Definition and Etiology

Physitis is a term used to describe a developmental orthopedic condition in which there is a disturbance in endochondral ossification at the physis, or growth plate. Of the developmental orthopedic diseases—osteochondrosis, physitis, subchondral bone cysts, flexural limb deformities, cuboidal bone malformation, acquired angular limb deformities, and juvenile arthritis—physitis is the most common.^1,2 In one study of 1711 Irish thoroughbred foals, 67% had signs of developmental orthopedic disease.² The term physitis may better be defined as “physeal dysplasia” because typically there is no evidence of an inflammatory process.³

Physitis has been seen in growing cattle as a result of copper deficiency and interactions with molybdenum, zinc, and sulfates, as well as in calves raised on slatted floors.⁴ Two common antagonists of copper include zinc, which at high levels prevents absorption of copper by the body, and molybdenum, which is found in alfalfa.⁵ Other animals in which physitis has been reported include show rams being heavily fed and sheep and goats with pregnancy-associated ephiphysitis.⁴

Physitis typically affects the given physis during its active growth phases. Factors implicated as causing physitis in horses include the following⁴:

Clinical Signs

Physitis in horses is seen mainly in three specific locations at certain ages. Foals ranging in age from 3 to 6 months most often have signs of physitis at the distal metacarpal/metatarsal growth plate (with or without involvement of the proximal physis of the first phalanx). Older foals (8 to 24 months) may have signs of physitis at the physis of the distal radius.⁶ Less frequently the distal physis of the tibia may be involved. Physitis is characterized by firm swellings that may be warm and painful on palpation. Typically the swellings are medial because of increased weight bearing on this portion of the limb.⁶ Foals may or may not be lame. Radiographic changes include a sclerotic, roughened physis with an irregular metaphyseal shape.² If the physitis continues, the growth plate may close prematurely, leading to an irreversible angular limb deformity (usually a varus deformity because of decreased growth on medial physis).⁶

Diagnosis

A diagnosis of physitis is usually made by appreciation of the clinical signs, including warm, sometimes painful, firm swellings in the locations previously cited. Physitis at the fetlock may appear to have an hourglass appearance if the proximal physis of the first phalanx is affected. A convex appearance just proximal to the distal tibial and radial physis may be seen early in the disease process.⁶ Recently, a quantitative method for detection of physitis was investigated in thoroughbred foals.² This method is based on the observation that when the physis is enlarged, both the metaphysis and the ephiphysis are more concave.⁷ Results of this study show that epiphyseal concavity may indicate the degree of physeal swelling by using the maximum second derivative value of that contour. Radiographically, physitis is characterized by a growth plate that is irregularly thickened with sclerotic adjacent bone.²

Treatment and Prognosis

Treatment of physitis should begin with management changes. Special attention should be given to the nutrition of these foals and weanlings. Ensuring proper balance of minerals, especially calcium and phosphorus, as well as adequate amounts of trace minerals such as copper and zinc, is necessary. Copper is required for successful cross-linking of collagen. When a copper deficiency exists, the cartilage matrix weakens and microfractures occur. Because mare’s milk is very low in copper, foals rely on hepatic stores gained during the last trimester of gestation.⁵ One study showed that supplementation of mares with copper during gestation significantly reduced radiographic signs of physitis in their foals at 150 days of age. Supplementation of foals did not affect the incidence of physitis in the same study. Based on these results, supplementation of mares during the second half of gestation with copper on farms with a high incidence of physitis may be beneficial in preventing physitis in their foals.⁸ A general reduction in energy is needed to slow growth rates and, when necessary, decrease body weight. Total concentrate for nursing foals should be 0.5 to 0.75 kg/100 kg body weight, 1 to 1.5 kg/100 kg for weanlings, and 0.5 to 1 kg/100 kg for yearlings.⁴

Varying degrees of discomfort are associated with physitis. For horses with very painful, warm physes, the judicious use of nonsteroidal antiinflammatory drugs (NSAIDs) is indicated. Exercise restriction, specifically stall rest, is indicated in affected horses. Without exercise restriction, these horses continue to load the physes, which may lead to permanent conformational changes, such as angular limb deformities.

With early detection and treatment, the prognosis for physitis is good for athleticism.

Definition and Etiology

Osteochondrosis is a developmental orthopedic disease characterized by failure of, or defect in, endochondral ossification that can lead to cartilage flaps, osteochondral fragments, or subchondral bone cysts. It is classified as a developmental orthopedic disease (DOD) along with physitis, angular limb deformities, subchondral bone cysts, flexural deformities, incomplete ossification of the cuboidal bones, and juvenile arthritis.⁹Chondrodysplasia and dyschondroplasia are more descriptive terms because they imply a primary defect in cartilage maturation, but their use is generally reserved for abnormalities of limb and vertebral development. The terms osteochondrosis, osteochondritis, and osteochondritis dissecans have all been used synonymously in discussing the condition. To maintain consistency and avoid confusion, the following designations are used: osteochondrosis refers to the disease, osteochondritis refers to the synovial inflammatory response caused by the disease, and osteochondritis dissecans refers to the condition when a cartilaginous flap is identified.¹⁰

Osteochondrosis has been recognized in most domestic species, including horses, swine, and less often in cattle, sheep, and goats. The main focus has been in horses because of the economic impact and performance-limiting characteristics of the disease and in swine because of effects on production traits¹¹ and the development of comparative models for study of the disease.¹²

Clinical Signs and Differential Diagnosis

Osteochondrosis can present with a variety of clinical signs that are frequently recognized in juvenile animals. Effusion of the affected joint with or without accompanying lameness is common. The tarsocrural and femoropatellar joints are most often affected, but the condition can be seen in any joint. Physitis, or inflammation at the physeal plate, in young animals can have a similar appearance, with generalized enlargements adjacent to synovial structures. Osteomyelitis can cause a periosteal reaction that, if located in the area of a joint, can have a similar appearance. Septic arthritis can closely mimic the signs of osteochondrosis, but the associated lameness is often much more severe. Physitis, osteomyelitis, synovitis, and septic arthritis should all be considered in the differential diagnosis of osteochondrosis in juvenile animals. In older animals the clinician should consider synovitis, osteoarthritis, and trauma in the differential diagnosis.

Osteochondrosis is generally diagnosed in horses when they are started into training programs or begin athletic activity. They often present with a complaint of joint effusion that can be acute or insidious. Lameness is usually nonapparent to mild, except in cases with large osteochondral fragments or subchondral bone cysts. Severe cases seem to be more common in the stifle, and associated clinical signs may be present in foals as young as 6 months. Warmblood horses generally present later, at 3 to 4 years of age, because it is common practice to delay training until this stage.

Reports in cattle indicate that young, intact male, purebred animals are most often affected. The typical clinical signs are lameness with associated joint effusion. Osteochondrosis in swine has been associated with a syndrome known as “leg weakness.” Affected animals can show a range of signs, from mild lameness to inability to rise and inability or refusal to mount.¹³ Evaluation of performance data from swine herds can be a useful indicator of osteochondrosis because it has been shown to have a significant effect on production traits.^11,14 Cattle and swine are production animals slaughtered before 2 years of age, so clinical signs may only be recognized in purebred animals used for breeding purposes.

Sites of Predilection

Osteochondrosis can be found in any diarthrodial joint, but sites of predilection exist in all species affected. In horses the stifle and hock are most frequently affected. In the stifle, in order of frequency, the lateral trochlear ridge of the femur, medial trochlear ridge of the femur, trochlear groove, and distal end of the patella are affected.¹⁵ The medial femoral condyle is the site of predilection for subchondral cystic lesions. In the hock, in order of frequency, the distal intermediate ridge of the tibia, lateral trochlear ridge of the talus, and the medial malleolus are affected.¹⁵ Predilection sites in cattle are similar to those in horses, with the hock and stifle most often affected and similar distribution in the joints.¹⁶ Swine show a slightly different pattern, with the medial condyle of the humerus and femur most frequently affected.¹⁴

Diagnostic Tests

Animals presenting with signs of joint effusion and lameness should undergo a thorough physical examination. Complete blood count (CBC) indicating a septic process along with radiography help differentiate osteomyelitis, septic physitis, or septic arthritis from osteochondrosis. In cases with any indication of a septic process, appropriate cultures should be taken. Horses should be observed in motion along with flexion tests, using local and intraarticular anesthesia to localize the site of lameness. Swine and cattle can be observed in their normal surroundings for signs of lameness. Once localized, the affected joint should be radiographed along with the corresponding joint on the contralateral limb in the tarsocrural and femoropatellar joints because the lesions are often bilateral in nature (Fig. 38-1). If lesions are detected in the metacarpophalangeal or metatarsophalangeal joint, the remaining three limbs should be radiographed because these can occur quadrilaterally.¹⁷

Fig. 38-1 Osteochondrosis in the tarsocrural joint of a horse. Note the characteristic osteochondral fragments located at the distal intermediate ridge of the tibia.

Lameness and effusion are more reliably seen in cases of osteochondritis dissecans and subchondral bone cysts than in osteochondrosis. Intraarticular anesthesia of the affected joint will alleviate the lameness, localizing the source. After the lameness has been localized, appropriate radiographs of the affected area should be obtained (Fig. 38-2), as well as of the contralateral or quadrilateral limbs, as described previously.

Fig. 38-2 Osteochondrosis in the femorotibial joint of a horse. Note the large subchondral cystic lesion in the medial femoral condyle, a typical location for these types of lesions.

Swine and cattle will often present with signs of lameness and mild joint effusion. Careful physical examination of the restrained animal should allow localization of the affected area and appropriate radiographs to be obtained. As with equine patients, the lesions are rarely unilateral, and corresponding limbs should be radiographed. Reviewing production records of finishing or breeding swine herds may also be of diagnostic value because osteochondrosis has been shown to cause significant reductions in performance and production traits.¹¹

The manifestations of osteochondrosis may not be adequately represented by clinical signs and radiographs. Clinical signs of lameness and joint effusion have been shown to precede changes within the joint, and serial radiographs may be needed to diagnose the condition.¹⁸ Also, radiographic abnormalities consistent with osteochondrosis of the distal intermediate ridge of the tibia and lateral trochlear ridge of the femur can return to a normal appearance by 5 and 8 months, respectively, in warmblood foals.¹⁹ Radiographs also often underrepresent the severity or size of the lesion seen at surgery.

Pathophysiology

Endochondral ossification is the process of bone formation that begins with a cartilage scaffold arranged in zones that are gradually replaced by bone. It occurs at the articular/epiphyseal and metaphyseal growth plates and secondary centers of ossification, such as the carpal and tarsal bones. Directly beneath the articular cartilage is a zone of resting chondrocytes that divide to form the next zone, the proliferating chondrocytes. These proliferative cells divide rapidly, organizing into columns perpendicular to the long axis of growth. The cells progress to the hypertrophic zone, where they swell and become vacuolated, and the columns become more organized. The chondrocytes in this zone also become surrounded by increasing amounts of extracellular matrix, which becomes mineralized in the zone of calcification. These columns of chondrocytes are invaded by metaphyseal blood vessels, and bone forms on these calcified cartilage columns, creating the primary spongiosa, which is subsequently remodeled into mature bone.

The exact pathogenesis of osteochondrosis is still undefined. The traditional theory is that the process of endochondral ossification is disrupted, resulting in areas of thickened cartilage. The deeper layers of these retained cartilage plugs do not receive adequate nutrients by diffusion from the synovium, and necrosis of the cells develops. These areas of cartilage have less structural integrity than normal cartilage and are prone to damage. Shear forces acting on the abnormal cartilage can lead to fissure formation. These fissures can then form dissecting cartilage flaps, free flaps, or fragments of cartilage and subchondral bone. When compressive forces predominate on an area of thickened cartilage, it can cause infolding of the cartilage plug. Normal endochondral ossification proceeds around the infolded plug, forming a subchondral bone cyst.

This traditional theory of defective endochondral ossification is still well accepted, but recent literature suggests this may be a simplistic view of a multifactorial condition. Limited reparative responses of bone and cartilage make it difficult to determine whether the origin of a lesion is developmental or traumatic. A recent report failed to distinguish articular cartilage differences in naturally occurring osteochondrosis versus healing osteochondral fragments.²⁰ Arthroscopic observations of normal-thickness cartilage defects and normal subchondral bone, as well as lesions occurring preferentially at single sites at the limits of articulation, suggest causative factors other than defective endochondral ossification.¹⁷ The development and spontaneous regression of osteochondrosis lesions suggest that the condition is a dynamic process that can be affected by numerous intrinsic and extrinsic factors, and a “window of susceptibility” may exist whereby lesions are repaired and normal articular development proceeds.²¹ These findings and observations suggest that multiple pathologic pathways exist and that a single etiologic explanation of osteochondrosis is unlikely.

Etiology

As with the pathophysiology, the exact etiology of osteochondrosis is unclear and likely multifactorial in origin. Several factors, including biomechanical forces, failure of vascularization, nutrition, growth rate, genetics, and hormones, have been implicated and are likely interrelated in the etiopathogenesis of the disease.

The consistent distribution of lesions at specific anatomic sites within the joint implicate trauma as a causative factor. The bilateral or quadrilateral nature of the disease would indicate that trauma or biomechanical stress is a necessary factor rather than direct cause. It has been established in pigs that microtrauma or disruption of the blood vessels in the developing cartilage canals causes ischemic necrosis, failure of mineralization, and a retained cartilage plug.²² This mechanism has not been elucidated or studied in horses or cattle; therefore, while offering a plausible explanation, the results cannot be applied across species lines.

Nutritional influences have been extensively studied in relationship to osteochondrosis. The studies have focused mainly on dietary energy levels and mineral composition (copper and zinc). The growth rate of the animal is directly affected by energy intake as well as the genetic predisposition of the animal for growth and size. Animals fed high-energy levels for accelerated growth rates have a much higher incidence of osteochondrosis than those fed for lower rates of growth.^12,23,24 Low copper levels and increased zinc concentrations have both been implicated in the etiology of the disease. Low copper is thought to exert its effect through lysyl oxidase, a copper-dependent enzyme essential in the cross-linking of collagen molecules. Increased levels of zinc antagonize copper and could work indirectly through a similar mechanism. There is conflicting evidence on the causative nature of low copper levels, and lesions seen in copper-deficient animals do not always mimic those of naturally occurring osteochondrosis. More recently, evidence suggests that neonatal copper levels exert a positive effect on the resolution of osteochondrosis lesions but are not directly involved in the pathogenesis of the disease.²⁵

Genetics have been shown to be at least partially responsible in the etiopathogenesis of osteochondrosis in different species. Landrace and Yorkshire breeds of swine show a high frequency of osteochondrosis, whereas domestic pigs crossed with wild hogs do not develop the disease.¹² Heritability has also been demonstrated in standardbred trotters in the tibiotarsal and metacarpal/metatarsal phalangeal joints.^26,27 A genetic component may also be related to nutrition levels because an animal must have the genetic capacity for increased growth rates and size while at high planes of nutrition.

Alterations in hormone concentrations have been implicated in the etiology of osteochondrosis, but the mechanisms remain in question. Numerous hormones, such as insulin, somatotropin, and thyroxine, are involved in the process of endochondral ossification. Physiologic or iatrogenic alterations of these hormones or their derivatives could theoretically lead to the development of osteochondrosis. The contribution of these factors to the etiology of osteochondrosis will likely not be elucidated until the molecular mechanisms of endochondral ossification are better understood.

Treatment and Prognosis

The treatment of osteochondrosis should take into account several factors. The clinical signs; severity of the lesion; species, age, intended use, and relative value of the animal; and owner expectations should all be considered. Treatment options include both nonsurgical and surgical management.

Nonsurgical management should consist of rest, controlled exercise, and dietary evaluation. The mineral and carbohydrate levels of the diet should be evaluated carefully and any deficiency or excess corrected. Systemic NSAIDs and intraarticular medications such as corticosteroids, hyaluronic acid, and polysulfated glycosaminoglycans (GAGs) can all be administered, but minimal clinical evidence exists to support their use. In food-producing animals the clinician must take into consideration that these are not approved treatments and that withdrawal times may not be established. Given the nature of the disease, nonsurgical management may provide a favorable outcome only in very young animals with regenerative capacity or in those with very mild lesions and minimal to no clinical signs.

Animals with osteochondritis dissecans are best treated with arthroscopic surgery. Cases with no radiographic evidence of degenerative joint disease (DJD) before surgery and minimal articular damage at arthroscopy carry a favorable prognosis. Animals that show radiographic evidence of DJD before surgery or considerable damage to the articular surfaces at arthroscopy carry a guarded prognosis. Arthroscopic approaches to the joints of cattle have been described, but the procedure is more difficult than in the horse.¹⁶ In select cases, reattachment of large cartilage flaps with absorbable poly-p-dioxanone pins may be warranted.²⁸ Diet evaluation should be included with the surgical patients and appropriate adjustments made.

Treatment of subchondral cystic lesions is still controversial, and many options are available. Nonsurgical management can be attempted and should consist of rest, controlled exercise, and intraarticular injection of corticosteroids along with hyaluronic acid or polysulfated GAGs. The prognosis is guarded except in cases with very narrow openings into the synovial cavity, and alternate treatments should be considered in refractory cases. Cysts can be treated with ultrasonographically or arthroscopically guided intralesional deposition of corticosteroids, bone marrow aspirates, or a combination of the two. Studies are lacking as to the efficacy of this treatment. Arthroscopic debridement and curettage of the cystic lesion is another option, and horses less than 3 years of age carry a better prognosis. Recent investigations show promise for arthroscopic debridement and curettage of lesions followed by packing of the remaining defect either with a cancellous bone graft covered by a chondrocytic growth factor or with various bone substitutes.²⁸ Cysts located in the proximal interphalangeal joint are generally nonresponsive to conventional treatment, and arthrodesis of the joint offers the best prognosis.

