1.6 to 1.7 m (15.5 to 17 hands). This size was optimal for the multipurpose activities these horses performed on most farms and ranches. They pulled the plow, mowed and racked hay, helped round up cattle, and often took the family to church on Sunday. Draft horses today are more frequently in the range of 820 to 1000 kg (1800 to 2200 lb) and measure 1.8 to 2 m (17.5 to 19.5 hands) in height. As a result of selection based on size as the dominant characteristic, conformation and quality have suffered in some respects. Distribution of lameness also has changed. Foot size and quality have not increased proportionately with body size and weight. Osteoarthritis is common in Draft horses and likely is related to body size rather than the use of the horse. Hybrid vigor, once thought to be advantageous, has decreased by using the practice of line breeding for selected traits. The large size of a Draft horse sometimes misleads one to think the horse can withstand greater stress and disease than can light horses, but I have not found this to be true. Draft horses may not recover as well as light horses with the same injury or disease. Because Draft horses have a tendency to be stoic, recognizing a severe problem early in the disease process may be difficult. This tendency may cause a costly delay in diagnosis and management. The physical size of Draft horses today has hindered veterinary care and treatment. Veterinarians tend to be unsure of drug dosage and appropriate treatment schedules because of the large body size. Many hobby horse owners do not have facilities adequate to handle a 1000-kg horse and may not be knowledgeable in Draft horse care. Draft horses are not always well trained or easy to handle, and owners are sometimes unable to lend assistance when needed. These facts have curtailed the interest of many practicing veterinarians who have difficulty rationalizing being stepped on by a l000-kg Draft horse as fun. In addition, finding quality foot care for a Draft horse is sometimes difficult, because most farriers are experienced with light horses. Farriers feel similar to veterinarians: “Why hold up a 1000-kg horse twice as long as needed to hold up a 500-kg horse?” In addition, farriers who shoe Draft horses have to stock nails, shoes, and bar stock often on special order or low-volume items, a fact that dramatically increases overhead expenses. Thankfully, some veterinarians and farriers are willing to treat and specialize in Draft horse care. The following discussions related to Draft horse lameness are my personal clinical experiences and do not necessarily reflect what may be in the equine literature. Lameness distribution may vary from my observations depending on the use, location, individual draft breed studied, or other factors associated with different populations of horses.

TEN MOST COMMON LAMENESS PROBLEMS Over the last several years I have evaluated 745 Draft horses admitted with a chief complaint of lameness. The following list shows the top 10 lameness conditions that I have observed in order of decreasing frequency (33 horses had other problems): 1. Foot lameness (abscess, hoof cracks, laminitis, and sidebone) ...................................................... 260 2. Tarsal lameness (osteoarthritis, bog spavin, and osteochondrosis).................................................. 207 3. Splints ................................................................. 84 4. Tendonitis and suspensory desmitis ..................... 45

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5. Osteoarthritis of the distal interphalangeal or proximal interphalangeal joints ........................... 6. Fetlock lameness (sesamoiditis, osteoarthritis, and osteochondrosis) ........................................... 7. Thoroughpin ....................................................... 8. Carpal lameness (traumatic or infectious carpitis) ............................................................... 9. Stifle lameness (traumatic, upper fixation of the patella, and osteochondrosis) ........................ 10. Myopathy ............................................................

44 23 18 13 10 8

LAMENESS EXAMINATION Diagnosis and management of lameness in a Draft horse may seem more intimidating simply because of the large size of the horse and the infrequency with which requests are made for examination compared with light horses. In reality, Draft horses suffer from the same problems as do light horses, although the distribution is different, and the principles of diagnosis and management are the same. The lameness examination is the same as in light horses, and any deficiency of hands-on experience can be overcome by a systematic and thorough examination. Palpation of peripheral nerves (palmar and plantar digital nerve, in particular) can be difficult because of thick skin and hair, and veterinarians are sometimes reluctant to attempt perineural or intra-articular blocks. The anatomy is the same, but the ability to palpate the nerves is diminished by these factors and also by subcutaneous thickening that some Draft horses develop in the lower limb. Draft horse lameness diagnosis and management lagged behind that of light horses for many years. First, as long as the horse could still accomplish farm work, less concern was shown for a horse that limped slightly. Possibly the person behind the plow or cultivator also limped and accepted it as part of doing the job. Second, economic considerations were a major factor in the farming operation. This does not reflect necessarily a lack of care, but it was simply an accepted part of working in that day and time. But today, Draft horses are afforded the same concerns and care given to the light horse, and only modification of most treatment protocols needs to be made. Detailed description of the lameness examination can be found in earlier chapters. Special attention should be paid to several critical points, however. Draft horses are more stoical than light horses and, as a result, lameness may be advanced when first recognized. For example, Draft horses with osteoarthritis of the proximal interphalangeal or distal interphalangeal joints may have severe radiographic changes, but the owner may report that the horse only recently showed signs of lameness. Granted, many owners are inexperienced, but even the experienced owner may not recognize a problem until it is well advanced. This can be explained partially by the fact that a Draft horse often is used at a gait (walk) that makes lameness less obvious, and the horse frequently is hitched with one to seven additional horses, and an individual horse’s problems are less discernible in a group. When possible, observing the horse at a walk and trot on soft and hard surfaces is useful. Hoof tester examination, in my experience, is less reliable in Draft horses than in light horses. Small hoof testers are of questionable value. Even with longhandled hoof testers, it is difficult to apply enough pressure to produce a positive response in many horses. Foot lameness should be suspected if a horse shows grade 1 of 5 lameness on soft footing but grade 3 of 5 lameness on a hard surface. The examination always should include backing the horse at least two or three times and observing the horse at the walk and trot in a circle and in tight turns. Sometimes conditions such as shivers, stringhalt, or intermittent upward fixation of the patella are seen only during these maneuvers.

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Lower limb flexion tests are less rewarding in Draft horses than in light horses. It is difficult to apply sufficient pressure during the flexion test to accentuate pain in this region. A Draft horse may be less willing to trot after a flexion test, making it difficult to determine a true positive response. Most light horses will trot after flexion, even when the reaction is highly positive, but a Draft horse will not trot off as readily without strong urging. In addition, Draft horses often are not accustomed to being trotted in hand routinely. Hindlimb upper limb flexion tests in a Draft horse are a more reliable indicator of hindlimb lameness than in a light horse. I prefer to perform diagnostic nerve blocks with the horse in a standing position, rather than having an assistant elevate the limb. This is especially true when attempting the palmar digital nerve block or abaxial sesamoid block. Palpating anatomical landmarks in this area when a Draft horse is weight bearing is easier than when the limb is elevated. To maintain the limb in an elevated position or to restrain the limb in this position can be difficult. Adequate restraint usually can be achieved by the application of a nose twitch.

LAMENESS COMMON TO THE FORELIMB AND HINDLIMB Foot The foot is the most common source of pain causing lameness in Draft horses. A thorough and complete examination of the foot is paramount to diagnosis and management of lameness. Hoof quality and conformation have suffered in modern-day breeding selection, and as a result we tend to have large horses that are supported on feet that lack hoof size and quality. I suggest that breeders of Draft horses give strong consideration to hoof conformation when making critical selections for breeding programs.

at least initially. Thorough flushing of the foot with povidoneiodine or chlorhexidine diacetate solutions should be done at least once a day for 3 days or until the drainage has stopped. The foot can be soaked in a saturated solution of magnesium sulfate for 3 to 5 days to reduce inflammation and to aid in drainage. Finding a soak boot large enough for Draft horse feet at a reasonable cost is difficult, and I have found an easy solution by using a 1 m length of truck tire inner tubing. The tubing is slipped half its length over the foot, and then up the leg, with the remaining half doubled back up the leg and secured in place by a wrap of choice (Fig. 126-1). The tube then can be filled with the soak solution. Draft horses with an uncomplicated subsolar abscess do not need to be treated with systemic antibiotics. However, if cellulitis of the coronary band and pastern region is present, the administration of antibiotics is indicated. Trimethoprim-sulfadiazine (15 mg/kg PO bid) or ceftiofur sodium (1 mg/kg IV bid or IM) is my usual choice. Judicious use of non-steroidal anti-inflammatory drugs (NSAIDs) is indicated, but theses drugs should not used for extended periods of time or at levels that may mask a more serious problem. Phenylbutazone, 4 g PO or 2 g IV, on the first day is sufficient. Thereafter, 3 g and then 1 g is given orally on the second and third days, respectively. A tetanus booster should be administered if the horse’s vaccination status is not current or is unknown. If the horse’s condition is not improved in 3 days, the horse should be re-examined. Plain radiographs and positive contrast fistulography should be performed. A fistulogram is performed using contrast material administered through a Foley catheter. The foot should be held off the ground when contrast media is infused and held up for 2 minutes thereafter. The foot is then placed in a weight-bearing position, and radiographs are obtained immediately. During weight bearing, a fistulous tract

Subsolar Abscess The most common cause of foot lameness in a Draft horse is a subsolar abscess, a problem most frequently encountered in a forelimb. The high incidence of subsolar abscess formation in Draft horses can be related to several factors. First, obtaining consistent farrier care may be difficult in many locations, and foot care may be neglected. Second, Draft horses often have poor hoof quality and easily develop hoof cracks or severely chipped and broken hoof walls. Clydesdales often have poor hoof quality. Many Draft horses have dropped soles, predisposing them to bruising and subsolar abscess formation. A pair of large, good quality hoof testers provides the simplest method of determining the location of the abscess. Tapping the hoof wall or sole with a hammer (or the hoof testers) can help locate the abscessed area. In horses that recently have been shod or reset, each nail should be examined. An abscess associated with a nail usually develops 5 to 11 days after shoeing. Hoof cracks causing instability of the hoof capsule can cause lameness even though the area of abscessation may have resolved. If a foreign body is lodged in the hoof (nail, glass, or other penetrating object), a fistulogram (contrast radiograph) should be performed. A subsolar abscess can become a life-threatening problem if osteitis of the distal phalanx develops or penetration of the distal interphalangeal joint, deep digital flexor tendon, or navicular bursa occurs. Proper diagnosis is mandatory; otherwise, the long-term prognosis becomes worse. Once the abscess is located, the sole should be pared with caution, especially if the horse has a dropped sole or has a concomitant full-thickness hoof wall crack. Overzealous sole paring may result in extensive mechanical damage to laminae and loss of hoof wall strength. Adequate drainage is paramount, but removing a large amount of sole is not necessary, even when substantial undermining has occurred. In Draft horses, it is important to err toward a conservative approach,

Draft horse with rubber inner tube in place and used as a soak boot for a foot abscess.

Fig. 126-1

CHAPTER 126 often is closed by soft tissue compression. If deeper structures are involved (distal interphalangeal joint, deep digital flexor tendon, distal phalanx, or navicular bursa), an extensive treatment program is initiated, including bacterial cultures, surgical drainage or curettage, lavage of the affected area, and the administration of broad-spectrum intravenous antibiotics. The initial antibiotic treatment usually includes 20,000 IU/kg of potassium penicillin 4 times a day and 6.6 mg/kg of gentamicin once a day. Bacterial culture and sensitivity results may require changing the antibiotic regimen.

Hoof Wall Cracks Forelimb hoof wall cracks were found in 67% of the 165 Draft horses examined for lameness, although not all were the primary cause of the horse’s current problem. Full-thickness hoof wall cracks need to be stabilized when they cause lameness. The crack should be cleaned carefully and curetted, and normal hoof wall should be present on each side of the defect. The technique of dovetailing may provide additional support if hoof repair material is used. Dovetailing is accomplished most easily using a 1-cm ( 3⁄8-inch) round burr on an electric drill and undermining the hoof wall at about a 45º angle, leaving a shelf of hoof wall down to the white line on each side of the defect for the full length of the crack. This provides additional surface area for a stronger repair and reduces the likelihood that the repair material will come out. Care must be exercised to avoid damage to the sensitive laminae or to create bleeding during this procedure because these may predispose to abscess formation beneath the repair material. If the horse is initially unshod, a shoe with clips may be sufficient to provide support and to immobilize the defect. Radiator hose clamps and 1-cm long, No. 8 metal screws can be used to stabilize the crack. Because infection is often a problem, the radiator clamp method can be used initially, when filling the defect with repair material is contraindicated. Antibiotic-impregnated repair material has been used, but my success with this material in Draft horses has been limited, and my preferred method is a shoe and the radiator clamp/ screw combination. It is important to have at least two screws through each piece of clamp and on each side of the defect to add stability. The top clamp should be placed at the proximal limit of the crack. I generally space the clamps 1.9 cm ( 3⁄4 inch) apart, and the number of clamps needed depends on the length, depth, and the amount of instability in the crack and on the size of radiator clamp used. The clamps are removed as the defect grows and replaced if broken. The clamps must be tightened carefully, because lameness from laminar pain will be worse if the

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clamps are too tight. This problem is corrected by adjusting the clamp with a screwdriver.

Laminitis Laminitis in Draft horses is a serious lameness condition, and prognosis for complete resolution often is guarded to unfavorable. Regardless of the cause (grain overload, colitis, metritis, retained placenta, toxemia, and so on), once the pathophysiological process of laminitis is in motion, the end results are similar. The solution to the primary cause often is solved more easily than the secondary problem of laminitis. This is especially true in mares with retained placenta in which the retained placenta and metritis are solved easily, but secondary complications may be devastating. Many of these mares develop severe laminitis with distal displacement (sinking) of the distal phalanx. I would like to contrast my observations of Draft horses with laminitis to similar conditions in light horses. Laminitis carries a more guarded or unfavorable prognosis in Draft horses for many reasons. Our ability to manage secondary problems is less satisfactory in Draft horses. Size, when we consider a 1000-kg as opposed to a 400- to 500-kg horse, is the most important factor. Slings are seldom big enough, and hoists or hoist support systems may not be available to lift a Draft horse safely. Locating a farrier who will work on a chronically lame Draft horse and forge therapeutic shoes on a consistent basis is often difficult. Management of Draft horses with myositis, decubital ulcers, infections, pneumonia, and other secondary complications is more difficult and costly. The owner must be informed clearly of cost, and a dedicated team (owner, farrier, and veterinarian) must be assembled to manage these complications. I generally tell clients that at least 1 year will pass before the horse’s level of function can be assessed reasonably. Classification of laminitis is confusing, and I make little attempt to classify laminitis based on chronicity or by using the Obel grading system (see Chapter 35). Regardless of classification used, prognosis for return to function is poor if lameness is severe and persists for longer than 10 days with intensive treatment. In my experience, two major differences exist between Draft horses and the light horses. First, Draft horses develop laminitis more frequently and severely in the hindlimbs. Second, Draft horses are more likely to develop distal displacement (sinking) of the distal phalanx once laminitis occurs (Fig. 126-2). This latter difference may be related to hoof quality or hoof care in general and the important role that body weight plays in causing distal displacement. In addition,

Lateromedial radiographic view of the front foot of a Draft horse mare that had developed laminitis in all four limbs within 24 hours of foaling and retention of the placenta. The radiograph waas obtained 10 days after foaling. The proximal end of the radiopaque marker on the dorsal hoof wall is at the level of the coronary band. There is both extensive sinking and rotation of the distal phalanx. Note also the broad radiolucent line in the dorsal hoof wall, the result of laminar necrosis. The mare was managed until the foal was weaned but humane destruction was ultimately necessary.

Fig. 126-2

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shoeing methods that flair the hoof wall simply to give the impression of a large foot weaken laminar support. Distal displacement can occur in horses with traumatic laminitis without a traditional laminitic episode. Traumatic laminitis and sinking can occur unilaterally, only to then occur weeks to months later in the opposite foot. Traumatic laminitis caused by incorrect shoeing can be reduced greatly or eliminated when proper shoeing is provided on a regular basis. Diagnosis of laminitis is not difficult except in Draft horses with traumatic laminitis that is slowly progressive, without an acute episode typically seen with laminitis in a light horse. These horses often have a dropped sole (including the frog in many horses), with the entire sole at a level below the hoof wall. Increased digital pulse amplitudes may be missed easily in a Draft horse, but hoof tester sensitivity and abnormal stance are important clinical signs. Initial and follow-up radiographs should always be obtained. Management of Draft horses with laminitis is similar to that in light horses, but some precautions need to be taken. Pain amelioration is important but often difficult to achieve. Clydesdales, for instance, are susceptible to gastric and colonic ulcers when treated with phenylbutazone. The Belgian horses that I have treated with phenylbutazone seem less susceptible to ulcers than do Clydesdales. In Clydesdales I seldom if ever administer more than 4 g phenylbutazone orally daily, or do not exceed 3 g intravenously daily, unless no other alternative is available. The dose should be lowered as quickly as possible, and the high dose should be maintained for a maximum of 5 to 7 days. Although this dose is low based on milligrams per kilogram, Clydesdales have many gastrointestinal complications with higher doses. Flunixin meglumine, meclofenamic acid, and other NSAIDs can be used, but phenylbutazone is the most frequently used and cost-effective drug. Butorphanol tartrate (0.01 to 0.02 mg/kg) can be used with phenylbutazone to lower the necessary dose of NSAIDs. Butorphanol tartrate alone is not a satisfactory analgesic for Draft horses with laminitis, but it is useful with NSAIDs, and can be repeated 3 to 4 times each day. To provide frog support initially, I use pieces of rubber stall matting, 1.9 cm ( 3⁄4 inch) thick. The matting is cut to fit the foot and frog and then secured with fiberglass cast material. To increase thickness, two rubber pads can be glued together. To raise the heels in Draft horses with acute laminitis, a hand grinder can be used to make a wedge pad from the rubber mat. I believe raising the heels helps to reduce pain and rotation of the distal phalanx. Heels should be elevated 10º to 14º, however. The single most important factor in Draft horses with laminitis is to avoid excessive paring of the sole. Paring the sole away to make it look like a normal sole is putting the curse of death on Draft horses with laminitis. This practice removes natural protection from rotation or sinking, and the sole supports the foot better than anything we can apply externally. Radical hoof wall resection should be avoided. I recall two horses that were referred after complete dorsal hoof wall resection. In both horses the remaining hoof wall lacked strength, and although one horse was shod and the other was unshod, the distal phalanx rotated and sank through the remaining hoof wall in both horses, which were euthanized. If hoof wall resection is indicated, a shoe with side or quarter clips is applied before the procedure is performed. The entire hoof wall should not be removed at one time, but resection should be staged over 2 to 3 weeks. If the hoof wall spreads and crowding of the side clips occurs or if further rotation or sinking of the distal phalanx is observed, any further resection is delayed. The coronary band should be assessed each day for signs of sinking (depression at the top of the coronary band). Radiography is helpful but does not replace careful physical examination. Horses with subsolar abscesses are treated by

drilling small holes (3 to 5 mm) through the hoof rather than by resection of large portions of hoof wall and sole. Two or more holes may need to be placed in the hoof wall or sole to provide adequate drainage and to flush the site. Drilling small holes does not reduce hoof wall strength compared with paring or removing large portions using conventional methods.

Sidebone Mineralization of the cartilages of the foot (sidebone) is a common radiographic finding in Draft horses, particularly in the forelimbs, but is an infrequent cause of lameness. Of 113 Draft horses with sidebones, 80 had the condition bilaterally in the forelimbs, and 28 horses had it bilaterally in the hindlimbs. Five horses had unilateral involvement. Draft horses with angular limb deformities are more likely to develop sidebone than are horses with normal bone structure. Sidebone is more common in Draft horses with poor hoof quality than in horses with normal hooves. Trauma to the heels and quarters and reduced palmar support are contributing factors. If sidebone is the cause of lameness, lameness grade is usually mild (1 to 2 of 5). Lameness is most common in horses 4 to 7 year of age. Sidebone fractures, occurring in older horses, can cause acute lameness. Lameness is usually most apparent when the horse is working on pavement or other hard surfaces. On soft surfaces the hoof can tip or angle, whereas on hard surfaces the bony column cannot move. Lameness is most obvious when the horses are working in circles or tight turns. Lameness associated with sidebone can be difficult to confirm. Palmar or plantar digital nerve blocks usually greatly improved clinical signs, and abaxial sesamoid blocks abolish signs. Both nerve blocks provide analgesia to numerous other structures that are more frequent causes of lameness, however. Physical examination is more helpful than is diagnostic analgesia. Tapping on the upper one fourth of the hoof wall (while avoiding hitting the coronary band) with hoof testers or a hammer may elicit pain. A lateral or medial wedge test often causes lameness (see Chapter 8). Thermography is valuable in some horses, showing increased temperature in the area of the sidebone. Radiography is of limited value, because the mere presence of mineralization is not conclusive evidence for lameness diagnosis. Treatment includes rest and hoof care. The hoof should be trimmed level. Hoof strike should be evaluated dynamically (how it strikes the ground) rather than by just viewing the hoof in a static position. Vertical and parallel grooving may allow the hoof wall to expand and may reduce pressure, but I have not found grooving highly rewarding. The horse should have stall rest or small paddock confinement for 4 to 8 weeks and NSAID therapy. The foot must be balanced properly before the horse resumes a normal exercise program. Fractures associated with large sidebones may be accompanied by osteoarthritis of the distal interphalangeal joint. Rarely the proximal interphalangeal joint is involved. Surgical management of Draft horses with sidebone fractures often is unrewarding, and I do not recommend it unless conservative management efforts have failed. Conservative management includes an extended period of stall rest (8 to 12 weeks) and then small, level paddock exercise for 6 to 8 months. Healing as shown on radiographs may require extensive time, and even then the fracture still may be evident, surrounded by proliferative exostosis. Unilateral palmar digital neurectomy also can be performed. This will provide relief in most horses unless there is concurrent osteoarthritis of the distal interphalangeal or proximal interphalangeal joints.

Quittor Quittor is defined as a chronic infectious condition associated with one of the cartilages of the foot. A mixed bacterial infection causing chronic or recurrent drainage at or near the coronary band is most common (Fig. 126-3). Trauma is the most common cause of the condition referred to as necrosis of the

CHAPTER 126 cartilage. Wire cuts and wounds incurred from large calks on the shoes when horses are working in harness or being transported are common histories. Quittor is considerably less common today than it once was. Surgical management is the only option, because scar tissue and limited circulation preclude successful conservative management with local or systemic antibiotics. Excision of necrotic cartilage and scar tissue is best. Samples should be submitted for aerobic and anaerobic bacterial culture. Standing surgery can be performed, but I prefer to use general anesthesia, which reduces the chance of the distal interphalangeal joint being penetrated, improves the ability to provide hemostasis, and provides maximal restraint during surgery. A tourniquet at the level of the fetlock joint provides excellent surgical hemostasis, and as a precaution I always administer prophylactic broad-spectrum antibiotics before surgery. The distal interphalangeal joint occasionally is opened, and although penetration does not necessarily indicate surgical failure, an open joint alters the post-operative management protocol. If necrotic material (cartilage or scar tissue) extends distal to the coronary band, adequate distal drainage and flushing requires drilling a hole in the hoof wall.1

Osteitis of the Distal Phalanx Many Draft horses have flat soles and bear significant weight on the sole, and thus are prone to sole bruising and osteitis of the distal phalanx. The condition is most prevalent in the forelimbs and often is associated with improper shoeing or lack of proper hoof care. Draft horses with osteitis of the distal phalanx may assume a stance similar to that seen with traumatic laminitis. Hoof tester examination may be helpful to differentiate these conditions. A laminitic horse is most sensitive immediately dorsal to the apex of the frog in line with the dorsal one third of the toe. With osteitis of the distal phalanx, hoof tester pain response usually is less severe and more likely involves the sole in general. Soles may be pink or red, showing indications of bruising, and lameness is worse on hard surfaces or gravel. Mildly affected horses warm out of the lameness,

Draft horse foot showing chronic scar and granulation tissue associated with quittor.

Fig. 126-3

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but in horses with severe pain lameness increases as exercise continues. Radiographs can be difficult to interpret, and a definitive diagnosis is best reached using nuclear scintigraphy, observing increased radiopharmaceutical uptake in the distal phalanx. Management includes the judicious administration of NSAIDs and corrective shoeing. The sole should be protected and minimally pared. Pads frequently are used initially but may be counterproductive in the long run, because the sole has a tendency to become soft and lose thickness. Pads are needed for the first few shoe changes but then should be removed, and the sole should be hardened. To harden the sole, a common mixture referred to as sole paint (comprised of equal parts of 7% iodine, buffered formalin, and liquid phenol) is applied. This solution is applied to the sole once each day for 3 to 5 days or until the sole becomes hard. Overzealous application can cause the sole to become too hard. Paddock rest for 45 to 60 days is given. If shorter rest periods are given, recurrence is common. Hard, frozen, or rough surfaces should be avoided.

Canker Canker is not common but is a difficult problem to solve. Canker is proliferative pododermatitis of the frog that may extend to undermine the sole and heel bulbs. The condition can occur in one or all feet and has no predilection for forelimbs or hindlimbs. Often horses are thought to have nonresponsive thrush, but later when the problem persists, canker is diagnosed (Fig. 126-4). Canker is seen more commonly in Draft horses than in light horses, a fact that may reflect differences in hoof care and environment or simply may represent a breed predisposition. Two clinical signs that differentiate canker from thrush are a foul odor (necrotic) and the presence of granulation-like tissue that bleeds easily when manipulated (Fig. 126-5). Lameness is highly variable depending on the severity and number of feet involved. Once the superficial layer of tissue is removed, bleeding is often profuse. Creamy exudate is typical initially, especially if the owner has initiated treatment with caustic preparations. Successful treatment of canker requires patience on the part of the owner and the veterinarian because recurrence is common. The application of a hospital plate shoe is critical,

Fig. 126-4 Draft horse foot showing the typical appearance of thrush complicated by canker beneath the superficial layer of the frog.

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Fig. 126-5 Chronic canker with proliferative granulation tissue. Infected granulation tissue has undermined the sole and heels. because this shoe allows for long-term treatment and protects the sole. Importantly, pressure on the sole appears beneficial to healing, similar to that seen with granulation tissue at any site. Hospital plate shoes reduce the cost associated with daily care and management of a bandage. The shoe allows the horse to be exercised. The hospital plate shoe is made and fitted to the foot, and then the foot is blocked. A tourniquet is placed at the level of the fetlock joint, because bleeding during debridement is often profuse. Complete debridement of all abnormal proliferative tissue is often not possible and in fact may be counterproductive, because aggressive debridement may expose uninvolved deep tissue. Dry gauze sponges are packed to apply pressure on the frog and sole when the plate is replaced. Metronidazole appears to be the best topical agent, but I have used tetracycline and sulfapyridine powder successfully. The dressing should be changed daily for the first 10 to 14 days and then as needed. Debridement often needs to be repeated several times. Long-term treatment is necessary, and the owner needs to be prepared to provide it. Caustic compounds are not effective and in fact may worsen the condition. In the final stages of healing, when cornification of the frog is complete, caustic agents may be applied. Sole paint is applied to the sole for 8 to 10 days before the hospital plate shoe is removed. Horses are administered trimethoprim-sulfamethoxazole (15 mg/kg) for 3 weeks starting the day before initial debridement. Penicillin (20,000 IU/kg IM) is also effective, but oral antimicrobial agents are administered more easily.

Osteoarthritis of the Proximal and Distal Interphalangeal Joints, Ringbone Osteoarthritis of the proximal interphalangeal or distal interphalangeal joint was diagnosed in 26 Draft horses in my series. Ringbone has been described classically as being periarticular or articular in nature. The prognosis for Draft horses

with articular ringbone is worse than for those with the periarticular form. Pulling horses (heavy loads) are affected most commonly, especially in the hindlimbs. Osteoarthritis of the proximal interphalangeal and distal interphalangeal joints appears to occur with similar frequency, because in 26 horses, 11 had proximal interphalangeal, 10 had distal interphalangeal, and 5 had proximal interphalangeal and distal interphalangeal involvement. Horses with osteoarthritis of the proximal interphalangeal joint remained serviceably sound for 2.6 years, whereas horses with osteoarthritis of the distal interphalangeal joint or in both joints were serviceably sound for only 11 months. Early diagnosis appears to be an important criterion for an improved prognosis, and reducing workload, instituting corrective shoeing, and providing medical management can make a substantial difference in delaying the progression of osteoarthritis. Draft horses with short, upright pasterns are predisposed to osteoarthritis of the proximal interphalangeal and distal interphalangeal joints, and other factors such as angular limb deformities, toed-in or toed-out conformation, hoof imbalance, and trauma may play a substantial role. Horses required to work on pavement are predisposed to osteoarthritis of the proximal interphalangeal and distal interphalangeal joints. Proliferative peri-articular changes often result from lacerations or wire cuts. Horses with moderate to severe lameness have obvious enlargement of the pastern or coronary band area and heat. The degree of lameness varies from grade 1 to 5, and it worsens with lower limb flexion or after rotation of the digit. Rotation causes a substantial positive response if collateral ligaments are involved in horses with the peri-articular form. In horses with osteoarthritis of the distal interphalangeal joint, a palmar digital nerve block generally results in substantial improvement in lameness score. Thorough examination of the foot must be done to eliminate other potential causes of lameness. If the diagnosis is unclear after radiography, intra-articular analgesia should be performed. In horses with osteoarthritis of the proximal interphalangeal joint, a palmar digital nerve block may provide some improvement in lameness score, but an abaxial sesamoid block is needed to improve lameness substantially. Intra-articular analgesia can also be used. Management depends on when the diagnosis is first made. Horses with osteoarthritis and mild lameness should be given rest in a small level paddock for 4 months. I do not use stall rest unless horses are very active, because I have had greater success allowing the horse to walk in a confined area. Hoof balance should be corrected, and the horse should be shod with flat shoes without calks, toe grabs, or borium. I recommend oral glucosamine or chondroitin sulfate supplementation or intramuscular injection of a polysulfated glycosaminoglycan. I also inject the joints with a corticosteroid and hyaluronan. Initial and follow-up radiographic examination is recommended. If the horse is sound and radiographic changes do not progress, the horse is put back into a light exercise program, whereas if radiographic changes progress, additional rest and injections are given. Many horses with osteoarthritis perform for extended periods of time without recurrence of lameness. Horses with severe osteoarthritis of the proximal interphalangeal or distal interphalangeal joints have an unfavorable prognosis for athletic use. Medical management is of little benefit, and although spontaneous fusion of the proximal interphalangeal joint may occur, giving an accurate time estimate of when this may occur is difficult. Spontaneous fusion of the distal interphalangeal joint seldom occurs. Surgical arthrodesis of the proximal interphalangeal joint can be performed by using bone plates or the three-screw technique with 5.5-mm bone screws (see Chapter 36). A half-limb cast is placed for at least 4 to 6 weeks after surgery. In Draft horses the surgical procedure is difficult compared with light horses

CHAPTER 126 because the joints are large, removing articular cartilage is difficult, and horses may have difficulty with anesthetic recovery. Draft horses in general do not recover well from extended periods (>2 hour) of general anesthesia. The surgical procedure can be long, in particular if there is substantial peri-articular bone formation and fibrosis. Implants can break because of the large size of a Draft horse. Because of this, I have used an alternative technique of drilling across the joint with a 4.5- or 5.5-mm drill bit and then applying a half-limb cast without using implants. In horses with substantial peri-articular bone proliferation or fibrosis, this technique is my method of choice. Intraoperative radiographs are mandatory to assure proper placement of the drill bit within the joint. I drill at three to five sites in a fan-shape pattern from each side of the joint to destroy as much articular cartilage as possible. Breaking a drill bit in the joint is possible, and if this happens, removing the bit generally is not worth the extra time required. The palmar digital artery, vein, and nerve must be avoided during this procedure. A half-limb cast encompassing the foot is applied and maintained for 12 to 16 weeks. Advantages of this technique over those involving implants are that this technique is faster, requires shorter anesthesia periods, and requires no major skin incisions, and implant failure is not a concern. Pain control must be used to maintain reasonable comfort to avoid contralateral laminitis, which is always a concern.

Metacarpophalangeal (Fetlock) Joint Lameness Problems associated with the fetlock joint are less frequent in Draft horses than in other breeds, and most result from direct trauma. Fetlock joint problems plague horses that perform at speed, and therefore Draft horses seldom have lameness in this region. Sesamoiditis does occur in Draft horses and usually results from suspensory desmitis and insertional injury at the level of the proximal sesamoid bone. Sesamoiditis is more common in the hindlimbs. An unusual problem of the fetlock joint in young Draft horses is osteochondritis dissecans.

Splints Exostoses of the second and fourth metacarpal or metatarsal bones (splints) most commonly affect the second metacarpal bone, similar to light horses. In 84 Draft horses diagnosed with splints, 71 horses had forelimb involvement. Lameness associated with true splint (tearing of the interosseous ligament) is not common in Draft horses. Lameness caused by splints is most prominent in the first 2 to 3 weeks after the condition is first recognized and usually resolves with 6 to 8 weeks of rest. Because Draft horses do not perform at speed or change direction quickly, splints do not cause long-term lameness. Splints can result from interference injury from the contralateral limb, a problem that usually is corrected by proper shoeing and trimming. Local infiltration of local anesthetic solution in the region of the splint may be performed if the diagnosis is in question. Although a splint may be painful during palpation, missing a more distal limb problem is easy; therefore diagnostic analgesia should be performed distal to the splint before local infiltration. Radiographs should be obtained to check for a fracture. To manage a Draft horse with lameness resulting from a splint, I administer NSAIDs for 5 to 7 days and recommend stall rest. If the condition is acute, I use cold water therapy or ice boots for 20 to 30 minutes twice daily and apply support wraps. The horse should be hand walked for 10 minutes twice daily. In horses with chronic splints, I recommend a sweat (50/50 mixture of glycerine and alcohol) for 7 to 10 days. Paddock exercise can be given for 12 hours each day. A total rest period of 60 to 90 days is usually adequate. I avoid overzealous treatment with topical or internal blisters. Fractures of the splint bones are rare but usually involve the fourth metatarsal bone, and they often occur from kick

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wounds. These fractures often are comminuted and usually infected, because owners do not seek veterinary attention until 2 to 3 weeks after injury. Severe lameness often is not seen or is short lived, so the owner usually is not concerned until drainage starts. If the tarsometatarsal joint is involved and infected, the prognosis for return to original use is unfavorable. Many of these fractures heal if horses are given rest and treated with antibiotics. If the articular surface of the tarsometatarsal joint is not involved, displacement of fragments is minimal, and if the horse is not an athlete, many times this injury can be treated conservatively. Standing curettage of a draining tract and removal of sequestra can be accomplished in many patients using sedation and local analgesia. A culture is performed, and the horse is placed on appropriate antibiotics for 3 to 4 weeks, and the outcome is often satisfactory. For economic reasons this method also is chosen by some owners for horses intended for athletic use. However, I believe the problem is best treated surgically in those horses that are expected to be athletes. Surgical removal of the distal fractured segment of the fourth metacarpal bone is recommended occasionally, and horses usually have a good prognosis. If greater than 80% of the total length of the fourth metacarpal bone is removed, I use a screw to stabilize the proximal fragment. I do not like placing a screw into an area of known infection if I can avoid doing so. In those horses with substantial displacement or a fracture involving the articular surface, internal fixation to realign the fracture is indicated, if the injury is less than 3 weeks old. Fractures older than 3 weeks can be difficult to realign because callus formation occurs quickly.

Tendonitis and Suspensory Desmitis Flexor tendonitis and suspensory desmitis are not as common in the Draft horse as one might expect. Of 45 horses examined for these soft tissue problems, the distribution of these combined soft tissue injuries between the forelimbs and hindlimbs was similar, in contrast to most sport horses. Suspensory desmitis is more common in the hindlimb and often is seen with sesamoiditis. Tendonitis and suspensory desmitis are more common in horses that pull heavy loads or weighted sleds. Clinical signs include heat, pain, swelling, and lameness, and diagnosis is usually straightforward. Horses with hindlimb proximal suspensory desmitis may have more subtle clinical signs, and diagnostic analgesia is usually necessary. In horses with early forelimb superficial digital flexor tendonitis, the anastomosing branch of the palmar nerves may be enlarged and sensitive to palpation before the tendon itself shows clinical abnormalities. Ultrasonographic examination should be performed. Management of Draft horses with tendonitis and suspensory desmitis is similar to that in light horses. Ultrasonographic examination, rest, and a staged return to work are important. I am an advocate of percutaneous tendon or suspensory ligament splitting under ultrasonographic guidance in Draft horses. The surgery can be accomplished in a standing horse, using local analgesia and sedation, thus avoiding the need for general anesthesia. Prognosis is guarded to favorable in Draft horses with forelimb tendonitis and suspensory desmitis. Draft horses with hindlimb injury, however, have a guarded to unfavorable prognosis, especially if horses are used for pulling heavy loads. Broodmares with chronic, severe suspensory desmitis must be given special attention during late pregnancy because of weight gain. These mares should be housed on level surfaces and alone. Situations that require the mare to move quickly to avoid an aggressive pasture mate, or to slip while going over rough terrain, should be avoided. Muddy or slick footing also should be avoided. Stall rest, while advantageous for healing of the suspensory ligament, is avoided, because these broodmares usually develop substantial ventral edema.

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Other Forelimb Lameness Other causes of forelimb lameness are unusual. Upper limb lameness usually is caused by direct trauma and is not the result of athletic use. Carpal, elbow, or shoulder joint lameness is not common. I have examined only 13 Draft horses with carpal lameness. Various manifestations of osteochondrosis are seen in the elbow and shoulder joints. Sweeny, a neuromuscular disorder thought to be associated with injury of the suprascapular nerve, does occur with some frequency in Draft horses. Muscle atrophy may not be obvious for weeks to months, depending on the extent of the injury. Sweeny may result from acute direct trauma, but in Draft horses insidious trauma from a collar is the most common cause. This is especially true of poorly fitting collars, or old and worn collars in which the padding is no longer adequate. Collars of inadequate size often are used on today’s largesized Draft horses. Some Draft horses with sweeny continue to perform adequately despite muscle atrophy. Diagnosis is made by observing muscle atrophy over the scapula, especially affecting the supraspinatus muscle. Lameness is most likely functional and not related to pain, because horses cannot extend the shoulder joint normally. In some horses, however, the shoulder joint actually may subluxate, when the horse is walking or especially while turning in a circle. Subluxation results more frequently from external trauma from being kicked or from running into a solid object rather than from collar injury and may involve additional nerve injury. Management of horses with acute trauma of the shoulder area includes the administration of NSAIDs, corticosteroids, and dimethylsulfoxide and by performing physical therapy. A water hose with a hard stream of water can be useful for physical therapy. Liniments, massage, handheld muscle stimulators, and heating pads can be useful physical therapeutic modalities as well. The administration of dimethylsulfoxide (0.3 g/kg sid IV for 3 to 5 days) is recommended in the acute phase. Prognosis is difficult to assess, but if improvement is not seen in the first 6 to 8 weeks after diagnosis, prognosis becomes less favorable. I have not attempted scapular notch resection in Draft horses, but knowing the complications associated with the procedure in light horses leads me to hesitate recommending it.

Unusual Signs Consistent with Lameness Caused by Mange Mites In the United Kingdom a significant incidence of mange occurs in draft breed horses.2 Draft horses often are presented for evaluation of presumed lameness because of a stiff, stilted gait and with abnormal stamping of the limbs to the ground. In these horses careful lameness evaluation reveals areas of dermatitis, but this condition can be confused easily with musculoskeletal pain. I have not seen this to be a problem in Draft horses in the United States.

Hindlimb Lameness Hindlimb lameness occurs frequently in Draft horses, and the most common cause is lameness associated with the tarsus (hock joint). Draft horses in general have a predisposition to develop tarsitis, and lameness does not seem to be related to use. The custom of lowering the inside wall of the hoof and attempting to turn the hocks, a shoeing change thought to improve the horse’s pulling ability, may predispose a Draft horse to tarsitis. To my knowledge, however, this has never been proved in a controlled study. Draft horse shoes often have a large calk on the heel of the lateral branch, increasing torque and shear stress on the entire limb. Heel calks are especially detrimental in horses that work on hard surfaces, because the calk does not sink into the surface, thus putting even greater stress on the limb. This method of shoeing causes a flaring of the lateral hoof wall and predisposes the hooves to

separation and breakdown of laminae. Even if this method of shoeing is abandoned, at least 12 to 18 months are required for the foot to return to normal.

Tarsus Draft horses with hock lameness show a variety of clinical signs. The perceived problems by the owner also vary considerably. The horse may stop pulling or may rest its butt on the stall wall when in the barn. Breeding stallions may be reluctant to mount a mare, and when mounted, they may be unable to maintain erection. Horses may be reluctant to back up, back in crooked fashion, and have difficulty going up and down inclines. The horse may take short strides in harness or may have a change in attitude, sometimes biting other horses. Because the prevalence of hock joint lameness is high, carefully considering this region when evaluating a Draft horse with hindlimb lameness is always wise. Diagnosis may be straightforward, based on clinical signs, or may require diagnostic analgesia to pinpoint the problem. Upper limb flexion tests in Draft horses appear to be slightly more accurate as an indicator of hock lameness than the same test is in light horses, but false-negative results do occur. Pulling the medial splint bone with the fingers (Churchill test) with the limb in flexion also may be of value. The horse may show a positive response while standing, or lameness may be exacerbated after performing this maneuver. When the horse is trotting, careful attention is given to the vertical movement of the wings of the ilium (hip or pelvic hike), but if the problem is bilateral, a pelvic hike may not be obvious. Stride length may be shortened when viewed from the side, and when evaluated from behind or in front, horses have a tendency to swing the limb toward the midline and then place the limb laterally as it strikes the ground. Horses may scuff the toes because of the low arc of limb flight. Bony exostosis on the dorsal medial aspect of the hock joint may be obvious or absent. Tarsocrural effusion, or bog spavin, is observed commonly in Draft horses. This clinical observation often does not correlate with the source of pain. Even if osteochondrosis is suspected or confirmed, intra-articular analgesia always should be performed (Fig. 126-6). Although present, osteochondritis dissecans fragments may not be causing the major source of pain, and surgical removal of these fragments may not resolve lameness. Arthroscopic removal of osteochondral fragments is often less rewarding in adult horses. In Draft horses less than 2 years of age, arthroscopic removal of osteochondritis dissecans fragments is more likely to resolve lameness, however. The decision to perform surgery is based on the level of performance, cosmetic considerations related to joint distention, location of the lesion, and most importantly, whether lameness resolves with tarsocrural analgesia. Horses with osteochondritis dissecans lesions located more distally on the trochlear ridges have a more favorable prognosis that those with lesions located on the proximal aspect. Horses with osteochondritis dissecans lesions associated with the cranial intermediate ridge of the distal tibia have a favorable prognosis if lesions are removed early before chronic synovitis or capsulitis occurs. With only a limited number of horses from which to draw experience, lesions seemingly occur more frequently on the lateral trochlear ridge of the talus (tibial tarsal bone) than in any other location in a Draft horse. Lameness associated with osteoarthritis of the centrodistal and the tarsometatarsal joints is common. Intra-articular analgesia is often necessary, although some veterinarians medicate these joints and assess the clinical response to this treatment. I prefer to perform intra-articular analgesia and consider management options once a definitive diagnosis is made, however. In my opinion, conservative management should be attempted before using corticosteroids. I block the tarsometatarsal and the centrodistal joints first with the horse standing squarely on

CHAPTER 126

Dorsomedial-plantarolateral oblique radiographic view of a hock of a yearling Draft horse. The radiograph was deliberately underexposed to highlight the extensive osteochondritic lesion involving the distal half of the lateral trochlear ridge of the talus.

Fig. 126-6

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vation improves breakover and comfort. If the lateral hoof wall is flared, it must be rasped at each shoeing, and the lateral branch of the shoe gradually must be adjusted to conform properly to a more normal hoof shape. If borium is needed for traction on hard surfaces, it should be placed so that it provides a level surface on the bottom of the shoe. Uneven stress from borium points may cause hoof wall cracks. Usually, using six to 10 spots of borium on the shoe adequately supports the foot and also provides adequate traction. Medical management may include oral supplementation, intramuscular administration of polysulfated glycosaminoglycan, and intravenous administration of hyaluronan. NSAIDs are recommended at the time of shoeing changes, but longterm use of NSAIDs is usually not a solution in the management of chronic distal hock joint pain. Chronic administration often results in gastrointestinal ulceration and additional problems such as colic or colitis. Horses with distal hock joint pain can be given 2 to 3 g of phenylbutazone daily. Intraarticular injection with hyaluronan alone has limited value in Draft horses with osteoarthritis of the distal hock joints, and I prefer to use hyaluronan with methylprednisolone acetate. If treatment involves economic considerations, the corticosteroid is most important and can be injected alone. The dose of these compounds is similar to that used in the light horse and is not based necessarily on body weight. I increase the corticosteroid dose by about 25% using methylprednisolone acetate (100 mg) in each of the centrodistal and the tarsometatarsal joints. If treating bog spavin, I use methylprednisolone acetate (120 mg) and hyaluronan (40 mg). I seldom if ever use triamcinolone acetonide in Draft horses, because of a concern about laminitis induction and the fact that I often am injecting several joints simultaneously. Cunean tenectomy is used in some horses, especially those that have obvious enlargement on the medial aspect of the hock (Fig. 126-7). Cunean tenectomy is accomplished in a standing horse using local analgesia and sedation. Horses often are put back into work once the skin sutures are removed, 12 to 14 days after surgery.

Stifle Joint each limb. In Draft horses with exostoses on the medial aspect, confidently blocking the centrodistal joint may be difficult. Seven to 12 ml 2% mepivacaine hydrochloride is injected into each joint using a 20- to 22-gauge, 2.5- to 4-cm needle in the standard locations (see Chapter 10). In most Draft horses a twitch is adequate for restraint. Radiographs should be obtained, but unfortunately they are unreliable in confirming the diagnosis of osteoarthritis. In some Draft horses with substantial radiographic changes, lameness may originate elsewhere, whereas in some horses with minor or equivocal radiographic changes, severe lameness from early osteoarthritis of these joints is diagnosed. Radiographic examination helps to select management options and to determine prognosis, however. Management of the Draft horse with osteoarthritis of the distal hock joints includes physical and medical and surgical options. Correction of any shoeing or trimming problems should be performed before any other treatment. The foot is balanced in a medial to lateral direction according to conformation to achieve a level foot strike. My definition of a level foot strike means that the foot lands evenly when contacting the ground during movement. I remove the large calks and trailers that often are placed on the lateral branch of the shoes. If the horse is not going to be worked for a period of time, I prefer to shoe the horse without any special trim (calks, toe grabs, or inside rims). The dorsal aspect of the shoe is placed at the white line, and the toe is rasped back to the level of the shoe. Squared-toe shoes also can be used. The heels of the shoe should extend far enough behind to support the plantar aspect of the heel completely. In some horses slight heel ele-

Draft horses have long been thought to have more stifle joint lameness than do light horses, but when reviewing the records of 745 Draft horse lameness examinations, only 10 horses had primary lameness of the stifle joint. Perhaps long ago, when Draft horses were used daily to pull heavy loads, the frequency of stifle lameness may have been far greater than it is today. Of these 10 horses, three had bilateral idiopathic effusion of the femoropatellar joint. One horse had bilateral subchondral bone cysts of the medial femoral condyles, one had upward fixation of the patella, and five had trauma from kick injuries. Poor conformation and extended stall confinement predispose some Draft horses to upward fixation of the patella. Emaciated horses or those with significant weight loss also are predisposed to the condition. I make every attempt to correct upward fixation of the patella by using conservative management including foot care, improving muscle tone or conditioning, and improving nutritional intake. Raising the heels often alleviates the problem, and block wedges to raise the angle of the foot 6º to 10º are needed. Heel elevation is reduced gradually as the problem is rectified. Improved muscle tone and exercise is beneficial, as is avoiding prolonged periods of stall confinement. Backing exercise strengthens the quadriceps muscles and is a useful form of physical therapy. Internal blisters, injected at the origin and insertion of the patellar ligaments, may cause mild fibrosis and thus tighten the joint. This treatment is used less frequently now than in the past because the preparations need to be special ordered. I seldom if ever elect medial patellar desmotomy as my initial treatment. If conservative management is unsuccessful, desmotomy needs to be performed. The procedure should be

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Lameness in the Sport Horse formed erroneously. Muscle biopsy to check for polysaccharide storage myopathy and treatment with high-fat, lowcarbohydrate diets may be warranted, but definitive proof that polysaccharide storage myopathy is the cause of shivers may be difficult to substantiate. Horses still can be worked, but often owners elect to use them sparingly.

LAMENESS OF FOALS, WEANLINGS, AND YEARLINGS Young Draft horses require careful monitoring and early attention to lameness conditions. Lameness is often multifactorial and is related to nutrition, genetics, and environment. Early diagnosis and management of lameness appears more critical in Draft horse foals than in light horse foals. Often the size and strength of Draft horse foals gives the erroneous impression that they can overcome many problems.

Infectious Arthritis Infectious arthritis is common in Draft horse foals and may be related to a high frequency of umbilical problems. Umbilical hernias, umbilical infections, and patent urachus are more common in Draft horse foals than in light horses. Careful examination and treatment of the umbilicus at birth is mandatory, and the umbilicus should be monitored closely for a minimum of 3 weeks. Compared with light horse foals, Draft horse foals are often slower to stand and nurse after birth, leading to many infectious processes. Owner education is important, not only in assisting slow foals up to nurse but also in careful, daily evaluation of joints. Early and aggressive management of infectious arthritis and umbilical remnant infections should be performed (see Chapter 66).

Developmental Orthopedic Disease The dorsal aspect of the left hock of Draft horse showing bony exostosis of the dorsal medial surface. If lameness were confirmed to originate from the lower hock joint region, this horse would be a candidate for cunean tenectomy.

Fig. 126-7

done in the standing horse and not under general anesthesia and should be done with a sharp, strong-backed bistoury. This procedure should not be attempted in a Draft horse with an ordinary scalpel handle and blade, because the risk of the blade breaking during the surgery is real.

