Fig. 16–2. Midline deviation of the foal’s knees and enlargement of the distal radial growth plates just above the knees.

Wobblers Syndrome

Swelling of the growth plates of the vertebrae of the neck causes compression and, if sufficiently severe, damage to the spinal cord. This can be detected radiographically as a narrowing of the vertebral canal. The onset of clinical signs often, but not always, occurs after a traumatic incident, such as being tied up for the first time, being cast, or falling. Clinical signs include an incoordinated gait, a wide-base stance, going down, and spasticity. These signs generally occur on both sides and first and most severely in the back legs. They are most noticeable when the horse is walking slowly or in tight circles, and frequently can be exaggerated by exercising the horse on a slope with the head elevated. Incoordination may be more obvious when the horse is backed. Because of these symptoms, it is commonly referred to as “wobblers syndrome.”

Wobblers syndrome may occur as a result of anything that causes spinal cord damage. In 383 cases seen in one university veterinary clinic, 45% were due to EDM (equine degenerative myeloencephalopathy) (discussed in that section in Chapter 2), 31% to a protozoan organism, and 24% to a swelling of the vertebral growth plates. However, spinal cord damage due to a swelling, of the vertebral growth plates is the most common cause of wobblers syndrome in horses less than 4 years old. Less frequent causes of posterior incoordination in the horse include rhinopneumonitis (see Chapter 9), injury, tumors, infarcts, inter-vertebral disc protrusion, Sudan grass toxicosis (discussed in section on Neurologic-Disease-Inducing Plants in Chapter 18), equine infectious anemia, (swamp fever, see Chapter 9) and a migrating parasite larvae (see Strongyles, Chapter 9).

Growth plate swelling-induced spinal cord compression rarely may be so severe the neck is fixed in a flexed position (Type I), with the onset of signs occurring anytime from birth to several years of age. Compression may instead occur only during neck flexure (Type II), which occurs primarily in nursing and weanling foals. Most often, however, compression is neither relieved nor worsened by neck flexion (Type III), with the onset of signs occurring at 1 to 3 years of age after the horse is put into training, but they may not occur until up to 10 years of age. Compression is often, but not always, continuous by the time it is diagnosed. With all types, an acute onset of signs is often triggered by a traumatic incident.

Dietary management, as described later for all DOD effects, is fairly effective for prevention and for treatment prior to obvious signs. Once signs are obvious, surgery may be indicated. The shorter the duration of clinical signs before surgery and the further forward the compression, the greater the chance of success.

Angular Leg Deformities

Impaired cartilage nutrition due to its thickening slows bone growth. If this occurs unevenly, with one side growing slower than the other, an angular leg deformity occurs. Anything causing more pressure on one side of the growth plates can also cause angular leg deformities. Such factors may include joint laxity, malpositioning in the uterus, poor foot trimming, and excessive trauma due to a large body size for the bone size, excessive physical activity, or lameness in the opposite leg. Excess feed intake during the latter half of pregnancy by previously poorly fed mares was the only common factor recognized on one farm in which angular leg deformities were present in 17 of 30 foals born. It was proposed that the excess feed intake may have resulted in sufficient abdominal fat to compress the uterus, causing fetal malpositioning resulting in congenital angular leg deformities. Impaired or delayed, conversion of bone growth cartilage into bone may result in collapse of the small bones in the knee or hock, or traumatic luxation or fracture of these bones, will also cause angular leg deformity. Angular deformities are most common at the knee, followed by the hock and fetlocks.

Fig. 16–3(A,B). Distal radial metaphyseal or bone growth plate enlargements giving the knee a dished-in appearance in front, referred to as “open knees,” and enlarged fetlocks due to enlargements of cannon bone growth plates. Upright or straight-appearing pasterns due to the occurrence of mild acquired flexure leg deformities are also evident.

Foals may have congenital angular leg deformities present at birth or occurring within the first few days of life, or the deformities may be acquired within several weeks to months of age (Fig. 16–1). Varying degrees of knee joint laxity may be present in newborn foals, particularly those that are premature. The surrounding tissues are not strong enough to support the knee and an angular leg deformity occurs. Unless the deformity is quite mild (less than 5° deviation), it is best to keep the affected foal and its dam confined to a stall and ran until muscle tone increases sufficiently to tighten the support and bring about correction. Hoof trimming and balancing should also be done. Squaring or rounding of the toe may help force a more normal break over the foot. However, if the deformity worsens, if substantial improvement has not occurred by 2 weeks of age, or if the deviation exceeds 12° to 15°, thorough investigation as to the cause, and treatment accordingly, should be instituted. Delaying treatment greatly decreases the chances for recovery and future athletic performance ability.

