Congenital deformities are present at birth, and the cause is often unknown. Although uterine malposition of the fetus is often discussed, because of the voluminous nature of the uterus and the ability of the foal to move, uterine malposition is an improbable cause of flexural deformity in most instances. Other documented causes include exposure of the mare to influenza and ingestion of Sudan grass, locoweed, or other teratogenic agents during development of the fetus.2,3,7 Equine goiter, neuromuscular disorders, and defects in elastin formation or collagen cross-linking may be involved in the pathogenesis.
Congenital flexural deformities most commonly involve the distal interphalangeal (DIP) joints, carpus, tarsus, and metacarpophalangeal and metatarsophalangeal joints, singularly or in combination.2 Both forelimbs are usually involved, and occasionally other variations of skeletal deformities are evident, such as hindlimb deformity (windswept), spinal deformity, rye nose, and cleft palate. Sporadically occurring deformities involving the scapulohumeral, cubital, coxofemoral, or femorotibial joints may occur in combination with other congenital skeletal anomalies. Congenital flexural deformities are a common cause of dystocia in the broodmare, resulting in loss of the foal and subsequent reproductive loss of the mare.
Treatment for congenital flexural deformities varies with the anatomical location involved and severity of the condition. Therapeutic intervention for foals with severe flexural deformities associated with arthrogryposis or gross spinal deformities should be discouraged, and humane destruction is recommended. Surgical transection of the digital flexor tendons and palmar carpal fascia generally fails to alleviate this deformity. Splinting and casting is also futile, although rarely a foal has survived with limited athletic potential.
Mild flexural deformities of the carpal, metacarpophalangeal or metatarsophalangeal, or DIP joints resolve spontaneously if the foal has the ability to stand, nurse, and ambulate on its own. Most foals with mild and moderate deformities of these sites respond favorably to physiotherapy, by manually extending the limbs every 4 to 6 hours for 15-minute sessions, or forcing the foal to ambulate (Figure 59-1). Heavy bandaging, splinting or casting, and the administration of oxytetracycline can be helpful.2,8 Foals with deformities advanced enough to require assistance to stand respond more rapidly after application of a cast, which should be changed every 2 to 3 days (Figure 59-2). If a carpal deformity severe enough to prevent standing is recognized at parturition, the foal should be heavily sedated, within 30 to 45 minutes, and full-leg casts should be applied with the limbs placed in extension. These should be changed within 24 hours and reset. Generally a rapid response is seen after the first or second application of casts. If the foal develops any complications with the casts or becomes distressed, casts should be removed. Commercially available articulating braces (Almanza Corrective Boot, www.redboot.com.ar/home.html; Equine Bracing Solutions, Trumansburg, New York, United States; Dynasplint Systems, Serverna Park, Maryland, United States) are available and allow adjusting the degree of extension in a specific region of the limb (Figure 59-3). As with all splints, caution must be exercised to prevent pressure sores. It is important to assist the foal in nursing and to provide supportive care in an intensive neonatal facility, because these horses are at high risk for developing complications with other body systems.
Oxytetracycline (2 to 4 g) administered slowly intravenously is also beneficial, but it should not be used in a neonate until serum creatinine is within normal limits.8
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