Shivers Shivers is considered a progressive, degenerative neuromuscular disease predominantly affecting Draft horses or other large breed horses (see Chapter 49). Various causes have been suggested, including immune-mediated disease following viral infection or strangles and exposure to organophosphates. Presently, polysaccharide storage myopathy has been put forth as a possible cause, but like previous proposed causes, this one may go by the wayside. Clinical signs include an involuntary jerking or twitching most frequently affecting the hindlimbs and the tail. A reflex-like maximum degree of flexion can be seen. Clinical signs often are noticed first by the farrier, because manually picking up the hindlimb frequently stimulates the jerking movements. Signs may be most obvious when the horse first starts to walk, or is backed, or is turned sharply. On occasion, twitching of the muzzle, lips, and ears and forelimb involvement occurs. The condition may improve with rest but usually returns when the horse is put back into work. Currently, no effective treatment is available. Shivers has been confused with stringhalt in some horses, and the surgical procedure, lateral digital flexor tenectomy, has been per-

Draft horses are affected by all of the various manifestations of developmental orthopedic disease, including flexural deformities, epiphysitis/physitis, osteochondrosis, angular limb deformities, and vertebral malformations (wobbler syndrome). A multifactorial cause is suspected, including nutrition (calcium/ phosphorous ratios and trace mineral levels) and hereditary factors (certain bloodlines have a high prevalence). Hereditary factors are complex and include high growth rate, feed deficiency conversion, milk production, and individual horse size.

Physitis/Epiphysitis and Flexural Deformities These conditions are closely related and seldom if ever a single problem. These conditions are seen over a wide age range from 6 weeks to 24 months, but peak occurrence is in foals 4 to 12 months of age. When raising large horses, owners have a tendency to overfeed, resulting in high-energy rations, fast growth, and nutritional stress, all of which include the possibility of developmental orthopedic disease. My experience with some 300 Draft horse foals suggests a distinct correlation between the frequency of developmental orthopedic disease and nutritional management. Foals having the highest frequency of developmental orthopedic disease were fed free choice high-quality alfalfa hay, approximately 0.015 kg feed/kg body weight/day, of a 16% protein grain ration and two vitamin/mineral supplements. Foals were fed in groups of six to 10 in 5- to 6-acre paddocks. Group feeding allowed the aggressive eater to consume far more than the prescribed amount of grain, and of course hay was fed free choice. None of the foals was thin or malnourished, but numerous foals were obese. Overweight foals, yearlings, or 2-year-olds do not exercise properly, a fact that exacerbates problems associated with excess ration. Under these conditions, two to four foals per group were affected with developmental orthopedic disease each year. To correct this problem, the nutritional program was revamped. The owner accepted the fact that yearling size may

CHAPTER 127 be slightly less than previously attained, but that developmental orthopedic disease would occur less frequently. Anecdotally, buyers of yearlings from this group had complained in previous years that 2-year-olds had become lame when training had started. The nutrition was changed as follows. The hay ration was given at a 50/50 mixture of alfalfa to timothy. Hay was fed at a rate of 0.015 kg/kg body weight/day, or the amount the foals could consume in about 16 hours. The grain ration was reduced to approximately 0.01 kg/kg body weight/day of a 14% protein ration. Only one vitamin/mineral supplement was given. Foals were grouped according to size, age, and disposition and were monitored closely and checked every 2 weeks by the farm veterinarian. Changes in conformation (becoming upright in the pastern and fetlock) or enlargement (heat and pain) of the growth plates were noted. Any foal with a change in the pastern or fetlock angle (developing more upright conformation), joint effusion, or physitis was treated immediately. Stall rest was given for 7 to 10 days, the feed intake was reduced, and the foal subsequently was given controlled exercise in a small paddock. Foals were fed only timothy hay, and the grain ration was reduced to 0.002 kg/kg body weight/day. They were placed on phenylbutazone (2.2 mg/kg bid for 3 consecutive days and then every other day for 3 more days). They were maintained in this environment until the problem resolved. Any hoof imbalance or growth abnormality was treated. A 60% decrease in developmental orthopedic disease was noted the first year, and now that farm management has become more attentive to noticing early signs of developmental orthopedic disease, the frequency of this complex of diseases is now less than 10%.

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Osteochondritis Dissecans and Osteochondrosis In my experience, osteochondrosis is observed more commonly in Draft horse foals than in light horse foals. In Draft horse foals the tarsocrural and femoropatellar joints are affected most commonly. Any joint can be affected, including the cervical vertebrae. Horses affected with osteochondrosis show varying degrees of lameness from 1 to 4 of 5 degrees lame. Lameness is less frequent with osteochondrosis lesions of the tarsocrural joint than with osteochondrosis of the stifle. Loose osteochondral fragments in the femoropatellar joint should be removed as soon as possible. Arthroscopic surgery does not guarantee success but improves the prognosis for athletic use. In my experience, Draft horses have a more guarded prognosis for future soundness with osteochondrosis of the stifle than do light horses. I am unsure if this is related simply to the size of the horse or the amount of pulling many of these Draft horses are expected to do, but only about 50% of Draft horses are sound after surgery. Early diagnosis and surgical management improves prognosis considerably. In some foals, without loose fragments, conservative management has resulted in a favorable outcome. Large osteochondritis dissecans defects involving the lateral trochlear ridges have healed based on radiographic examination, but this process may take up to 6 months to occur.

REFERENCES 1. Stashak TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 2. Dyson SJ: Personal communication, 2001.

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orses under the height of 14 hands, 2 inches (148 cm) at the withers generally are recognized as ponies. Despite this classification some pony breeds are referred to as horses; for example, Icelandic (toelter) horses. Many native pony breeds occur throughout the world; for example, Asturian (Spain), Connemara (Ireland), Fell (England), Gerrano (Portugal), Highland (Scotland), M’Bayar (Senegal), Merens (Pyrenees), Ob (Russia), Pindos (Greece), and Welsh ponies. Several small island breeds also occur; for example, Barearic, Eriskay, Faeroe island horse, and Chincoteague ponies. The size and conformation of most pony breeds has evolved over centuries because of specific work requirements and geographical isolation. Several breeds are endangered, including the Yonaguni and Noma in Japan and Sorraia in Spain, and some have become extinct; for example, the Fen, Galloway, and Tarpan. Attempts are being made actively to prevent extinction for several breeds; for example, the Kerry bog pony in Ireland and the Taishuh in Japan. In recent times new breeds of pony have evolved, including the Welara and Pony of the Americas. Despite this, most ponies are crossbred.

H

Ponies have a considerable range of height, weight, and conformation and are involved in most spheres of equine work, including show jumping, eventing, dressage, driving, and general pleasure activities. Many ponies show great athletic ability and, when used for show jumping, they often jump heights similar to their own height at the withers. Ponies have a long life expectancy and can remain in athletic work well into the twenties. Although a small number of ponies are used for high-level competition work such as eventing and show jumping, most are used for general purpose work, when they may be ridden only in the summer months. General purpose ponies tend to be much less valuable than horses and are ridden predominantly by children, which may create emotional and financial conflicts for owners (parents) when deciding the appropriate treatment of a seriously injured pony. Many general purpose ponies remain at grass all year round and do not have access to a stable. Competition ponies often change ownership, at high prices, every 2 or 3 years, as children outgrow them. Few reports in the literature describe orthopedic conditions specifically affecting the pony. In this chapter I hope to

CHAPTER 127 be slightly less than previously attained, but that developmental orthopedic disease would occur less frequently. Anecdotally, buyers of yearlings from this group had complained in previous years that 2-year-olds had become lame when training had started. The nutrition was changed as follows. The hay ration was given at a 50/50 mixture of alfalfa to timothy. Hay was fed at a rate of 0.015 kg/kg body weight/day, or the amount the foals could consume in about 16 hours. The grain ration was reduced to approximately 0.01 kg/kg body weight/day of a 14% protein ration. Only one vitamin/mineral supplement was given. Foals were grouped according to size, age, and disposition and were monitored closely and checked every 2 weeks by the farm veterinarian. Changes in conformation (becoming upright in the pastern and fetlock) or enlargement (heat and pain) of the growth plates were noted. Any foal with a change in the pastern or fetlock angle (developing more upright conformation), joint effusion, or physitis was treated immediately. Stall rest was given for 7 to 10 days, the feed intake was reduced, and the foal subsequently was given controlled exercise in a small paddock. Foals were fed only timothy hay, and the grain ration was reduced to 0.002 kg/kg body weight/day. They were placed on phenylbutazone (2.2 mg/kg bid for 3 consecutive days and then every other day for 3 more days). They were maintained in this environment until the problem resolved. Any hoof imbalance or growth abnormality was treated. A 60% decrease in developmental orthopedic disease was noted the first year, and now that farm management has become more attentive to noticing early signs of developmental orthopedic disease, the frequency of this complex of diseases is now less than 10%.

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Osteochondritis Dissecans and Osteochondrosis In my experience, osteochondrosis is observed more commonly in Draft horse foals than in light horse foals. In Draft horse foals the tarsocrural and femoropatellar joints are affected most commonly. Any joint can be affected, including the cervical vertebrae. Horses affected with osteochondrosis show varying degrees of lameness from 1 to 4 of 5 degrees lame. Lameness is less frequent with osteochondrosis lesions of the tarsocrural joint than with osteochondrosis of the stifle. Loose osteochondral fragments in the femoropatellar joint should be removed as soon as possible. Arthroscopic surgery does not guarantee success but improves the prognosis for athletic use. In my experience, Draft horses have a more guarded prognosis for future soundness with osteochondrosis of the stifle than do light horses. I am unsure if this is related simply to the size of the horse or the amount of pulling many of these Draft horses are expected to do, but only about 50% of Draft horses are sound after surgery. Early diagnosis and surgical management improves prognosis considerably. In some foals, without loose fragments, conservative management has resulted in a favorable outcome. Large osteochondritis dissecans defects involving the lateral trochlear ridges have healed based on radiographic examination, but this process may take up to 6 months to occur.

REFERENCES 1. Stashak TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 2. Dyson SJ: Personal communication, 2001.

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orses under the height of 14 hands, 2 inches (148 cm) at the withers generally are recognized as ponies. Despite this classification some pony breeds are referred to as horses; for example, Icelandic (toelter) horses. Many native pony breeds occur throughout the world; for example, Asturian (Spain), Connemara (Ireland), Fell (England), Gerrano (Portugal), Highland (Scotland), M’Bayar (Senegal), Merens (Pyrenees), Ob (Russia), Pindos (Greece), and Welsh ponies. Several small island breeds also occur; for example, Barearic, Eriskay, Faeroe island horse, and Chincoteague ponies. The size and conformation of most pony breeds has evolved over centuries because of specific work requirements and geographical isolation. Several breeds are endangered, including the Yonaguni and Noma in Japan and Sorraia in Spain, and some have become extinct; for example, the Fen, Galloway, and Tarpan. Attempts are being made actively to prevent extinction for several breeds; for example, the Kerry bog pony in Ireland and the Taishuh in Japan. In recent times new breeds of pony have evolved, including the Welara and Pony of the Americas. Despite this, most ponies are crossbred.

H

Ponies have a considerable range of height, weight, and conformation and are involved in most spheres of equine work, including show jumping, eventing, dressage, driving, and general pleasure activities. Many ponies show great athletic ability and, when used for show jumping, they often jump heights similar to their own height at the withers. Ponies have a long life expectancy and can remain in athletic work well into the twenties. Although a small number of ponies are used for high-level competition work such as eventing and show jumping, most are used for general purpose work, when they may be ridden only in the summer months. General purpose ponies tend to be much less valuable than horses and are ridden predominantly by children, which may create emotional and financial conflicts for owners (parents) when deciding the appropriate treatment of a seriously injured pony. Many general purpose ponies remain at grass all year round and do not have access to a stable. Competition ponies often change ownership, at high prices, every 2 or 3 years, as children outgrow them. Few reports in the literature describe orthopedic conditions specifically affecting the pony. In this chapter I hope to

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give an overview of some of the conditions that are recognized as affecting the pony.

LAMENESS AFFECTING THE PONY Ponies suffer from orthopedic problems similar to those horses suffer, but the overall prevalence of lameness in the pony is less than in the horse. This may be because of differences in temperament and body weight. With a relatively older population the incidence of some specific orthopedic conditions affecting older ponies may appear higher than in horses, but the prevalence is often unclear and may, for some conditions, be similar; for example, Cushing’s disease.

the lower limb is generally easier, some important lesions may be more subtle than in the horse, particularly involving the distal interphalangeal joint and navicular bone. Conversely, one should note that a substantial amount of joint degeneration can be present in some sound ponies (Fig. 127-1). It is therefore important in the pony to undertake intrasynovial analgesia to confirm that any peri-articular and intra-articular abnormalities are associated with joint pain. In some ponies, particularly those kept at grass, a prominent increased thickness of skin in the distal limbs, pelvis, and thoracolumbar areas can be present and reduces skin penetration by ultrasound waves, resulting in poor ultrasonographic images. I have found that shaving the hair and hosing the area to be scanned with warm water for 15 minutes often substantially improves the quality of the image.

LAMENESS EXAMINATION Gait assessment in ponies can be challenging because they can have a higher limb speed than horses, and the larger, heavier pony breeds (e.g., Highland) often have a base-wide gait behind, which may make assessment of hindlimb lameness difficult. Several breeds also have gaits additional to walk, trot, and canter; these include the South African, Basotho pony, and Icelandic horses. In small ponies the handler may have to walk when leading a trotting pony, rather than run, to keep the limb speed to a rate at which the observer can detect lowgrade lameness. The low height of some ponies compared with most veterinary surgeons may create difficulties with assessment of the lower limb, and excessive force or torsion can be applied easily to the distal joints while performing a flexion test. In small ponies, care should be taken not to apply excessive pressure with hoof testers and, if the veterinary surgeon is tall, not to flex or twist the lower limb excessively in an effort to raise the foot to a convenient height to use the testers. Paradoxically, in comparison with horses many ponies have harder hoof horn, making eliciting foot pain difficult, so care always should be taken when assessing the response to hoof testers. The use of small or adjustable hoof testers is advisable for ponies. Ponies can have a positive response to lower limb flexion tests despite being sound and performing to the owner’s expectations.

B

A

DIAGNOSTIC ANALGESIA Some ponies are strong-willed, which can limit a conventional lameness evaluation using perineural or intrasynovial analgesia. Using a nose twitch or a low dose of an α2-sedative may aid this (e.g., 40 to 60 μg/kg romifidine or 0.6 to 0.9 mg/kg xylazine intravenously). In some ponies the lower limbs may have thick skin and be very hairy, making accurate palpation of the structures difficult, particularly finding the site for a palmar digital nerve block. I am conscious that because of the relatively shorter limbs in ponies, local anesthetic solution may diffuse farther than in the horse, and a reduced amount of local anesthetic solution is used for perineural analgesia (e.g., 1 ml of mepivacaine hydrochloride for each nerve when performing a palmar digital or palmar [abaxial sesamoid] analgesia).

IMAGING CONSIDERATIONS For most clinical situations a similar number of radiographic projections are required to examine the lower limb of a pony as for a horse. Although obtaining good-quality radiographs of

Fig. 127-1 Lateromedial radiographic view of the metacarpophalangeal joint of a 12-year-old jumping pony. Peri-articular osteophytes on the articular margins of the proximal and distal aspect of the proximal sesamoid bones reflect osteoarthritis. There is also evidence of supracondylar lysis (A) on the palmar aspect of the third metacarpal bone and villonodular (proliferative) synovitis (B) on the dorsal border. This pony had met the owners’ expectation until 5 weeks before this examination.

CHAPTER 127 MOST COMMON CONDITIONS AFFECTING COMPETITION PONIES Competition ponies appear to have a reduced prevalence of lameness in comparison with horses, but the conditions that they suffer tend to mimic competition horses. • Laminitis • Distal hock joint pain—osteoarthritis of the distal tarsal joints (bone spavin) • Desmitis of the accessory ligament of the deep digital flexor tendon (ALDDFT) • Palmar and plantar annular desmitis • Osteoarthritis of the metacarpophalangeal joint • Superficial digital flexor tendonitis • Exertional rhabdomyolysis • Osteoarthritis of the carpus

LIMB DEFORMITIES Mild angular limb deformities in ponies are common, but few affect performance or require medical or surgical correction. In many native breeds in the United Kingdom a small degree of carpus and fetlock valgus deviation is common. The persistence of a full-length ulna and fibula has been associated with the development of severe angular limb deformities in Shetland ponies.1 This may be a form of atavism, the inheritance of a characteristic from remote rather than recent ancestors. Congenital laxity of the flexor tendons in the hindlimb of Shetland ponies is not uncommon and can be associated with hyperextension of the distal interphalangeal joint. Treatment is similar to that in the horse. Adactyly (absence of all or part of a normal digit) and polydactyly (duplication of all or part of a digit beyond the normal number) and other congenital musculoskeletal defects have been recorded in ponies.2

JOINT DISEASE Osteochondrosis Rarely do ponies have lameness associated with osteochondritis dissecans. Histopathological evidence of osteochondrosis specifically in ponies has been reported only in the lateral trochlear ridge of the femur.3 Based on a limited number of ponies, in my opinion the most commonly affected joints are the tarsocrural and femoropatellar joints, and lesions are found at the same recognized sites as in the horse, that is, the cranial aspect of the distal intermediate ridge of the tibia, trochlear ridges of the talus, medial and lateral malleoli of the tibia, and lateral trochlear ridge of the femur. Osteochondrosis has been seen particularly in ponies bred for showing,4 and this may be because these animals were receiving high feed intakes in an effort to improve their show ring appearance. Lameness associated with a subchondral bone cyst in the medial femoral condyle in the stifle is not uncommon in the pony.

Osteoarthritis Ponies suffer from osteoarthritis in similar joints as do horses. However, many ponies have mild to moderate joint degeneration, are clinically sound, and perform to the level of the owner’s expectation (Fig. 127-1). Osteoarthritis in ponies tends to be primary rather than secondary to a previous intra-articular condition, such as intra-articular chip fractures, osteochondritis dissecans, osseous cyst-like lesions, or ligamentous damage.

Scapulohumeral Joint Shetland ponies have a higher prevalence of osteoarthritis of the scapulohumeral joint than do other equine breeds. This

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typically occurs in young ponies; mean age in one survey was 5.2 years. The lameness is usually unilateral but can be bilateral and is sudden and severe (grade 4 to 5 of 5) in onset. Lameness is characterized by a reduction in the cranial phase of the stride and a low arc of foot flight. Radiographic abnormalities may not be present in the acute stage.5 No reported treatment has resulted in successful resolution of the lameness. Shetland ponies have a flatter and shallower glenoid cavity of the scapula than other equine breeds, and this may be caused by a primary joint dysplasia that could predispose Shetland ponies to osteoarthritis of the scapulohumeral joint.6

Carpus Older ponies appear to have an increased incidence of osteoarthritis of the carpometacarpal joint, often referred to as carpal spavin. The radiographic abnormalities found within the carpometacarpal joint are similar to osteoarthritis of the distal tarsal joints, and periosteal and enthesophyte formation on the abaxial margins of the second and fourth metacarpal bones also may be present.7 I have observed several lame ponies with restricted flexion of the carpus and radiographic evidence of carpal joint degeneration, but the lameness was abolished by perineural or intrasynovial analgesia in the more distal limb. Restricted carpal flexion, without overt lameness, may result in a pony being presented for a history of tripping and concern for the safety of a child rider.

Stifle In a retrospective study of stifle lameness, a higher incidence of osteoarthritis of the femorotibial joints was noted in Highland ponies compared with the normal referral horse population at the University of Edinburgh.8 The condition presents as sudden-onset, severe (grade 4 to 5 of 5) lameness associated with substantial damage to the menisci and collateral or cruciate ligaments. Ultrasonography and arthroscopy are useful to assess the extent of the soft tissue damage. In some of these ponies concurrent abnormalities in the surface of the medial femoral condyle, as described in horses, were present.9 The extent of the meniscal and ligament damage was such that treatment was generally unsuccessful. Osteoarthritis of the femoropatellar joint can occur in Shetland and Miniature Shetland ponies secondary to chronic lateral luxation of the patella10 (see following discussion).

Hock Osteoarthritis of the distal tarsal joints (bone spavin) is a common cause of hindlimb lameness in ponies, but as in other joints, intrasynovial or perineural analgesia is advisable to confirm the relevance of any radiographic changes. Icelandic horses appear to be predisposed to osteoarthritis of the distal hock joints.11 An epidemiological study showed that 23% of Icelandic horses in Sweden had radiographic signs of bone spavin.12 A causal relationship has been found between hindlimb lameness and radiographic evidence of bone spavin and the animals’ ages and hock angles. No relationship was found with environmental factors such as training and showing.13 The lameness found in Icelandic horses is often mild, despite moderate to severe radiographic changes.11

Other Specific Joint Conditions Luxation of the Coxofemoral Joint Rupture of the coxofemoral ligaments and secondary luxation of the coxofemoral (hip) joint has a higher prevalence in the pony than in the horse (Fig. 127-2).14 This may be because in the horse, unlike in ponies, the ilium tends to fracture before luxation of the hip occurs.15 In the pony, ligament rupture usually occurs after trauma, and the head of the femur is often displaced in a craniodorsal direction. Affected ponies adopt a characteristic posture with outward rotation of the foot and stifle, inward rotation of the tarsus, and a pronounced shortening of the affected limb. Open or closed reduction has been

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A

B

Fig. 127-2 A, Typical appearance of luxation of the coxofemoral joint in a pony. Note the outward rotation of the stifle and foot, inward rotation of the tarsus, and shortening of the right hindlimb. B, Ventrodorsal radiographic view of the right coxofemoral joint demonstrating the caudodorsal luxation of the head of the femur.

used to treat the luxation, but the prognosis for long-term soundness is poor.14 Ponies with unsuccessful reduction or irreducible luxation can be salvaged for breeding or companion purposes by excision arthroplasty.16 Coxofemoral luxation often is complicated by upward fixation of the patella.15,16 Ligament rupture may occur without luxation of the coxofemoral joint, and the clinical signs are similar to luxation except for the absence of limb shortening.15

Dysplasia of the Coxofemoral Joint Hip dysplasia has been reported in the Norwegian Dole and a Shetland pony colt.17 In the Shetland pony, hip dysplasia was associated with the development of osteoarthritis in the coxofemoral joint.

Luxation of the Patella Lateral (sub)luxation of the patella in Shetland ponies is common.18 The condition is usually congenital, but can be acquired, and affects one or both hindlimbs. A distinction should be made between (sub)luxation and congenital permanent lateral luxation (see the following discussion). The cause of the condition is thought to be malformation of the trochlear ridges and groove, but rupture of the medial femoropatellar ligament has been reported in one pony.19 Post-mortem examination usually reveals that (sub)luxation is associated with a

broadening and flattening of the medial and lateral trochlear ridges, particularly the distal aspect of the medial trochlear ridge. Whether these changes are congenital or are caused by bone modeling is unknown. The clinical signs vary, but in most ponies the patella can be easily manipulated laterally and then replaced in the trochlear groove, and in some ponies the (sub)luxation can be observed during motion. The degree of (sub)luxation varies between ponies and can vary during an individual pony’s life. Patellar luxation can be observed on lateromedial and caudocranial radiographs, but to confirm (sub)luxation a cranioproximal-craniodistal oblique (skyline) projection of the patella is required. In ponies with (sub)luxation the patella may appear an abnormal shape on the skyline projection, but this is caused by rotation and abnormal positioning and not by bone modeling.18 Lateral luxation has been treated successfully by medial imbrication and lateral release incision,10 or imbrication and recession sulcoplasty.19 Hermans et al.,18 using a limited breeding experiment with a group of Shetland ponies, found evidence to suggest monogenic autosomal recessive hereditary transmission of this defect. Congenital permanent lateral luxation of the patella also is seen in Shetland ponies. Affected newborn foals are unable to extend the stifle fully and therefore have a crouched, squat-

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ting position when standing. The lateral trochlear ridge in affected foals is often flat rather than convex.18 The prognosis for successful treatment is poor.

Upward Fixation of the Patella Intermittent upward fixation of the patella is a not uncommon condition in ponies, affecting young ponies (typically 2 to 3 years old), and older ponies secondary to an orthopedic problem in the limb. The clinical presentation is similar to that in the horse.

Hemarthrosis A higher incidence of hemarthrosis has been noted in ponies than horses,20 and this is often secondary to a systemic disease such as a blood clotting disorder or hepatopathy. Affected ponies have acute-onset lameness with a severely painful joint effusion(s).

Subluxation of the Proximal Interphalangeal Joint Non-traumatic dorsal subluxation of the proximal interphalangeal (pastern) joint has been recorded in the hindlimbs of ponies.21 The condition usually occurs bilaterally in young ponies (Fig. 127-3). Dorsal proximal interphalangeal joint subluxation is observed when the affected limb is not bearing weight. The subluxation is reduced as weight is borne on the affected limb, and an audible clink often accompanies joint reduction. Tenotomy of the medial head of the deep digital flexor tendon in the proximal metatarsal region has produced good results in treating this condition.21 Unilateral proximal interphalangeal joint dorsal subluxation has been recorded in a 3-year-old pony secondary to infectious arthritis of the tarsocrural joint.22 The subluxation resolved after successful treatment of the infectious arthritis.

Treatment of Joint Disease Non-steroidal anti-inflammatory drugs should be used with care in lightweight ponies, because they may be more susceptible to phenylbutazone toxicity.24 (Recommendations by some phenylbutazone-supplying drug companies in the United Kingdom state the maximum level of phenylbutazone in ponies is 4.4 mg/kg orally on alternate days compared with a maximum level of 4.4 mg/kg twice daily for horses.) The ulcerogenic properties of orally administered phenylbutazone are possibly more pronounced in ponies because of less efficient gut absorption. Systemic and intra-articular corticosteroid use in ponies also has to be undertaken with caution because of the potential for development of laminitis.25 If arthroscopy or arthrotomy is undertaken in the diagnosis or treatment of joint disease, one should note before giving a prognosis that ponies appear to accommodate greater cartilage degeneration than horses. A Fell pony foal with infectious arthritis should be checked for immunodeficiency syndrome before treatment is initiated.23

FRACTURES Common fractures seen in horses (i.e., third metacarpal/ metatarsal bone condylar, proximal phalanx, and third carpal bone slab fractures) are rare in ponies. Most fractures are secondary to trauma. Hindlimb fractures, particularly involving the lateral splint bone (fourth metatarsal bone), often result from kicks from other horses. Because of the reduced value of ponies, owners may not opt for surgical intervention to repair fractures. In some ponies, closed fracture reduction and using a cast alone may result in successful bony union in fractures that would require internal fixation in a horse. The lighter weight of most ponies also means that the use of internal or external fixation of long bone fractures is more successful than in a horse. Repair of some complete fractures of the humerus, tibia, and radius that would require euthanasia in a horse can

Bilateral non-traumatic dorsal subluxation of the proximal interphalangeal joints in a 3-year-old Welsh pony. The condition resolved after tenotomy of the medial head of the deep digital flexor tendon.

Fig. 127-3

be attempted in lightweight ponies (50,000/μl), and degenerate neutrophils predominate. Epiphyseal type (E-type) infectious arthritis involves the joint and adjacent epiphysis. Foals are generally several weeks of age or older. One or more joints may be infected, and other systemic illnesses may occur concomitantly. Radiographic evidence of epiphyseal involvement commonly is seen. Physeal type (P-type) may occur in foals from 1 week to 4 months of age. Degrees of soft tissue swelling and lameness may vary, and generally only one site is involved. Sympathetic effusion eventually may occur in a nearby joint (articular structure in close proximity). Lesions may be seen radiographically in the metaphysis, physis, or epiphysis (Fig. 129-11). Pathological fracture may result because of weakening of the involved structure. Small tarsal or carpal cuboidal bone (T-type) osteomyelitis may result in collapse of the central or third tarsal bones (Fig. 129-12). Several joints commonly are affected. Invasion into a physis or joint from a peri-articular soft tissue abscess is called I-type infection. Most commonly, joints of the upper limb such as the hip or stifle are involved. If soft tissue abscessation is detected early, infectious arthritis often can be avoided. Most commonly foals with osteomyelitis have acute onset lameness, diffuse regional swelling, heat, and detectable pain of the involved area. Fever is generally present before and at the onset of lameness but may go undetected. Degree of lameness depends on what bone is involved, the time frame, and stage of detection. Owners often erroneously assume lameness

results from trauma because signs occur acutely. A common assumption is that the mare stepped on the foal (the Editors). Diagnosis of complex infection is based on physical examination findings and the results of arthrocentesis (if intrasynovial involvement occurs) and radiographic examination.2,10,12,14,15 Foals with infectious osteitis or early osteomyelitis may have no or subtle radiographic changes, but within 1 to 2 weeks radiographic changes consist of erosive, radiolucent changes with sclerosis and eventual proliferation of new bone. It is therefore important to perform follow-up radiographic evaluation to monitor the progression of the disease. Other imaging modalities are of limited value. Sensitivity of nuclear scintigraphy alone is questionable in young foals because of the high metabolic activity of developing bone.10 White cell imaging using nuclear medicine techniques is useful, but adds expense and radiation exposure, and has not gained widespread acceptance in private practice. Ultrasonographic examination is most helpful in identifying soft tissue injury or inflammatory processes of the upper limb. Abscessation of the soft tissue adjacent to the infected bone is a common finding in foals with physeal infection. Using ultrasonographic guidance, abscesses can be aspirated for culture and susceptibility testing and opened, drained, and lavaged. Arthrocentesis is the key in diagnosing infectious arthritis, but a negative culture does not rule out infection.4,10-14,19 Joint fluid should be obtained in EDTA tubes to evaluate the differential and total nucleated white blood cell count and protein concentration and for cytological evaluation. Anaerobic and aerobic culture and susceptibility tests should be performed. Using an antimicrobial removal device may be of benefit to potentiate a positive culture if the foal is receiving antimicrobial drugs. Blood cultures should be collected.

Dorsopalmar radiographic view of the carpus of a foal with P-type osteomyelitis of the distal radial physis. Lateral is to the right. Note the soft tissue swelling and the extensive lytic areas in the physis, metaphysis, and epiphysis. Infection has caused fragmentation of the lateral aspect of the metaphysis.

Fig. 129-12 Dorsoplantar radiographic view of a hock of a young foal with type T osteomyelitis involving the cuboidal bone of the tarsus. Lateral is to the right. Note the mottled opacity of the central and third tarsal bones and the proximolateral aspect of the third and fourth metatarsal bones. These extensive lesions warrant a grave prognosis.

Fig. 129-11

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In horses suspected of having infectious arthritis, synovial fluid cultures are positive 64% of the time.11,13,16,17,19 In our practice, of 158 synovial samples submitted in 1 year, there were only 64 (40%) positive isolates. Reasons for low positive culture results include previous administration of antimicrobial agents, partial success of the immune system, the intrinsic bacteriocidal properties of infected synovial fluid, poor storage, or no bacteria present in the synovial fluid. If there is radiographic evidence of osteomyelitis well away from a joint, a sample of bone and debris may be obtained using a Michelle’s trephine. An alternative technique is to use a 2.5- or 3.2-mm drill bit and collect the shavings for culture and sensitivity testing.10 This tract then may be used for intraosseous infusion of an antimicrobial agent. The results of hematological testing can be confusing. Complete blood count and fibrinogen level should be assessed, but results are often within normal limits initially because infection is localized. Serial hemograms should be performed in this instance. Any elevation in the white blood cell count or fibrinogen level in a lame foal with fever should be assumed to reflect bone or joint infection until proved otherwise. A normal hemogram does not rule out infectious arthritis or osteomyelitis. Foals less than 1 month of age should have immunoglobulin G levels checked to evaluate for failure of passive transfer. Treatment of foals with infectious arthritis consists of joint lavage with sterile polyionic fluids through large-bore needles or by using an arthroscope. If a large amount of fibrin and cellular debris is in the synovial fluid, arthrotomy and lavage with or without primary closure of the joint may be indicated. Joint lavage may be repeated every 1 to 3 days depending on the clinical response. A long-term closed suction drainage system may be used as well.10 Broad-spectrum systemic antimicrobial drugs should be started immediately and adjusted accordingly based on the clinical progression and culture and sensitivity testing. Other treatments for joint and bone infection include local intraosseous injection or regional hyperperfusion with anti-

microbial agents. To perform intraosseous injection, an 18- or 20-gauge needle is inserted into the physis or adjacent bone. An aminoglycoside such as amikacin (250 to 500 mg) may be used. To perform regional hyperperfusion, a site over the abaxial digital neurovascular bundle is prepared aseptically and a rubber tourniquet is placed in the proximal metacarpal region. A 23-gauge butterfly catheter is inserted in the digital vein. An antimicrobial solution (500 mg amikacin diluted in 10 ml sterile water) is infused into the digital vein (Fig. 129-13). The tourniquet is removed after 15 minutes, and a lower-limb bandage is applied. The procedure may be repeated as necessary. Regional digital hyperperfusion is especially useful in treating infectious osteitis of the distal phalanx and distal limb infectious arthritis or osteomyelitis. I have not encountered complications from tourniquet application such as distal limb ischemia. Foals with infectious arthritis should be allowed to rest for a minimum of 3 to 4 weeks to prevent further traumatic cartilage damage.2 Systemic administration of chondroprotective agents or intra-articular administration of hyaluronan may be of benefit. Severe erosive lesions of the physis and metaphysis may result in pathological fracture and collapse of the bony column, resulting in an unstable fracture or severe angular deviation. Surgery may be indicated, but prognosis is poor for soundness if this occurs. The prognosis for foals with infectious arthritis and osteomyelitis depends on the antimicrobial susceptibility of the organism and how early effective treatment is instituted.11-19 In general, foals treated early for articular infections have a good prognosis for full recovery. Foals with articular infection with subchondral bone involvement have a poor prognosis, and the clinical course of disease and treatment are prolonged. Foals with focal bony lesions, involving only the physis without bone instability, have a good prognosis. Those with a pathological fracture or severe angular limb deformities have a poor prognosis and may be candidates for humane destruction.

Fig. 129-13 Regional intravenous hyperperfusion of an antimicrobial solution for treatment of infection of the digit. A needle has been placed into the lateral digital vein. There is a tourniquet around the proximal metacarpal region.

CHAPTER 129 Immune-Mediated Synovitis Immune-mediated synovitis is a sequella to a primary inflammatory focus such as pneumonia, umbilical remnant infection, or a peripheral abscess.10,20 Rhodococcus equi pneumonia is the most common primary focus of infection. The syndrome results from the deposition of immune complexes in the synovial lining and complement activation, resulting in synovitis. The condition usually involves more than one synovial structure. Foals usually have a stiff gait resulting from the synovial distention, and severe lameness is unusual. The primary rule out for immune-mediated synovitis is early infectious polyarthritis, causing only moderate lameness and mild synovial fluid distention. Cytological evaluation of joint fluid in foals with immune-mediated synovitis commonly reveals nucleated cell counts of less than 20,000 nucleated cells/μl. The cells are well-preserved neutrophils and large mononuclear cells. Foals with infectious arthritis generally have nucleated cell counts greater than 50,000 nucleated cells/μl, and neutrophils are degenerative. Therapy for foals with immune-mediated synovitis is based on identifying and resolving the underlying disease. Synovitis is self-limiting once the offending cause is removed. Systemic chondroprotective agents may be of benefit to the health of the joint, because prolonged inflammation may cause cartilage damage.

Infection of the Digit Infection of the digit is a frequent cause of substantial lameness in foals. Infection may be contained to the subsolar or hoof wall regions, or it may involve the distal phalanx or the distal interphalangeal joint. It is critical to differentiate between these sites as soon as possible. Infection at all sites causes increased intensity of the digital pulse amplitudes and, at some stage, increased temperature of the hoof capsule. With subsolar or wall abscessation, pressure applied with hoof testers usually produces a painful response along the toe and sole, unless overlying horn is separated from the sensitive tissue caused by accumulation of purulent material. Radiographs in these foals reveal gas accumulation in the involved area. If the distal phalanx is infected, radiolucency or sequestration may be evident. Diffuse swelling at the coronary band usually means involvement of the distal interphalangeal joint, and arthrocentesis should be performed in an area remote from the swelling. Subsolar abscesses should be drained early to prevent involvement of deeper tissues. To facilitate drainage, the foot can be soaked in hot water and bandaged with an Animalintex pack (3M Animal Care Products, St. Paul, MN). Both procedures soften the horn. Surgical curettage of the distal phalanx and lavage of the infected bone should be performed in foals with sequestration. A sterile, antiseptic bandage should be maintained after surgery for a minimum of 3 to 4 weeks or until a healthy keratin covering has grown over the exposed bone. Ancillary treatment includes regional digital hyperinfusion using a dilute antimicrobial solution. A good prognosis is warranted in foals with infection of the distal phalanx if the disease is detected and treated early. If more than 25% of the distal phalanx is involved, prognosis for future soundness worsens. Recurrence of infection after initial curettage requires additional surgery. Because of the limited surface area and porous nature of the distal phalanx in the foal, recurrence worsens the prognosis considerably.

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REFERENCES 1. Stashak TS: Diagnosis of lameness. In Stashak TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 2. Bohanon TC: Developmental musculoskeletal disease. In Kobluk CN, Ames TR, Geor RJ, editors: The horse: diseases & clinical management, vol 2, Philadelphia, 1995, WB Saunders. 3. Douglas J: The pathogenesis and clinical manifestations of equine osteochondrosis, Vet Med 87:826, 1992. 4. Stashak TS: Diseases of joints, tendons, ligaments, and related structures. In Stashak TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, 1987, Lea & Febiger. 5. Dutton DM, Watkins JP, Honnas CM, et al: Treatment response and athletic outcome of foals with tarsal valgus deformities: 39 cases (1988-1997), J Am Vet Med Assoc 215:1481, 1999. 6. Dutton DM, Watkins JP, Walker MA, et al: Incomplete ossification of the tarsal bones in foals: 22 cases (19881996), J Am Vet Med Assoc 213:1590, 1998. 7. Embertson RM, Bramlage LR, Herring DS, et al: Physeal fractures in the horse: classification and incidence, Vet Surg 15:223, 1986. 8. Pool R: Pathologic manifestations of osteochondrosis. Proceedings of the Developmental Orthopedic Disease Symposium, Dallas, April 1986. 9. Dik KJ, Enzerink E, van Weeren PR: Radiographic development of osteochondral abnormalities in the hock and stifle of Dutch Warmblood foals, from age 1 to 11 months, Equine Vet J Suppl 31:9, 1999. 10. Madison JB: Infectious orthopedic disease in foals. In Robinson NE, editor: Current therapy in equine medicine, ed 4, Philadelphia, 1997, WB Saunders. 11. Vatistas NJ, Wilson WD, Pascoe JR, et al: Septic arthritis in foals: bacterial isolates, antimicrobial susceptibility, and factors influencing survival, Proc Am Assoc Equine Pract 39:259, 1993. 12. Firth EC: Infectious arthritis in foals. In White NA, Moore JN, editors: Current practice of equine surgery, Philadelphia, 1990, JB Lippincott. 13. Madison JB, Sommer M, Spencer PA: Relations among synovial membrane histopathologic findings, synovial fluid cytologic findings, and bacterial culture results in horses with suspected infectious arthritis: 64 cases (1979-1987), J Am Vet Med Assoc 198:1655, 1991. 14. Martens RJ, Auer JA: Haematogenous septic arthritis and osteomyelitis in the foal, Proc Am Assoc Equine Pract 26:47, 1980. 15. Schneider RK, Bramlage LR, Moore RM, et al: A retrospective study of 192 horses affected with septic arthritis/tenosynovitis, Equine Vet J 24:436, 1992. 16. McIlwraith CW: Treatment of septic arthritis. In Turner A, editor: The veterinary clinics of North American large animal practice: equine orthopedic surgery, Philadelphia, 1983, WB Saunders. 17. Bertone AL: Infectious arthritis in adult horses, Proc Am Coll Vet Intern Med 9:409, 1991. 18. Wagner PC, Watrous BJ, Darien BJ: Septic arthritis and osteomyelitis. In Robinson NE, editor: Current therapy in equine medicine, ed 3, Philadelphia, 1992, WB Saunders. 19. Steele CM, Hunt AR, Adams PLE, et al: Factors associated with prognosis for survival and athletic use in foals with septic arthritis (1987-1994), J Am Vet Med Assoc 215(7):973, 1999. 20. Madison JB, Scarratt WK: Immune-mediated polysonovitis in four foals, J Am Vet Med Assoc 192:1581, 1988.

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PART X

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Lameness in the Sport Horse

CHAPTER •

130

Pleasure Riding Horse Herbert J. Burns

leasure riding horses are a vital part of the equine industry and many owners devote great amounts of time, money, and emotion to them. Although pleasure riding horses are of far less monetary value than competition horses, the overall importance to the owner should never be underestimated. Pleasure riding horses often tend to be used seasonally and somewhat episodically. Uses include trail riding, hunting, gymkhana-type activities, showing, lesson horses (teaching horses), the pasture pet, and eating grass. Pleasure riding horses can be divided loosely into two categories, ex-professionals and others. The ex-professionals are horses that formerly were used for a specific athletic use such as racing, but are no longer able to perform in the sport, and have been demoted. The others include potential athletes that were unable to be used for the intended purpose because of lack of ability, poor conformation, or temperament and horses and ponies that were bred casually as pets. The common causes of lameness in these two groups differ to some extent. It is vital to be able to relate to the owners of pleasure riding horses, who often are inexperienced with horses, have little veterinary knowledge, but have tremendous emotional involvement with the horse and are often anxious. It is vital to first establish communication with the owner and try to relieve any anxieties. The veterinarian should explain the intended examination and treatment and why in straightforward, non-technical language. Facilities for examination may be far from ideal and may complicate the examination. The veterinarian should not over-interpret a short striding gait shown by a horse trotting on an uneven paddock or a rocky driveway. The clinician should start from the basics and evaluate left-right symmetry, with the horse standing on a flat, level surface, if available, and then assess the horse moving in straight lines and circles. The veterinarian should be aware that the horse may have been living with a low-grade lameness, unrecognized by the owner, for a considerable time. If the owner is concerned about a severe left forelimb lameness, the veterinarian would be prudent to avoid mentioning a lowgrade left hindlimb lameness observed concurrently, because the lameness is probably not of material relevance and will only further worry the owner. Interpretation of findings is in part dictated by the age and previous occupation of the horse. Many ex-professional horses have previous soft tissue injuries or show lameness after flexion of a variety of joints, and it is important to try to establish which is the current active disease process causing lameness. Many clinical observations reflect previous injuries and are unrelated to the current lameness. Local analgesic techniques are useful in some situations, but the temperament of the horse, difficulties in adequate restraint, or examination facilities available may mitigate against them. Owners of pleasure riding horses may resist techniques that are invasive or potentially painful to the horse, whereas they may be fully prepared to pay large sums for advanced diagnostic techniques. The clinician should bear in mind that a twitch in the inexperienced hands of an owner

P

may be dangerous and should consider using tranquilization (e.g., 1 ml of acepromazine) in the horse to facilitate local analgesic techniques. In some situations an owner prefers a step-by-step diagnosis reached by assessing the response to treatment, even without a definitive diagnosis. This can provide the slow acquisition of useful information. For example, assessment of the response to non-steroidal anti-inflammatory drug treatment can be helpful. Lameness associated with a subsolar abscess is likely to deteriorate, whereas lameness from navicular disease or osteoarthritis of the proximal interphalangeal joint is likely to improve. In ex-professional horses, osteoarthritis and previous tendon and ligament injuries are common. Minor trauma to a joint in a horse with pre-existing osteoarthritis may result in severe, persistent lameness, whereas similar trauma to a normal joint probably would not result in chronic lameness. Commonly injured joints include the carpus, fetlock, hock, and stifle. Superficial digital flexor tendonitis, suspensory desmitis, and distal sesamoidean ligament injuries are common chronic injuries in ex-professional horses, but re-injury is comparatively unusual unless the horse is subjected to a sudden and substantial increase in exercise intensity; for example, a horse is ridden hard for 2 hours after 3 months of little or no exercise. Previous sites of chronic inflammation may become a long-term problem. For example, a horse may lose a shoe and then gallop about on hard ground, resulting in solar bruising. However, lameness may persist and radiographs may reveal osteitis of the palmar processes of the distal phalanx. A horse with toed-out conformation may traumatize the medial proximal sesamoid bone, resulting in acute lameness, but radiographic examination may reveal pre-existing abnormalities. Many causes of lameness in pleasure riding horses relate to the lifestyle of pampered pets, and the environment in which they are kept. Subsolar abscesses are common and often result in a severe lameness, creating panic for an owner, who assumes the horse must have sustained a fracture. Managing the owner is equally as important as treating the horse. Subsolar abscesses also may be sequelae to previous laminitis. Creation of effective drainage is essential for successful management of subsolar abscesses. Without drainage the use of systemic antimicrobial drugs is contraindicated in my experience, because such drugs may prolong the course of the infection. In some pleasure riding horses with a hard hoof capsule, determining accurately the site of abscess may not be possible initially. I recommend intensive soaking with Epsom salts and warm water and poultice at night. Periodic survey radiographs can be useful. Up to 30 days may pass before the abscess can be located accurately and drainage can be established. Once the abscess has opened or been opened, systemic antimicrobial drugs may be useful, especially if a large area of the foot is damaged. Pleasure riding horses are at high risk for sustaining lacerations or puncture wounds, often resulting from impact with less than ideal fencing such as barbed wire or a jagged post. Injuries vary from minor to severe, resulting in long-term lame-

CHAPTER 130 ness. Injuries may go unrecognized for several days because not all pleasure riding horses are inspected carefully and regularly. Many pleasure riding horses are kept in groups at pasture, and the introduction of a new horse can result in disruption of the hierarchy and the risk of horse-induced injury. The veterinarian also should recognize that many pleasure riding horses have major conformational abnormalities that predispose them to the early development of osteoarthritis. Many pleasure riding horses live to an old age, and age-related osteoarthritis is not uncommon. Farrier care may be less than ideal and may predispose the horses to chronic foot pain and osteoarthritis of the distal limb joints. Nail bind and excessive shortening of the toe are common farriery-related causes of lameness. It is important to establish the time of onset of lameness relative to when the horse was last shod. These problems are usually apparent within 48 hours. If a nail was driven inside the white line and immediately removed, this may predispose the horse to a subsolar abscess, which usually causes lameness within 7 to 10 days. If foot lameness develops more than 2 weeks after trimming and shoeing, the lameness is unlikely to be related to the farrier. Other primary foot problems include solar bruising, sheared heels, puncture injuries, and thrush. The relative incidence of these problems may be related to the ground conditions if the horse lives out. Early, wet springs increase the incidence of thrush. Long, dry summers resulting in hard ground are associated with an increased incidence of bruising and sore feet. Laminitis is a problem seen most commonly in two types of pleasure riding horse, obese ponies and older horses and ponies with a pituitary adenoma. Laminitis is often seasonal, occurring most in the spring and early summer and also in the autumn, if a flush of grass occurs late. Navicular disease is not uncommon, and an irregular exercise history may be a predisposing factor. Navicular disease is less common in horses that have never been shod. Cellulitis can create an acute-onset, non–weight-bearing lameness associated with pyrexia and inappetence. In some horses minor skin abrasions can be identified through which infection was initiated, but in others the primary cause may not be identified. The incidence of tendon and ligament injuries is low and may be related to the weather and environmental conditions, or to the age of the horse. Excessively deep, muddy pastures and extremely icy conditions may predispose horses to tendonitis or desmitis. Age-related degenerative changes take place in some tendons and ligaments, and in older pleasure

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riding horses, even those receiving no ridden exercise, sudden onset of a severe, progressive tendonitis of the forelimb superficial digital flexor tendons may develop. Progressive stretching of the hindlimb suspensory apparatus, resulting in dropping of the fetlocks, also occurs in older horses. Neurological problems such as radial nerve paralysis may result from trauma induced by a kick from another horse in the same field or from a collision with another horse or a static object such as a gate post. In older horses neoplastic lesions may result in secondary lameness. For example, a large melanoma in the gluteal region in a horse I examined created pressure on the sciatic nerve and thus lameness. Pleasure riding horses are often kept at pasture in a group, with access to field shelters of variable design. Long bone fractures, the result of a kick from a companion horse, are not uncommon, especially during the winter months. Splint bone fractures are also common. Treatment of many of these conditions is no different than in other athletic sport horses; however, certain constraints may apply that must be considered. No facilities may be available to restrict the horse’s exercise or to keep it on its own. Some facilities are completely inadequate for performing clean procedures, such as intra-articular medication, in a safe manner. However, owners often are prepared to spend a disproportionate amount of their income on treating a condition in their much loved horse, despite a guarded prognosis, so it is important to describe all available treatment options. It is also critically important to explain carefully the treatment protocol, and writing it down can be useful to ensure owner compliance. The veterinarian can create a chart that the owner should complete as medication is administered. In managing osteoarthritis, the fact that a pleasure riding horse lives out and is constantly exercising actually may be of benefit. I prefer to start with the least invasive therapy first and only use alternative methods if that does not work. Some oral nutraceutical agents may be of benefit, as may be intramuscular administration of polysulfated glycosaminoglycans. Management of wounds can be difficult because client compliance is often poor. I treat wounds in anticipation of the worst-case scenario, using non-steroidal anti-inflammatory drugs, broad-spectrum antimicrobial drugs, and confinement. Complete stall rest is often impossible, and restricted area turnout is a frequent compromise. If a penetrating injury possibly may have entered a joint or tendon sheath, I recommend referral for intensive therapy, stressing to the owner that this injury is potentially life threatening.

