Page 1122 - Adams and Stashak's Lameness in Horses, 7th Edition

1088 Chapter 10

Perinatal and Congenital Conditions This pathology is frequently mistaken for flexural limb
deformity.
Foals may be born with musculoskeletal conditions
VetBooks.ir that result in lameness or they may develop them shortly ical evaluation. Lateral and common digital extensor
The two conditions may be differentiated with phys­
after birth. These conditions are relatively infrequent
tendon rupture may be recognized by the presence of a
but worthy of mention because historically they have
either been misdiagnosed or erroneously given a poor characteristic swelling over the dorsal lateral surface of
the carpus at the musculotendinous junction where the
prognosis. As a result, foals that might have matured rupture occurs. The limb also may readily be placed in
and had normal athletic potential have been humanely a normal position, whereas this is not possible in foals
destroyed. Lameness may be directly caused by these with flexural deformity.
conditions or it may be secondary to their occurrence. Treatment is aimed at protecting the limb from exco­
Two such conditions of the neonate are flexural riation of the dorsum of the fetlock with bandaging until
limb deformities and excessive laxity of flexor tendons, the foal acclimates to walking. Continuous splinting or
both of which are relatively common and may result in casting is not usually necessary but may be applied inter­
secondary lameness. Flexural limb deformity may pro­ mittently to facilitate use of the limb. Surgery is not nec­
duce mechanical limitations on ambulation, or it may essary or advisable because the tendons generally heal
cause pain associated with attempts to correct the uneventfully over several weeks.
deformity. The most common cause of lameness from Ruptured gastrocnemius muscle is recognized in
flexural deformity is excessive trauma to the sole of the neonates following both normal deliveries and dysto­
foot at the toe region, which causes bruising and cias, but larger foals appear to be predisposed to this
abscess formation. condition. Rupture may be partial or total. With par­
24
Flexor tendon laxity causes lameness from decubital tial rupture there is moderate flexion of the tarsus, but
sores, bruising, and abscess in the heel bulbs of the hind­ the foal can still bear weight on the limb. With a com­
feet. These may be prevented by lightly bandaging the plete tear the foal is unable to extend the limb and will
heel bulbs for protection and preventing luxation of the collapse with weight‐bearing, and the excessive flexion
distal limb by applying extended heels. of the hock with the stifle in a fixed position results
Certain structures in the neonate and young foal are in a typical, crouched position on the affected side
prone to rupture, including that of the common and lat­ (Figure 10.60). Prognosis for future soundness is good
eral digital extensor tendons of the forelimb, which usu­ with conservative treatment, providing the foal is not
ally occurs within 72 hours of birth. Foals with mild compromised with other concomitant disease pro­
flexural deformities may be predisposed to develop cesses. 24,44 Splinting is usually required, and bandages
these problems. In these contracted individuals, the con­ must be changed frequently to prevent focal pressure
dition may develop at 2–3 weeks of age. The predomi­ necrosis, adequately support the limb, and support
nant clinical sign is knuckling forward on the ankle and ambulation while healing occurs.
carpus and initially failure to advance the limb.

Figure 10.60. Excessive flexion of the hock in a foal with rupture of the left gastrocnemius muscle.