Operative Orthopedics of the Fetlock Joint of the Horse: Traumatic and Developmental Diseases of the Equine Fetlock Joint

MILNE LECTURE Part I: Operative Orthopedics of the Fetlock Joint of the Horse: Traumatic and Developmental Diseases of the Equine Fetlock Joint Larry R. Bramlage, DVM, MS The invitation to present the Frank J. Milne State-of-the-Art Lecture is a special degree of flattery for one’s career. The flattery comes with a degree of responsibility to present the current state of practice and, to a certain extent, challenge doctrine and lay out theories of practice that result from one’s years of practice in a specialty area. The lecture should, therefore, enjoy the possibility of moving the “state of the art” forward. In areas where the author of this manuscript has a view of pathology that varies from the current concepts, the views will be presented as theories based on years of observation and, where possible, controlled studies. The object is to lay them out for examination and challenge or refutation by future practitioners of this specialty. I want to thank the members of the American Association of Equine Practitioners for this opportunity. Author’s ad- dress: Rood and Riddle Equine Hospital, PO Box 12070, Lexington, Kentucky 40580; e-mail: [email protected]. © 2009 AAEP. “An orthopedic surgeon must be able to think like a bone, and feel like a joint.”—Anonymous 1. Introduction constructed like a suspension bridge with structural The fetlock joint is, arguably, the joint that makes a members incapable of supporting its loads until the horse a horse. Its unique anatomy and physiology appropriate ligament tenses and supports the bone. allow the high-speed, medium-distance activity that It is the most fascinating of the complex of joints has lead to the unique place for the horse in society, that allows a horse to move at high speeds and over historically and currently. Its evolution allowed rough terrain with little conscious concern. Be- the horse to become a single-digit quadraped. The cause of its complexity, it is vulnerable to a variety fetlock is a joint, a shock absorber, an energy storage of traumatic and developmental problems that are system, and a stabilizer of the distal limb.1,2 It is the veterinarian’s purview. This paper will discuss the traumatic and developmental diseases of the fetlock joint and concen- Unreferenced statements are the opinion of the author. trate on the physical causes and surgical treatment NOTES 96 2009 ր Vol. 55 ր AAEP PROCEEDINGS MILNE LECTURE of diseases of the fetlock joint. Space and time lim- Degenerative arthritis certainly will occur if the itations will preclude details of surgical technique inciting cause is left unattended and the destruction for most procedures. Concepts will be presented progresses to the point that it will proceed unabated and surgical techniques will be referenced where even if the cause is removed. But, fortunately, possible. lameness and decreased performance usually occur in horses in strenuous activities before the joint 2. Defining the Problem reaches this state, providing the opportunity for diagnosis and treatment of the primary disease before Short of a fracture needing the reconstruction of an it becomes irreversible. articular surface, the majority of clinical problems in The clinical signs can be subtle, especially if the the fetlock joint present a risk for secondary degen- level of the horse’s activity is moderate. In the erative arthritis as their sequelae. To reach the author’s experience, the attending veterinarian for point of a decision to treat the fetlock joint surgi- high-level equine athletes has an advantage in that cally, we must be able to understand the concept of horses in heavy work will show more significant progressive degeneration, to assess the current sta- signs than horses in light activity, although the tus of the joint, and to understand when the surgeon joint’s response is the same in total. High-level can make a difference. activity elevates the rate of debris shedding and Primary degenerative arthritis is rare in the 3 magnifies the joint response, but hypothetically, the horse. What we see in the horse is degenerative amount of debris shedding seems to be a direct prod- arthritis secondary to an insult of traumatic or de- uct of the severity of the problem and the activity velopmental origin. The overwhelming volume of level of the horse. Horses with small problems or literature in recent years has concentrated on the low levels of activity may shed debris at a rate that biology of the degenerative arthritis cycle. This pa- causes a subtle joint response, creating lameness per will concentrate on debris in the joint, the re- that remains subclinical. But low-level clinical sultant physical damage, and the biologic responses 3,4 signs are indications for concern and eventually, can that it initiates. cause acute significant lameness, because, in