Postural Deformities

Carter E. Judy • John Maas

A postural deformity in horses or ruminants is an abnormal stance caused by neurologic deficit, pain, or a musculoskeletal problem. Postural deformities can range from subtle confor­mational faults such as broken forward foot axis to severe and unusual positions, such as when the animal is camped out in front.

Mechanisms of Postural Deformities

Postural deformities can be either congenital or acquired and result from maldevelopment, trauma, or disease. Congenital deformities may be caused by tendon contracture or laxity, osseous malformation, and hypoplasia or aplasia of osseous structures or soft tissues. Acquired deformities are most often caused by trauma or disease. Disuse atrophy secondary to an unrelated musculoskeletal abnormality can result in abnormal posture. Occasionally diseases affecting proprioception and consciousness may cause an abnormal stance that appears as

■ TABLE 13.4

■ BOX 13.4

Examples of Postural Deformities and Possible Origins for Horses

a postural deformity (e.g., head pressing) but is unrelated to neurologic pain or a musculoskeletal problem.

Approach to Diagnosis of Postural Deformities in Horses

A history can help the examiner determine if a postural deformity is congenital, as with arthrogryposis, or acquired. Because most postural deformities in horses (Box 13.4) arise from traumatic injuries or overuse, a complete lameness examination is essential. Occasionally a postural deformity does not cause lameness; in these instances the veterinarian must consider nontraumatic causes associated with abnormal development, improper nutrition, and seemingly unrelated disease such as carpal valgus deformity.

Diagnosis of the cause of a postural deformity begins with a detailed description of the deformity and assessment of the position and asymmetry of the anatomic structures involved. If the nature and severity of the deformity cannot be determined by direct observation, palpation and manipulation of the affected structure are required. Radiography and ultrasonography can also assist in the diagnosis and provide information on which to base treatment recommendations and prognosis.

Approach to Postural Deformities in Ruminants

Sarel R. Van Amstel • Jan K. Shearer

The causes of postural deformities in cattle vary widely and may be congenital, nutritional, environmental, traumatic, and infectious. History, visual inspection, manipulation, and palpa­tion are important in the diagnosis of postural deformities in ruminants. Postural deformities in ruminants including the origin are shown in Box 13.5.

Overall symmetry of the limbs may be changed because of swellings originating from muscle, bones, or joints and muscle

Causes of Postural Deformities in Horses

Common Causes

Infections of the foot Hoof wall defects

Fractures

Septic (infectious) arthritis Secondary (degenerative) joint disease Laminitis

Angular limb deformities Osteomyelitis

Sprain

Strain

Tenosynovitis Contracted tendons (flexural deformity) Laxity of flexor tendons in foals

Tendon rupture, damage, tendonitis (bowed tendon) Upward fixation of the patella (locking patella) Epiphysitis

Septic tenosynovitis

Muscle injury, soreness, bruise, trauma, compartment syndrome Navicular disease

Cuboidal bone hypoplasia

Less Common Causes

Disruption of the suspensory apparatus (broken down) Lateral or medial patellar luxation

White muscle disease (nutritional myodegeneration) Brucellosis

Sesamoiditis

Hypertrophic osteopathy or osteodystrophy Ankylosis or arthrogryposis

Luxation or subluxation Snakebite

Equine monocytic ehrlichiosis (Potomac fever) Spondylitis, Cliskospondylitis

Spinal or vertebral neoplasia

Tick paralysis Vertebral column malformation

Nigropallidal encephalomalacia (star thistle poisoning) Postanesthetic equine myasthenia

Abscess caused by Clostridium perfringens Hyperparathyroidism

Osteomalacia, osteodystrophy (rickets)

Uncommon Causes

Lupus erythematosus (rheumatoid arthritis) Osteochondrosis

Cruciate or meniscal rupture Patellar ligament injury

Malnutrition

Splenic rupture

Neonatal maladjustment

Subcutaneous abscess, cellulitis, foreign body Vesicular stomatitis

Bucked shins (dorsal metacarpal disease) Hemimelia (radial, tibial, ulnar hypoplasia, agenesis) Botulism (shaker foal)

Myotonia congenita Skeletal neoplasia

Shivers (shivering) Borreliosis (Lyme disease)

atrophy.

swelling is hard and often not painful to pressure. Swellings of the muscle could be hard (vitamin E/selenium deficiency); soft and fluctuant, such as with subcutaneous hematoma or abscesses; or crepitant, such as with subcutaneous emphysema or gangrenous myositis (e.g., blackleg).

