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Congenital and Acquired Orthopedic Disorders in Foals
by Alan J. Ruggles, D.V.M., Equine Veterinary Surgeon
Rood and Riddle Equine Hospital, Lexington, Kentucky



Orthopedic problems in foals can be both congenital and acquired. Congenital problems are present at birth and are usually obvious. Acquired deformities occur some time after birth. Congenital angular (knock-kneed or bow-legged) and flexural (relaxed or contracted tendons) deformities can lead to difficulty in delivering the foal (dystocia) and, in some cases, necessitate Cesarean section.

Many foals are born with some degree of flexural or angular limb problem. The most common appearance is a degree of flexor laxity (loose tendons) and/or a mild carpal (knockkneed) and/or tarsal (cow-hocked) angular deformity. Fortunately, many of these deformities self correct with exercise and age and should be considered normal findings in a newborn foal rather than manifestations of developmental orthopedic disease. Likewise, congenital flexural deformity of the fetlock (metacarpal/tarsal phalangeal) joint, coffin (distal interphalangeal) joint, and carpus may be present. Mild forms of these conditions will usually self correct with age and exercise.

Developmental Orthopedic Disease
Acquired conditions, such as moderate to severe angular deformity, flexural deformity, physitis, and osteochondrosis (OC), fall under a broad category of disorders referred to as developmental orthopedic disease. Developmental orthopedic disease (DOD) is recognized as an important problem in juvenile horses. This disease is not a disease the foal catches from another horse, but rather a metabolic disorder the foal or weanling develops. Developmental orthopedic disease can lead to conformational abnormalities, joint swelling (effusion), and/or lameness.

Developmental orthopedic disease can be caused by many factors and more than one factor may be responsible. Some factors which have been identified as being related to DOD include dietary imbalances, genetic predisposition, trauma, and rapid growth rates. Recognition and early intervention are the keys to successful treatment and, whenever possible, preventative measures should be taken.

Various manifestations of DOD are seen most prevalently in fastgrowing foals on a high plane of nutrition. Studies have implicated high-carbohydrate (high-grain) diets and diets low in copper or high in zinc (which competes with copper uptake) as being associated with the development of DOD. As a preventative measure, it is essential to feed pregnant mares and young horses appropriate amounts of high-quality feed (hay and concentrates) including trace minerals to meet their nutrient needs. Although this seems obvious, the pressures of showing young horses and preparing sales yearlings do not always allow this to occur. In cases of DOD, it is a very common historical finding that the weanling or yearling had recently gone through a growth spurt, even when on a proper diet. This occurs most frequently in cases of flexural deformity (contracted tendons). This implicates both dietary and possible genetic factors responsible for fast growth as important causes in the development of DOD.

Clients frequently ask about the genetic implications of DOD. It is difficult to determine why an individual horse develops DOD. It is even more difficult to predict whether any of its offspring will develop DOD. Moreover, it is impossible to predict if an identical breeding, which produced an affected animal, will produce another horse with DOD. Some studies have made a genetic link to some forms of osteochondrosis. As a general rule, we do not consider DOD to be strictly inherited, so no breeding restrictions are generally recommended. If, however, a specific mare or stallion or a specific breeding consistently produces affected foals, common sense would dictate to avoid such a breeding.

Trauma is a potential cause of damage to growing cartilage. Damage to the growing cartilage at the joint or at the growth plate can lead to osteochondrosis or angular deformity. If trauma is suspected, radiographic evaluation may aid diagnosis.

It is often impossible to determine which factors contributed to DOD in a foal. However, some things should be considered. If the incidence of DOD on a farm is more than sporadic, then nutrition, feed management, and breeding programs should be examined. It may not be possible to change the broodmare pool or stallion, but one can certainly provide proper amounts of a well-balanced ration in an attempt to eliminate any nutritional or feed management causes of DOD.

Specific Disorders
Flexor Laxity .....Many foals are born with flexor laxity, or looseness of their tendons. Flexor laxity is a congenital disorder and not a manifestation of DOD. Usually, it is most obvious in the hind limbs with the fetlock dropping close to the ground, and occasionally the toe will lift off the ground when the foal is bearing weight on that leg. In general, this laxity self corrects over a few days as muscle tone improves with exercise. In some circumstances, the laxity is severe enough to prevent the foal from getting up to nurse or is such that the back of the fetlock develops abrasions. In these cases, lowering the heels with a rasp or using glue-on shoes with extended heels and/or using compounds, such as Equilox,ョ* are helpful in providing heel support. Exercise should be encouraged, but limited to prevent fatigue. The use of bandages (except to protect the soft tissues) and splints is generally counter indicated, since they encourage further laxity. The use of casts is discouraged. Most foals improve significantly once normal loading of the flexor tendons occurs.

Flexural deformity (contracted tendons) of the coffin joints in a weanling. This is an acquired deformity in this foal, which was normal at birth. Flexural Deformity (contracted tendons) Flexural
deformity can be congenital or acquired. The congenital form may involve the carpus, fetlock, and/or coffin joints and is not a manifestation of DOD. Acquired flexural deformity of the coffin joint typically occurs in four- to eight month- old horses (see Figure 1). Flexural deformity of the fetlock joint occurs in eight- to fourteen-month-old horses. Acquired flexural deformities of the fetlock and coffin joints are manifestations of DOD.

