Osteochondritis Dissecans of the Shoulder

Osteochondrosis is a developmental disease affecting the growth plates and joint cartilage in medium and large breed dogs. Abnormal endochondral ossification of the deep layers of articular cartilage results in focal areas of thickened cartilage that are prone to injury. Normal activity may cause enough stress to create a fissure in the articular cartilage. Contact of the synovial fluid with the deep layers of degenerating cartilage may cause synovitis. In the absence of further stress, the lesion may heal. However, further stress on the cartilage may result in formation of a cartilage flap. This condition is termed osteochondritis dissecans (OCD). Osteochondritis dissecans has been described in various joints of the dog, but occurs most commonly in the caudal aspect of the humeral head. The etiology is multifactorial in all species. Risk factors in dogs include young age, large and giant breeds, rapid growth (high calorie diet), and excess calcium consumption.¹

Dogs are typically presented with mild to moderate weight-bearing lameness between 4 and 8 months of age. Many dogs have bilateral lesions, although one side may be clinically more severe. Muscle atrophy may be apparent in the affected limb if the dog has had a chronic lameness. Pain may be elicited on extreme flexion or extension of the shoulder. Radiographs may demonstrate a defect in the subchondral bone under the cartilage flap on the caudal aspect of the humeral head (Figure 32-1). Uncommonly, advanced imaging or arthroscopy is needed to confirm the diagnosis.²

If shoulder osteochondrosis is diagnosed early, decreased activity may prevent cartilage flap formation. Cryotherapy and NSAIDs may be used to limit inflammation. Use of disease-modifying osteoarthritis agents (DMOAs), such as glucosamine and chondroitin sulfate, may support cartilage health. Passive range of motion exercises help to maintain joint range of motion and provide joint nutrition and stress along normal lines of movement.³ Once a flap has formed it will not heal and should be removed. If the dog is more than 7 months of age or the lameness has persisted more than 4 to 6 weeks, surgery is indicated.⁴

Surgery is generally the treatment of choice in dogs with clinical signs. It is performed via arthrotomy or arthroscopy to remove the defective cartilage and forage or curettage the bed of the lesion (Figure 32-2). This encourages vascular ingrowth and healing by the formation of fibrocartilage. After surgery NSAIDs, cryotherapy, PROM, and controlled leash walks are instituted for the first 2 to 4 weeks (Table 32-2). After this initial healing period the duration of the leash walks is progressively intensified. In addition treadmill walking, UWTM exercise, and swimming may be initiated. By 6 weeks, light jogging usually can be started.³ Seroma formation is a common complication after shoulder surgery by arthrotomy, but is usually self-limiting and resolves with rest. If a shoulder seroma is observed, the activity level should be reduced until it resolves. The value of treating a seroma with hot packs or cold packs has not been documented, but is commonly recommended. Long-term management of OCD is focused on limiting or treating osteoarthritis (OA). The long-term prognosis for shoulder OCD is excellent in most cases.^2,5

Bicipital Tenosynovitis

Bicipital tenosynovitis is a degenerative or failed healing response of the tendon and tendon sheath of the biceps brachii muscle.6,7 Inflammation is not consistently present. Tendonitis implies the presence of inflammation in the tendon and musculotendinous junction, and may not be accurate for many cases of tendon pain.^8,9 Tendinopathy is an inclusive term used to describe tendon pathologies such as tendonitis, tendinosis, or paratenonitis. Tendon injuries may be caused by acute trauma or repetitive loading. Repetitive tendon overload tends to respond with tendon sheath inflammation, tendon degeneration, or both. There is some evidence that acute tendinitis is quickly replaced by tendon degeneration.¹⁰ Tendon pain should not be assumed to be caused by inflammation, but can occur with tendinosis as well.

Bicipital tenosynovitis is commonly seen in middle- to older-age large-breed dogs. Affected dogs usually have a weight-bearing forelimb lameness that is insidious in onset, progressive or intermittent, and exacerbated by exercise. Pain is not a consistent finding, but may be elicited on direct palpation of the bicipital groove on the proximal craniomedial aspect of the humerus. The pain response may be increased by flexing the shoulder with simultaneous elbow extension, which increases biceps tendon tension. Bicipital tenosynovitis may occur in conjunction with OA of the shoulder or glenohumeral ligament damage. Atrophy of the supraspinatus and infraspinatus muscles may be palpable, particularly in chronic cases. Mineralization of the biceps tendon, osteophytes in the intertubercular groove, or other degenerative changes may be seen on radiographs. Diagnosis can be difficult and is sometimes made by diagnostic ultrasound, magnetic resonance imaging (MRI), or observation during arthroscopy.

