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Acutely developing carpal deformities are a common problem in medium to large, rapidly growing puppies. The condition has been referred to as carpal hyperextension, carpal hyperflexion, carpal flexural deformity, or, most recently, carpal laxity syndrome (1). It involves excessive hyperextension or hyperflexion at the carpus, often with some varus or valgus deformity (Figure 1). Affected puppies are most often between 6- to 12-weeks old, but cases can rarely be seen as late as 7 mo of age (1,2). There appears to be some predisposition in male puppies with many breeds represented. Reports list dobermans and shar peis as being over-represented (1). Affected dogs are not in pain, but may display a mechanical lameness if the deformities are severe enough. Aside from the obvious deformities, the results of physical examination, radiography, and clinical pathologic testing of all sorts are unremarkable.
The cause of carpal flexural deformity is unknown. It has been suggested that this condition represents a temporary imbalance in growth rates between the bones and tendons of the front limbs. If the bones grow more rapidly than the flexor or extensor tendons one can imagine how these deformities would occur. Other proposed etiological factors include genetic influences, malnutrition, or “over-nutrition” of dietary energy or vitamin and minerals. Little evidence exists to support any of these theories.
The range of proposed therapies is also wide and includes rearing the puppy on surfaces with good traction, providing a balanced diet, providing a diet with less caloric energy than conventional puppy foods, splinting the limb, NOT splinting the limb, regular exercise, restricted exercise, or benign neglect (1). Again, little or no evidence exists to buttress any of these recommendations, save for the well-accepted observation that splinting of limbs in young pups tends to cause hyperextension rather than resolve it.
What is clear is that the prognosis for these puppies is almost always very good. Nearly all will return to normal, regardless of treatment (or lack of same) within 4 wk; most are resolved in the first 2 wk (1). The rare exception seems to be in cases characterized by severe carpal hyperextension alone. While most of these cases will return to good function without major treatment, their course may be longer and they may not resolve completely.
Another source of forelimb lameness centered in the carpal joint area is stenosing tenosynovitis of the abductor pollicis longus muscle (3).
The abductor pollicis longus muscle originates on the lateral surface of the proximal radius and ulna, crosses the extensor carpi radialis muscle in the region of the distal radial metaphysis, passes through a tendon sheath, under the medial collateral ligament of the carpus and inserts on the proximal aspect of metacarpal I (4). Chronic strain of the tendon leads to a fibrotic, or occasionally ossifying, tenosynovitis which restricts movement of the tendon in its sheath inducing pain and lameness. Affected dogs are generally large breeds that present with mild to moderate forelimb lameness. There is usually palpable swelling or thickening of the medial metaphyseal area of the distal radius and proximal carpus combined with pain on hyperflexion of the joint. Radiographic signs may show soft tissue swelling of the same region along with boney proliferation in the area of the radial styloid (Figure 2). The condition can be bilateral. A similar condition, De Quervain’s tenosynovitis, has been described in humans, and is associated with repetitive thumb movements such as in video game enthusiasts, for example. The diagnosis in dogs is generally made on radiographs of the affected area combined with appropriate clinical signs.
Non-steroidal anti-inflammatory medications are seldom of much help in relieving the symptoms. In mild to moderate cases, especially those that are not chronic, injections of long-acting corticosteroids can be very helpful. Maximum doses of 20 to 40 mg methylprednisolone acetate (Depomedrol; Upjohn, Mississauga, Ontario), depending on the size of the patient, can be injected into the area of the tendon sheath on the distal medial surface of the radius in the area of the radial styloid. The treatment can be repeated in 2 to 3 wk. Some advocate splinting of the carpus in the interim although the importance of this is unclear, especially since it does not appear to be important and has generally been abandoned in the treatment of the condition in humans (3).
In chronic cases, or in the event of poor results with medical management, surgical release of the tendon sheath can be performed. This is accomplished through a longitudinal incision in the area of the radial styloid which identifies the tendon and its sheath. The sheath is incised and fibrous or osseous adhesions are released until the tendon is seen to freely move. Surgical tendonotomy has been associated with relief of clinical signs but also appears to lead to the development of significant carpal osteoarthritis. This suggests that the abductor pollicis longus tendon contributes to carpal stability. Consequently, tendonotomy cannot be recommended as a primary form of surgical therapy (3).
The author thanks Dr. Cheryl Good for Figure 1.
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