Conversion of growth cartilage to bone in the small bones of the knee and hock normally occurs during the last few weeks of pregnancy and continues during the first month of life. In some foals this may not be sufficiently complete at birth as a result of normal variation, immaturity, or inadequate thyroid function. Hypothyroidism delays bone formation. This may result not only in the collapse of these bones, but also in bone cysts, contracted flexor tendons, extensor tendon rupture, mandibular prognathism (overbite or parrot mouth) and/or scoliosis (abnormal curvature of the back). As described in Chapter 2, hypothyroidism in the foal may be caused by either inadequate or excessive iodine intake by the mare during pregnancy or lactation.

Radiographs of at least one knee and one hock should be taken of foals that appear immature at birth. If normal ossification of the small bones isn’t complete, the foal and the dam should be kept confined until ossification is complete. Radiographs to determine this should be taken every few weeks. Exercise prior to complete ossification may result in collapse of these bones or abnormal ossification with subsequent development of juvenile arthritis. Stall confinement for a maximum of 2 months may be the only management necessary.

Collapse of the small bones of the knee will result in angular deformity of the knee, whereas collapse of the small bones of the hock will result in an increased flexion angle, or sickle hocks. These deformities may be present without improvement since birth. Both knee and hock bone collapse, if treated prior to secondary changes, can usually be straightened under general anesthesia and a splint changed every few days, or a tube cast changed every 1 to 2 weeks, until there is radiographic evidence of adequate symmetrical ossification. This usually takes 2 to 4 weeks but may take as long as 2 months. The cast or splint is stopped at the fetlock, because if the foot is included, dropped fetlocks may occur when support is removed. The leg is usually wrapped for several days after the cast or splint is removed to provide some transitional support.

With acquired angular leg deformities, the foal is born with relatively straight legs that after a few weeks to months of life begin to deviate. The cause may be an unrecognized angular leg deformity present at birth (congenital) that becomes more severe, a growth plate injury, or the other causes of other DOD effects as discussed in that section later in this chapter. Poor conformation or improper hoof trimming that result in more weight and as a result pressure on one part of the growth plate than another have also been thought to cause angular leg deformities. However, it is doubtful that poor hoof trimming is a cause, as it has been shown that altered pressures resulting from attaching a wedge to the hoof, which elevated the lateral aspect 12° to 15°, progressively returned to normal within 10 days. In cases that don’t respond to more conservative management or that are severe (in excess of 12° to 15° angulation), both conservative management and surgery are necessary for correction.

Joint Cartilage Damage

Joint cartilage damage may occur because inhibited nutrient diffusion through the thickened noncalcified cartilage results in degeneration of its basal layers. Subsequent physical stress may result in the cracking or fissuring at the periphery of the affected joint. Joint swelling, pain, and lameness may occur as a result of these effects. Avulsion of a piece of the damaged cartilage may occur, resulting in what is referred to as OCD or osteochondrosis dissecans. This damaged piece of cartilage may remain attached or become detached and form “joint mice”. In either case this loose piece of cartilage or bone may cause erosions of the opposing joint surface, resulting in juvenile arthritis (also referred to as degenerative joint disease and osteoarthrosis). This is the major cause of juvenile arthritis in the horse and leads to chronic lameness.

The sites most commonly affected by OCD include the stiffle, hock, and less commonly the fetlocks and shoulder. Often multiple joints are affected to varying degrees.

Most horses with OCD of the stifle or hock joints are ½ to 2 years of age but may be older or younger. The majority are 1 year of age or less when signs first become apparent, and lesions tend to be more severe the younger the horse. In slightly over one-half of the cases both hocks are affected.

Typically there is joint distention and mild lameness, which are increased following holding the leg for several minutes in a position to flex the joint (flexion test). Lameness may be severe and worsened by training, or not obvious, although affected horses may have an asymmetric or awkward gait that minimizes flexion of the affected joint. Mature horses frequently present with a sudden onset of clinical signs thought to be associated with the development of osteochondral fragments. Young foals that are affected may have difficulty getting up or are lame. Radiographic changes are usually evident.

