Skeletal disorders

Skeletal disorders

Developmental disorders

Deformities of the axial skeleton (Figs. 7.17.4)

A wide variety of skeletal deformities occurs in horses, although individually most are rare. The importance of such abnormalities rests both in their heritability and their immediate and long-term effects upon posture and locomotion. Even if severe, the consequences of these deformities may not be life-threatening, but they may lead to significant disorders of gait as the animal grows or comes into work.

Deformities of the vertebral column

Deformities of the vertebral column are most common in the cervical (wry neck) and lumbar (kyphosis, lordosis, scoliosis) regions. Deviations and distortions of the skull are also encountered. While such defects are visually dramatic, there is commonly little or no material effect upon the growth or natural behavior of the horse but they will become important when ridden work is required. Severe deformities, especially of the cervical vertebrae, may result in dystocia as the fetus cannot be positioned normally for delivery. Most deviations of the axial skeleton are sporadic occurrences and there is little evidence of heritability. Such defects are thought to be the result of fetal malpositioning when, during the later rapid phases of growth, fetal movement is naturally suppressed. However, many other factors may be involved and the more severe deviations may be the result of growth deformities, arising from a number of factors such as maternal viral or bacterial infections or toxemia during gestation.

Congenital deformities of the limbs and joints (arthrogryposis) (Figs. 7.6 & 7.7)

These developmental defects are relatively common and usually obvious from birth and frequently cause significant dystocia. The extent of deformity ranges from mild deviations of limb position, resulting from relatively minor deformities in the long bones, to gross distortion of the bones, joints, ligaments and tendons of the limbs, with consequent severely restrictive, postural deformities. It is more usual for the front legs to be involved, although hind leg deviations are sometimes encountered, either on their own, or in conjunction with fore-limb distortions. It is unlikely that the disorders are the result of genetic factors, although they are more often encountered in Thoroughbred horses and in the small European draught breeds. They are generally regarded as accidents of gestation, possibly associated with developmental infections, toxins and nutritional deficiencies or excesses. In spite of their relatively high incidence, a definitive etiology and pathogenesis has not been established. In most cases no apparent cause can be identified, and fetal malpositioning is then commonly blamed for the misshapen axial or appendicular skeleton. These abnormalities are often complicated by the co-existence of flexural and soft tissue deformities. Complex developmental deformities involving skeletal, cardiac and other defects are frequently found concurrently.

Figure 7.7 Arthrogryposis (same foal as Fig. 7.6). This is a post-mortem image demonstrating section of the tendons above and below the carpus with no change in the contracture.

Collapse of carpal and/or tarsal bones and incomplete ossification (Figs. 7.87.11)

Incomplete ossification occurs commonly in premature or dysmature foals. Collapse of the tarsal or carpal bones can occur secondary to incomplete ossification and abnormal weight distribution on the developing bones. In some cases it may occur secondary to trauma or infection.

The grade of incomplete ossification may be appreciated by radiographic examination:

Diagnosis and treatment

• Radiographic examination to assess degree of ossification, extent of bone compression and some cases may have concurrent infections. Assessment of white cell count and fibrinogen if there is any doubt about whether there may be a septic element.

• Foals should be restricted from excessive exercise to prevent compression of the tarsal cuboidal bones and slowly reintroduced to normal turnout even after complete ossification has occurred.

• The tarsus should be radiographed every 10–14 days. If sepsis is suspected based on blood work and radiographic findings, foals should also be started on broad-spectrum antibiotics.

• Once collapse of the tarsal or carpal bones has occurred, the condition is easily recognized clinically by the abnormal angles adopted by the affected limb(s). Concurrent flexural deformities and other developmental defects may be found in some cases. Prognosis is usually poor for severe cases.

Congenital luxation of the patella (Fig. 7.12)

This is an uncommon condition that is most frequently identified in miniature horses and Shetland ponies. It can be unilateral or bilateral, intermittent or complete, and frequently in a lateral direction. The more severely affected bilateral cases have difficulty standing or if standing carry their pelvis lower than the lumbar spine. Unilateral cases show intermittent lameness. Shetland ponies appear to be able to tolerate the condition quite well and some are even capable of mild work, although osteoarthritis usually develops over time. The etiology is not well understood but is thought to be related to a dysmaturity of the trochlear ridges and relative laxity of the femoro-patellar joint.

