Shoulder pain in horses is a common suspicion among riders and owners; in reality, however, it is an uncommon origin of lameness. Chronic upper limb lameness frequently includes atrophy of the proximal limb muscles (especially supraspinatus, infraspinatus, cranial shoulder muscles, and muscles of the cranial antebrachium), which helps to differentiate it from distal limb lameness.
Diagnosis is based on careful examination, including manipulative tests. Intrasynovial anesthesia of the shoulder joint or bicipital bursa can be used to diagnose pain in these specific areas. Scintigraphy and thermography are physiological imaging modalities that can help in the diagnosis of shoulder lameness. Radiography (usually caudolateral-craniomedial or proximocranial-proximodistal) and ultrasonography are essential for full assessment of the shoulder region.
Developmental Diseases of the Shoulder in Horses
Developmental orthopedic disease (osteochondrosis) in horses manifests in the scapulohumeral (shoulder) joint principally as subchondral cystlike lesions (SCLs or bone cysts) affecting the glenoid of the scapula or as osteochondritis dissecans (OCD) of the humeral head. In addition, a condition almost exclusive to miniature ponies is caused by joint dysplasia and is attributable to hypoplasia of the joint surfaces that results in instability and secondary arthritis.
Osteochondrosis of the equine shoulder is most commonly diagnosed in weanlings and yearlings. Of all anatomical sites where osteochondrosis occurs, the shoulder is the least forgiving; obvious and persistent lameness is a typical finding of osteochondrosis in the shoulder. The primary cartilage lesion is located in the glenoid, humeral head, or both (most commonly), and the disease often affects a large portion of the cartilage surface.
Subchondral Cystlike Lesions
SCLs in horses typically develop in the glenoid of the scapula. They may or may not communicate with the shoulder joint, and they respond variably to intra-articular anesthesia. Although SCLs are part of the developmental orthopedic disease complex, clinical signs might not be apparent until the animal is mature. Like other manifestations of this syndrome, lameness might not become a feature until the animal begins work (typically breaking in or early ridden exercise).
Occasionally, SCLs cause lameness in an older horse, having remained quiescent for most of the animal’s life. The reason for these later-onset cases is not clear. In some cases, SCLs are traumatic rather than developmental in origin.
Generally, radiography is necessary to definitively diagnose the lesion; for some subtle lesions, however, scintigraphy and/or diagnostic arthroscopy might be necessary for diagnosis. Intra-articular anesthesia to localize lameness to the shoulder area can be extremely helpful.
SCLs are treated with conservative therapy, in the hope that cysts will remodel and become nonpainful. Treatment consists of combinations of rest, controlled exercise, anti-inflammatory therapy, and intra-articular therapies, including corticosteroids, hyaluronic acid, and interleukin receptor antagonist protein (IRAP). Recommended rest periods range from a few weeks to 3 months.
Arthroscopy and debridement are required for larger lesions; however, these techniques can be difficult because the cyst and articular cartilage damage within the glenoid can be difficult to access. Secondary osteoarthritis can limit the effectiveness of any treatment.
Osteochondritis Dissecans
In the equine shoulder, the formation of a bone defect with a cartilage flap (OCD) usually occurs on the caudal humeral head. Radiography is important to determine the extent of the lesion. Intra-articular osseous free bodies are unusual; when present, however, they settle in either the caudal or cranial recesses of the joint.
Treatment of OCD in the shoulder is similar to that for SCLs, but conservative therapy is less successful. Arthroscopic debridement of the lesion can be effective; however, cases should be selected carefully because of the pathological changes that could be present. Limited arthroscopic access to the medial aspect of the humeral head makes debridement of lesions in this location extremely difficult. Radiographic evidence of degenerative joint disease before surgery indicates a poor prognosis.
Scapulohumeral Dysplasia
Seemingly unique to miniature horse breeds, scapulohumeral dysplasia arises from a size mismatch between the glenoid and the humeral head. This mismatch causes joint instability and secondary arthritis. Although this problem is undoubtedly developmental and can be heritable, the condition commonly does not become evident until the animal is an adult, often with sudden-onset lameness.