Hock joint distention, or bog spavin without lameness, in horses from 6 to 18 months, but up to 3 years of age, is the most common manifestation of OCD in the hock. However, lameness may occur, particularly in horses over 2 years of age in training, and may be worsened by flexion for several minutes. It is a common problem in Standardbreds, with twice as many males as females affected. In one study of 114 cases, joint swelling was evident in 62% and lameness in 43% of affected horses, but previously affected horses had similar lifetime race earnings as did nonaffected horses regardless of whether they had been treated surgically or conservatively. Those affected did have significantly fewer race starts, particularly affected females. Surgical removal of OCD fragments preferably via arthroscopic surgery is recommended for those with joint swelling or lameness.

Horses with OCD or bone cysts, of the shoulder are usually younger than 12 to 18 months and have an intermittent foreleg lameness of insidious onset. In a series of 43 cases, in 37 only 1 shoulder, and in 6, both shoulders were affected. The lameness may have a swinging component and stumbling. Flexing and extending the shoulder joint may cause pain. A loss of muscle size over the shoulder and a smaller foot may be evident. Joint swelling generally is not evident. Arthroscopic surgery is often necessary, but difficult, with about one-half achieving athletic soundness.

OCD in the fetlock joints causes thickening over the front aspect of the joint, and joint swelling. Lesions, although not clinical signs, are frequently present in the legs on both sides. No lameness is usually present, although some may have severe joint pain, and lameness may be worsened by flexing the fetlock for several minutes.

Instead of cracking and fissuring at the periphery of the thickened degenerative joint cartilage, resulting in OCD, this may occur at the center of the joint, leaving an entrance for synovial fluid and creating a bone cyst. Sites in which this most commonly occurs in decreasing order of incidence are the stifle, knee, fetlock, pastern, and the hock. Problems due to bone cysts are usually recognized at a later age than those due to OCD and generally occur after the horse is put into training. They can generally be detected on radiographs.

Bone cysts in the hock typically result in an intermittent gait abnormality worsened by exercise and alleviated following rest. However, in some cases acute lameness may occur. Horses from 3 months to 5 years of age, but most commonly from 5 to 24 months old are most commonly affected. The onset of lameness may be associated with some traumatic event, such as the commencement of training. There is a supporting leg lameness with a shortened stride generally noticeable only at a trot. As with OCD of most joints, flexion may worsen the lameness. Swelling and joint effusion generally doesn’t, but may, occur as a result of bone cysts.

Bone cysts in the knee, hock, or fetlock joints usually cause no effects until the horse is put into training and these effects are worsened by several minutes of flexion. In contrast, cystic lesions in the pastern and coffin joints generally result in obvious lameness and swelling. Lameness often occurs suddenly when the coffin joint is affected.

Surgery (generally arthroscopically) is usually recommended for removal of fragmented OCD chips, and for debridement of bone cysts. If chips or fragmentation are not evident, and initially for bone cysts without radiographic evidence of juvenile arthritis, surgery may not be necessary. Injections into the affected joints of substances that decrease inflammation and prevent or slow joint degeneration, along with rest may be adequate. Rest is an important aspect of therapy to give the articular cartilage time to repair. Rest for at least 3 months is necessary and should be followed by radiographic and lameness evaluation to determine if continued rest is necessary. A longer period of rest is required in some cases. The younger the horse and the smaller the bone cyst, the better the prognosis. However, if lameness persists, arthritis is present, or the bone cysts are large, surgery should be considered. Surgery has been recommended over nonsurgical treatment of bone cysts of the elbow, hock, and shoulder joints.

Lesions believed to have a high probability of affecting athletic performance, regardless of treatment, include all OCD of the shoulder and elbow; major OCD lesions of the stifle and hip joints; bone cysts of the distal cannon bones and the phalanges, and lesions that have already initiated juvenile or degenerative arthritis. The clinical course is unpredictable for cartilage flap lesions of the stifle and OCD lesions. With proper treatment, athletic performance may not be affected by small OCD lesions at the rear surface of the first phalanx, most fragments within the hock, and small fragments of the front of the fetlock joints.

Contracted Flexor Tendons (Leg Flexure Deformities)

Flexure deformities of the legs are often referred to as contracted flexor tendons. However, the tendons are not contracted; the effective functional length of the muscletendon unit is less than necessary to maintain normal leg extension, resulting in a flexure deformity. Flexure deformities may be present at birth or develop within the first few days of life (congenital), or they may be acquired during growth following birth. Most congenital flexure deformities affect both front fetlocks. Less commonly knee flexion may be present. All flexure deformities associated with bone malformation are fixed and generally not treatable. More than one-half of the lethal congenital defects, which are present in about 1% of Thoroughbred foals, are reported to be due to fixed leg flexure deformities.

