Contracted flexor tendons are probably the most prevalent abnormality of the musculoskeletal system of newborn foals and calves. An autosomal recessive gene causes this condition. In utero positioning may also affect the degree of disability.
At birth, the pastern and fetlocks of the forelegs and sometimes the carpal joints are flexed to varying degrees due to shortening of the deep and superficial digital flexors and associated muscles. A cleft palate may accompany this condition in some breeds. Slightly affected animals bear weight on the soles of the feet and walk on their toes. More severely affected animals walk on the dorsal surface of the pastern and fetlock joint. If not treated, the dorsal surfaces of these joints become damaged, and suppurative arthritis develops. Rupture of the common digital extensor can occur as a sequela. This condition should be differentiated from arthrogryposis.
Mildly affected animals recover without treatment. In moderate cases, a splint can be applied to force the animal to bear weight on its toes. The pressure from the splint must not compromise the circulation, or the foot may undergo ischemic necrosis. Frequent manual extension of the joints, attempting to stretch the ligaments, tendons, and muscles, aids in treating these intermediate cases. Severe cases require tenotomy of one or both flexor tendons. A plaster-of-Paris cast may also be indicated in some cases. Extreme cases may not respond to any treatment. (See also flexion deformities, Flexion Deformities.)