Treatment of osteochondrosis in food animals is generally limited by the economic value of the animal. Show animals or valuable breeding animals may be treated by any of the methods previously described, and the surgical options will offer a better prognosis than nonsurgical treatment. In production herds, ration evaluation and genetic predisposition may be the only variables that can be addressed. A review of production records and estimates of monetary loss will indicate whether intervention is necessary.

Definition, Etiology, and Clinical Signs

Angular limb deformities are deviations in the axis of the forelimbs or hindlimbs in the frontal plane. Valgus deformity denotes a lateral deviation of the limb distal to the origin of the deformity; varus deformity denotes a medial deviation. The deformity is further described by naming the joint adjacent to the origin of the deformity; for example, carpus valgus describes an angular deformity arising in the carpal region with lateral deviation of the metacarpus (knock-kneed conformation) (Fig. 38-3).

Fig. 38-3 Carpus valgus deviation.

Angular limb deformities may be either congenital or acquired. In general, they are caused by laxity of periarticular supporting structures, incomplete ossification, or asynchronous growth rate. Although the underlying cause of these abnormalities remains undefined, potential causes include intrauterine malpositioning, relative immaturity, hereditary predisposition, rapid growth, dietary imbalances, osteochondrosis, and trauma.^29-31

Congenital angular deformities frequently are attributed to intrauterine malpositioning and laxity of periarticular supporting structures. They typically originate in the region of the carpus and tarsus, resulting in bilateral valgus deformity. It is also common to identify a “windswept” foaling in which valgus deformity of one limb is accompanied by varus deformity of the contralateral limb. Acquired angular deformities usually occur secondary to asynchronous growth. Additionally, a foal born with incomplete ossification may acquire an angular deformity secondary to crushing of the cartilaginous precursors of the cuboidal bones. A hereditary angular limb deformity of Suffolk, Suffolk crossbred, and Hampshire sheep is known as spider lamb syndrome (see later discussion).

Pathophysiology

Incomplete ossification is an important cause of angular deformities originating at the carpus and tarsus. The epiphyses and cuboidal bones of the carpus (ulnar, third, and fourth carpal bones) and tarsus (central and third tarsal bones) are primarily affected.²⁹ Ossification of the cartilaginous precursors of these bones occurs in late gestation; prematurity or relative immaturity results in the birth of a foal before these precursors are completely ossified (Figs. 38-4 and 38-5). If laxity of the periarticular supporting structures accompanies incomplete ossification, the deformity is congenital and may progressively worsen with weight bearing. If laxity is not present, the foal may be born with straight legs and may acquire an angular deformity after deformation of the precursors of the cuboidal bones during weight-bearing activity.

Fig. 38-4 Premature foal with incomplete ossification of the cuboidal carpal bones showing marked bilateral carpus valgus.

Fig. 38-5 Specimen from a foreleg of the premature foal in Figure 38-4, cut in the frontal plane. Note the thick cartilage surrounding the centers of ossification of the cuboidal carpal bones.

Foals can acquire an angular limb deformity as a result of asynchronous growth at the metaphyseal and epiphyseal growth cartilages.^30,31 An important cause of asynchronous growth is trauma to a portion of the growth cartilage of the physis.³² In many foals this trauma is in the form of nonphysiologic compression of the growth cartilage. Excessive exercise in foals with mild angulation and normal activity in foals with moderate to severe preexisting angular deformity may cause sufficient trauma to the growth cartilage to cause progressive deformity.

Asymmetric loading also occurs when severe lameness is present. With the change from a rectangular stance with four weight-bearing limbs to a triangular stance with three weight-bearing limbs, asymmetric, nonphysiologic loading of the weight-bearing limb occurs, which predisposes it to develop an angular deformity. Because compressive forces are concentrated along the medial aspect of the growth cartilages, a varus deformity usually develops in the overloaded limb. Abnormalities of the growth cartilage that affect ossification, such as osteochondrosis, also may be responsible for angular deformities caused by asynchronous growth. Foals with a predisposition for rapid growth or those that are exposed to nutritional imbalances appear to be at greatest risk for developing the disease. Rapid growth also may result in a foal with a large body size disproportionate to its skeletal structures. This condition may cause increased compressive forces, nonphysiologic loading of the growth cartilages, and angular deformity.³²

Ruminants raised in confinement may experience endochondral dysplasia and angular limb deformities if dietary iron is high or dietary vitamin D is low³³ (rickets). Elevated dietary iron results in elevations in serum phosphorus, which may in turn inhibit 1,25-dihydroxycholecalciferol synthesis by the kidney, resulting in rickets.³³ Pregnancy-associated epiphysitis in primiparous dairy goats³⁴ also may result in angular limb deformities.

Evaluation and Radiographic Findings

In the evaluation of a foal with an angular deformity, important historical information includes age, onset and progression of the deformity, and intended use of the foal. The foal should be observed carefully while standing and walking to characterize the degree of deformity and determine the presence of compensatory problems or lameness. Physical examination includes careful palpation of the affected limb and a determination of whether the deformity can be corrected by manual manipulation of the limb. If the foal is examined before ossification has progressed, deformities resulting from laxity of periarticular supporting structures and incomplete ossification can be corrected manually. On the other hand, if deformities in foals born with incomplete ossification are left untreated and the cuboidal bones are in a collapsed configuration, or if deformities are the result of asynchronous growth, they cannot be corrected manually.

An arthropathy should be suspected if lameness is present. Collapse of incompletely ossified cuboidal bones may result in deformation of articular surfaces and subsequent DJD. When this occurs in the carpus, the prognosis for athletic performance is guarded to poor. If the cuboidal bones of the tarsus are affected, mild collapse may not adversely affect performance, but with significant collapse, degenerative change is likely. A less common cause of lameness in foals with angular limb deformity is osteochondrosis. The prognosis for athletic performance in foals with osteochondrosis-associated angular limb deformities is guarded, depending on the severity of the cartilage lesions.

The importance of early radiographic evaluation of foals with angular deformity cannot be overemphasized. If a diagnosis of incomplete ossification is delayed, irreparable damage, as described previously, may occur. In fact, a strong argument can be made for radiographic evaluation of all foals shortly after birth before uncontrolled exercise is allowed. Radiographic evaluation is mandatory to determine the degree of ossification in premature foals, twins, foals that appear to be relatively immature at birth, and foals born with angular deformities.

Radiographic evaluation allows the examiner to identify the origin of the deformity and determine its severity. Dorsopalmar views for the carpus and fetlock using 7 × 17–inch film cassettes and a lateromedial view of the tarsus are recommended. In the carpus and fetlock the origin of the deformity may be subjectively determined by two geometric methods (Fig. 38-6). One is to draw longitudinal lines bisecting the long bones above and below the joint. Where these lines intersect is the pivot point, which is considered the origin of the deformity. In addition, the angle of incidence of these lines is an estimation of the degree of deformity. Another method, which the author prefers for the carpus and fetlock, is to draw lines through the joints and adjacent physes. These lines should be parallel to each other and perpendicular to the long axis of the long bones proximal and distal to the affected joint. The origin and degree of deformity are estimated by determining where and by what degree these lines deviate from normal. Both asynchronous growth and incomplete ossification can occur concurrently, which is most easily determined with the latter method of geometric evaluation²⁹ (Fig. 38-7). Geometric examination to determine the degree of deformity in the tarsus is less reliable because the tibia and third metatarsus are not in the same frontal plane. The severity of the angular deformity in this location is best determined by a careful visual assessment.

Fig. 38-6 Two methods for geometric evaluation of an angular deformity at the carpus. Lines A and B are drawn through the long axis of the radius and metacarpus, respectively. The angle of incidence is 15 degrees. Lines a, b, c and d are drawn through the distal radial physis, antebrachiocarpal (radiocarpal), middle, and carpometacarpal joints, respectively. Line a′ is drawn parallel to line b, and line a″ is perpendicular to A. Their angle of incidence is 15 degrees.

Reprinted with permission from Compend Cont Educ (Pract Vet)4:S330, 1982.

Fig. 38-7 Geometric evaluation of an angular deformity at the carpus caused by a combination of asynchronous growth and incomplete ossification. The pivot point, c, identified by lines A and B, indicates that the origin of the deformity is in the distal radial epiphysis. However, lines a, b, c and d are not parallel to each other; and lines a, b and c are not perpendicular to the long axis of the metacarpus and radius. Their orientation indicates that the deformity is in the distal radial physis and the cuboidal carpal bones as well. Note that the sum of angles of a-a′, b-b′, and c-c′ equals the angle of incidence of lines A and B.

Reprinted with permission from Compend Cont Educ (Pract Vet) 4:S330, 1982.

Radiographic examination of foals with incomplete ossification reveals a rounded contour to the affected bones instead of their normal angular appearance. The width of the radiolucent cartilage is increased, appearing radiographically as an increase in the width of the joint space (Fig. 38-8). As ossification progresses, the bones may appear wedge shaped or crushed because of deformation of the cartilage during weight bearing. This phenomenon often is noted in the ulnar, fourth, and lateral aspect of the third carpal bones in the forelimb and the central and third tarsal bones in the hindlimb. In severe cases the affected bones may be grossly deformed and appear to be partially extruded from the joint (Fig. 38-9). In the tarsus, lateromedial radiographs are used to determine whether ossification is complete (Fig. 38-10).

Fig. 38-8 Dorsopalmar radiograph of a foal with mild incomplete ossification of the cuboidal carpal bones. Note the difference in width of the medial aspect, a, and the lateral aspect, b, of the third carpal bone. Normally, width a should be approximately three-fourths the width of b.⁴¹ Also note the appearance of an increase in the width of the joint space, c, as a result of incompletely ossified joint cartilage.

Fig. 38-9 Dorsopalmar radiograph of a foal with incomplete ossification that was not externally supported. Severe deformation and collapse of the fourth and third carpal and proximal fourth metacarpal bones have occurred.

Fig. 38-10 Lateral-to-medial radiograph of a tarsus from a foal with incomplete ossification. Note the lack of an angular appearance of the central tarsal bone and incomplete ossification of the third tarsal bone.

Radiographic evaluation of foals with angular deformity caused by asynchronous growth may show wedging of the epiphysis (Fig. 38-11), widening of the physis, and sclerosis adjacent to the physis. Geometric evaluation places the deviation in the metaphysis or the epiphysis of the long bone proximal to the affected joint. The joints are parallel each other and are perpendicular to the longitudinal axis of the adjacent long bones.

Fig. 38-11 Dorsopalmar radiograph of a foal with angular deformity caused by wedging in the distal radial epiphysis, the result of asynchronous growth of the epiphyseal growth cartilage.

Treatment and Prognosis

Neonatal foals with an angular deformity should be confined to a stall until clinical and radiographic examinations are completed. If the deformity is 10 degrees or less and radiographs reveal normal ossification, stall confinement with periods of controlled exercise is recommended. This regimen promotes continued development of the supporting structures while minimizing trauma to growth cartilages that could result if the foal were allowed uncontrolled exercise.

Foals with a congenital angular deformity of more than 10 degrees accompanied by incomplete ossification or ligamentous laxity failing to improve with controlled exercise should be externally supported. If incomplete ossification is present and the limb is not supported in axial alignment, continued weight bearing can cause deformation of the cartilaginous structures. Subsequent ossification results in a permanent deformity of the affected bones (see Fig. 38-9).

Methods of externally supporting the carpus and tarsus vary from the application of tube casts or rigid splints to custom-made orthotic devices. Tube casts have been recommended and used successfully for several years.^29-31 Although tube casts provide the rigid external support needed to maintain axial alignment while ossification progresses, several potential complications are associated with their use. The most serious complication is the potential for coxofemoral luxation when tube casts are used on the hindlimbs. In addition, foal skin is easily traumatized by a poorly fitting cast, and deep ulcerations may occur. Other considerations include the cost of materials and need for constant monitoring to detect signs of a poorly fitting cast. Monitoring the status of a cast requires daily evaluation by a trained individual, and owners are seldom capable or willing to take on this responsibility; therefore hospitalization is recommended. Rigid splints are an alternative method of support. The leg is protected with a padded support bandage, and the splint is applied with nonelastic tape while the limb is held in alignment by an assistant. These splint bandages are changed every third or fourth day. Pressure sores beneath the splint bandage are a concern and must be prevented. A splint for the tarsus may be fashioned from synthetic casting material molded lengthwise over the cranial aspect of a padded bandage centered at the joint. Once the material has dried, the splint is taped to the dorsal surface of the bandage.

Regardless of the means of external support used for the carpus or tarsus, it should not extend beyond the distal metacarpus or metatarsus. Continued weight bearing by the suspensory apparatus of the fetlock helps prevent the development of fetlock hyperextension after removal of the external support. A degree of carpal hyperextension is usually present immediately after removal of external support from the forelimb, and exercise should be controlled until the tendons and periarticular supporting structures regain their normal tone.

Foals with angular deformity resulting from asynchronous growth should also be confined to a stall and allowed only controlled exercise to minimize the magnitude of asymmetric loading at the growth cartilages and encourage spontaneous correction. In these cases, reducing the magnitude of the forces acting asymmetrically at the growth cartilage should encourage compensatory growth to occur and correct the deformity. Additional therapy consists of corrective hoof trimming. Because foals with valgus deformity typically have a toe-out conformation, emphasis in the past has been to lower the lateral hoof wall of the affected limb. If this mode of therapy is vigorously pursued, compensatory varus deformity may develop in the fetlock region. This form of corrective trimming concentrates forces asymmetrically on the medial aspect of the distal metacarpal and proximal phalangeal growth cartilages. Currently, trimming the hoof level and squaring the toe to promote breakover at the toe are recommended. If the lateral hoof wall is to be lowered; only a few millimeters should be removed each week.

Foals with angular limb deformities that fail to respond to stall confinement are candidates for surgical therapy. Although it was previously believed that animals with angular deformities arising distal to the physis were not candidates for surgical therapy, it has been shown that they can respond favorably to surgery.^35,36

The decision for surgery should take into account the amount of correction required (degree of deformity) and the age of the foal. The more severe the deformity, the earlier should be the surgical intervention. Timing of surgery should consider the periods of rapid and predictable growth at the physis. The most rapid and predictable rate of growth occurs from birth to 10 weeks of age.³⁷ In the distal radius, continuous but declining growth occurs until 60 weeks of age. In the distal third metacarpal and metatarsal bones, growth rate slows dramatically by 10 weeks of age and stops shortly thereafter.

Surgical manipulation of physeal growth is intended to alter asymmetrically the elongation occurring at the physis, thereby realigning the axis of the limb. Growth at the physis can be altered surgically in one of two ways: retardation or acceleration. Growth retardation is accomplished by bridging the physis with metallic implants. When applied to the convex side of the affected physis, growth is disallowed on the long side of the bone while continued growth on the opposite of the bone brings the limb into alignment. As long as the implants are in place, the effect continues and is limited only by the amount of growth remaining at the physis. If the physis is still active once the limb is aligned, it is extremely important that the implants be removed, or overcorrection will occur. Techniques of transphyseal bridging include stapling, screw and wire implants, the use of a small bone plate, and more recently, a single transphyseal screw. Indications for transphyseal bridging include deformities that present after the period of rapid and reliable physeal growth, severe angulations, and based on the author’s experience, deformities of the carpus and tarsus resulting from cuboidal bone malformations.

In the second surgical approach to altering physeal growth, periosteal transection and elevation (stripping) is aimed at promoting growth acceleration on the concave side of the bone.³⁸ Reported advantages include rapid correction without the potential for overcorrection.^35,38 Periosteal transection does not require implants; therefore the likelihood of infection and excessive fibrosis is reduced. Implant failure is not a consideration, and a second surgery for implant removal is not required. The procedure does not require specialized equipment and is technically easy to perform. In one series of foals, correction of the deformity occurred in 22 of 25 limbs treated with periosteal transection.³⁸ In a second series of 23 foals, 83% had straight limbs and were sound for their intended use at long-term follow-up.³⁵ The success rate was not affected by the origin of the deformity, degree of deviation, or presence of mild to moderate morphologic changes in the involved bones.³⁸ Indications include mild to moderate deformities present during the rapid, reliable growth at the involved physis. The periosteum will reestablish itself, so the surgical effect is short-lived, and if correction is not adequate within 4 to 6 weeks, additional therapy is indicated.

Definition and Etiology

Spider lamb syndrome is characterized by generalized chondrodysplasia and is apparently a semilethal autosomal recessive trait. Variable expressivity of the trait may occur in the homozygous animal.^40-42 It has been seen in Suffolk, Suffolk crossbred, and Hampshire sheep (Hampshire sheep often have some Suffolk breeding). At this time, no chondrodysplastic lambs from any white-face breeds of sheep have been reported.

Clinical Signs

Lambs affected with spider lamb syndrome are characterized by overall appendicular and axial deformities, including one or more of the following conditions^40,42: kyphosis, scoliosis, concavity of the sternum, lateroventral deviation of the maxilla (crooked nose and Roman nose), and angular limb deformities. The limb deformities usually include a “knock-kneed” appearance at the carpus (carpus valgus) and lateral deviation with rotation of the metacarpus or metatarsus (Fig. 38-12). In addition, these lambs show extreme height, fineness of bone, poor muscling, and failure to thrive (Fig. 38-13).

Fig. 38-12 Rotation and deviation of front legs (carpus valgus) characteristic of spider lamb syndrome in a 16-week-old Suffolk lamb.

Fig. 38-13 Twin Suffolks (12 weeks old), with normal lamb (78 pounds) at left and lamb with spider syndrome (37 pounds) at right. Note extreme height, narrow chest, scoliosis, kyphosis, and facial deformity of affected lamb.