Congenital Leg Flexure Deformities

Congenital flexure deformities have classically been attributed to malpositioning or a lack of normal fetal movement in the uterus. Obesity during pregnancy has been proposed as a cause. Genetic factors and intrauterine insults to the fetus, such as infectious or toxic agents, may also be responsible in some cases. Dietary nutrient intake by the mare is not known to be a factor, although if obesity is a cause, excess dietary energy intake during pregnancy would be responsible.

Most congenital flexure deformities do not involve the bone and are not fixed. Most of these are alleviated shortly after the foal stands if the foal is able to place the bottom of the toe or the sole on the ground. However, if they do not correct within a few days, early and effective therapy is necessary to prevent juvenile arthritis or degenerative joint disease which may limit the horse’s future athletic performance ability. The earlier adequate therapy is begun, the greater the chance of success.

Box stall confinement of the mare and foal for several days may be sufficient for spontaneous correction to occur. Oxytetracycline is commonly given during this period. It has been shown to be a safe and effective method of decreasing the young foal’s fetlock joint angles. But it may not be safe for foals with existing renal compromise, septicemia, or other extensive medical problems, or if diuretics or methoxyflurane anesthesia is administered.

Leg wraps from the coronary band to the elbow may be beneficial in some cases. If used, the leg should be rewrapped daily and carefully managed to prevent formation of pressure sores. Correction of nonfixed congenital flexure deformities should occur within 1 week. If it does not, or if the foal cannot stand, or stands on the front surface of the hoof, pastern or fetlocks, splints or casts are generally needed to apply forced extension. Pneumatic splints may work well for this. Forced extension is generally successful if the foal can walk on the sole of the foot so that weight-bearing causes extensor tension, and if pressure sores from the splint or cast can be minimized. If not, they are generally unsuccessful, and surgery may be necessary, although in these cases prognosis for normal limb function is guarded.

Acquired Leg Flexure Deformities

Acquired flexure deformities occur in horses born with straight legs. They may occur gradually over several months or more rapidly over several weeks. They may occur on either one or both sides, although one leg is generally worse than the other. There are two major types: those involving primarily the deep digital flexor tendon, and therefore the coffin joint, and those involving primarily the superficial digital flexor tendon, and, therefore, the front leg fetlock joint.

Acquired flexure deformities involving primarily the coffin joint are characterized by a raised heel and a “club footed” appearance. As a result, the heel tends to grow long and the toe stays worn off. Sole bruises and abscesses in the toe area may occur. In severe cases the front aspect of the hoof wall is past vertical, and knuckling over of the fetlock joint may occur. Flexure involving primarily the coffin joint tends to occur most often in nursing or weanling foals 6 weeks to 6 months of age, whereas flexure involving primarily the fetlock joint or superficial digital flexor tendon tends to occur in older weanlings and in yearlings.

Flexure involving primarily the fetlock joint is characterized by a moving of the pastern and fetlock joint forward and a knuckling at the fetlock joint, with the sole of the foot remaining level so the heel remains on the ground (Fig. 16–4). The leg may at first appear to be upright or straight at the pastern and fetlock (Fig. 16–3). As the horse walks, the fetlock may occasionally knuckle forward. As this condition worsens, the horse may stand with the fetlock in a knuckled-over position. Prolonged abnormal flexion results in a failure of structures (tendons, ligaments, and joint capsules) to elongate normally with growth so that straightening becomes more difficult with time. Thus, the longer a flexure deformity exists, the less likely it can be successfully corrected.

Chronic leg pain, such as that due to OCD, bone cysts, arthritis or degenerative joint disease, chronic joint infections, fractures, or soft tissue damage, causes a shifting of body weight to the nonpainful leg. The pain may result in a contraction of the flexor muscle-tendon unit of either the painful or non-painful leg. A low heel, rapid growth rate, and inadequate exercise have each been thought to predispose to acquired flexure deformities. However, even all three of these factors together did not result in flexure deformities in Quarter Horse weanlings studied from the age of 4 to 10 months.

Fig. 16–4. Acquired leg flexure deformity involving primarily the superficial flexor tendon and fetlock joint. The right fetlock is abnormally straight and the left knuckled forward, but the heel remains on the ground, helping to differentiate the deformity from one involving primarily the deep digital flexor tendon and coffin joint.

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