Fractured ribs (Figs. 7.137.16)

Rib fractures are commonly found in newborn foals and minimally displaced fractures are perhaps underdiagnosed. The majority of foals with rib fractures suffer no related clinical abnormalities but moderately or severely displaced fractures can be a significant cause of death in this age group. Inappropriate or poorly timed assistance during foaling is a significant cause of rib fractures. Hospitalized patients, whether presented for rib fractures or other problems are overrepresented in numbers of mortalities. The additional manipulation of hospitalized patients may be a factor in the increased mortality rate of this group when compared with foals that have no additional abnormalities or illnesses.

Palpation of the thoracic wall should be a part of any routine neonatal examination. Signs that should direct an examiner’s attention to the possibility of rib fractures include groaning or grunting in the foal, respiratory distress, plaques of subcutaneous edema overlying the ribs or along the ventrum of the thorax, especially behind the elbows, and flinching when the rib area is palpated.

Audible or palpable crepitation or a clicking sensation when the hand is gently pressed over an affected area is common with moderately to severely displaced fractures but is rarely present with minimally displaced fractures. The level of pain experienced by the foal is very variable with some showing marked pain, including grunting, while others display normal activity despite the presence of multiple fractures.

Flail chest occurs when several consecutive ribs are fractured, leading to an incompetent segment of chest wall. When a flail chest is present, the involved segment of chest wall will sink inwards during the inspiratory excursions of the abdomen and diaphragm.


• Four to six weeks are considered to be necessary for stabilization of the thoracic wall following rib fractures. Foals are normally box rested for 2–3 weeks and then reassessed ultrasonographically before commencing paddock turnout. Administration of analgesics is generally avoided as some pain limits movement and helps avoid additional displacement of fracture segments as a result of exercise.

• The formation of a hematoma or thrombus at the broken bone ends is typical of a rib fracture injury in the acute stages. Serial examinations document the evolution of this finding to bony callus formation, and eventual smoothing and remodeling of the callus with time.

• Deformation of the lung surface and thickening of the visceral pleura may be semi-permanent to permanent findings in the long-term assessment of these foals.

• Foals that have severely displaced fractures that are adjacent to the heart or causing significant pulmonary contusions are considered surgical candidates.

Hereditary multiple exostoses (multiple osteochondroma, multiple cartilagenous exostosis, diaphyseal aclasis or endochondromatosis) (Fig. 7.17)

This is an uncommon hereditary skeletal disorder characterized by mulitple bony projections, often bilateral and symmetrical on the long bones, ribs and pelvis. A single autosomal dominant gene is thought to be responsible. Histologically the exostoses appear to be osteochondromas. They remain benign and no transformation to malignancy has been reported.

The condition may be associated with lameness if an exostosis impinges on surrounding muscle or tendon. In those cases excision of the extosis may be indicated.

Developmental disorders: Acquired conditions

Osteochondrosis (Figs. 7.187.24)

Osteochondrosis has often been defined as failure of endochondral ossification resulting in either osteochondritis dissecans (OCD) or subchondral bone cysts. Besides defects in the process of endochondral ossification, other causes have been suggested, including loss of blood supply, genetic, gender specific, dietary, endocrine, biomechanical, traumatic and toxic. The level of exercise young horses receive has also been implicated in the development of osteochondrosis, with excessive exercise and lack of exercise in young foals both being implicated as causing osteochondrosis. Subchondral bone cysts are now speculated to originate from possible mechanical insults when compared to osteochondritis.

Osteochondrosis commonly occurs in the tarsus, stifle and fetlock joints. Though uncommon, osteochondrosis can occur in the scapulohumeral, elbow and hip joints. Tables 7.1 and 7.2 list the most common locations of lesions within each joint. Lesions can potentially regress. In the hock, 5 months has been used as a possible cut off for lesions regressing. After 5 months, lesions will typically not regress. In the stifle, 8 months is the cut off for a lesion regression involving the lateral trochlear ridge.

