Shoulder lameness in horses is less common than many lay persons expect. Although cases are often described as having a typical gait (reduced protraction/cranial phase; wearing of the toe; a swinging lameness) they are still difficult to diagnose simply from analysis of the animal's walk or trot. However, almost all cases have atrophy of the proximal limb muscles (especially supraspinatus, infraspinatus, the cranial shoulder muscles, and muscles of the cranial antebrachium) beyond that which would normally be expected for lameness caused by distal limb disease. This is associated not with shoulder pathology per se, but is a feature of proximal limb lameness. Intra-articular anesthesia, medication, and centesis can be accomplished by passing a long (preferably spinal-type) needle between the cranial and caudal parts of the lateral tuberosity of the humerus, angling caudodistally, from above. Radiography is limited to the mediolateral projection, with the limb extended, and in some cases oblique projections (usually caudolateral-craniomedial or proximocranial-proximodistal). Ultrasonography can be useful in certain situations.
Developmental orthopedic disease manifests in the scapulohumeral (shoulder) joint principally as subchondral cyst-like lesions (bone cysts) affecting the glenoid of the scapula or as osteochondritis dissecans of the humeral head. Also, a condition almost exclusive to miniature ponies, caused by dysplasia of the joint and attributable to hypoplasia of the joint surfaces, results in instability and secondary arthritis.
Subchondral Cyst-like Lesions
Bone cysts may develop in the glenoid, or socket, of the shoulder joint. They may or may not communicate with the shoulder joint and respond variably to intra-articular anesthesia. Although part of the developmental orthopedic disease complex, signs may not be apparent until the animal is mature. In common with other manifestations of this syndrome, lameness may not become a feature until the animal begins work (typically breaking in or early ridden exercise). Occasionally bone cysts may be a cause of lameness in the older horse, having remained quiescent for most of the animal's life; the reason for these later onset cases is not clear.
Diagnosis is made by localization with intra-articular anesthesia, by exclusion of lower limb disease, or occasionally by gamma scintigraphy. Radiographs should document the lesion, although some cysts are too small to be seen.
Treatment in young horses consists of rest in the hope that the cyst will remodel to become nonpainful; however, this happens only rarely. Intra-articular medication can provide relief from lameness, but usually only transiently. Some newer disease-modifying preparations show promise (eg, autologous conditioned serum) and some clinicians favor the use of systemic glycosaminoglycans. Surgical debridement is very difficult in the majority of cases because of the cyst location and articular cartilage damage that causes secondary osteoathritis. Injection of corticosteroids directly into the cyst via an extra-articular approach could be appropriate, but the lack of 3-dimensional imaging of this region in horses makes the approach hard to plan.
Derangement of cartilage and bone development on the humeral head can result in weakness within the articular cartilage that may lead to erosion or formation of a free flap of cartilage. Typically the caudal part of the head is affected, or at least it is the part most evident on radiographs. In other joints, osteochondritis dissecans often can be treated successfully with arthroscopic debridement. Unfortunately, access to the shoulder joint is severely restricted and in most cases the full extent of the lesion cannot be seen or treated. Clinical resolution in all but the mildest cases in young horses is rare. Rest and various medications have been tried with little documented success.
Seemingly unique to the miniature breeds, this condition arises from a mismatch between the size of the glenoid and humeral head. This causes instability of the joint and secondary arthritis. Although undoubtedly a developmental problem, probably with a significant degree of heritability, many cases do not present until the animal is an adult. The history is often of sudden onset lameness. On physical examination, proximal limb muscle atrophy is often profound and lameness considerable. These factors, along with the breed disposition and the often present sign of resentment of proximal limb manipulation, make localization straightforward. Radiographs reveal the presence of osteoarthritis and variable subluxation of the scapulohumeral articulation. Oblique views may demonstrate deep erosion of the humeral head in severe cases. The generalized destruction of the joint produces a “hot spot” on a bone scan, if performed. There is no simple treatment. Most cases present at such an advanced stage that even palliative care is impossible; euthanasia on humane grounds should be considered in such situations. Surgical arthrodesis has been described but is rarely performed.
Serious trauma can result in fracture to any part of the shoulder region. However, the main sites affected are the supraglenoid tuberosity of the scapula (which serves as the origin of the biceps brachii muscle), the mid to distal scapula, and the proximal humeral metaphysis.