INDEX A A nerve fiber in arthritic pain, 607 AAEP. See American Association of Equine Practitioners. Abaxial, non-articular fragmentation of metatarsophalangeal joint, 428-429 Abaxial extension for shoe, 264 Abaxial fracture of proximal sesamoid bone, 354 Abaxial sesamoid nerve block, 102-103, 115, 244 in European Thoroughbred, 885 Abdominal palpation, 51 Abduction of hindlimb during advancement, 70 lateral placement of foot during, 69 Abductor digitus longus muscle anatomy, 692-693 Ablation, chemical, for navicular disease, 302 Abscess bone, ultrasonographic examination of, 197 foot in broodmare, 1082 in Draft horse, 1060-1061 in European Thoroughbred, 887 in foal, 1093 in North American Standardbred, 903-904 in North American Thoroughbred, 873 perineural nerve block for, 102 in pleasure riding horse, 1094 poultice for, 770 in show hunter and jumper horses, 968 muscular, 734, 735 cervical, 527 post-injection, 734 staphylococcal on back of metacarpophalangeal joint in European Thoroughbred, 891 Accessory carpal bone fracture, 391, 686 Accessory ligament of deep digital flexor tendon anatomy of, 82, 433-434, 644, 684 biochemical parameters for, 616-617 desmitis of, 644, 650-653 in acute-onset, severe lameness, 147 in Arabian and Half-Arabian show horse, 1048-1049 desmotomy for, 653 in dressage horse, 981 in driving horse, 1057-1058 in polo pony, 1011 in pony, 1074 in show hunter and show jumper horses, 975 in team roping horse, 1023-1024 desmotomy of for acquired flexural deformity, 564 palpation of, 47 tenoscopy of, 233-234 ultrasonographic imaging of, 176-182 Accessory ligament of superficial digital flexor tendon desmitis of, 685 in polo pony, 1016-1017 transection of for tendonitis, 635-639 in Three Day Event horses, 994 Acepromazine, 1079 for laminitis, 330 in endurance horse, 1000 for post-anesthetic myopathy, 735 Acetabular lip, 86 Acetabulum anatomy of, 484 fracture of, 488-489, 490

Acetazolamide, 739 Acetylpromazine for chemical restraint during diagnostic analgesia, 99 during lameness examination, 62 in pelvic fracture management, 490 in rhabdomyolysis management, 729, 731 in North American Standardbred, 912 for warming in bone scintigraphy, 204 Acid firing, 779 Acoustic enhancement, 172 Acoustic shadowing, 172-173 Activated charcoal, 330 Active training, 790 Acupressure, 794 Acupuncture, 792-803 for back pain, 520, 796 for diagnostic examination, 795-796 for lameness therapy, 796 for pain associated with lower limb lameness, 796-797 scientific basis of, 792-893 techniques and instrumentation in, 793-795 traditional Chinese medical theories and, 793, 794 Acute-onset, severe lameness, 143, 145-149 ADAM enzymes, 578 ADAMTS enzymes, 578 Adequan. See Polysulfated glycosaminoglycans. Adhesives for glue-on shoes, 267, 274-275 Advancement abduction of hindlimb during, 70 lateral placement of foot during, 69 A-FAS. See Average fiber alignment score, ultrasonographic. Age in clinical history, 9-11 of fracture, 160 Age factors in biochemical markers of bone cell activity in racehorses, 844-845 in desmitis of accessory ligament of deep digital flexor tendon, 650-651 in epidemiology of racehorse injuries, 865 in navicular disease, 287-288 in tendon injury, 622-624 Aggrecan, 574-575, 621 Aggrecanase, 578 Albumin, cerebrospinal fluid, 127-128 ALDDFT. See Accessory ligament of deep digital flexor tendon. Alfalfa in cervical vertebral malformation therapy, 548 mineral requirements of for weanlings, 544 overfeeding and, 546 Aliasing, 220 Alkaline phosphatase as biochemical marker in arthritis, 592 of bone formation in racehorses, 842-843 All-weather racetrack surface, 881 Alpha-adrenergic agonists, epidural, 768 ALSDFT. See Accessory ligament of superficial digital flexor tendon. Alternative therapy. See Complementary therapy. Altrenogest, 481 Aluminum horseshoe, 262 in laminitis treatment, 334-335 in metatarsophalangeal joint osteoarthritis, 427 Ambulance, 856 Ambulation for flexural limb deformities, 562 American Association of Equine Practitioners, humane destruction guidelines of, 149 American Saddlebred, 1035-1040

Amikacin for infectious arthritis, 600, 601 in foal, 1092 for tenosynovitis of extensor tendon sheaths, 695 Aminoglycosides, 600 Aminoproprionitrile fumarate, 633-634 for desmitis of accessory ligament of deep digital flexor tendon, 653 for superficial digital flexor tendonitis in event horses, show jumpers, and dressage horses, 641 in racehorses, 633-634 for suspensory desmitis, 663 in driving horse, 1053 Anabolic process, 592 Analgesia, 93-124, 243-244 of bursae and tendon sheaths forelimb, 113-115 hindlimb, 121-122 carpal, 378 in cervical stenotic myelopathy, 569 of crus, 450 dangerous horses and, 140 in distal hock joint pain, 441 of distal interphalangeal joint, 310-311 of distal phalanx, 322 in dressage horse, 979 in driving horse, 1052 of elbow, 400-401 false-negative responses to, 135-137 flexion tests and, 80-81 injection technique in, 99-100 intra-articular in forelimb, 107-113 in hindlimb, 117-120, 121, 122, 764-769 local infiltration in, 122-123 in metacarpal region, 363-364 of metacarpophalangeal joint, 348-349 of metatarsal region, 434 of metatarsophalangeal joint, 422 in metatarsophalangeal joint osteoarthritis, 427 in National Hunt, point to point, and timber racing horses, 941 in navicular disease, 289, 290 negative responses to, 140-141 opiate for post-anesthetic myopathy, 735 patient preparation in, 99 in pelvic injury, 492 perception of by laypersons, 98 perineural in forelimb, 100-107 in hindlimb, 115-117 in pony, 1070 polo, 1005 in poor performance, 831 potentially confusing responses to, 137-138 for primary lesion of deep digital flexor tendon within hoof capsule, 306 in proximal suspensory desmitis of forelimb, 655 of hindlimb, 658 radiation therapy and, 783 role of chemical restraint in, 98-99 of sacroiliac joint, 506-507 of shoulder, 400-401 in Standardbred European, 916 North American, 901-902 in stifle, 456 strategy, methodology, and other considerations in, 94-96, 97, 98 therapeutic ultrasound for, 813 of thoracolumbar spine, 513

1097

1098

Index

Analgesia—cont’d in Thoroughbred European, 885-886 North American, 871 in Three Day Event horses, 987-988 Anamnesis, 9-14. See also History. Anchorin, 575 Anechogenic ultrasound image, 172 Anemia, equine infectious, 733 Anesthesia in diagnostic analgesia, 93-124, 243-244 dangerous horses and, 140 false-negative responses to, 135-137 of forelimb bursae and tendon sheaths, 113-115 of hindlimb bursae and tendon sheaths, 121-122 injection technique in, 99-100 intra-articular in forelimb, 107-113 intra-articular in hindlimb, 117-120, 121, 122 local infiltration in, 122-123 negative responses to, 140-141 patient preparation in, 99 perception of by laypersons, 98 perineural in forelimb, 100-107 perineural in hindlimb, 115-117 potentially confusing responses to, 137-138 role of chemical restraint in, 98-99 strategy, methodology, and other considerations in, 94-96, 97, 98 general neck stiffness and cervical vertebral mobilization under, 531 pelvic fracture and, 485-486 myopathy following, 735 ultrasound of, 195 Angles assessment in conformation evaluation, 20, 21 Angular limb deformity, 557-561, 1071 Animation, horseshoes for, 268 Ankylosis in osteoarthritis, 583 of thoracolumbar synovial intervertebral articulations, 518 Anlehung, 977 Annular ligament anatomy of, 674-675, 716 avulsion fracture of at origin of suspensory ligament, 666, 667 desmitis of, 678-681, 682, 721 in dressage horse, 982 in polo pony, 1015-1016 in pony, 1074 desmotomy of, 232, 637, 641 in polo pony, 1007 diagnostic techniques for, 675 disease of, 682, 683 Annular ligament syndrome, 678-681 Antebrachium, 394-399 compartment-like syndrome in, 735 diagnostic analgesia of intra-articular, 110-111 perineural, 106-107 direct trauma to in driving horse, 1057, 1058 palpation of, 50 in European Thoroughbred, 883 Antibiotics. See Antimicrobials. Antibody testing in neurologic examination, 126 Anti-endotoxin hyperimmune serum, 329 Anti-inflammatory effects of radiation, 783 Antimicrobials. See also specific drugs. for deep penetrating injury of sole, 279 for infectious arthritis, 600-602 for peri-tarsal cellulitis, 448 for tenosynovitis of extensor tendon sheaths, 695, 696 Anti-proliferative effects of radiation, 783-784 Aorto-iliac-femoral thrombosis, 497-499 in breeding stallions, 1079 Apical fracture of proximal sesamoid bone, 354

Aquatreds, 790 Arabian racehorse, 931-933 Arabian show horse, 1040-1049 conformation of, 958, 1042 diagnosis and management of lameness in, 1044-1049 diagnostic analgesia in, 1044 history of breed and sport, 1040-1041 lameness examination of, 1042-1044 neurologic examination of, 1044 ten most common causes of lameness in, 1042 training of, 1041-1042 undiagnosed lameness in, 1044 Arachidonic acid cascade, 746 Arena polo, 1003 Arm anatomy of, 399-400 diagnosis of lameness in, 400-401 imaging of, 401-403 palpation of, 50 Arnica montana, 817 Arquel. See Meclofenamic acid. Artemesia vulgaris, 794 Arthritis, 571-613 infectious, 598-606 antimicrobial therapy for, 600-602 causes of, 598 diagnosis of, 599-600 examination and initial management of, 598-599 in foal, 1089-1093 future treatments of, 604 joint drainage and debridement for, 602-603 models of, 596 pain management for, 603 prognosis for, 604 synovial fluid cytology for, 582 topical treatment, bandaging, and alternative therapy for, 603-604 in young Draft horse, 1068 models of, 594-598 non-infectious, 606-610 osteoarthritis, 572-594. See also Osteoarthritis. clinical evaluation of, 580-584 etiopathogenesis of, 576-577 markers of, 591-594 normal joint function and structure and, 572-576 role of synovium in, 577 radiography of, 161 treatment of, 746-764 biologically based, 756-757 corticosteroids, 748-749, 751, 752 glucosamine and chondroitin sulfate, 751, 753 hyaluronan, 749-750, 753 intra-articular, 753 joint resurfacing, 756 nonsteroidal antiinflammatory drugs, 746-748, 751 pentosan polysulfate, 750 polysulfated glycosaminoglycan, 750, 753 surgical, 754-756 Arthrocentesis forelimb, 107-113 hindlimb, 117-120, 121, 122 in infectious arthritis, 599 in foal, 1091 synovial fluid cytology for, 582 Arthrodesis, 755-756 carpal, 391 for distal hock joint pain, 443 in driving horse, 1055 for osteoarthritis in breeding stallion, 1078 of proximal interphalangeal joint, 346, 550-551 for traumatic disruption of suspensory apparatus, 360-361

Arthropathy, steroid, 608 Arthroplasty, mosaic, 229 Arthroscopic examination and surgery, 226-230 carpal, 380, 385, 386 for cruciate ligament injury, 463 of distal interphalangeal joint, 312 in femoropatellar joint osteochondrosis, 458 in fragmentation of proximal plantar processes of proximal phalanx, 428 for infectious arthritis, 602 for joint disease, 754 for meniscal ligament injury, 462, 463 of metatarsophalangeal joint, 426 for scapulohumeral joint osteochondrosis, 408 Arthrotomy, arthroscopic surgery versus, 226-230 Articular cartilage arthroscopic examination of, 227, 228 damage to in femorotibial joint, 464 in interphalangeal joint, 314 magnetic resonance imaging of, 220 models of, 596 normal structure and function of, 573-575, 591 Articular disease of stifle, 458-465 femoropatellar joint, 458-461 femorotibial joint, 461-465 of tarsus, 440-443 Articular fracture radiography, 159-160 Artifacts magnetic resonance imaging, 220 scintigraphic, 208 ultrasonographic, 169-173 Artificial gaits, 60-61 Artificial insemination, 1083 Aseptic bursitis of intertubercular bursa, 412 Aseptic necrosis of proximal sesamoid bone, 667, 668 Aspartate aminotransferase in immune-mediated myopathy, 733 in muscle disorders, 724 in neurologic examination, 126 in rhabdomyolysis, 494, 730 Aspiration, cerebrospinal fluid, 126-128 Aspirin, 1079 for aorto-iliac-femoral thrombosis, 499 for metatarsophalangeal joint osteoarthritis, 427 for navicular syndrome in reined cow horse, 1029 for sesamoiditis in reined cow horse, 1029 AST. See Aspartate aminotransferase. Asymmetry of front feet in purchase examination of Thoroughbred sales yearling in Europe, 839 in growth of distal physis, 558 in height or shape of tuber sacrale, 35, 36, 495, 503 of muscle in performance horse, 959 of thoracolumbar synovial intervertebral articulations, 518 Ataxia in cervical stenotic myelopathy, 566 performance horse and, 960 Atlantoaxial joint anatomy, 522 Atlanto-occipital joint anatomy, 522 Atlas anatomy of, 522 fracture of, 529 Atrophy forelimb, 31-32 hindlimb, 33-34 supraspinatus and infraspinatus muscle, 413-414 Atropine for hygroma, 611 for tenosynovitis, 695

Index Atypical myoglobinuria, 737 Australian form of stringhalt, 478 Autoimmune-mediated arthritis, 607-608 Average fiber alignment score, ultrasonographic, 183 Avulsion hoof, 281 at the origin of peroneus tertius and long digital extensor tendon, 467 at origin of suspensory ligament palmar annular ligament, 666, 667 third metacarpal bone, 367-368 third metatarsal bone, 436 patellar, 465 of proximal digital annular ligament, 682, 683 sesamoidean from palmar aspect of proximal phalanx, 352 of superficial digital flexor tendon in polo pony, 1013 Axial articular fragmentation of metatarsophalangeal joint, 428 Axial sesamoid fracture, 356 Axial skeleton, 483-532 cervical spine and soft tissues of neck, 522-531 anatomy of, 522 clinical examination of, 522-523 clinical presentation of, 522 congenital abnormalities of, 525-526 cyst-like lesions of, 530 diskospondylitis of, 529 fracture of, 529-530 imaging of, 523-525 insertional desmopathy of nuchal ligament and injury to semispinalis in, 526-527 jugular vein thrombophlebitis of, 530-531 muscle abscess of, 527 musculature disorders of, 527 myeloma of, 530 occipito-atlantoaxial malformations of, 525, 548 osteoarthritis of, 527-529 osteomyelitis of, 530 stiffness and mobilization of under general anesthesia, 531 digital compression of followed by movement in lameness examination, 79-80 osteopathic treatment of, 819-824 pelvic injuries of in non-racehorse, 484-490 in Thoroughbred racehorses, 484-490, 893 sacroiliac joint injuries of, 501-508 anatomy and, 501-502 clinical presentation of, 503-504 diagnostic imaging of, 507 differential diagnosis of, 507 pathological conditions in, 502-503 physical examination of, 504-506 prognosis for, 508 regional analgesia in, 506-507 treatment of, 507-508 thoracolumbar spine, 509-521 anatomy and function of, 509-510 diagnosis of pain in, 510-514, 515 imaging of, 513-514, 515 lesions of, 514-521 on the track injury of in Thoroughbred racehorse, 859-860 Axillary intertrigone infection, 891-892 Axis anatomy of, 522 fracture of, 529 Azium. See Dexamethasone. Azoturia, 728, 1075. See also Rhabdomyolysis. B Back, 509-521 anatomy and function of, 509-510 imaging of, 513-514, 515

Back—cont’d injury of in cutting horse, 1020-1021 in team roping horse, 1025 lesions of, 514-521 muscular tension and spasm in, 727 palpation of, 51 in European Standardbred, 916 in performance horse, 959 standard radiographic projection and suggested extra views of, 166 thermography of, 238 Back pain, 509-521 acupuncture for, 796 in American Saddlebred, 1037-1038 anatomy and function of thoracolumbar spine and, 509-510 in Arabian and Half-Arabian show horse, 1047 in Arabian racehorse, 932-933 in breeding stallions, 1077-1078 in cutting horse, 1020-1021 diagnosis of, 510-514, 515 in dressage horse, 983 in endurance horse, 1001 in National Hunt, point to point, and timber racing horses, 944 in pony, 1075 polo, 1013-1014 in poor performance of sports horse, 830 in show hunter and show jumper horses, 971-972 in Three Day Event horses, 992-993 Back-at-the-knee conformation, 25-26, 27 carpometacarpal osteochondral fragmentation and, 382 Background radiation, scintigraphic, 203 Backing, 61 Bacteria as trigger factor in laminitis, 328 Bacterial infection in infectious arthritis, 598 lameness in European Thoroughbred secondary to, 891-892 in mud fever, 151 in quittor, 1062 in thrush, 277 Balance conformation and, 18-20, 252-255 dorsopalmar, 248 foot, 252-255 in European Standardbred, 915 loading of superficial digital flexor tendon and, 625 in performance horse, 958 horseshoes for, 267 trimming of barefooted horse for natural, 272-273 Ballottement, 44 Bamboo fever, 1012 Banamine. See Flunixin meglumine. Bandaging, 769-771 cast, 772-773 following fetlock arthrodesis for traumatic disruption of suspensory apparatus, 361 for deep digital flexor tenosynovitis in driving horse, 1055, 1056 for flexural limb deformities, 562 following debridement of infectious osteitis of distal phalanx, 280 for infectious arthritis, 603-604 for injury prevention in metacarpal region, 375 for superficial digital flexor tendonitis in Three Day Event horses, 993 Bandy-legged conformation, 22-23 Bar firing, 779 Bar for horseshoe, 265 Bar stock, 262 Barefooted horse, natural balance trimming for, 272-273 Barley, mineral requirements for, 544

1099

Barrel-racing horse, 1030-1032 Baseline lameness in lameness examination, 4, 62 manipulation and, 74-81 Base-narrow conformation, 22, 23, 29 in show hunter and show jumper, 966 Base-wide conformation, 21, 22, 29 in show hunter and show jumper, 966 Basic fibroblast growth factor, 579 Basilar fracture of proximal sesamoid bone, 354-355, 356 Basisesamoid block, 115 Beam angle, ultrasonographic, 169-170 Beat, 61 Bedding material for hoof care in laminitis, 332 Being broke in the middle, term, 1036 Belly lift, 816 Bench-knee conformation, 23, 24 Bending, 85 Beta-aminoproprionitrile fumarate for desmitis of accessory ligament of deep digital flexor tendon, 653 for superficial digital flexor tendonitis in event horses, show jumpers, and dressage horses, 641 in racehorses, 633-634 for suspensory desmitis, 663 in driving horse, 1053 Betamethasone, 748 for digital flexor tendon sheath disease, 677 for distal hock joint pain in show hunter and show jumper, 970 for stifle synovitis and osteoarthritis in show hunter and show jumper, 973 for suspensory desmitis in show hunter and show jumper, 971 for tarsal tenosynovitis, 690 BEVA. See British Equine Veterinary Association. Biceps brachii muscle enthesopathy of, 404, 405 injury of, 727 lesions of, 413 strain of, 146 tearing of, 404 tendonitis of, 411-412 Bicipital bursa. See Intertubercular bursa. Biglycan, 621 Bilaterally symmetrical lameness, 66 Biodegradable delivery system of antimicrobials, 602 Biologically based therapy, 756-757 Biomarkers of bone cell activity in racehorses, 842-847 of osteoarthritis, 591-594 Biomechanics in applied anatomy, 84 of articular cartilage, 576 of fibrotic myopathy, 477 of foot, 247-248 in mechanical lameness, 475-479 in models of joint disease, 596 role of in osteochondrosis, 540 of shivers, 479 of stringhalt, 477 of tendons, 616-617 of upward fixation of patella, 477 Biopsy, muscle, 725 in chronic exertional rhabdomyolysis, 731 in immune-mediated myopathy, 733 in mechanical lameness, 475 in polysaccharide storage myopathy, 732 in rhabdomyolysis, 494 Biotin, 968 Bizolin 200. See Phenylbutazone. Bladder uptake, bone scintigraphy and, 202-203 Bleeding from arthrocentesis, 599 within carpal sheath, 685 into a joint. See Hemarthrosis. muscular, 726

1100

Index

Bleeding—cont’d at site of fracture or blunt trauma, 32, 35 in superficial digital flexor tendonitis in racehorses, 629 Blind spavin, 55-56, 440 Blindness, 18-20 Blister beetle-related myopathy, 737 Blistering for counterirritation, 778 for metatarsophalangeal joint osteoarthritis, 427 for superficial digital flexor tendonitis in racehorses, 630, 632-634 Block, 243-244. See also Diagnostic analgesia. bone scan and, 208 dangerous horse and, 140 dorsal ring of pastern, 115 failure to perform appropriate, 136 fibular, 116-117 median, ulnar, and medial cutaneous antebrachial, 106-107 mid-pastern ring, 100-102 negative responses to, 140-141 palmar, 243-244 high, 104-105 lateral, 105-106 low, 103-104 palmar digital, 100, 101, 102 plantar, 243-244 high, 115-116 low, 115 sequential, 94, 95, 96, 97, 98 sesamoid abaxial, 102-103, 115, 244 basisesamoid, 115 sources of pain that cannot be desensitized by, 136-137 tibial, 116-117 of wrong limb, 136 Block for horseshoe, 265 Blood culture in infectious arthritis, 598-599 Blood flow therapy for laminitis, 330 Blood spavin, 55 Blood supply of tendon, 618, 625 degeneration and, 625 Blood test in prepurchase examination of performance horse, 952, 963 Blunt trauma deep digital flexor tendon injury in pastern region caused by, 648 periosteal new bone in response to, 155 swelling at site of, 32 Body posture assessment in lameness examination, 37-41 Body size, osteochondrosis and, 536-537 Body temperature assessment, 59 Body weight femur fracture and, 474 management of in breeding stallions, 1080 in laminitis treatment, 338 osteochondrosis and, 536-537 in overfeeding assessment, 546 Bog spavin, 443-444, 551 in Draft horse, 1066 tarsal palpation in, 55, 56 Bone abscess of, ultrasonographic examination of, 197 articular, structure and metabolism of, 591 biomarkers of cell activity of in racehorses, 842-847 bruising of computed tomography of, 214-215 magnetic resonance imaging of, 218, 219 degenerative disease of, radiation therapy for, 786-787 fatigue of in bucked shins, 847-854 intercalated, anatomy of, 86 lameness development and length of, 17 new formation of, 154-158, 159 biochemical markers of in racehorses, 843

Bone—cont’d new formation of—cont’d on caudal aspect of wing of sacrum, 497 on dorsal aspect of middle phalanx, 315 radiation therapy for, 785, 787 subchondral. See Subchondral bone. thermography of, 237 of thoracolumbar spine, 509 Bone islands of humerus, 407 Bone marrow components, 673-674 Bone scintigraphy, 198-212 of brachium, 401-403 carpal, 378-379, 380 of cervical spine, 524-525 computed tomography versus, 214 in confusing or equivocal radiographic changes, 211 in damaged skeletal muscle, 211-212 in distal hock joint pain, 442 of distal interphalangeal joint, 312, 313 of distal phalanx, 322 of elbow, 401-403 equipment used in, 199, 200 of European Thoroughbred, 884 of foot, 246 general considerations in, 198 image acquisition in, 199-204 indications and case selection for, 208-209 of metatarsophalangeal joint, 423-424, 425 in muscle disorders, 724 in navicular disease, 294-295 of North American Standardbred, 902 in North American Thoroughbred, 872 in osteoarthritis, 583 pelvic, 211, 486, 487, 488, 489, 493 phases in, 204 in prepurchase examination of performance horse, 962 in primary lesion of deep digital flexor tendon within hoof capsule, 307 in proximal suspensory desmitis in forelimb, 656 in hindlimb, 659, 661 radiation safety in, 204 radioisotope and radiopharmaceutical, 198-199 in rhabdomyolysis, 494 in sacroiliac injury, 495-497, 507 scan interpretation in, 204-208 of shoulder, 401-403 of stifle, 457-458 in stress-related bone injury in cortical and subchondral bone, 209-211 of thoracolumbar spine, 514, 515 of Three Day Event horses, 988 Bone spavin, 440. See also Distal hock joint pain. in pony, 1071 tarsal palpation in, 55, 57 Bone-on-bone grafting, 36 Bone-specific alkaline phosphatase, 843 Bony asymmetry, 35-37 Bony swelling, 32 Boot use of in Three Day Event horses, 992 use of to prevent injury in metacarpal region, 375 Borrelia burgdorferi, 126, 143, 609 Bow-legged conformation, 22-23, 29 Box rest, 788, 789 in cervical stenotic myelopathy, 569 for chronic exertional rhabdomyolysis, 731 for desmitis of accessory ligament of deep digital flexor tendon, 652-653 following transection of accessory ligament of superficial digital flexor tendon in racehorses, 636 for pelvic fracture in Thoroughbred racehorse, 489 for proximal suspensory desmitis, 656, 660 for radial management, 395, 396

Brachial plexus anatomy of, 399-400 damage to, 414 Brachium anatomy of, 399-400 diagnosis of lameness in, 400-401 imaging of, 401-403 palpation of, 50 Brachytherapy, 784 interstitial, 784-785 intra-cavitary, 786 surface, 785-786 Bracing for flexural limb deformities, 562 Braciocephalicus muscle injury to, 727 lesions of, 413 Breaching, 756 Breakover horseshoes for modification of, 267-268 lameness and, 248 in stride biomechanics, 247, 251 Breed biochemical markers of bone cell activity in racehorses and, 845 in clinical history, 11 in epidemiology of racehorse injuries, 865 Breeder’s Cup, 868 Breeding management, 1080-1082, 1083 Breeding stallions, 1077-1082 Bridging, transphyseal, 560 Brisket, traumatic injury to in driving horse, 1057, 1058 British Equine Veterinary Association humane destruction guidelines of, 149 prepurchase examination worksheet of, 953-957 Broad-spectrum antimicrobials, 600 Broodmare, 1082-1083 nutritional requirements of, 546-548 positioning of for breeding, 1080 Brucella neck pain and, 525 in supraspinous bursitis, 705 in vertebral osteomyelitis, 530 Bruising of foot, 276-277 in Arabian and Half-Arabian show horse, 1044-1045 in driving horse, 1054 in European Thoroughbred, 887 in North American Standardbred, 903-904 in North American Thoroughbred, 872 in reined cow horse, 1029 in show hunter and show jumper horses, 968 in Three Day Event horses, 993 Brushing interference, 69 in European Thoroughbred, 886 horseshoes for prevention of, 268 Bucked shins, 435 cryotherapy for, 781 in racehorses, 847-854 European Thoroughbred, 892 North American Standardbred, 898 North American Thoroughbred, 876 racing Quarter Horse, 929 radiation therapy for, 785 thermography in, 237 Bucked-knee conformation, 25, 27 Buckling forward at knee, 38 Bursa, 705-708 applied anatomy of, 86 diagnostic analgesia of, 244 in forelimb, 113-115 in hindlimb, 121-122 Bursitis aseptic intertubercular, 412 calcaneal, 705-706 infectious of extensor tendon, 697, 698 navicular, 288 in North American Thoroughbred, 873 supraspinous, 705 trochanteric, 472-473, 499

Index Bursoscopy, 230-231, 234-235 Butorphanol, 1079 for acute rhabdomyolysis, 729 for chemical restraint during bone scintigraphy, 203 epidural, 767, 768 for laminitis in Draft horse, 1062 for post-anesthetic myopathy, 735 for sedation in extracorporeal shock wave therapy, 825 Buttress foot, 31 C C nerve fiber in arthritic pain, 607 cryotherapy for destruction of, 780 Calcaneal bursa, 705-706 arthrocentesis of, 122 Calcaneus anatomy of, 440 enthesitis of in North American Standardbred, 908-909 osteitis of, 447-448 symmetry assessment and, 36-37 tendonitis of, 709 Calcinosis circumscripta, 467-468 Calcitonin in arthritic pain, 607 for splints in polo pony, 1012 Calcitonin gene-related peptide, 285 Calcium developmental orthopedic disease and, 543-544 exertional rhabdomyolysis and, 730, 731 fractional exertion of in recurrent exertional rhabdomyolysis, 494 for hypocalcemia, 738 osteochondrosis and, 538, 541 requirements of during pregnancy, 547 for yearlings, 544 Calcium gluconate, 739 Calf roping horse, 1025-1026 Calf-knee conformation, 25-26, 27 Calks for horseshoe, 265-266 in driving horse, 1053 in polo pony, 1004 Camera for gait analysis, 224 Camped under, 39 Camped-out conformation, 24, 25, 26 Camped-under conformation, 24, 25 Canker, 1063-1064 Canter, 61 back disorder evaluation during, 512 Saddlebred, 1036 Cantharides, 778 Capped elbow, 706 Capped hock, 706 tarsal palpation in, 54, 55 Capsaicin, 607 Capsulitis of metacarpophalangeal joint, 349 Carbohydrate intake in chronic exertional rhabdomyolysis, 731 in developmental orthopedic disease, 544 osteochondrosis and, 537 Carbonic anhydrase III, 723 Carboxy propeptide of type II collagen, 592 Carboxyterminal cross-linked telopeptide of type I collagen, 844 Carboxyterminal propeptide, 843 Carpal canal, 684-687 Finnish lameness of, 949 Carpal flexor tendon sheath analgesia, 114 Carpal joint anatomy of, 376 arthrocentesis of, 110-111 flexion testing of, 76, 77 lameness of in dressage horse, 982 in European Standardbred, 920

Carpal joint—cont’d lameness of—cont’d in European Thoroughbred, 888-889 in steeplechasers, hurdlers, and point to point horses, 945 Carpal synovial sheath, 684-687 tenoscopy of, 233-234 tenosynovitis of, 629 Carpometacarpal joint inadvertent penetration of in high palmar nerve block, 104, 105 osteoarthritis of, 368, 369, 382 Carprofen, 747 Carpus, 376-393 anatomy of, 376-377 three-dimensional, 92, 93 arthrocentesis of, 110-111 canal and synovial sheath of, 684-687 clinical characteristics and diagnosis of lameness of, 377-380 conformation of, 377 diagnostic analgesia of, 106-107 disorders of, 380-393 accessory carpal bone fractures, 391, 686 arthrodesis, 391 articular fracture of distal radius, 392 comminuted fractures, 390 hygroma, 392-393, 611 hypertrophic osteopathy, 393 neoplasia, 393 in North American Standardbred, 898 osseous cyst-like lesion, 391 osteoarthritis, 380-382, 1071 osteochondral fragmentation, 382-390, 930, 933 osteochondromatosis, 391 osteochondrosis, 391 in pony, 1073 in racing Quarter Horse, 930 radiation therapy for, 785 soft tissue injuries, 392 synovitis of in racing Quarter Horse, 930 on the track fracture of in Thoroughbred racehorse, 858 field management of traumatic injury to, 146-147 flexion testing of, 76, 77 flexural limb deformity of, 562-565 National Hunt, point to point, and timber racing horse lameness of, 945 North American Standardbred lameness of, 905-906 nuclear scintigraphy of, 209, 210 palpation of, 48-50 in European Standardbred, 915 polo pony lameness of, 1016 previously unrecognized causes of lameness proximal to, 141 radiography of in European Thoroughbred, 884 retinacular release of for superficial digital flexor tendonitis, 637-638 standard radiographic projection and suggested extra views of, 164-165 synovitis of in Finnish horses, 949 Thoroughbred lameness of European, 888-889 North American, 874-875 Carpus valgus, 22, 23, 557-561 Carriage horse. See Driving horse. Carrot stretches, 816 Cartilage arthroscopic resurfacing of, 229, 756 models of, 596 for osteochondral fragmentation in carpometacarpal joint, 385 articular models of, 596 normal structure and function of, 573-575, 591

1101

Cartilage—cont’d of foot disease of, 323-325 functional anatomy of, 283-284 involvement of canals in osteochondrosis, 539-540 replacement of by bone, 534-535 failure of. See Osteochondrosis. traumatic damage to in distal interphalangeal joint, 314 in femorotibial joint, 464 Cartilage oligomeric matrix protein, 575, 592, 621, 622-624 Case selection for arthroscopic surgery, 636 for transection of accessory ligament of superficial digital flexor tendon, 636 Cassia occidentalis–related myopathy, 737 Cast bandage, 772-773 following fetlock arthrodesis for traumatic disruption of suspensory apparatus, 361 Casting for digital extensor tendon laceration, 693 for flexural limb deformities, 562 following surgery for ringbone in Draft horse, 1064, 1065 for superficial digital flexor injury management in racehorses, 630 Catabolic process, 592-593 Catastrophic injury in Thoroughbred, 854-861, 863-864 equipment used in, 856 euthanasia and insurance in, 861 management of, 855-856 public relations and media issues in, 857 during racing, 857-860 regulatory considerations in, 861 role of regulatory veterinarian in, 855 during training, 856-857 Cathepsin B, 578 Catheter placement, epidural, 766-767 Caudal antebrachial myositis, 398 Caudal phase of stride, 247 in lameness examination, 67-68 Cautery, 778-780 for bucked shins in North American Thoroughbred, 876 for curb management, 702 CCM. See Cervical compressive myelopathy. CDET. See Common digital flexor tendon. Ceftiofur for infectious arthritis, 600 for subsolar abscess in Draft horse, 1060 Celestone. See Betamethasone. Cellular components of tendons, 618-619, 620, 621 Cellulitis, 32, 35, 151 antebrachial, 398 metatarsal, 439 in pleasure riding horse, 1095 of superficial digital flexor tendon in steeplechaser, hurdlers, and point to point horses, 942 tendonitis-associated, 374 after topical application, 374 tarsal, 448 in acute-onset, severe lameness, 148 in European Thoroughbred, 891 Center of gravity, 4, 5 Central pattern generator, 819 Central tarsal bone, incomplete ossification of, 543 Centrodistal joint analgesic arthrocentesis of, 117-118 false-negative response to, 135 distal hock joint pain and, 440, 441 osteoarthritis of in Arabian and Half-Arabian show horse, 1047-1048 in Draft horse, 1066-1067

1102

Index

Centrodistal joint—cont’d osteoarthritis of—cont’d in dressage horse, 981-982 in Three Day Event horses, 993 pain in reined cow horse, 1029 Centroquatral joint fragments, 444 Cephalosporins for infectious arthritis, 600 for tenosynovitis of extensor tendon sheaths, 695 Cerebellar abiotrophy in pony, 1075 Cerebrospinal fluid aspiration and analysis in cervical stenotic myelopathy, 566-567 in neurologic disorders, 126-128 Cervical compressive myelopathy, 128 Cervical spinal cord compression, 130-131, 143 Cervical spine, 522-531 anatomy of, 522 clinical examination of, 522-523 clinical presentation of, 522 congenital abnormalities of, 525-526 cyst-like lesions of, 530 diskospondylitis of, 529 forelimb posture seen in pain of, 38-39 fracture of, 529-530 imaging of, 523-525 insertional desmopathy of nuchal ligament and injury to semispinalis, 526-527 jugular vein thrombophlebitis of, 530-531 muscle abscess of, 527 musculature disorders of, 527 myeloma of, 530 myositis of in American Saddlebred, 1040 occipito-atlantoaxial malformations of, 525 nutritional management of, 548 osteoarthritis of, 527-529 osteomyelitis of, 530 palpation of, 50-51 soreness and restriction of in Three Day Event horses, 992-993 standard radiographic projection and suggested extra views of, 166 stenotic myelopathy of, 566-570 stiffness and mobilization of under general anesthesia, 531 thermography of, 238 Cervical vertebral interbody fusion, 569-570 Cervical vertebral malformation, 548 in breeding stallion, 1078 Chain, cross-ties and overhead, 789 Chemical ablation for navicular disease, 302 Chemical fusion with sodium monoiodoacetate for distal hock joint pain, 443 Chemical restraint during bone scintigraphy, 203 for cerebrospinal fluid analysis, 127 for diagnostic analgesia, 98-99, 140 in pony, 1070 during lameness examination, 62 of breeding stallion, 1077 of European Standardbred, 916 Chemical shift artifact, 220 Chest acute-onset, severe lameness in, 146-147 width of in conformation assessment, 20 Chinese medicine, traditional, 793, 794 Chip fracture arthroscopic examination of, 229 carpal, 382-390 in Arabian racehorse, 933 in European Thoroughbred, 889 in North American Thoroughbred, 875 osteoarthritis versus, 380-381 in racing Quarter Horse, 930 in steeplechasers, hurdlers, and point to point horses, 945 of carpometacarpal joint, 382-390 of distal interphalangeal joint, 551 of extensor process of distal phalanx, 316-317 of femur in cutting horse, 1019

Chip fracture—cont’d in fibular tarsal bone, 445 of metacarpophalangeal joint in racing Quarter Horse, 930 of metatarsophalangeal joint, 428-429 in North American Standardbred, 907 of middle phalanx, 315, 351 models of, 596 of proximal phalanx, 351-353, 550 in North American Thoroughbred, 874 radiography of, 160 Chiropractic, 803-811 adjunct recommendations and prognosis, 810 approaches, 804-805 for clinical evaluation, 805-808 complications or adverse effects, 810 contraindications, 809 history of, 804 indications for, 808-809 manual therapy and, 803, 804 pathophysiology and mechanism of action of, 805 practitioner qualifications in, 803-804 for sacroiliac joint injury in show hunter and show jumper, 972 techniques, 809-810 Chloride, fractional exertion of in recurrent exertional rhabdomyolysis, 494 Chondrocoronal ligament, 283 Chondrocyte in endochondral ossification, 534-535 normal structure and function of, 575 role of in osteoarthritis, 577-580 Chondroitin sulfate, 592, 750, 751, 753 Chondromatosis, synovial, 612 Chondroprotection, 746 Chondroungular ligament, 283 Churchill hock test, 56-58 in lameness of metatarsal region, 434 in North American Thoroughbred, 871 Chymotrypsin, 578 Circadian variability, biochemical markers of bone cell activity and, 844 Circling, lameness examination during, 71-72 Circumferential fibrocartilage, 86 Citation. See Flunixin meglumine. CK. See Creatine kinase. Claiming races, 869 Claudication, defined, 4 Cleansing of tendon laceration wound, 714 Clinical history, 9-14. See also History. Clinical Radiology of the Horse, 162 Clip, horseshoe, 267 Close nail, 270, 275-276 in Three Day Event horse, 993 Clostridium species in infectious arthritis, 598 in myonecrosis, 733-734 Clubfeet, 32 natural balance trimming for barefooted horse with, 272-273 Cobalt toxicity in developmental orthopedic disease, 544 Cobra venom, 302 Coexistent lameness, 4 Cold edema, 150-152 Cold firing, 779 Cold shoeing, 266 Cold therapy. See also Cryotherapy. for foot bruising in Arabian and HalfArabian show horse, 1045 for splints, 437 for superficial digital flexor injury management in racehorses, 630 Cold water hosing. See also Cryotherapy. for acute caudal antebrachial myositis, 398 for splints, 437 for tarsal tenosynovitis, 690 Cold-backed behavior, 829-830 Cold-blooded trotters, Scandinavian, 946-950

Collagen of articular cartilage, normal structure and function of, 573, 574 carboxyterminal propeptide of as biochemical marker of bone formation in racehorses, 843 crossed-linked telopeptides of as biochemical marker of bone absorption in racehorses, 843 fibrils in, diameter of, 618 pyridinium cross-links of as biochemical marker of bone absorption in racehorses, 843 in tendons, 619-621 Collagenases, 578, 579 Collateral ligament carpal, injury to, 392 of distal interphalangeal joint desmitis of, 315 injury to in show hunter and show jumper horses, 970 of elbow anatomy of, 399 injury to, 404 of metacarpophalangeal joint, injury to, 359 of metatarsophalangeal joint, injury to, 432, 610, 611 of navicular bone desmotomy of, 302 functional anatomy of, 284 of proximal interphalangeal joint, 717 of stifle anatomy of, 456 injury to, 463-464 palpation of, 54 ultrasound of, 457 of tarsus anatomy of, 440 entheseopathy of, 447 injury to, 447 ultrasonographic examination of, 192, 193, 194 Collateral ligament test, 456 Collision injury in foal, 1089 to shoulder, 146 during training of Thoroughbred racehorse, 856-857 Comfrey, 817 Comminuted fracture carpal, 390 of distal phalanx, 320, 344 patellar, 465 of second and fourth metacarpal/metatarsal bone in European Thoroughbred, 893 of third metatarsal bone, 435 tibial in European Thoroughbred, 892 Common calcaneal tendonitis, 709 Common digital extensor muscle, 692 Common digital extensor tendon anatomy of, 716 rupture of, 694 Common digital flexor tendon, 617 Communication with vendor in prepurchase of performance horse, 952, 953-957 COMP. See Cartilage oligomeric matrix protein. Compartment-like syndrome in antebrachium, 735 Compensatory lameness, 4, 62-63 Complementary therapy, 792-826 acupuncture, 792-803 for back pain, 796 for diagnostic examination, 795-796 for lameness therapy, 796 for pain associated with lower limb lameness, 796-797 scientific basis of, 792-893 techniques and instrumentation, 793-795 traditional Chinese medical theories and, 793, 794 for back pain, 521

Index Complementary therapy—cont’d chiropractic, 803-811 adjunct recommendations and prognosis, 810 approaches, 804-805 for clinical evaluation, 805-808 complications or adverse effects, 810 contraindications, 809 history of, 804 indications for, 808-809 manual therapy and, 803, 804 pathophysiology and mechanism of action of, 805 practitioner qualifications in, 803-804 techniques, 809-810 extracorporeal shock wave therapy, 825-826 herbal, 817 homeopathy, 816-817 for infectious arthritis, 603-604 laser therapy, 812-813 magnetic and electromagnetic therapy, 813 massage, 815, 818 osteopathy, 819-824 physical therapy and rehabilitation, 817-818 stretching, 815-816 ultrasonographic, 811-812 Complete immobilization, 789 Complex tenosynovitis of digital synovial sheath, 676 Complimentary lameness, 4, 62-63 Compression, 85 cartilage matrix resistance of, 576 cervical spinal cord, 130-131, 143 nerve root in cervical stenotic myelopathy, 566 Computed tomography, 213-215 of cervical spine, 525 of foot, 247 magnetic resonance imaging versus, 221 in navicular disease, 295, 296, 297 in primary lesion of deep digital flexor tendon within hoof capsule, 307-308 Concours Complet, 984 Condylar fracture of third metacarpal bone, 357-358, 367 in steeplechasers, hurdlers, and point to point horses, 943 in Three Day Event horse, 995 of third metatarsal bone, 431, 432 in North American Standardbred, 907 in steeplechasers, hurdlers, and point to point horses, 943 in Three Day Event horses, 995 tibial, 466 Confidence, 144 Conflicts of interest in prepurchase examination of performance horse, 952 Conformation, 6, 15-31 of Arabian and Half-Arabian show horse, 1042 balance and, 252-255 of barrel-racing horse, 1030 carpal, 377 curb and, 699 of digit, 30-31 of dressage horse, 977 of driving horse, 1051 in epidemiology of racehorse injuries, 865 of European Standardbred, 915 evaluation of, 15-21 in sales yearling, 836 of event horse, 997 of Finnish and other Scandinavian cold-blooded trotters, 948 of forelimb, 21-26, 27 forelimb/hindlimb weight distribution ratio and, 5 hereditary aspects of, 15 of hindlimb, 26-30 of metatarsophalangeal joint, 421 of National Hunt horse, 939 of North American Standardbred, 898

Conformation—cont’d of North American Thoroughbred, 870 osteochondrosis and, 540 of pleasure riding horse, 1095 of polo ponies, 1004 poor, imbalance and, 253-255 treatment of, 258-261 of racing Quarter Horse, 928 of reined cow horse, 1027 relevance of, 15 of roping horse, 1022, 1026 of show hunter and show jumper horses, 966 in Standardbred yearling sales, 841 of Three Day Event horses, 986 Congenital disorders of first rib, 143 flexural limb deformity, 562-563 lateral luxation of patella in pony, 1072-1073 Connecting fibrocartilage, 86 Consignor, 840 Contact with the bit, dressage horse and, 977 Contract between veterinarian and purchaser of performance horse, 951-952 Contracted heels in North American Standardbred, 904 Contrast, radiographic, 154 Controlled exercise, 818. See also Exercise. for superficial digital flexor injury management in racehorses, 632-633 in Three Day Event horses, 994 for suspensory desmitis body, 663 proximal, 656, 660 Coon footed, 30 Copper developmental orthopedic disease and, 544, 547 osteochondrosis and, 537, 538 requirements of for yearlings, 544 Corns, 276 in driving horse, 1054 in European Thoroughbred, 887 mineral requirements for, 544 in North American Standardbred, 903-904 in polo pony, 1011 Coronary band, 281-282 palpation of, 43, 44 Corrective shoeing, 269-270. See also Shoeing. Cortical bone fracture bone scan of, 209-211 in third metatarsal bone, 435 Corticosteroids for acute rhabdomyolysis, 729 for digital flexor tendon sheath disease, 677 for distal hock joint pain, 442, 443 in show hunter and show jumper, 970 for distal interphalangeal joint pain in Arabian and Half-Arabian show horse, 1045 for equine protozoal myelitis, 130 for fracture and exostoses of second and fourth metatarsal bone, in North American Standardbred, 911 laminitis and, 328 for metacarpophalangeal joint capsulitis/synovitis, 349 for myopathy immune-mediated, 733 polysaccharide storage, 732 for osteoarthritis, 748-749, 751, 752 in dressage horse, 981 of metatarsophalangeal joint, 428 for splints in polo pony, 1012 for superficial digital flexor tendonitis in polo pony, 1007 in racehorses, 630, 634 for suspensory desmitis body, 663 in dressage horse, 980 in endurance horse, 999 proximal, 660

1103

Corticosteroids—cont’d for tarsocrural joint capsule distention, 444 for tenosynovitis, 695 tarsal, 690 for thoracolumbar spine injury, 520 for upward fixation of patella in cutting horse, 1020 Corynebacterium pseudotuberculosis, 734 Cosmesis with arthroscopic surgery, 226 Count numbers, scintigraphic, 201 Count stealing in scintigraphy, 201 Counterirritation, 778-780 in gluteal syndrome, 472 for metatarsophalangeal joint osteoarthritis, 427 for stifle joint osteoarthritis in Arabian and Half-Arabian show horse, 1047 for superficial digital flexor injury management in polo pony, 1007 in racehorses, 630, 633 for trochanteric bursitis, 473 for upward fixation of patella, 477 Cow-hocked conformation, 29 in North American Standardbred, 898 COX. See Cyclooxygenase. Coxofemoral joint anatomy of, 484 arthrocentesis of, 120, 121, 122 in pelvic fracture, 492 injury of, 499-500 luxation of in pony, 1071-1072 radiography of, 492 Cracking off, 319 Cracks, foot, 280-281 in Draft horse, 1061 in North American Standardbred, 903, 904 in North American Thoroughbred, 872 perineural nerve block for, 102 in reined cow horse, 1029 Cranial cruciate ligament anatomy of, 455 injury of, 610 in show hunter and show jumper horses, 973 ultrasound of, 457 Cranial gluteal artery, 501-502 Cranial gluteal nerve, 501-502 Cranial gluteal vein, 501-502 Cranial phase of stride, 247 in lameness examination, 67-68, 248 Cranialis tibialis muscle, 450 Creases of shoe, 263 Creatine kinase in immune-mediated myopathy, 733 in muscle disorders, 723-724 in neurologic examination, 126 in polysaccharide storage myopathy, 732, 733 in post-anesthetic myopathy, 735 in rhabdomyolysis, 148, 494 chronic exertional, 730 in driving horse, 1055 ilial wing fracture and, 486 Crepitus assessment of using palpation, 42 in femur fracture, 473 in pelvic injury, 36 Crimp, 616, 618 Crossed-linked collagen telopeptides, 843 Cross-sectional area measurement, ultrasonographic, 174-175, 182 Cross-ties chains, 789 Croton oil, 778 Croup pain, 1047 Cruciate ligaments anatomy of, 455, 654 ultrasonographic, 717 desmitis of, 721 injury of, 610-611 in stifle, 463, 464, 973 ultrasound of, 457

1104

Index

Cruciate test in stifle lameness, 456 Crus, 450-454 direct trauma to in driving horse, 1057, 1058 palpation of, 54 Cryoneurectomy, 782 for navicular disease, 302 Cryotherapy, 780-782 for acute caudal antebrachial myositis, 398 for bruised feet in Arabian and Half-Arabian show horse, 1045 for laminitis, 330 for splints, 437 in polo pony, 1012 for superficial digital flexor injury management in racehorses, 630 for suspensory desmitis, 663 in North American Standardbred, 910 for tarsal tenosynovitis, 690 Crystalline penicillin, 734 CS. See Chondroitin sulfate. Cs packs, 787 CS-846 epitope, 592 CSA. See Cross-sectional area. CSF. See Cerebrospinal fluid aspiration and analysis. CT. See Computed tomography. C-telopeptides, 592 CTX. See C-telopeptides. Cubital joint arthrocentesis, 111-113 Cuboidal bone injury in foal, 1086, 1087 Cunean tendon anatomy of, 450 bursa on, 706 arthrocentesis for, 121-122 cryotherapy for tendonitis of, 782 tenectomy of in distal hock joint pain, 443 in Draft horse, 1067, 1068 Curb, 699-704 cryotherapy for, 782 in European Standardbred, 918 in Finnish horse, 950 local infiltration of anesthetic solution in, 122-123 in North American Standardbred, 912 tarsal palpation in, 56 Curby, 27 Cushing’s disease, 328, 330-331 Cushion, digital, 284 Cut-out-under-the-knee conformation, 26 Cutting horse, 1017-1021 Cyanoacrylate adhesive, 274 Cyclooxygenase, nonsteroidal antiinflammatory drugs for inhibition of, 746-747 Cyclooxygenase II inhibitors for infectious arthritis, 603 Cyst, subchondral bone, 158 in cutting horse, 1019-1020 in femorotibial joint, 461-462 relationship between physeal dysplasia, osteochondrosis, and, 536 in scapulohumeral joint, 408-409 in show hunter and show jumper horses, 973 Cytokines corticosteroids in inhibition of synthesis of, 748 role of in osteoarthritis, 577, 579-580 D Dally team roping, 1021-1022 Dandelion toxicity, 478 Dangerous horse, nerve block and, 140 Dantrolene sodium for rhabdomyolysis, 729 in endurance horse, 1000 in North American Standardbred, 912 Data collection in gait analysis, 222, 224 DDFT. See Deep digital flexor tendon. Death, racetrack-associated, 864 in National Hunt horses, 938 Debridement of canker, 1064 of deep penetrating injury of sole, 280