The number and severity of the deformities seen in individual lambs vary widely. Spider lamb syndrome can occur in two types of lambs: those that are obviously abnormal at birth and, more often, those that develop abnormalities at 3 to 8 weeks of age. Lambs that are abnormal at birth may have kyphosis, scoliosis, facial deformities, deformed sternum, and angular limb deformities.⁴⁰ Lesions may be present as early as day 100 of gestation but are not detectable by radiographic or ultrasound examination.⁴² The lambs may be stillborn or die within a few days of birth because of their inability to stand or nurse. If these lambs are maintained by good nursing care, they fail to gain weight normally and usually die of secondary problems (e.g., scours, pneumonia) by 4 weeks of age. In lambs that are apparently normal at birth but develop angular limb deformities at 3 to 8 weeks of age, one to four limbs may be affected; and close examination may show curvature of the spine and concavity of the sternum. Often these lambs are unusually tall, long necked, fine boned, and poorly muscled. The growth rate of these “spider lambs” decreases after 4 to 8 weeks of age, and the various deformities become more marked until the lambs can no longer walk; chronic bacterial pneumonia and pathologic fractures are common.

Attempts to maintain spider lambs for research are rarely successful beyond 6 months to 1 year of age. In Illinois an affected ram lamb was able to breed seven ewes before he died, but in California, two affected ram lambs failed successive semen evaluations from 7 to 12 months of age and were euthanized because of their poor condition.

Diagnosis

Currently, spider lamb syndrome is diagnosed on the basis of appearance, radiographic changes, and pathology (gross and microscopic). Radiographic changes are diagnostic, although serial radiographs may be necessary in some cases. There are widened, irregular growth plates with retained islands of cartilage in the olecranon, sternum, shoulder, long bones, and spine (Fig. 38-14). The most constant radiographic lesion is in the olecranon, which exhibits multiple islands of ossification instead of the uniform, nonmineralized cartilage surrounded by dense bone in a normal lamb.^40,43 The olecranon should be radiographed lateral to medial with the elbow flexed. The changes in the olecranon usually begin by 1 to 3 weeks of age and are progressive. Lambs that are stillborn or die in the first week of life may not exhibit radiographic abnormalities in growth plates associated with spider syndrome.

Fig. 38-14 Lateral radiograph of front leg of a lamb with spider syndrome. Note thick, irregular growth plates and multiple ossification centers near the olecranon and distal humerus.

Chromosomal evaluation, hematology, and standard serum chemistry, as well as morphologic and biochemical evaluations of growth plate, have not been abnormal in spider lambs.^42-44 Circulating levels of insulin-like growth factor type I (IGF-I) and its associated hepatic messenger ribonucleic acid (mRNA) are increased in very young spider lambs. The proliferative zone of the growth plate is a major target of IGF-I.⁴⁵

Differential diagnosis includes other diseases that result in congenital defects (scoliosis, kyphosis, and arthrogryposis, often associated with hydranencephaly), including Cache Valley virus, bluetongue virus, lupine ingestion, and the bent leg syndrome.^40,43 The bent leg syndrome is believed to be a dietary problem in young lambs suckling ewes on unimproved pasture; chondrodysplasia of the elbow is not present.

Epidemiology

Limited breeding trials, pedigree analysis of breeding stock producing “spiders,” and the wide geographic distribution of spider lambs indicates that the spider syndrome is an inherited defect and is probably an autosomal recessive gene.^41,42 Some workers believe that the selection for very tall sheep within the Suffolk breed resulted in selection for the recessive trait. Affected lambs are double recessive (ss), and both the parents must be carriers (heterozygotes Ss) to produce a spider lamb (Fig. 38-15). Carrier sheep appear to be fairly common within the seed stock of the Suffolk breed and presently can be identified only when they produce a spider lamb. The appearance of a clinically affected lamb may lag years behind the introduction of carrier breeding stock, especially if a carrier ram is crossed into a ewe flock free of the trait. It is important that the diagnosis of a spider lamb is made correctly and with care, particularly in lambs that die before 3 weeks of age, because the condition may be confused with other congenital defects causing scoliosis, kyphosis, and arthrogryposis. Not all lambs suspected as being spider lambs can be confirmed as such.

Fig. 38-15 Spider syndrome is believed caused by an autosomal recessive trait. This figure illustrates probable mode of inheritance in two possible matings that could produce spider lambs. SS, Normal; Ss, carrier; ss, affected.

Necropsy Findings

Gross postmortem examination findings are similar to radiographic changes (generalized chondrodysplasia). Joint cartilage may show erosion, and excess cartilage is evident in thickened, irregular growth plates and in the olecranon. Retained cartilage cores are apparent on the metaphyseal side of affected growth plates. Dysplastic growth plates of spider lamb syndrome are characterized by thickened, proliferative, and hypertrophic zones and a failure to form organized columns. Histologically, chondrocytes exhibit a chaotic pattern of ossification, with chondrocyte proliferation in areas of maturation and loss of normal pattern and direction.^40,44

Prevention and Control

Carrier rams should be destroyed, but carrier ewes can be used to produce market lambs or to progeny-test rams for the spider trait. Ram lambs produced from carrier ewes must not be used for crossbreeding on commercial ewes of any breed, except for terminal cross-market lambs, because crossbred Suffolk lambs can carry the trait into the commercial sheep industry. A ram can be progeny-tested by breeding to ewes that have produced spider lambs or by breeding to its own daughters. If a ram produces 16 normal offspring from matings with known carrier ewes or 32 normal offspring from mating with his own daughters, the probability that he is a carrier is less than 1 in 100. This procedure is costly to the breeder, and the temptation to retain a ram without an adequate number of test progeny is great. Rams that have enough normal progeny to reduce the probability of being a carrier to less than 5 in 100 have produced spider lambs from the next test breedings needed to complete the progeny test.* Within the purebred industry, breeding stock is classified as “white” (no known spider progeny), “gray” (sire or dam or sibling has produced a spider lamb, but this individual has not), or carrier or “black” (individual has produced a spider lamb). Inaccuracies in sheep pedigrees make prediction of the genetic makeup of any individual risky, and classification without proper testing may be potential grounds for legal action. If parentage of a spider lamb is in question, blood-typing of the sire, dam, and offspring may be helpful.^†‡

Incidence and Risk Factors

Septic arthritis can result from extension of a periarticular wound infection, traumatic inoculation, iatrogenic inoculation, or hematogenous inoculation. The hematogenous route is the most common avenue of inoculation of organisms in a joint in foals, and bacteremia and septicemia are the most important risk factors for septic arthritis in foals. In one study, septicemia was the most common cause of death (30%) in foals under 7 days of age; septic arthritis was identified as the cause of death in 12.5% of foals age 8 to 31 days.⁴⁶ In adults, articular wounds are reported to be the most common cause of joint infection, followed closely by iatrogenic intraarticular injection; postsurgical infection and idiopathic (unidentified cause) are also reported in association with septic arthritis in adult horses.^47,48 Although uncommon, hematogenous spread from a distant focus is possible in adult horses.

Establishment of infection depends on several factors, including size of inoculum, host defense, virulence of the organisms, and local joint factors. In foals, host defense is mainly associated with passively acquired immunity. Failure of transfer of passive immunity (FTPI) is the greatest risk factor for development of septicemia in foals.⁴⁹ The incidence of disease resulting from FTPI has been reported to be as high as 78%. Organism virulence is related to the ability to establish infection. Attachment factors, ability to resist phagocytosis, and resistance to cell killing all contribute to the establishment of infection. Local joint factors that may predispose to establishment or maintenance of infection include low blood flow, particularly in end-loop capillaries, and poor blood supply, more prominent in bone. In adults, certain intraarticular medications (e.g., corticosteroids, hyaluronate, polysulfated GAGs) have been associated with a higher risk for septic arthritis, potentially by decreasing articular defense.^50,51

In calves, septic arthritis is associated with FTPI and septicemia and with feeding of mastitic milk (Mycoplasma). In older cattle, direct spread from a perisynovitis is the most common cause, and the distal interphalangeal joint is most often involved.

Pathogenesis

Articular blood supply is provided through a main arteriole that branches to the synovial membrane and epiphysis. Blood supply to the metaphysis is provided by the nutrient artery, but in young foals, transphyseal vessels exists that connect the metaphyseal and epiphyseal blood supply.⁵² Experimental intravenous (IV) injection of bacteria results in rapid inoculation of articular and periarticular capillaries. Five types of hematogenous articular infection have been described: type S (synovial), where a septic arthritis results from inoculation of the synovial membrane; type E (epiphysis), where subchondral bone infection is present (Fig. 38-16); type P (physis), where infection of the physis occurs on the metaphyseal side of the growth plate (Fig. 38-17); type T, observed in premature foals, with infection of the small tarsal or carpal bones (Fig. 38-18); and type I, where joint invasion occurs after a periarticular soft tissue abscess (Fig. 38-19).⁵³ In young foals, functional transphyseal vessels allow communication of the metaphysis and epiphysis, such that bacteria localize preferentially in the synovial membrane and subchondral bone. Thus, young foals predominantly have infectious arthritis types S and E. Closure of transphyseal vessels occurs after about 7 to 10 days of age, such that localization of infection to the metaphyseal vessel loops occurs in older foals.⁵² Although bone inoculation can occur simultaneously with synovial inoculation in young foals, determination of bone involvement can be delayed until radiographs identify the lesions. In foals the hock, carpus, and stifle are frequently involved in hematogenous joint infection, but it is important to remember that any joints, including those of the vertebral column, can be affected. In young foals, Actinobacillus equuli, Salmonella species, Escherichia coli, and other Enterobacteriaceae are often involved; in older foals, Streptococcus species and Rhodococcus equi are common isolates. In foals with type P (physeal) involvement, Salmonella and Rhodococcus species are typically involved.

Fig. 38-16 Radiograph of a foal with type E septic arthritis showing involvement of the distal femoral epiphysis (arrow).

Fig. 38-17 Radiograph of a foal with type P septic arthritis showing involvement of the distal metacarpal physis (arrows).

Fig. 38-18 Radiograph of the tarsus of a premature foal with type T septic arthritis showing involvement of the distal tarsal bones (arrows).

Fig. 38-19 Foal with type I septic arthritis where a soft tissue abscess (arrow) dissected down into the coxofemoral joint.

In adults, inoculation of the joint from an articular wound is the most common cause of joint sepsis. The establishment of infection will depend on size of the inoculum, pathogenicity of the bacteria, and duration before treatment. In one study, 53% of horses examined within 24 hours of an open joint wound developed septic arthritis, versus 92% of horses examined within 2 to 7 days of injury and 100% of horses examined after 7 days.⁵⁴ Joints of the lower limb (fetlock, coffin joint) are often involved in open joint injuries because of the poor tissue coverage in those areas.^48,55 Organisms frequently encountered in open joint wounds include Enterobacteriaceae, streptococci, and staphylococci.^48,55 These injuries are also likely to have multiple bacterial infections. Wounds near the hoof are more likely to have anaerobic infection, and Clostridium is the most common isolate. Fungal organisms are a rare cause of septic arthritis in horses but should be considered if isolated in pure culture more than once.⁵⁶

Iatrogenic joint injection is the second most common cause of septic arthritis in adults, followed by postoperative infection. The tarsus is the joint most often involved in septic arthritis after joint injection, whereas the carpus is the most common joint involved after surgery.^47,48 Staphylococci, particularly Staphylococcus aureus, are the most common organism isolated after iatrogenic joint injections or surgery. When S. aureus is isolated from a joint infection, care should be taken to identify further the possibility of methicillin resistance.^57,58 The risk of septic arthritis after arthroscopic surgery is low, 8 of 627 joints (1.3%) in one study.⁵⁹ Interestingly in these horses, clinical signs did not develop until several days after discharge.

In adult cattle, common pathogens involved in septic arthritis include Mycoplasma bovigenitalium, Mycoplasma mycoides, Brucella species, and Arcanobacterium (Actinomyces) pyogenes, which is most often involved.⁶⁰ In sheep, goats, and calves, Chlamydia psittaci polyarthritis can occur as an endemic or epidemic disease and may be accompanied by keratoconjunctivitis.^61,62 In lambs, Erysipelothrix rhusiopathiae is also a cause of polyarthritis, gaining systemic entrance through the stump of docked tails or castration site. Improving hygiene during these procedures helps prevent the disease.⁶¹

Diagnosis

Septic arthritis, osteomyelitis, or physitis should be ruled out in any lame foal. Foals with septicemia are at high risk of developing septic arthritis, which generally is noted clinically hours to days after the initial signs of septicemia. Although owners often complain of external trauma, septic arthritis is the most common cause of lameness in foals. In young foals with types S and E arthritis, inoculation of the synovial membrane is the first event, which the astute clinician can identify as periarticular edema. Joint effusion rapidly follows. Involvement of multiple joints is common, and identification of all affected joints is essential for successful management. Because effusion of the shoulder, elbow, or hip joints is more difficult to detect by palpation, arthrocentesis of these joints should be performed in foals with an unidentified lameness. In the stifle, femoropatellar joint involvement results in marked effusion; however, femorotibial joint effusion is usually more difficult to discern. Because of the usual communication between the femoropatellar and the medial femorotibial joint, both are usually involved concurrently. Lateral femorotibial infection is more subtle to identify and can occur separately. Distention of the long extensor pouch is often present in lateral femorotibial infection and suggests involvement of that joint. In foals older than 7 days, physeal infection may be observed. With physeal infection, presence of concurrent synovial effusion depends on the intraarticular or extraarticular localization of the growth plate. For example, distal metacarpal physeal infection results in periphyseal edema, initially without joint effusion. The infection can break through the skin, rather than involving the joint. In foals with septic arthritis, the CBC is consistent with an inflammatory response and includes a neutrophilic leukocytosis and hyperfibrinogenemia.

Adult horses usually show minimal changes on the CBC and little change in systemic signs; therefore the development or increasing lameness after a wound, joint injection, or surgery indicates the need for further examination. Because of their potent antiinflammatory properties, corticosteroids may delay the onset of clinical signs of septic arthritis after joint injection. In one study of experimentally induced septic arthritis, changes in synovial fluid were present before the onset of clinical signs, and clinical signs of lameness were delayed for 3 days in these horses.⁶³

Arthrocentesis is the mainstay of diagnosis of septic arthritis.⁶³ Table 38-1 lists the characteristics of synovial fluid according to conditions in large animals. A high protein concentration (>2.5 g/dL) and high white blood cell (WBC, leukocyte) count are observed. Classic counts diagnostic for septic arthritis in foals exceed 30,000 cells/μL, with greater than 90% neutrophils; however, cell counts greater than 10,000/μL may indicate early infection. Neutrophils are not always degenerate. Gram stain is a useful diagnostic tool because it may identify the etiologic agent in up to 25% of cases in which culture results are negative.⁶⁴ In foals with a separate physeal infection, where the physis is extraarticular, sympathetic joint inflammation and effusion can occur.⁶⁵ This manifests as a moderate increase in WBC count, with less than 90% neutrophils. The presence of such cytologic findings should alert the clinician and practitioner to the presence of physeal sepsis.

Table 38-1 Characteristics of Synovial Fluid According to Condition in Large Animal

In adult horses with a wound localized near a synovial structure, it is crucial to identify as early as possible whether there is synovial involvement. The most convincing evidence is demonstration of synovial communication with a wound by injecting a sterile solution in the synovial structure and observing fluid exiting from the wound. For this purpose, a site remote from the wound and covered with normal skin should be prepared aseptically, and depending on the structure involved, 20 to 200 mL of a sterile solution (e.g., saline, balanced electrolyte) is injected, after collection of synovial fluid samples using aseptic technique.⁶⁶ If synovial involvement is detected, therapy is immediately instituted.

Radiographs of all affected joints are essential. The presence of osteomyelitis may affect prognosis and dictate prolonged antibiotic therapy. Radiographs should be repeated weekly until resolution of clinical signs, or any time there is deterioration in the clinical condition. Radiographs are also indicated whenever a change in therapy is planned (e.g., from IV to oral antibiotics).

Nuclear scintigraphy has been used to diagnose infectious foci in odd localizations in foals. For example, vertebral and atlantooccipital involvements have been diagnosed using this imaging modality. It must be remembered that local bone infarcts, which are often present in osteomyelitis, will result in areas of decreased rather than increased uptake. Scintigraphy using technetium-99 m (^{99 m}Tc)–labeled WBCs or ciprofloxacin labels has potential uses in foals with multiple-limb involvement and warrants further investigation as an imaging modality for septic arthritis.⁶⁷ Newer imaging capabilities (e.g., MRI, CT) may evolve as diagnostic modalities in septic arthritis (Fig. 38-20).

Fig. 38-20 Computed tomography scan of a foal with septic arthritis of the left coxofemoral joint showing osteomyelitis of the acetabulum (arrows) that was not radiographically evident.