In neonates with congenital flexural deformity, exercise, splints, casts, and oxytetracycline have been used to achieve tendon laxity. In mild cases of flexural deformity, corrective hoof trimming and exercise are often curative. Polyvinyl chloride (PVC) splints placed over a padded bandage are used to place the limb in a weight bearing position. In is important to reset the splints daily and to use well padded bandages to prevent rub sores which easily occur in foals. Splints may be placed in the morning and removed at night. The procedure should be repeated daily. Casting will cause flexor tendon laxity. Casts should not be left on longer than 10 days, and early removal may be necessary if a cast rub is suspected.

Acquired flexural deformity of the coffin joint is usually seen in foals between four and eight months of age and is associated with large, fast-growing foals on a high plane of nutrition. These foals may appear completely normal until they develop this deformity, usually associated with a rapid period of growth. Nonsurgical methods of correction, chosen for mild cases, include extended toe shoes, phenylbutazone, and exercise. In cases which are moderate to severe in nature or unresponsive to medical treatment, surgically incising the inferior check ligament is recommended. Correction after this procedure is usually dramatic and immediate. Prognosis for athletic soundness is good after correction. Corrective shoes usually are necessary for four to eight weeks post-operative. Early recognition and intervention are the keys for optimum results.

Acquired flexural deformity of the fetlock joint is usually seen between eight and 14 months of age and is also associated with large, fast growing foals on a high plane of nutrition. In general, nonsurgical methods are only helpful with mild cases and consist of raising the heel with a wedge pad, phenylbutazone, and exercise. For cases which are moderate to severe or unresponsive to medical treatment, surgical correction by making an incision in the superior check ligament is recommended. To achieve maximize tendon/muscle unit lengthening in severe cases, an incision in the distal check ligament and splinting are often combined with making an incision in the proximal check ligament.

Angular Deformities Most foals are born with some degree of ?cow-hocked? (tarsal valgus) and/or ?knock-kneed? (carpal valgus) deformity. This is generally considered normal. As the foal matures,
many angular deformities completely improve. Moderate to severe (>10 degrees) valgus deformities that are still present at six weeks are considered abnormal and require evaluation (see Figure 2). Radiographs are required to diagnose the source of the problem and to ensure the carpal bones have developed normally.

Fortunately, most of the bony causes of angular limb deformities occur in the growth plate, which are surgically correctable.

Growth acceleration is induced by a procedure known as periosteal elevation and transection. The accelerated growth occurs on the operated side and overcorrection is not possible. Surgical correction for fetlock deformities should be performed before eight weeks of age and for carpal deformities by four months of age. The earlier the surgery is performed, the more rapid the correction; however, case selection is important since some deformities will self correct. In cases of severe angular deformity, it is necessary to stop the growth on one side of the leg by the use of screws and wires. Removal of the screws and wires is necessary when the leg straightens to prevent overcorrection. This procedure is often combined with periosteal elevation and transection on the opposite side of the leg.


Osteochondrosis (OC) is a disorder of the growing horse caused by failure of cartilage to form bone. All limb bone is originally cartilage which, through the process of mineralization, becomes bone. This process, called endochondral ossification, occurs at the growth plates. When most people think of a growth plate, they think of the areas at the ends of a long bone (the radius, for example) which are
responsible for longitudinal growth of the bone. There is another type of growth plate associated with the joints called the articular growth plate. The cartilage at these growth plates also undergoes the process of endochondral ossification. If this process does not occur, then bone is not properly formed and fragments of bone and cartilage may become loose or cysts may form. The result is joint swelling (see Figure 3). The degree of lameness present is variable and is dependent upon the site of abnormality and degree of joint swelling.

Diagnosis of OC is by evaluation of clinical signs and radiography. Osteochondrosis can occur anywhere cartilage forms bone, including the articular growth plates of the neck vertebrae. Some cases of Wobbler?s Syndrome are caused by OC. In general, however, OC is found in limb joints. Commonly affected joints include the hocks, fetlocks, and stifles. The carpus (knee), shoulder, elbow, and hip are less likely to be affected. When a joint is found to be affected, radiographs of the corresponding joint on the opposite limb should be taken. In approximately 50% of the cases, a less severe form of OC will be present in the corresponding joint of the opposite leg. Most horses are between six months and two years when the signs of OC become obvious. In some circumstances, the clinical signs do not become obvious until the horse is placed in a training program.

When a diagnosis of OC is made, consideration should be given to surgical removal of the abnormal cartilage and bone. With the advent of arthroscopic surgery, most OC lesions can be removed easily and completely through minimal incisions. Prognosis varies depending on the joint involved and site of the lesion within the joint. In general, a good (80%) prognosis for full athletic soundness is possible for horses with lesions of the hock and fetlock and with most stifle lesions. Lesions of the shoulder and cysts within the stifle have a lower prognosis due to the location within the joint. Most joints have a significant improvement in cosmetic appearance after surgery. In some cases where joint swelling has existed for a few months, complete resolution of the joint swelling may not be possible due to loss of joint elasticity.

Congenital and acquired orthopedic disorders commonly occur in foals. Developmental orthopedic disease is the most important cause of conformational, cosmetic, and functional abnormalities in the growing horse. Prevention, early recognition, and prompt intervention are the keys to successful management of DOD. In an affected horse, a specific cause may be difficult to determine. When herd problems are found to exist, nutritional imbalances and genetic factors should be considered. Well-balanced rations and the availability of minerals are important to help prevent DOD in growing horses. When necessary, surgical correction of angular and flexural deformities and osteochondrosis is successful in most cases.

*Not a trademark of ADM Alliance Nutrition Inc.


ADM Alliance Nutrition, Inc. , a wholly owned subsidiary of the Archer Daniels Midland Company