Debridement—cont’d for digital extensor tendon laceration, 693 in femoropatellar joint osteochondrosis, 458-459 in femorotibial cartilage trauma, 464 for infectious arthritis, 602-603 of osseous cyst-like lesion of distal radius, 397 for scapulohumeral joint osteochondrosis, 408 of subchondral lucency of third carpal bone, 390 of sub-solar abscess, 279 of tendon laceration wound, 714 in tenosynovitis of extensor tendon sheaths, 695-696 Decompression, osseous, 755 Decorin, 575, 621-622 Deep digital flexor tendon, 644-650 accessory ligament of. See Accessory ligament of deep digital flexor tendon. anatomy of, 82, 287, 433-434, 618-622, 644, 650, 684, 716 three-dimensional, 91 ultrasonographic, 717 biochemical parameters for, 616-617 bursoscopy of, 234-235 imaging of, 175-182, 717 infection of, 373 injuries of in pastern region, 647-648, 718 laceration of, 712-715 marginal tears of, 647 mineralization and fibrosis of, 646-647 primary lesion of in hock and proximal metatarsal regions, 649 puncture wound of, 648 rupture of, 648 tendonitis of, 644-647, 686 cryotherapy and, 782 in curb, 704 in pastern region, 647-648 perineural nerve block for, 102 in pony, 1074 tenoscopy of, 233-234 tenotomy of for laminitis, 335-338 Degeneration of intersesamoidean ligament, 667 of tendons, 624-625 Degenerative joint disease. See also Osteoarthritis. radiation therapy for, 786-787 radiographic diagnosis of, 161 Degenerative myeloencephalopathy, 131, 566-567 Delayed-phase bone scan image, 204 Deltoid anatomy of, 399 fracture of tuberosity of, 405, 406 Demineralization. See Osteopenia. Deoxypyridinoline, 844 Depo Medrol. See Methylprednisolone. Depo-Provera. See Medroxyprogesterone acetate. Derby, 868 Dermatitis, pastern, 151 Derotation of distal phalanx for laminitis, 338 Desmitis of accessory ligament of deep digital flexor tendon. See Accessory ligament of deep digital flexor tendon. of superficial digital flexor tendon, 685, 1016-1017 of collateral ligaments in distal interphalangeal joint, 315 in metatarsophalangeal joint, 432 of distal sesamoidean ligament oblique, 670-671, 719-720, 721 perineural nerve block for, 102 in polo pony, 1016 straight, 668-670, 720-721 in team roping horse, 1023-1024 on the track in Thoroughbred racehorse, 860

Desmitis—cont’d low plantar, 704 of palmar annular ligament, 678-681 in dressage horse, 982 in polo pony, 1015-1016 in pony, 1074 of proximal digital annular ligament, 682, 683 of sacroiliac ligament, 502-503 in cutting horse, 1021 of suspensory ligament in American Saddlebred, 1039 in Arabian and Half-Arabian show horse, 1046 in Arabian racehorse, 932 in barrel-racing horse, 1031-1032 body lesions, 662-663, 1009-1010 branch lesions, 663-666, 876, 921-922, 980, 1009-1010 as compensatory lameness, 63 cryotherapy for, 781-782 in Draft horse, 1065 in dressage horse, 979-980 in driving horse, 1053 in endurance horse, 998-999 in European Standardbred, 920-922 in European Thoroughbred, 888 extracorporeal shock wave therapy for, 826 in Finnish horse, 950 in metatarsal region, 437-438 in National Hunt, point to point, and timber racing horses, 943 in North American Standardbred, 910-911 in North American Thoroughbred, 875-876 in polo pony, 1009-1010 proximal in forelimb, 654-657, 658 proximal in hindlimb, 658-662 radiation therapy for, 785 in reined cow horse, 1028-1029 in show hunter and show jumper horses, 970-971 stem cell and marrow components for, 673 in team roping horse, 1024-1025 in Three Day Event horses, 994-995 Desmopathy insertional of nuchal ligament, 526-527 of medial collateral ligament, ultrasound of, 191, 192 of supraspinous ligaments, 515-516 Desmotomy of accessory ligament of deep digital flexor tendon for acquired flexural deformity, 564 for desmitis, 653 navicular suspensory, 302 of palmar annular ligament, 232, 637, 641, 680 in polo pony, 1007 of superficial digital flexor tendon, 637 in Three Day Event horse, 994 for upward fixation of patella, 477 Destruction of injured horse, 149 Detomidine, 1079 for acute rhabdomyolysis, 729 for chemical restraint during bone scintigraphy, 203 epidural, 767, 768 for sedation in extracorporeal shock wave therapy, 825 Developmental anatomy of stifle, 455 Developmental orthopedic disease, 533-570 angular limb deformities, 557-561 cervical stenotic myelopathy, 566-570 flexural limb deformities, 562-565 in foals, 1088-1089 nutrition and, 543-548 osteochondrosis, 534-543, 549-554 causes of, 536-541 characteristics of lesions in, 535-536 of distal interphalangeal joint, 551 of metacarpophalangeal and metatarsophalangeal joints, 549-550

Index Developmental orthopedic disease—cont’d osteochondrosis—cont’d of proximal interphalangeal joint, 550-551 relationship between physeal dysplasia, subchondral bone cysts, and, 536 of scapulohumeral joint, 551 of stifle, 554 of tarsocrural joint, 551-554 physitis, 554-556 in young Draft horse, 1068-1069 Devil’s claw, 817 Dexamethasone for digital flexor tendon sheath disease, 677 for hormone-related performance problems in mares, 481 for immune-mediated myopathy, 733 for superficial digital flexor injury management in racehorses, 630 for thoracolumbar myositis in cutting horse, 1020 for thoracolumbar spine injury, 520 for upward fixation of patella in cutting horse, 1020 Dextrose for hyperkalemic periodic paralysis, 739 DFTS. See Digital flexor tendon sheath. Diagnosis of lameness. See Diagnosis of lameness. of navicular disease, 288-297 clinical signs in, 289 computed tomography and magnetic resonance imaging in, 295, 296, 297 endoscopy in, 297 history in, 288-289 local analgesic techniques in, 289, 290 nuclear scintigraphy in, 294-295 radiographic examination in, 289-294 of neurologic disorders, 125-129 of swollen limb, 150-152 Diagnosis of lameness, 1-124, 135-239 acupuncture for, 795-796 acute-onset, severe, 145-149 chiropractic, 805-808 diagnostic imaging in, 153-239 arthroscopic, 226-230 computed tomography, 213-215 gait analysis, 222-225 magnetic resonance imaging, 216-221 nuclear medicine, 198-212 radiography, 153-166 tenoscopy and bursoscopy, 230-235 thermographic, 236-239 ultrasonography, 166-194 examination in baseline and induced lameness in, 4 clinical history in, 9-14 coexistent lameness in, 4 components of, 7-8 conformation and, 6, 15-31 diagnostic analgesia used in, 93-124 distribution of lameness in, 4-6 historical perspective of, 2-3 localization of pain in, 4 during movement, 60-73 musculoskeletal system anatomy and, 81-93 neurologic examination and neurologic conditions causing gait deficits and, 124-135 palpation in, 42-60 poor performance and, 6-7 symmetry and posture assessment in, 31-41 unexplained lameness and, 7 using manipulation, 74-81 unexplained, 135-144 apparent only during riding, 142 dangerous horse and nerve blocks and, 140 false-negative responses to local analgesic techniques, 135-137 identifiable lesions and, 142 lameness that varies within and between examinations and, 139

Diagnosis of lameness—cont’d unexplained—cont’d misinterpreted imaging findings that result in misdiagnosis and, 141-142 neck lesions and forelimb lameness and, 141 negative responses to nerve block and, 140-141 potentially confusing responses to local analgesic techniques in, 137-138 previously unrecognized causes of lameness proximal to carpus and tarsus, 141 referred pain and, 141 very intermittent or sporadic lameness and, 138-139, 140 using high-speed treadmill, 834-835 Diagnostic analgesia, 93-124, 243-244 in Arabian and Half-Arabian show horse, 1044 of bursae and tendon sheaths forelimb, 113-115 hindlimb, 121-122 carpal, 378 in cervical stenotic myelopathy, 569 of crus, 450 dangerous horses and, 140 in distal hock joint pain, 441 of distal interphalangeal joint, 310-311 of distal phalanx, 322 in dressage horse, 979 in driving horse, 1052 of elbow, 400-401 false-negative responses to, 135-137 flexion tests and, 80-81 injection technique in, 99-100 intra-articular in forelimb, 107-113 in hindlimb, 117-120, 121, 122 local infiltration in, 122-123 of metacarpal region, 363-364 of metacarpophalangeal joint, 348-349 of metatarsal region, 434 of metatarsophalangeal joint, 422 in metatarsophalangeal joint osteoarthritis, 427 in National Hunt, point to point, and timber racing horses, 941 in navicular disease, 289, 290 negative responses to, 140-141 in North American Standardbred, 901-902 patient preparation in, 99 in pelvic injury, 492 perception of by laypersons, 98 perineural in forelimb, 100-107 in hindlimb, 155-117 in polo pony, 1005 in pony, 1070 in poor performance, 831 potentially confusing responses to, 137-138 in proximal suspensory desmitis of forelimb, 655 of hindlimb, 658 role of chemical restraint in, 98-99 of sacroiliac joint, 506-507 of shoulder, 400-401 in Standardbred European, 916 North American, 901-902 of stifle, 456 strategy, methodology, and other considerations in, 94-96, 97, 98 of thoracolumbar spine, 513 in Thoroughbred European, 885-886 North American, 871 in Three Day Event horses, 987-988 Diagnostic imaging. See Imaging. Diaphysis of elbow, anatomy of, 399

1105

Diaphysis—cont’d fracture of of humerus, 405-407 of third metatarsal bone, 435 tibial, 451, 452, 453 Diarthrosis, 85 Diazepam for enhancement of libido and facilitation of ejaculation, 1079 for opioid respiratory side effects, 768 Diclazuril, 130 Diet acquired flexural deformities and, 563, 564 biochemical markers of bone cell activity and, 844 cervical stenotic myelopathy and, 569 in chronic exertional rhabdomyolysis, 731 in clinical history, 13 developmental orthopedic disease and, 544-546 in laminitis management, 338 osteochondrosis and, 537 in polysaccharide storage myopathy, 732 shivers and, 479 Differential cell count, synovial, 599 Diffuse filling in metacarpal region, 372-375 in metatarsal region, 439 Digit conformation of, 30-31 infection of in foals, 1093 Digital annular ligament anatomy of, 674-675, 716 desmitis of, 682, 721 diagnostic techniques for, 675 disease of, 682, 683 Digital blood flow therapy for laminitis, 330 Digital compression of painful area followed by movement in lameness examination, 79-80 Digital cushion, functional anatomy of, 284 Digital extensor muscle, 692 Digital extensor tendon anatomy of, 716 laceration of, 693-694 rupture of, 694 Digital flexor tendon sheath analgesia of, 102, 113-114 for metacarpal pain or disease, 364 anatomy of, 674-675 three-dimensional, 89 annular ligament syndrome and, 678-681 diagnostic techniques for, 675 disease of, 676-678 imaging of, 675-676 palpation of, 46, 47 primary injury of, 688 in steeplechasers, hurdlers, and point to point horses, 945 synovial ganglion and hernia of, 682-683 tenoscopy of, 231-232 tenosynovitis of, 629 in dressage horse, 982 in driving horse, 1055-1056 in Finnish horses, 950 in polo pony, 1015-1016 in show hunter and show jumper horses, 975 on the track injuries of in Thoroughbred racehorse, 860 wind puffs or wind galls of, 47 Digital nerve block of, 100, 101, 102, 243-244 in European Standardbred, 916 for hind foot and pastern lameness, 419 in North American Standardbred, 902 for proximal suspensory desmitis, 658 in Three Day Event horses, 987 neurectomy of, 303 in North American Thoroughbred, 873 neuritis/neuroma of, 722 ultrasonographic anatomy of, 718

1106

Index

Digital pulse monitoring of in laminitis, 339 palpation of, 42, 47, 83 in swollen limb, 151 Digital radiography, 162 Dimethylsulfoxide for acute rhabdomyolysis, 729 for cervical stenotic myelopathy, 569 for infectious arthritis, 603 for laminitis, 330 in endurance horse, 1000 synovial fluid cytology for, 582 DIP. See Distal interphalangeal joint. Dirt on racetrack, 863, 864 Disease modification, 746 Diskospondylitis, 132 of cervical spine, 529 Disputes, resolution of in Standardbred sales, 840 Disruption of caudal component of reciprocal apparatus, 40 Distal forelimb nuclear scintigraphy of, 209, 210 perineural nerve block in, 103 ultrasonographic zone designations for, 175-178, 179 Distal hindlimb palpation of in European Standardbred, 915-916 ultrasonographic zone designations for, 178-180, 181 Distal hock joint pain, 440-443 in American Saddlebred, 1037 in Arabian and Half-Arabian show horse, 1047-1048 in Arabian racehorse, 932 in barrel-racing horse, 1031 cryotherapy for, 782 in cutting horse, 1018-1019 in Draft horse, 1067 in driving horse, 1054-1055 in endurance horse, 1001 in North American Standardbred, 898-899, 907-909 in North American Thoroughbred, 877 in polo pony, 1013 in racing Quarter Horse, 930 in show hunter and show jumper horses, 969-975 in team roping horse, 1025 Distal interphalangeal joint, 310-316 anatomy of functional, 285, 310 three-dimensional, 89 articular chip fracture of middle phalanx and, 315 clinical signs of lameness in, 310 damaged distal sesamoidean impar ligament of, 315 desmitis of collateral ligaments of, 315 diagnostic analgesia of, 107-108, 244, 310-311 for distal interphalangeal joint pain, 310 in Three Day Event horses, 987-988 effusion of, palpation of, 44 flexural limb deformity of, 563 of hindlimb, 419-420 history, 310 imaging of, 311-312 injury of in show hunter and show jumper horses, 970 joint capsule trauma in, 314, 315 osseous cyst-like lesion of, 314-315 osseous fragments on dorsal aspect of, 315 osteoarthritis of, 313, 314 in Arabian and Half-Arabian show horse, 1045-1046 in Draft horse, 1064-1065 in dressage horse, 981 in driving horse, 1056-1057 in European Standardbred, 919-920 in North American Standardbred, 905 in North American Thoroughbred, 873

Distal interphalangeal joint—cont’d osteoarthritis of—cont’d perineural nerve block for, 102 in polo pony, 1011 in show hunter and show jumper horses, 970 in Three Day Event horses, 993 osteochondrosis of, 551 pain in reined cow horse, 1029 palisading new bone on dorsal aspect of middle phalanx and, 315 subchondral bone in, 314 perineural nerve block for, 102 synovitis of in dressage horse, 981 in driving horse, 1054 perineural nerve block for, 102 in racing Quarter Horse, 929 in show hunter and show jumper horses, 970 traumatic damage to articular cartilage of, 314 Distal limb flexion test of, 243 passive stay apparatus of, 87 Distal phalanx derotation of for laminitis, 338 disease of collateral cartilage of, 323-325 fractures and fragmentation of, 318-321, 419 in American Saddlebred, 1038 in breeding stallions, 1078 in extensor process, 316-317 in foals, 1086-1088 in North American Standardbred, 904-905 in North American Thoroughbred, 873 in polo pony, 1010 in Three Day Event horses, 995 nuclear scintigraphy of, 209, 210 osseous cyst-like lesion in, 317 osteitis of in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045 in Draft horse, 1063 infectious, due to penetrating injury, 280 of palmar processes, 322-323 pedal, 321 in polo pony, 1011 in reined cow horse, 1029 radiography of, weight-bearing oblique of, 246 three-dimensional anatomy of, 89 on the track fracture of in Thoroughbred racehorse, 857 Distal radius osseous cyst-like lesion of, 397-398 traumatic physitis and closure of physis of, 394-395 Distal sesamoidean ligament anatomy of, 89, 91, 675, 716, 717 desmitis of, 719-721 perineural nerve block for, 102 in polo pony, 1016 in show hunter and show jumper, 974 in team roping horse, 1024 on the track in Thoroughbred racehorses, 860 palpation of, 46 Disuse atrophy related to, 31-32, 33 models of, 596 DMSO. See Dimethylsulfoxide. Documentation, ultrasonographic, 167-168 Dorsal longitudinal ligament, 522 Dorsal metacarpal disease. See Bucked shins. Dorsal metatarsal artery, 433 Dorsal metatarsal disease. See Bucked shins. Dorsal ring block of pastern, 115 Dorsal spinous process fracture of in withers region, 142-143 in polo pony, 1014 impingement of, 123, 514-515, 516 in polo pony, 1013-1014

Dorsolateral aspect of fetlock, ultrasonographic examination of, 189 Dorsomedial articular fracture of third metacarpal bone, 367 Dorsomedial aspect of fetlock, ultrasonographic examination of, 189 Dorsopalmar balance, 248 Dorsopalmar imbalance, 254-255, 257-258 treatment of, 258-259 Dorsopalmar view of foot, 245 Dorsoproximal-palmarodistal oblique view of foot, 245 DPr-PaDiO view. See Dorsoproximalpalmarodistal oblique view. Draft horse, 1058-1069 foot lameness in, 1060-1064 hindlimb lameness in, 6 lameness examination of, 1059-1060 modern-day, 1059 osteoarthritis of proximal and distal interphalangeal joint in, 1064-1065 ringbone in, 1064-1065 ten most common lameness problems in, 1059 Drainage articular for infectious arthritis, 602-603 of hygroma, 611 of tarsal tenosynovitis, 690 Draining tracts, ultrasonographic examination of, 195 Dressage horse, 975-983 diagnostic analgesia in, 979 explanation of sport, 975-977 imaging of, 979 lameness examination of, 978-979 superficial digital flexor tendonitis in, 642, 643 tack, 978 ten most common lameness conditions in, 979-983 training surfaces used by, 977-978 Drifting, 67 Drilling, surgical, 303 for third metacarpal bone stress fracture, 853 Driving horse, 1049-1058 conformation of, 1051 description of sport, 1049-1050 diagnosis and management of lameness in, 1053-1058 diagnostic analgesia in, 1052 difficulties in diagnosis of, 1052-1053 ground conditions for, 1051 imaging of, 1052 lameness examination of, 1052 shoeing of, 1053 ten most common lameness conditions of, 1051 training of, 1050-1051 types of horses used as, 1050 Dropped elbow, 38 Dropped fetlock, 33, 37 Drug testing of polo pony, 1004 Drugs in clinical history, 13 for navicular disease, 301-302 used in on the track catastrophe in Thoroughbred racehorse, 856 Dryness, excessive, of racetrack, 862 Duct tape, 332, 333 Dummy mount, 1080 Duration of current lameness, 12 Duty cycle, 811-812 Dynamic acquisition in bone scintigraphy, 201, 202 Dynamic balance, conformation and, 253 Dyschondroplasia, 535 Dysplasia of coxofemoral joint, 499 in pony, 1072 physeal, relationship between subchondral bone cysts, osteochondrosis, and, 536 of scapulohumeral joint, 410

Index Dystocia, obturator nerve paralysis secondary to, 1083 Dystrophic mineralization, 161 Dystrophy, neuroaxial, 131 E Ear tick-associated muscle cramping, 738 Echogenicity, 173, 174 Eclampsia, 737-738 Edema, 32 cold, 150-152 in superficial digital flexor tendonitis in racehorses, 629 EDM. See Equine degenerative myeloencephalopathy. Effusion, 32 in arthritis, 606-607 in carpal lameness, 378, 381 in digital flexor tendon sheath disease, 677 of distal interphalangeal joint, palpation of, 44 of joint in purchase examination of Thoroughbred sales yearling in Europe, 839 in metatarsophalangeal joint lameness, 422 in osteoarthritis, 581 of tarsal sheath. See Thoroughpin. tarsocrural. See Bog spavin. Egg bar shoe fitting in navicular disease, 300, 301 in subsolar bruising, 968 EHV. See Equine herpesvirus. Eight Principles, 793, 794 Ejaculation, management and pharmacologic aids for enhancement of, 1079 Elasticity, modulus of, 617, 644 Elastin, 622 Elbow anatomy of, 399-400 arthrocentesis of joint of, 111-113 capped, 706 diagnosis of lameness of, 400-401 disorders of, 403-405 dropped, 38 imaging of, 401-403 palpation of, 50 standard radiographic projection and suggested extra views of, 165 Electroacupuncture, 794 Electrolytes, 494, 730 Electromagnetic therapy, 813 Electromyography in mechanical lameness, 475 in muscle disorders, 725-726 in neurologic disorder diagnosis, 129 Embedded hoof, ultrasonographic appearance of, 196 Emergency management of fracture in broodmare, 1083 of tendon lacerations, 713-714 of on the track catastrophe in Thoroughbred, 854-861 equipment used in, 856 euthanasia and insurance in, 861 management of, 855-856 public relations and media issues in, 857 during racing, 857-860 regulatory considerations in, 861 role of regulatory veterinarian in, 855 during training, 856-857 En bloc resection for carpal hygroma, 393 Endochondral ossification, 534-535 failure of. See Osteochondrosis. Endoscopy of deep digital flexor tendon, 308-309 in navicular disease, 297 in purchase examination of Thoroughbred sales yearling in North America, 837 of tarsal sheath, 690 in transection of accessory ligament of superficial digital flexor tendon, 636

Endosteal new bone, 155, 156 Endotoxin contamination in reactive synovitis, 608 Endurance horse, 996-1002 Energy dissipation, functional anatomy of palmar aspect of foot and, 284 Energy intake in chronic exertional rhabdomyolysis, 731 developmental orthopedic disease and, 544 osteochondrosis and, 537-538 Enhancement, acoustic, 172 Enostosis, defined, 407 Enostosis-like lesion, 156 of humerus, 407 of metacarpal region, 374 of radius, 396, 397 of third metatarsal bone, 437 tibial, 453 Enrofloxacin, 600 Enterobacter cloacae, 448 Enteseophyte, 156, 157 Enthesopathy of biceps brachii, 404, 405 of insertion of extensor carpi radialis tendon, 695 of lateral collateral ligaments of tarsocrural joint, 447 Environmental contamination development in developmental orthopedic disease, 544 Enzyme/cytokine ratio in infectious arthritis diagnosis, 600 Enzymes activation of in laminitis, 325, 327 matrix-degrading, 577-579 muscle, 723-724 in superficial injury, 728 proteolytic, tendon degeneration and, 625 EORL. See Equine Orthopedic Research Laboratory. Eosinophilic synovitis, 608 Epaxial muscles, 510 Epidural analgesia for hindlimb lameness, 764-769 Epidural narcotics for infectious arthritis, 603 Epinephrine, 739 Epiphysis of elbow, 399 endochondral ossification in, 534-535 Epiphysitis, 1068-1069 Epitopes, 592 EPM. See Equine protozoal myeloencephalitis. Epoxy resin, 274 Epsom salts soaking for foot abscess, 279 in North American Thoroughbred, 873 in show hunter and show jumper, 968 for foot bruising, 277 in Arabian and Half-Arabian show horse, 1045 EPSSM. See Equinepolysaccharide storage myopathy. Equiflex. See Hyaluronan. Equine Cushing’s disease, 328, 330-331 Equine degenerative myeloencephalopathy, 131, 566-567 Equine herpesvirus, 132 cerebrospinal fluid analysis in, 128 serologic testing in, 126 Equine infectious anemia, 733 Equine lower motor neuron disease, 131, 143 Equine Orthopedic Research Laboratory, 595 Equine protozoal myeloencephalitis, 129-130, 143, 567 antibody titer testing in, 126 in breeding stallion, 1078 mechanical lameness in, 475 in polo pony, 1017 Equine sports medicine, computed tomography in, 214-215 Equinepolysaccharide storage myopathy, 475 Equipalazone. See Phenylbutazone.

1107

Equiphen paste. See Phenylbutazone. Equipment acupuncture, 793-795 arthroscopic, 226, 227-229 computed tomography, 213-214 cryotherapy, 780-781 in high-speed treadmill assessment, 833-834 for hoof examination, 43 magnetic resonance imaging, 216 radiographic, 244 scintigraphic, 199, 200 tenoscopic and bursoscopic, 230-231 ultrasonographic, 167 therapeutic, 811-812 used in on the track catastrophe in Thoroughbred racehorse, 856 Equron. See Hyaluronan. Erector spinae muscle, 510 Escherichia coli in calcaneal osteitis, 448 in infectious arthritis, 598 Estradiol benzoate, 481 Estradiol cypionate, 477 Estrogenic compounds, 477 Estrone sulfate, 1001 Estrous cycle athletic mare performance and, 480-482 stopping of, 144 Ethanolamine oleate injection, 477 Ether bandage, 770 Etiquette, examination, 7 Eupatorium rugosum-related myopathy, 737 European Standardbred, 879-894 approaching lameness problems in, 914 corrective shoeing for, 918-919 diagnostic analgesia in, 916 dimensions and characteristics of, 913, 914 final diagnosis, prognosis, and treatment options for, 918 hoof pain in, 919 imaging of, 916-918 lameness examination of, 914-916 metatarsophalangeal joint lameness in, 922 middle carpal joint lameness in, 920 osteoarthritis of distal interphalangeal joint in, 919-920 osteoarthritis of metacarpophalangeal joint in, 920 proceeding without a diagnosis, 919 proximal palmar metacarpal pain including proximal suspensory desmitis in, 920-921 sesamoiditis in, 921 superficial digital flexor tendonitis in, 922-923 tarsocrural joint osteochondrosis in, 923 ten most common lameness conditions in, 914 training programs for, 919 European Thoroughbred, 879-894 clinical examination of, 882-884 diagnostic analgesia in, 885-886 exostosis of second and fourth metacarpal/metatarsal bones in, 893 foot-related lameness in, 887-888 fractures of proximal phalanx and condyles of distal third metacarpal/metatarsal bones in, 893-894 history in assessment of, 882 history of sport, 879-894 imaging of, 884-885 lameness subsequent to bacterial infection in, 891-892 middle carpal joint-related lameness in, 888-889 pain associated with tarsometatarsal joint in, 894 pattern of racing in, 879-880 purchase examination sales yearling, 838-839, 840 shoeing considerations for, 886-887

1108

Index

European Thoroughbred—cont’d stress fractures of long bones and pelvis in, 892-893 subchondral bone injuries to distal third metacarpal/metatarsal bone in, 889-891 suspensory desmitis in, 888 training regimen for, 879-880 undiagnosed hindlimb lameness in, 893 European Western performance horse, 1032-1033 Euthanasia guidelines for, 149 for on the track catastrophe in Thoroughbred racehorse, 861 Event horse superficial digital flexor tendonitis in, 639-641 Three-Day, 984-996 conformation of, 986 diagnosis and management of lameness in, 992-995 diagnostic analgesia in, 987-988 history in assessment of, 986 imaging of, 988-989, 990 influence of sport on lameness of, 985 lameness examination of, 986-987 prevention of lameness in, 995-996 proceeding without a diagnosis in, 989-990 saddle pressure analysis of, 989, 991 shoeing of, 990-991, 992 sport of, 984 tack considerations in, 991-992 ten most common lameness conditions in, 986 training of, 985-986 types of horses in, 984-985 Examination of acute-onset, severe lameness, 145-149 of American Saddlebred, 1036-1037 of Arabian and Half-Arabian show horse, 1042-1044 of barrel-racing horse, 1030-1031 baseline and induced lameness in, 4 of breeding stallion, 1077 clinical history in, 9-14 coexistent lameness in, 4 components of, 7-8 conformation in, 6, 15-31 digit, 30-31 evaluation of, 15-21 forelimb, 21-26, 27 hereditary aspects of, 15 hindlimb, 26-30 relevance of, 15 of cutting horse, 1018 diagnostic analgesia in, 93-124 false-negative responses to, 135-137 of forelimb bursae and tendon sheaths, 113-115 of hindlimb bursae and tendon sheaths, 121-122 injection technique in, 99-100 intra-articular in forelimb, 107-113 intra-articular in hindlimb, 117-120, 121, 122 local infiltration in, 122-123 patient preparation in, 99 perception of by laypersons, 98 perineural in forelimb, 100-107 perineural in hindlimb, 115-117 potentially confusing responses to, 137-138 role of chemical restraint in, 98-99 strategy, methodology, and other considerations in, 94-96, 97, 98 distribution of lameness in, 4-6 of Draft horse, 1059-1060 of dressage horse, 978-979 of driving horse, 1052 of European Standardbred, 914-916 of European Thoroughbred, 882-884 sales yearling, 838-839, 840 of event horse, 998

Examination—cont’d of Finnish and other Scandinavian coldblooded trotters, 948-949 of foot, 242-249 historical perspective of, 2-3 localization of pain in, 4 movement during, 60-73 circling, 71-72 determination, grading, and characterization of lameness, 62-64 foot placement evaluation, 70-71 gait, 60-62 on hard and soft surfaces, 71 lameness detection during, 67-70 lameness score, 66-67 location of lameness determination during, 64-66 riding observation in, 72-73 using treadmill or gait analysis, 73 musculoskeletal system anatomy and, 81-93 forces in, 85 language of, 85 passive stay apparatus in, 87-88 specialized structures in, 85-87 three-dimensional, 88, 89, 90, 91, 92, 93 of National Hunt, point to point, and timber racing horses, 940-941 in neurologic disorders, 124-129 of North America Thoroughbred, 870-871 sales yearling, 836-837 of North American Standardbred, 900-901 palpation in, 42-60 art of, 42-60 of cervical spine, 50-51 Churchill hock test in, 56-58 of external genitalia, 51 of forelimb, 42-50 of hindlimb, 53-56, 57 of lateral and ventral thorax and abdomen, 51 of pelvis, 52 of pelvis per rectum, 52-53 saphenous filling time in, 58-59, 60 of thoracolumbar spine, 51 of polo pony, 1005 of pony, 1070 poor performance and, 6-7 posture assessment in, 37-41 prepurchase of performance horse, 951-964 blood tests in, 963 communication with vendor in, 952, 953-957 at a distance, 952-958 evaluation of identified problems in, 960 gait assessment in, 960 goals of, 951 guidelines for reporting, 964 nerve blocks in, 963-964 nuclear scintigraphic examination in, 962 radiographic examination in, 960-962 rectal examination in, 960 at rest, 958-959 summary of observations in, 964 thermographic examination in, 963 Three Day Event horse, 986 ultrasonographic examination in, 962-963 veterinarian contract in, 951-952 of reined cow horse, 1027-1028 relationship of lameness and conformation in, 6 of roping horse, 1022-1023 of show hunter and show jumper horses, 966 of swollen limb, 150-152 symmetry assessment in, 31-37 of Tennessee Walking Horse, 1034 of Three Day Event horse, 986-987 in unexplained lameness, 135-144 unexplained lameness following, 7 Exercise, 789-790, 818 of breeding stallion, 1080 bucked-shin complex and, 849-851

Exercise—cont’d effects of in tendon injury, 622-624 following blistering, 778 foot function at, 251-252 forced, models of, 596 in gluteal syndrome therapy, 472 graduated in tendon laceration, 715 hyperthermia induced by, tendon degeneration and, 624-625 level grading scale for, 168, 169 lunging in prepurchase examination of performance horse, 960 osteochondrosis and, 540 for proximal suspensory desmitis, 663 for superficial digital flexor injury management in racehorses, 631-632, 633-634 in Three Day Event horse, 994 tendon blood flow and, 618 testing in chronic exertional rhabdomyolysis, 730 in muscle disorders, 724 in upward fixation of patella management, 477 use of bone markers to study effects of, 545 in vasodilatory therapy for laminitis, 330 Exertional myopathy, 1000 Exertional rhabdomyolysis, 728-732 in driving horse, 1055 in endurance horse, 1000 in iliac wing fractures, 486 in North American Standardbred, 912 in North American Thoroughbred, 878 in ponies, 1075 in Three Day Event horse, 995 Exostosis. See Splints. Exposure factors, 154 Exposure latitude, 154 Extension for horseshoe, 263-265 Extensor carpi obliquus muscle, 692-693 Extensor carpi radialis muscle, 692 Extensor tendon, 692-699 anatomy of, 692-693 diagnostic techniques in, 693 disorders of, 693-697, 698 in American Saddlebred, 1040 laceration of, 712 surgical management of, 714 rupture of, flexural limb deformity versus, 565 External beam irradiation, 784 External fixation for distal phalanx fracture, 344, 345 skeletal, 774-777 External genitalia palpation, 51 External rotation of hindlimb, 39 Extracorporeal shock wave therapy, 825-826 for distal hock joint pain, 443 for metatarsophalangeal joint osteoarthritis, 427 for proximal suspensory desmitis, 656-657, 660 F Facet joint anatomy of, 509-510 modeling of, 527 radiography of, 513, 514 Falls in National Hunt horse, 939, 940 False thoroughpin, 706-708 False-negative findings in local analgesic techniques, 135-137 in nuclear medicine, 206-207 False-positive findings in nuclear medicine, 206 Far gain setting, ultrasonographic, 170 Farrier, 300, 338 lameness in European Thoroughbred from pricking by, 887 Fasciculation, muscle, 737-738 Fasciotomy, proximal metacarpal, 637-638 Fast spin echo sequence in magnetic resonance imaging, 217

Index Fatal injury, racetrack, 864 in National Hunt horses, 938 Fatigue failure of third metacarpal bone. See Bucked shins. Fatigue fracture incomplete palmar cortical of third metacarpal bone, 364-366 radiography of, 159 Federation Equestre Internationale dressage rules of, 975 European Championship of, 996 Feeding systems to prevent developmental orthopedic disease, 546-548 Feedstuffs in ration evaluation, 545 Femoral head separation, 490 Femoral nerve paresis, 40, 41, 132 Femoropatellar joint anatomy of, 455 diagnostic analgesia of, 119, 456 disease of, 458-461 ultrasonographic examination of, 191 Femoropatellar ligament, 455 Femorotibial joint anatomy of, 455-456 diagnostic analgesia of, 119 disease of, 461-465 in North American Standardbred, 911 pain in cutting horse, 1020 palpation of, 53 in European Standardbred, 916 ultrasonographic examination of, 191-192, 193 Femur anatomy of, 455 displacement of head of, 500 fractures of, 473-474, 493, 500 in foal, 1085-1086 swelling caused by, 34-35 on the track in Thoroughbred racehorse, 859 osteochondrosis of in cutting horse, 1019 subchondral bone cyst of in cutting horse, 1019-1020 Fence hurdle racing, 934-935 Fences, rushing, 829 Fetlock acquired bursa on dorsal aspect of hind, 706 American Saddlebred lameness of, 1038 arthrodesis of for traumatic disruption of suspensory apparatus, 361 deep digital flexor tendonitis within tendon sheath in region of, 645-647 dressage horse lameness of, 982 dropped, 33, 37 flexion testing of, 75, 76, 78 height of in symmetry assessment, 33, 37 intersesamoidean ligament injury of, 666-667, 668, 681-682 joint of. See Metacarpophalangeal joint. North American Thoroughbred lameness of, 873-874 palpation of, 46-47 in European Standardbred, 915 physitis of, 555 scab on palmar aspect of, 151 show hunter and show jumper lameness of, 972-973 soft tissue injuries of in hindlimb, 431-432 standard radiographic projection and suggested extra views of, 163-164 ultrasonographic examination of, 189, 190, 191 varus deformity of, 557-558 Fetlock drop, 67 Fever, 59 bamboo, 1012 mud, 151 FFD. See Focus film distance. Fiber alignment pattern assessment, 173-174 Fiberglass cast, 361 Fibril diameter, 618

Fibroblasts in tendon healing, 625-626 Fibrocartilaginous structure anatomy, 86-87 Fibroma, 612 Fibromodulin, 575, 621 Fibronectin, 575, 622 Fibrosis, 32 within deep digital flexor tendon, 646-647 muscular, 726 subcutaneous in region of palmar annular ligament, 680, 681 Fibrotic myopathy, 34, 70, 476, 477-478 thigh palpation in, 53 Fibula anatomy of, 450 fracture of, 445, 454, 467 Fibular nerve analgesic block of, 116-117 in pelvic fracture, 492 anatomy of, 450 Fibularis tertius altered hindlimb posture seen in, 40, 41 anatomy of, 450 avulsion of origin of, 467 rupture of, 708-709 in acute-onset, severe lameness, 148 in North American Standardbred, 909 Field diagnosis of injured horse, 145-149 Filled legs, 150-152 Filly. See Mare. Film and screen factors in imaging, 154 Finnish horse, 946-950 Firing, 778-780 for bucked shins in North American Thoroughbred, 876 for curb management, 702 First rib fracture, 415 Fistula, synovial, 612 of extensor tendon, 697 Fitness of breeding stallions, 1080 training in Three Day Event horse, 986 Five Element theory, 793, 794 Fixation for distal phalanx fracture, 343, 344, 345 external, 344, 345, 774-777 of intra-articular fracture, 754 patellar, 70, 459-460, 465, 475-477 altered hindlimb posture seen in, 39-40 coxofemoral joint luxation with or without, 499-500 in cutting horse, 1020 in pony, 1073 stifle palpation in, 53-54 for proximal interphalangeal joint lesions, 550 of proximal physeal tibial fracture, 452 of slab fracture of third carpal bone, 388-389 of tarsal bone fracture, 445 of tibial tuberosity fracture, 467 Flap shoe, 920 Flare as diagnostic analgesia complication, 94 Flat feet, natural balance trimming for barefooted horse with, 272 Flat racing, 880 Flat walk, Saddlebred, 1036 Flatweed toxicity, 478 Flexibility assessment of neck, 523 in performance horse, 959 Flexion tests, 74-79, 243 in Arabian and Half-Arabian show horse, 1043 carpal, 378 in distal hock joint pain, 441 in Draft horse, 1060 in European Standardbred, 916 during fetlock palpation, 47 in Finnish horse, 949 in hind foot and pastern lameness, 419 in North American Thoroughbred, 871 in pelvic fracture, 492 in prepurchase examination of performance horse, 960 training in Three Day Event horse, 987

1109

Flexor deformity of metatarsophalangeal joint, 431 Flexor tendon common digital, 617 deep digital. See Deep digital flexor tendon. laceration of, 712 surgical treatment of, 714 palpation of, 58 radiation therapy for tendonitis/desmitis, 785 superficial digital. See Superficial digital flexor tendon. thermography of, 237 Flexural limb deformity, 562-565 in young Draft horse, 1068-1069 Flight phase of stride, 251 Flip-flop shoe, 920 Floating the hoof wall, 262 Flooring material for breeding shed, 1081 Flucort. See Flumethasone. Fluid therapy for post-anesthetic myopathy, 735 for rhabdomyolysis, 729 in driving horse, 1055 in endurance horse, 1000 in tendon laceration emergency management, 713 Flumethasone, 748 Flunixin meglumine, 747, 1079 for digital flexor tendon sheath disease, 677 for distal hock joint pain in cutting horse, 1019 for distal interphalangeal joint synovitis in driving horse, 1054 for laminitis, 329-330 in endurance horse, 1000 for post-anesthetic myopathy, 735 for rhabdomyolysis, 729 in endurance horse, 1000 Fluoride toxicity in developmental orthopedic disease, 544 Fluoroscopy of foot, 246 Foal, 1084-1093 angular limb deformities of, 557-561 cervical stenotic myelopathy of, 566-570 developmental orthopedic disease in, 533-570 Draft horse, lameness of, 1068-1069 evaluation of, 1084-1085 flexural limb deformities of, 562-565 fractures in acetabular, 490 odontoid peg, 526 sesamoid, 356, 357 in solar margin of distal phalanx, 318-319 tibial, 451-452, 453 infectious causes of lameness in, 1089-1093 with myotonia congenita in, 738 non-infectious causes of lameness in, 1085-1089 pelvic fracture radiography in, 485-486 rupture of common digital extensor tendon in, 694 Foaling-related injuries in broodmare, 1083 Foam for solar support in laminitis, 332, 333, 334, 335 Focal hypoechogenic lesion, 646 Focal peritarsal cellulitis, 891 Focal tear of intersesamoidean ligament, 297, 298, 666-667 Focal zone, improper use of, 170, 171 Focus film distance, 153, 154 Folate, 1079 Foot, 241-340 appearance of self-maintained, 271-272 Arabian and Half-Arabian show horse lameness of, 1044-1045 Arabian racehorse lameness of, 933 attachment of shoe to, 266-267 balance and conformation of, 252-255 in European Standardbred, 915 loading of superficial digital flexor tendon and, 625 in performance horse, 958

1110

Index

Foot—cont’d biomechanics of, 247-248 breeding stallion lameness of, 1078 broodmare lameness in, 1082 care of in laminitis, 332-335, 336 detailed examination of, 242-243 disease of cartilages of, 323-325 distal interphalangeal joint pain in, 310-316 distal phalanx disorders of, 316-325 Draft horse lameness in, 1060-1064 driving horse lameness of, 1053-1054 endurance horse lameness in, 999-1000 evaluation of placement of, 70-71 examination of, 242-247 computed tomography, 247 diagnostic ultrasonographic, 246-247 distal limb flexion test in, 243 fluoroscopic, 246 frog pressure test in, 243 hoof tester examination in, 44-46, 243 hoof wall surface evaluation in, 242 magnetic resonance imaging, 247 nerve and joint blocks in, 243-244 palpation in, 42-44, 242-243 radiographic, 244-246 reverse wedge test in, 243 scintigraphic, 246 in Three Day Event horse, 986 visual examination in, 242 function of, 250-252 functional anatomy of palmar aspect of, 282-286 hind, 418-421 horseshoes and shoeing of, 262-271 adhesive type, 274-275 attachment of shoe to hoof in, 266-267 bars for, 265 calks, grabs, and other devices added to ground of shoe, 265-266 corrective, 269-270 cross-sectional profile of shoe stock for, 263, 264 effects of on foot function, 269 extensions for, 263-264 functions of, 267-269 hot versus cold, 266 lameness associated with, 270 materials and size of horseshoe in, 262-263 pads for, 266 of sound horses for performance, 269 imbalance and poor conformation of, 253-255 clinical identification of, 255-258 in proximal suspensory desmitis, 655 in purchase examination of Thoroughbred sales yearling in Europe, 839 treatment of, 258-261 interference, 68-69 keratoma, neoplastic, and non-neoplastic occupying lesions in, 317-318 laminitis of, 325-339 deep digital flexor tenotomy for, 335-338 diagnosis of, 329 enzymatic theory of, 327 histological grading of, 325-327 hoof care in, 332-335, 336 medical therapy of, 329-331 natural trigger factors in, 327-328 pathophysiology of, 325 lateral placement of during advancement, 69 National Hunt, point to point, and timber racing horse lameness of, 944-945 natural balance trimming of, 272-273 navicular disease of, 286-297 diagnosis of, 288-297 fracture, 304-305 pathophysiology of, 286-288 treatment and prognosis of, 299-304 North American Standardbred lameness of, 903-905 pain of in European Standardbred, 919 polo pony lameness in, 1010

Foot—cont’d pony lameness in, 1074 poultice application, 770 primary lesion of deep digital flexor tendon within capsule of, 305-309 primary lesion of deep digital flexor tendon within hoof capsule, 305-309 reined cow horse lameness in, 1029 saphenous filling time assessment in, 59, 60 show hunter and show jumper lameness in, 967-969 size of, asymmetry and, 32-33 soft tissue causes of palmar heel pain in, 297-298 soreness of in racing Quarter Horse, 930 in Three Day Event horse, 993 thermography of, 236 Thoroughbred lameness of European, 887-888 North American, 872-873 trauma to sole and wall of, 275-282 penetrating, 278-282 problems associated with horseshoe nails in, 275-278 traumatic injury to, 147 Foot poultice, 770 Footbath for foot abscess, 279 in North American Thoroughbred, 873 in show hunter and show jumper, 968 for laminitis, 330 for solar bruising, 277 Forage inappropriate grain for, 546 nutrient analysis of, 545 Force musculoskeletal, 85 used in flexion tests, 74-75 Force plate quantification of ground reaction force, 223-224 Forearm, 394-399 compartment-like syndrome in, 735 diagnostic analgesia of intra-articular, 110-111 perineural, 106-107 direct trauma to in driving horse, 1057, 1058 palpation of, 50 in European Thoroughbred, 883 Foreign body in reactive synovitis, 608 solar, 279 ultrasonographic examination of, 195-196 Forelimb, 341-416 analgesia in blocking strategy in, 95, 96 of bursa and tendon sheath, 113-115 intra-articular, 107-113 local infiltration in, 122-123 perineural, 100-107 antebrachial disorders of, 394-399 brachium of anatomy of, 399-400 diagnosis of lameness of, 400-401 imaging of, 401-403 brushing interference of in European Thoroughbred, 886 carpus of, 376-393 anatomy of, 376-377 clinical characteristics and diagnosis of lameness of, 377-380 conformation of, 377 specific conditions of, 380-393 common abnormalities of limb flight in, 69 conformation of, 21-26, 27 in performance horse, 958 elbow of anatomy of, 399-400 diagnosis of lameness of, 400-401 disorders of, 403-405 imaging of, 401-403

Forelimb—cont’d field assessment of traumatic injury to, 147 flexion testing of, 75-77 fracture of, 147 on the track in Thoroughbred racehorse, 857-859 humeral disorders of, 405-407 intertubercular bursa disorders of, 411-412 lameness of assessment of during circling, 72 bilaterally symmetrical, 66 in Draft horse, 1066 hindlimb lameness versus, 65-66 neck lesions and, 141 recognition of, 64-65 upper in polo pony, 1016 metacarpal region of, 362-376 anatomy of, 362-363 diagnosis of lameness of, 363-364 disorders of, 364-375 imaging of, 364 use of boots and bandages to prevent injury to, 375 metacarpophalangeal joint of, 348-362 acute or repetitive overload injuries of, 349-351 anatomy of, 348 diagnosis of lameness of, 348-349 imaging of, 349 proximal phalanx injuries in, 351-354 proximal sesamoid bone conditions in, 354-356, 357 third metacarpal bone fracture in, 357-361 types of fetlock lameness of, 349 palpation of, 42-50 passive stay apparatus of, 87 posture assessment of, 37-39 proximal and middle phalanx and proximal interphalangeal joint of, 342-348 proximal suspensory desmitis in, 654-657, 658 in dressage horse, 980 shoulder of anatomy of, 399-400 diagnosis of lameness of, 400-401 imaging of, 401-403 intertubercular bursa disorders of, 411-412 local analgesia of, 400-401 muscle disorders of, 413 nervous disorders of, 413-415 scapular disorders of, 412-413 scapulohumeral joint disorders of, 408-411 symmetry assessment of, 31-33 ultrasonographic zone designations for, 175-178, 179 Forelimb/hindlimb weight distribution ratio, 4, 5, 6 Forging, 69 in European Thoroughbred, 886-887 Fortification, inadequate in grain, 546 Fourth metacarpal bone exostoses of, 369-371 in European Thoroughbred, 893 in North American Standardbred, 911 in racing Quarter Horse, 929 fracture of, 371-372 cryotherapy for, 781 in North American Standardbred, 911 in pony, 1073 in Three Day Event horse, 995 palpation of, 47 Fourth metatarsal bone anatomy of, 433 exostoses of, 437 in European Thoroughbred, 893 in North American Standardbred, 911 fractures of, 437 cryotherapy for, 781 in North American Standardbred, 911 in pony, 1073 palpation of, 58

Index Fox hunting, 934 Fox trot, 60 Fracture. See also specific fracture. acute-onset, severe lameness following, 148 emergency repair of in broodmare, 1083 endosteal new bone in response to, 155, 156 internal fixation of, 754 radiographic diagnosis of, 158-160 stress. See Stress fracture. swelling at site of, 32, 34 ultrasonographic examination of, 196 Fragmentation arthroscopic examination of, 229 carpal, 380-381, 382-390 in Arabian racehorse, 933 in European Thoroughbred, 889 in North American Thoroughbred, 875 osteoarthritis versus, 380-381 in racing Quarter Horse, 930 in steeplechasers, hurdlers, and point to point horses, 945 of carpometacarpal joint, 382-390 of distal interphalangeal joint, 551 of distal phalanx, 316-317 in European Standardbred, 922 on dorsal aspect of interphalangeal joint, 315 of femur in cutting horse, 1019 in fibular tarsal bone, 445 of metacarpophalangeal joint in racing Quarter Horse, 930 of metatarsophalangeal joint, 428-429 in North American Standardbred, 907 of middle phalanx, 315, 351 models of, 596 patellar, 460, 465 in American Saddlebred, 1039 of proximal phalanx, 351-353, 550, 874 in North American Thoroughbred, 874 radiography of, 160 of stifle, 466 in talocalcaneal-centroquatral joint, 444 Free radical scavengers, 330 Freeze firing, 780. See also Cryotherapy. Freezing, 780. See also Cryotherapy. Frog pressure test, 243 proliferative pododermatitis of in Draft horse, 1063 support of in American Saddlebred, 1038 in laminitis, 332, 338, 1062 in pelvic fracture, 490 Front foot asymmetry of in purchase examination of Thoroughbred sales yearling in Europe, 839 interference, 68-69 lameness of in National Hunt, point to point, and timber racing horses, 944-945 in North American Standardbred, 903-905 standard radiographic projection and suggested extra views of, 162-163 symmetry of, 32 Front perspective in forelimb conformation, 21-24, 25 Frontal carpal slab fracture, 387 Fullering of shoe, 263 Function, loss of, assessment of using palpation, 42 Fungal infection in mud fever, 151 Furosemide for opioid respiratory side effects, 768 Fusion, cervical vertebral interbody, 569-570 Fusobacterium necrophorum, 277 Future directions of magnetic resonance imaging, 221 for quantification of lameness, 224 of Standarbred sales yearling, 841 in studies of racing injuries, 866