Conservative management of tendinopathies or tendinitis in humans primarily consists of rest, icing, and eccentric strengthening exercises. There are little data to support the use of therapeutic ultrasound, shock wave therapy, orthotics or massage,⁸ but these are used in some cases. Analgesics are indicated, but not necessarily NSAIDs or corticosteroids. Deep transverse friction massage has been advocated as part of the treatment for tendinopathy pain. Studies of the effectiveness of deep transverse friction massage for the treatment of tendinopathies in humans are inconclusive.¹¹ Common recommendations for the conservative management of tendinopathies in dogs include 4 to 12 weeks of rest and NSAIDs as needed (Table 32-3). As an alternative to oral NSAID therapy, intraarticular corticosteroids may be administered because the shoulder joint communicates with the biceps tendon sheath. Pulsed-mode 3-MHz therapeutic ultrasound is advocated over the tendon and musculotendinous junction to promote tissue healing. Because of the close proximity to bone, the dog must be monitored for any signs of pain, and the ultrasound intensity adjusted accordingly. Pulsed-mode ultrasound should not result in significant tissue temperature increase. Laser therapy may also be used to decrease pain and aid healing. Cryotherapy may be prescribed to reduce inflammation and pain. Response to conservative therapy varies, and may be related to the inciting cause of the tendinopathy.^12,13 Full recovery can be expected to require 3 to 6 months of therapy.⁸

Surgical treatment is recommended for dogs that do not respond to medical treatment or have significant tears of the tendon. Surgical techniques include tenodesis or tendon release, both of which have been described as arthroscopic or open procedures.12,14–16 Cryotherapy, PROM, and short leash walks (preferably with a harness that does not rub over the surgical site) are used for the first 3 postoperative weeks to promote normal joint movement while the tendon has minimal strength. Joint mobilizations may also help increase joint ROM. Exercises to gradually increase limb strength and promote remodeling of the peritendinous scar are performed after 3 weeks. Exercises should emphasize strengthening of the brachialis muscle, to improve the dog’s ability to flex the elbow joint. Shake hands exercises with limb weights that are gradually increased, as well as walking over cavaletti rails with limb weights, are specific exercises to increase the strength of elbow flexor muscles. Aquatic therapy and treadmill exercises may be beneficial. Superficial heat therapy may be used before exercise to facilitate tissue extensibility. Neuromuscular electrical stimulation may be applied to the brachialis muscle. Cross-fiber frictional massage can be used to prevent or diminish adhesions. Cryotherapy may help to minimize postexercise inflammation. Most surgically treated dogs regain near normal function and gait.^12,13

Supraspinatus Tendinopathy

Supraspinatus tendinopathy may cause mild to moderate lameness in medium and large breed dogs. The etiology of supraspinatus tendinopathy is unknown, but it is speculated to be caused by overuse and repetitive trauma.¹⁷ Affected dogs typically have chronic, intermittent, unilateral lameness. Palpation of the greater tubercle, near the tendon insertion, is usually painful. Mineralization may be observed on radiographs, and may contribute to bicipital tenosynovitis or impingement of the biceps tendon. However, the presence of mineralization can also be asymptomatic and may be an incidental finding. Diagnostic ultrasound or MRI may be needed to identify nonmineralized tendinopathy. Medical treatment includes rest, PROM, NSAIDs, local steroid injection, heat or cold therapy, deep massage therapy, and therapeutic ultrasound. Response to these treatments is limited. However, pulsed therapeutic ultrasound resulted in some clinical improvement in one study of calcific tendonitis in humans.¹⁸ Extracorporeal shock wave therapy may decrease the size of the mineralized region in dogs.¹⁹ If medical treatment is inadequate, surgical excision of the mineralized tissue is recommended.^17,20–22 After surgery, a carpal flexion bandage may be applied for 2 weeks to prevent weight bearing. Activity is limited for an additional 2 to 3 weeks. Swimming may cause too much tendon stress and is not advised for several months. The prognosis varies with the severity of the mineralization.¹⁷ Most dogs will be sound within 3 to 4 weeks. Lameness may recur with persistent bicipital tenosynovitis or recurrence of supraspinatus mineralization.