Horses with scapulohumeral dysplasia often have profound proximal limb muscle atrophy and considerable lameness. These factors, along with the breed disposition and the resentment of proximal limb manipulation, make lesion localization straightforward.
Radiography reveals the presence of osteoarthritis and variable subluxation of the scapulohumeral articulation. Oblique views can demonstrate deep erosion of the humeral head in severe cases. The generalized joint destruction produces an area of increased uptake on a bone scan.
There is no simple treatment for scapulohumeral dysplasia in horses. 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; however, it is rarely performed.
Fractures of the Shoulder in Horses
Fractures of the shoulder are uncommon in horses. Scapular fractures involve the spine, supraglenoid tubercle, body, neck, and glenoid cavity. Proximal humeral fractures involve the humeral head, greater tubercle, and deltoid tuberosity. Supraglenoid tubercle fractures are the most common of these. Fractures are usually caused by direct trauma or by falls sustained during racing or jumping.
Supraglenoid tubercle fractures are the most common scapular fractures in horses, accounting for 30–50% of scapular fractures. These fractures are often simple; however, they can be comminuted and are frequently intra-articular. Radiography is required to make a definitive diagnosis.
Treatment options for supraglenoid tubercle fractures depend on the nature and duration of the fracture, economics, and performance expectations. Conservative therapy consisting of NSAID administration with stall rest for 3–4 months, followed by 6–9 months of pasture rest, can be successful for minimally displaced fractures with minimal articular involvement. Shoulder fractures are best treated with surgery—either surgical resection of the fragment or internal fixation with or without biceps brachii tenotomy.
The prognosis for restoration of normal function after supraglenoid tubercle fracture depends on many factors. Conservative therapy gives the horse a good prognosis for return to performance if the fracture is nonarticular and minimally displaced; for any other supraglenoid tubercle fracture, however, the prognosis is poor. Surgical resection of these complicated fractures results in a much better prognosis, with nearly 60% of treated horses returning to performance. The prognosis after internal fixation is good, and when it is combined with biceps brachii tenotomy, the prognosis is excellent.
Fractures of the scapular spine, body, neck, and glenoid cavity in horses can be difficult to diagnose. Radiography of the region is important; however, the thickness of the body mass and thinness of the scapula can make it very difficult to see minimally displaced fractures of the spine and body. The neck and glenoid can usually be visualized well enough to see fractures. Scintigraphy could be necessary to locate injured bone in this region. Ultrasonography can accurately reveal the integrity of the bone surface and can be very helpful in determining the fracture location.
Fractures of the scapular spine usually do not require surgery unless they develop into sequestra, in which case the fragment is removed. Minimally displaced nonarticular fractures of the body and neck can be treated conservatively, with a good prognosis.
Transverse fractures of the scapular body and proximal neck can be treated by internal fixation, giving the horse a fair to good prognosis for performance. However, comminuted fractures, fractures of the distal neck, and fractures of the glenoid all have poor prognosis. Immediate euthanasia is recommended for horses with extensive joint involvement or severe joint instability.
Stress fractures of the scapula occur in racehorses. Scintigraphy and/or ultrasonography can be used to diagnose these injuries. 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.
Fractures of the humeral head, greater tubercle, and deltoid tuberosity usually present as marked lameness that improves over 48 hours to moderate lameness. Pain and swelling can be detected over the fracture area.
Radiography is needed for definitive diagnosis of shoulder fractures in horses. Multiple oblique radiographic projections are usually necessary to identify them. Treatment can be conservative or surgical, depending on the configuration and displacement of the fracture.
Fractures of the proximal humeral head (Salter-Harris Type I or II) are rarely displaced, because of the stabilizing effect of the shoulder muscles (supraspinatus, infraspinatus, subscapular, and deltoid).
Unstable or large greater tubercle fractures can be treated by removal or lag screw fixation.
Deltoid tuberosity fractures are uncommon.