G GAG. See Glycosaminoglycan. Gain setting, improper, 170, 171 Gait abnormalities of. See Gait abnormalities. analysis of, 73, 222-225 in distal hock joint pain, 441 on high-speed treadmill, 834-835 for lameness in stifle, 73, 222-225 defined, 60 of dressage horse, 975 forelimb/hindlimb weight distribution ratio and, 4, 5 lameness examination during, 60-62 in pony, 1070 in prepurchase examination of performance horse, 960 Saddlebred, 1036 of show horses, 1035 “stabby,” 69-70 Gait abnormalities caused by neurologic conditions, 124-135 cervical spinal cord compression, 130-131 diagnosis of, 125-129 equine degenerative myeloencephalopathy and neuroaxial dystrophy, 131 equine herpes virus I infection, 132 equine lower motor neuron disease, 131 equine protozoal myelitis, 129-130 peripheral nerve injuries, 132-133 caused by tendon lacerations, 712 in elbow or shoulder lameness, 400 in gluteal syndrome, 472 hindlimb, 70 not caused by lameness, 7 in sacroiliac joint injury, 504 in stringhalt, 478 in trochanteric bursitis, 473 Gallop, 61 prevention of bucked shins and, 852 Gamma camera images, 199, 200 Ganglion, 611-612 of digital synovial sheath, 682-683 Gastrocnemius bursa, 706 Gastrocnemius muscle anatomy, 450, 709 Gastrocnemius tendon rupture of altered hindlimb posture seen in, 40 in foal, 1085 tendonitis of, 709-710 Gelatinases, 578, 579 Gender factors in biochemical markers of bone cell activity in racehorses, 845 in clinical history, 11 in osteochondrosis, 539 General anesthesia neck stiffness and cervical vertebral mobilization under, 531 pelvic fracture and, 485-486 Gene-related peptide, 607 Genetic factors in acquired flexural deformity, 564 in conformation, 15 in osteochondrosis, 538-539 Genitalia, external, palpation of, 51 Gentamicin for infectious arthritis, 600, 601, 602 for suspensory desmitis in reined cow horse, 1029 synovial fluid cytology for, 582 Geometric design of racetrack, 862 Geriatric horse, lameness conditions of, 10-11 Getting stung, term, 1010 Ghosting, 220 Gibbs effect, 220 Gibbs-Donnan ionic equilibrium, 576 Gloving for diagnostic analgesia, 99 Glucocorticoids for cervical stenotic myelopathy, 569

1111

Glucocorticoids—cont’d for hormone-related performance problems in mares, 481 Glucosamine, 751, 753 Glucose, laminitis and changes in metabolism of, 328 Glue-on shoes, 274-275 for European Thoroughbred, 887-888 Gluteal muscle atrophy of, 33-34 myositis of in North American Thoroughbred, 878 Gluteal pain and disorders, 471-472 in American Saddlebred, 1037-1038 in Arabian and Half-Arabian show horse, 1047 in endurance horse, 1001 in polo pony, 1013-1014 in show hunter and show jumper horses, 974 Glycemic response test, 544 Glyceryl trinitrate for laminitis, 330 Glycogen storage disorder, 731-732 Glycoproteins in tendons, 621-622 Glycosaminoglycan, 592, 621-624, 750 for arthroscopic surgery postoperative care, 385 for carpal lameness in North American Standardbred, 906 for distal hock joint pain, 442, 443 in show hunter and show jumper, 970 for distal interphalangeal joint pain and disease, 313 in Arabian and Half-Arabian show horse, 1045 in dressage horse, 981 for navicular disease, 302 for osteoarthritis, 750, 753 metatarsophalangeal joint, 427, 428 in North American Thoroughbred, 874, 875 for superficial digital flexor injury management in racehorses, 630, 634 Gonadotropin-releasing hormone, 1079 Grabs for horseshoe, 265-266 in North American Thoroughbred, 872 Gracilis muscle tear, 1017 Gradient echo sequence in magnetic resonance imaging, 217 Grading of lameness, 62-64, 66-67 of laminitis, 325-327 for navicular bone evaluation, 290 Grafting arthroscopic, 229 bone-on-bone, 36 of joint, 756 Grain intake developmental orthopedic disease and, 546, 548 physitis and, 548 Gram stain synovial fluid culture, 598-599 Grand Prix, 975 Grass hay in cervical vertebral malformation therapy, 548 mineral requirements for, 544 overfeeding and, 546 Gravel, 278-279 in Draft horse, 1060-1061 in North American Standardbred, 904 perineural nerve block for, 102 in show hunter and jumper horses, 968 Gravity, center of, 4, 5 Greater trochanter, 493 swelling in, 36 GRF. See Ground reaction forces. Grid use in radiography, 153 Grooving of hoof capsule, 262 Ground reaction forces, 65, 66, 223, 247, 251 Ground surface. See Surface. Group races, 880

1112

Index

Growth asymmetrical of distal physis in angular limb deformities, 558 bone, 154-158, 159 biochemical markers of in racehorses, 843 on caudal aspect of wing of sacrum, 497 on dorsal aspect of middle phalanx, 315 radiation therapy for, 785, 787 osteochondrosis and, 536-537 Growth factors in bone marrow, clinical use of, 673 in osteoarthritis development, 579 role of in osteochondrosis, 540 for superficial digital flexor injury management in racehorses, 634 in Three Day Event horse, 994 in tendons, 619 Growth plate injury, 554-556 GSH-Px. See Selenium-dependent glutathione peroxidase. H Hair, cleansing and clipping of for diagnostic analgesia, 99 for ultrasound, 167 of thoracolumbar spine, 514 Half round shoe, 263 Half-Arabian show horse, 1040-1049 conformation of, 1042 diagnosis and management of lameness in, 1044-1049 diagnostic analgesia in, 1044 lameness examination of, 1042-1044 neurologic examination of, 1044 ten most common causes of lameness in, 1042 training of, 1041-1042 undiagnosed lameness in, 1044 Halicephalobus deletrix, 132 Hamstring stretch, 816 Hand walking, 636, 790 Hand-forged shoe, 262 Hanging-knee conformation, 25, 27 Haplopappus heterophyllus-related myopathy, 737 Hard surface, lameness examination on, 71 Harness, back pain examination of horse in, 512-513 Head conformation of, 18 elevation of in forelimb lameness, 64-66 injury to on the track in Thoroughbred racehorse, 859-860 Healing of fracture, 160 Health in clinical history, 13 Heart rate in tendon laceration emergency management, 713 Heat in digital flexor tendon sheath disease, 677 in superficial digital flexor tendonitis, 629 Heel bruised, 276 in North American Thoroughbred, 872 crack, 281 in North American Standardbred, 903, 904 perineural nerve block for, 102 elevation of for navicular disease, 300 pain in in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045-1046 in driving horse, 1054 in North American Standardbred, 906 in polo pony, 1010-1011 sheared, 277 foot palpation in assessment of, 43 in North American Standardbred, 904 perineural nerve block for, 102 in show hunter and show jumper horses, 969

Heel—cont’d underrun foot palpation in assessment of, 43 natural balance trimming for barefooted horse with, 273 in show hunter and show jumper, 966 that accompany mediolateral imbalance, 259 Heel extension for shoe, 264-265 Heights assessment of in conformation evaluation, 20, 21 in symmetry assessment, 33, 35, 37 Hemangiosarcoma, 612 ultrasound of, 195 Hemarthrosis in acute-onset, severe lameness, 148 in arthritis, 608-609 in pony, 1073 Hematology in neurologic disorders, 126 Hematoma soft tissue swelling due to, 35 in stifle region, 468 ultrasonographic monitoring of, 194-195 Hemicircumferential periosteal transection and elevation, 560 Hemorrhage from arthrocentesis, 599 within carpal sheath, 685 into a joint. See Hemarthrosis. muscular, 726 at site of fracture or blunt trauma, 32, 35 in superficial digital flexor tendonitis in racehorses, 629 Hemorrhagic shock in tendon laceration, 713 Herbal therapy, 817 Hereditary factors in conformation, 15 in osteochondrosis, 538-539 Hernia of digital synovial sheath, 682-683 synovial, 611 ventral body wall, 1083 Herpesvirus, 126, 128, 132 High palmar nerve block, 104-105 High plantar nerve block, 115-116 High ringbone, 345 High-density foam for solar support in laminitis, 332, 333, 334, 335 High-speed treadmill in lameness assessment, 73 for poor performance assessment, 832-835 for rehabilitation, 790 Hill training, 790 Hind foot, 418-421 interference, 68-69 radiographic assessment of, 163, 245 Hindlimb, 417-482 analgesia in blocking strategy in, 97-98 epidural, 764-769 local infiltration in, 122-123 perineural, 115-117 brushing injuries of in European Thoroughbred, 886 common abnormalities of limb flight in, 69-70 conformation of, 26-30 crus of, 450-454 estrous cycle and performance in athletic mares and, 480-482 external rotation of, posture seen in, 39 flexion testing of, 77-79 fracture of on the track in Thoroughbred racehorse, 859 hind foot and pastern of, 418-421 lameness in, 4-6 assessment of during circling, 72 bilaterally symmetrical, 66 in cutting horse, 1018 in Draft horse, 1066-1068 forelimb lameness versus, 65-66 mechanical, 475-479

Hindlimb—cont’d lameness in—cont’d in polo pony, 1016 recognition of, 65 undiagnosed in European Thoroughbred, 893 metatarsal region of, 433-439 metatarsophalangeal joint of, 421-433 anatomy of, 421 clinical characteristics and diagnosis of lameness of, 421-422 disorders of, 426-432 imaging of, 422-426 palpation of, 53-56, 57 in European Thoroughbred, 886 passive stay apparatus of, 87-88 posture assessment of, 39-41 progressive atraumatic breakdown of suspensory ligament of, 671-672 proximal suspensory desmitis in, 658-662 in dressage horse, 979-980 resting a, 39 stifle of, 455-470 anatomy of, 455-456 articular disease of, 458-465 avulsion of origin of peroneus tertius and long digital extensor tendon in, 467 calcinosis circumscripta in, 467-468 diagnosis of lameness in, 456 diagnostic analgesia in, 456 fractures of, 465-467 hematoma in, 468 imaging of, 456-458 symmetry assessment of, 31-33 tarsus of, 440-449 anatomy of, 440 articular disease of, 440-443 fractures and luxation of, 444-447 osteitis of, 447-448 peri-articular cellulitis of, 448 soft tissue injuries of, 447 thigh of, 471-474 traumatic injury to, 147-148 ultrasonographic zone designations for, 178-180, 181 Hindlimb varus posture, 39 Hip arthrocentesis of joint of, 120, 121, 122 knocked-down, 35 Hip hike, 65 Histological grading of laminitis, 325-327 Historical perspective of lameness examination, 2-3 History, 9-14 of Arabian and Half-Arabian show horse, 1040-1041 in driving horse assessment, 1052 of equine chiropractic, 804 of horseracing in United Kingdom, 879 patient in Arabian and Half-Arabian show horse assessment, 833 in assessment of acute-onset, severe lameness, 145-148 in desmitis of accessory ligament of deep digital flexor tendon, 651 in European Thoroughbred examination, 882 in high-speed treadmill assessment, 833 in muscle disorders, 723, 728 in navicular disease, 288-289, 304 in North American Standardbred examination, 899-900 in North American Thoroughbred examination, 870 in osteopathic treatment, 821 in pelvic injury, 491 in poor performance, 828-830, 833 in primary lesion of deep digital flexor tendon within hoof capsule, 306 in swollen limb diagnosis, 150

Index History—cont’d of polo, 1003 of Scandinavian horse, 946-947 of show hunting and show jumping, 965 Hock acute-onset, severe lameness following trauma to, 148 capped, 706 tarsal palpation in, 54, 55 Churchill test of, 56-58 deep digital flexor tendon primary lesion in region of, 649 extension test of, 78, 79 joint pain in distal in American Saddlebred, 1037 in Arabian and Half-Arabian show horse, 1047-1048 in Arabian racehorse, 932 cryotherapy for, 782 in cutting horse, 1018-1019 in driving horse, 1054-1055 in endurance horse, 1001 in North American Standardbred, 898-899, 907-909 in North American Thoroughbred, 877-878 in polo pony, 1013 in racing Quarter Horse, 930 in show hunter and show jumper horses, 969-975 lameness associated with in National Hunt, point to point, and timber racing horses, 943 osteoarthritis of, 440-443 in pony, 1071 palpation of, 54-56, 57 sickle, 16 standard radiographic projection and suggested extra views of, 165 ultrasonographic examination of, 192, 193, 194 Hock-hitting interference, 69 Homeopathy, 816-817 Hoof. See also Foot. attachment of shoe to, 266-267 balancing of in metatarsophalangeal joint arthritis, 427 care of in laminitis, 332-335, 336 clinical identification of imbalance of, 255-258 cracks of in North American Standardbred, 904 in reined cow horse, 1029 detailed examination of, 242-243 embedded, ultrasonographic appearance of, 196 height of in lameness assessment, 248 injury of in polo pony, 1010 in reined cow horse, 1029 keratoma, neoplastic, and non-neoplastic occupying lesions in, 317-318 pain of in European Standardbred, 919 preparation of for horseshoe, 262 primary lesion of deep digital flexor tendon within capsule of, 305-309 thermography of, 236 Hoof tester examination, 44-46, 243 in Arabian and Half-Arabian show horse, 1043 in Draft horse, 1060 in European Standardbred, 915 in European Thoroughbred, 883 induced lameness after, 80 in North American Thoroughbred, 872 in show hunter and show jumper, 967 Hoof wall cracks of, 280-281 in Draft horse, 1061 floating the, 262 laceration of, 280-281 poor quality of, 278 separation of, 277-278 in North American Standardbred, 904 Hoof-strike, 247

Horn tubule, 242 Horse Trials, 984 Horseracing. See also Racehorse. history of, 868-870 of National Hunt horses, 937-938 poor performance in of North American Standardbred, 897 in United Kingdom history of, 879 North America versus, 880-881 pattern of, 879-880 Horseshoe, 262-271. See also Shoeing. adhesive type, 274-275 attachment of to hoof, 266-267 bars for, 265 calks, grabs, and other devices added to ground of, 265-266 corrective, 269-270 cross-sectional profile of shoe stock for, 263, 264 effects of on foot function, 269 in epidemiology of racehorse injuries, 865 extensions for, 263-264 foot preparation for, 262 functions of, 267-269 hot versus cold shoeing of, 266 instrumented, 65, 224 lameness associated with, 270 in natural balance shoeing, 273 for navicular disease, 300-301 pads for, 266 problems associated with nails used in, 275-278 for racing Quarter Horse, 928 for sound horses for performance, 269 for Standardbred European, 918-919 North American, 903 for Thoroughbred European, 886-887 North America, 872 Hosing, cold water. See also Cryotherapy. for acute caudal antebrachial myositis, 398 for splints, 437 for tarsal tenosynovitis, 690 Hot shoeing, 266 Hot water footbath for bruised feet in Arabian and Half-Arabian show horse, 1045 for foot abscess in North American Thoroughbred, 873 for laminitis, 330 Housing in clinical history, 13 Humane destruction of injured horse, 149 Humerus anatomy of, 399 enostosis-like lesions of, 407 fractures of, 405-407 in European Thoroughbred, 893 in foal, 1085-1086 in North American Thoroughbred, 878 in pony, 1073 during training of Thoroughbred racehorse, 856 luxation of, 410-411 osteitis of tubercles of, 412 osteochondrosis of, 551 proximal physeal injuries of, 407 ultrasound of, 401, 402 Hunter’s bump, 36 Hurdle race, 934, 935 Husbandry management, 1083 HY-50. See Hyaluronan. Hyaline cartilage in foot, 283 Hyalovet. See Hyaluronan. Hyaluronan, 607, 749-750 in arthroscopic surgery postoperative care, 385 for digital flexor tendon sheath disease, 677 for distal hock joint pain, 442, 443 in barrel-racing horse, 1031 in cutting horse, 1018-1019

1113

Hyaluronan—cont’d for distal hock joint pain—cont’d in North American Thoroughbred, 877-878 in show hunter and show jumper, 970 for distal interphalangeal joint pain, 313 in Arabian and Half-Arabian show horse, 1045 for metacarpophalangeal joint capsulitis/synovitis, 349 for metatarsophalangeal joint osteoarthritis, 427, 428 for osteoarthritis, 749-750, 753 femorotibial in North American Standardbred, 911 for proximal suspensory desmitis in dressage horse, 980 for superficial digital flexor tendonitis in racehorses, 634 for tarsocrural joint capsule distention, 444 Hycoat. See Hyaluronan. Hydrochlorothiazide, 739 Hydrotherapy for acute caudal antebrachial myositis, 398 for splints, 437 for superficial digital flexor injury management in racehorses, 630 for suspensory desmitis, 663 Hydroxylysine glycosides, 843, 844 Hydroxyproline, 843, 844 Hygroma, 392-393, 611 Hylartil Vet. See Hyaluronan. Hylartin V. See Hyaluronan. Hypaxial muscle, 510 Hyperechogenic ultrasound image, 172 Hyperkalemic periodic paralysis, 738-739 Hyperthermia, induced by exercise, tendon degeneration and, 624-625 Hypertrophic osteopathy, 157 antebrachial, 398 carpal, 393 metacarpal, 374 Hypocalcemia, 737-738 in acute rhabdomyolysis, 729 Hypochoeris radica, 478 Hypoderma species, 132 Hypoechogenic ultrasound image, 172, 173 HyPP. See Hyperkalemic periodic paralysis. Hysteresis, 617 Hyvisc. See Hyaluronan. I Icing. See Cryotherapy. ICR. See Instant center of rotation. Idiopathic arthritis, 608 IGF. See Insulin-like growth factor. IgG. See Immunoglobulin G. Iliocostalis muscle, 510 Ilium anatomy of, 484 fracture of diagnostic ultrasonography of, 485 in European Thoroughbred, 893 scintigraphic diagnosis of, 486 shaft, 487-488 treatment of, 489 wing, 486-487 Image acquisition, scintigraphic, 199-204 Image contrast, 154 Image resolution, 153 Image sharpness and resolution, 154 Imaging, 84-85, 153-239 of American Saddlebred, 1037 arthroscopic, 226-230 carpal, 378 of cervical spine, 523-525 computed tomography, 213-215 of crus, 451 of digital synovial sheath, palmar annular ligament, and digital annular ligament, 675-676

1114

Index

Imaging—cont’d of distal interphalangeal joint, 311-312 of distal phalanx, 322, 323 of dressage horse, 979 of driving horse, 1052 of Finnish and other Scandinavian cold-blooded trotters, 949 gait analysis, 222-225 magnetic resonance imaging, 216-221 of metacarpal region, 364 of metacarpophalangeal joint, 349 of metatarsal region, 434-435 of metatarsophalangeal joint, 422-426 of National Hunt, point to point, and timber racing horses, 940-941 nuclear medicine, 198-212 in confusing or equivocal radiographic changes, 211 in damaged skeletal muscle, 211-212 equipment used in, 199, 200 general considerations in, 198 image acquisition in, 199-204 indications and case selection for, 208-209 in pelvic lameness, 211 phases in, 204 radiation safety in, 204 radioisotope and radiopharmaceutical, 198-199 scan interpretation in, 204-208 in stress-related bone injury in cortical and subchondral bone, 209-211 in pelvic injury, 485-486, 492-493 of polo pony, 1006 of pony, 1070 in poor performance, 831 in primary lesion of deep digital flexor tendon within hoof capsule, 306-308, 309 of proximal and middle phalanx and proximal interphalangeal joint, 342-343 in proximal suspensory desmitis of forelimb, 655-656, 657 of hindlimb, 659, 661 of racing Quarter Horse, 928 radiographic, 153-166 of degenerative joint disease, 161 detail in, 153-154 dystrophic and metastatic mineralization in, 161 of fracture, 158-160 interpretation of, 161-162 of luxation and subluxation, 161 safety in, 154 technique, 161, 162-166 Wolff’s law and, 154-158, 159 of reined cow horse, 1028 of sacroiliac joint, 507 of show hunter and show jumper horses, 967 of Standardbred European, 916-918 North America, 902 of stifle, 456-458 tenoscopy and bursoscopy, 230-235 thermography, 236-239 of thoracolumbar spine, 513-514, 515 of Thoroughbred European, 884-885 North America, 871-872 of Three Day Event horse, 988-989, 990 ultrasound, 166-194 artifacts in, 169-173 of bone, 196-197 clinical, 182-185 of draining tracts, 195 equipment used in, 167 exercise levels and, 169 of fetlock, 189, 190, 191 of foreign bodies, 195-196 of nerves, 195 patient preparation for, 167 of penetrating injuries, 195 recording of, 167-168

Imaging—cont’d ultrasound—cont’d scanning technique in, 169 of skeletal muscle, 194-195 of stifle, 191-192, 193 terminology and quantitative measurements in, 173-175 zone designations in, 175-182 Imbalance foot in proximal suspensory desmitis, 655 in Three Day Event horse, 993 of hoof, 255-258 poor conformation and, 253-255 treatment of, 258-261 Imipramine, 1079 Immobilization. See also Casting; Splinting. complete, 789 for digital extensor tendon laceration, 693 Immune-mediated arthritis, 608 Immune-mediated myopathy, 733, 734 Immune-mediated synovitis, 143-144 in foals, 1093 Immunoglobulin G, 128 in immune-mediated arthritis, 608 Immunohistochemistry in neurologic disorder diagnosis, 129 Impact phase of stride, 251 Impingement in caudal neck, 528 of spinous process, 123, 514-515, 516 in polo pony, 1013-1014 in show hunter and show jumper horses, 972 Implant local infiltration of anesthetic solution in, 123 ultrasonographic examination of, 197 Impregnated polymethylmethacrylate for infectious arthritis, 601-602 In vitro models of joint disease, 595 In vivo models of joint disease, 595-596 In-at-the-hock conformation, 27, 29, 30 curb and, 699 In-at-the-knee conformation, 22, 23 Inclines, observation of during lameness examination, 73 Incomplete fracture ilial wing, 486-487 of metacarpal region, 364-366 of proximal phalanx, 343 of third metacarpal bone, 364-366 of third metatarsal bone, 436 Incomplete ossification of central and third tarsal bones, 443 Increased radiopharmaceutical uptake character of, 205-206 intensity of, 205 location of, 204-205 Indoor polo, 1003 Induced lameness, 4, 74-81 Infarction, vascular, in immune-mediated myopathy, 733 Infection after arthroscopic surgery, 230 of axial aspect of proximal sesamoid bones, 668, 669 bacterial in infectious arthritis, 598 lameness in European Thoroughbred secondary to, 891-892 in mud fever, 151 in quittor, 1062 in thrush, 277 cellulitis caused by, 151 of digit in foals, 1093 equine herpes virus I, 132 cerebrospinal fluid analysis in, 128 serologic testing in, 126 of intertubercular bursa, 412 in lameness of foals, 1089-1093

Infection—cont’d in osteitis and osteomyelitis, 157-158 of distal phalanx due to penetrating injury, 280 in foal, 1089-1093 parasitic of spinal cord, 132 of superficial digital flexor tendon or deep digital flexor tendon, 373 Infectious arthritis, 598-606 antimicrobial therapy for, 600-602 causes of, 598 diagnosis of, 599-600 examination and initial management of, 598-599 in foal, 1089-1093 future treatments of, 604 joint drainage and debridement for, 602-603 models of, 596 pain management for, 603 prognosis for, 604 synovial fluid cytology for, 582 topical treatment, bandaging, and alternative therapy for, 603-604 in young Draft horse, 1068 Infectious bursitis of extensor tendon, 697, 698 Infectious myositis, antebrachial, 398 Infectious tenosynovitis of digital flexor tendon sheath, 677-678 of extensor tendon, 695-696 of tarsal sheath, 688, 690-691 Infestation, Otobius megnini, 738 Inflammation, 32 arthritic, 607 of bone. See Osteitis. of curb, 702-703 of foot in Arabian and Half-Arabian show horse, 1044-1045 muscular, thermography of, 237-238 in tendon injury, 625 Inflammatory myopathies, 733-735 Influenza in myopathy development, 733 Information, subjective versus objective, 9 Infrared thermographic imaging, 821-822 in back pain, 514 of cervical spine, 525 in muscle disorders, 724 Infraspinatus muscle atrophy of, 413-414 ultrasound of, 401, 402 Injection for back pain, 520 bone marrow, 674 diagnostic analgesia, 99-100. See also Diagnostic analgesia. intra-articular, 753 of antimicrobials for infectious arthritis, 601 irritant for sacroiliac joint injury, 508 muscle soreness and abscessation following, 734 Injury. See also specific injury. angular limb deformities related to, 558 blunt deep digital flexor tendon injury in pastern region caused by, 648 periosteal new bone in response to, 155 swelling at site of, 32 in breeding stallions, 1078 cellulitis caused by, 151 in driving horse, 1057, 1058 field diagnosis of, 145-148 history of in lameness examination, 11-12 humane destruction following, 149 interference in driving horse, 1057 horseshoes for prevention of, 268-269 in North American Standardbred, 899 penetrating fractures of distal phalanx associated with, 320 solar, 278-282 ultrasonographic examination of, 195

Index Injury—cont’d in purchase examination of Thoroughbred sales yearling in Europe, 839 role of in osteochondrosis, 540 synovitis following, 608 tendon blood flow and, 618 transportation following, 149 use of boots and bandages for injury prevention in metacarpal region, 375 Innervation of distal forelimb, 285-286 of hind foot and pastern, 418 Insertional desmopathy of nuchal ligament, 526-527 Insertional injury of intersesamoidean ligament, 667, 668 Inside rim shoe, 263, 264 Instability models of, 596 sacroiliac joint, 503 shoulder, 414 Instant center of rotation, 15 Instrumentation. See also Equipment. acupuncture, 793-795 arthroscopic, 226, 227-229 cryotherapy, 780-781 for hoof examination, 43 Instrumented horse shoe, 65, 224 Insulation for solar support in laminitis, 332, 333, 334, 335 Insulin administration of in polysaccharide storage myopathy, 732 serum in osteochondrosis, 537, 538 Insulin-like growth factor in osteoarthritis development, 579 role of in osteochondrosis, 540 for superficial digital flexor injury management in racehorses, 634 Insurance mortality, 149 in prepurchase examination of performance horse, 952 for on the track catastrophe in Thoroughbred racehorse, 861 Interarticular fibrocartilage, 86 Interbody fusion, cervical vertebral, 569-570 Intercalated bone anatomy, 86 Intercarpal ligament anatomy of, 377 injury to, 392 in North American Thoroughbred, 875 Interference brushing, 69 in European Thoroughbred, 886 horseshoes for prevention of, 268 injury from in driving horse, 1057 horseshoes for prevention of, 268-269 in North American Standardbred, 899 types of, 68-70 Interleukin, 579 Interleukin-1 receptor antagonist protein, 579 Intermittent lameness, challenge of diagnosis in, 138-139, 140 Intermittent upward fixation of patella, 53-54 Internal fixation, 754. See also Fixation. for fracture of distal phalanx, 343 for tibial tuberosity fracture, 467 Interphalangeal joint, 310-316 anatomy of, 342 three-dimensional, 89 arthrodesis of, 346 articular chip fracture of middle phalanx and, 315 breed predilection in disorders of, 343 clinical signs, 310 damaged distal sesamoidean impar ligament of, 315 desmitis of collateral ligaments of, 315

Interphalangeal joint—cont’d diagnostic analgesia of, 102, 107-108, 109, 244 for navicular disease, 289, 290 in Three Day Event horse, 987-988 examination of, 342 flexion testing of, 76, 78 flexural limb deformity of, 563 of hindlimb, 419-420 history, 310 imaging of, 311-312, 342-343 joint capsule trauma in, 314, 315 osseous cyst-like lesion of, 314-315 osseous fragments on dorsal aspect of, 315 osteoarthritis of, 313, 314, 345-346 in Arabian and Half-Arabian show horse, 1045-1046, 1048 cryotherapy for, 782 in Draft horse, 1064-1065 in dressage horse, 981 in driving horse, 1056-1057 in European Standardbred, 919-920 in North American Thoroughbred, 873 perineural nerve block for, 102 in polo pony, 1011, 1014, 1015 radiation therapy for, 785 in show hunter and show jumper horses, 974 in Three Day Event horse, 993 osteochondrosis of, 344-345, 550-551 pain of in reined cow horse, 1029 palpation of, 46, 47 in effusion, 44 radiography of, 246 subchondral bone in perineural nerve block for, 102 trauma to, 314 subluxation of, 346-347 in pony, 1073 synovitis of in dressage horse, 981 in driving horse, 1054 perineural nerve block for, 102 in racing Quarter Horse, 929 traumatic damage to articular cartilage of, 314 Intersesamoidean ligament anatomy of, 654, 675 injury to, 681-682 Interspinous ligament anatomy, 509-510 Interstitial brachytherapy, 784-785 Intersynovial fistula of extensor tendon, 697 Intertrigone infection, 891-892 Intertubercular bursa, 411-412 analgesia of, 114-115, 401 anatomy of, 400 bursoscopy of, 234 infection of, 412 Intra-articular analgesia. See also Diagnostic analgesia. in distal hock joint pain, 441 in forelimb, 107-113 in hindlimb, 117-120, 121, 122 in polo pony, 1005 of sacroiliac joint, 506-507 for shoulder and elbow lameness, 400-401 Intra-articular injection, 743 of antimicrobials for infectious arthritis, 601 reactive synovitis following, 608 Intra-articular volume and pressure, 576 effusion and ischemia in arthritis and, 606, 607 Intra-cavitary brachytherapy, 786 Intrasynovial analgesia, 99-100, 113-115. See also Diagnostic analgesia. Intra-thecal analgesia, 401 Inversion recovery sequence in magnetic resonance imaging, 217 Involucrum, 157, 158 Iodine in oil for stifle osteoarthritis in Arabian and Half-Arabian show horse, 1047 for upward fixation of patella, 477

1115

Iodine toxicity in developmental orthopedic disease, 544 Ionophore toxicity, 737 Iron toxicity in developmental orthopedic disease, 544 Irradiation. See Radiation therapy. Irritant injection for sacroiliac joint injury, 508 IRU. See Increased radiopharmaceutical uptake, location of. Ischemia, arthritic, 607 Ischium anatomy of, 484 fracture of, 488 Isoechogenic ultrasound image, 172 Isoflupredone acetate, 748 for femorotibial osteoarthritis in North American Standardbred, 911 for metatarsophalangeal joint osteoarthritis, 428 for suspensory desmitis in show hunter and show jumper, 971 Isonicotinate, 520 Isopropyl alcohol injection in gluteal syndrome, 472 in trochanteric bursitis, 473 Isotonic fluid therapy, 713 Isoxsuprine, 1079 for aorto-iliac-femoral thrombosis, 499 for metatarsophalangeal joint osteoarthritis, 427 for navicular disease, 301-302 in reined cow horse, 1029 for sesamoiditis in European Standardbred, 921 in reined cow horse, 1029 IUFP. See Intermittent upward fixation of patella. J Jack spavin, 440 cryotherapy for, 782 Jack tendon, 121, 450 Japanese approach to acupuncture, 794 Jaw, large, neck pain and, 522 Jogging, prevention of bucked shins and, 852 Joint. See also specific joint. anatomy of, 85-86 assessment of in prepurchase examination of performance horse, 959 bleeding into. See Hemarthrosis. cartilage of arthroscopic examination of, 227, 228 damage to, 314, 464 magnetic resonance imaging of, 220 models of, 596 normal structure and function of, 573-575, 591 disease of. See also Arthritis. degenerative. See Osteoarthritis. of stifle, 458-465 of tarsus, 440-443 drainage and debridement of for infectious arthritis, 602-603 fracture of of carpal distal radius, 392 dorsomedial of third metacarpal bone, 367 dorsoproximolateral aspect of third metatarsal bone, 436-437 radiography of, 159-160 grafting of, 756 mobilization of, 803, 804 neoplasia of, 612 normal structure and function of, 572-576 osteochondromatosis of, 612 pain of in osteoarthritis, 580-581 pathophysiology of in arthritis, 606 physiology of, 606 in pony, 1071-1073 resurfacing of. See Resurfacing of cartilage. secondary, 161

1116

Index

Joint—cont’d soft tissue, 610-612 tarsal, 440-443 thermography of, 236-237 Joint block, 243-244 Joint capsule anatomy of, 572 distention of in tarsocrural joint, 443-444 trauma to in distal interphalangeal joint, 314, 315 in scapulohumeral joint, 410 Jugular vein thrombophlebitis, 530-531 Jumping sport horse show jumper, 965-975 back pain in, 971-972 characteristics of horse, 965 competition surfaces used in, 966 desmitis of accessory ligament of deep digital flexor tendon in, 975 distal hock joint pain in, 969-970 distal interphalangeal joint synovitis and early osteoarthritis in, 970 failure to make a diagnosis in, 967 fetlock joint lameness in, 972-973 gluteal myositis in, 974 historical perspective, 965 imaging of, 967 lameness examination of, 967 palmar foot pain in, 967-969 pastern lameness in, 974 sheared heels in, 969 stifle joint pain in, 973-975 structure of sport, 965 superficial digital flexor tendonitis in, 641-642, 974-975 suspensory desmitis in, 970-971 ten most common lameness problems in, 966-967 tenosynovitis of digital flexor tendon sheath, 975 training of, 965-966 treatment of lameness in, 967 Three Day Event horse, 984-996 conformation of, 986 diagnosis and management of lameness in, 992-995 diagnostic analgesia in, 987-988 history in assessment of, 986 imaging of, 988-989, 990 influence of sport on lameness of, 985 lameness examination of, 986-987 prevention of lameness in, 995-996 proceeding without a diagnosis in, 989-990 saddle pressure analysis of, 989, 991 shoeing of, 990-991, 992 sport of, 984 tack considerations in, 991-992 ten most common lameness conditions in, 986 training of, 985-986 types of horses in, 984-985 Juvenile spavin, 440 Juxtavertebral muscle, 510 K Kallikrein, 578 Keg shoe, 262 Kentucky Equine Research Inc., 544 Keratan sulfate, 592 Keratoma of hind foot and pastern, 419, 420 in hoof, 317-318 Ketamine, epidural, 767 Ketofen. See Ketoprofen. Ketoprofen, 747, 1079 for bruised feet in Arabian and Half-Arabian show horse, 1045 for distal hock joint pain in cutting horse, 1019 for laminitis, 330 for rhabdomyolysis, 729

Kinematic analysis of gait, 222-223 in distal hock joint pain, 441 during high-speed treadmill assessment, 833 Kinetic analysis of gait, 223-224 Kissing spines, 514-515, 516 Klebsiella species, 678 Knee, buckling forward at, 38 Knee-sprung conformation, 25, 27 Knocked-down hip, 35 Knock-kneed conformation, 22, 23 Knuckling forward of fetlock joint, 33 KS. See Keratan sulfate. Kyphosis, lumbar, 510 L Labeling of radiographic image, 162 of ultrasonographic image, 168 Labrum acetabulare, 86 Laceration, 142 of digital extensor tendon, 438-439, 693-694 in steeplechasers, hurdlers, and point to point horses, 945 of hoof wall, 280-281 in pleasure riding horse, 1094-1095 of tendon, 712-715 Lactate dehydrogenase, 724 Lactation, feeding systems to prevent developmental orthopedic disease during, 547 Lactation tetany, 737-738 Lactide-glycolide copolymers, 602 Lag screw fixation, 754 for patellar fracture, 465 Lameness acute-onset, severe, 143, 145-149 associated with shoeing, 270 baseline and induced, 4, 62 manipulation and, 74-81 biomechanics of foot and, 248 coexistent, 4 conformation and, 6, 15-31 digit, 30-31 evaluation of, 15-21 forelimb, 21-26, 27 hereditary aspects of, 15 hindlimb, 26-30 relevance of, 15 defined, 2-3 diagnosis of, 1-239 acupuncture for, 795-796 acute-onset, severe, 145-149 chiropractic, 805-808 clinical history in, 9-14 components of examination in, 7-8 determination, grading, and characterization of in, 62-64 diagnostic analgesia in, 93-124 diagnostic imaging in, 153-239 historical perspective of, 2-3 localization of pain in, 4 during movement, 60-73 musculoskeletal system anatomy and, 81-93 neurologic examination and neurologic conditions causing gait deficits and, 124-135 palpation in, 42-60 poor performance and, 6-7 swollen limb in, 150-152 symmetry and posture assessment in, 31-41 unexplained lameness and, 135-144. See also Unexplained lameness. using manipulation, 74-81 distribution of, 4-6 gait abnormalities not caused by, 7 imbalance and poor conformation as cause of, 255 in sport horse, 827-1095 poor performance, 828-835 racehorse, 836-950. See also Racehorse.

Lameness—cont’d warming into, 12 warming out of, 12 Laminitis, 325-339 analgesic techniques for, 102 false-negative response to, 125-136 associated with pelvic fracture, 490 in breeding stallions, 1078 in broodmare, 1082 deep digital flexor tenotomy for, 335-338 diagnosis of, 329 in Draft horse, 1061-1062 in endurance horse, 1000 enzymatic theory of, 327 of hind foot and pastern, 419 histological grading of, 325-327 hoof care in, 332-335, 336 medical therapy of, 329-331 natural trigger factors in, 327-328 pathophysiology of, 325 in pleasure riding horse, 1095 in pony, 1074 scintigraphic examination of, 246 thermography in, 236 Laser therapy, 812-813 Latent period, radiographic, 154 Lateral digital extensor muscle anatomy, 692 Lateral palmar block, 105-106 in proximal suspensory desmitis, 655 Lateral perspective in forelimb conformation, 24-26, 27 in hindlimb conformation, 26-29 Lateral thorax palpation, 51 Latex gloving for diagnostic analgesia, 99 Lathyrus odoratus, 633 Lavage for digital extensor tendon laceration, 693 for infectious arthritis, 600, 602 in tenosynovitis of extensor tendon sheaths, 695 tarsal, 690 Laxity, peri-articular in angular limb deformity, 557-558 LDH. See Lactate dehydrogenase. Lead toxicity in developmental orthopedic disease, 544 Lead use in radiography, 153 Leading of horse during lameness examination, 62 Leg circles, 816 Legend. See Hyaluronan. Lengths assessment in conformation evaluation, 20, 21 Lesion of deep digital flexor tendon within hoof capsule, 305-309 identifiable in unexplained lameness, 142 neck, 141 radiography in determining age of, 162 ultrasonographic assessment of, 183-185 Leukocytes cerebrospinal fluid, 127 synovial, 582 Libido, management and pharmacologic aids to enhance, 1079 Lidocaine for diagnostic analgesia, 94 in mesotherapy for thoracolumbar spine injury, 520 Liftex sling, 789 Ligament. See also specific ligament. articular anatomy of, 572 injury of, 610-611 assessment of in prepurchase examination of performance horse, 959 magnetic resonance imaging of, 219-220 therapeutic ultrasound for, 812 thermography of, 237 ultrasonographic characterization of lesion of, 173-175 Ligamentum flava anatomy, 522

Index Ligamentum nuchae anatomy, 522 Lily pads for frog support in laminitis, 332 Limb angular deformities of, 557-561 in pony, 1071 assessment of in acute-onset, severe lameness, 145-146 evaluation of conformation of, 20-21 flexural deformities of, 562-565 in young Draft horse, 1068-1069 lameness development and length of, 17 swollen or enlarged in broodmare, 1082 Limb flight, 67-70 in metatarsophalangeal joint lameness, 421 Line firing, 779 Linear assessment of conformation, 15, 16, 17, 18 Listed races, 880 Live sole, 272 Load distribution ratio, 4, 5, 6 Local analgesic techniques. See Analgesia. Local diagnostic techniques of metacarpophalangeal joint, 348-349 Local infiltration of anesthesia, 122-123 Localization of pain, 4 Locking stifle, 475-477 Long bone fracture of in European Thoroughbred, 892-893 in foals, 1085-1086 thermography of, 237 Long digital extensor muscle, 693 Longissimus dorsi muscle, 510 Longitudinal ligament, 522 Lope, 61 Lordosis, thoracic, 511 Loss of function assessment using palpation, 42 Low palmar analgesia, 103-104 in European Thoroughbred, 885 in North American Thoroughbred, 871 Low plantar block, 115 in North American Thoroughbred, 871 Low plantar desmitis, 704 Lower limb acupuncture for pain associated with lameness of, 796-797 chronic osteoarthritis of in driving horse, 1056-1057 flexion testing of, 75-76, 77-79 stretching therapy for, 816 Lower motor neuron disease, 131, 143 Lubrication, articular, 575-576 in arthritis, 607 Lucent line in fracture radiography, 159 Lumbar kyphosis, 510 Lumbosacral pain in endurance horse, 1001. See also Thoracolumbar spine. Lumican, 621 Lunge line examination of Arabian and Half-Arabian show horse, 1043-1044 Lunging exercise in prepurchase examination of performance horse, 960 Lutamate Plus. See Progesterone. Luxation of coxofemoral joint, 499-500 in pony, 1071-1072 of elbow joint, 404 of metatarsophalangeal joint, 432 patellar, 460-461 in American Saddlebred, 1039 in pony, 1072-1073 radiographic diagnosis of, 161 of sacroiliac joint, 507 scintigraphic diagnosis of, 486 of scapulohumeral joint, 410-411 of superficial digital flexor tendon, 710-711 palpation of, 710-711 of tarsal joint, 446-447 Lyme disease, 126, 143, 609 Lymphangitis, 32, 151-152 in broodmare, 1082

M Mach line, fracture versus, 158 Magic angle effect, 220 Magnesium depletion in exertional rhabdomyolysis, 730 Magnetic resonance imaging, 216-221 of distal interphalangeal joint, 312 of foot, 247 in navicular disease, 295, 296, 297 in osteoarthritis, 583-584 in primary lesion of deep digital flexor tendon within hoof capsule, 308, 309 Magnetic susceptibility artifact, 220 Magnetic therapy, 813 Malleolus fracture of, 452-453 osteochondritis dissecans in, 552 Management changes in clinical history, 12-13 Mandible, large, neck pain and, 522 Manganese toxicity in developmental orthopedic disease, 544 Mange mite-associated lameness, 1066 Manica flexoria, 675 Manipulation testing, 74-81 for lameness in stifle, 456 in North American Thoroughbred, 871 sacroiliac joint, 503, 505-506 Manual therapy, chiropractic and, 803, 804 Manufactured shoe, 262 MAP-5. See Hyaluronan. Mare broodmare, 1082-1083 nutritional requirements of, 546-548 positioning of for breeding, 1080 chronic exertional rhabdomyolysis in, 730 estrous cycle and performance in, 480-482 feeding systems to prevent developmental orthopedic disease during pregnancy in, 547 reproductive problems in, 144 Marginal tears of deep digital flexor tendon, 647 Marie’s disease, 157 antebrachial, 398 carpal, 393 metacarpal, 374 Markers of bone cell activity in racehorses, 842-847 of osteoarthritis, 591-594 Marrow components to stimulate regeneration of suspensory ligament, 673-674 Massage, 815, 818 Mastitis, 144 Matrilysin, 579 Matrix articular, 575 of tendon, 619-622 Matrix metalloproteinases, 577-579, 756 corticosteroids in inhibition of synthesis of, 748 Maximal injury fiber alignment score, ultrasonographic, 182 Maximal injury zone, ultrasonographic, 182 Maximal injury zone echo score, ultrasonographic, 182 Maximal injury zone lesion cross-sectional area, ultrasonographic, 182 Maximal injury zone type score, ultrasonographic, 182 Maximal zone cross-sectional area, ultrasonographic, 182 McII. See Second metacarpal bone. McIII. See Third metacarpal bone. McIV. See Fourth metacarpal bone. Meadowsweet, 817 Mechanical forces in osteoarthritis development, 577 Mechanical lameness of hindlimb, 475-479 limb flight and, 70 Meclofenamic acid, 747 Media issues, 857

1117

Medial aspect of fetlock, ultrasonographic examination of, 189, 190 Medial cutaneous antebrachial block, 106-107 Medial palmar vein thrombosis, 373 Median nerve analgesic block of, 106-107 in European Thoroughbred, 886 for shoulder and elbow lameness, 400-401 injury of, 132 Medical history. See History. Medical records, ultrasonographic, 167-168 Medication. See also specific medications. in clinical history, 13 for navicular disease, 301-302 used in on the track catastrophe in Thoroughbred racehorse, 856 Mediolateral balance, 248 Mediolateral imbalance, 253-254, 255, 256-257 treatment of, 258-259 Medroxyprogesterone acetate for hormone-related performance problems in mares, 481 for splints in polo pony, 1012 Meflosyl. See Flunixin meglumine. Megestrol acetate, 481 Membrane-type 1-metalloproteinase, 578, 579 Menisci anatomy of, 86 of femorotibial joint, ultrasound of, 191, 193 of stifle, injury to, 462-463 Mepivacaine for diagnostic analgesia, 94 in proximal suspensory desmitis, 655 of thoracolumbar spine, 513 Mesotendon, 85 Mesotherapy for back pain, 520 Metabolic disease in endurance horse, 1002 myopathies, 731-733 nutrition and, 537-538 Metabolism articular bone, 592-593 articular cartilage, 592, 593 glucose, laminitis and, 328 tenocyte, 619 Metacarpal bone Arabian racehorse disease of, 931 cryotherapy for periostitis of, 781 European Standardbred lameness in, 920-921 exostoses of, 369-371. See also Splints. in European Thoroughbred, 893 in North American Standardbred, 911 in racing Quarter Horse, 929 fatigue failure of. See Bucked shins. fracture of, 357-361, 364-368, 371-372, 431 in acute-onset, severe lameness, 147 cryotherapy for, 781 in pony, 1073 in racehorses, 853-854, 858, 889-891, 893-894, 911, 943 in Three Day Event horse, 995 North American Standardbred lameness in, 910 North American Thoroughbred disease of, 873-874 osseous cyst-like lesion of, 368-369, 550 osteochondrosis of sagittal ridge of, 549-550 palpation of, 47, 48 in North American Thoroughbred, 871 periostitis of. See Bucked shins. physitis of, 555 radiation therapy for new growth on, 785 Metacarpal nerve anatomy of, 654 diagnostic analgesia of, 104-105 in proximal suspensory desmitis, 655 Metacarpal region, 362-376 anatomy of, 82, 362-363 deep digital flexor tenotomy for laminitis in, 336, 337 diagnosis of lameness of, 363-364 diagnostic analgesia of, 104-105 diffuse filling in, 372-375

1118

Index

Metacarpal region—cont’d exostoses of second and fourth metacarpal bones in, 369-371 fracture in avulsion of third metacarpal bone at origin of suspensory ligament, 367-368 dorsomedial articular of third metacarpal bone, 367 incomplete longitudinal palmar cortical fatigue or stress of third metacarpal bone, 364-366 of second and fourth metacarpal bones, 371-372 transverse stress of distal metaphyseal region of third metacarpal region, 366-367 imaging of, 364 osseous cyst-like lesion in proximal aspect of second metacarpal bone in, 368-369 osteoarthritis of carpometacarpal joint in, 368, 369 palpation of, 47-48, 363 in Finnish horse, 948 in North American Thoroughbred, 871 proximal fasciotomy of for superficial digital flexor tendonitis, 637-638 standard radiographic projection and suggested extra views of, 164 ultrasonographic zone designations for, 175 use of boots and bandages to prevent injury to, 375 Metacarpophalangeal joint, 348-362 acute or repetitive overload injuries of, 349-351 analgesia of, 103, 108-110 anatomy of, 348 Arabian racehorse disease in, 933 diagnosis of lameness of, 348-349 Draft horse lameness of, 1065 flexural limb deformity of, 562-565 fracture of in racing Quarter Horse, 930 third metacarpal bone, 357-361 on the track in Thoroughbred racehorse, 857-858 imaging of, 349 National Hunt, point to point, and timber racing horse lameness associated with, 945 osseous cyst-like lesion of, 550 osteoarthritis of in Arabian and Half-Arabian show horse, 1047, 1048 in Arabian racehorse, 933 in dressage horse, 982 in driving horse, 1056-1057 in endurance horse, 1000-1001 in European Standardbred, 920 in polo pony, 1008-1009 radiation therapy for, 785 in show hunter and show jumper, 972-973 in Three Day Event horse, 993 osteochondrosis of, 549-550 palpation of, 46, 47 in European Standardbred, 915 in European Thoroughbred, 883 proximal phalanx injuries in, 351-354 proximal sesamoid bone conditions in, 354-356, 357 staphylococcal abscess on back of in European Thoroughbred, 891 subluxation of, 432 in acute-onset, severe lameness, 147 synovitis of, 349-350 in Arabian and Half-Arabian show horse, 1047, 1048 in barrel-racing horse, 1032 in dressage horse, 982 in North American Thoroughbred, 873 in racing Quarter Horse, 929 in show hunter and show jumper, 972-973

Metacarpophalangeal joint—cont’d types of fetlock lameness of, 349 ultrasonographic zone designations for, 175 Metal horseshoe, 262 Metalloproteinase, 756 corticosteroids in inhibition of synthesis of, 748 in osteoarthritis development, 577-579 Metalloproteinase inhibitors, 327-328 Metastatic mineralization, 161 Metatarsal artery anatomy, 433 Metatarsal bone anatomy of, 433 disease of in North American Thoroughbred, 873-874 exostoses of, 437. See also Splints. in European Thoroughbred, 893 in North American Standardbred, 911 fractures of, 431, 432, 435-437 in acute-onset, severe lameness, 147 cryotherapy for, 781 in European Thoroughbred, 889-891, 893-894 in National Hunt, point to point, and timber racing horses, 943 in North American Standardbred, 907, 911 in pony, 1073 on the track in Thoroughbred racehorse, 859 osseous cyst-like lesion of, 550 osteochondrosis of sagittal ridge of, 549-550 palpation of, 58 Metatarsal region, 433-439 acute-onset, severe lameness following trauma to, 148 anatomy of, 433-434 clinical characteristics and diagnosis of lameness in, 434-435 deep digital flexor tendon primary lesion in region of, 649 saphenous filling time assessment in, 58 specific conditions of, 435-439 standard radiographic projection and suggested extra views of, 164 Metatarsophalangeal joint, 421-433 anatomy of, 421 clinical characteristics and diagnosis of lameness of, 421-422 dressage horse lameness in, 982 European Standardbred lameness in, 922 flexural limb deformity of, 431, 562-565 fractures of, 429-431, 432 in North American Standardbred, 906-907 imaging of, 422-426 North American Standardbred lameness in, 906-907, 911 osseous cyst-like lesion of, 550 osteoarthritis of, 426-428 in Arabian and Half-Arabian show horse, 1047, 1048 in dressage horse, 982 osteochondral fragmentation of, 428-429, 430 osteochondrosis of, 549-550 in North American Standardbred, 907 palpation of in European Standardbred, 916 reined cow horse lameness of, 1029 saphenous filling time assessment in, 58-59 sesamoiditis of, 431 soft tissue injuries of, 431-432, 610, 611 stress-related subchondral bone injury and osteoarthritis of, 426-428 Methionine, 968 Methocarbamol, 1079 for gluteal myositis in show hunter and show jumper, 974 for rhabdomyolysis, 729 in North American Standardbred, 912 for thoracolumbar myositis in cutting horse, 1020