Clinical signs can include joint effusion and lameness. However, in certain situations lameness and joint effusion may not be present. Joint effusion is more common with a dissecting lesion. Lameness can be present with both dissecting lesions and cysts, but cysts can often be asymptomatic until horses begin training. In some cases, joint effusion is present but radiographs show no significant findings. In these cases, serial radiographs over 4–6-week intervals may be required to ensure the absence or presence of an osteochondritis lesion. It is very important to examine the contralateral joint for the presence of an osteochondral lesion as lesions are frequently bilateral.

Diagnosis and treatment

• Diagnosis of osteochondritis is often easily made based on signalment, history, clinical signs and radiographic findings. Ultrasound examination of affected joints can also help to evaluate and confirm the presence of a cartilaginous flap.

• Treatment of osteochondral lesions involves conservative or surgical management. Conservative management involves limiting exercise and chondroprotective therapy and is indicated in young foals and those which do not have any effusion or lameness associated with their OCD lesion(s).

• Surgical management of osteochondritis dissecans typically involves surgical debridement of the fragment and the fragment bed. Surgical management of subchondral bone cysts has included debridement, cartilage replacement, packing the cyst with bone marrow or injection of corticosteroids. Surgical treatment should be considered for foals with joint effusion and lameness. Prophylactic removal may also be considered in young horses intended for sale.


Prognosis for osteochondritis dissecans and subchondral bone cysts varies based on location, number of joints involved, size of the lesion, presence of osteoarthritis and the degree of lameness.

• Fetlock. Many fetlock lesions can improve radiographically over time with conservative management. Surgical treatment should be considered only in foals that demonstrate joint effusion and lameness. Lesions of the palmar/plantar aspect of P1 do not often require surgery.

• Hock (tarsus). The distal intermediate ridge of the tibia is the most common site of lesions and these are rarely associated with effusion and lameness. Lesions of the medial malleolus are more likely to result in joint effusion and lameness requiring surgical treatment. Lesions of the lateral trochlear ridge can be quite variable in size but if large may result in effusion and lameness. Most medial trochlear ridge lesions are incidental findings and do not require treatment.

• Shoulder and elbow. OCD lesions of the shoulder and elbow are normally only recognized when associated with lameness. The lameness in these cases may develop insidiously or acutely and identifiying the site of the lesion is often difficult. Surgery should only be considered in foals less than 8–10 months of age if they are intractably lame as some cases may improve with rest. Radiography may also underestimate the size of the lesions making pre-surgical assessments of future athletic function difficult.

Angular limb deformities (Figs. 7.257.28)

Angular deformities of limb joints, particularly of the knee (carpus), hock (tarsus) and fetlock (metacarpophalangeal joint), are frequently encountered in all breeds. They may be congenital or acquired, and can be related to certain management and nutritional factors. Valgus deformities occur when the lower limb deviates laterally. This gives the foal a ‘knock-kneed’ appearance. Varus deformities occur when the lower limb deviates medially and results in a ‘bowlegged’ appearance. The condition may be unilateral or bilateral with single or multiple joints affected in a given limb. The forelimbs are more commonly affected but hindlimbs can also be affected. Occasionally, a foal may have a valgus deformity of one limb and varus on the other, giving a ‘windswept’ appearance. Although deviations occurring at the fetlock are usually less dramatic in appearance, they are regarded as being more urgent, as growth in the distal metacarpal physis ceases at an earlier age than growth in the distal radial physis. Once the growth plate has closed, the potential for therapeutic intervention involving growth acceleration/retardation is lost. Even before physeal closure, the extent of the deviation may be such that there is exceptional weight-bearing on the concave side and much less on the convex. This results in a slower growth rate (and often premature closure) of the physis on the ‘short’ side of the joint. Thus, the condition becomes progressively worse, and effective therapeutic measures are correspondingly less feasible.

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Feb 27, 2017 | Posted by in EQUINE MEDICINE | Comments Off on Skeletal disorders

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