Medial Shoulder Instability

Medial glenohumeral instability is thought to result from chronic repetitive activity or overuse, such as jumping. Dogs typically develop a chronic, intermittent weight-bearing lameness that is nonresponsive to treatment with NSAIDs. Instability may be assessed subjectively by palpating for increased translocation of the humerus.²³ Medial instability can be confirmed by goniometric measurements of shoulder abduction,²⁴ although the clinician should consider the role of pain-related muscle atrophy as a potential cause for increased shoulder abduction as opposed to true instability of the shoulder. The normal abduction angle in a large breed dog is approximately 30 degrees.²⁴ The affected shoulder will have a much larger abduction angle as compared with the normal shoulder.²⁴ The degree of instability may be characterized as mild, moderate, or severe.²⁵ Mild instability is associated with minimal pathologic changes and abduction angles of 35 to 45 degrees. Dogs with moderate instability have abduction angles of 45 to 65 degrees and more advanced pathology is seen arthroscopically. Dogs with severe instability typically have shoulder abduction angles greater than 65 degrees. Severe disruption of the medial glenohumeral ligament, subscapularis tendon, and joint capsule are seen arthroscopically.²⁵

Conservative treatment with the shoulder supported and restricted by shoulder hobbles can be used in mild cases. Extracorporeal shockwave treatment to the medial shoulder structures may be beneficial. As healing progresses, strengthening of the medial supporting muscles may be achieved by walking on a treadmill with lateral tension supplied by an elastic band during the swing phase of gait. As strength improves progressively stiffer elastic bands may be used. Dogs with moderate shoulder instability are treated arthroscopically with imbrication, thermal capsulorrhaphy, reconstruction of the medial glenohumeral ligament, or transposition of the biceps tendon.26,27 After surgery a shoulder support wrap with hobbles is applied to protect the surgical repair. Cryotherapy, PROM, and strictly controlled activity are instituted for the first 3 postoperative weeks.²⁵ After 3 weeks weight-bearing exercises are gradually introduced. Function improves within three to four months, and optimal function is not attained until 5 to 6 months following thermal capsulorrhaphy.²⁶ Severe shoulder instability is usually caused by trauma and is treated as for acute shoulder luxation.

Shoulder Luxation

Shoulder luxation is usually a result of trauma, but may also be seen with congenital joint malformation. Shoulder luxation may be apparent on physical examination, but radiographs are recommended to evaluate for concomitant fractures or congenital bony malformations. If it is a recent injury with no evidence of fracture or malformations, closed reduction and immobilization in a sling for 1 to 3 weeks may be successful. Medial shoulder luxations are immobilized with the limb flexed in a Velpeau sling, whereas lateral luxations are immobilized with a spica splint. After the sling is removed, gentle PROM is initiated. Motion is limited to the sagittal plane to avoid excess stress on the affected joint capsule and ligament. Weight-bearing exercises are also limited.

If conservative management is unsuccessful or fractures are present, surgical stabilization is indicated. Surgical techniques for medial shoulder luxation include imbrication or reconstruction of the medial glenohumeral ligament and joint capsule, or transposition of the biceps tendon to a more medial position to assist with joint stability. Postoperatively treatment with cryotherapy and NSAIDs can be initiated to minimize inflammation, and the shoulder may be placed in a Velpeau sling for 2 weeks. After the Velpeau sling is removed the front limbs may be placed in hobbles to prevent abduction of the limb, but ROM must be restored. Passive ROM exercises are performed, but are limited to the sagittal plane (flexion and extension) to avoid stressing the medial or lateral joint capsule. Exercise is initially restricted, with gradual progression of weight-bearing exercises. Full recovery may require 1 to 3 months.

The prognosis is generally good, although OA may develop. In the case of severe congenital malformations or irreparable joint fractures, a salvage procedure may be indicated. Salvage procedures of the shoulder include excision arthroplasty (glenoid excision), arthrodesis, or amputation.