Methylprednisolone, 748, 749, 751 for acute rhabdomyolysis, 729 for digital flexor tendon sheath disease, 677 for distal hock joint pain, 443 in barrel-racing horse, 1031 in cutting horse, 1018 in North American Thoroughbred, 877, 878 in show hunter and show jumper, 970 for distal interphalangeal joint synovitis and osteoarthritis in dressage horse, 981 for fracture and exostoses of second and fourth metatarsal bone, 911 for metacarpophalangeal joint osteoarthritis in endurance horse, 1001 for metatarsophalangeal joint osteoarthritis, 427 for paravertebral myalgia in endurance horse, 1001 reactive synovitis associated with, 608 for sacroiliac desmitis in cutting horse, 1021 for splints, 437 for stifle synovitis and osteoarthritis in show hunter and show jumper, 973 for superficial digital flexor injury management in racehorses, 630 for tarsocrural joint capsule distention, 444 for tenosynovitis, 695 tarsal, 690 for thoracolumbar myositis in cutting horse, 1020 for thoracolumbar spine injury, 520 Metronidazole, 714 Microfracture, 229 Micropicking, 756 MicroSteed, 544, 545 Middle carpal joint anatomy of, 376 diagnostic analgesia of in proximal suspensory desmitis, 655 lameness of in dressage horse, 982 in European Standardbred, 920 in European Thoroughbred, 888-889 in steeplechasers, hurdlers, and point to point horses, 945 Middle phalanx anatomy of, 342 three-dimensional, 89 breed predilection in disorders of, 343 examination of, 342 imaging of, 342-343 palisading new bone on dorsal aspect of, 315 on the track fracture of in Thoroughbred racehorse, 857 Midline-to-lateral pelvic width, 36 Mid-pastern area deep digital flexor tenotomy for laminitis in, 336, 337 ring block of, 100-102 Mid-shaft fracture of third metatarsal bone, 435 Mid-swing, 247 Mineral oil for laminitis, 330 Mineralization within deep digital flexor tendon, 306, 646-647 metastatic versus dystrophic, 161 muscular, 726 Minerals deficiency of in developmental orthopedic disease, 543, 544 excess of in developmental orthopedic disease, 543-544 intake of in cervical stenotic myelopathy, 569 Miniature breed. See Pony. Minimal sagittal diameter in radiographic diagnosis of cervical compressive myelopathy, 128-129 Mini-skirt walk, term, 142 Mirror image artifact, 173 Misdiagnosis, 141-142 Mixed lameness, 63-64

Index MIZ. See Maximal injury zone, ultrasonographic. MIZ-CSA. See Maximal zone cross-sectional area, ultrasonographic. MIZ-ES. See Maximal injury zone echo score, ultrasonographic. MIZ-FAS. See Maximal injury fiber alignment score, ultrasonographic. MIZ-LCA. See Maximal injury zone lesion cross-sectional area, ultrasonographic. MIZ-TS. See Maximal injury zone type score, ultrasonographic. MMPs. See Matrix metalloproteinases. Mobilization of joint, 803, 804 Modeling of bone, 292 radiography of, 154-158, 159 of synovial facet joints, 527 Models of joint disease, 594-598 Modulus of elasticity, 617, 644 Moisture content of racetrack, 862, 863 Molecular composition of tendon matrix, 619-622 Monday morning disease, 728 Mononuclear cells, synovial, 582 Morphine, epidural, 767, 768 Mortality, racetrack-associated, 864 in National Hunt horses, 938 Mosaic arthroplasty, 229 Motion, scintigraphic, 203 Motor neuron disease, 131, 143 Movement lameness examination during, 60-73 back pain and, 511, 512 circling in, 71-72 determination, grading, and characterization of lameness in, 62-64 direct or local palpation in, 79-80 of European Standardbred, 916 foot placement evaluation in, 70-71 gait, 60-62 on hard and soft surfaces, 71 lameness detection during, 67-70 lameness score in, 66-67 location determination of lameness in, 64-66 of North American Standardbred, 901 of North American Thoroughbred, 871 observation during riding, 72-73 using treadmill or gait analysis, 73 osteopathic examination during, 821 reduction of excessive in rehabilitation, 789 MRI. See Magnetic resonance imaging. MSD. See Minimal sagittal diameter. MtII. See Second metatarsal bone. MtIII. See Third metatarsal bone. MtIV. See Fourth metatarsal bone. Mu points, 794 Mucous membrane assessment in swollen limb, 151 Mud fever, 151 Multifidus muscle, 510 Muscle articular, anatomy of, 572 disorders of, 723-743 cervical, 527 diagnosis of, 723-726 exertional rhabdomyolysis, 728-732 hyperkalemic periodic paralysis, 738-739 non-exertional rhabdomyolysis, 732-735 nutritional myodegeneration, 736-738 pain, strain and tears, 726-728 pelvic, 494-495 scapular, 413 in show hunter and show jumper horses, 972 tumor, ultrasound of, 195 magnetic resonance imaging of, 220 post-injection soreness and abscessation of, 734 scintigraphy of, 211-212 soreness of in North American Standardbred, 912

Muscle—cont’d stimulation of, 818 in superficial muscle injury diagnosis, 728 symmetry assessment in prepurchase examination of performance horse, 959 thermography of, 237-238 thoracolumbar, 510 ultrasonographic examination of, 194-195 Muscle atrophy of supraspinatus and infraspinatus muscle, 413-414 symmetry assessment in, 31-32, 33-34 Muscle biopsy, 725 in chronic exertional rhabdomyolysis, 731 in immune-mediated myopathy, 733 in mechanical lameness, 475 in polysaccharide storage myopathy, 732 in rhabdomyolysis, 494 Muscle cramping, ear tick-associated, 738 Muscle enzyme testing, 723-724 in superficial injury, 728 Muscle relaxants for acute rhabdomyolysis, 729 for thoracolumbar myositis in cutting horse, 1020 Muscle stimulation, 818 in superficial muscle injury diagnosis, 728 Muscle weakness in cervical stenotic myelopathy, 566 Muscular dystrophy, nutritional, 736-738 Musculoskeletal system. See also Muscle. anatomy of, 81-93 forces in, 85 language of, 85 passive stay apparatus in, 87-88 specialized structures in, 85-87 three-dimensional, 88, 89, 90, 91, 92, 93 scintigraphy of, 211-212 thermography of, 236-239 ultrasonographic examination of, 194-195 Myalgia in endurance horse, 1001 Myeloencephalitis, equine protozoal, 129-130, 143, 567 antibody titer testing in, 126 in breeding stallion, 1078 mechanical lameness in, 475 in polo pony, 1017 Myeloencephalopathy, equine degenerative, 131, 566-567 Myelography, 129 in cervical stenotic myelopathy, 568-569 Myeloma of cervical spine, 530 Myelopathy cervical compressive, 128 cervical stenotic, 566-570 Myodegeneration, nutritional, 736-738 Myofascial release, 815 Myoglobin in muscle disorders, 724 Myoglobinuria, atypical, 737 Myonecrosis, clostridial, 733-734 Myopathy equinepolysaccharide storage, 475 exertional, 1000 fibrotic, 34, 70, 476, 477-478 thigh palpation in, 53 immune-mediated, 733, 734 pasture, 737 polysaccharide storage, 731-733 post-anesthetic, ultrasonography of, 195 thermography in, 238 toxic, 737 traumatic, 735 virus-associated, 733-734 Myorelaxants, 520 Myositis in American Saddlebred, 1039, 1040 antebrachial, 398 cervical, 1040 in endurance horse, 1000, 1002 gluteal in American Saddlebred, 1037-1038

1119

Myositis—cont’d gluteal—cont’d in polo pony, 1013 in show hunter and show jumper horses, 974 in North American Standardbred, 912 in North American Thoroughbred, 878 pelvic, 471 suppurative, 734 thoracolumbar in cutting horse, 1020-1021 Myotenectomy, semitendinosus, 478 Myotherapy, 815 Myotonia, 737-738 N Nail bind, 270, 275-276 in Three Day Event horse, 993 Nail prick, 270, 276 Nails for horseshoe attachment, 266-267 problems associated with, 275-278 Naloxane for opioid respiratory side effects, 768 Napping, 828, 830 Naproxen, 747 Narcotics, epidural, 603 National Hunt horse, 934-942 National Research Council, 545 Natural balance shoeing for, 273 trimming of barefooted horse for, 272-273 Natural gaits, 60 NAV terms. See Nomina Anatomica Veterinaria terms. Navicular bone bursoscopy of, 234-235 deep digital flexor tendon’s relationship to, 305 diagnostic analgesia of, 113, 114, 244 disease of, 286-297 diagnosis of, 288-297 in driving horse, 1054 in hindlimb, 419 in North American Standardbred, 905 in North American Thoroughbred, 873 pathophysiology of, 286-288 perineural nerve block for, 102 in polo pony, 1011 radiation therapy for, 785 in reined cow horse, 1029 scintigraphic examination of, 246 in show hunter and show jumper horses, 968-969 treatment and prognosis of, 299-304 fracture of, 304-305, 419, 420 suspensory apparatus of, 284-285 three-dimensional anatomy of, 89, 90 Navicular bursa bursitis of, 288 in North American Thoroughbred, 873 contrast radiography of, 294 endoscopic evaluation of, 297 three-dimensional anatomy of, 89 Navicular suspensory desmotomy, 302 Near gain setting, ultrasonographic, 170, 171 Neck, 522-531 anatomy of, 522 clinical examination of, 522-523 in performance horse, 959 clinical presentation, 522 congenital abnormalities of, 525-526 cyst-like lesions of, 530 direct trauma to in driving horse, 1057, 1058 diskospondylitis of, 529 elevation of in forelimb lameness, 64-66 forelimb lameness and lesion of, 141 forelimb posture seen in pain of, 38-39 fracture of, 529-530 imaging of, 523-525 insertional desmopathy of nuchal ligament and injury to semispinalis, 526-527

1120

Index

Neck—cont’d jugular vein thrombophlebitis of, 530-531 length of in conformation assessment, 20 lesion of in National Hunt, point to point, and timber racing horses, 944 muscle abscess of, 527 musculature disorders of, 527 myeloma of, 530 occipito-atlantoaxial malformations of, 525 nutritional management of, 548 osteoarthritis of, 527-529 osteomyelitis of, 530 palpation of, 50-51 reining of in polo pony, 1004 soreness in Three Day Event horse, 992-993 standard radiographic projection and suggested extra views of, 166 stiffness and mobilization of under general anesthesia, 531 Necrosis aseptic of proximal sesamoid bone, 667, 668 of superficial digital flexor tendon in steeplechaser, hurdlers, and point to point horses, 942 after topical application, 374 Needle acupuncture, 794 for cerebrospinal fluid aspiration, 126, 127 for epidural analgesia, 765-766 for intra-articular analgesia carpal, 111 distal interphalangeal joint, 107, 108 elbow joint, 111, 112 hip joint, 120, 121 metacarpophalangeal joint, 108, 110 proximal interphalangeal joint, 108, 109 sacroiliac joint, 506 shoulder joint, 113 stifle, 119-120 tarsometatarsal, 117-118, 119 for intrasynovial analgesia, 99 bicipital bursa, 114 digital flexor tendon sheath, 114 podotrochlear bursa, 113, 114 for perineural analgesia, 99 abaxial sesamoid, 103 fibular and tibial, 116-117 high palmar, 104-105 high plantar, 116 lateral palmar, 106 low palmar, 103-104 median nerve, 106 mid-pastern ring, 102 palmar digital, 100, 101 ulnar nerve, 106 Negative responses to nerve blocks, 140-141 Neoplasm carpal, 393 in hoof, 317-318 joint-associated, 612 muscular, ultrasonography of, 195 spinal cord, 132 Neospora, 126, 129 Nerve traumatic injury to in foals, 1089 ultrasonographic examination of, 195 Nerve block, 243-244. See also Diagnostic analgesia. bone scan and, 208 dangerous horse and, 140 dorsal ring of pastern, 115 failure to perform appropriate, 136 fibular nerve, 116-117 median, ulnar, and medial cutaneous antebrachial, 106-107 mid-pastern ring, 100-102 negative responses to, 140-141 palmar, 100, 101, 102, 243-244 high, 104-105 lateral, 105-106 low, 103-104

Nerve block—cont’d plantar, 243-244 high, 115-116 low, 115 in prepurchase examination of performance horse, 963-964 sesamoid abaxial, 102-103, 115, 244 basisesamoid, 115 sources of pain that cannot be desensitized by, 136-137 tibial nerve, 116-117 of wrong limb, 136 Nerve conduction studies, 129 Nerve root compression in cervical stenotic myelopathy, 566 Neurectomy chemical for navicular disease, 302 palmar digital, 303 in North American Thoroughbred, 873 tibial for proximal suspensory desmitis, 662 Neuritis of palmar/plantar digital nerves, 722 Neuroaxial dystrophy, 131 Neurogenic atrophy, 31, 33-34 Neurokinin A, 284, 285 Neurologic examination, 125-129 in Arabian and Half-Arabian show horse, 1044 in breeding stallion, 1077 in North American Standardbred, 903 Neurologic system disorders of, 124-135, 143 in breeding stallions, 1078, 1079 in broodmare, 1083 cervical spinal cord compression, 130-131 cervical stenotic myelopathy as, 566-570 diagnosis of, 125-129 equine degenerative myeloencephalopathy and neuroaxial dystrophy, 131 equine herpes virus I infection, 132 equine lower motor neuron disease, 131 equine protozoal myelitis, 129-130 peripheral nerve injuries, 132-133 in pleasure riding horse, 1095 of shoulder, 413-415 of distal forelimb, 285-286 of hind foot and pastern, 418 thoracolumbar, 510 Neuroma of palmar/plantar digital nerves, 722 Neuromuscular therapy, 815 Neuropeptides in arthritic pain, 607 Neurotransmitters, 285 Neutrophils, synovial in arthritic disease and therapeutic manipulation, 582 in infectious arthritis, 599, 600 in tenosynovitis of extensor tendon sheaths, 695 New bone, 154-158, 159 associated with osteoarthritis of cervical synovial articulations, 527-528 biochemical markers of in racehorses, 843 on caudal aspect of wing of sacrum, 497 on dorsal aspect of middle phalanx, 315 endosteal, 155, 156 periosteal, 155 radiation therapy for, 785, 787 of unknown origin, 157 Wolff’s law and, 155 Nitazoxanide, 130 Nitric oxide, 579, 580 NMD. See Nutritional myodegeneration. Nomina Anatomica Veterinaria terms, 85 Non-adaptive remodeling of metatarsophalangeal joint in North American Standardbred, 906 of third carpal bone and radial carpal bones in North American Thoroughbred, 874-875 Non-exertional rhabdomyolysis, 732-735 Non-neoplastic space-occupying lesion in hoof, 317-318

Non-racing sport horse, 951-1095 American Saddlebred, 1035-1040 Arabian and Half-Arabian horse, 1040-1049 conformation of, 1042 diagnosis and management of lameness in, 1044-1049 diagnostic analgesia in, 1044 history of breed and sport, 1040-1041 lameness examination of, 1042-1044 neurologic examination of, 1044 ten most common causes of lameness in, 1042 training of, 1041-1042 undiagnosed lameness in, 1044 breeding stallions, 1077-1082 broodmares, 1082-1083 Draft horse, 1058-1069 foot lameness in, 1060-1064 lameness examination of, 1059-1060 modern-day, 1059 osteoarthritis of proximal and distal interphalangeal joint in, 1064-1065 ringbone in, 1064-1065 ten most common lameness problems in, 1059 dressage horse, 975-983 diagnostic analgesia in, 979 imaging of, 979 lameness examination of, 978-979 the sport, 975-977 tack, 978 ten most common lameness conditions in, 979-983 training surfaces used by, 977-978 driving horse, 1049-1058 conformation of, 1051 description of sport, 1049-1050 diagnosis and management of lameness in, 1053-1058 diagnostic analgesia in, 1052 difficulties in diagnosis of, 1052-1053 ground conditions for, 1051 imaging of, 1052 lameness examination of, 1052 shoeing of, 1053 ten most common lameness conditions of, 1051 training of, 1050-1051 types of horses used as, 1050 endurance horse, 996-1002 polo pony, 1003-1017 history of sport, 1003 imaging of, 1006 lameness examination of, 1005 polo as an industry and, 1003-1005 superficial digital flexor tendonitis in, 1006-1008 ten most common lameness patterns in, 1005 undiagnosed lameness of, 1005-1006 pony, 1069-1076 back pain in, 1075 cerebellar abiotrophy in, 1075 diagnostic analgesia in, 1070 foot-related problems in, 1074 fractures in, 1073 imaging of, 1070 joint disease in, 1071-1073 lameness examination in, 1070 limb deformities in, 1071 most common conditions affecting, 1071 recurrent exertional rhabdomyolysis in, 1075 soft tissue injuries in, 1074 wounds in, 1075 prepurchase examination of, 951-964 blood tests in, 963 communication with vendor in, 952, 953-957 at a distance, 952-958 evaluation of identified problems in, 960

Index Non-racing sport horse—cont’d prepurchase examination of—cont’d gait assessment in, 960 goals of, 951 guidelines for reporting, 964 nerve blocks in, 963-964 nuclear scintigraphic, 962 radiographic, 960-962 rectal, 960 at rest, 958-959 summary of observations in, 964 thermographic, 963 ultrasonographic, 962-963 veterinarian contract in, 951-952 show hunter and show jumper, 965-975 back pain in, 971-972 characteristics of horse, 965 competition surfaces used in, 966 desmitis of accessory ligament of deep digital flexor tendon in, 975 distal hock joint pain in, 969-970 distal interphalangeal joint synovitis and early osteoarthritis in, 970 failure to make a diagnosis in, 967 fetlock joint lameness in, 972-973 gluteal myositis in, 974 historical perspective, 965 imaging of, 967 lameness examination of, 967 palmar foot pain in, 967-969 pastern lameness in, 974 sheared heels in, 969 stifle joint pain in, 973-975 structure of sport, 965 superficial digital flexor tendonitis in, 974-975 suspensory desmitis in, 970-971 ten most common lameness problems in, 966-967 tenosynovitis of digital flexor tendon sheath, 975 training of, 965-966 treatment of lameness in, 967 Tennessee Walking Horse, 1033-1034 Three Day Event horse, 984-996 conformation of, 986 diagnosis and management of lameness in, 992-995 diagnostic analgesia in, 987-988 history in assessment of, 986 imaging of, 988-989, 990 influence of sport on lameness of, 985 lameness examination of, 986-987 prevention of lameness in, 995-996 proceeding without a diagnosis in, 989-990 saddle pressure analysis of, 989, 991 shoeing of, 990-991, 992 sport of, 984 tack considerations in, 991-992 ten most common lameness conditions in, 986 training of, 985-986 types of horses in, 984-985 Western performance horse, 1017-1033 barrel-racing horse, 1030-1032 cutting horse, 1017-1021 European, 1032-1033 reined cow horse, 1026-1029 roping horse, 1021-1026 Nonsteroidal antiinflammatory drugs for acute caudal antebrachial myositis, 398 for acute rhabdomyolysis, 729 for arthritis, 607, 746-748, 752 infectious, 603 in pony, 1073 for bruised feet in Arabian and Half-Arabian show horse, 1045 for carpal lameness in North American Standardbred, 906 for cervical stenotic myelopathy, 569

Nonsteroidal antiinflammatory drugs—cont’d for distal hock joint pain, 442 in North American Standardbred, 907 enostosis-like lesion of radius, 396 for laminitis, 329-330 for metacarpophalangeal joint capsulitis/synovitis, 349 for metatarsophalangeal joint osteoarthritis, 427, 428 for navicular disease, 301 for pelvic fracture, 489 for physitis, 556 for post-anesthetic myopathy, 735 for radial fracture, 396 for splints, 437 for superficial digital flexor injury management in racehorses, 630 for suspensory desmitis, 663 for thoracolumbar spine injury, 520 for upward fixation of patella in cutting horse, 1020 North America Standardbred, 895-912 carpal lameness in, 905-906 conformation of, 898 curb and superficial digital flexor tendonitis in, 912 description of sport, 895 diagnostic analgesia in, 901-902 distal hock joint pain and other tarsal lameness in, 907-909 distribution of lameness in, 898 front foot lameness in, 903-905 history in assessment of, 899-900 imaging of, 902 lameness in young, 898-899 metatarsophalangeal joint lameness in, 906-907, 911 physical examination of, 900-901 poor racing performance of, 897 proceeding without diagnosis of lameness in, 902-903 rhabdomyolysis and muscle soreness in, 912 sales yearling, 839-841 shoeing of, 903 split bone disease in, 911 stifle joint lameness in, 911-912 suspensory desmitis in, 910-911 ten most common lameness conditions in, 898 track size and lameness in, 897-898 track surface and lameness in, 897 training of, 895-897 Thoroughbred bucked shins in, 876 carpal lameness in, 874-875 conformation of, 870 description of sport, 868-870 distal hock joint pain in, 877-878 fetlock joint lameness in, 873-874 foot-related lameness in, 872-873 imaging of, 871-872 lameness examination in, 870-871 myositis in, 878 osteochondral fragmentation in carpometacarpal joint in, 382-383 purchase examination of sales yearling, 836-837 secondary shoulder region pain in, 879 shoeing of, 872 stifle lameness in, 879 superficial digital flexor tendonitis in, 876-877 suspensory desmitis in, 875-876 tibial stress fractures in, 877 top ten common lameness diagnosis in, 870 track surface and lameness in, 870 unexplained lameness in, 872 NRC. See National Research Council.

1121

NSAIDS. See Nonsteroidal antiinflammatory drugs. Nuchal ligament, insertional desmopathy of, 526-527 Nuclear scintigraphy, 198-212 of brachium, 401-403 carpal, 378-379, 380 of cervical spine, 524-525 computed tomography versus, 214 in confusing or equivocal radiographic changes, 211 in damaged skeletal muscle, 211-212 in distal hock joint pain, 442 of distal interphalangeal joint, 312, 313 of distal phalanx, 322 of elbow, 401-403 equipment used in, 199, 200 of European Thoroughbred, 884 general considerations in, 198 image acquisition in, 199-204 indications and case selection for, 208-209 of metatarsophalangeal joint, 423-424, 425 in muscle disorders, 724 in navicular disease, 294-295 negative responses to nerve blocks, no clinical clues, and negative findings with, 140-141 in neurologic disorder diagnosis, 129 in North American Standardbred, 902 in North American Thoroughbred, 872 in osteoarthritis, 583 pelvic, 211, 486, 487, 488, 489, 493 phases in, 204 in prepurchase examination of performance horse, 962 in primary lesion of deep digital flexor tendon within hoof capsule, 307 in proximal suspensory desmitis in forelimb, 656 in hindlimb, 659, 661 radiation safety in, 204 radioisotope and radiopharmaceutical, 198-199 in rhabdomyolysis, 494 in sacroiliac injury, 495-497, 507 scan interpretation in, 204-208 of shoulder, 401-403 of stifle, 457-458 in stress-related bone injury in cortical and subchondral bone, 209-211 of thoracolumbar spine, 514, 515 in Three Day Event horse, 988 Nucleated cell count in digital flexor tendon sheath disease, 675, 678 in infectious arthritis, 599-600 in infectious conditions in foals, 1091, 1093 in tenovaginocentesis, 690 Nutrient artery, inadvertent transection of during transection of accessory ligament of superficial digital flexor tendon, 636 Nutrient foramen, 83 fracture versus on radiography, 159 Nutrients in ration evaluation, 545-546 Nutrition acquired flexural deformities and, 563, 564-565 of articular cartilage, 575 cervical stenotic myelopathy and, 569 osteochondrosis and, 537-538 role of in developmental orthopedic disease, 543-548 Nutritional muscular dystrophy, 736-738 Nutritional myodegeneration, 736-738 O OAAM. See Occipito-atlantoaxial malformations. Oats, mineral requirements for, 544 Objective information, 9

1122

Index

Oblique distal sesamoidean ligament desmitis of, 719-720, 721 palpation of, 46 ultrasonographic anatomy of, 717 Oblique muscles, 510 Obturator nerve paralysis secondary to dystocia, 1083 OC. See Osteocalcin. Occipito-atlantoaxial malformations, 525, 567-568 nutritional management of, 548 Occult osteochondral fragmentation, arthroscopic examination of, 229 Occult spavin, 55-56, 440 Occult spiral fracture, 142 Occult stress fracture of sacroiliac joint, 507 Ocular abnormalities, 18-20 Odontoid peg fracture in foal, 526 Offset conformation, 23, 24 Olecranon analgesia of, 114 anatomy of, 399 fracture of, 146, 147, 404-405 “On Call” program, 857 On the track catastrophe in Thoroughbred, 854-861 equipment used in, 856 euthanasia and insurance in, 861 management of, 855-856 public relations and media issues in, 857 during racing, 857-860 regulatory considerations in, 861 role of regulatory veterinarian in, 855 during training, 856-857 Onchocerca cervicalis, 705 One Day events, 984 Opacity, radiographic, 154 modification of in thoracolumbar synovial intervertebral articulations, 518 Operator errors in ultrasonographic artifacts, 169-172 Opioids epidural, 767-768 for post-anesthetic myopathy, 735 Organic matter content on track, 862 Orthopedic disease developmental, 533-570 angular limb deformities, 557-561 cervical stenotic myelopathy, 566-570 flexural limb deformities, 562-565 in foals, 1088-1089 nutrition and, 543-548 osteochondrosis, 534-543. See also Osteochondrosis. physitis, 554-556 in young Draft horse, 1068-1069 purchase examination of Thoroughbred sales yearling in Europe and, 838-839 Orthopedic implants, 123 Orthopedic laminitis, 419 Osselets, 46-47 Osseous cyst-like lesion, 158 carpal, 391 in coxofemoral joint, 499 in distal interphalangeal joint, 314-315 in distal phalanx, 317, 344 in distal radius, 397-398 in elbow, 403, 404 femorotibial, 461 navicular, 419, 420 in proximal aspect of second metacarpal bone, 368-369 in scapulohumeral joint, 408-409 in third metacarpal bone of metacarpophalangeal joint, 358 tibial, 453-454 Osseous decompression, 755 Ossification endochondral, 534-535 failure of. See Osteochondrosis. incomplete of central and third tarsal bones, 443

Ossification—cont’d of lateral cartilage of foot, 323-325. See also Sidebone. Ossifying spondylosis, 157 Osteitis, 157 of distal phalanx in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045 in Draft horse, 1063 of palmar processes, 322-323 of pedal, 321 in polo pony, 1011 in reined cow horse, 1029 of humeral tubercles, 412 infectious, 157-158 of distal phalanx due to penetrating injury, 280 in foal, 1089-1093 of metacarpal region, 375 navicular, radiation therapy for, 785 pedal, perineural nerve block for, 102 sacroiliac, 495 of second and fourth metatarsal bone, 439 tarsal, 447-448 ultrasonographic examination in, 196-197 Osteoarthritis, 572-594 in breeding stallions, 1078 in broodmare, 1082 carpal, 380-382, 875 in pony, 1071 radiation therapy for, 785 in steeplechasers, hurdlers, and point to point horses, 945 of carpometacarpal joint, 368, 369, 382 of centrodistal joint in Arabian and Half-Arabian show horse, 1047-1048 in Draft horse, 1066-1067 in dressage horse, 981-982 cervical, 527-529 clinical evaluation of, 580-584 controversy surrounding use of corticosteroids in, 748 of coxofemoral joint, 499 defined, 576 of distal hock joint, 440-443 in Draft horse, 1067 of distal interphalangeal joint, 313, 314, 419-420, 873 in Arabian and Half-Arabian show horse, 1045-1046 in Draft horse, 1064-1065 in dressage horse, 981 in driving horse, 1056-1057 in European Standardbred, 919-920 in North American Standardbred, 905 in North American Thoroughbred, 873 perineural nerve block for, 102 in polo pony, 1011 in show hunter and show jumper horses, 970 in Three Day Event horse, 993 of distal tarsus in cutting horse, 1018-1019 of elbow, 403 etiopathogenesis of, 576-577 of femoropatellar joint, 461 of femorotibial joint, 464-465 in North American Standardbred, 911 of hock, 440-443 in pony, 1071 of lower limb in driving horse, 1056-1057 markers of, 591-594 of metacarpophalangeal joint in Arabian and Half-Arabian show horse, 1047, 1048 in Arabian racehorse, 933 in dressage horse, 982 in driving horse, 1056 in endurance horse, 1000-1001 in European Standardbred, 920 in North American Standardbred, 911

Osteoarthritis—cont’d of metacarpophalangeal joint—cont’d in polo pony, 1008-1009 in show hunter and show jumper horses, 972-973 in Three Day Event horse, 993 of metatarsophalangeal joint, 426-428 in Arabian and Half-Arabian show horse, 1047, 1048 in dressage horse, 982 normal joint function and structure and, 572-576 in North American Thoroughbred, 873, 874, 875 in pleasure riding horse, 1094, 1095 in pony, 1071 of proximal interphalangeal joint, 345-346 in Arabian and Half-Arabian show horse, 1048 cryotherapy for, 782 in Draft horse, 1064-1065 in polo pony, 1014, 1015 in show hunter and show jumper horses, 974 in Three Day Event horse, 993 radiation therapy for, 786 radiographic diagnosis of, 161 role of synovium in, 577 of sacroiliac joint, 507 of scapulohumeral joint in miniature breeds, 409, 410 of stifle in American Saddlebred, 1038-1309 in Arabian and Half-Arabian show horse, 1046-1047 in pony, 1071 in show hunter and show jumper horses, 973-974 synovial fluid cytology for, 582 of synovial intervertebral articulations, 520 of talocalcaneal joint, 443 of tarsocrural joint, 443 in American Saddlebred, 1038 in North American Standardbred, 908 of tarsometatarsal joint in Arabian and Half-Arabian show horse, 1047-1048 in Draft horse, 1066 in dressage horse, 981-982 in Three Day Event horse, 993 in Three Day Event horse, 993 treatment of, 746-764 biologically based, 756-757 corticosteroids, 748-749, 751, 752 glucosamine and chondroitin sulfate, 751, 753 hyaluronan, 749-750, 753 intra-articular, 753 joint resurfacing, 756 nonsteroidal antiinflammatory drugs, 746-748, 751 pentosan polysulfate, 750 polysulfated glycosaminoglycan, 750, 753 surgical, 754-756 Osteoarthrosis, radiographic diagnosis of, 161 Osteocalcin, 592, 843 Osteochondral fragmentation arthroscopic examination of, 229 carpal, 382-390 in Arabian racehorse, 933 in European Thoroughbred, 889 in North American Thoroughbred, 875 osteoarthritis versus, 380-381 in racing Quarter Horse, 930 in steeplechasers, hurdlers, and point to point horses, 945 of carpometacarpal joint, 382-390 of distal interphalangeal joint, 551 of extensor process of distal phalanx, 316-317 of femur in cutting horse, 1019 in fibular tarsal bone, 445 of metacarpophalangeal joint, 930

Index Osteochondral fragmentation—cont’d of metatarsophalangeal joint, 428-429 in North American Standardbred, 907 of middle phalanx, 315, 351 models of, 596 of proximal phalanx, 351-353, 550 in North American Thoroughbred, 874 radiography of, 160 Osteochondritis dissecans, 534, 535-536, 1069. See also Osteochondrosis. Osteochondroma solitary, deep digital flexor tendonitis in carpal sheath secondary to, 644, 686 tibial, 453 Osteochondromatosis, 612 carpal, 391 of extensor tendon, 697 Osteochondrosis, 158, 159, 534-543, 549-554 bone scan in, 208 carpal, 391 causes of, 536-541 characteristics of lesions in, 535-536 defined, 534 of distal interphalangeal joint, 551 of elbow, 403, 404 of femoropatellar joint, 458-459 in foal, 1089 of metacarpophalangeal and metatarsophalangeal joints, 549-550 nutritional management of, 548 in pony, 1071 of proximal interphalangeal joint, 344-345, 550-551 in racing Quarter Horse, 930 relationship between physeal dysplasia, subchondral bone cysts, and, 536 of scapulohumeral joint, 408, 409, 551 of stifle, 554 in American Saddlebred, 1038-1039 in Arabian and Half-Arabian show horse, 1047 in cutting horse, 1019 in North American Standardbred, 912 in show hunter and show jumper horses, 973 of tarsocrural joint, 551-554 in American Saddlebred, 1038 in Arabian racehorse, 932 in European Standardbred, 923 of third metacarpal bone, 358 in young Draft horse, 1069 Osteolysis, 155 Osteomyelitis articular, drainage and debridement for, 603 of cervical spine, 530 infectious, 157-158 in foal, 1089-1093 of metacarpal region, 375 of proximal sesamoid bone, 668 ultrasonographic examination in, 196-197 vertebral, 132 Osteonecrosis, magnetic resonance imaging of, 218 Osteopathy, 819-824 hypertrophic, 157 antebrachial, 398 carpal, 393 metacarpal, 374 Osteopenia, 155 radiation-related, 784 Osteophyte, 156, 157, 583 Otobius megnini infestation, 738 Out-at-the-knee conformation, 22-23 Outdoor polo, 1003 Outside rim shoe, 263, 264 Ovaban. See Megestrol acetate. Ovariectomy, 482 Over track, 61 Overall gain setting, ultrasonographic, 170 Over-at-the-fetlock conformation, 26 Over-at-the-knee conformation, 25, 27, 38 in show hunter and show jumper, 966

Overfeeding acquired flexural deformities and, 563, 564 in developmental orthopedic disease, 546 Overhead chains, 789 Overload injury of metacarpophalangeal joint, 349-351 Over-reach in acute-onset, severe lameness, 147 in European Thoroughbred, 886-887 Ovnicek aluminum shoe, 334 Oxytetracycline for flexural limb deformities, 563 for peri-tarsal cellulitis, 448 P P block for navicular disease, 302 P2G injection, 711 Pace, 61 Pacers. See Standardbred. Paddock rest, 789 Pain arthritic, 607 associated with distal interphalangeal joint, 310-316 associated with navicular disease, 288 associated with tarsometatarsal joint in European Thoroughbred, 894 back, 509-521 acupuncture for, 796 in American Saddlebred, 1037-1038 anatomy and function of thoracolumbar spine in, 509-510 in Arabian and Half-Arabian show horse, 1047 in Arabian racehorse, 932-933 in breeding stallions, 1077-1078 in cutting horse, 1020-1021 diagnosis of, 510-514, 515 in dressage horse, 983 in endurance horse, 1001 in National Hunt, point to point, and timber racing horses, 944 in polo pony, 1013-1014 in pony, 1075 in poor performance of sports horse, 830 in show hunter and show jumper horses, 971-972 in Three Day Event horse, 992-993 causes of during flexion testing, 75 distal hock joint, 440-443 in American Saddlebred, 1037 in Arabian and Half-Arabian show horse, 1047-1048 in Arabian racehorse, 932 in barrel-racing horse, 1031 cryotherapy for, 782 in cutting horse, 1018-1019 in Draft horse, 1067 in driving horse, 1054-1055 in endurance horse, 1001 in North American Standardbred, 898-899, 907-909 in North American Thoroughbred, 877 in polo pony, 1013 in racing Quarter Horse, 930 in show hunter and show jumper horses, 969-975 in team roping horse, 1025 heel in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045-1046 in driving horse, 1054 in North American Standardbred, 906 in polo pony, 1010-1011 hoof in European Standardbred, 919 localization of in lameness diagnosis, 4 muscular, 726-728 neck forelimb posture seen in, 38-39 in Three Day Event horse, 992-993

1123

Pain—cont’d in osteoarthritis, 580-581 palmar foot in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045-1046 navicular disease in, 286-297, 299-304 in show hunter and show jumper horses, 967-969 soft tissue causes of, 297-298 proximal palmar metacarpal in European Standardbred, 920-921 referred, 141 sacroiliac joint in Arabian and Half-Arabian show horse, 1047 in endurance horse, 1001 in show hunter and show jumper horses, 972 in Three Day Event horse, 995 secondary in shoulder region in North American Thoroughbred, 879 tack-induced, 144 temporomandibular joint, 143 PAL. See Palmar annular ligament. Palisading new bone on dorsal aspect of middle phalanx and, interphalangeal joint, 315 Palmar annular ligament anatomy of, 674-675, 716 avulsion fracture of at origin of suspensory ligament, 666, 667 desmitis of, 678-681, 721 in dressage horse, 982 in polo pony, 1015-1016 in pony, 1074 desmotomy of, 232, 637, 641 in polo pony, 1007 diagnostic techniques for, 675 Palmar aspect of fetlock scab on, 151 ultrasonographic examination of, 189, 191 Palmar digital nerve block of, 100, 101, 102, 243-244 for deep digital flexor tendon primary lesions, 306 for distal interphalangeal joint pain, 310 in European Standardbred, 916 for metacarpal pain and disease, 363-364 in North American Standardbred, 902 in Three Day Event horse, 987 neurectomy of, 303 in North American Thoroughbred, 873 neuritis/neuroma of, 722 ultrasonographic anatomy of, 718 Palmar foot pain in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045-1046 due to navicular disease, 286-297, 299-304 due to soft tissue causes, 297-298 in polo pony, 1010-1011 in show hunter and show jumper horses, 967-969 Palmar ligament of proximal interphalangeal joint, 717-178 Palmar metacarpal nerve, 654 anatomy of, 654 diagnostic analgesia of, 104-105 in proximal suspensory desmitis, 655 Palmar pastern, ultrasonographic zone designations for, 180-182 Palmar vein thrombosis, 373 Palmaroproximal-palmarodistal oblique view of foot, 245-246 Palpation, 42-60 of Arabian and Half-Arabian show horse, 1043 art of, 42-60 of cervical spine, 50-51 chiropractic, 806-807 Churchill hock test in, 56-58 of crus, 450 direct or local followed by movement, 79-80

1124

Index

Palpation—cont’d in European Standardbred examination, 915-916 in European Thoroughbred examination, 883-884 of external genitalia, 51 of Finnish horse, 948-949 of forelimb, 42-50 antebrachium, 50 brachium, 50 carpus, 48-50 elbow, 50 fetlock, 46-47 foot, 42-44, 242-243 hoof tester examination, 44-46, 243 metacarpal region, 47-48, 363 pastern, 46, 47 in gluteal syndrome, 471-472 of hindlimb, 53-56, 57 of lateral and ventral thorax and abdomen, 51 of metatarsal region, 434 in North American Standardbred examination, 900-901 in North American Thoroughbred examination, 870-871 pelvic, 52, 491 of pelvis per rectum, 52-53 of performance horse, 958-959 saphenous filling time in, 58-59, 60 sensitivity to in superficial digital flexor tendonitis, 629 of shoulder, 400 in tendon laceration, 712-713 of thoracolumbar spine, 51, 511 of Three Day Event horse, 986-987 PaPr-PaDiO view. See Palmaroproximalpalmarodistal oblique view. Paralysis hyperkalemic periodic, 738-739 obturator nerve secondary to dystocia, 1083 of radial nerve, 132, 414-415 Paralytic myoglobinuria, 728 Parasitic infection of spinal cord, 132 Paravertebral myalgia, 1001 Paresis in cervical stenotic myelopathy, 566 femoral nerve, 40, 41, 132 Partial volume effect in magnetic resonance imaging, 220 PASM. See Periodic acid–silver methanamine staining. Passive exercise, 789-790 Passive stay apparatus anatomy, 87-88 Pastern, 418-421, 716-723 acute-onset, severe lameness following trauma to, 148 anatomy of, 716-718 angle and length of in digital conformation, 30-31 deep digital flexor tendon injuries in region of, 647-648 dermatitis of, 151 distal sesamoidean desmitis in, 719-720 dorsal ring block of, 115 fracture of in Thoroughbred racehorse during racing, 857, 859 joint abnormalities in, 721-722 neuritis and neuroma in, 722 palpation of, 46, 47 polo pony lameness in, 1014, 1015 saphenous filling time assessment in, 59 show hunter and show jumper lameness in, 974 standard radiographic projection and suggested extra views of, 163 superficial digital flexor tendonitis in region of, 641, 718-719 swelling in, 721 tendon injury limited to, 630 ultrasonographic zone designations for, 180-182, 716-718 wounds in, 347

Pasture myopathy, 737 Pasture turnout, 630, 633 Pasture-associated stringhalt, 478 Patella fractures of, 465-466 in Three Day Event horse, 995 fragmentation of, 460 in American Saddlebred, 1039 locking mechanism of, 87 luxation of, 460-461 in American Saddlebred, 1039 in pony, 1072-1073 upward fixation and delayed release of, 70, 459-460, 475-477 altered hindlimb posture seen in, 39-40 coxofemoral joint luxation with or without, 499-500 in cutting horse, 1020 in pony, 1073 stifle palpation in, 53-54 Patella ligament anatomy of, 455 injuries of, 461 palpation of, 53 ultrasound of, 457 Patellar displacement test, 456 Patient history in Arabian and Half-Arabian show horse assessment, 833 in assessment of acute-onset, severe lameness, 145-148 in desmitis of accessory ligament of deep digital flexor tendon, 651 in European Thoroughbred examination, 882 in high-speed treadmill assessment, 833 in muscle disorders, 723, 728 in navicular disease, 288-289, 304 in North American Standardbred examination, 899-900 in North American Thoroughbred examination, 870 in osteopathic treatment, 821 in pelvic injury, 491 in poor performance, 828-830, 833 in primary lesion of deep digital flexor tendon within hoof capsule, 306 in swollen limb diagnosis, 150 Patient preparation for diagnostic analgesia, 99 for ultrasound, 167 Patient selection for arthroscopic surgery, 636 for transection of accessory ligament of superficial digital flexor tendon, 636 PCR. See Polymerase chain reaction. Pectorals muscle injury to, 146, 727 lesions of, 413 Pedal osteitis of distal phalanx, 321 in polo pony, 1011 perineural nerve block for, 102 Pelvic injury, 484-500 asymmetry in height of tubera coxae in, 35, 36 in foal, 1086 in non-racehorse, 491-500 Aorto-iliac-femoral thrombosis, 497-499 clinical signs of, 491-492 coxofemoral joint, 499-500 desmitis of dorsal sacroiliac ligament, 497 diagnostic imaging of, 492-493 equine rhabdomyolysis, 493-494 fracture of third trochanter of femur, 500 fractures, 493 muscular, 494-495 new bone on caudal aspect of wing of sacrum, 497 in polo pony, 1016 sacroiliac, 495-497 in team roping horse, 1025 sacroiliac, 501-508

Pelvic injury—cont’d in Thoroughbred racehorse, 484-490, 878-879 acetabulum fracture, 488-489 diagnostic techniques, 484-486 European, 893 ilial shaft fracture, 487-488 ilial wing fracture, 486-487 pubis and ischium fractures, 488 during racing, 859 treatment of, 489-490 tuber coxae fracture, 486 Pelvis anatomy of, 484 bone scan of, 202-203, 206, 211 hike of in hindlimb lameness, 65-66 injury of. See Pelvic injury. myositis in, 471 National Hunt, point to point, and timber racing horse lameness and, 943-944 palpation of, 52 in European Thoroughbred, 884 standard radiographic projection and suggested extra views of, 166 Pelvis per rectum palpation, 52-53 Penetrating injury fractures of distal phalanx associated with, 320 solar, 278-282 ultrasonographic examination of, 195 Penicillin for calcaneal osteitis, 448 before canker debridement in Draft horse, 1064 for immune-mediated myopathy, 733 for infectious arthritis, 600 for muscle abscess, 734 Pentosan polysulfate, 750 Pentoxyfyline for laminitis in endurance horse, 1000 for navicular disease, 301 Penumbra, radiographic, 154 Peptides, 285 Percussion, tibial, 54 Performance horse, 951-1034 dressage horse, 975-983 diagnostic analgesia in, 979 imaging of, 979 lameness examination of, 978-979 the sport, 975-977 tack, 978 ten most common lameness conditions in, 979-983 training surfaces used by, 977-978 estrous cycle in mares and, 480-482 polo pony, 1003-1017 history of sport, 1003 imaging of, 1006 lameness examination of, 1005 polo as an industry and, 1003-1005 superficial digital flexor tendonitis in, 1006-1008 ten most common lameness patterns in, 1005 undiagnosed lameness of, 1005-1006 prepurchase examination of, 951-964 blood tests in, 963 communication with vendor in, 952, 953-957 at a distance, 952-958 evaluation of identified problems in, 960 gait assessment in, 960 goals of, 951 guidelines for reporting, 964 nerve blocks in, 963-964 nuclear scintigraphic, 962 radiographic, 960-962 rectal, 960 at rest, 958-959 summary of observations in, 964 ultrasonographic, 962-963 veterinarian contract in, 951-952 rest and, 788

Index Performance horse—cont’d show hunter and show jumper, 965-975 back pain in, 971-972 characteristics of horse, 965 competition surfaces used in, 966 desmitis of accessory ligament of deep digital flexor tendon in, 975 distal hock joint pain in, 969-970 distal interphalangeal joint synovitis and early osteoarthritis in, 970 failure to make a diagnosis in, 967 fetlock joint lameness in, 972-973 gluteal myositis in, 974 historical perspective, 965 imaging of, 967 lameness examination of, 967 palmar foot pain in, 967-969 pastern lameness in, 974 sheared heels in, 969 stifle joint pain in, 973-975 structure of sport, 965 superficial digital flexor tendonitis in, 974-975 suspensory desmitis in, 970-971 ten most common lameness problems in, 966-967 tenosynovitis of digital flexor tendon sheath, 975 training of, 965-966 treatment of lameness in, 967 Three Day Event horse, 984-996 conformation of, 986 diagnosis and management of lameness in, 992-995 diagnostic analgesia in, 987-988 history in assessment of, 986 imaging of, 988-989, 990 influence of sport on lameness of, 985 lameness examination of, 986-987 prevention of lameness in, 995-996 proceeding without a diagnosis in, 989-990 saddle pressure analysis of, 989, 991 shoeing of, 990-991, 992 tack considerations in, 991-992 ten most common lameness conditions in, 986 training of, 985-986 types of horses in, 984-985 Western, 1017-1033 barrel-racing horse, 1030-1032 cutting horse, 1017-1021 European, 1032-1033 reined cow horse, 1026-1029 roping horse, 1021-1026 Perfusion, regional, of antimicrobials for infectious arthritis, 602 Pergolide mesylate, 328, 330-331 Periarterial sympathectomy, 302 Peri-articular laxity in angular limb deformities, 557-558 Peri-articular soft tissue, 572 Peri-articular tarsal cellulitis, 448 Perineural analgesia. See also Diagnostic analgesia. in distal hock joint pain, 441 in forelimb, 100-107 in hindlimb, 115-117 technique, 99 Periodic acid-Schiff staining in laminitis, 325-326 in polysaccharide storage myopathy, 732 Periodic acid-silver methanamine staining, 325-326 Periosteal new bone, 155 Periostitis. See Bucked shins. Peripheral nerve deficit of, hindlimb posture seen in, 40, 41 injury to, 132-133 Peroneal nerve. See Fibular nerve. Peroneus tertius altered hindlimb posture seen in, 40, 41 anatomy of, 450

Peroneus tertius—cont’d avulsion of origin of, 467 rupture of, 708-709 in acute-onset, severe lameness, 148 in North American Standardbred, 909 Petroleum jelly, 778 Phalanx breed predilection in disorders of, 343 disease of collateral cartilage of, 323-325 examination of, 342 fractures and fragmentation of, 318-321, 343-344, 345, 353, 419, 428-430, 431, 500 in American Saddlebred, 1038 in breeding stallions, 1078 in European Standardbred, 922 in European Thoroughbred, 893-894 in extensor process, 316-317 in foals, 1086-1088 in North American Standardbred, 904-905, 906 in North American Thoroughbred, 873, 874 in polo pony, 1010 of proximal plantar processes of, 428-429, 922 in Three Day Event horse, 995 on the track in Thoroughbred racehorse, 857 imaging of, 342-343 infectious osteitis of due to penetrating injury, 280 injuries to, 351-354 nuclear scintigraphy of, 209, 210 osseous cyst-like lesion in, 317 osteitis of in American Saddlebred, 1038 in Arabian and Half-Arabian show horse, 1045 in Draft horse, 1063 of palmar processes, 322-323 pedal, 321 in polo pony, 1011 in reined cow horse, 1029 palisading new bone on dorsal aspect of, 315 palpation of, 46, 47, 58-59 radiography of, 246 three-dimensional anatomy of, 89 Phenothiazine for chemical restraint in breeding stallion, 1077 Phenylbutazone, 747, 1079, 1080 for acute rhabdomyolysis, 729 for Aorto-iliac-femoral thrombosis, 499 for assessment of interference gait abnormalities versus lameness in North American Standardbred, 902 for bruised feet in Arabian and Half-Arabian show horse, 1045 for digital flexor tendon sheath disease, 677 for distal hock joint pain, 442, 443 in cutting horse, 1018, 1019 in North American Standardbred, 907 for distal interphalangeal joint pain in Arabian and Half-Arabian show horse, 1045 in driving horse, 1054 for enostosis-like lesion of radius, 396 for infectious arthritis, 603 for laminitis, 330 for metatarsophalangeal joint osteoarthritis, 427 for navicular disease, 301, 303 for osteoarthritis in breeding stallion, 1078 for pelvic fracture, 489 for peri-tarsal cellulitis, 448 for post-anesthetic myopathy, 735 for subsolar abscess in Draft horse, 1060 for superficial digital flexor injury management in racehorses, 630 for suspensory desmitis in European Standardbred, 922 in show hunter and show jumper, 971