the The physical debris liberated into the joint as part author’s opinion, when debris shedding approaches of the original insult and by the joint’s attempt to a critical mass, the clinical damage will be similar. heal mediates most of the ongoing damage after a The need for treatment is obvious with acute dam- traumatic or developmental osteochondral frag- age such as a dorso-medial proximal phalanx (P-I) ment. If the cause is developmental or traumatic, chip fracture of the fetlock joint in a racehorse, be- the secondary reaction of the joint is remarkably cause the debris shedding is acute, the damage to 5 similar. So, it follows that the treatment will be the joint is rapid, and it causes lameness early in the similar as well. When one examines the reaction of course of the disease. But, a show horse or a plea- the joint to a traumatic disease such as an osteo- sure horse with a similar lesion may show only mild chondral fragment or to a developmental abnormal- signs, such as effusion and pain on flexion, but no ity such as an osteochondritis dessicans (OCD), the lameness. Although the debris shedding may be place where the two inciting causes are similar is in slower in less strenuous activity, clinical observa- the shedding of debris into the joint. tion suggests slower shedding causes lameness and Debris is physical (particulate) and biologic (in- causes joint damage after a comparable amount of flammatory cytokines/mediators of inflammation debris is shed. that are liberated by the chondrocytes and synovio- The need for treatment in the racehorse is obvious cytes, and inflammatory cells recruited to the joint when it cannot perform because of lameness. The by response to the physical insult). As the debris is need for treatment for a similar injury in the horse liberated the joint responds to the insult. Injection of less strenuous activity may be less clear when of cartilage particles experimentally can create sy- debris shedding causes only the synovial effusion, novitis and mechanical injury to cartilage, but bone but the horse can still perform. The permanent debris is likely more important and more damag- damage accumulating in the joint is less obvious, ing.6,7 Removal of the inciting lesion and its asso- because the rate of damage is slow but the end effect ciated debris allows the joint to return normal if the is no less severe. After the same amount of debris secondary arthritis has not reached the critical is liberated, although it takes a much longer time, threshold of self-perpetuating degeneration. the end result is equally severe.8 Degenerative joint disease (DJD) has sometimes The determination of the need for treatment in erroneously become a “catch all” for any change seen the pleasure or working horse with subclinical dis- on radiographs. Most joint inflammation seen in ease is more difficult. Not all horses’ careers are the equine athlete is not degenerative, especially in valuable enough to warrant surgical intervention for young horses; it is the response to traumatic or all conditions. Simply the fact that the horse can developmental insult. The response to trauma or a perform is not an indication that the fragment is developmental OCD lesion is often reversible early innocuous, especially if the horse requires ongoing in the course by removing the inciting cause, and intra-articular therapy to mitigate the signs. Often therefore, it is not degenerative. a fragment will be tolerable for a prolonged period of AAEP PROCEEDINGS ր Vol. 55 ր 2009 97 MILNE LECTURE time, especially with intra-articular medication. to a deficit in proteoglycan balance, but simple pro- If the horse is easily replaceable or its use can be teoglycan depletion is reversible. easily changed, then the decision may be to tolerate The lubricating function of the proteoglycan pro- the problem. But, if it is unacceptable to risk hav- tects the collagen in the normal joint. In the dis- ing the horse’s disease progress and potentially eased joint, the proteoglycan becomes depleted, and shorten the athletic career, then fragment removal the collagen becomes exposed and vulnerable. So, is the best treatment. So, each diagnosis of poten- any measure that preserves proteoglycan function, tial damaging traumatic fragmentation or develop- its lubrication of the cartilage surface, and there- mental bone malformation must be evaluated in fore, its protection of the collagen is likely worth- light of the long-term effect on the horse’s career and while to consider for the prevention of collagen performance level. The decision to remove or to degeneration and degenerative joint disease/degen- tolerate the presence of a fragment needs to be an erative arthritis. This is where the disease-modi- active one and not simply a matter of assuming that fying medications have an important potential for minimal clinical lameness means no harm.

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