Identification of the organism should be attempted in all cases of septic arthritis. Gram stains, culture of synovial fluid in blood culture bottles, and culture of synovial biopsies have been suggested to increase the likelihood of identification of the organism. In general, the positive culture rate from synovial fluid samples is approximately 50%, and synovial biopsy culture has a low yield to increase this figure.⁶⁴ Appropriate culture techniques should be used for organisms such as Chlamydia or Mycoplasma species, and special stains may be required. In foals, because bacteremia or septicemia precedes the local signs, blood cultures should be obtained. In addition, any other local sites of infection should be cultured. In cases of septic physitis, needle aspiration of the affected site under radiographic or fluoroscopic guidance can be performed. In the future, other techniques for early identification of synovial sepsis may become available.⁶⁸

Treatment

Septic arthritis is an emergency. Immediate assessment followed by institution of treatment should be done as soon as possible after problem identification. Treatment of septic arthritis includes systemic broad-spectrum antibiotics, local joint lavage and debridement, and local antibiotics. Systemic antibiotics are best administered intravenously to ensure adequate tissue concentrations. Most often the combination of a β-lactam and an aminoglycoside or fluoroquinolone is used in adults; a β-lactam and aminoglycoside combination is most often used in foals because fluoroquinolones may have detrimental effects on articular cartilage in young animals. In open joint injuries, particularly if an anaerobic organism is suspected, metronidazole may be added to the antibiotic regimen. Gram-positive organisms can be isolated from blood cultures in up to 33% of foals with sepsis, so gram-positive coverage is also important.⁶⁹ In foals with physeal involvement, Gram stain and culture of a physeal aspirate are helpful to identify the causative agent. The most common organisms isolated from septic physitis are Salmonella species and Rhodococcus equi. If R. equi is identified, appropriate therapy with erythromycin, azithromycin, or clarithromycin and rifampin should be instituted, keeping in mind that resistance to rifampin and erythromycin has been reported; therefore, obtaining susceptibility patterns may be warranted.⁷⁰ In general, the presence of osteomyelitis may warrant an antibiotic combination that reaches effective bone levels; rifampin with another antibiotic is often used. Rifampin should not be used as the sole antimicrobial because resistance is acquired rapidly with this antibiotic. Other antibiotics that reach effective bone concentrations include tetracyclines, chloramphenicol, fluoroquinolones, and cephalosporins. If cephalosporins are chosen, third-generation agents (e.g., ceftiofur, cefotaxime, ceftriaxone, ceftazidime) are preferred because they are more effective against gram-negative bacteria. In foals, fluoroquinolones should be reserved for organisms that are only susceptible to this class of drugs because evidence shows cartilage lesions developing in immature animals with their use.^71,72

Local lavage of the joint or synovial structure is an important component of therapy; removal of debris, fibrin, and inflammatory mediators helps minimize damage and eliminate the organism. In foals, joint lavage can be performed under heavy sedation or short-term general anesthesia. In adults, sedation and a regional block can be used or short-term general anesthesia. Joint lavage can be performed using through-and-through needle technique; use of a pressure bag or a pump will facilitate efficient lavage of several liters of fluids through the joint. This technique may be sufficient in joints where the diagnosis was made early, where the infection is not severe, and in simple joints (fetlock, carpus). If there is poor response to treatment after one or two sequential joint lavages, arthrotomies should be performed without hesitation. Often, fibrin accumulation in the affected joint precludes effective lavage and allows sequestration of bacteria. Once arthrotomies have been performed, the affected joint will need to be covered with a sterile bandage. During subsequent lavages, a teat cannula inserted in the arthrotomies may be used to lavage the joint. The arthrotomies are left to heal by second intention; the joint will need to remain bandaged until the arthrotomies are closed. Occasionally, delayed closure of the arthrotomies is necessary, particularly in arthrotomies localized over high-motion joints. In joints with multiple compartments (stifle, hock), in severe infection or osteomyelitis, in cases of longer duration, or in animals with poor response to joint lavage, arthroscopic debridement is indicated.⁷³ Arthroscopy has several advantages over simple needle lavage. It allows thorough debridement, removal of fibrin, and lavage of all compartments, as well as evaluation and debridement of cartilage and underlying bone lesions. In addition, arthroscopy may have prognostic value when radiographic lesions are equivocal. The arthroscopic portals can be left open for drainage and subsequent lavage but must be kept under a sterile bandage.

Intraarticular antibiotics are advocated for the management of septic arthritis. Delivery of local antibiotics to the affected joint can be achieved by intraarticular injection, regional IV or intraosseous (IO) perfusion, continuous antibiotic delivery, or implantation of antibiotic-impregnated, biocompatible materials. Aminoglycosides (gentamicin, amikacin) and ceftiofur have been shown to maintain levels above the minimum inhibitory concentration (MIC) for 24 hours after a single intraarticular injection.^74,75 Other third-generation cephalosporins are also routinely used in the treatment of joint sepsis, at least until the susceptibility patterns are obtained. Antibiotic-impregnated polymethylmethacrylate (PMMA) beads can also be used, although direct implantation into a joint can result in cartilage damage.^76-78 PMMA implants are fabricated by mixing the desired antibiotic with the powder before adding the polymerizer. Antibiotics evaluated for inclusion in PMMA include gentamicin, metronidazole, vancomycin, ceftiofur, cefazolin, and amikacin.^79-87 Tetracyclines do not elute from PMMA and should not be used. Antibiotic combinations have also been used; metronidazole and gentamicin elute well from PMMA, but the combination of cefazolin and gentamicin is not recommended.^85,86 The implant is then molded into beads and strung on nonabsorbable suture material. The implant is placed into the affected joint or bone, and elution usually persists for approximately 7 days, with peak levels in the first 24 to 48 hours depending on the antibiotic used; the implant is then removed and may be replaced. Antibiotic-impregnated implants, such as gentamicin-impregnated collagen sponges,* have been evaluated experimentally and are commercially available in Europe.^88-90 Garamycin sponges consist of highly purified cattle collagen; the gentamicin molecules are embedded within the pores of the collagen. No stabilizing agents or foreign substances are added. A 50 × 50-mm sponge contains 32.5 mg of gentamicin base and 70 mg of collagen. The main advantage of these implants is that a separate procedure for their removal is not needed.

Regional intravenous perfusion (RIP) or intraosseous perfusion (ROP) are also advocated for the treatment of septic arthritis complicated with osteomyelitis.^91,92 The techniques are performed by first placing a tourniquet around the limb proximal to the location of the joint and/or bone involved. Regional perfusion cannot be performed for joints above the carpal/tarsal region because of the inability to place a tourniquet in those locations. After tourniquet placement, a regional vein is catheterized using a 23-gauge butterfly catheter for RIP; an IO screw is inserted for ROP.^† The antibiotic is subsequently injected and the tourniquet left in place for 30 to 45 minutes. Antibiotics, particularly aminoglycosides and enrofloxacin, should be diluted in 20 to 40 mL of saline to avoid phlebitis at the injection site.

Continuous infusion of antibiotics can also be accomplished by placing a small catheter into the joint and attaching it to an infusion system^‡ (pump syringe, balloon infuser).⁹³ In foals it is difficult to maintain these catheters in place, and considering the concentration of antibiotics achieved after intermittent intraarticular injection or regional perfusion, the aggravation of trying to make the system work is probably not warranted.

With extensive physeal lesions in foals, curettage, autologous bone grafting, and external coaptation may be required.^94,95 The addition of tricalcium phosphate granules or bioresorbable paste may be considered.⁹⁶ Angular limb deformities may result from growth disturbances or collapse of the physis on the affected side. In adults with septic arthritis and osteomyelitis, curettage of the bone lesion followed by bone grafting and external coaptation may also be indicated.⁹⁷ Adjunctive therapies that may help alleviate inflammation include sodium hyaluronate, polysulfated GAGs, and dimethyl sulfoxide (DMSO). Sodium hyaluronate and polysulfated GAGs can be used systemically or locally, but local use should be reserved for when infection is under control because these agents decrease joint defense mechanisms.^51,98 Although DMSO has significant antiinflammatory properties in joints, it should be used with caution because of its negative effects on cartilage metabolism.⁹⁹

In addition to specific therapies, management of pain, stress, and other metabolic disturbances are indicated. Pain can be managed by judicious use of NSAIDs, using the smallest dose that will keep the animal comfortable. If a foal continues to show severe pain despite appropriate treatment, it is important to ensure that other joints in the limb are not involved. Other pain management modalities, such as opiates, fentanyl patches, and epidural analgesia, can be attempted. It is important to remember that in foals, continued pain in one limb may result in development of a varus deformity in the contralateral weight-bearing limb, because of the tripod stance that these foals acquire to maintain the weight-bearing limb under the center of gravity. Application of a lateral extension to the contralateral foot may help increase the weight-bearing surface and prevent the development of this complication. Continued pain is a negative prognostic indicator in the affected foal. In adults, continued pain in one limb may result in the development of contralateral limb laminitis.¹⁰⁰ When continued pain in the treated limb is a problem, preventive measures (e.g., hoof support, therapeutic shoeing) should be undertaken.

The use of antiulcer agents is indicated in foals and adult horses that are in pain, stressed, and receiving high doses of NSAIDs. Omeprazole is currently the only medication that has been shown significantly to prevent formation of gastric ulcers and promote healing of existing ulcers in adult horses. Although evidence for its efficacy in preventing and treating NSAID-induced ulcers is lacking, omeprazole is still indicated when NSAIDs are used in stressed animals.

In cattle, facilitated ankylosis is a reasonable alternative when the disease is too advanced, and it is a particularly good option for involvement of the distal interphalangeal joint. Articulations of the distal limb in general are well suited to facilitated ankylosis. In brief, the involved joint is opened and debrided of all debris, all infected tissue is curetted and removed, and a cast is applied and maintained until ankylosis is achieved.¹⁰¹ Alternatively, the digit may be amputated, although a reduced production life should be expected.¹⁰²

Prognosis

Despite the relatively high prevalence of septic arthritis or osteomyelitis in foals, few studies have examined long-term outcome in affected foals. Furthermore, treatment is often limited by economic considerations, and therefore the true long-term outcome of treatment is not known. Prognosis for septic arthritis should always be guarded. Factors that will influence prognosis are systemic condition of the foal, number of joints involved, localization of joint involvement, severity of the infection, early versus delayed identification and institution of treatment, presence of osteomyelitis, and virulence of the organisms. In one study, 73/93 (78%) of foals survived to discharge, but only a third reached racing performance.¹⁰³ Isolation of Salmonella species and presence of multisystem diseases were negatively associated with survival and ability to race. In another study, 58/69 (84%) of foals survived to discharge, although signs were present for less than 24 hours in 74% of foals, only five foals had more than one joint involved, and only one foal had osteomyelitis.¹⁰⁴ This population of foals therefore appeared less severely affected. Of the affected foals, only 40.5% started in one race, and of the affected foals that were discharged, only 48.3% raced versus 66.2% in the control (sibling) group. This study concluded that even if foals are successfully discharged from the hospital, they are significantly less likely to start in at least one race than their siblings. Furthermore, these foals took significantly longer to appear on the track than their siblings.

In adults with open joint injuries, the prognosis can be favorable if the joint is contaminated but not yet infected, and if aggressive treatment is immediately started. However, with established infection, the prognosis should always be guarded. In one study of horses with open joint injury, 53% of those examined within 24 hours developed septic arthritis, and overall survival was 65%. In horses presented within 2 to 7 days of injury, septic arthritis developed in 92%, and survival was 38.5%; in horses examined more then 7 days after injury, septic arthritis developed in all, and survival was 50%.⁵⁴ In one study of 101 horses with heel bulb lacerations, those with involvement of synovial structures had worse outcomes then those that did not; 5 of 17 horses with synovial involvement were euthanized.⁵⁵ Horses with contaminated or infected synovial structures treated by arthroscopic debridement appeared to have a better long-term outcome, with 106 of 118 (90%) surviving and 96 (81%) returning to previous use.⁵⁵ In a study of horses with septic tenosynovitis, 40 of 51 horses (78%) were discharged, and 37 of 40 (73%) survived long term, with 21 (57%) returning to intended use.¹⁰⁵ Surgical technique did not influence outcome in this study. Owners should be informed of the prognosis and high cost of treatment of infected synovial structures.

In cattle the prognosis for septic arthritis is generally better than in horses, probably because of the lack of expectation for athletic use. The prognosis depends on time of presentation, degree of bone involvement, and degree of extracapsular ankylosis. In two studies the success rate was reported as 72% and 85%; cattle with septic tarsi had a worse prognosis.^105a,105b In another study, arthroscopic lavage and implantation of gentamicin-impregnated collagen sponges resulted in recovery in 12 of 14 cattle.¹⁰⁶ After arthrodesis of the distal interphalangeal joint, 85% success was reported.¹⁰² For carpal arthrodesis, 87% success was reported if no carpal bone was removed, 72% success if one row of carpal bones was removed, and 35% if both carpal rows were removed. Tarsal arthrodesis has a reported success rate of 87% in cattle.¹⁰²

Definition and Etiology

Mycoplasma mycoides subspecies (ssp.) mycoides is a pathogenic mycoplasma that causes a variety of clinical syndromes in goats. Although the organism was formerly considered exotic to the United States, several large herd outbreaks have been described.^107,108 In most outbreaks the predominant clinical signs are polyarthritis and pneumonia in goat kids, occurring concurrently with mastitis in does. Abortions also may occur in pregnant does. Overwhelming generalized infection can occur in kids or adults, resulting in death.

Clinical Signs and Differential Diagnoses

Affected kids are from a few days of age to weaning age and have multiple warm swollen joints, elevated body temperatures of 40.8° C to 41.5° C (105.4° F to 106.7° F), pneumonia, and weight loss. They may have conjunctivitis. Many kids are unable to arise or reluctant to move. The acute febrile phase lasts 1 to 3 days, after which polyarthritic kids will be bright and alert and continue to eat. In addition, a few very young kids may exhibit central nervous system (CNS) signs (opisthotonos) or sudden death. Failure to respond to conventional antibiotic treatment or rapid relapse after treatment also characterizes outbreaks. Acute mastitis caused by M. mycoides ssp. mycoides is characterized initially as an agalactia with a firm, hot gland(s); the milk is brownish and watery with sandy clots. The affected doe is febrile, depressed, and anorexic; has diarrhea; may abort; and may have swollen joints or pneumonia. Some does develop a toxic shock—like syndrome and die rapidly, whereas others make an apparent clinical recovery with variable amounts of udder fibrosis and atrophy remaining. The milk becomes normal in appearance, but intermittent chronic shedding of M. mycoides ssp. mycoides may occur.

Differential diagnosis in kids includes septic arthritis caused by bacteria, chlamydial polyarthritis, or white muscle disease, whereas in adult does the mastitis must be differentiated from that caused by Mycoplasma putrefaciens and other bacteria. Other Mycoplasma species, particularly M. putrefaciens, occasionally cause polyarthritis in goat kids.

Clinical Pathology and Laboratory Aids

Most affected kids have an increased WBC count (>13,000 WBCs/mm³ with neutrophilia >7200 cells/mm³, monocytosis >530 cells/mm³) and plasma fibrinogen (>400 mg/dL). Peracutely affected kids and does have a CBC typical of toxic shock, with neutropenia and a degenerative left shift. The joint fluid is increased in volume and contains large fibrin clots with increased numbers of neutrophils and lymphocytes. The organism is usually cultured on mycoplasma media from the most applicable affected site (joint fluid, milk, tracheal wash).

Pathophysiology

M. mycoides ssp. mycoides infection leads to mycoplasmemia and multiple organ involvement of varying degrees, with pyrexia, fibrinopurulent polyarthritis, pneumonia, pleuritis, pericarditis, peritonitis, mastitis, abortion, and encephalitis the most common clinical expressions of infection. Recovery is accompanied by the conversion to carrier status in many animals with intermittent shedding of M. mycoides ssp. mycoides in milk and in ocular and nasal secretions. Pathogenic mycoplasmas are thought to produce toxins, but little is known of the pathogenesis of mycoplasmal diseases.

Epidemiology

M. mycoides ssp. mycoides is usually a milk-borne infection that enters herds through inapparent carriers (usually adult milking does). The organism is an obligate intracellular parasite and survives poorly in the environment. It is easily transmitted to other does during normal milking operations and to young stock by ingestion. One milliliter of infected milk contains enough organisms (10⁶) to cause polyarthritis in kids.¹⁰⁹ In reported outbreaks the morbidity is high (60% to 90%), and the mortality is 15% to 91%. The morbidity and mortality are highest in young animals. Transmission by contact occurs in conjunction with high-density stocking rates. Environmental and other stressors (transport, kidding, kid processing, changes in herd grouping) induce shedding in chronic carrier animals and may facilitate herd outbreaks. The goat ear mite (genus Psoroptes) may play a role in maintaining a reservoir for M. mycoides ssp. mycoides.¹¹⁰ Numerous isolations have been made from the external ear canals of clinically normal goats infected with mites.

Necropsy Findings

Gross necropsy findings may include fibrinopurulent polyarthritis, with erosions of articular surfaces, fibrinous pleuritis, fibrinous pericarditis, pneumonia, mastitis, peritonitis, and conjunctivitis. Subcutaneous edema often extends into soft tissues above and below the joint. In addition, meningoencephalitis may be appreciated on gross examination. Histologically, affected tissues exhibit neutrophilic infiltration with perivascular infiltration of plasma cells and lymphocytes.^107,108

Treatment and Prognosis

There is no effective treatment for M. mycoides ssp. mycoides. Treatment with antibiotics may result in complete or transient remission followed by relapse. Naturally recovered animals are considered to be carriers, although the number of exposed-recovered kids that remain carriers is not well understood. Treatment with tylosin (10 to 50 mg/kg three times daily) may result in apparent clinical improvement, but the associated risk of producing carrier animals weighs against treatment. Newly developed antibiotics may make successful treatment possible in the future.

Prevention and Control

M. mycoides ssp. mycoides can be prevented from entering goat dairies by isolating and performing milk cultures on new herd additions. Milk cultures should be performed at purchase and 2 and 4 weeks later, before the doe is declared free of M. mycoides ssp. mycoides. If the doe is dry at purchase, isolation should be maintained until she is cultured at kidding and 2 and 4 weeks fresh. Herd outbreaks are controlled by feeding cow colostrum, cows’ milk, or milk replacer to kids and by performing milk cultures on individual does. Initially, each doe should have a composite milk sample cultured for mycoplasma.