1125

Phenylbutazone—cont’d for tarsocrural joint capsule distention, 444 for upward fixation of patella in cutting horse, 1020 use of in broodmare, 1083 Phenytoin, 478 Phosphorus fractional exertion of in recurrent exertional rhabdomyolysis, 494 osteochondrosis and, 538 requirements of during pregnancy, 547 for yearlings, 544 Photopenia, 206 Physical examination, 1-149 of acute-onset, severe lameness, 145-149 of American Saddlebred, 1036-1037 of Arabian and Half-Arabian show horse, 1042-1044 of barrel-racing horse, 1030-1031 baseline and induced lameness in, 4 of breeding stallion, 1077 clinical history in, 9-14 coexistent lameness in, 4 components of, 7-8 conformation in, 6, 15-3 digit, 30-31 evaluation of, 15-21 forelimb, 21-26, 27 hereditary aspects of, 15 hindlimb, 26-30 relevance of, 15 of cutting horse, 1018 diagnostic analgesia in, 93-124 false-negative responses to, 135-137 of forelimb bursae and tendon sheaths, 113-115 of hindlimb bursae and tendon sheaths, 121-122 injection technique in, 99-100 intra-articular in forelimb, 107-113 intra-articular in hindlimb, 117-120, 121, 122 local infiltration in, 122-123 patient preparation in, 99 perception of by laypersons, 98 perineural in forelimb, 100-107 perineural in hindlimb, 115-117 potentially confusing responses to, 137-138 role of chemical restraint in, 98-99 strategy, methodology, and other considerations in, 94-96, 97, 98 distribution of lameness in, 4-6 of Draft horse, 1059-1060 of dressage horse, 978-979 of driving horse, 1052 of European Standardbred, 914-916 of European Thoroughbred, 882-884 sales yearling, 838-839, 840 of event horse, 998 of Finnish and other Scandinavian coldblooded trotters, 948-949 of foot, 242-249 historical perspective of, 2-3 localization of pain in, 4 movement during, 60-73 back pain, 512 circling, 71-72 determination, grading, and characterization of lameness, 62-64 foot placement evaluation, 70-71 gait, 60-62 on hard and soft surfaces, 71 lameness detection during, 67-70 lameness score, 66-67 location of lameness determination during, 64-66 riding observation in, 72-73 using treadmill or gait analysis, 73 musculoskeletal system anatomy and, 81-93 forces in, 85 language of, 85

1126

Index

Physical examination—cont’d musculoskeletal system anatomy and—cont’d passive stay apparatus in, 87-88 specialized structures in, 85-87 three-dimensional, 88, 89, 90, 91, 92, 93 of National Hunt, point to point, and timber racing horses, 940-941 in neurologic disorders, 124-129 of North America Thoroughbred, 870-871 sales yearling, 836-837 of North American Standardbred, 900-901 palpation in, 42-60 art of, 42-60 of cervical spine, 50-51 Churchill hock test in, 56-58 of external genitalia, 51 of forelimb, 42-50 of hindlimb, 53-56, 57 of lateral and ventral thorax and abdomen, 51 of pelvis, 52 of pelvis per rectum, 52-53 saphenous filling time in, 58-59, 60 of thoracolumbar spine, 51 of polo pony, 1005 of pony, 1070 poor performance and, 6-7 posture assessment in, 37-41 prepurchase of performance horse, 951-964 blood tests in, 963 communication with vendor in, 952, 953-957 at a distance, 952-958 evaluation of identified problems in, 960 gait assessment in, 960 goals of, 951 guidelines for reporting, 964 nerve blocks in, 963-964 nuclear scintigraphic examination in, 962 radiographic examination in, 960-962 rectal examination in, 960 at rest, 958-959 summary of observations in, 964 thermographic examination in, 963 in Three Day Event horse, 986 ultrasonographic examination in, 962-963 veterinarian contract in, 951-952 of reined cow horse, 1027-1028 relationship of lameness and conformation in, 6 of roping horse, 1022-1023 of show hunter and show jumper horses, 966 of swollen limb, 150-152 symmetry assessment in, 31-37 of Tennessee Walking Horse, 1034 of Three Day Event horse, 986-987 unexplained lameness and, 7, 135-144 Physical therapy, 817-818 for bruised feet in Arabian and Half-Arabian show horse, 1045 for superficial digital flexor injury management in racehorses, 630, 634 Physiotherapy for flexural limb deformities, 562 following transection of accessory ligament of superficial digital flexor tendon in racehorses, 636 Physis asymmetrical growth of in angular limb deformity, 558 endochondral ossification in, 534-535 fracture of femoral, 474 in fibular tarsal bone, 445 in foals, 1086, 1087 in third metatarsal bone, 435-436 tibial, 452 Physitis, 554-556 closure of distal radius and, 394-395 nutritional management of, 548

Physitis—cont’d relationship between subchondral bone cysts, osteochondrosis, and, 536 in young Draft horse, 1068-1069 Picker PQ 5000 Helical computed tomography scanner, 213 Pin, transfixation, 774 Pin firing, 779 for curb management, 702 Pitting edema, 32 Pixels, tomographic, 213 Plaiting in American Saddlebred horse, 1037 forelimb, 69 hindlimb, 70 Plant material, ultrasonographic appearance of, 195-196 Plant toxicity in stringhalt, 478 Plantar annular ligament desmitis, 982 PLANTAR block, 342 Plantar digital nerve block of, 115, 243-244 for hind foot and pastern lameness, 419 in North American Standardbred, 902 for proximal suspensory desmitis, 658 neuritis/neuroma of, 722 ultrasonographic anatomy of, 718 Plantar ligament of proximal interphalangeal joint, ultrasonographic anatomy of, 717-178 of tarsus, anatomy of, 440 Plantar pastern, ultrasonographic zone designations for, 180-182 Plantar process osteochondral fragmentation, 428-429 Plasmin, 578 Platelet-derived growth factor, clinical use of, 673 Pleasure riding horse, 1094-1095 Plesiotherapy, 785-786 Plumb lines in limb conformation assessment, 20-21 PM/CHMA system. See Polymethyl/cyclohexyl methacrylate system. PMMA. See Polymethylmethacrylate. Podotrochlear bursa analgesia, 113, 114 Pointing, forelimb, 37-38 Point to point horse, 934-935, 936, 937, 938-942 Polo plate, 263 Polo pony, 1003-1017 history of sport, 1003 imaging of, 1006 lameness examination of, 1005 polo as an industry and, 1003-1005 superficial digital flexor tendonitis in, 1006-1008 ten most common lameness patterns in, 1005 undiagnosed lameness of, 1005-1006 Polyester resin, 274 Polymerase chain reaction, 128 in infectious disease diagnosis, 600 in neurologic disorder diagnosis, 129 Polymerization in glue-on shoes, 274 Polymethyl/cyclohexyl methacrylate system, 274 Polymethylmethacrylate, 601-602 Polysaccharide storage myopathy, 731-733 Polysulfated glycosaminoglycans, 750 for arthroscopic surgery postoperative care, 385 for carpal lameness in North American Standardbred, 906 for distal hock joint pain, 442, 443 in show hunter and show jumper, 970 for distal interphalangeal joint pain and disease, 313 in Arabian and Half-Arabian show horse, 1045 in dressage horse, 981

Polysulfated glycosaminoglycans—cont’d for navicular disease, 302 for osteoarthritis, 750, 753 of femorotibial joint in North American Standardbred, 911 of metatarsophalangeal joint, 427, 428 in North American Thoroughbred, 874, 875 for proximal suspensory desmitis in dressage horse, 980 Polysynovitis, immune-mediated, 143-144 Polyurethane adhesive, 274 Polyvinyl chloride cast, 693 Ponazuril, 130 Pony, 1069-1076 back pain in, 1075 cerebellar abiotrophy in, 1075 diagnostic analgesia in, 1070 foot-related problems in, 1074 fractures in, 1073 imaging of, 1070 joint disease in, 1071-1073 lameness examination in, 1070 limb deformities in, 1071 most common conditions affecting, 1071 osteoarthritis of scapulohumeral joint in, 409, 410 polo, 1003-1017 history of sport, 1003 imaging of, 1006 lameness examination of, 1005 polo as an industry and, 1003-1005 superficial digital flexor tendonitis in, 1006-1008 ten most common lameness patterns in, 1005 undiagnosed lameness of, 1005-1006 recurrent exertional rhabdomyolysis in, 1075 soft tissue injuries in, 1074 wounds in, 1075 Pool-phase bone scan image, 204 Poor performance, 6-7, 828-835 assessment of challenge of, 828 clinical, 830-831 history in, 828-830 using high-speed treadmill, 832-835 common problems in, 831-832 of North American Standardbred, 897 Popliteal tendon anatomy, 456 Positional tendons, 617-618 Post leg conformation, 26-27 Post-mortem examination of catastrophic racehorse injury, 866 Postoperative management following arthroscopy, 754 following repair of third metacarpal bone stress fracture in racehorse, 854 following transection of accessory ligament of superficial digital flexor tendon, 636-637 Posture assessment, 37-41 Potassium depletion of in exertional rhabdomyolysis, 730 fractional exertion of in recurrent exertional rhabdomyolysis, 494 high intake of in hyperkalemic periodic paralysis, 738 Poultice, foot, 770 Predef 2X. See Isoflupredone acetate. Prednisolone sodium succinate, 1002 Prednisone, 733 Pre-existing pathological condition in epidemiology of racehorse injuries, 865 Pregnancy feeding systems to prevent developmental orthopedic disease during, 547 nutritional requirements during, 546-548 pelvic fracture and, 489-490 as treatment for problem mare, 481-482

Index Prepubic tendon rupture, 1083 Prepurchase examination of non-racing sport horse, 951-964 blood tests in, 963 communication with vendor in, 952, 953-957 at a distance, 952-958 evaluation of identified problems in, 960 gait assessment in, 960 goals of, 951 guidelines for reporting, 964 nerve blocks in, 963-964 nuclear scintigraphic examination in, 962 radiographic examination in, 960-962 rectal examination in, 960 at rest, 958-959 summary of observations in, 964 thermographic examination in, 963 ultrasonographic examination in, 962-963 veterinarian contract in, 951-952 of Thoroughbred sales yearling Europe, 838-839, 840 in North Amercia, 836-837 of Three Day Event horse, 986 Pressage bandage, 770 Prick from nail, 276 Primary lameness in lameness examination, 4, 62 manipulation and, 74-81 Probe point counting, 199 Procaine penicillin, 734 Progesterone for hormone-related performance problems in mares, 481 impregnated microspheres for hormonerelated performance problems in mares, 481 Progestins, 481 Prognosis assessment, 8 Proliferative synovitis, 349-350, 431-432, 608, 612 in European Standardbred, 933 palpation of, 47 in polo pony, 1008-1009 radiation therapy for, 785 Propenrofylline, 301 Prostaglandins, 577, 579, 580, 746 Protease, 625 Protection, horseshoes for, 267 Protein articular, 575 normal structure and function of, 575 cerebrospinal fluid, 127 dietary osteochondrosis and, 537-538 requirements during pregnancy, 547 synovial in arthritic disease and therapeutic manipulation, 582 in infectious arthritis, 599 in tenosynovitis of extensor tendon sheaths, 695 Proteoglycans, 592 articular, 573-575 corticosteroids in inhibition of synthesis of, 748 in osteoarthritis development, 577, 578 in tendons, 621-622 Proteolytic enzymes, tendon degeneration and, 625 Protozoal myeloencephalitis, 129-130, 143, 567 antibody titer testing in, 126 in breeding stallion, 1078 mechanical lameness in, 475 in polo pony, 1017 Proud flesh, term, 1075 Provocative testing. See Manipulation testing. Proximal check desmotomy, 635-639 Proximal digital annular ligament anatomy of, 716 desmitis of, 682, 721

Proximal interphalangeal joint analgesia of, 102, 108, 109 anatomy of, 342, 717 arthrodesis of, 346 breed predilection in disorders of, 343 examination of, 342 imaging of, 342-343, 717 osteoarthritis of, 345-346 in Arabian and Half-Arabian show horse, 1048 cryotherapy for, 782 in Draft horse, 1064-1065 in driving horse, 1056-1057 in polo pony, 1014, 1015 radiation therapy for, 785 in show hunter and show jumper horses, 974 in Three Day Event horse, 993 osteochondrosis of, 344-345, 550-551 palpation of, 46, 47 subluxation of, 346-347 in pony, 1073 Proximal metacarpal fasciotomy of superficial digital flexor tendon, 637-638 Proximal palmar metacarpal bone fracture of in dressage horse, 983 pain of in European Standardbred, 920-921 in North American Standardbred, 910 Proximal parts of limb, ultrasonographic zone designations for, 182 Proximal phalanx anatomy of, 342 breed predilection in disorders of, 343 examination of, 342 fractures of, 343-344, 345, 353, 429-430, 431 in European Thoroughbred, 893-894 in North American Standardbred, 906 fragmentation of, 428-429, 430, 500 in European Standardbred, 922 in North American Thoroughbred, 874 in proximal plantar processes of, 428-429, 922 imaging of, 342-343 injuries to, 351-354 palpation of, 46, 47, 58-59 on the track fracture of in Thoroughbred racehorse, 857 Proximal plantar process fracture of metatarsophalangeal joint, 429 Proximal sesamoid bone anatomy of, 86 disorders of, 354-356, 357 enlargement of in purchase examination of Thoroughbred sales yearling in Europe, 839 fractures of, 430-431 in Arabian racehorse, 933 in foals, 1088 in North American Standardbred, 906 on the track in Thoroughbred racehorse, 858 infection of axial aspect of, 668, 669 palpation of, 47 in North American Thoroughbred, 871 sesamoiditis of, 431 Proximal suspensory desmitis in Arabian and Half-Arabian show horse, 1046 in barrel-racing horse, 1031-1032 in dressage horse, 979-980 in European Standardbred, 920-921 in European Thoroughbred, 888 extracorporeal shock wave therapy for, 826 in forelimb, 654-657, 658 in hindlimb, 658-662 in North American Standardbred, 910-911 in North American Thoroughbred, 875-876 in polo pony, 1009 diagnostic analgesia in, 1005 in show hunter and show jumper, 970-971 in Three Day Event horse, 994-995

1127

PSB. See Proximal sesamoid bone. PSD. See Proximal suspensory desmitis. PSGAGs. See Polysulfated glycosaminoglycans. Psoas minor and major muscle, 510 Psoas stretch, 816 PSSM. See Polysaccharide storage myopathy. Pubic symphysis anatomy, 484 Pubis anatomy of, 484 examination of, 485 fracture of, 488 Public relations issues, 857 Pulse palpation, 42, 47, 83 Puncture wound in broodmare, 1082 of deep digital flexor tendon, 648 in pleasure riding horse, 1094-1095 of second and fourth metatarsal bone, 439 solar, in driving horse, 1053-1054 Purchase examination of non-racing sport horse, 951-964 blood tests in, 963 communication with vendor in, 952, 953-957 at a distance, 952-958 evaluation of identified problems in, 960 gait assessment in, 960 goals of, 951 guidelines for reporting, 964 nerve blocks in, 963-964 nuclear scintigraphic examination in, 962 radiographic examination in, 960-962 rectal examination in, 960 at rest, 958-959 summary of observations in, 964 thermographic examination in, 963 ultrasonographic examination in, 962-963 veterinarian contract in, 951-952 of Thoroughbred sales yearling Europe, 838-839, 840 in North Amercia, 836-837 of Three Day Event horse, 986 Purchase of performance horse for resale, 952 Purpura hemorrhagica, 152 PVC. See Polyvinyl chloride cast. Pyridinium cross-links of collagen, 843 Pyridinoline, 844 Pyrimethamine, 1079 for equine protozoal myelitis, 130 Q QH. See Quarter Horse. Quantification of lameness analysis, 222-225 Quantitative analysis, ultrasonographic, 182 Quantitative measurement, ultrasonographic, 173-175 Quantitative terms, ultrasonographic, 182-185 Quarter, bruised in North American Thoroughbred, 872 Quarter cracks, 281 in North American Standardbred, 903, 904 in North American Thoroughbred, 872 perineural nerve block for, 102 Quarter Horse, 927-930 osteochondral fragmentation in carpometacarpal joint, 383 Queckenstedt’s test, 127 Quickening, 270, 276 Quittor in Draft horse, 1062-1063 perineural nerve block for, 102 R Racehorse, 836-950 Arabian, 931-933 biochemical markers of bone cell activity in, 842-847 bucked-shins complex in, 847-854 carpal osteoarthritis in, 381

1128

Index

Racehorse—cont’d compensatory lameness development in, 63 epidemiology of injuries in, 861-867 effects of racetrack surface in, 862-863 epidemiological studies of racetracks in, 863-864 future initiatives in, 866 during racing, 866 trainer-related factors and effects in, 865 European Standardbred, 913-924 approaching lameness problems in, 914 corrective shoeing for, 918-919 diagnostic analgesia in, 916 dimensions and characteristics of, 913, 914 final diagnosis, prognosis, and treatment options for, 918 hoof pain in, 919 imaging of, 916-918 lameness examination of, 914-916 metatarsophalangeal joint lameness in, 922 middle carpal joint lameness in, 920 osteoarthritis of distal interphalangeal joint in, 919-920 osteoarthritis of metacarpophalangeal joint in, 920 proceeding without a diagnosis, 919 proximal palmar metacarpal pain including proximal suspensory desmitis in, 920-921 sesamoiditis in, 921 superficial digital flexor tendonitis in, 922-923 suspensory branch desmitis in, 921-922 tarsocrural joint osteochondrosis in, 923 ten most common lameness conditions in, 914 training programs for, 919 European Thoroughbred, 879-894 clinical examination of, 882-884 diagnostic analgesia in, 885-886 exostosis of second and fourth metacarpal/metatarsal bones in, 893 foot-related lameness in, 887-888 fractures of proximal phalanx and condyles of distal third metacarpal/ metatarsal bones in, 893-894 history in assessment of, 882 history of sport, 879-894 imaging of, 884-885 lameness subsequent to bacterial infection in, 891-892 middle carpal joint-related lameness in, 888-889 pain associated with tarsometatarsal joint in, 894 pattern of racing in, 879-880 shoeing considerations for, 886-887 stress fractures of long bones and pelvis in, 892-893 subchondral bone injuries to distal third metacarpal/metatarsal bone in, 889-891 suspensory desmitis in, 888 training regimen, 881-882 undiagnosed hindlimb lameness in, 893 Finnish and other Scandinavian cold-blooded trotters, 946-950 National Hunt, point to point, and timber racing, 934-946 North American Standardbred, 895-912 carpal lameness in, 905-906 conformation of, 898 curb and superficial digital flexor tendonitis in, 912 description of sport, 895 diagnostic analgesia in, 901-902 distal hock joint pain and other tarsal lameness in, 907-909 distribution of lameness in, 898 front foot lameness in, 903-905 history in assessment of, 899-900 imaging of, 902

Racehorse—cont’d North American Standardbred—cont’d lameness in young, 898-899 metatarsophalangeal joint lameness in, 906-907, 911 physical examination of, 900-901 poor racing performance of, 897 proceeding without diagnosis of lameness in, 902-903 rhabdomyolysis and muscle soreness in, 912 shoeing of, 903 split bone disease in, 911 stifle joint lameness in, 911-912 suspensory desmitis in, 910-911 ten most common lameness conditions in, 898 track size and lameness in, 897-898 track surface and lameness in, 897 training of, 895-897 North American Thoroughbred, 868-879 bucked shins in, 876 carpal lameness in, 874-875 conformation of, 870 description of sport, 868-870 distal hock joint pain in, 877-878 fetlock joint lameness in, 873-874 foot-related lameness in, 872-873 imaging of, 871-872 lameness examination in, 870-871 myositis in, 878 secondary shoulder region pain in, 879 shoeing of, 872 stifle lameness in, 879 superficial digital flexor tendonitis in, 876-877 suspensory desmitis in, 875-876 tibial stress fractures in, 877 top ten common lameness diagnosis in, 870 track surface and lameness in, 870 unexplained lameness in, 872 osteochondral fragmentation in carpometacarpal joint in, 382-390 pelvic injury in, 484-490 acetabulum fracture, 488-489 anatomy of pelvis and, 484 diagnostic techniques, 485-486 ilial shaft fracture, 487-488 ilial wing fracture, 486-487 pubis and ischium fractures, 488 treatment of, 489-490 tuber coxae fracture, 486 prognosis assessment in, 8 Quarter Horse, 927-930 sales yearling Standardbred, 830-841 Thoroughbred, 836-839, 840 stress-related subchondral bone injury and osteoarthritis in, 426-428 superficial digital flexor tendonitis in, 628-635 acute phase management of, 630 clinical signs of, 629-630 injury assessment and goals for athletic outcome, 630 subacute phase treatment and long-term rehabilitation, 631-634 ultrasonographic evaluation and categorization of injuries, 630-631 timber, 934-935, 936, 937, 938-942 on the track catastrophe in Thoroughbred, 854-861 equipment used in, 856 euthanasia and insurance in, 861 management of, 855-856 public relations and media issues in, 857 during racing, 857-860 regulatory considerations in, 861 role of regulatory veterinarian in, 855 during training, 856-857

Racetrack epidemiological studies of, 863-864 Finnish and other Scandinavian cold-blooded trotters and, 947 size of and North American Standardbred lameness, 897-898 study of accidents on, 866 surface of, 862-863 National Hunt racehorse, point to point horse, and timber racing horse lameness and, 938-942 North American Standardbred lameness and, 897 North American Thoroughbred lameness and, 870 racing Quarter Horse lameness and, 927 Thoroughbred racehorse catastrophes on, 857-860 Racing history of in North America, 868-870 of National Hunt horses, 937-938 poor performance of North American Standardbred on, 897 in United Kingdom history of, 879 North America versus, 880-881 pattern of, 879-880 Racing Quarter Horse, 927-930 Rack, 60 Saddlebred, 1036 Racking Horse, 1033-1034 Radial nerve paralysis, 132, 143, 414-415 Radiation therapy, 783-788 safety in, 204 Radiography, 153-166 bone scan in confusing or equivocal changes in, 211 brachial, 401 carpal, 378-379, 380 in osteochondral fragmentation, 383-384 of cervical spine, 523-524 in cervical stenotic myelopathy, 566-567 computed tomography versus, 214 of degenerative joint disease, 161 detail in, 153-154 in digital flexor tendon sheath disease, 676 in distal hock joint pain, 441-442 of distal interphalangeal joint, 311-312 of distal phalanx, 322, 323 dystrophic and metastatic mineralization in, 161 of elbow, 401 of European Standardbred, 916-918 of European Thoroughbred, 884, 885 of foot, 244-246 of fracture, 158-160 interpretation of, 161-162 of luxation and subluxation, 161 of metatarsophalangeal joint, 422-423 in navicular disease, 289-294 in neurologic disorder diagnosis, 128-129 of North American Standardbred, 902 of North American Thoroughbred, 871-872 in osteoarthritis, 581-583 pelvic, 485-486, 492 in prepurchase examination of performance horse, 960-962 in primary lesion of deep digital flexor tendon within hoof capsule, 306 in proximal suspensory desmitis in forelimb, 656 in hindlimb, 659, 661 in purchase examination of sales yearling in North America Standardbred, 841 Thoroughbred, 837 in sacroiliac joint injury, 507 safety in, 154 of shoulder, 401 of stifle, 456-457 of tarsal sheath, 688-689

Index Radiography—cont’d technique, 161, 162-166 of thoracolumbar spine, 513, 514 of Three Day Event horse, 988 Wolff’s law and, 154-158, 159 Radioisotope, 198-199 Radiolucency of tibia and talus, 444 Radiopacity, 154 Radiopharmaceutical uptake, 198-199 increased character of, 205-206 intensity of, 205 location of, 204-205 Radius distal osseous cyst-like lesion of, 397-398 traumatic physitis and closure of physis of, 394-395 enostosis-like lesion of, 396, 397 fractures of, 395-396 in foal, 1086 in pony, 1073 on the track in Thoroughbred racehorse, 858 non-adaptive remodeling of carpal bones of in North American Thoroughbred, 874-875 physitis of, 555, 556 radiography of, 165, 401 Range of motion of fetlock joint in European Standardbred, 915 limited in osteoarthritis, 581 Ration evaluation in developmental orthopedic disease, 544-546 Rayless goldenrod-related myopathy, 737 Reactive synovitis, 608 Rear perspective in hindlimb conformation, 29-30 Rearing, 830 Reciprocal apparatus anatomy of, 88 disruption of caudal component of, 40 of stifle, 455 Recording of ultrasonographic images, 167-168, 171, 172 Rectal examination palpation in, 52-53 in pelvic fracture in Thoroughbred racehorse, 485 in prepurchase examination of performance horse, 960 Rectal temperature in focal peritarsal cellulitis in European Thoroughbred, 891 monitoring of in pelvic fracture, 489 Rectus abdominis muscle, 510 Recurrent exertional rhabdomyolysis, 729-731 in North American Standardbred, 912 pelvic injury and, 493-494 in ponies, 1075 in Three Day Event horse, 995 Red blood cell count, cerebrospinal fluid, 127 Red mercuric iodide, 778 Redden Ultimate wedge system, 332, 334 Redness, assessment of, 42 Referred pain, 141 Refractive scattering, 172 Regional perfusion of antimicrobials, 602 Regulatory considerations in on the track catastrophe in Thoroughbred racehorse, 861 Regu-Mate. See Altrenogest. Rehabilitation, 788-791, 817-818 following external skeletal fixation, 776-777 following repair of third metacarpal bone stress fracture in racehorse, 854 following transection of accessory ligament of superficial digital flexor tendon, 636-637 Reined cow horse, 1026-1029

Re-injury of suspensory ligament in Thoroughbred racehorse, 860 tendon, 626 Remodeling, 154, 292 exercise-induced bone fatigue and, 849-851 following tendon injury, 626 of metatarsophalangeal joint in North American Standardbred, 906 in osteoarthritis, 583 of third carpal bone and radial carpal bones in North American Thoroughbred, 874-875 of third metatarsal bone in European Standardbred, 922 Renal compromise in acute rhabdomyolysis, 729 Repetitive overload injury of metacarpophalangeal joint, 349-351 Repetitive trauma in osteoarthritis development, 577 Reporting of prepurchase examination of performance horse, 964 Reproductive system exertional rhabdomyolysis and, 480-481 problems associated with, 144, 480-481 RER. See Recurrent exertional rhabdomyolysis. Resale, purchase of performance horse for, 952 Research in bucked-shin complex in racehorses, 848-851 Resection of hoof capsule, 262 synovial, 755 Resolution of disputes in Standardbred sales, 840 radiographic, 153, 154 Resorption, bone, biochemical markers of in racehorses, 843-844 Rest, 788, 789 for cervical stenotic myelopathy, 569 for chronic exertional rhabdomyolysis, 731 for desmitis of accessory ligament of deep digital flexor tendon, 652-653 following transection of accessory ligament of superficial digital flexor tendon in racehorses, 636 foot function at, 250-252 for pelvic fracture in Thoroughbred racehorse, 489 for physitis, 556 for radial management, 395, 396 rehabilitation and, 788-791 for suspensory desmitis, 656, 660 in North American Standardbred, 910 Resting a hindlimb, 39 Restraint, chemical during bone scintigraphy, 203 for cerebrospinal fluid analysis, 127 for diagnostic analgesia, 98-99, 140 in pony, 1070 during lameness examination, 62 of breeding stallion, 1077 of European Standardbred, 916 Resurfacing of cartilage, 229, 756 models of, 596 for osteochondral fragmentation in carpometacarpal joint, 385 Retraining a racehorse, 897 Reverberation, ultrasonographic, 173 Reverse wedge test, 243 Rhabdomyolysis, 728-735 in acute-onset, severe lameness, 148 in breeding stallions, 1078, 1079 in broodmare, 1082 in driving horse, 1055 in endurance horse, 1000 in iliac wing fractures, 486 in North American Standardbred, 912 in North American Thoroughbred, 878 pelvic injury and, 492, 493-494 in non-racehorse, 492, 493-494 in Thoroughbred racehorse, 489

1129

Rhabdomyolysis—cont’d in pony, 1075 polo, 1016-1017 in Three Day Event horse, 995 Rheumatoid arthritis, 607-608 Rhodococcus equi in bone abscess, 197 in immune-mediated arthritis, 608 in immune-mediated synovitis in foal, 1093 in infectious arthritis, 598 in vertebral osteomyelitis, 530 Rhus toxicodendron, 817 Rib congenital abnormalities of, 143 fracture of, 146, 415 lesion of as cause of lameness, 142 Ridden horse back pain examination in, 512-513 in prepurchase examination of performance horse, 960 Ridden walking, 789 Rider lameness assessment and, 72-73, 830 lameness induced by, 144 in dressage horse, 978 Riding lameness assessment during, 72-73 odd lameness apparent only during, 142 Rifampin, 734 Rim shoe, 263, 264 Rimadyl. See Carprofen. Ring block, 99 mid-pastern, 100-102 Ringbone in Draft horse, 1064-1065 high, 345 Robaxin. See Methocarbamol. Robert Jones bandage, 770-771, 772 Rocker toe shoe, 264 Roller motion shoe, 263 Rolling of shoe, 263, 264 Romifidine, 1070 Root signature, 39 thermography of, 238 Roping horse, 1021-1026 Rump length and angle in conformation assessment, 20, 21 Run, 61 Running walk, 60 Rupture of common digital extensor tendon, 694 flexural limb deformity versus, 565 of coxofemoral joint in pony, 1071-1072 of deep digital flexor tendon, 648 of extensor carpi radialis tendon, 694-695 of fibularis tertius, 708-709 in acute-onset, severe lameness, 148 of gastrocnemius tendon altered hindlimb posture seen in, 40 in foal, 1085 of intersesamoidean ligament, 667 of oblique distal sesamoidean ligament, 719 of prepubic tendon, 1083 of serratus ventralis muscle, 413 of superficial digital flexor tendon, 147, 718 of teres ligament, 500 Rushing fences, 829 Ruta graveolins, 817 S Sacroiliac joint anatomy of, 484, 501-502 pain and injury in, 495-497, 501-508 in Arabian and Half-Arabian show horse, 1047 clinical presentation of, 503-504 in cutting horse, 1021 diagnostic analgesia of, 506-507 diagnostic imaging of, 492, 507 differential diagnosis of, 507

1130

Index

Sacroiliac joint—cont’d pain and injury in—cont’d in dressage horse, 983 in endurance horse, 1001 luxation, scintigraphic diagnosis of, 486 in North American Thoroughbred, 879 physical examination of, 504-506 prognosis for, 508 in show hunter and show jumper horses, 972 in Three Day Event horse, 995 treatment of, 507-508 Sacroiliac joint provocation test, 503, 505-506 Sacroiliac ligament anatomy of, 501 desmitis of, 497 injury to, 503 Sacrosciatic ligament anatomy of, 501 lameness in, 471 Sacrum anatomy of, 484 fracture of, 485, 493 new bone on caudal aspect of wing of, 497 Saddle examination under in Arabian and HalfArabian show horse, 1043-1044 pressure analysis of in Three Day Event horse, 989, 991 tack-induced pain from ill-fitting, 144 Three Day event horse performance and, 991-992 Safety high-speed treadmill, 834 radiation, 204 radiographic, 154 Safing of shoe, 263 Sagittal fracture carpal, 388 in North American Thoroughbred, 875 patellar, 465 of proximal phalanx in European Thoroughbred, 893-894 in North American Standardbred, 906 of talus in North American Standardbred, 908, 909 tarsal, 444, 445 Sagittal ratio in radiographic diagnosis of cervical compressive myelopathy, 128-129, 567 Sales yearling Standardbred, 830-841 Thoroughbred purchase examination of in Europe, 838-839, 840 purchase examination of in North America, 836-837 Salter-Harris fracture of distal third metatarsal physis, 435 of femur, 466, 473 of growth plate, 554-556 of proximal humeral physis, 407 of proximal phalanx, 343-344 tibial, 452 Saphenous filling time, 58-59, 60 Sarapin for navicular disease, 302 for paravertebral myalgia in endurance horse, 1001 for sacroiliac desmitis in cutting horse, 1021 for splints, 437 in North American Standardbred, 911 for suspensory desmitis in show hunter and show jumper, 971 for thoracolumbar myositis in cutting horse, 1020 for thoracolumbar spine injury, 520 Sarcocytis neurona, 126, 129-130 Sarcocytosis, 734-735 Sarcoma, synovial cell, 612 Scab on palmar aspect of fetlock, 151

Scalping interference, 69 in European Thoroughbred, 886-887 Scandinavian cold-blooded trotters, 946-950 Scapula anatomy of, 399 fractures of, 146, 412-413 in Thoroughbred racehorse, 858, 878 height of, asymmetry and, 33 palpation of, 50 subchondral bone cyst of, 408-409 Scapulohumeral joint anatomy of, 400 arthrocentesis of, 113 articular surface fracture of distal scapula of, 411 dysplasia of, 410 field diagnosis of traumatic injury to, 146 luxation of, 410-411 osteoarthritis of in miniature breeds, 409, 410, 1071 osteochondrosis of, 408, 409, 551 periarticular trauma to, 411 radiography of, 401 subchondral bone cysts and osseous cyst-like lesions of, 408-409 tearing of joint capsule in, 410 Scar tissue formation, 32. See also Fibrosis. Schirrhous cord, 144 Sciatic nerve anatomy of, 501-502 damage to, 40-41, 132 Scintigraphy, 198-212 brachial, 401-403 carpal, 378-379, 380 of cervical spine, 524-525 computed tomography versus, 214 in confusing or equivocal radiographic changes, 211 in damaged skeletal muscle, 211-212 in distal hock joint pain, 442 of distal interphalangeal joint, 312, 313 of distal phalanx, 322 of elbow, 401-403 equipment used in, 199, 200 of European Thoroughbred, 884 of foot, 246 general considerations in, 198 image acquisition in, 199-204 indications and case selection for, 208-209 of metatarsophalangeal joint, 423-424, 425 in muscle disorders, 724 in navicular disease, 294-295 negative responses to nerve blocks, no clinical clues, and negative findings with, 140-141 in neurologic disorder diagnosis, 129 of North American Standardbred, 902 of North American Thoroughbred, 872 in osteoarthritis, 583 pelvic, 211, 486, 487, 488, 489, 493 phases in, 204 in prepurchase examination of performance horse, 962 in primary lesion of deep digital flexor tendon within hoof capsule, 307 in proximal suspensory desmitis in forelimb, 656 in hindlimb, 659, 661 radiation safety in, 204 radioisotope and radiopharmaceutical, 198-199 in rhabdomyolysis, 494 in sacroiliac injury, 495-497, 507 scan interpretation in, 204-208 of shoulder, 401-403 of stifle, 457-458 in stress-related bone injury in cortical and subchondral bone, 209-211 of thoracolumbar spine, 514, 515 of Three Day event horse, 988 Sclerosing agent injection, 508

Sclerosis, 155-156, 583 in European Thoroughbred, 888-889 in North American Thoroughbred, 874-875 Scoring system for cervical stenotic myelopathy, 567-568 for lameness, 66-67 Scratches, 151 Screen factors in imaging, 154 Screw fixation, 754 for patellar fracture, 465 for proximal interphalangeal joint lesions, 550 of proximal physeal tibial fracture, 452 for slab fracture of third carpal bone, 388-389 for tarsal bone fracture, 445 Screw-in calks, 265 Scrotal intertrigone infection, 891-892 Scutum, 674 SDFT. See Superficial digital flexor tendon. Seasonal factors in biochemical markers of bone cell activity, 844 Seating out of shoe, 263 Second metacarpal bone exostoses of, 369-371. See also Splints. in European Thoroughbred, 893 in North American Standardbred, 911 in racing Quarter Horse, 929 fracture of, 371-372 cryotherapy for, 781 in North American Standardbred, 911 in pony, 1073 in Three Day event horse, 995 osseous cyst-like lesion in proximal aspect of, 368-369 palpation of, 47 Second metatarsal bone anatomy of, 433 exostoses of, 437. See also Splints. in European Thoroughbred, 893 in North American Standardbred, 911 fractures of, 437 cryotherapy for, 781 in North American Standardbred, 911 in pony, 1073 palpation of, 58 Secondary joint disease, 161 Secondary lameness, 4, 62-63 Sedatives for chemical restraint during bone scintigraphy, 203 during lameness examination, 62 for extracorporeal shock wave therapy, 825 in tendon laceration emergency management, 713 Seedy toe, 242, 277-278 Selenium cervical stenotic myelopathy and, 569 deficiency of in exertional rhabdomyolysis, 730 nutritional myodegeneration and, 736, 737 toxicity of in development of developmental orthopedic disease, 544 Selenium-dependent glutathione peroxidase, 736 Semen collection, 1078, 1082 Semimembranosus myositis, 1039 Semispinalis injury, 526-527 Semitendinosus muscle myositis of in American Saddlebred, 1039 tearing of in fibrotic myopathy, 477, 478 Sequential blocking, 94, 95, 96, 97, 98 Sequestrum, 157, 158 Serology in neurologic disorders, 126 Serotonin in arthritic pain, 607 Serratus ventralis muscle rupture, 413 Serum aspartate aminotransferase in immune-mediated myopathy, 733 in muscle disorders, 724 in neurologic examination, 126 in rhabdomyolysis, 494 chronic exertional, 730 pelvic injury and, 492

Index Serum creatine kinase in ear tick-associated muscle cramping, 738 in immune-mediated myopathy, 733 in muscle disorders, 723-724 in neurologic examination, 126 in polysaccharide storage myopathy, 732, 733 in post-anesthetic myopathy, 735 in rhabdomyolysis, 148, 494 chronic exertional, 730 in driving horse, 1055 ilial wing fracture and, 486 pelvic fracture and, 492 Serum insulin, 537 Serum lactate dehydrogenase, 724 Serum muscle enzyme concentration, 492 Serum myoglobin, 724 Sesamoid bone anatomy of, 86 disorders of, 354-356, 357 enlargement of in purchase examination of Thoroughbred sales yearling in Europe, 839 fractures of, 430-431 in Arabian racehorse, 933 in foals, 1088 in North American Standardbred, 906 on the track in Thoroughbred racehorse, 858 infection of axial aspect of, 668, 669 palpation of, 47 in North American Thoroughbred, 871 Sesamoid nerve block abaxial, 102-103, 115, 244 basisesamoid, 115 Sesamoidean ligament anatomy of, 89, 90, 284, 654, 675, 716, 717 avulsion of from palmar aspect of proximal phalanx, 352 desmitis of, 719-721 in polo pony, 1016 in show hunter and show jumper, 974 in team roping horse, 1024 on the track in Thoroughbred racehorses, 860 focal tear of, 297, 298 palpation of, 46 Sesamoiditis in European Standardbred, 921-922 forelimb, 354 hindlimb, 431 in polo pony, 1014-1015 radiation therapy for, 785 in reined cow horse, 1029 in show hunter and show jumper horses, 973 Setaria species, 132 7D4 epitope, 592 Severe, acute-onset lameness, 143, 145-149 Sex in clinical history, 11. See also Gender factors. Sharpness, radiographic, 154 Shear force, 85 cartilage matrix resistance of, 576 Sheared heels, 277 foot palpation in assessment of, 43 in North American Standardbred, 904 perineural nerve block for, 102 in show hunter and show jumper horses, 969 Shearing strength, racetrack and, 863 Sheep-knee conformation, 25-26, 27 Shielding, scintigraphic, 202-203 Shin, bucked and sore, 435 cryotherapy for, 781 in racehorses, 847-854, 876, 892, 898, 929 radiation therapy for, 785 thermography in, 237 Shin-hitting interference, 69 Shivers, 70, 133, 143, 476, 478-479 in Draft horse, 1068 Shock, treatment of in tendon lacerations, 713-714

Shock wave therapy, 825-826 for distal hock joint pain, 443 for metatarsophalangeal joint osteoarthritis, 427 for proximal suspensory desmitis, 656-657, 660 Shoeing adhesive type, 274-275 of American Saddlebred, 1037 for angular limb deformities, 557-558 attachment of shoe to hoof in, 266-267 of barrel-racing horse, 1032 bars for, 265 calks, grabs, and other devices added to ground of shoe for, 265-266 clinical examination of hind foot and pastern and, 418 in clinical history, 12 corrective, 269-270 cross-sectional profile of shoe stock for, 263, 264 for distal hock joint pain, 442-443 of driving horse, 1053 effects of on foot function, 269 in epidemiology of racehorse injuries, 865 extensions for, 263-264 of Finnish and other Scandinavian cold-blooded trotters, 947-948 foot palpation in assessment of, 44 foot preparation for, 262 functions of, 267-269 in gluteal syndrome, 472 high-speed treadmill assessment and, 834 hot versus cold, 266 instrumented, 65, 224 lameness associated with, 270 in laminitis, 332-335, 338 materials and size of horseshoe in, 262-263 in metatarsophalangeal joint osteoarthritis, 427 of National Hunt, point to point, and timber racing horses, 941-942 natural balance, 273 for navicular disease, 300-301 in show hunter and show jumper, 969 pads for, 266 problems associated with horseshoe nails used in, 275-278 of racing Quarter Horse, 928 of roping horse, 1025, 1026 of show hunter and show jumper horses, 966 of sound horses for performance, 269 of Standardbred European, 918-919 North American, 903 for sub-solar bruising in show hunter and show jumper, 968 in tendon laceration, 715 of Thoroughbred European, 886-887 North America, 872 in Three Day event horse, 990-991, 992 Shoulder acute-onset, severe lameness in, 146-147 in Draft horse, 1066 anatomy of, 399-400 angle of in conformation assessment, 20 arthrocentesis of, 113 diagnosis of lameness of, 400-401 fracture of on the track in Thoroughbred racehorse, 858-859 imaging of, 401-403 intertubercular bursa disorders of, 411-412 length of in conformation assessment, 20 limb flight in lameness of, 69 local analgesia of, 400-401 muscle disorders of, 413 thermography of, 238 nervous disorders of, 413-415 scapulohumeral joint disorders of, 408-411 secondary pain in region of in North American Thoroughbred, 879

1131

Shoulder—cont’d standard radiographic projection and suggested extra views of, 165 Show horse American Saddlebred, 1035-1040 Arabian and Half-Arabian horse, 1040-1049 conformation of, 1042 diagnosis and management of lameness in, 1044-1049 diagnostic analgesia in, 1044 history of breed and sport, 1040-1041 lameness examination of, 1042-1044 neurologic examination of, 1044 ten most common causes of lameness in, 1042 training of, 1041-1042 undiagnosed lameness in, 1044 Tennessee Walking Horse, 1033-1034 Show hunter, 965-975 back pain in, 971-972 characteristics of horse, 965 competition surfaces used in, 966 desmitis of accessory ligament of deep digital flexor tendon in, 975 distal hock joint pain in, 969-970 distal interphalangeal joint synovitis and early osteoarthritis in, 970 failure to make a diagnosis in, 967 fetlock joint lameness in, 972-973 gluteal myositis in, 974 imaging of, 967 lameness examination of, 967 palmar foot pain in, 967-969 pastern lameness in, 974 sheared heels in, 969 stifle joint pain in, 973-975 structure of sport, 965 superficial digital flexor tendonitis in, 974-975 suspensory desmitis in, 970-971 ten most common lameness problems in, 966-967 tenosynovitis of digital flexor tendon sheath, 975 training of, 965-966 treatment of lameness in, 967 Show jumper, 965-975 back pain in, 971-972 characteristics of horse, 965 competition surfaces used in, 966 desmitis of accessory ligament of deep digital flexor tendon in, 975 distal hock joint pain in, 969-970 distal interphalangeal joint synovitis and early osteoarthritis in, 970 failure to make a diagnosis in, 967 fetlock joint lameness in, 972-973 gluteal myositis in, 974 historical perspective, 965 imaging of, 967 lameness examination of, 967 palmar foot pain in, 967-969 pastern lameness in, 974 sheared heels in, 969 stifle joint pain in, 973-975 structure of sport, 965 superficial digital flexor tendonitis in, 641-642, 974-975 suspensory desmitis in, 970-971 ten most common lameness problems in, 966-967 tenosynovitis of digital flexor tendon sheath, 975 training of, 965-966 treatment of lameness in, 967 Shu points, 794 Sialoprotein, 592-593 Sickle-hocked conformation, 16, 27-29 curb and, 699 in North American Standardbred, 898 in show hunter and show jumper, 966

1132

Index

Sidebone, 323-325 in Draft horse, 1062 in Finnish horses, 950 in North American Standardbred, 904 palpation of, 44 in pony, 1074 Sideways belly lift, 816 Signalment in clinical history, 9-11 Sinus, 157-158 Skeletal fixation, external, 774-777 Skeletal muscle disorders of, 723-743 diagnosis of, 723-726 exertional rhabdomyolysis, 728-732 hyperkalemic periodic paralysis, 738-739 non-exertional rhabdomyolysis, 732-735 nutritional myodegeneration, 736-738 pain, strain and tears, 726-728 scintigraphy of, 211-212 ultrasonographic examination of, 194-195 Ski jump deformation, 519 Skin cleansing of before diagnostic analgesia, 99 for ultrasound, 167, 514 damage to from radiation therapy, 784 mud fever of, 151 necrosis of in steeplechaser, hurdlers, and point to point horses, 942 of superficial digital flexor tendon after topical application, 374 ultrasonographic artifacts and, 169, 172 Skin fold infection in European Thoroughbred, 891-892 Skin markers in conformation assessment, 16, 17 SL. See Suspensory ligament. Slab fracture carpal, 386-390, 391 in North American Standardbred, 906 radiography of, 160 of third tarsal bone in North American Standardbred, 907 Sling, 789 Slow gait, Saddlebred, 1036 Snow polo, 1003 Sodium depletion of in exertional rhabdomyolysis, 730 fractional exertion of in recurrent exertional rhabdomyolysis, 494 Sodium acetylsalicylate, 921 Sodium chloride, 1002 Sodium hyaluronate. See Hyaluronan. Sodium monoiodoacetate, chemical fusion with, 443 Soft surface, lameness examination on, 71 Soft tissue, anatomy and disorders of, 615-743 altering hindlimb posture seen in, 39-40, 41 articular disease, 610-612 bursae, 705-708 capped elbow, 706 capped hock, 706 of carpal and carpal region, 392 carpal canal and carpal synovial sheath, 684-687 common calcaneal tendonitis, 709 of crus, 454 curb as, 699-704 digital synovial sheath, palmar annular ligament, and digital annular ligament, 674-684 fibularis tertius rupture, 708-709 field assessment of, 147 gastrocnemius tendonitis, 709-710 in metatarsophalangeal joint, 431 mineralization, 161 normal structure and function of, 572, 616-618 palmar heel pain due to, 297-298

Soft tissue, anatomy and disorders of—cont’d pastern, 716-723 anatomy of, 716-718 joint abnormalities in, 721-722 neuritis and neuroma in, 722 in show hunter and show jumper horses, 974 swelling in, 721 tendon and ligament injuries of, 718-721 ultrasound of, 716-718 in pony, 1074 suspensory ligament, 654-672 anatomy and pathophysiology of, 654 avulsion fracture of palmar annular ligament at insertion on, 666, 667 desmitis of body of, 662-663 desmitis of medial or lateral branches of, 663-666 infection of axial aspect of proximal sesamoid bones and, 668, 669 intersesamoidean ligament injury, 666-667, 668 oblique distal sesamoidean desmitis and, 670-671 progressive atraumatic breakdown of in hindlimb, 671-672 proximal desmitis of in forelimb, 654-657, 658 proximal desmitis of in hindlimb, 658-662 stem cells and marrow components to stimulate regeneration of, 673-674 straight distal sesamoidean desmitis and, 668-670 tarsal, 447 tarsal sheath, 447, 687-692 tendons anatomy of, 618-622 deep digital flexor. See Deep digital flexor tendon. extensor, 692-699 hypothesized mechanisms of degeneration of, 624-625 lacerations of, 712-715 mechanism of injury to, 622-624 phases of healing of, 625-626 superficial digital flexor. See Superficial digital flexor tendon. types of, 622 thoroughpin, 706-708 on the track injury in Thoroughbred racehorse, 860 Soil on track, 862, 863 Sole abscess of, 278-279 in broodmare, 1082 in Draft horse, 1060-1061 in European Thoroughbred, 887 in foal, 1093 foot poultice for, 770 in North American Standardbred, 904 perineural nerve block for, 102 in pleasure riding horse, 1094 in show hunter and jumper horses, 968 live, 272 trauma to penetrating, 278-282 problems associated with horseshoe nails in, 275-278 Sore shins, 435 Soreness foot in breeding stallions, 1078 in broodmare, 1082 in show hunter and show jumper horse, 967-968 in Three Day event horse, 993 muscular, 726 neck and back in breeding stallions, 1077-1078 in Three Day event horse, 992-993 Sound, use of in lameness examination, 67

Spasm, muscular, 727 Spasticity in cervical stenotic myelopathy, 566 Spavin, 440. See also Distal hock joint pain. bog, 443-444, 551 in Draft horse, 1066 bone in pony, 1071 carpal, 1071 cryotherapy for, 782 tarsal palpation in, 55-56, 57 Spavin test, 441 Speedy cutting interference, 69 Spin echo sequence in magnetic resonance imaging, 217 Spinal cord cervical, compression of, 130-131, 143 disease of, 132 cervical stenotic myelopathy as, 566-570 Spinosus muscle, 510 Spinous process anatomy of, 509 fracture of in withers region, 142-143 in polo pony, 1014 impingement of, 123, 514-515, 516 in polo pony, 1013-1014 in show hunter and show jumper horses, 972 radiography of, 513, 514 scintigraphic imaging of, 514, 515 ultrasound of, 513-514 Spiral fracture, occult, 142 Splinting for digital extensor tendon laceration, 693 for flexural limb deformities, 563 of traumatic disruption of suspensory apparatus, 360 Splints, 369-371, 437, 771-772 in American Saddlebred, 1039 in Arabian and Half-Arabian show horse, 1048 cryotherapy for, 781 in Draft horse, 1065 in endurance horse, 1001 in European Thoroughbred, 893 in Finnish horses, 950 fracture versus on radiography, 159 local infiltration of anesthetic solution in, 122 in North American Standardbred, 911 young, 898 in polo pony, 1012 in racing Quarter Horse, 929 radiation therapy for, 785 Split bone disease, 911 Splitting, tendon for superficial digital flexor tendonitis, 638 in North American Thoroughbred, 877 in polo pony, 1007 therapeutic ultrasound for, 812 in Three Day event horse, 994 for suspensory desmitis, 663 Spoiled gradient echo sequence in magnetic resonance imaging, 217 Spondylosis, 157, 519 Sporadic exertional rhabdomyolysis, 728-729 Sporadic lameness, challenge of diagnosis in, 138-139, 140 Sport horse, 827-1095 non-racing, 951-1095 Arabian and Half-Arabian horse, 1040-1049 breeding stallions, 1077-1082 broodmares, 1082-1083 Draft horse, 1058-1069 dressage horse, 975-983 driving horse, 1049-1058 endurance horse, 996-1002 polo pony, 1003-1017 pony, 1069-1076 prepurchase examination of, 951-964 show hunter and show jumper horse, 965-975 Tennessee Walking Horse, 1033-1034 Three Day event horse, 984-996 Western performance horse, 1017-1033