Fibrotic Contracture of the Infraspinatus Muscle

Contracture is a shortening of the tendon-muscle unit that is not caused by active muscle contraction. Most or all of the muscle and/or associated tendon is replaced by fibrous tissue. Most cases of contracture have a history of acute injury with lameness and inflammation that subsides with supportive care. Weeks to months later the animal is presented with clinical signs, which may include pain, weakness, firmness within the muscle, and an abnormal posture and gait.²⁸ Proposed causes include infection, trauma, repetitive strains, fractures, infectious diseases, immune-mediated diseases, ischemia, and eosinophilic myositis. Muscle contracture leads to permanent shortening of the affected muscle and can limit ROM of the associated joint. Muscle contracture can occur in any muscle, but has been reported in the infraspinatus, supraspinatus, teres minor, brachialis, quadriceps, semitendinosus, gracilis, and sartorius.²⁸ If the contracture is not severe, splinting with the muscle and tendon in tension and stretching activities may lengthen the tendon-muscle unit. In many cases, surgery is recommended to lengthen or transect the tendon.

Contracture in the front limb has been most commonly reported in the infraspinatus muscle. Infraspinatus contracture causes a mild weight-bearing lameness mainly in hunting or working dogs. The cause is hypothesized to be acute muscle trauma, which results in incomplete rupture of the infraspinatus muscle. The injury leads to inflammation and subsequent compartment syndrome.28–30 Replacement of muscle fibers by fibrous tissue occurs over days to weeks. The supraspinatus and deltoid muscles also may be involved and undergo atrophy or contracture.³¹ The humerus is held in adduction, whereas the antebrachium is externally rotated with the foot abducted. The scapulohumeral joint cannot fully extend. There is a weight-bearing lameness in which the limb circumducts as it is advanced during the stride and the paw flips into extension before foot placement.

Physical rehabilitation may be beneficial if the condition is diagnosed early. Continuous mode therapeutic ultrasound with stretching exercises may help to lengthen contracted tissues, but the degree of contracture is usually so severe at the time of diagnosis that it is difficult to improve the condition.³ When the dog is presented with contracture, the treatment of choice is surgical transection of the infraspinatus tendon and associated fibrous tissue.³¹ This immediately restores motion of the shoulder joint and the prognosis is good.

Postoperatively full weight bearing is allowed, but activity should be restricted for the first few weeks. Uncontrolled activity may cause tissue damage and recurrence of fibrous tissue.³ Passive ROM exercises to the forelimb joints several times daily maintain joint ROM and promote normal alignment of the healing tissues.³ Cryotherapy may be used to reduce inflammation after exercise. In cases in which there is significant disuse atrophy of the forelimb muscles, general conditioning exercises for the limb are used to gradually return the muscle to normal size and strength. Conditioning exercises include walking, jogging, and aquatic therapy. Neuromuscular electrical stimulation (NMES) may be used if the atrophy is severe and the dog is too weak to use the leg well.

Teres Minor Strain

Teres minor strain has been reported in athletic dogs of various breeds.³² All dogs in one report had front limb lameness that was improved by rest, but recurred with return to activity. The shoulder was painful on full extension and pain was elicited with direct palpation of the teres minor muscle. Treatment included ultrasound, stretching, balancing exercises, leash walking, gait retraining, and acupuncture point stimulation. All dogs returned to previous levels of activity.³²

Elbow Dysplasia

Elbow dysplasia includes fragmented medial coronoid process (FCP), osteochondritis dissecans (OCD), and ununited anconeal process (UAP). Dogs with elbow dysplasia usually have only one of the three conditions. Elbow incongruity may also be present. The pathogenesis is poorly understood. Factors that have been implicated include genetics, improper nutrition, and trauma. Other proposed mechanisms are osteochondrosis, trochlear notch dysplasia, and asynchronous growth of the radius and ulna.³⁶ Elbow dysplasia usually occurs in large or giant breeds of dogs. Affected dogs typically have bilateral problems, although one elbow may be more severely affected.

Fragmented Medial Coronoid Process of the Ulna

Dogs with FCP are presented with a mild to moderate weight-bearing lameness, which is usually noted between 4 and 7 months of age.³⁷ Physical exam findings include pain on flexion and extension of the elbow, pain on palpation of the medial aspect of the joint, and palpable joint effusion. In dogs older than 11 months, crepitus, decreased ROM, and general joint thickening may be evident. Radiographs often show degenerative changes in the joint, but the actual lesion may not be seen (Figure 32-7). In many cases, computed tomography or arthroscopy is needed to make a definitive diagnosis.