Supraglenoid tuberosity fractures, if complete, invariably displace in a craniodistal direction, due to the pull of the biceps. Large fractures can be surgically repaired. This is not easy, however, as the fragments are often difficult to reduce and the implants are difficult to place and prone to failure during recovery from anesthesia or during convalescence. Smaller fragments can be removed, but the involvement of the biceps tendon of origin has to be resected. Very large fragments can involve the joint surface. Cases usually present with severe lameness and a history of trauma (eg, a fall during jumping or collision with a fixed object). On manipulation, there is often a sense of disarticulation between the lower limb and shoulder as the biceps is disrupted. Crepitus may be felt. In most cases, because the inciting cause is significant trauma, there are other signs such as soft tissue abrasions or swelling that pinpoint the shoulder as the site of pain. Radiographs will reveal the fracture and ultrasonography can be very useful to assess the biceps tendon. Management varies and depends on intended use, age, size of fragment, size of horse, etc. The prognosis for restoration of normal function is guarded. The degree of biceps disruption, along with the severity of lameness and the intended use for the horse, are probably the most important prognostic factors.
Mid to distal scapula fractures occur through trauma or, in racehorses, as stress fractures associated with cumulative cyclical fatigue. Trauma can result in complete or (presumably due to the flexibility of the bone, especially in foals) incomplete fractures. Radiographs rarely help, because of the difficulty in obtaining diagnostic images of the area. Ultrasonography can accurately assess the integrity of the bone surface and is the technique of choice. Scintigraphy can also detect the injuries. Comminuted fractures can occur and the prognosis worsens with increased complexity of the fracture. Simple, nondisplaced or minimally displaced fractures usually heal well with rest alone.
Ultrasonography can be used to monitor healing. Stress fractures are almost always incomplete and heal very well, carrying an excellent prognosis for return to training. Very rarely, scapula fractures manifest as severe, unstable, comminuted injuries necessitating euthanasia on humane grounds. The clinical appearance is the key to making a decision in these circumstances—although painful, scapula fractures with a good prognosis cause no observable limb instability.
Rarely, fractures affect the tuberosities of the proximal humerus and the deltoid tuberosity. The principles described above can be extrapolated to these injuries. The majority heal with conservative therapy and very good outcomes.
Stress fractures affect the proximal humerus also, almost exclusively in the caudal metaphyseal region. They are an uncommon but important cause of lameness in racehorses (the craniodistal metaphysis of the humerus is also affected, see Fractures). The typical history is one of sudden onset, often moderate to marked lameness closely associated with recent exercise, in an animal usually but not always in faster work. Lameness is usually transient, and the horse generally becomes sound within a short time (days to a week). If exercise resumes, lameness recurs. Localization is difficult; many are detected following elimination of the lower limb as the source of pain, or with scintigraphy. Radiographs can identify periosteal and endosteal new bone at the site of injury. Recovery is usually uncomplicated and complete with a few weeks' rest. Prolonged confinement may be counterproductive, and light exercise (walking only) may be introduced surprisingly quickly once the initial painful period has subsided. The injury remains evident on radiographs long after the bone is strong enough to withstand exercise, but a gradual smoothing and resolution of the callus will be seen as remodelling proceeds. Undetected humeral stress fractures can result in failure of the bone during exercise and complete breakdown, necessitating euthanasia.
The tendon of the biceps brachii runs over the cranioproximal humerus, protected by a synovial bursa. Inflammation of this structure can cause lameness and is usually secondary to a more serious inciting cause. Trauma to the proximal humerus, cystic lesions in the underlying bone, and injury to the tendon itself will cause secondary bursitis; it is important to recognize the primary lesion and treat appropriately. Occasionally, idiopathic primary bursitis arises and responds very well to medication of the bursa with corticosteroids. Bacterial contamination and, rarely, fungal infections can cause bicipital bursitis. In most cases, a wound in the vicinity of the bursa alerts the clinician to this possibility but, very rarely, closed sepsis can occur. Treatment for septic bursitis follows the same pattern as for other synovial structures. Radiography and ultrasonography complement each other in the diagnosis and management of primary and secondary bursitis. Repeat examinations may be necessary if a primary lesion cannot be detected, as it may become obvious with time. Scintigraphy is useful in cases in which the primary lesion remains elusive, because small areas of bone damage or cavitation can go undetected radiographically.