Does with positive cultures are culled to slaughter or are housed together and milked last until they can be sold to slaughter. At weekly intervals after the milk tank has been emptied, a culture is taken after each string is milked, and the identity of each doe that contributed to the can or tank string sample is recorded. If a positive culture occurs in a string, individual cultures must be performed on that string to identify the doe(s) shedding M. mycoides ssp. mycoides. After 1 to 2 months of weekly cultures, monthly string cultures are adequate, combined with individual cultures for all does kidding. After 6 to 8 months, monthly bulk tank samples and fresh doe samples are monitored for 1 more year. The majority of infected lactating does are identified in the first 4 weeks of milk culturing. Some does infected with M. mycoides spp. mycoides may remain undetected for years even with intensive surveillance, thereby leading to sporadic disease. All kids that were being fed milk on the dairy during the outbreak should be sold for meat if they are in satisfactory condition, whereas clinically affected kids should be euthanized because, even with treatment, they may become carriers.

Definition and Etiology

Caprine arthritis-encephalitis virus (CAEV) is an RNA-enveloped lentivirus from the Retroviridae family that infects cells of the monocyte-macrophage lineage, with manifestations ranging from subclinical disease to severe encephalitis. Time from infection by the virus to clinical disease may vary from months to years. Infection with CAEV is lifelong, so efforts to eradicate and control its prevalence and incidence are paramount to maintaining successful goat herds. The economic impact of this disease in herds and the goat industry involves loss of productivity, death, and restrictions on the export of diary goats in the United States.

Clinical Signs

Clinically, only approximately 20% of CAEV-infected goats display signs of disease during their lifetime. Recognized forms of disease include a leukoencephalomyelitis, interstitial pneumonia, chronic mastitis, and debilitating polysynovitis-arthritis. Leukoencephalomyelitis is observed primarily in kids 2 to 6 months of age, although cases have been reported in adults.¹¹¹ This form of CAEV infection is characterized by an ascending paresis leading to paralysis, beginning in the hindlimbs and sometimes involving the forelimbs. These signs may or may not be accompanied by a mild interstitial pneumonia. Goat kids surprisingly may continue to be bright, alert, and appetent. The most severe manifestation of leukoencephalomyelitis is progressive paresis to paralysis to urinary retention and bloating. Chronic interstitial pneumonia with progressive weight loss and dyspnea is another recognized form of CAEV infection. Primary ruleouts for this form should include lung worms, pulmonary abscessation, and chronic bronchopneumonia. The mammary gland is a target organ for CAEV, resulting clinically in a firm udder with decreased milk production (chronic mastitis). Although quantity of milk is reduced, grossly, there are no apparent abnormalities.

The most common form of CAEV infection is polysynovitis-arthritis, which can be recognized in goats as young as 6 months but more frequently is observed in mature goats. Lameness caused by this form is intermittent and insidious in onset; eventually, however, affected joints become painful and enlarged. Enlargement of the joints is most often caused by hyperplasia of the synovial tissues and their associated sheaths, rather than increased volume of joint fluid. The carpus is most frequently involved, but the stifle, coxofemoral, atlantooccipital, and hock joints are also potential locations. Affected goats have a stiff, stilted gait and progress to walking on their carpus or recumbency. Range of motion is greatly affected, which contributes to chronic contracture of the soft tissue. This polysynovitis-arthritis form of CAEV infection can be accompanied by chronic interstitial pneumonia and weight loss and typically is also associated with some form of mammary involvement.¹¹¹

Diagnosis and Clinical Pathology

On suspicion of the polysynovitis-arthritis form of CAEV infection, arthrocentesis usually yields a brown to red-tinged fluid, with an increased cell count and decreased protein. Joint fluid cell counts in affected joints are dominated by mononuclear cells, which differs from the bacterial synovitis usually observed, consisting predominantly of neutrophils. This predominance of mononuclear cells is also seen in the cerebrospinal fluid (CSF) of goats affected with the leukoencephalomyelitis form. Radiographs may be a useful tool in the diagnosis of CAEV polysynovitis-arthritis in that early cases display soft tissue swelling dorsal to the carpus. Later, as the disease progresses, mineralization can be observed in the periarticular tissue, tendon sheaths, joint capsules, and ligaments. Roughened bone proximal and distal to the joint becomes apparent, along with a periosteal reaction.

The U.S. Department of Agriculture (USDA) recognizes agar gel immunodiffusion (AGID) using ovine progressive pneumonia virus antigen as the official test for CAEV. However, an enzyme-linked immunosorbent assay (ELISA) has been developed for detection of whole-virus, core, or envelope proteins. Both AGID and ELISA are considered reliable enough to be incorporated into prevention and control programs. The AGID test is reportedly more specific, but less sensitive, than the ELISA.¹¹² Detection of antigen in milk, tissue, and blood can be facilitated through polymerase chain reaction (PCR) techniques. A positive AGID or ELISA in adults is synonymous with lifelong viral infection. Generally, time from infection to seroconversion ranges from 4 to 16 weeks, although some infected goats shed virus for long periods without seroconversion.¹¹³ Goat kids may be transiently positive for the presence of antibodies during the first 8 to 16 weeks of life after consuming CAEV antibody—containing colostrum; however, because of the nonprotective nature of the maternal antibodies, such kids may seroconvert from true viral infection due to shedding of the virus from the infected dam.

Pathophysiology

The characteristic granulomatous inflammatory pathology produced in affected tissues is thought to be caused by immune complexes generated by the interaction of nonneutralizing antibodies produced by lymphocytes and associated virus-infected macrophages. Localization of such inflammatory lesions occurs where tissue-associated macrophages are found. Tissues of importance in CAEV localization include the synovium, mammary gland, and CNS; therefore the clinical manifestations of the disease are logical.

Epidemiology

Transmission involves the transfer of virus-laden cells from one animal to the next. Transfer of CAEV to neonates through colostrum and later milk is a highly efficient, natural mode of transmission.^114,115 Transmission has also been reported through direct contact; consequently, herds that do not practice segregation of seropositive animals have ongoing difficulty controlling and eradicating the disease.^114-117 Complete separation of kids from the dams immediately after parturition and during the periparturient period is necessary because even kids not allowed to nurse become infected. CAEV proviral DNA has been recently detected in the female caprine genital tract,¹¹⁸ and experimental infection of goat embryos with CAEV has been reported.¹¹⁹ Intramammary and in utero transmission also have been described.^117,120 All these means of acquiring CAEV are potential explanations for continued transmission in herds that practice segregation and sound colostrum and milk management.

Maedi-visna virus (MVV), also known as “ovine progressive pneumonia,” is another lentivirus that, together with CAEV, is often referred to as “small ruminant lentivirus” (SLV). Although sheep are most likely to display clinical signs of MVV and goats to have signs of CAEV, studies have shown that these viruses can be transmitted from sheep to goats, and vice versa.¹²¹ Therefore, eradication programs aimed at eliminating SLV from herds and flocks should not allow contact between sheep and goats.

The last study examining the prevalence of antibody to CAEV in the United States found that 31% of all goats tested were seropositive and that 73% of herds had at least one seropositive member. Serum samples in this study were obtained from 28 states. The prevalence was highest in the western Pacific and northern plains regions, on family-owned farms, and increased with age. Prevalence in this study was lowest in the Angora breed.¹²²

Necropsy Findings

Grossly, goats affected with the polysynovitis-arthritis form of CAEV have thickened, sometimes folded synovium consistent with synovial hyperplasia resulting from chronic inflammation. Microscopically, synovial hyperplasia is characterized by mononuclear infiltration of lymphocytes, plasma cells, and macrophages. Synovial spaces contain fibrin, whereas synovial villi and collagen are necrotic.¹¹¹

No gross lesions are apparent in the CNS of goats affected with the leukoencephalomyelitis form of CAEV; microscopically, however, perivascular infiltration of lymphocytes, macrophages, and plasma cells are observed. Perivascular infiltration is often accompanied by malacia of the brain and spinal cord in addition to loss of myelin. Occasionally, degenerative lesions are seen in the gray matter.¹²³

Treatment and Prognosis

Prognosis for CAEV infection varies because most goats do not show clinical disease; once signs begin, however, rapid deterioration ensues. Arthritis and accompanying weight loss are progressive, and there is no treatment. Kids or mature goats affected with the leukoencephalomyelitis form do not survive and should be euthanized for humane reasons. Reportedly, a genetically determined predisposition for development of the CAEV arthritis exists and can be identified through the use of DNA fingerprinting.¹²⁴

Prevention and Control

Prevention and control are based on colostrum and milk management, although kids should also be prevented from any contact with the dam after parturition. Heat treatment of colostrum by holding it at 45° C (113° F) for 1 hour is effective in inactivating the virus.¹¹⁷ Kids can then be fed pasteurized milk until weaning. Goats’ milk from seronegative dams that is not pasteurized is a risky substitute for heat-treated milk because some seronegative goats shed virus for long periods before seroconversion occurs. Pooling of colostrum increases the prevalence of disease on goat dairies, so this practice should be restricted. Kids should be tested serologically at periodic intervals to detect and remove infected individuals. Seronegative goats should be isolated from seropositive ones by a minimum of 6 feet (1.8 m).¹¹⁷ Sharing of feed and water troughs should not be allowed, nor should the use of common needles during routine vaccination or administration of medication. During breeding, seronegative does should not be housed with seropositive bucks; however, they can be hand-mated and quickly reisolated. New additions to the herd should be tested and isolated until seronegative status is confirmed before entry into the herd.

Despite diligent prevention and control programs based on elimination of colostrum and milk transmission, isolation of seronegative goats, and serologic monitoring, obstacles to a CAEV-free herd are often encountered. Detection of virus has been reported in properly treated colostrum.¹¹⁴ Colostrum that is overheated denatures immunoglobulin, thereby preventing effective passive transfer of immunity, and colostrum not heated long enough or at sufficiently high temperature fails to inactivate the virus. Feeding overheated colostrum may also cause diarrhea in the kids.¹²⁵ Therefore, attention to times and temperatures during heat treatment of colostrum and pasteurization of milk is crucial for effective colostrum and milk management. Some farms routinely feed cow colostrum; however, neonatal isoerythrolysis has been reported in kids consuming cows’ milk, and the lack of goat-specific immunoglobulin transfer is less than ideal.¹²⁵ Serologic monitoring can be complicated by shedding of the virus before seroconversion. All goats must therefore be tested at least twice yearly to ensure that new cases are detected and managed accordingly. Unfortunately, no vaccine is currently available for CAEV.

Definition

The term osteoarthritis (OA) encompasses a large group of joint disorders that are characterized by progressive, permanent deterioration of the articular cartilage.^126-129 Cartilage damage is often accompanied by changes in the adjacent bone and soft tissue structures, including subchondral bone sclerosis, periarticular new bone formation, and synovial inflammation. Unfortunately, some confusion and debate surround the best term to use for this broad group of disorders. Osteoarthritis, degenerative joint disease (DJD), osteoarthrosis, and secondary joint disease have been used almost interchangeably in veterinary medicine.^126,127 However, osteoarthritis emphasizes the characteristic synovial inflammation detected in most patients, and this term is used here.

Interestingly, OA is one of the oldest documented orthopedic conditions. In fact, the fossilized remains of early dinosaurs suggest that OA predates the evolutionary development of mammals. Unfortunately, however, questions remain regarding the etiopathogenesis of OA, and this condition is still regularly diagnosed in most large animal species, including horses, cattle, and small ruminants. In goats, OA is frequently associated with CAEV (see previous discussion).^130,131 In pigs, OA is a common debilitating sequela of infectious arthritis or osteochondrosis.¹³² Although not routinely diagnosed in sheep, OA has been reported to develop in individuals infected with ovine progressive pneumonia.¹³⁰ In contrast, joint disease is a common and expensive problem in the equine industry, and a wide variety of athletic injuries can progress to a common endpoint with stereotypic features of chronic OA.^126-128

Etiology and Classification

Many factors, including athletic performance, repetitive trauma, and age, are thought to influence cartilage homeostasis and contribute to degenerative changes in the joint. Contrary to the traditional view of articular cartilage as a passive bystander subjected to overexertion and traumatic wear-and-tear damage, it is now recognized that both resident and infiltrating articular cells have a critical role in the development of OA. Cartilage degeneration is an active process ultimately resulting from the inability of resident cells to maintain a normal balance between matrix synthesis and degradation. This occurs when chondrocytes and synovial cells are exposed to various nonphysiologic stimuli, including trauma and inflammation. Once the balance is disrupted, proteoglycans within the hyalin cartilage matrix are depleted and reduced in size, while the collagen meshwork progressively deteriorates. These changes in turn alter the mechanical properties of articular cartilage. A variety of different joint problems can initiate an imbalance between the rates of cartilage degradation and repair and, if left untreated, will ultimately progress to a common endpoint of OA.

Although a number of initiating and predisposing conditions have been identified, it is generally thought that trauma, either a single severe injury or low-grade repetitive damage, is the most important basis for the development of OA in large animal species.^126-128 In many cases the traumatic damage is augmented by abnormal weight bearing, poor-quality cartilage, or congenital joint instability, such as that seen with hip dysplasia in calves. In addition, OA frequently develops in joints that have unresolved or untreated osteochondrosis, subchondral bone collapse, or septic arthritis. In all these cases, the link between the cause and the end result of OA is a series of complex biochemical and metabolic events that are not yet fully understood. Regardless of the inciting etiology, advanced OA is characterized by fibrillated and ulcerated cartilage, eburnation and sclerosis of the subchondral bone, hyperplasia of the synovial membrane, and development of periarticular osteophytes.

Several classification schemes have been proposed to group clinical OA conditions in both human and veterinary medicine. One useful classification developed for equine OA defines three main categories of disease based on predisposing causes and clinical findings.¹³¹ The categories include OA associated with synovitis and capsulitis (type 1), OA secondary to other identified injuries or disorders (type 2), and incidental or nonprogressive articular cartilage erosion (type 3).¹²⁷ For example, type 2 OA would include the chronic degenerative changes typically associated with intraarticular fractures, septic arthritis, osteochondrosis, and traumatic cartilage or ligament injuries. All three categories are routinely identified in equine athletes, but this simple scheme can easily be applied to other large animal species as well. For example, cattle most often develop type 2 OA as a consequence of septic arthritis, cruciate rupture, osteochondrosis, or nutritional deficiencies.¹³²

A second way of classifying OA is based on the possible deleterious effects of biomechanical forces on normal and abnormal joints.¹²⁸ According to this scheme, the first of two major causes of OA is the concentration of abnormal forces on a previously normal joint. For example, OA can develop when there is increased weight bearing on one limb to protect a painful contralateral limb. The second major cause is the concentration of normal forces on an abnormal articulation, such as the joint damage that occurs when normal weight-bearing forces are applied to cartilage previously exposed to infection.

Pathology and Pathogenesis

Despite the many pathways by which OA may develop, the resulting changes in the joint are essentially indistinguishable regardless of the initiating cause. By definition, this condition has a characteristic picture of cartilage damage with variable amounts of hypertrophic cartilage and bone remodeling. Pathologic features include different degrees of cartilage splitting and fragmentation, extending to complete erosion and loss of articular cartilage.^126-128 Typically, the rate of disease progression and severity of OA are related to the nature and severity of the primary insult, the animal’s age at the time, the joint location, and the animal’s type and level of activity.

The pathogenesis of these changes is only partially understood. Several explanations have been proposed for the failure of resident chondrocytes to maintain the extracellular matrix. Mechanical trauma to the joint surface could initiate matrix damage, and repetitive microtrauma could damage chondrocytes and physically disrupt the joint surface. Leukocytes in an inflamed joint release destructive enzymes, which can degrade the cartilage surface. Recent work has also demonstrated that various polypeptide mediators released in inflamed joints can stimulate chondrocytes to degrade their surrounding matrix. Regardless of the initiating factor, once the balance of chondrocyte-matrix turnover is shifted toward degradation, proteoglycans are rapidly depleted from the extracellular matrix, and collagen fibers are exposed to direct traumatic and enzymatic breakdown. Unfortunately, hyaline cartilage has no effective intrinsic repair mechanism.

Articular cartilage damage is accompanied by changes in the adjacent subchondral bone (e.g., sclerosis), joint capsule (e.g., synovial hyperplasia, thickening of fibrous joint capsule), and joint margin (e.g., osteophyte formation, enthesophyte formation at joint capsule and ligament insertions).¹²⁸ Subchondral bone sclerosis may develop from an abnormal distribution of forces under damaged articular cartilage, or it may actually precede the cartilage damage. It is now known that bone remodeling and subchondral bone sclerosis occur in response to repetitive cyclic compression during exercise and, in certain cases, could result in trauma to the overlying articular cartilage and predispose to the development of OA (e.g., third carpal bone disease in horses). Joint margin changes occur as a result of progressive cartilage deterioration and subchondral remodeling (osteophytes) or joint instability (enthesophytes).

Clinical Signs

History and occupation are important for identifying animals at risk for developing OA. Typically, the first sign that an owner or caretaker recognizes in an affected animal is lameness or stiffness. Whereas the pain and dysfunction may develop insidiously, the owner will often report a sudden onset of clinical signs. Flexion and extension of an involved joint frequently exacerbates the lameness or elicits a pain response. Because articular cartilage is aneural, pain is thought to result from joint inflammation and secondary changes in adjacent tissues. Pain receptors are abundant in joint capsule, articular ligaments, and subchondral bone. Joint stiffness may be associated with guarding of a painful joint. Decreased range of motion with joint capsule inflammation is also common. Osteophytes and enthesophytes may be palpable in chronic cases of bone spavin and ringbone. A postural deformity may be evident if articular degeneration progresses to ankylosis. It is also important to remember that OA may exist in the absence of any clinical signs.