Treatment is removal of the abnormal process via arthrotomy or arthroscopy, with possible subtotal coronoidectomy or ulnar osteotomy in some cases. Postoperatively activity is limited for 2 to 4 weeks. The prognosis is good if FCP is removed before there is advanced OA. Osteoarthritis will progress regardless of treatment, but changes are thought to be more severe in untreated cases. If the OA is severe at the time of diagnosis, the value of surgical treatment must be questioned. These dogs may be better managed by conservative treatment for the OA.³⁷ In all cases rehabilitation is directed toward preventing, slowing, or treating OA to maintain an acceptable quality of life. Therapy includes maintaining an appropriate body weight, controlled low-impact exercise, aquatic exercise, monitoring pain, NSAIDs, and chondroprotective agents. See section on OA for guidelines on rehabilitation.

Osteochondritis Dissecans of the Elbow

Dogs with elbow OCD are typically presented with mild to moderate lameness between 4 and 9 months of age. Many dogs have bilateral lesions, although one side may be clinically more severe. Atrophy of the muscles may be apparent in the affected limb if the dog has been lame for several weeks. Pain may be elicited on extreme flexion or extension of the affected joint. Chronic elbow OCD may also have signs of OA such as joint effusion, thickening of the periarticular soft tissues, decreased ROM, and crepitus. Radiographs may demonstrate a defect in the subchondral bone under the cartilage flap on the medial humeral condyle. Fragmented medial coronoid process can create an erosive lesion on the medial humeral condyle, called a kissing lesion, which can look very similar to OCD at the time of surgery (Figure 32-8). In some cases especially with elbow OCD, the diagnosis may be difficult and is best made by computed tomography or arthroscopy.

Surgery is usually the treatment of choice in dogs with clinical signs. It is performed via arthrotomy or arthroscopy to remove the defective cartilage and forage or curettage of the lesion. After surgery NSAIDs, cryotherapy, PROM, and controlled leash walks are instituted for the first few weeks (see Table 32-2). After the initial healing period, the duration of the leash walks are progressively intensified. Long-term management of OCD is focused on limiting or treating OA. See section on OA for guidelines on rehabilitation. The prognosis for elbow OCD is good if surgery is performed before OA is advanced, but it is more guarded than for OCD of the shoulder.

Ununited Anconeal Process

Ununited anconeal process (UAP) is a failure of the anconeal process to fuse with the olecranon by 5 months of age, and is apparent on a flexed lateral radiograph (Figure 32-9).³⁷ Instability of the anconeal process causes inflammation and eventual OA. The dog usually is presented with a weight-bearing lameness. Decreased range of motion and joint effusion of the caudolateral aspect of the elbow may be apparent on palpation

Treatment options include surgical removal of the anconeal process, screw fixation combined with osteotomy of the proximal ulna, or osteotomy of the proximal ulna alone to relieve joint incongruity and allow healing of the anconeal process. Regardless of the treatment, OA progresses, therefore ongoing treatment is directed at managing OA. (See the section on OA for guidelines on rehabilitation.)

If the UAP is treated by screw fixation, the rehabilitation program should have a slower progression of weight-bearing activities until there is radiographic evidence of healing. This may take as long as 12 weeks in some cases. If the UAP was treated by removal, the rehabilitation program may progress more rapidly, as dictated by the degree of joint effusion, pain, ROM, and weight bearing. Immediately after surgery PROM, aquatic therapy, and light leash walks are recommended. Cryotherapy and NSAIDs may be used as needed to control inflammation and pain. Aquatic activity can be very beneficial because of the active ROM while weight bearing in a buoyant environment.38,39

Elbow Incongruity

Asynchronous growth of the radius and ulna can cause elbow incongruity in chondrodystrophoid dogs, and is usually evident by 4 to 5 months of age. Ununited anconeal process and FCP have been associated with elbow incongruity, although they can occur in the absence of incongruity. Traumatic closure of a radial or ulnar physis also leads to asynchronous growth with elbow subluxation and angular limb deformity.

Surgical options to improve congruity include corrective osteotomy or ostectomy of the radius or ulna, and may involve stabilization with a bone plate or external fixator. The prognosis is worse if the incongruity is severe and the animal is older (>9 months of age).⁴⁰

After surgery normal ROM of the joints proximal and distal to the repair should be maintained. Pain and edema may be controlled by NSAIDs and cryotherapy. If the goal was to lengthen the limb following surgery, increased tension on the soft tissues may result in decreased ROM, joint stiffness, and lameness. In these cases therapeutic ultrasound with simultaneous stretching and ROM activities may be helpful. As bone healing progresses more aggressive weight-bearing exercises may be initiated.

