The Management of Congenital and Acquired Flexural Deformities

Acquired flexural deformities of the coffin and fetlock joints are an important problem in foals and young horses, respectively. Deformities at the coffin joint can lead to clubfoot and caudal heel syndrome, while deformities at the fetlock joint can lead to degenerative joint disease. This issue of Large Animal Veterinary Rounds discusses the etiology and treatment of flexural deformities.

Acquired flexural deformities of the coffin and fetlock joint are well-recognized developmental orthopedic conditions in foals and juvenile horses. Early descriptions termed the condition “contracted tendons”; however, this is a misnomer, since tendons have little capacity to contract. In the truest sense, muscle contraction leads to flexion and persistent flexion leads to a state of contracture. Abnormal flexion at the coffin joint generally occurs in foals <4 months of age, whereas involvement at the fetlock joint typically develops in juvenile horses between 10 and 18 months of age. The condition is frequently bilateral.

Etiology

When first described, acquired flexural deformities were attributed to an imbalance of growth between the long bones of the limb and the soft-tissue structures, specifically, the digital flexor tendons and accessory ligaments of the deep digital flexor (DDF) and superficial digital flexor muscles. Early support for the “imbalance of growth” theory was based on knowledge of the periods of growth in the metacarpus and radius.While growth may play a role, the imbalance theory fails to explain the sudden onset of the condition at a time when long bone growth has essentially stopped. It is known that growth of the metacarpus is minimal after 90 days of age; yet, flexural deformities at the coffin joint develop after that time.

Previously, animals with unilateral involvement were believed to have developed flexural deformity secondary to an injury, resulting in a period of reduced weight bearing on the affected limb. Proponents of this pathogenesis believed that during periods of reduced weight-bearing, the softtissue structures on the flexor surface of the limb become shortened because they are not repeatedly stretched during the stance phase. Firth dispelled this theory by clearly demonstrating that failure to bear weight alone does not result in the development of a flexural deformity.1

Acquired flexural deformities have often been associated with high-energy diets and foals pushed for development in preparation for autumn futurities were thought to be particularly at risk. In humans, limb pain associated growth is referred to as “growing pains.” Most clinicians now believe pain is likely the precipitating factor in the development of acquired flexural deformities in horses. A natural reaction to limb pain is “stenting” or persistent contraction of the muscles in the limb. The stronger digital flexor muscles overcome and fatigue the extensors, resulting in abnormal flexion at the coffin or fetlock joints. The capacity of the coffin and fetlock joints to resist flexion is determined not only by the opposition of the digital extensor muscles, but also by the simple lever arm mechanics of the individual joints. In foals, mechanical resistance to flexion of the coffin joint is initially less than that of the fetlock joint. As the hoof grows – effectively lengthening the lever arm of the coffin joint – the fetlock becomes easier to flex than the coffin...