Gait abnormalities compatible with OA include shortened stride length, limb abduction, and dragging the toe. Increased lameness after sustained flexion of a single joint suggests that the joint is involved. Horses with OA often present early in the course of disease with a primary complaint of poor performance. These individuals can warm out of the lameness, or temporarily improve with rest, and are often difficult to diagnose. In contrast, food animals typically present in the advanced stages of OA. Rams and bulls may stand post-legged and appear weak in the rear when the hindlimbs are severely affected. In all species the severity of signs varies with the joint affected, stage of disease, amount of inflammation, cartilage degeneration, and periarticular changes.

Diagnosis

Regional nerve blocks and intraarticular anesthesia can be useful for determining the origin of lameness. Unfortunately, standard synovial fluid analysis typically shows only minimal, nonspecific changes. Although not useful for determining the severity of cartilage destruction, cytology is often useful for differentiating OA from other causes of synovial inflammation (e.g., septic arthritis). A variety of synovial fluid markers have been evaluated as possible diagnostic aids for evaluation of equine synovitis and joint disease (e.g., cytokines, eicosanoids, GAG concentrations, immune complexes, collagen type-specific antibodies and propeptides, cartilage wear fragment, free-radical oxidation products, polymerization of hyaluronate, chondroitin sulfate epitopes). Current detection techniques for cytokines and eicosanoids may prove useful diagnostically and prognostically.

After identification of an involved joint, radiographs are used to determine the severity and extent of disease. Articular cartilage is not visualized but may be indirectly assessed by evaluating joint space width. In contrast, the associated subchondral and periarticular bone reaction can be directly evaluated. Radiographic signs of OA develop gradually, affect opposing joint surfaces, and may include destructive as well as productive lesions. Changes typical of advanced OA include marginal osteophyte proliferation, periosteal new bone production at sites of joint capsule and ligamentous attachments (enthesophytes), narrowing or obliteration of the joint space, subchondral bone sclerosis, and occasionally, subchondral lysis. Early in the disease, no bony lesions may be detected, and clinical findings from the entire examination must be considered. Radiographic changes associated with OA must be differentiated from similar bone reactions caused by active infection, fractures, osteochondrosis, and invasive tumors. Infectious arthritis classically causes rapid, widespread osteochondral destruction. Minimally displaced fractures may mimic OA but are usually discrete, isolated lesions. Knowledge of the characteristic site distribution and site-respective appearances of osteochondroses in each species is useful for differentiation from OA. The presence of OA in joints with osteochondrosis usually worsens the prognosis.

Scintigraphy is particularly valuable in early disease states when conventional diagnostic methods have not revealed bone or soft tissue changes. Increased scan activity is associated with soft tissue inflammation or increased bone remodeling, but alone it is not diagnostic for OA. Arthroscopy is the best method for gross evaluation of articular cartilage and is most useful when lameness has been localized to a specific joint but no bony changes are detected radiographically. This technique provides the added therapeutic benefit of simultaneous joint lavage. Although arthroscopy was initially promoted for diagnostic and therapeutic use in equine patients, these techniques are gaining popularity in food animal practice as well.¹³³

Treatment

The choice and efficacy of treatment depend on the inciting cause of OA, stage of cartilage degradation, joint involved, and degree of active inflammation. In general the treatment of OA should be directed at eliminating any primary causes, reducing active joint inflammation, and treating articular cartilage loss or degeneration.^126,127,134 Early treatment of primary problems minimizes the extent of secondary joint damage. For example, fractures and osteochondritis dissecans can often be managed successfully with arthroscopic surgery; however, early intervention is essential to avoid the secondary changes of OA.

Many therapeutic options are designed to treat active soft tissue inflammation and prevent progression of articular cartilage damage. Rest is the simplest but often the most difficult recommendation to enforce, especially when dealing with elite performance horses. There are also valid concerns that complete rest may result in resorption of subchondral bone and predispose the horse to subsequent injury. Other treatments for soft tissue disturbances in the joint include physical therapy and controlled exercise, systemic NSAIDs (e.g., phenylbutazone, flunixin meglumine), joint lavage, and topical application of antiinflammatory products.

Numerous medications have been specifically designed and marketed for treating OA in human and veterinary patients. However, many of these products remain controversial in terms of their safety and efficacy in large animals. The most popular formulations include intraarticular corticosteroids, intraarticular and intramuscular polysulfated glycosaminoglycans (GAG), intraarticular and intravenous hyaluronan, and oral GAG supplements.

Intraarticular steroids are the most potent antiinflammatory agents available; historically, however, they have been associated with progressive cartilage damage.^134,135 Nevertheless, investigations critically evaluating the effects of corticosteroids in equine joints suggest that when administered at physiologic doses, these drugs may have beneficial protective effects.^134,135 Current recommendations emphasize the need for appropriate caution and encourage the use of low doses of steroids in conjunction with other antiinflammatory medications. Hyaluronan (sodium hyaluronate) is currently used both intravenously and intraarticularly to treat synovial inflammation and OA in the horse.^134,136 The intraarticular products vary in molecular weight and cost and include cross-linked hylans, which may prolong intraarticular retention. Clinical reports document the efficacy of hyaluronan for mild to moderate synovitis, and some research supports an inhibition of proteoglycan degradation and inhibition of synoviocyte release of various inflammatory mediators. Other studies failed to demonstrate beneficial effects in joints with significant articular cartilage damage or osteochondral fragmentation.

The intraarticular administration of polysulfated GAG has been reported to reduce progressive degenerative changes in articular cartilage, but is controversial in terms of its ability to augment the chondrocyte repair response.^134,137 Intramuscular use is advocated because intraarticular use has been associated with adverse reactions and potentiates the risk of iatrogenic joint infection.^134,137

There is still great interest in the use of nutritional supplements to prevent and treat OA, with a proliferation of products promoted as beneficial to joint health and cartilage regeneration.¹³⁸ Among the most popular are the oral glucosamine sulfate and chondroitin sulfate preparations. However, oral absorption of chondroitin sulfates has not been documented in the horse, and although clinical reports suggest a beneficial effect from these supplements, additional controlled studies are needed to confirm these effects. Methylsulfonylmethane (MSM), a dietary derivative of DMSO, is also being used as a dietary supplement to control the inflammation associated with OA. Again, minimal documentation exists regarding its value in treating joint disease in large animals. Other compounds to treat OA include S-adenosyl-L-methionine and various vitamins known to provide antioxidant protection.

The most challenging aspect of OA management is treatment of existing articular cartilage degeneration and loss. Partial-thickness cartilage defects do not heal, and full-thickness defects heal with inferior fibrocartilaginous tissue. Some surgical techniques (e.g., curettage, subchondral bone drilling, microfracture) facilitate defect repair by enhancing fibrocartilage ingrowth from the underlying subchondral bone; however, fibrocartilage is biomechanically inferior to normal hyaline cartilage. Grafting cartilage defects with periosteum, perichondrium, and sternal cartilage has not been encouraging. More recent work focuses on transplantation resurfacing using chondrocyte grafts and growth factors to stimulate repair.¹³⁹

Prognosis

Prognosis for animals with OA depends on the initiating factor(s), extent of the secondary disease, joint affected, and intended use of the animal. With early and aggressive treatment, many animals can return to soundness and athletic performance. In other cases, salvage in the form of surgical arthrodesis may provide the most favorable outcome.

Definitions

Sprains and luxations have been classified as a type 2a traumatic arthritis.¹⁴⁰ These injuries have been categorized in three forms: mild, moderate, and severe. Mild sprains constitute injuries that involve the tearing or disruption of minimal number of ligament fibers, with no loss of integrity to the ligament. Hemorrhage and edema typically are present in the ligament. Injuries that involve a portion of the ligament, with loss of integrity, are considered moderate sprains. Laxity of the joint is often present with moderate injury; however, complete separation of the ligament from the bone or complete separation of the body of the ligament is not seen. Significant hemorrhage and edema are present in the ligament. Injuries that involve tearing of the ligament, resulting in either complete separation from the bone or widening of the tendon fibers, are considered severe sprains. These injuries will result in some form of joint instability, especially when the affected joint is manually stressed.

Luxations and subluxtions are usually the result of severe sprains of periarticular or articular ligaments. Luxations represent the complete dislocation of the articular surfaces, with subluxations having only partial and incomplete disarticulation (Fig. 38-21).

Fig. 38-21 Dorsopalmar radiograph of a subluxated metacarpophalangeal joint after the joint has been manually stressed.

Etiology and Pathophysiology

Sprains can be associated with acute injuries in which there is excessive strain on the ligament fibers, on ligamentous attachments, or secondary to repetitive actions on the ligament. The latter results when there is maximal or near-maximal loads repeatedly applied to the ligaments and associated structures, causing a degenerative type of lesion. Age can also be a contributing factor to these degenerative changes. Furthermore, muscle fatigue can contribute to the weakening of adjacent structures, increasing the stresses applied to the supporting ligaments.

Typically, hemorrhage and edema form within the ligament(s) surrounding the joint capsule, or in severe lesions the hemorrhage can be periligamentous or intraarticular. Inflammation ensues, and the ligamentous or capsular lesion heals through fibrosis, forming a scar, with type III collagen the predominant type produced. Type III collagen contains a smaller fibril diameter and has fewer cross-links then type I collagen, which is the predominant collagen type in normal tendons and ligaments. As the lesion matures, the fibril diameter will increase along with the number of cross-links, in addition to the proportion of type I collagen. This will increase the strength of the injury, which can take weeks to months to heal but will ultimately be weaker than the normal tissue.¹⁴¹ Often the affected joint capsule and surrounding ligaments become fibrotic as healing occurs, resulting in a decreased range of motion in the affected joint. Secondary calcification of the affected soft tissue structures may occur and adversely affect the joint’s mobility.

Luxations of the coxofemoral joint in calves may be associated with calving injuries during a dystocia or in cows being ridden while in estrus, or with a traumatic fall in the immediate postpartum period.^142,143 Shoulder joint luxations are usually the result of trauma.¹⁴⁴

Clinical Signs and Differential Diagnosis

The clinical signs vary depending on the severity of the sprain and the duration from the initial injury. The animal may have a history of mild lameness or decreased performance, as well as a history of a positive response to NSAIDs or stall rest. Patients with moderate to severe sprains will typically have a more pronounced, acute lameness or may be non—weight bearing on the affected limb. There may also be localized swelling, heat, increased joint effusion, or pain elicited on palpation or manipulation of the affected joint. Other signs may include abnormal limb positioning, decreased range of motion, crepitus, and joint laxity. Injuries may present after an acute or traumatic insult, as a chronic lameness, or a chronic mild injury can present acutely with severe lameness if the ligament completely separates. Chronic injuries are characterized by a thickening of the joint capsule or enthesophyte formation at the origin and insertion of the affected ligament.

Subluxations and luxations result in the loss of joint function and mobility and may present with a varus or valgus deformity. Complete luxations in the horse are most common with the pastern, fetlock, and hock joints.¹⁴⁰ Luxations can occur in the shoulder, carpus, and coxofemoral joint; however, these luxations are less common in horses. Coxofemoral luxations are the second most common type of luxation in cattle.¹⁴³

Differential diagnoses vary depending on the region affected and duration of injury but may include soft tissue contusion, synovitis and capsulitis, osteoarthritis, bursitis, musculotendinous injuries, fractures, physeal fractures, septic arthritis, tenosynovitis, and flexural or angular limb deformities.

Diagnostic Tests

A thorough history and physical examination should be performed at presentation. The exam should include assessment of pain, swelling, heat, effusion, or instability of the joint. Patients able to ambulate with only mild lameness should have a lameness examination that includes perineural anesthesia to localize the affected region or joint. The clinician should take extra caution if there is any evidence of joint laxity or instability or severe lameness.

Radiographs should be obtained to assess the bony structures of the joint because concurrent factures are common with traumatic insults resulting in luxation. Stress views can be performed to assess the level of instability of joints (see Fig. 38-21). Fractures of the proximal or middle pastern bones can cause luxation or subluxation of the proximal or distal interpastern joint. Furthermore, radiographs are useful in detecting avulsion fractures or insertional desmopathies and enthesophytes associated with chronic disease. Nuclear scintigraphy can also be used to evaluate insertional desmopathies that may not be radiographically apparent. Arthroscopy may be indicated as a diagnostic aid if disruptions of intraarticular ligaments are suspected or if damage to the articular cartilage is suspected. Ultrasonography is used to locate the ligamentous lesions and characterize the extent of the lesion. Ultrasound should also be used to evaluate the joint because arthritis is a common sequela. Magnetic resonance imaging (MRI) is becoming more readily available in the veterinary field and has been found useful in identifying and characterizing lesions in ligaments. In addition, there may be concurrent damage to adjacent structures of the joint or avulsion fractures that might not be ultrasonographically or radiographically detectable but that can significantly influence the prognosis.^142,145-147

Treatment

Treatment is largely based on the severity of the lesion and associated structures involved. Mild sprains can be treated conservatively with support bandages, NSAIDs, polysulfated GAGs, and rest for 3 to 4 weeks, followed by a controlled exercise program before returning to normal activity. Adjunctive physiotherapies may also be considered, such as hydrotherapy or shock wave treatment. Moderate sprains involving significant ligament damage may necessitate the use of a cast or splint to provide joint stability during the initial healing process. In acute cases, ultrasound evaluation of the affected joint often shows hemorrhage within the joint capsule (Fig. 38-22). This hemorrhage usually resolves after 7 to 10 days; however, it can also subsequently form a fibrinous clot within the joint capsule, resulting in a chronic mild synovitis that can be treated with intraarticular medications, such as sodium hyaluronic acid, triamcinolone, and amikacin antibiotic. Arthroscopy should be considered to treat joints with persistent fibrin accumulation. Arthroscopy has the advantage of further evaluating damaged cartilage or intraarticular ligaments and serving as a portal for high-volume flush. If arthroscopic surgery is performed, a cast or splint should be applied to the affected limb during recovery from anesthesia to prevent luxation of the affected joint and further injury. Severe sprains may need some form of internal or external coaptation or arthrodesis of the joint, depending on the degree joint instability. Support of the contralateral limb should be considered for non—weight-bearing injuries.

Fig. 38-22 Ultrasound image of a metacarpophalangeal joint from a horse with an acute sprain. Note the hemorrhage accumulation within the joint capsule. Mt3, Third metatarsal bone of fetlock joint.

Luxations of the coxofemoral joint in cattle can be repaired by open or closed techniques, and success depends on duration of the luxation, concurrent fractures or soft tissue injury, and age. Open reduction was reported as being more successful than closed reduction, although closed reduction should be attempted immediately after the injury if possible.¹⁴³ Shoulder joint luxations can also be reduced by closed and open techniques.¹⁴⁴ Open reduction with internal stabilization seems to result in a better survival outcome for the animal.¹⁴⁴

Prognosis

Prognosis depends on the severity of damage to the intraarticular cartilage and surrounding soft tissue structures. Horses sustaining mild joint or ligamentous strains have a good prognosis for returning to previous athletic use. Horses sustaining moderate or severe sprains or joint luxations usually develop secondary DJD in the affected joint, which may require intraarticular medications and NSAIDs to return to previous use. The long-term prognosis for returning to athletic performance in these cases is poor. Simple shoulder luxations in large animals generally carry a guarded to poor prognosis. Simple coxofemoral luxations in cattle have a fair to good prognosis, with calves having a better prognosis than adult cows.

Definition and Etiology

Ankylosis is the abnormal adhesion or fusion of the bones in a joint. This process is naturally occurring, resulting in a consolidation of two or more bones into one structure.¹⁵⁶ Development of ankylosis is often the result of disease or traumatic injury to the region involved. Septic arthritis may be an inciting factor for secondary ankylosis, as can DJD, severe articular or periarticular trauma, and prolonged joint immobilization from bandaging, splinting, or casting.^157,158 Congenital ankylosis (absence of an articulation) may occur, but it is rare in horses and cattle and is often associated with other congenital abnormalities.¹⁵⁹

The process of joint fusion is initiated by biomechanical and biochemical factors, leading to joint instability and degeneration of cartilage and chondrocytes. Joint immobility occurs from periarticular contracture, capsular fibrosis, and chronic muscle spasm, leading to synovitis and cartilage destruction. Ossification of the periarticular soft tissue structures begins to develop, resulting in partial bone bridging of the joint. The final stage of ankylosis is complete bone bridging with trabecular bone and joint obliteration.¹⁶⁰

Common sites of ankylosis in the horse include the tarsometatarsal joint, distal intertarsal joint, thoracolumbar intervertebral articulations, proximal interphalangeal joint, and distal interphalangeal joint. In high-motion joints, naturally achieving complete bony bridging across the articular surface is rare, and the resulting cartilage degeneration leads to severe lameness.¹⁵⁶ Low-motion joints are more likely to achieve complete ankylosis without intervention. Large animals with vertebral ankylosis may show neurologic deficits caused by bony impingement of the spinal cord or by dynamic compression leading to abnormal motion or spinal ligament hypertrophy.¹⁶⁰ Pathologic fractures may occur near joints that are ankylosed because of abnormal biomechanical forces on the limb, and animals are prone to secondary injuries and osteoarthritis from abnormal stresses imposed on neighboring normal joints.¹⁶¹

Facilitated ankylosis refers to a procedure in which the joint is stimulated by a method intended to promote joint fusion. The speed at which ankylosis occurs may be enhanced through the use of chemical destruction of the chondrocytes or surgical obliteration of the joint.¹⁶² A recent study evaluating surgical drilling to achieve ankylosis of the distal intertarsal joint and tarsometatarsal joint reported that 59% of the horses were sound and able to perform at their previous level of athletic performance.¹⁶³ A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser has also been used for facilitated ankylosis in the distal tarsal joints.¹⁶⁴ Chemical fusion options include the use of ethyl alcohol or sodium monoiodoacetate (MIA) injected into the intraarticular space.^156,162,165 A study comparing surgical drilling, laser surgery, and injection of MIA into the distal tarsal joints revealed that bone bridging was greater in the MIA and surgically drilled horses at 6 and 12 months after treatment; however, animals receiving laser treatment were more comfortable after surgery and less lame on the treated limb.^156,164 Injection of 70% ethyl alcohol into the tarsometatarsal joint of healthy horses resulted in progression to joint fusion 4 months posttreatment, although complete obliteration of the joint had not occurred by 12 months after treatment.¹⁶²

Arthrodesis involves surgical fixation of a joint using procedures designed to promote joint fusion. An arthrodesis therefore may be considered a type of ankylosis.¹⁵⁶ A typical arthrodesis involves the use of stainless steel screws and dynamic compression plates, after removal of the articular cartilage.¹⁵⁶

Clinical Signs and Differential Diagnosis

Typical indications of ankylosis include fused joint bones evident on radiography, stiffness of the joint and joint immobility, and decreased range of joint motion. Limited joint mobility is most obvious if high motion or multiple joints are involved. In the early stages, there may be local signs of inflammation with a corresponding lameness. The degree of lameness ranges from mild to severe. Enlarged and thickened periarticular structures, conformational abnormalities, disuse atrophy of muscles, and gait stiffness may also be identified. Once ankylosis is complete and no cartilage remains, the condition is nonpainful and the articulation will be immobile.