Elbow incongruity invariably results in some degree of OA of the elbow. Some dogs may not present for rehabilitation until they have end-stage OA. In either case rehabilitation is directed at managing OA so as to maintain an acceptable quality of life. (See the section on OA for guidelines on rehabilitation.) Conservative management of OA includes NSAIDs, chondroprotective agents, cryotherapy, PROM, and physical rehabilitation. Dogs with end-stage OA often have chronic synovial effusion, reduced ROM, crepitus of the joint, pain on manipulation of the elbow, muscle atrophy, and lameness. Physical rehabilitation cannot correct the underlying problem, but efforts to improve joint health, increase ROM, reduce weight, and rebuild atrophied muscles may significantly improve the patient’s quality of life. Physical rehabilitation considerations would include PROM and stretching, active ROM activities, redeveloping muscle strength with exercise or neuromuscular electrical stimulation, low-impact exercises, laser, extracorporeal shock wave, and aquatic therapy. Careful monitoring of ROM is important with a home program to avoid permanent losses in ROM.

Elbow Luxation

Elbow joint luxations are generally a result of trauma, although congenital malformations of the elbow can predispose to luxation. Traumatic elbow luxations are usually lateral and can be diagnosed by palpating the radial head laterally displaced relative to the humeral condyle. Radiographs are recommended to assess for concomitant fractures and for congenital malformations. Radiographic findings may affect the treatment choice and the prognosis.

If there are no congenital malformations or concurrent fractures, closed reduction of the elbow is usually successful because the joint is inherently quite stable, despite significant collateral ligament damage. Open reduction and surgical stabilization are indicated if closed reduction is not achieved, closed reduction fails, or congenital abnormalities or articular fractures are present. Surgical repair often involves direct repair of the collateral ligaments or replacement of the collateral ligaments with a suture prosthesis (e.g., heavy suture secured by bone anchors or screws). After closed or open reduction, joint healing is protected by maintaining the elbow in an extended position. This is accomplished by placing the limb in a spica splint for 1 to 4 weeks.

Regardless of whether closed or open reduction is performed, rehabilitation is begun after the spica splint is removed. Range of motion must be restored without causing the joint to reluxate. Cryotherapy and NSAIDs are used to minimize inflammation in the early postoperative period. After elbow luxation, passive and active ROM exercises should be limited to the sagittal plane, and internal, external, varus or valgus stresses should be minimized. Activity is gradually increased, but aggressive activities such as jogging, swimming, or uncontrolled play are limited until the joint has healed. This may take 1 to 3 months, depending on the degree of tissue damage. The prognosis for traumatic joint luxations is generally good, although OA is a common sequela.

Joint reduction and preservation of the joint may not be recommended if there are irreparable fractures involving the joint or severe congenital malformations. In these cases a joint salvage procedure, such as elbow arthrodesis, may be a better choice. Total elbow replacement surgery is relatively new in dogs and is not commonly performed, but may result in better function.⁴¹ Limb amputation may be elected in some cases.

Angular Limb Deformities

Angular limb deformities can occur as a developmental abnormality or as a result of trauma to a physis. The most common deformity is carpal valgus as a result of fracture of the distal antebrachium. As the animal continues to grow, it may develop subluxation of the elbow and carpal joints with subsequent OA in these joints. Correction of angular limb deformities involves a corrective osteotomy of the affected bone(s) and stabilization with a bone plate or external fixator. In some cases, a circular fixator is used to gradually correct the angular deformity and lengthen the bones by distraction osteogenesis. After surgery cryotherapy and NSAIDs may be used to limit inflammation and pain. It is important to maintain normal ROM of the joints proximal and distal to the repair. This is particularly important for animals undergoing distraction osteogenesis, because the concurrent stretching of soft tissues in the region may cause reduced joint ROM, stiffness, and lameness. Stretching and ROM activities with simultaneous application of heat or therapeutic ultrasound may be beneficial. As bone healing progresses the intensity or duration of aquatic therapy and weight-bearing therapeutic exercises may be increased.

Contracture of the Flexors of the Antebrachium

After limb immobilization or prolonged disuse, the antebrachial flexor muscles may undergo contracture (shortening of the tendon-muscle unit). The result is limited extension of the joints distal to the elbow, which can impair normal weight-bearing. Methods of lengthening and stretching the contracted tendon-muscle units include 3-MHz therapeutic ultrasound or hot packs, manual stretching, exercises, and massage.42–44 If stretching is too aggressive it may cause damage to soft tissues or bone fractures. A prolonged stretch may be applied with a custom splint on the distal limb. The splint should be applied intermittently to minimize the risk of pressure injuries from the splint. The splint may be applied for longer periods each day until it can be worn all day, if desired. The goal is to stretch and realign the tissues without damaging them.