Sepsis of the shoulder joint occurs most commonly as a result of penetrating injury. Diagnosis and treatment proceed as for other joints. In foals (and rarely, weanlings or yearlings) infection can spread hemato-genously and become established in the growth plates or ends of the bones (physeal or epiphyseal infection). These infections, provided they are not associated with contamination of the synovial structures, can be treated with high levels of antimicrobials systemically before resorting to surgical intervention. Methods of providing high quantities of antimicrobials at the site of infection exist (eg, intraosseus perfusion).
This syndrome describes the physical appearance of the horse's shoulder. It is not a diagnosis in itself, as there are a number of potential causes. The most common cause is injury to the suprascapular nerve.
All cases have atrophy of the supraspinatus and infraspinatus muscles that cover the scapula. This results in the scapular spine becoming prominent—in severe cases the muscles virtually disappear. The atrophy is unusual in that it is often profound and very localized, which are hallmarks of an injury to a single lower motor nerve. The nerve involved is the suprascapular. Although the site of damage is rarely documented clinically, most cases involve trauma to the cranial shoulder at the point where the nerve is exposed to potential compression as it courses over the cranial aspect of the scapula. The severity of damage determines the degree of atrophy and the chances of recovery. If nerve function is severely compromised, the shoulder joint becomes unstable (it is a synarthrosis relying on the surrounding muscles to support it) and the joint “pops out” sideways as the horse bears weight. This subluxation does not appear overtly painful to the horse but does have significant implications for the longterm health of the joint and the horse's athletic career.
Therapy is aimed at maintaining muscle health during the period of nerve recovery and maximizing neurogenesis. Horses should be restricted to stable rest or a very small paddock. Complete immobilization may negatively impact the nerve and muscles, but activity probably hastens joint degeneration. A surgical procedure for removing part of the scapula over which the nerve courses has been described, aiming to provide optimal conditions for nerve recovery. This should be considered, but its usefulness is open to debate. Muscle stimulation, under the guidance of a trained physiotherapist, will help to limit muscle fibrosis and may encourage nerve regeneration. The vast majority of cases seem to be a result of neuropraxia or axonotmesis (based on clinical observations and rates of recovery) and will recover function with time. However, this process can take many months and frequently some loss of muscle bulk will remain. The prognosis seems most affected by duration of injury before diagnosis, degree of atrophy at diagnosis, and willingness of the owner to perform time-consuming physical treatments for many months.
Other causes of sweeney include disuse atrophy (which does not appear focal and is rarely severe), brachial plexus injury (which usually disrupts a number of nerves, atrophy is not focal but observable in a number of muscle groups), and caudal cervical disease resulting in spinal nerve radiculopathy (in which a number of motor nerves will be affected so that other muscles atrophy). Careful assessment of the muscles involved and radiography of the neck and shoulder will aid differentiation. Scintigraphy is useful for rapid screening of the proximal limb and cervical and thoracic vertebra for damage that may have an adverse effect on prognosis.
Degenerative joint disease affecting the shoulder joint poses the same problems here as it does elsewhere. If no primary cause is identified that is amenable to correction and if radiographic signs (periarticular osteophytes, etc) are established, it is safe to assume that cartilage destruction is well underway. Signs can be ameliorated, but not cured, with the use of anti-inflammatory, analgesic, and disease-modifying therapies.
Last full review/revision March 2012 by Stephen B. Adams, DVM, MS, DACVS; Joerg A. Auer, DrMedVet, Dr h c, MS, DACVS, DECVS; James K. Belknap, DVM, PhD, DACVS; Jane C. Boswell, MA, VetMB, CertVA, CertES (Orth), DECVS, MRCVS; Peter Clegg, MA, Vet MB, PhD, CertEO, DECVS, MRCVS; Andrew L. Crawford, BVetMed, CertES (Orth), MRCVS; Jean-Marie Denoix, DVM, PhD, Agregé; Marcus J. Head, BVetMed, MRCVS; C. Wayne McIlwraith, BVSc, PhD, DSc, FRCVS, DACVS; James Schumacher, DVM, MS, DACVS, MRCVS; John Schumacher, DVM, MS, DACVS, MRCVS; Roger K. W. Smith, MA, VetMB, PhD, DEO, DECVS, MRCVS; Chris Whitton, BVSc, FACVSc, PhD