Small fracture fragments can become sequestra and need to be removed.
Large fragments require lag screw fixation to reestablish cortical continuity of the bicipital groove.
The prognosis in cases of nondisplaced fractures after conservative therapy is generally good. For displaced greater tubercle and deltoid tuberosity fractures, internal fixation produces a very good prognosis.
Stress fractures also affect the proximal humerus, almost exclusively in the caudal lateral cortex. They are an uncommon but important cause of lameness in racehorses (the craniodistal metaphysis of the humerus is also affected). Typically, the patient presents with sudden-onset, often moderate to marked lameness closely associated with recent exercise, usually in faster work.
Lameness due to stress fractures is usually transient, and the horse generally becomes sound within a few days to a week, if it rests. If exercise resumes, lameness recurs. Localization is difficult; many stress fractures are detected after the lower limb has been eliminated as the source of pain, or via scintigraphy. Radiography can detect periosteal and endosteal new bone at the site of injury.
Recovery from stress fractures is usually uncomplicated; however, ample rest (6–8 months) and gradual return to training are important for successful outcome.
Walking exercise can be introduced surprisingly quickly once the initial painful period of a stress fracture has subsided. The injury remains evident radiographically long after the bone is strong enough to withstand exercise; however, the callus gradually smooths and resolves as remodeling proceeds.
Undetected humeral stress fractures or fractures that have not sufficiently healed can result in complete bone fracture during exercise and necessitate euthanasia.
Bicipital Bursitis in Horses
The biceps brachii tendon runs over the cranioproximal humerus, protected by a synovial bursa. Inflammation of the bursa in horses can cause lameness and is usually secondary. Trauma to the proximal humerus, cystic lesions in the underlying bone, or injury to the tendon can cause secondary bursitis; the primary lesion must be identified and treated appropriately. Poorly fitting tack (blankets, breast collars) has caused bursitis in a few cases.
Clinical signs of bicipital bursitis include a shortened cranial phase of stride, decreased flight arc of the foot, decreased carpal flexion, and markedly decreased shoulder movement. When the horse is trotted in a circle, lameness is usually worse in the outside leg. Pressure applied over the bicipital tendon or bursa and manipulation of the shoulder in flexion cause a painful response.
Diagnosis of bicipital bursitis is based on local anesthetic injection into the bursa. However, radiography and ultrasonography are important to assess osseous and soft tissues in the region. Scintigraphy and thermography can also be useful diagnostic imaging modalities.
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; very rarely, however, closed sepsis can occur. With infection, the bursa needs to be drained, debrided, and thoroughly lavaged arthroscopically. This treatment is followed by prolonged administration of appropriate antimicrobials and NSAIDs.
Nonseptic bursitis responds favorably to rest, parenteral or topical NSAIDs, and/or intrasynovial injection of the bursa with corticosteroids or IRAP. The length of rest depends on the underlying injury to the humerus or bicipital tendon. In the absence of identifiable injury, rehabilitative exercise can begin a few days after injection. If the bicipital tendon has been injured, rest periods of up to 3 months have been recommended.
Extracorporeal shock wave therapy has been beneficial for treatment of the biceps tendon or bursa in horses. Surgery is required in cases of fracture or infection. If the tendon has calcified or adhered because of chronic inflammation, removal of the calcified portion or bicipital tenotomy has shown favorable results.
Infection of the Shoulder in Horses
Sepsis of the shoulder joint in horses is usually the result of penetrating injury. Diagnosis and treatment proceed as for other joints. In foals (and, rarely, weanlings or yearlings), infection can be transmitted hematogenously and become established in the growth plates or ends of the bones (physeal or epiphyseal infection). If not associated with contamination of synovial structures, these juvenile bony infections of the shoulder can be treated with systemic antimicrobials before surgical intervention (arthroscopic lavage and debridement) is undertaken. Intraosseous perfusion can provide high quantities of antimicrobials at the site of infection.