Leg Angles

Straight hocks in excess of 175 degrees may predispose to degenerative joint disease. Bilateral excessive hock angle (sickle hock) is often associated with shallow toe angles and low heels. Cow hocks (inward hock rotation), on the other hand, are often associated with unbalanced weight bearing and overgrowth of the outer claws. Abduction of a single leg usually indicates pain in the outer claw, whereas a basewide stance in the front legs is indicative of pain in the outer claws. In the rear legs, a basewide stance may also be due to obturator nerve paralysis, which affects the adductor muscles of the inner thigh of the rear legs. Apart from a basewide stance, animals affected by obturator nerve paralysis appear ataxic and are predisposed to splaying their back legs. With a “camped under” posture, more weight is shifted to the rear legs and is often associated with pain in the front feet due to laminitis. Laminitis and pain may also cause the animal to cross the front legs in an effort to remove weight from the medial claws. Partial flexion of the front leg with inability or difficulty in advancing the leg may be associated with suprascapular or radial nerve injury or bicipital bursitis. The leg is held in semiflexion, and the elbow is dropped in case of damage to the radial nerve at the level of the brachial plexus.

POSTURAL CHANGES ASSOCIATED WITH STIFLE JOINT. Instability within the stifle joint associated with cranial cruciate rupture is often seen when the animal is walking and may be accompanied by an audible sound (Video 13.3). This is caused by sliding of the femoral condyles over the tibial plateau. The animal tends to stand with the fetlock slightly flexed and the heel raised. Weight bearing is on the tip of the toe. In cases of medial collateral ligament instability, the leg is held in an abducted position to relieve weight bearing on the medial side of the stifle and weight is placed on the medial claw when walking. With upward fixation of the patella the limb will “lock” while in full extension.

POSTURAL CHANGES ASSOCIATED WITH HOCK JOINT. Drop­ping (overflexion) of the hock during standing, but more so during walking, is often indicative of gastrocnemius rupture (Video 13.4). Tibial nerve paralysis also results in a dropped hock and slight knuckling of the fetlock. The hock remains dropped while the animal is walking but does not sink during weight bearing, in contrast to rupture of the gastrocnemius muscle. Overextension of the hock is associated with peroneal nerve damage, peroneus tertius rupture, upward fixation of the patella, flexor tendon contracture, and advanced degenerative joint disease. Intermittent spastic contracture of both legs with flexion of the hocks is caused by spastic (spasmotic) syndrome (Video 13.5). In contrast, spastic contracture of one or both hind legs with overextension of the hock is due to spastic paresis. Cattle with damage to the peroneal nerve will stand with the foot knuckled over onto the dorsum of the pastern and fetlock joint. At the same time the hock joint will appear to be overextended. In mild cases, the fetlock tends to knuckle over intermittently when the cow walks.

POSTURAL CHANGES ASSOCIATED WITH FETLOCK AND INTERPHALANGEAL JOINTS. Knuckling of the fetlock joint is associated with neuropathy of the sciatic nerve and its branches, the peroneal and tibial. Other causes include lesions of the palmar or plantar aspect of the foot or sole, as well as conditions of the spinal cord (e.g., lymphosarcoma) or vertebral column.

POSTURAL CHANGES ASSOCIATED WITH NERVES, TENDONS, AND JOINTS OF FRONT LEGS. Postural changes and clinical signs of suprascapular nerve injury include stumbling, inability to support weight in severe cases, inability to support and extend the shoulder, a shortened stride, and abduction of the leg. Reflexes and sensation in the lower limb remain normal if the suprascapular is the only nerve affected, and atrophy of the supraspinatus and infraspinatus muscles can become visible in 5 to 7 days after injury.

In calves, contracture of the flexors may cause flexion of both the carpus and fetlock. In such cases, the leg usually cannot be straightened. Semiflexion of the knee can also be due to abnormal conformation or metabolic bone disease. Depending on the level of contracture of the flexors, only the fetlock may be affected. In more severe cases, the carpus may also be affected because of contracture of the flexor carpi radialis and ulnaris or, additionally, because of fibrosis of the joint capsule. In milder cases, the animal may be able to walk on its toes and knuckle forward during weight bearing. In more severe cases, the animal bears weight on the dorsum of the foot or is unable to walk.

POSTURAL CHANGES ASSOCIATED WITH CONDITIONS OF FOOT (DEFINED AS PART OF LIMB BELOW FETLOCK). A sym­metric swelling of the foot sometimes extending to and above the fetlock is usually associated with foot rot, whereas a unilateral swelling of the digit is more often associated with a septic tenosynovitis, retroarticular space abscess formation, or sepsis of the distal interphalangeal joint. This can be confirmed through an aspirate of the distal interphalangeal joint and ultrasound of the flexor tendons and structures in the heel. Toe ulcers may cause a heel-first foot placement or weight bearing toward the heel when standing; these can be seen in the apex of zone 5 (see Fig. 13.1). The proximal interphalangeal joint may become subluxated with superficial flexor tendon contracture, resulting in knuckling of the joint.

Septic arthritis of the distal interphalangeal joint results in severe lameness with little to no weight bearing during both standing and walking. White line disease in zone 3 of the rear outer claw often prompts the animal to abduct the limb to move weight bearing to the medial claw. Ulcers or hemorrhage in zones 4 and 6 could also be responsible for changes in gait and posture, which may include inward rotation of the hocks to reduce weight bearing on the outer claws of the rear legs, knuckling of the fetlock, crossing of the front legs, and abduction or adduction of the leg. White line disease in zones 1, 2, and 3 could also result in postural change.