In calves and foals, congenital ankylosis may occur between vertebrae (i.e., block vertebrae) or in multiple joints of the limbs, resulting in dystocia related to musculoskeletal inflexibility.¹⁶⁰

Differential diagnoses should include soft tissue injuries or contracture, intraarticular or periarticular adhesions, luxation of a joint, joint or bone neoplasia, arthrodesis, spondylosis, an intraarticular mass, osteomyelitis, and fracture. Diagnosis of ankylosis should be based on a complete physical examination, lameness evaluation, and radiographs. Multiple radiographic views should be acquired for definitive diagnosis; however, other imaging techniques such as ultrasonographic evaluation, computed tomography (CT), and MRI may be useful and provide more detailed information.

Treatment and Prognosis

Early treatment focuses on making the animal comfortable because ankylosis is a chronic and progressive disease process. Treatment may include antiinflammatory medications, polysulfated polysaccharides (Adequan), hyaluron, oral joint supplements, joint immobilization, and a decrease in the level of athletic performance required. Common antiinflammatory medications include systemic phenylbutazone and intraarticular administration of corticosteroids.¹⁶² A low level of exercise appears to be beneficial in some animals and may increase and stimulate the development of new bone, resulting in a more rapid and complete ankylosis. In unstable joints, immobilization with splints or casts may be necessary to allow the fusion to progress. Although further studies are warranted, the neurolytic properties of intraarticular 70% ethyl alcohol may allow the horse to continue in athletic work during the fusion process.¹⁶² In horses that remain lame, have end-stage joint osteoarthritis, or are not completing ankylosis naturally, facilitated ankylosis and arthrodesis are viable treatment options that may result in a usable animal.

Ankylosis may require 6 to 12 months for completion and in some animals may take longer.^158,165 Prognosis depends on which joint is involved and the intended use of the animal. Low-motion joints (distal tarsal joints in horse) hold a good prognosis for return to soundness and athletic activities after completion of the fusion process. Animals requiring the use of a high-motion joint to sustain their athletic career have a poor prognosis for return to function. Once the bony bridge is complete, ankylosis is not painful, but it is irreversible, and joint mobility is absent.

Definition and Etiology

Osteomyelitis is an infectious inflammatory disease of the substance of bone and its marrow cavity. Most large animal bone infections are of bacterial origin; mycotic infections rarely occur. Osteomyelitis may be acute or chronic and may involve the epiphyseal, metaphyseal, or diaphyseal region of a bone. Osteomyelitis can originate hematogenously, secondary to a contiguous focus of infection, or by direct bacterial inoculation (e.g., trauma, orthopedic surgery).^166,167

Clinical Signs and Differential Diagnosis

Diagnosis is based on history, physical examination findings, microbiologic culture results, and radiographic findings. Clinical signs vary with the length and severity of infection and the organism involved.

Animals with acute osteomyelitis usually exhibit localized inflammation and soft tissue swelling, may resent palpation of the affected area, and often have an obvious lameness. Fever, anorexia, depression, and general malaise may be observed. Acute bacterial osteomyelitis is seen most often in very young animals and is usually of hematogenous origin.^166,168 In the neonate it is frequently secondary to other foci of infection (e.g., respiratory or gastrointestinal tract) or umbilical remnant.¹⁶⁸ There is often a history of prematurity, failure of passive transfer of colostral immunoglobulins, or peripartum difficulties. Osteomyelitis in foals, calves, kids, and lambs is typically associated with septic arthritis and may or may not involve infection of the epiphyseal, physeal, and metaphyseal regions of the long bones.¹⁶⁸

The acute form of osteomyelitis is rare in adults and usually is associated with direct bacterial inoculation during trauma or open reduction of a fracture. Clinical signs of fever, localized pain, inappetence, and soft tissue swelling often make differentiation between infection and postoperative inflammation difficult. Persistent elevation in rectal temperature for more than 48 hours may be more indicative of an acute infectious process.

Fever and depression are usually not observed in chronically affected animals. In adults, infection is usually localized and the result of direct trauma to bone. Clinical signs typically observed in chronic osteomyelitis include firm swelling of the affected area, reluctance to bear weight on the limb, mild to moderate lameness, and presence of a draining fistulous tract. Drainage may be constant or intermittent and is usually purulent.

Radiographic signs of acute osteomyelitis are often subtle and can be difficult to interpret. Soft tissue swelling adjacent to the affected area may be the only radiographically visible abnormality during the initial signs of infection. Osteolysis may be observed as early as 3 days; however, serial radiography is often necessary to visualize bony changes, which may lag 7 to 14 days behind the evolution of infection.¹⁶⁸ Destruction of cortical bone initially appears as focal radiolucent holes that subsequently enlarge and coalesce to involve a region of bone (Fig. 38-24). Radiographic changes frequently noted in animals with chronic osteomyelitis include sclerotic bone, cortical resorption and thinning, and periosteal proliferation that may be smooth, expansile, or spiculated.¹⁶⁶ A sequestrum, a necrotic portion of cortical bone devoid of an osseous blood supply, is a classic radiographic observation. It appears radiodense and is surrounded by an area of cortical lysis¹⁶⁹ (Fig. 38-25). As the body’s defenses attempt to isolate the area of infection, periosteal new bone forms an involucrum, or bony sheath, around the sequestrum with a cloaca that allows inflammatory debris an avenue to egress through a fistulous tract to the skin¹⁶⁹ (Fig. 38-26).

Fig. 38-24 Osteomyelitis of the distal metaphyseal, physeal, and epiphyseal regions of the third metacarpal bone of a 3-week-old foal that did not receive colostral immunity at birth. Bony destruction is advanced. Note the associated soft tissue swelling.

Fig. 38-25 Cortical sequestration of the dorsal aspect of the third metatarsal bone in a horse 4 weeks after blunt trauma to the region.

Fig. 38-26 Lateral radiograph of the third metacarpal bone of a cow with chronic osteomyelitis. A sequestrum is visible surrounded by an area of osteolysis. An involucrum formed by medullary sclerosis and periosteal new bone and a cloaca (arrows) are evident.

Osteomyelitis at a fracture repair site delays healing and fracture instability is often noted clinically. Radiographically, lysis or bone resorption around implants may be observed, and fracture gap widening or nonunion is frequently seen.¹⁶⁶ Implant loosening and fixation collapse may occur with progression of bone lysis.

A definitive diagnosis of osteomyelitis is made by culture of the suspected focus of infection. Samples for culture may be obtained from deep needle aspirates, sequestra, and necrotic tissue removed during surgical debridement or metallic implants removed from the affected area. It is not recommended to culture draining tracts because tract organisms are not usually the pathogen(s) responsible for bone infection. Blood cultures are advisable in the neonate. Culture for both aerobic and anaerobic bacterial pathogens is indicated. Clinical characteristics suggestive of, but not limited to, anaerobic infection include a fetid odor, presence of bony sequestra, and purulent discharge. Anaerobic infection should be suspected if bacteria are identified on cytologic analysis but routine aerobic cultures show no bacterial growth.¹⁶⁶ Anaerobes are frequently associated with infection after surgical repair of an open fracture. Culture results will most accurately reflect the causative bacteria if samples have been collected and transported properly.

Clinical Pathology

The WBC count is usually elevated in animals with acute osteomyelitis. A degenerative left shift in the leukogram is often present. In neonates an initial leukopenia may be observed as the result of a primary disorder such as generalized septicemia or enteritis. Plasma fibrinogen also may be elevated in acute infection. The leukogram tends to return to normal with chronicity.

Osteomyelitis is frequently associated with septic arthritis in the neonate.^167,168 Synovial fluid of affected joints has an elevated leukocyte count and total protein concentration. Gram stain of synovial fluid can be helpful initially in determining the type of bacteria present, to aid in the selection of appropriate antimicrobial therapy before culture results are known. Blood cultures also may be helpful for identification of causative organism(s) in the neonate.

Pathophysiology

Sequestration of cortical bone results from mechanical trauma to the periosteum and overlying soft tissues, which compromises the defenses of normal cortical bone and leads to regional vascular injury and venous stasis.^166,167,169 Increased capillary permeability permits inflammatory cells to infiltrate the injured area and engulf bacteria. Lysed neutrophils release proteolytic lysosomal enzymes that induce local tissue and bone necrosis; and an exudate composed of serum, neutrophils, bacteria, and nonviable tissue accumulates.¹⁶⁷ If host defense mechanisms are inadequate to contain the infection, bacterial colonization of adjacent periosteal, cortical, and medullary regions ensues.¹⁶⁷ Antibodies and antibiotics cannot easily penetrate the infected area because of the compromised blood supply. The necrotic cortical bone or sequestrum is enveloped by granulation tissue and new bone, forming an involucrum in an effort to contain the infection.¹⁶⁷ Draining sinus tracts may eventually form as the disease progresses. Acute hematogenous osteomyelitis has historically been attributed to sluggish blood flow in the metaphyseal region of long bones in young, growing animals.^166,167 It was thought that vascular stasis in the capillary loops of the primary spongiosa resulted in localization of blood-borne bacteria in the metaphysis. Recently it has been shown that the endothelial lining of the capillaries pervading the primary spongiosa of neonates is incomplete and allows extravasation of bacteria and erythrocytes.¹⁶⁶ Because leukocytes are absent from this location in the young animal, macrophages provide the sole defense against bacterial colonization in this region.¹⁶⁶ The inability of these macrophages to eliminate bacteria effectively appears to be a critical factor in the development of hematogenous osteomyelitis in young animals.

Treatment

Selected cases of acute osteomyelitis may respond to aggressive antimicrobial treatment in the early stages, but once infection is established in bone, it is difficult to resolve without surgical intervention. Broad-spectrum antimicrobial administration in combination with surgical management constitutes the hallmark of treatment for osteomyelitis.^166,167

The goal of surgical treatment is to facilitate the penetration of blood-borne antibiotics to the site of infection by eliminating necrotic debris and encouraging vascular access to compromised tissues. The most important precepts are careful and thorough debridement of all nonviable tissue and sequestrated bone fragments, establishment of open drainage, and removal of foreign material implants.^166,167 Certain bacteria (e.g., staphylococci) are capable of producing a viscous substance that enshrouds bacterial colonies and facilitates adhesion of bacteria to necrotic bone and foreign implants.¹⁶⁶ When combined with host-derived matrix proteins and cellular debris, this biofilm protects bacteria from host defenses and may actually alter bacterial susceptibility to certain antibiotics.¹⁶⁶

The exception to implant removal arises when the implant is required for fracture stabilization. Although healing is delayed, stable fractures can heal in the presence of infection.¹⁶⁶ Therefore it is advisable to maintain implants until they are no longer necessary for fracture stability while treating the infection. However, delayed healing can lead to excessive cycling of the implant and fixation failure.

Initially the choice of appropriate antibiotic is based on known susceptibilities of the organism suspected to be responsible for infection. Antibiotic therapy may require modification after a definitive organism(s) is isolated and in vitro susceptibilities determined. The ideal antibiotic demonstrates the greatest bactericidal activity against the offending organism, with the least toxicity to the patient, and is economically feasible. Duration of antibiotic therapy is empirical and depends on clinical response. Because compromised bone requires 4 to 6 weeks for revascularization, this time frame has generally been accepted for treatment duration in cases of chronic osteomyelitis.^166,170

The most common aerobic bacterial groups isolated from musculoskeletal infections in horses include Enterobacteriaceae, streptococci, and staphylococci.¹⁷¹Actinomyces pyogenes is the most frequent isolate recovered from adult cattle, sheep, and goats. Neonates appear particularly susceptible to infection from Escherichia coli and Salmonella species.¹⁶⁸ Bacteroides species is the most predominant obligate anaerobic genus encountered; however, most infections include a mixture of anaerobes or a combination of aerobes and anaerobes.

Parenteral administration of antibiotics constitutes the mainstay of antimicrobial therapy in the treatment of osteomyelitis.¹⁷⁰ Localized antibiotic therapy, however, is a useful adjunct to systemic antibiotic treatment. Regional limb antibiotic perfusion, local implantation of polymethylmethacrylate (PMMA) antibiotic-impregnated beads, and use of autogenous cancellous bone grafts enhance the resolution of osteomyelitis.^172-174

Regional limb perfusion delivers a systemic dose of antibiotic to an isolated area of infected tissue,^172,173 subjecting the tissue to antibiotic concentrations in excess of the MIC for the infectious agent. This technique is particularly useful for cases of septic arthritis in which vascular compromise of synovial membrane may prevent adequate antimicrobial distribution.¹⁷² A tourniquet is placed proximal to the site of infection. A systemic dose of antibiotic is administered through a catheterized vein distal to the site of infection,^172,173 or through a single, 4.5-mm-diameter hole into the medullary cavity and allowed to perfuse the isolated area for 30 minutes. In horses, cattle, and rabbits, synovial antibiotic concentrations are significantly greater than peak serum concentrations associated with systemic administration.^172,173 We have used regional limb perfusion as an adjunct treatment in selected cases of septic tenosynovitis and navicular bursitis and osteomyelitis of the calcaneus, phalanges, and distal sesamoid bone.

Antibiotic-impregnated PMMA beads are an effective drug delivery system for bone and soft tissue infections in human medicine.^166,174 Although this treatment is gaining popularity in large animal orthopedics, there are no published reports of its efficacy in veterinary medicine. Gentamicin is the traditional antibiotic impregnated in beads and elutes over time to yield local concentrations well above the therapeutic concentration range for as long as 80 days postimplantation.¹⁷⁴ Aminoglycoside toxicity does not appear to be a problem, with human serum and urine concentrations below those associated with systemic administration.¹⁷⁴ Gentamicin-impregnated PMMA beads are used routinely in our hospital in the repair of open fractures and in the internal fixation of closed fractures that incurred significant soft tissue trauma.

The use of autogenous cancellous bone graft has been advocated as an ancillary treatment in some cases of septic navicular bursitis and osteomyelitis of the navicular bone in horses.¹⁷⁵ Placement of the graft in a surgically created defect underlying the navicular bone may reduce dead space, provide protection of the deeper tissues from environmental contamination, and afford a temporary scaffold for the ingrowth of capillaries and precursor cells of granulation tissue.¹⁷⁴ We believe this modality has merit for continued clinical application and routinely use it for deep-seated infections of the foot.

Prevention and Control

Early and aggressive medical therapy for neonates suspected to be at risk for developing septicemia is prudent in the prevention of acute hematogenous osteomyelitis. Therapy may include administration of prophylactic antibiotics and hyperimmune plasma in animals with failure of passive transfer of colostral antibodies. Prompt and meticulous debridement of avascular and necrotic tissue in treatment of soft tissue wounds and repair of open fractures cannot be overemphasized. Delayed wound closure may be desirable in select cases of overwhelming contamination or infection.

Many infections associated with fracture repair occur during open reduction and internal fixation of closed fractures.¹⁶⁶ Strict adherence to the principles of aseptic technique is imperative to a successful outcome. Prophylactic antibiotics are often used because the risk of infection increases with metallic implants. The timing of antibiotic administration is crucial for efficacy and should achieve sufficient blood antibiotic levels while the amount of bacteria in the exposed tissues exceeds the host’s ability to eliminate the organisms and allow tissue healing to commence.¹⁶⁷ For elective uncomplicated orthopedic procedures, antibiotics should be administered 1 to 2 hours before surgery and continued for no more than 72 hours after surgery.¹⁶⁷ For long-bone fracture repair, the risk of infection is much greater because of increased operative time, the presence of metallic implants, and the soft tissue trauma incurred during the injury and subsequent fixation.¹⁷¹ In this case, administration of the most effective broad-spectrum antibiotic combination for an extended period is advisable.

Diagnosis

The diagnosis of heel pain is not difficult when a horse’s lameness resolves with a palmar digital nerve block. However, determining which foot structure is the source of pain and establishing correct treatment are becoming more difficult. It seems that the more we learn about diagnostic anesthesia, the more clouded the picture becomes. Horses with navicular or heel pain can be a diagnostic and therapeutic challenge to the owner, clinician, and farrier.