Suprascapular Neuropathy in Horses
The name "suprascapular neuropathy" (known also as sweeney) describes the physical appearance of the horse’s shoulder in this syndrome: atrophy of the supraspinatus and infraspinatus muscles is evident and results in subsequent shoulder instability. Suprascapular neuropathy is the most common abnormality of the equine shoulder. It is not a diagnosis in itself, because there are multiple potential causes. The most common cause is direct trauma to the suprascapular nerve.
Atrophy of the supraspinatus and infraspinatus muscles covering the scapula causes the scapular spine to become more prominent; in severe cases, these muscles virtually disappear. This atrophy is unusual in that it is often profound and very localized—hallmarks of an injury to a single lower motor nerve, the suprascapular nerve.
Although the site of damage is rarely documented clinically, most cases of suprascapular neuropathy in horses 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 extent of atrophy and the chances for recovery.
If nerve function is severely compromised, the shoulder joint becomes unstable because of a lack of support by the surrounding musculature, and the joint subluxates sideways as the horse bears weight. This subluxation does not appear overtly painful; an inability to stabilize the joint, however, could have important implications for longterm joint health and the horse’s athletic career.
Treatment of suprascapular neuropathy is aimed at maintaining muscle health during the period of nerve recovery and maximizing neurogenesis. Horses should be restricted to stable rest or to a very small paddock. Complete immobilization can negatively affect the nerve and muscles; however, excess activity can hasten joint degeneration.
Surgery to remove part of the scapula over which the nerve courses removes pressure and stretch on the nerve and provides optimal conditions for nerve recovery. This surgery should be considered, but its usefulness is debatable.
Muscle stimulation, under the guidance of a trained physiotherapist, helps to limit muscle fibrosis and can encourage nerve regeneration. Clinical observations and rates of recovery suggest that the vast majority of suprascapular neuropathy cases in horses result from neuropraxia (mild nerve damage from compression or stretching) or axonotmesis (damage to the nerve axon that leaves the connective tissue intact), and function is recovered over time. However, recovery can take many months, and frequently some loss of muscle mass remains.
The prognosis in cases of suprascapular neuropathy seems most affected by the duration of the injury before diagnosis, extent of atrophy at diagnosis, and willingness of the owner to perform time-consuming physical treatments for many months.
Other causes of suprascapular neuropathy in horses include disuse atrophy (which does not appear focal and is rarely severe), brachial plexus injury (which usually disrupts multiple nerves; atrophy is not focal but occurs in a number of muscle groups), and caudal cervical disease resulting in spinal nerve radiculopathy (in which a number of motor nerves are also affected, such that other muscles atrophy).
Careful assessment of the muscles involved and radiography of the neck and shoulder aid differentiation. Scintigraphy is useful for rapid screening of both the proximal limb and cervical and thoracic vertebrae for damage that could adversely affect the prognosis. Thermography can be useful for determining nerve or nerve root involvement.
Osteoarthritis of the Shoulder in Horses
Degenerative joint disease (osteoarthritis) affecting the shoulder joint in horses poses the same problems as in other joints. If no primary cause is identified that is amenable to correction, and if radiographic signs (eg, periarticular osteophytes) are established, cartilage destruction is likely well underway. These clinical signs can be ameliorated, but not cured, by anti-inflammatory, analgesic, and disease-modifying therapies.
Key Points
Developmental orthopedic disease of the equine shoulder (osteochondrosis dissecans and subchondral cystlike lesions) carries a guarded prognosis.
Shoulder dysplasia is a condition of miniature horses.
Various fracture configurations occur within the equine shoulder, including supraglenoid tubercle fractures and stress fractures of the humerus or scapula in racing Thoroughbreds.
Sweeney (suprascapular neuropathy) is the most common abnormality of the equine shoulder, resulting in severe atrophy of the supraspinatus and infraspinatus muscles.
For More Information
Garvican E, Clegg P. Clinical aspects of the equine shoulder and elbow joints. Companion Anim. 2008;13(5):5-12.
Also see pet owner content regarding disorders of the shoulder and elbow in horses.
