Diagnosis and treatment of surgical conditions of the carpal canal
Lameness originating in the carpal sheath has probably been underestimated and with the improvement in diagnostic techniques, several pathological conditions have been addressed as causes of carpal canal swelling and low grade lameness. Classic tenosynovitis, radial osteochondroma, tendonitis and myotendonitis of the flexor tendons and fracture of the accessory carpal bone have been recognized as causes of carpal canal syndrome. Recently, radial physeal caudal spikes, exostoses developing at the level of the closed physis, are reported as a cause of damage to the deep digital flexor tendon (DDFT) and as being responsible for carpal tenosynovitis with the same pathogenesis reported for the osteochondroma, from which they differ radiographically and histologically. Both kind of exostoses mentioned can be responsible for deep digital flexor tendon damage and consequently, for the clinical signs of tenosinovitis and mild lameness. In the author’s experience, carpal canal tenosinovitis is often related to the caudal exostosis, which can be under diagnosed especially if of small size.
Carpal sheath tenosinovitis results in intermittent and eventually chronic distension of the carpal sheath well clearly visible on the proximal lateral aspect with distension of its recess located between the ulnaris lateralis muscle caudally and lateral extensor tendon cranially. In more severe cases additional swelling can be encountered on the proximal medial aspect other than, obviously, on the distal recess in the proximal matacarpal area. Occasionally, the horse can be lame more often after the exercise when intense bleeding fluid is obtained through the centesis; this finding is frequently encountered in case of distal radial exostosis, which impinge and damage the DDFT. Verification of carpal sheath lameness requires intrathecal anesthesia. Follow-up radiographs are necessary to demonstrate the presence of ostochondroma or physeal spike, which aren’t always well noted especially if small in size. In these cases, the ultrasonography is of extreme value for the definitive diagnosis other than essential to evaluate the damage to the DDFT. It is predictable that the synovial effusion of the sheath, in the presence of an osteocondroma or physeal spike, is caused by the exostosis damaging the soft tissue structures and in particular the DDFT, due to its location next to the site where the osteochondromas are typically encountered.
The characteristic site where the osteochondroma develops is axial to the medial edge of the caudal cortex of the distal metaphysis of the radius although the lateral location is reported, and this explains the difficulty in detecting, radiographically, the small exostoses on the latero-medial and dorsomedialpalmarolateral oblique (Dm-PlO) radiographic views for the superimposition of both edges (lateral and medial) of the caudal cortex of the radius (LM views) due to its concave shape. On the other hand, the small size of the exostosis is clinically very important for their frequently sharp shape, as shown in our cases, where the osteochondromas were responsible for the damage to DDFT, in these cases ultrasonography can be quite accurate as diagnostic procedure even more than the radiography. Ultrasonography can also highlight primary tendinitis lesions encountered in the proximal metacarpal area especially of the superficial digital flexor tendon with its enlargement and core lesion, which is a good indication for carpal retinaculum desmotomy. In the proximal part of the sheath, the muscolotendineus junction is not to be mistaken for damaged tendons.