Diagnosis is based on historical data, clinical findings, and both routine and advanced imaging techniques to localize the structure causing pain within the hoof capsule. My approach to horses with lameness originating from the heel region is to determine which structure in the foot is causing the pain and then develop a therapeutic plan. Severity and duration of the lameness, the horse’s activity, and potential owner compliance, as well as the farrier’s experience, should be considered. The horse’s hoof wall quality, conformation, environment, and occupation will all affect therapy.

HISTORICAL DATA

Common complaints reported by owners of a horse exhibiting chronic foot pain include intermittent unilateral or bilateral forelimb lameness and increased severity of lameness for several days immediately after shoeing or at the end of the shoeing period (when the toes are long). Occasionally the horse may point the affected forelimb, stumbling, with a short, choppy gait and increased lameness when ridden on hard ground.

Horses sustaining acute injuries to soft tissue structures in the caudal aspect of the foot (e.g., impar or CSL of navicular suspensory apparatus, distal DDFT), laminar tearing, or severe bruising of the heel region may have a history of becoming acutely lame during or immediately after a performance event. Historical data are often overlooked but may suggest which foot structure is damaged.

LAMENESS EXAMINATION

Horses with bilateral forelimb involvement have a stiff, shuffling, short-strided gait that owners often perceive as shoulder lameness. The horse should be observed at a slow trot in a straight line and circled in both directions. A smooth, hard surface is optimal. In horses with heel pain the lameness will often be exacerbated when trotted on hard versus soft ground. The severity of lameness should be assessed before and immediately after application of hoof-tester pain. Horses with navicular area pain may have increased severity of lameness when trotted after the hoof-tester application in the central frog area. Several tests may exacerbate lameness in horses with navicular pain, such as allowing the horse to stand on a small block of wood centered over the frog for 60 seconds before trotting, or elevating the toe with a block of wood. A 30-second lower-limb “fetlock” flexion test may also exacerbate lameness in horses with navicular area pain.

DIAGNOSTIC ANESTHESIA

Perineural anesthesia of the palmar digital nerves (PDNs) with 1 to 2 mL of mepivacaine placed axial and distal to the proximal limits of the medial and lateral collateral ligaments will desensitize the palmar half of the foot, entire sole, and palmar aspect of the coffin joint. This block is performed just below the proximal limits of the collateral cartilages to avoid desensitizing the dorsal nerve branches. One study demonstrated that lameness secondary to solar pain created by a setscrew-induced pain model was eliminated 10 minutes after anesthesia using 2 mL mepivacaine over each PDN.¹⁷⁹ In the past, coffin joint (DIP) anesthesia was thought to be helpful in diagnosing navicular area pain, but investigators have recently demonstrated a lack of specificity with this block. DIP anesthesia has been shown to eliminate lameness associated with pain in the navicular bone itself, navicular suspensory apparatus, navicular bursa, and sole of the foot, because the sensory nerves to the navicular area are close to the DIP joint, and passive diffusion of the anesthetic occurs to the PDNs. Solar pain in the toe region was eliminated before solar pain in the heel region after DIP anesthesia, and a maximum 6 mL of anesthetic was recommended for analgesia of the DIP joint. This suggests that horses with heel bruises or laminar tearing in the heel region should not improve after DIP analgesia using low-volume anesthetic and evaluating the horse after 10 minutes.

The navicular bursa is a thin synovial structure located between the navicular bone and distal aspect of the DDFT. Analgesia of the navicular bursa may be more specific for navicular area pain. A positive response to navicular bursa analgesia probably reflects pathology in the navicular bursa, navicular bone, or supporting ligamentous structures. The normal navicular bursa has a 3-mL capacity, which may be reduced in horses with inflamed tissue or adhesions between the navicular bursa and DDFT. Synovial fluid is obtained infrequently when performing navicular bursa analgesia.

Horses that improve but do not have total resolution of the lameness until after a high palmar digital or abaxial nerve block may have pain associated with a desmitis of the DDFT within the hoof capsule or desmitis of the DIP joint collateral ligament. Horses with DDFT desmitis may also improve after DDFT analgesia.

RADIOGRAPHIC EXAMINATION

A minimum of three high-detail radiographic views should be used to evaluate the navicular bone; additional views are needed to evaluate the entire foot. Lateromedial (LM), 60-degree dorsoproximal-palmarodistal oblique with grid (D60Pr-PaDiO), and palmaroproximal-palmarodistal oblique (Pa45Pr-PaDiO) views of the navicular bone are obtained. Some clinicians also include two oblique views of the navicular bone. Abnormal radiographic changes include variation in size and shape of synovial foramina on the D60Pr-PaDiO projection; cystic changes within the navicular bone; enthesophyte formation at the attachment of the CSL ligament on the LM projection; flexor cortex erosions and loss of corticomedullary distinction, best viewed on the Pa45Pr-PaDiO projection; calcification of the flexor surface and distal DDFT; and osseous fragments associated with avulsion of the impar ligament. Previous studies have shown that abnormal synovial fossae are poorly correlated with lameness, rarely progress over time, and are inconclusive for the diagnosis of navicular disease. Radiographic abnormalities more strongly associated with lameness are flexor cortex defects, medullary sclerosis, proximal border remodeling, and loss of medullary trabecular pattern.

Although radiographic evaluation is important in the diagnostic workup of a horse showing palmar foot pain, it is not very sensitive in defining the actual pathologic condition of the navicular bone. Radiographs often underestimate the extent of pathology seen on necropsy in horses with navicular lesions.

NAVICULAR BURSOGRAPHY

Administration of a 3-mL mixture of 1:1 contrast media and anesthetic into the navicular bursa, followed by a Pa45Pr-PaDiO radiographic view, is used to evaluate pathologic changes on the flexor surface of the navicular bone and adhesions or scarring of the DDFT. The advantage of this technique is confirming pathologic changes on the flexor surface of the navicular bone, which may not be apparent on survey radiographs, and injection of the anesthetic into the navicular bursa. Navicular bursography identified pathology in the flexor region of the navicular bone 60% more often than plain radiographs.^179a The disadvantages are that some horses are not very tolerant of needle penetration of the DDFT and insertion into the navicular bursa, and the procedure carries risks such as trauma to the navicular bone, sepsis, acute synovitis of the bursa, and possibly DDFT damage secondary to needle penetration.

NUCLEAR SCINTIGRAPHY

Radiography has lower sensitivity than, but equal specificity as, scintigraphy for the diagnosis of navicular disease. For detecting abnormal bone activity within the hoof, nuclear scintigraphy is a sensitive but rather nonspecific imaging method. Scintigraphy detects increased ^99mTc uptake in areas of active osteoblastic activity; however, because of the proximity of anatomical structures in the caudal third of the foot, specific structural location of the source of pain in a horse with palmar foot pain is limited with scintigraphy. The reliability of scintigraphy in diagnosis of foot pain has been criticized because of common false-positive and false-negative results. Lateral bone-phase images were found to be less sensitive than palmar images, and views taken 1 hour after radioisotope administration were as diagnostic as those taken 2 to 4 hours after administration.

ULTRASONOGRAPHY

Diagnostic ultrasonographic images can be obtained for some structures in the foot region. Ultrasonographs of the collateral ligaments of the DIP joint are obtained by positioning a 7.5- or 10-MHz transducer on the firm part of the dorsolateral and dorsomedial aspects of the coronary band. The normal DIP joint collateral ligament for a large horse is about 0.66 cm.¹⁷⁷ The distal aspect of the DDFT can be visualized from between the heel bulbs in the palmarodistal aspect of the pastern joint. The frog of the foot can also be used as a window to image the DDFT and impar ligament near the flexor surface of the navicular bone. Before imaging, the frog should be trimmed to pliable tissue and the foot soaked in a water bath overnight. Limitations of ultrasound are that the images are restricted to the axial midline, and off-incidence artifacts can confuse image interpretation. If the frog is excessively hard or has deep sulci, poor contact between the frog and transducer may prevent propagation of the ultrasound beam. Variation in cross-sectional area and width of the DDFT and impar ligament both within and between limbs of normal horses also may make image interpretation difficult.

COMPUTED TOMOGRAPHY

CT is the best modality for detecting and evaluating bone pathologies in the cortex or trabecula and can also provide an accurate three-dimensional assessment of soft tissue structures of the foot. Although less expensive than MRI, CT is less versatile. Special contrast studies are needed to evaluate articular cartilage with CT, but not with MRI. One advantage over MRI is that CT can be used to assess accurate needle or scalpel placement for specific treatment options. One disadvantage for CT in horses is the need for general anesthesia and special equipment design to accommodate the horse.

MAGNETIC RESONANCE IMAGING

MRI offers a superior diagnostic tool to image soft tissue structures in the foot. The recent use of MRI in equine lameness has provided valuable insight into the pathologic problems occurring in horses with palmar foot pain. MRI is particularly useful in the recognition of abnormally high signal (fluid) in structures such as the DDFT, IL, and collateral ligaments. MRI also can detect navicular bone edema as well as articular cartilage damage in the navicular region. MRI can be performed under general anesthesia or in the standing horse, depending on the equipment available. In one study of 199 horses with lameness localized to the foot by clinical signs and perineural anesthesia, MRI was found to be superior to nuclear scintigraphy, ultrasound, or radiology in identifying the specific foot structure causing the pain. The most common injury was DDFT desmitis (59%), followed by desmitis of the DIP collateral ligament (31%); 17% of horses had injuries to multiple structures. Only 28% of horses with DDFT or collateral ligament injuries of the DIP joint returned to previous use.¹⁸⁰

MEDICAL THERAPIES

Basic Principles for Proper Hoof Balance

The configuration of the hoof capsule reflects the stresses applied to the foot during the previous months. Hoof balance refers to both mediolateral and dorsopalmar balance. Dorsopalmar balance refers to proper hoof-pastern alignment. Ideally, when viewed from the side, a line drawn through the central aspect of the first phalanx should bisect the hoof capsule, and the toe angle and heel angle should be parallel to this line. A broken back hoof-pastern axis is common in horses with long-toe low-heel conformation and results in increased stress on the phalangeal joint capsules, navicular suspensory apparatus, and distal DDFT and increases pressure between the navicular bone and DDFT.

Breakover (break-over point) of the foot is the terminal part of locomotion when the heel looses contact with the ground surface, followed by the toe. Tension of the DDFT over the navicular area and flexion of the coffin joint occur during breakover. A low hoof angle or long toe is associated with prolongation of breakover time. A high heel angle reduces breakover, causing a reduction of forces exerted on the caudal structures of the foot and limb (e.g., navicular suspensory apparatus, DDFT, suspensory ligament). Breakover should be made as easy as possible by decreasing toe length.

Corrective trimming is often more important but can be more difficult than corrective shoeing. The toe is shortened as much as possible, and the heels are trimmed back to the widest aspect of the frog. One of the most common problems I see is allowing the heels to grow forward, thus decreasing heel support and contributing to dorsopalmar hoof imbalance (Fig. 38-27); the heels lose mechanical strength and often collapse. In addition, the bars of the hoof flatten out and lose support. Proper trimming of the heels back to the widest aspect of the frog increases the functional weight-bearing surface of the foot. The ground surface of the properly trimmed foot has a more rounded appearance (Fig. 38-28). Palmar hoof support is essential for horses with navicular/heel pain. Full-fitting shoes provide more support hoof by increasing the weight-bearing surface. Ideally, the shoe should fit about 1/16 inch wider than the hoof behind the last shoe nail to allow heel expansion. The nails should be placed in a line parallel to the ground approximately 1 inch (2.5 cm) proximal to the shoe, and no nails should be placed behind the widest aspect of the hoof.

Fig. 38-27 Hoof with the heels allowed to run too far forward. The heels are located at the pointer but should be back at the widest aspect of the frog.

Fig. 38-28 Hoof from Figure 38-27 after trimming the heels back to the widest aspect of the frog. Note the larger, rounded shape to the hoof with increased heel support.

Using a wedged shoe or pad to elevate the heels by 2 to 3 degrees after the foot is properly trimmed decreases tension in the DDFT, thus reducing pressure applied to the navicular region. The effect of raising the heels is helped by rolling or rockering the toe to quicken the breakover of the foot. The use of an egg-bar shoe is controversial. Although horses with long-toe, low—heel-hoof conformation may gain caudal foot/heel support from the shoe, egg-bar shoes had no effect on reducing forces between the DDFT and navicular area.

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When selecting a particular corrective shoe or shoe/pad combination, the horse’s use is an important factor because the desired corrective shoe for the individual hoof conformation may not be suitable for the horse to perform its intended use. A compromise must be made between shoeing for the “ideal” and shoeing for athletic performance, taking into consideration such factors as weight of the shoe, traction, and interference of other limbs. Another important factor is hoof quality. The ideal shoe/pad selected for proper hoof balance may be impossible to apply if the hoof wall is thin or damaged. In these cases, a secondary shoeing regimen is selected that will accomplish similar results until hoof quality improves. Although no standard shoeing technique exists for horses with navicular pain, the following suggestions may be beneficial.

A rim shoe or half-round shoe has a rounded edge that will enhance breakover. The rim shoe has good traction and is useful in western performance horses, such as roping horses, barrel racers, and cutting horses. The Natural Balance Shoe has a rockered toe and, because of its design, artificially shortens the toe length and enhances breakover. It is made of aluminum or steel; owners of some western performance horses seem to prefer the steel shoe, which is thought to provide better traction than the aluminum shoe.

Acute ligamentous injuries involving the distal aspect of the DDFT or navicular suspensory apparatus require extended periods of rest. During the rest period, application of a 3- to 4-degree wedge pad to the shoeing regimen may decrease tension of these soft tissue structures. Controlled exercise is important in the treatment of these injuries. My group often begins with a 3- to 4-degree pad, depending on the horse’s hoof conformation, and gradually decreases the quantity of heel elevation over time.

Different shoeing techniques will accomplish the same goals of easing breakover, supporting the heels, and protecting injured areas of the foot.

Intraarticular Medications

Intraarticular medication of the DIP joint can be beneficial in horses with navicular area pain. Some horses fail to respond adequately to corrective shoeing, rest, and NSAID therapy, or the horse may have responded initially but no longer. If the lameness has been previously localized to the caudal aspect, intraarticular anesthesia of the DIP joint is performed at the recheck examination. If significant improvement is seen in the lameness, the client is offered intraarticular medication as a treatment option. Alternately, if the horse improves after PDN anesthesia in one limb and becomes lame in the opposite limb, anesthesia of the DIP joint is performed. If significant improvement is seen, medication of the DIP joint is offered as an initial treatment option. It is important to remember that DIP joint anesthesia is not specific for navicular area pain, as discussed earlier.

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Selection of intraarticular medication varies with the clinician, severity of disease, and client. I usually inject 20 mg of sodium hyaluronate and 6 to 9 mg of triamcinolone (Vetalog), which often alleviates clinical signs of lameness for 6 to 12 weeks. In severe cases of navicular disease, 20 to 40 mg of methylprednisolone acetate (Depo-Medrol) in combination with the sodium hyaluronate may provide a slightly longer duration of effect. Hyaluronate is used for joint lubrication and to increase the hyaluronan content of synovial fluid. Corticosteroids interact with steroid-specific receptors in the cytoplasm of cells and inhibit inflammatory infiltration into the joint and neutrophil function by impairing lysosomal enzymatic release. Corticosteroids also inhibit phospholipase A₂, preventing both cyclooxygenase and lipoxygenase inflammatory pathways.

The two primary reasons not to use intraarticular corticosteroids in horses with joint disease are risk of sepsis and potential adverse effects on articular cartilage and subchondral bone. Using aseptic technique and combining intraarticular antimicrobials with the injection medication should decrease the risk of synovial infection. I prefer to use 50 to 100 mg of amikacin sulfate for joint injections. To minimize the negative effects of intraarticular corticosteroids, the lowest clinically effective dose is used. Minimal research has been performed in this area, so clinician experience and empirical information are often consulted. Both systemic and intraarticular corticosteroids have been associated with laminitis in horses. DIP joint medication is injected using a 20-gauge sterile needle placed approximately 1 cm dorsal to the hoof capsule on midline, penetrating the extensor tendon while entering the DIP joint. The angle of needle insertion is about 45 degrees from perpendicular to the ground surface. Synovial fluid is usually obtained.

About 30% of horses with pain localized to the navicular area either do not improve or may improve but remain lame after DIP joint anesthesia, which may be associated with different diffusion properties of the local anesthetic versus the intraarticular medication. Drug treatment of the navicular bursa may be beneficial in some of these horses. We recently reported on 25 horses with pain localized to the navicular region that did not respond to corrective shoeing, phenylbutazone, or DIP joint medication.¹⁷⁸ These horses did improve after navicular bursa injection with 40 mg methylprednisolone and remained sound for a mean of 4 months. Most of the 25 horses had moderate to severe radiographic changes involving the navicular bone. Approximately half had an enthesophyte located at the proximal aspect of navicular bone at the attachment of the CSL, possibly indicating chronic CSL desmitis (Fig. 38-29). The technique for navicular bursa injection has been previously described.¹⁷⁸

Fig. 38-29 Lateral-to-medial radiograph of foot showing an enthesophyte at the proximal aspect of the navicular bone where the collateral suspensory ligament attaches. Horses with this type of radiographic abnormality usually respond better to medication of the navicular bursa than distal interphalangeal joint medication.

SURGICAL OPTIONS

SUMMARY

No single treatment option is suitable for all horses with heel or navicular area pain. Each horse must be evaluated individually to determine which structure in the palmar aspect of the foot is injured, severity of disease, horse and hoof conformation, and horse use and level of performance expectation before a treatment plan can be developed. Many treatment options are available to help these horses to perform.

SPONDYLITIS

SARAH M. REUSS

SPONDYLOSIS

SARAH M. REUSS