Index Sport horse—cont’d poor performance in, 828-835 racehorse, 836-950 Arabian, 931-933 biochemical markers of bone cell activity in, 842-847 bucked-shins complex in, 847-854 compensatory lameness development in, 63 epidemiology of injuries in, 861-867 European Standardbred, 913-924 European Thoroughbred, 879-894 Finnish and other Scandinavian coldblooded trotters, 946-950 National Hunt, point to point, and timber racing, 934-946 North American Standardbred, 895-912 North American Thoroughbred, 868-879 Quarter Horse, 927-930 on the track catastrophe in Thoroughbred, 854-861 Sports medicine, computed tomography in, 214-215 SR. See Sagittal ratio. Stabbing, 69-70 Stable bandage, 769 Stable rest for physitis, 556 for proximal suspensory desmitis, 656 Staining in laminitis, 325-326 in polysaccharide storage myopathy, 732 Stakes races, 869-870, 896-897 Stall rest, 788, 789 for cervical stenotic myelopathy, 569 for chronic exertional rhabdomyolysis, 731 for desmitis of accessory ligament of deep digital flexor tendon, 652-653 following transection of accessory ligament of superficial digital flexor tendon in racehorses, 636 for pelvic fracture in Thoroughbred racehorse, 489 for proximal suspensory desmitis, 660 for radial management, 395, 396 Stance phase biomechanics of, 247, 251 lameness in, 64 Standardbred. See also Racehorse. bucked-shins complex in, 847-854 European, 913-924 approaching lameness problems in, 914 diagnostic analgesia in, 916 dimensions and characteristics of, 913, 914 final diagnosis, prognosis, and treatment options for, 918 hoof pain in, 919 imaging of, 916-918 lameness examination of, 914-916 metatarsophalangeal joint lameness in, 922 middle carpal joint lameness in, 920 osteoarthritis of distal interphalangeal joint in, 919-920 osteoarthritis of metacarpophalangeal joint in, 920 proceeding without a diagnosis, 919 proximal palmar metacarpal pain including proximal suspensory desmitis in, 920-921 sesamoiditis in, 921 superficial digital flexor tendonitis in, 922-923 tarsocrural joint osteochondrosis in, 923 ten most common lameness conditions in, 914 training programs for, 919 forelimb/hindlimb weight distribution ratio in, 6 fracture of proximal sesamoid bones in, 430-431 hindlimb lameness in, 6

Standardbred—cont’d North American, 895-912 carpal lameness in, 905-906 conformation of, 898 curb and superficial digital flexor tendonitis in, 912 diagnostic analgesia in, 901-902 distal hock joint pain and other tarsal lameness in, 907-909 distribution of lameness in, 898 front foot lameness in, 903-905 history in assessment of, 899-900 imaging of, 902 lameness in young, 898-899 metatarsophalangeal joint lameness in, 906-907, 911 physical examination of, 900-901 poor racing performance of, 897 proceeding without diagnosis of lameness in, 902-903 rhabdomyolysis and muscle soreness in, 912 shoeing of, 903 split bone disease in, 911 stifle joint lameness in, 911-912 suspensory desmitis in, 910-911 ten most common lameness conditions in, 898 track size and lameness in, 897-898 track surface and lameness in, 897 training of, 895-897 osteochondral fragmentation in carpometacarpal joint in, 382, 383 prognosis assessment in, 8 sales yearling, 839-841 Standardized scoring system for lameness, 66-67 Standoff pads, 172 Staphylococci in calcaneal osteitis, 448 in digital flexor tendon sheath disease, 678 in immune-mediated myopathy, 733 in infectious arthritis, 598, 599 in metacarpophalangeal joint abscess in European Thoroughbred, 891 in muscle abscess, 734 in severe cellulitis of metatarsal region, 439 in supraspinous bursitis, 705 Starling forces, 606 Static balance, conformation and, 252-253 STB. See Standardbred. Steel horseshoe, 262 Steeplechasing, 935, 936 Stem cells, clinical use of, 673-674 Stenotic myelopathy, cervical, 566-570 Stent bandage, 770 Sternal injury, 142 Steroid arthropathy, 608 Sticker for horseshoe, 265 Stiff horse syndrome, 143, 479, 738 Stiffness measurement of in third metacarpal bone in bucked shins, 849 neck, 522-523 neurologic problems and, 143 in poor performance in sport horse, 829 Stifle, 455-470 acute-onset, severe lameness following trauma to, 148 anatomy of, 455-456 Arabian racehorse lameness in, 932 arthrocentesis of, 119-120, 456 in pelvic injury, 492 articular disease of, 458-465 femoropatellar joint, 458-461 femorotibial joint, 461-465 avulsion of origin of peroneus tertius and long digital extensor tendon in, 467 calcinosis circumscripta in, 467-468 cutting horse lameness in, 1019-1020 diagnosis of lameness in, 456

1133

Stifle—cont’d direct trauma to in driving horse, 1057, 1058 Draft horse lameness in, 1067-1068 driving horse lameness in, 1057 fractures of, 465-467 in Three Day event horse, 995 on the track in Thoroughbred racehorse, 859 hematoma in, 468 imaging of, 456-458 North American Standardbred lameness in, 911-912 North American Thoroughbred lameness in, 879 osteoarthritis of in American Saddlebred, 1038-1039 in Arabian and Half-Arabian show horse, 1046-1047 in pony, 1071 in show hunter and show jumper horses, 973-974 osteochondrosis of, 458-459, 554 in American Saddlebred, 1038-1039 in Arabian and Half-Arabian show horse, 1047 in cutting horse, 1019 in show hunter and show jumper, 973 pain in racing Quarter Horse, 930 in reined cow horse, 1029 palpation of, 53-54 in show hunter and show jumper lameness in, 973 standard radiographic projection and suggested extra views of, 165-166 ultrasonographic examination of, 191-192, 193 “Stifle flexion” test, 79 Stimulated endogenous repair, 756 Stocked-up, 32, 150-152 Stoved-up, 150-152 Stove-pipe swelling, term, 32 Straight behind conformation, 26-27 Straight distal sesamoidean ligament, ultrasonographic anatomy of, 717, 720-721 Straight hocks conformation, 26-27, 37 Strain bone, measurement of in bucked-shin syndrome, 849 muscular, 726-728 thermography of, 237-238 sacroiliac in cutting horse, 1021 ultimate tendon, 617 Strangles, 530 Streptococci in antebrachial myositis and cellulitis, 398 in calcaneal osteitis, 448 in digital flexor tendon sheath disease, 678 in infectious arthritis, 598 in laminitis, 328 in severe cellulitis of metatarsal region, 439 in supraspinous bursitis, 705 in vertebral osteomyelitis, 530 Stress fracture and injury in cortical and subchondral bone, bone scan of, 209-211 endosteal new bone in response to, 155, 156 of humerus, 405, 406 in European Thoroughbred, 893 in North American Thoroughbred, 878 in North American Standardbred, 906 pelvic in Thoroughbred racehorse, 485, 878-879 radiography of, 159 of sacroiliac joint, 507 scapular, 412-413 in North American Thoroughbred, 878 in subchondral bone of elbow, 403 of metatarsophalangeal joint, 426-428

1134

Index

Stress fracture and injury—cont’d of third metacarpal bone condylar, 367 palmar cortical, 364-366, 983 in racehorses, 853-854 transverse of distal metaphyseal region, 366-367 of third metatarsal bone in European Standardbred, 922 transverse, 436 in Thoroughbred European, 892-893 North American, 878-879 tibial, 451 in American Saddlebred, 1039 in European Thoroughbred, 892-893 in North American Thoroughbred, 877 vertebral lamina, 519 Stress test valgus, 80 of stifle, 54 varus, 80 Stress-strain curves for tendon, 616-617 Stretching, 815-816 Stride biomechanics of, 247 cranial and caudal phases of during lameness examination, 67-68 foot function and, 251-252 lameness and, 248 length of in lameness evaluation, 61 Stringhalt, 70, 133, 143, 476, 478 in American Saddlebred, 1039 from metatarsal region wounds, 439 Stromelysins, 578, 579 Strongylus species, 132 Stud for horseshoe in driving horse, 1053 in navicular disease, 300-301 Styrofoam insulation for solar support in laminitis, 332, 333, 334, 335 Subchondral bone changes of in osteoarthritis, 577 cyst of, 158 in cutting horse, 1019-1020 in femorotibial joint, 461-462 relationship between physeal dysplasia, osteochondrosis, and, 536 in scapulohumeral joint, 408-409 in show hunter and show jumper horses, 973 magnetic resonance imaging of, 218, 219 normal structure and function of, 572 stress fracture of bone scan of, 209-211 metatarsophalangeal joint, 426-428 trauma to in distal interphalangeal joint, 314 in distal phalanx, 320 in European Thoroughbred, 889-891 in metacarpophalangeal joint, 350-351 of tibia and talus, 444 Subchondral forage for distal hock joint pain, 443 Subchondral lucency of third carpal bone, 390 Subcutaneous fibrosis in region of palmar annular ligament, 680, 681 Subjective information, 9 Subluxation lumbar vertebra, 519 of metacarpophalangeal joint, 147 of metatarsophalangeal joint, 431, 432 of proximal interphalangeal joint, 346-347 in pony, 1073 radiographic diagnosis of, 161 sacroiliac, 495, 507 in cutting horse, 1021 of superficial digital flexor tendon from tuber calcanei, 710-711 Subsolar abscess, 278-279 in broodmare, 1082 in Draft horse, 1060-1061

Subsolar abscess—cont’d in European Thoroughbred, 887 in foal, 1093 foot poultice for, 770 in North American Standardbred, 904 perineural nerve block for, 102 in pleasure riding horse, 1094 in show hunter and jumper horses, 968 Subsolar bruising, 968 Substance P, 284, 285 Succinylcholine, 856 Suckling, feeding systems to prevent developmental orthopedic disease in, 547 Sulfadiazine, 130, 1079 Sulfamethoxazole, 130, 1079 Sulfoxide, 690 Summits fracture, 142-143 Superficial digital flexor tendon acute-onset, severe lameness following injury to, 147, 148 anatomy of, 82, 618-622, 674-675, 684, 716 ultrasonographic, 716-717 avulsion and dislocation of in polo pony, 1013 biochemical parameters for, 616-617 bursoscopy of, 234 cellulitis, skin necrosis and necrosis of after topical application, 374 desmitis of accessory ligament of, 685 in polo pony, 1016-1017 diagnostic techniques for, 675 disease of, 676-678 imaging of, 175-182, 675-676, 716-717 infection of, 373 laceration of, 712-715 in steeplechasers, hurdlers, and point to point horses, 945 pastern injuries of, 718 subluxation and luxation of, 710-711 palpation of, 55, 56 tendonitis of. See Superficial digital flexor tendonitis. tenoscopy of, 233-234 Superficial digital flexor tendonitis, 628-643, 686 in Arabian racehorse, 931-932 cellulitis associated with, 374 as compensatory lameness, 63 cryotherapy and, 782 in curb, 703-704 in dressage horse, 642, 643 in driving horse, 1058 in endurance horse, 1000 in European Standardbred, 922-923 in event horses, 639-641 factors effecting loading of tendon in, 625 in Finnish horse, 950 in metatarsal region, 438 in National Hunt, point to point, and timber racing horses, 942-943 in pastern, 718-719 in polo pony, 1006-1008 in pony, 1074 in racehorses acute phase management of, 630 clinical signs of, 629-630 injury assessment and goals for athletic outcome, 630 North American Standardbred, 912 North American Thoroughbred, 860, 876-877 subacute phase treatment and long-term rehabilitation, 631-634 on the track, 860 ultrasonographic evaluation and categorization of injuries, 630-631 in reined cow horse, 1029 in show hunter and show jumper horses, 974-975 in show jumpers, 641-642 surgical management of, 635-639 in Three Day event horse, 993-994 Superior check desmotomy, 635-639 Support, horseshoes for, 268

Supporting limb lameness, 63-64 Suppurative myositis, 734 Supraglenoid tubercle fracture, 412-413 Suprascapular nerve damage, 413-414 Supraspinatus muscle atrophy, 413-414 Supraspinous bursa, 705 Supraspinous ligament anatomy of, 509 injury to, 515-516 Surface back disorder evaluation and, 512 in clinical history, 13 during lameness examination, 62, 71 loading of superficial digital flexor tendon and conformation of, 625 of racetrack, 862-864 National Hunt racehorse, point to point horse, and timber racing horse lameness and, 938-942 North American Standardbred lameness and, 897 North American Thoroughbred lameness and, 870 racing Quarter Horse lameness and, 927 in United Kingdom, 880 stride characteristics and, 251-252 used by dressage horse, 977-978 used by driving horse, 1051 used by event horse, 997 used by reined cow horse, 1026-1027 used by show hunter and show jumper horses, 966 Surface brachytherapy, 785-786 Surgery for angular limb deformities, 558-561 arthroscopic, 226-230 carpal, 385, 386 for cruciate ligament injury, 463 in femoropatellar joint osteochondrosis, 458 in fragmentation of proximal plantar processes of proximal phalanx, 428 for joint disease, 754 for meniscal ligament injury, 462, 463 of metatarsophalangeal joint, 426 for back pain, 521 for cervical stenotic myelopathy, 569-570 for digital flexor tendon sheath disease, 678 external skeletal fixation as, 774-777 for fibrotic myopathy, 478 for laminitis, 335-338 in primary lesion of deep digital flexor tendon within hoof capsule exploration, 308-309 for problems with estrous cycle in performance mares, 482 for scapulohumeral joint osteochondrosis, 408 for stress fracture of third metacarpal bone in racehorses, 853-854 for stringhalt, 477 for tendon laceration, 714-715 tenoscopic and bursoscopic, 230-235 for traumatic disruption of suspensory ligament in metacarpophalangeal joint, 360-361 for upward fixation of patella, 460, 477 Surgical drilling, 303 Suspensory desmitis, 663-666 in American Saddlebred, 1039 in Arabian and Half-Arabian show horse, 1046 in Arabian racehorse, 932 in barrel-racing horse, 1031-1032 body lesions, 662-663, 876, 1009, 1010 branch lesions, 663-666, 876, 921-922, 980, 1009-1010 as compensatory lameness, 63 cryotherapy for, 781-782 in Draft horse, 1065 in dressage horse, 980 in driving horse, 1053 in endurance horse, 998-999 in European Standardbred, 920-922

Index Suspensory desmitis—cont’d in European Thoroughbred, 888 extracorporeal shock wave therapy for, 826 in Finnish horse, 950 in forelimb, 654-657, 658 in hindlimb, 658-662 in metatarsal region, 437-438 in National Hunt, point to point, and timber racing horses, 943 in North American Standardbred, 910-911 in North American Thoroughbred, 875-876, 876 in polo pony, 1009-1010 radiation therapy for, 785 in reined cow horse, 1028-1029 in show hunter and show jumper horses, 970-971 stem cell and marrow components for, 673 in team roping horse, 1023-1024 in Three Day event horse, 994, 995 Suspensory ligament, 654-672 anatomy and pathophysiology of, 82, 433, 654, 716 avulsion fracture at origin of palmar annular ligament, 666, 667 in third metacarpal bone, 367-368 in third metatarsal bone, 436 biochemical parameters for, 616-617 infection of axial aspect of proximal sesamoid bones and, 668, 669 local infiltration of anesthetic solution at origin of, 122 oblique distal sesamoidean desmitis and, 670-671 palpation of, 48, 58, 434 in European Thoroughbred, 883 in North American Thoroughbred, 871 progressive atraumatic breakdown of in hindlimb, 671-672 stem cells and marrow components to stimulate regeneration of, 673-674 straight distal sesamoidean desmitis and, 668-670 thermography of, 237 on the track injury to in Thoroughbred racehorse, 860 traumatic disruption of in metacarpophalangeal joint, 359-361 Sustentaculum tali osteitis, 448 Suture material, ultrasonographic appearance of, 195 Swedging of shoe, 263 Sweeny, 1066 Sweet pea, 633 Swelling of antebrachium associated with other conditions, 398 arthritic, 606-607 assessment of using palpation, 42 asymmetry assessment in, 32, 34-35 in carpal hygroma, 392-393 as diagnostic analgesia complication, 94 in hematoma of stifle region, 468 of limbs in broodmare, 1082 in metacarpal region, 372-375 in metatarsal region, 439 over greater trochanter, 36 in pastern, 721 in superficial digital flexor tendonitis, 629 in suspensory desmitis, 664 Swimming, 636, 790, 818 Swing phase of stride, 247-248 Swinging limb lameness, 63-64 Symmetry assessment in lameness examination, 31-37 of Three Day event horse, 987 in prepurchase examination of performance horse, 959 Sympathectomy, periarterial, 302 Symphysis, 86 pubic, 484 Synacid. See Hyaluronan.

Synovectomy, 755 Synovex C 6-8, 481 Synovex S 3-4, 481 Synovial fluid in carpal lameness, 378 changes in osteoarthritis, 581, 582 in digital flexor tendon sheath disease, 675 in infectious arthritis, 598-599 normal structure and function of, 85, 572 in tenosynovitis of extensor tendon sheaths, 695 Synovial structures anatomy, 85-86 Synoviocentesis, 675 Synoviocytes osteoarthritis and, 577 structure and function of, 572 Synovitis acute as diagnostic analgesia complication, 94 of carpal sheath, 378, 685 in Finnish horse, 949 in racing Quarter Horse, 930 in steeplechasers, hurdlers, and point to point horses, 945 of distal interphalangeal joint, 312-313 in dressage horse, 981 in driving horse, 1054 perineural nerve block for, 102 in racing Quarter Horse, 929 in show hunter and show jumper horses, 970 immune-mediated, 143-144, 608 in foals, 1093 of metacarpophalangeal joint, 349-350 in Arabian and Half-Arabian show horse, 1047 in barrel-racing horse, 1032 in dressage horse, 982 in European Standardbred, 920 in North American Thoroughbred, 873 in racing Quarter Horse, 929 in show hunter and show jumper horses, 972-973 of metatarsophalangeal joint in Arabian and Half-Arabian show horse, 1047 in dressage horse, 982 of middle carpal joint in dressage horse, 982 in non-infectious arthritis, 606 proliferative, 349-350, 431-432, 608, 612 in European Standardbred, 933 palpation of, 47 in polo pony, 1008-1009 radiation therapy for, 785 radiation therapy for, 786 reactive, 608 of stifle in show hunter and show jumper horses, 973-974 synovial fluid cytology for, 582 traumatic, 608 Synovium diagnostic analgesia injection in, 99-100. See also Diagnostic analgesia. fistula of, 612 hernia of, 611 magnetic resonance imaging of, 220 normal structure and function of, 572 role of in osteoarthritis, 577 Synthetic racetrack surface, 863 Systemic lupus erythematosus-like disease, 607 T T1-weighted image, 217 T2-weighted image, 217-218 T3. See Triiodothyronine. Tachycardia in tendon laceration emergency management, 713 Tack dressage horse and, 978 pain induced by, 144 in poor performance assessment, 831 Three Day Event horse and, 991-992

1135

Tail, abnormal position of in hindlimb pain, 39 Tail stretch, 816 Talocalcaneal joint anatomy of, 440 fragments in, 444 osteoarthritis of, 443 Talocalcaneal-centroquatral joint anatomy of, 455 fragmentation of, 444 Talus anatomy of, 440 osteochondrosis of trochlear ridge of, 552-553 sagittal fracture of in North American Standardbred, 908, 909 subchondral trauma and radiolucency of, 444 Tape, casting, 773 Tarsal sheath anatomy of, 687 arthrocentesis of, 122 injuries of, 688-690 tenoscopy of, 232-234 tenosynovitis of, 687-691 palpation of, 55, 56 Tarsocrural joint anatomy of, 440 arthrocentesis of, 118-119 distention of joint capsule of, 443-444 in cutting horse, 1019 effusion in. See Bog spavin. enthesopathy of lateral collateral ligaments of, 447 luxation and subluxation of, 446 North American Standardbred lameness of, 908 osteoarthritis of, 443 in American Saddlebred, 1038 in North American Standardbred, 908 osteochondrosis of in American Saddlebred, 1038 in Arabian racehorse, 932 in European Standardbred, 923 in North American Standardbred, 908 Tarsometatarsal joint analgesic arthrocentesis of, 117, 118 false-negative response to, 135 in proximal suspensory desmitis, 658 anatomy of, 440 distal hock joint pain and, 440, 441 luxation and subluxation of, 446 osteoarthritis of in Arabian and Half-Arabian show horse, 1047-1048 in Draft horse, 1066-1067 in dressage horse, 981-982 in Three Day Event horse, 993 pain in in European Thoroughbred, 894 in reined cow horse, 1029 Tarsus, 440-449 American Saddlebred lameness of, 1037 anatomy of, 440 angular limb deformity of, 557-561 arthrocentesis of, 117-119 articular disease of, 440-443 cellulitis of, 448 in acute-onset, severe lameness, 148 in European Thoroughbred, 891 cutting horse lameness of, 1018-1019 Draft horse lameness of, 1066-1067, 1068 Finnish horse lameness of, 949-950 flexural limb deformity of, 562-565 fractures and luxation of, 444-447 in North American Standardbred, 907-908 on the track in Thoroughbred racehorse, 859 North American Standardbred lameness of, 907-909 osteitis of, 447-448 palpation of, 54-56, 57 in European Thoroughbred, 883-884 in Finnish horse, 949 peri-articular cellulitis of, 448

1136

Index

Tarsus—cont’d previously unrecognized causes of lameness proximal to, 141 soft tissue injuries of, 447 ultrasound of, 700, 701 zone designations for, 178, 179 Tarsus valgus, 29, 30, 557-561 T-CSA. See Total cross-sectional area, ultrasonographic. Team roping horse, 1021-1025 Tears of deep digital flexor tendon, 647 of intersesamoidean ligament, 297, 298, 666-667 of medial palmar intercarpal ligament, 392 muscular, 726-728 gracilis in polo pony, 1017 pectoral, 146 of scapulohumeral joint capsule, 410 Teletherapy, 784, 785 Telopeptides, 843 Temperament, 144 lameness examination and, 61-62 Temperature assessment, 59 Temporomandibular joint pain, 143 Tenascin-C, 622 Tendon. See also specific tendons. anatomy of, 85, 618-622 articular, 572 blood supply, 618, 619 cellular components, 618-619, 620, 621 molecular composition of matrix, 619-622 morphology, 618-626 assessment of in prepurchase examination of performance horse, 959 function of, 616-618 hypothesized mechanisms of degeneration of, 624-625 laceration of, 712-715 magnetic resonance imaging of, 219-220 mechanism of injury to, 622-624 modulus of elasticity of, 617 phases of healing of, 625-626 therapeutic ultrasound for, 812 thermography of, 237 types of injury to, 622 ultimate strain of, 617 ultimate tensile force of, 616-617 ultrasonographic characterization of lesion of, 173-175 Tendon boot, 992 Tendon sheath analgesia of forelimb, 113-115 hindlimb, 121-122 anatomy of, 85-86 digital flexor analgesia of, 113-114 deep digital flexor tendonitis within, in fetlock region, 645-647 tenoscopy of, 231-232 tenosynovitis of, 629 extensor tendon, conditions affecting, 695-697, 698 laceration in, 715 tarsal anatomy of, 687 arthrocentesis of, 122 injuries of, 688-690 palpation of, 55, 56 tenoscopy of, 232-234 tenosynovitis of, 55, 56, 687-691 tenoscopy of, 231-234 Tendon splitting for superficial digital flexor tendonitis, 638 in North American Thoroughbred, 877 in polo pony, 1007 therapeutic ultrasound for, 812 in Three Day Event horse, 994

Tendonitis in American Saddlebred, 1039 of biceps brachii, 411-412 common calcaneal, 709 of cunean tendon, cryotherapy for, 782 of deep digital flexor tendon, 644-647, 686 cryotherapy and, 782 in curb, 704 in pastern region, 647-648 perineural nerve block for, 102 in pony, 1074 in European Thoroughbred, 881 gastrocnemius, 709-710 radiation therapy for, 785 of superficial digital flexor tendon. See Superficial digital flexor tendonitis. thermography in, 237 Tenectomy cunean in distal hock joint pain, 443 in Draft horse, 1067, 1068 semitendinosus, 478 Tennessee Walking Horse, 1033-1034 Tenocyte, 618-619 Tenoscopy, 230-234 in annular ligament syndrome, 681 in digital flexor tendon sheath disease, 676 of tarsal sheath, 690 Tenosynovitis of carpal tendon sheath, 629 of digital flexor tendon sheath, 629, 676-678 in dressage horse, 982 in driving horse, 1055-1056 in Finnish horse, 950 in polo pony, 1015-1016 in show hunter and show jumper horses, 975 of extensor tendon, 695-697 in American Saddlebred, 1040 in foal, 1089-1093 of superficial digital flexor tendon, 677 of tarsal sheath, 687-691 palpation in, 55, 56 Tenotomy of deep digital flexor tendon, 335-338 Tenovaginocentesis of tarsal sheath, 690 TENS. See Transcutaneous electrical nerve stimulation. Tensile force of tendons, 616-617 Tension, 85 muscular, 727 Teres ligament rupture, 500 T-ES. See Total echo score, ultrasonographic. Testicular palpation, 51 Tetanus antitoxin, 714 Tetanus toxoid, 714 T-FAS. See Total fiber alignment score, ultrasonographic. TGF. See Transforming growth factor. Therapeutics, 745-826 bandaging, splinting and casting, 769-773 complementary, 792-826 acupuncture, 792-803 chiropractic, 803-811 extracorporeal shock wave therapy, 825-826 laser therapy, 812-813 magnetic and electromagnetic therapy, 813 massage, stretching, homeopathy, and herbs, 815-817, 818 osteopathy, 819-824 physical therapy and rehabilitation, 817-818 ultrasonographic, 811-812 counterirritation, 778-780 cryotherapy, 780-782 epidural analgesia for hindlimb lameness, 764-769 external skeletal fixation, 774-777 for joint disease, 746-764 biologically based, 756-757 corticosteroids, 748-749, 751, 752 glucosamine and chondroitin sulfate, 751, 753

Therapeutics—cont’d for joint disease—cont’d hyaluronan, 749-750, 753 intra-articular, 753 joint resurfacing, 756 nonsteroidal antiinflammatory drugs, 746-748, 751 pentosan polysulfate, 750 polysulfated glycosaminoglycan, 750, 753 surgical, 754-756 radiation therapy, 783-788 rest and rehabilitation, 788-791 Thermal print storage envelope, 167-168 Thermocautery, 778-780 for bucked shins in North American Thoroughbred, 876 for curb management, 702 Thermography, 236-239, 821-822 in back pain, 514 of cervical spine, 525 in muscle disorders, 724 in poor performance assessment of sports horse, 831 in prepurchase examination of performance horse, 963 in sacroiliac joint injury, 507 in Three Day Event horse, 988-989, 990 Thermoplastic adhesive, 274 Thickening in superficial digital flexor tendonitis, 629 Thigh, 471-474 palpation of, 53 Thiocolchicoside, 520 Third carpal bone non-adaptive remodeling of in North American Thoroughbred, 874-875 nuclear scintigraphy of, 209, 210 slab fracture of frontal, 387-388 sagittal, 389 subchondral lucency of, 390 Third metacarpal bone cryotherapy for periostitis of, 781 disease of in Arabian racehorse, 931 in North American Thoroughbred, 873-874 fatigue failure of. See Bucked shins. fractures of, 357-361, 364-368 in acute-onset, severe lameness, 147 in dressage horse, 983 in racehorses, 853-854, 857, 858, 889-891, 893-894, 943 osseous cyst-like lesion of, 550 osteochondrosis of sagittal ridge of, 549-550 palpation of, 47, 48, 58 in European Thoroughbred, 883 in North American Thoroughbred, 871 periostitis of. See Bucked shins. physitis of, 555 radiation therapy for new growth on, 785 Third metatarsal bone anatomy of, 433 disease of in North American Thoroughbred, 873-874 enostosis-like lesion, 437 exostosis of, 437 fractures of, 431, 432, 435-437 in acute-onset, severe lameness, 147 in European Thoroughbred, 889-891, 893-894 in National Hunt, point to point, and timber racing horses, 943 in North American Standardbred, 907 on the track in Thoroughbred racehorse, 859 osseous cyst-like lesion of, 550 osteochondrosis of sagittal ridge of, 549-550 palpation of, 58 Third tarsal bone incomplete ossification of, 543 slab fracture of in North American Standardbred, 907

Index Third trochanter of femur fracture, 500 Third-generation cephalosporins, 600 Thoracic dorsal spinous processes fracture in polo pony, 1014 Thoracolumbar spine, 509-521 anatomy and function of, 509-510 imaging of, 513-514, 515 injury of in cutting horse, 1020-1021 in team roping horse, 1025 lesions of, 514-521 muscular tension and spasm in, 727 pain in, 509-521 acupuncture for, 796 in American Saddlebred, 1037-1038 in Arabian and Half-Arabian show horse, 1047 in Arabian racehorse, 932-933 in breeding stallions, 1077-1078 in cutting horse, 1020-1021 diagnosis of, 510-514, 515 in dressage horse, 983 in endurance horse, 1001 in National Hunt, point to point, and timber racing horses, 944 in polo pony, 1013-1014 in pony, 1075 in poor performance of sports horse, 830 in show hunter and show jumper horses, 971-972 in Three Day Event horse, 992-993 palpation of, 51 in European Standardbred, 916 in performance horse, 959 standard radiographic projection and suggested extra views of, 166 thermography of, 238 Thorax palpation, 51 Thoroughbred racehorse. See also Racehorse. bucked shins in, 847-854 compensatory lameness development in, 63 European, 879-894 clinical examination of, 882-884 diagnostic analgesia in, 885-886 exostosis of second and fourth metacarpal/metatarsal bones in, 893 foot-related lameness in, 887-888 fractures of proximal phalanx and condyles of distal third metacarpal/metatarsal bones in, 893-894 history in assessment of, 882 history of sport, 879-894 imaging of, 884-885 lameness subsequent to bacterial infection in, 891-892 middle carpal joint-related lameness in, 888-889 pain associated with tarsometatarsal joint in, 894 pattern of racing in, 879-880 sales yearling, 838-839, 840 shoeing considerations for, 886-887 stress fractures of long bones and pelvis in, 892-893 subchondral bone injuries to distal third metacarpal/metatarsal bone in, 889-891 suspensory desmitis in, 888 training regimen, 881-882 undiagnosed hindlimb lameness in, 893 forelimb/hindlimb weight distribution ratio in, 5 hindlimb lameness in, 4 North American, 868-879 bucked shins in, 876 carpal lameness in, 874-875 conformation of, 870 distal hock joint pain in, 877-878 fetlock joint lameness in, 873-874 foot-related lameness in, 872-873 imaging of, 871-872 lameness examination in, 870-871

Thoroughbred racehorse—cont’d North American—cont’d myositis in, 878 osteochondral fragmentation in carpometacarpal joint in, 382-384 sales yearling, 836-837 secondary shoulder region pain in, 879 shoeing of, 872 stifle lameness in, 879 superficial digital flexor tendonitis in, 876-877 suspensory desmitis in, 875-876 tibial stress fractures in, 877 top ten common lameness diagnosis in, 870 track surface and lameness in, 870 unexplained lameness in, 872 pelvic injury in, 484-490 acetabulum fracture, 488-489 anatomy of pelvis and, 484 diagnostic techniques, 485-486 ilial shaft fracture, 487-488 ilial wing fracture, 486-487 pubis and ischium fractures, 488 treatment of, 489-490 tuber coxae fracture, 486 stress-related subchondral bone injury and osteoarthritis in, 426-428 on the track catastrophe in, 854-861 equipment used in, 856 euthanasia and insurance in, 861 management of, 855-856 public relations and media issues in, 857 during racing, 857-860 regulatory considerations in, 861 role of regulatory veterinarian in, 855 during training, 856-857 Thoroughpin, 687-691 false, 706-708 tarsal palpation in, 55, 56 3B3 epitope, 592 Three Day Event horse, 984-996 conformation of, 986 diagnosis and management of lameness in, 992-995 diagnostic analgesia in, 987-988 history in assessment of, 986 imaging of, 988-989, 990 influence of sport on lameness of, 985 lameness examination of, 986-987 prevention of lameness in, 995-996 proceeding without a diagnosis in, 989-990 saddle pressure analysis of, 989, 991 shoeing of, 990-991, 992 sport of, 984 tack considerations in, 991-992 ten most common lameness conditions in, 986 training of, 985-986 types of horses in, 984-985 Three-dimensional anatomy, 88, 89, 90, 91, 92, 93 Thrombophlebitis, jugular vein, 530-531 Thrombosis aorto-iliac-femoral, 497-499 in breeding stallions, 1079 in foals, 1089 of medial palmar vein, 373 Thrombospondin 4, 622 Thrush, 277 Thyroxine in osteochondrosis, 537, 538 Tibia enostosis-like lesion of, 453 fractures of, 445-446, 451-453, 466-467 in American Saddlebred, 1039 in European Thoroughbred, 892-893 in foal, 1085-1086 in North American Thoroughbred, 877 in pony, 1073 neurectomy of for proximal suspensory desmitis, 662

1137

Tibia—cont’d osseous cyst-like lesions of, 453-454 osteochondroma of, 453 osteochondrosis of, 552, 553 palpation of, 54, 55 in European Thoroughbred, 884 subchondral trauma and radiolucency of, 444 Tibial nerve block, 116-117 in pelvic fracture, 492 Tied-in-below-the-knee conformation, 25-26, 27 Timber hurdles, 934 Timber racing horse, 934-935, 936, 937, 938-942 Time off for superficial digital flexor tendonitis long-term rehabilitation in racehorses, 632-634 Timothy hay, 569 TIMP-1. See Tissue inhibitor of matrix metalloproteinase-1. Ting points, 794, 795, 796 Tissue local anesthetic interactions with, 94-100 ultrasound interaction artifacts, 172-173 for in vitro study of joint disease, 595 Tissue inhibitor of matrix metalloproteinase-1, 578-579 Tocopherol concentration in neurologic examination, 126 Toe crack, perineural nerve block for, 102 long, natural balance trimming for barefooted horse with, 273 seedy, 242, 277-278 Toe extension for shoe, 264 Toed-in conformation, 21-22, 24, 25 in reined cow horse, 1027 in show hunter and show jumper, 966 Toed-out conformation, 21-22, 24, 25 metatarsophalangeal joint injury and, 421 in reined cow horse, 1027 in show hunter and show jumper, 966 Toltrazuril, 130 Topical application, cellulitis, skin necrosis and necrosis of superficial digital flexor tendon after, 374 Topical lavage. See Lavage. Torsion, 85 Torticollis, congenital, 525 Total alkaline phosphatase, 843 Total cross-sectional area, ultrasonographic, 182 Total echo score, ultrasonographic, 182 Total fiber alignment score, ultrasonographic, 182-183 Total leukocytes, synovial, 582 Total protein, synovial in arthritic disease and therapeutic manipulation, 582 in infectious arthritis, 599 in tenosynovitis of extensor tendon sheaths, 695 Total white blood cell count, 695 Toxemia, laminitis and, 329 Toxic myopathy, 737 Toxicity calcium, osteochondrosis and, 541 role of in developmental orthopedic disease, 544 role of in osteochondrosis, 541 in stringhalt, 478 zinc, osteochondrosis and, 541 Track epidemiological studies of, 863-864 size of and North American Standardbred lameness, 897-898 study of accidents on, 866 surface of, 862-863 National Hunt racehorse, point to point horse, and timber racing horse lameness and, 938-942 North American Standardbred lameness and, 897

1138

Index

Track—cont’d surface of—cont’d North American Thoroughbred lameness and, 870 racing Quarter Horse lameness and, 927 Thoroughbred racehorse catastrophes on, 857-860 used by European Standarbreds, 913, 914 Track up, 61 Traditional Chinese medicine, 793, 794 Trailers, 264-265 Trainer-related factors in epidemiology of racehorse injuries, 865 Training active, 790 of Arabian and Half-Arabian show horse, 1041-1042 of barrel-racing horse, 1030 in clinical history, 12-13 of cold-blooded trotter, 947 of cutting horse, 1017-1018 of dressage horse, 977-978 of driving horse, 1050-1051 of endurance horse, 997 hill, 790 management of in back pain, 521 of National Hunt horses, 936-938 to prevent bucked shins, 852 regimen of in United Kingdom horseracing, 881-882 of reined cow horse, 1026-1027 of roping horse, 1022 of show hunter and show jumper horses, 965-966 of Standardbred European, 919 North American, 895-897 in superficial digital flexor tendonitis in racehorses, 632 of Three Day Event horse, 985-986 on the track catastrophes in Thoroughbred racehorses during, 856-857 Tranquilizers for chemical restraint in breeding stallion examination, 1077 in diagnostic analgesia, 99 in lameness examination, 62, 916 for post-anesthetic myopathy, 735 in tendon laceration emergency management, 713 Transcutaneous electrical nerve stimulation, 818 Transducer, ultrasonographic, 167 incorrect frequency, 170 Transection of accessory ligament of superficial digital flexor tendon, 635-639 hemicircumferential periosteal, 560 Transforming growth factor in bone marrow, clinical use of, 673 role of in osteochondrosis, 540 for superficial digital flexor injury management in racehorses, 634 in Three Day Event horses, 994 in tendons, 619 Transphyseal bridging, 560 Transport tetany, 737-738 Transportation, 772 following traumatic injury, 149 in tendon laceration, 714 Transverse stress fracture of distal aspect of third metatarsal bone, 436 of distal metaphyseal region of third metacarpal bone, 366-367 Trauma. See Injury. Traumatic disruption of suspensory ligament in metacarpophalangeal joint, 359-361 Traumatic myopathies, 735

Traumatic physitis, 394-395 Traumatic tenosynovitis, 695 Traveling bandage, 769 Treading forelimb, 38 hindlimb, 39 Treadmill lameness evaluation using, 73 for poor performance assessment, 832-835 for rehabilitation, 790, 818 in water, 818 Trematone-related myopathy, 737 Triamcinolone, 748, 751 for digital flexor tendon sheath disease, 677 for distal hock joint pain, 443 in barrel-racing horse, 1031 in cutting horse, 1019 for distal interphalangeal joint synovitis and osteoarthritis in dressage horse, 981 for laminitis, 328 for metacarpophalangeal joint capsulitis/synovitis, 349 for metatarsophalangeal joint osteoarthritis, 428 for superficial digital flexor injury management in endurance horse, 1000 in racehorses, 630, 634 for suspensory desmitis in dressage horse, 980 in endurance horse, 999 in show hunter and show jumper, 971 for tenosynovitis, 695 tarsal, 690 for thoracolumbar myositis in cutting horse, 1020 Trigger factors in laminitis, 327-328 Trigger point therapy, 815 Triiodothyronine, 537, 538 Trimethoprim-sulfamethoxazole before canker debridement in Draft horse, 1064 for equine protozoal myelitis, 130 for sub-solar abscess in Draft horse, 1060 Trimming for distal hock joint pain, 442-443 in laminitis management, 338 in natural balance for barefooted horse, 272-273 for navicular disease, 300-301 in show hunter and show jumper, 969 of North American Thoroughbred, 872 Triple Crown, 868 Trochanter of femur fracture, 500 Trochanteric bursa arthrocentesis, 122 Trochanteric bursitis, 472-473, 499 Trochlear ridge fracture, of stifle, 466 talus, osteochondrosis of, 552-553 Trot back disorder evaluation during, 512 high-speed treadmill analysis during, 834 lameness examination during, 61 in North American Thoroughbred, 871 Saddlebred, 1036 Trot in hand, lameness examination during, 61 in North American Standardbred, 901 Truncation artifact, 220 Trypsin, 578 Tuber coxae anatomy of, 484 fracture of, 35, 484-485 in thoroughbred race horse, 486 height of assessment of, 52 asymmetry in, 35 Tuber ischium fracture, 493 Tuber sacrale anatomy of, 484 asymmetry of, 36, 495, 503

Tuberculosis, 530 Tuberosity fracture deltoid, 405, 406 tibial, 453 Tumor. See Neoplasm. Tumor necrosis factor, 579 Tuohy needle, 766 Turf racetrack, 863-864 Turnout for metatarsophalangeal joint osteoarthritis, 427 for superficial digital flexor injury management in racehorses, 630, 633 for suspensory desmitis in driving horse, 1053 Tying up. See also Rhabdomyolysis. in acute-onset, severe lameness, 148 in driving horse, 1055 pelvic injury and in non-racehorse, 492, 493-494 in Thoroughbred racehorse, 489 in polo pony, 1016-1017 U Ulna fracture in foal, 1086 Ulnar nerve analgesic block of, 106-107 in European Thoroughbred, 886 anatomy of, 399 injury of, 132 Ultimate tensile strain, 616-617 Ultimate tensile strength, 616-617 Ultrasound, 166-194 artifacts in, 169-173 of bone, 196-197 of brachium, 401, 402 of cervical spine, 525 clinical, 182-185 of deep digital flexor tendon desmitis of accessory ligament, 651-652 primary lesion within hoof capsule, 306-307 in digital flexor tendon sheath disease, 675-676 of distal interphalangeal joint, 312 of draining tracts, 195 of elbow, 401, 402 equipment used in, 167 of European Thoroughbred, 884-885 sales yearling, 837 exercise levels and, 169 of fetlock, 189, 190, 191 of foot, 246-247 of foreign bodies, 195-196 of metatarsophalangeal joint, 424-426 in muscle disorders, 724-725 of nerves, 195 in neurologic disorder diagnosis, 129 of North American Standardbred, 902 of North American Thoroughbred, 872 in osteoarthritis, 584 of pastern, 716-718 patient preparation for, 167 pelvic, 485, 486, 487, 488-489, 492-493 of penetrating injuries, 195 in prepurchase examination of performance horse, 962-963 in proximal suspensory desmitis of forelimb, 655-656, 657 of hindlimb, 659, 660, 661 recording of, 167-168 in sacroiliac joint injury, 507 scanning technique in, 169 of shoulder, 401, 402 of skeletal muscle, 194-195 of stifle, 191-192, 193, 457 in superficial digital flexor tendonitis in event horses, 640 in racehorses, 630-631

Index Ultrasound—cont’d of tarsal sheath, 689-690 of tendon lacerations, 713 terminology and quantitative measurements in, 173-175 therapeutic, 811-812 of thoracolumbar spine, 513-514 of Three Day Event horses, 988 zone designations in, 175-182 Underrun heels foot palpation in assessment of, 43 natural balance trimming for barefooted horse with, 273 in show hunter and show jumper, 966 that accompany mediolateral imbalance, 259 Undiagnosed lameness. See Unexplained lameness. Unexplained lameness, 135-144 apparent only during riding, 142 in Arabian and Half-Arabian show horse, 1044 in Arabian racehorse, 933 in Finnish and other Scandinavian coldblooded trotters, 949 identifiable lesions and, 142 local analgesic techniques in dangerous horses and, 140 false-negative responses to, 135-137 negative responses to, 140-141 potentially confusing responses to, 137-138 in metatarsal region, 438 misinterpreted imaging findings that result in misdiagnosis, 141-142 in National Hunt, point to point, and timber racing horses, 941 neck lesions and forelimb lameness and, 141 in polo pony, 1005-1006 previously unrecognized causes of lameness proximal to carpus and tarsus, 141 referred pain and, 141 in reined cow horse, 1028 in show hunter and show jumper horses, 967 in Standardbred European, 919 North American, 902-903 that varies within and between examinations, 139 in Thoroughbred racehorse European, 893 North American, 872 of Three Day Event horses, 989-990 very intermittent or sporadic, 138-139, 140 Ungular cartilage, 323 Uphill work in upward fixation of patella management, 477 Upper forelimb lameness of in polo pony, 1016 manipulation of during lameness examination, 76-77 Upper hindlimb manipulation, 78 Upper motor neuron deficit, 566 Upright pedal view of foot, 245 Upward fixation of patella, 70, 459-460, 475-477 altered hindlimb posture seen in, 39-40 coxofemoral joint luxation with or without, 499-500 in cutting horse, 1020 in pony, 1073 stifle palpation in, 53-54 Urine retention, bone scintigraphy and, 202203 Urine sample in recurrent exertional rhabdomyolysis, 494 V Valgus deformity, 557-561 Valgus stress test, 80 of stifle, 54

Varus conformation, 39 Varus deformity, 557-561 of metatarsophalangeal joint, 421 Varus stress test, 80 Vascular system applied anatomy of, 83-84 infarction of in immune-mediated myopathy, 733 of tendon, degeneration and, 625 thrombosis of in foals, 1089 Vasodilatory therapy for laminitis, 330 Vendor, communication with in prepurchase of performance horse, 952, 953-957 Venom, cobra, 302 Veno-venoanastomoses, 284 Ventral body wall hernia, 1083 Ventral thorax palpation, 51 Versican, 621 Vertebral body radiography, 513, 514 Vertebral column. See also Cervical spine; Thoracolumbar spine. chiropractic assessment of, 806-808 osteomyelitis of, 132 thermography of, 238 Vetalog. See Triamcinolone. Veterinarian in prepurchase examination of performance horse, 951-952 in Standardbred yearling sales, 836, 840-841 in on the track catastrophe in Thoroughbred racehorse, 855 Video-image analysis, 15-16, 828 during high-speed treadmill assessment, 833-834 Views, radiographic, 244-246 Villonodular synovitis, 349-350, 431-432, 608, 612 in European Standardbred, 933 palpation of, 47 in polo pony, 1008-1009 radiation therapy for, 785 Virus isolation in neurologic disorder diagnosis, 129 Virus-associated myopathy, 733 Vitamin A, 569 Vitamin E, 1079 cervical stenotic myelopathy and, 569 deficiency of in equine degenerative myelopathy, 131 in equine lower motor neuron disease, 131 in exertional rhabdomyolysis, 730 in neurologic examination, 126 nutritional myodegeneration and, 736, 737 supplementation of for equine degenerative myelopathy, 131 for equine lower motor neuron disease, 131 Vitamin intake, cervical stenotic myelopathy and, 569 W Walk, 60, 61 back disorder evaluation during, 512 high-speed treadmill analysis during, 834 Saddlebred, 1036 Walking for desmitis of accessory ligament of deep digital flexor tendon, 652-653 following blistering, 778 hand, 790 following transection of accessory ligament of superficial digital flexor tendon in racehorses, 636 in North American Standardbred assessment, 901 in pelvic fracture management, 490 for proximal suspensory desmitis, 656, 660 ridden, 789

1139

Walking Horse, Tennessee, 1033-1034 War Admiral, 868 Warfarin, 301 Warmbloods conformation of, 958 dressage horses as, 977 Warming into lameness, 12 Warming out of lameness, 12 Water content on racetrack, 862 on training surface for reined cow horse, 1027 Weakness in cervical stenotic myelopathy, 566 Weanlings Draft horse, lameness of, 1068-1069 feeding systems to prevent developmental orthopedic disease in, 547-548 mineral requirements for, 544 Weather Finnish and other Scandinavian cold-blooded trotters and, 947 racetrack surface and, 862-863 Website, 544 Wedge pad for horseshoe, 266 in laminitis treatment, 332-333, 335 Wedge test, 80 Weight femur fracture and, 474 management of in breeding stallions, 1080 in laminitis treatment, 338 osteochondrosis and, 536-537 in overfeeding assessment, 546 Weight distribution ratio, 4, 5, 6 Weight-bearing in foot function, 250-251 in hind foot and pastern lameness, 419 in laminitic hoof care, 332 tendons for, 617 Weight-bearing oblique of distal phalanx, 246 Western blot, cerebrospinal fluid, 128 Western performance horse, 1017-1033 barrel-racing horse, 1030-1032 European, 1032-1033 reined cow horse, 1026-1029 roping horse, 1021-1026 Wet-to-dry bandage, 770 Wheat block, 105-106 White blood cell count, 695 White line disease of, 277-278 visual examination of, 242 White muscle disease, 736-738 White snakeroot-related myopathy, 737 White willow bark, 817 Whole bone stiffness measurements of third metacarpal bone, 849 Whorl bone lameness, 473 Wind galls, 47 Wind puffs, 47 Window level in computed tomography, 213 Window width in computed tomography, 213 Winging in, 69 Winging out, 69 Withers fracture, 142 in polo pony, 1014 in show hunter and show jumper horses, 972 Withers stretch, 816 Wobbler syndrome, 566-570 Wolff’s law, 154-158, 159 Wood, ultrasonographic appearance of, 195 Wound bandaging of, 770-771 of metatarsal region, 438-439 of pastern region, 347 in ponies, 1075 puncture of deep digital flexor tendon, 648 solar, 279-280

1140

Index

X

Y

Z

X-ray. See Radiography. Xylazine, 1079 for chemical restraint in cerebrospinal fluid analysis, 99 during diagnostic analgesia, 99 during lameness examination, 62 in pony, 1070 epidural, 767, 768

Yearling Draft horse, lameness of, 1068-1069 feeding systems to prevent developmental orthopedic disease in, 548 prepurchase examination of European Thoroughbred, 838-839, 840 North America Thoroughbred, 836-837 Yucca, 817

Zinc osteochondrosis and, 537, 541 requirements of for yearlings, 544 toxicity of in development of in developmental orthopedic disease, 544 Zinc/copper ratio in femoropatellar joint osteochondrosis, 458 Zone designation, ultrasonographic, 175-182