Carpal Hyperextension

Carpal hyperextension injuries occur after jumping or falling from a height, spraining the palmar fibrocartilage and the carpal ligaments. Damage may occur to antebrachiocarpal, middle carpal, carpometacarpal joints, or any combination of these joints. Carpal hyperextension may also be caused by immune-mediated joint disease, or endocrinopathy such as hyperadrenocortism. Affected animals are lame and walk with the carpus in hyperextension. In severe cases, the carpus may touch the ground. In general healing of a sprain (ligament injury) may take months, and occurs by the formation of fibrous connective tissue to replace the torn ligament, rather than primary healing of the ligament. Conservative management of carpal hyperextension injuries is generally unsuccessful and results in subluxation.⁴⁵ The recommended treatment is panarthrodesis (surgical fusion of all three joint levels) or partial arthrodesis (fusion of only the middle and distal joints), depending on the level of the injuries (Figure 32-13). Rehabilitation is performed as for any arthrodesis, with an emphasis on gait training after the initial healing period (see General Physical Rehabilitation of Joint Arthrodesis). Although the limb function is not normal, prognosis for return to daily activity is good after carpal arthrodesis.⁴⁶ The prognosis is more guarded if instability is caused by rheumatoid arthritis because multiple joints are typically affected.

Carpal laxity syndrome has been described in puppies, which walk with the carpus in a hyperextended position.⁴⁷ The cause is unknown but is speculated to be caused by asynchronous growth between the skeleton and the musculature. Long-term application of supportive splints for hyperextension is avoided because it may lead to muscle atrophy and increased tendon weakness (Figure 32-14). Treatment recommendations generally include balanced diet and controlled exercise on surfaces that provide good traction. Carpal arthrodesis may be a treatment option for hyperextension that does not resolve with exercise and nutrition, but this cannot be performed until the physes are closed. Carpal laxity syndrome is usually self-limiting, with a short duration and good prognosis.

Carpal flexural contractures have also been recognized in puppies. Poor nutrition has been implicated as a factor, so altering the diet may be beneficial. Splinting may be helpful for puppies that are developing flexural contractures. In severe cases of flexural contracture, tenotomy may be performed.

Trauma of the Superficial and Deep Digital Flexor Tendons

Laceration or avulsion of superficial and deep digital flexor tendons are traumatic injuries that can occur in the front or rear feet. Avulsion or laceration of the tendon insertion on P2 and P3 results in abnormal toe carriage. The tendons may be reattached or repaired for cosmetic reasons and for improved athletic function. Postoperatively the foot is immobilized in a splint for 2 to 3 weeks to limit edema and provide support. Active motion is limited to prevent disruption of the weakened tissue and allow the tendons to heal with minimal adhesions.

Weekly splint changes with ROM exercises of adjacent joints should be performed if possible.³ Passive range of motion and light activity are used to maintain normal tissue length and encourage normal joint movement. Removal of the splint is recommended within 3 weeks of the injury, because prolonged immobilization may delay healing and weaken the repaired tissue. Some tendon motion promotes remodeling of the peritendinous scar, which allows the tendon to glide. However, restricted activity must be enforced, because running or jumping could place catastrophic stress on the healing tissues and result in failure. By 6 weeks the tendons should have achieved adequate strength to sustain normal physiologic stress. At this point the focus of therapy is to restore ROM and strength. If there is contracture of muscle-tendon units, 3-MHz continuous-mode therapeutic ultrasound or hot packs with simultaneous stretching is indicated.³

Luxation of the Metacarpophalangeal and Interphalangeal Joints

Metacarpophalangeal and phalangeal luxations are treated by closed reduction or surgical repair of the collateral ligaments and joint capsule. After repair the foot is splinted for 2 to 3 weeks. It is beneficial to change the splint once weekly so as to perform gentle PROM on the immobilized joints. After the splint has been permanently removed, ROM exercises in the sagittal plane are continued. Limited weight-bearing activities are initiated and gradually increased over another 3 weeks.

Other options for metacarpophalangeal and phalangeal luxations include arthrodesis of the joint or amputation of the digit. Arthrodesis is a better choice if a high level of function, such as racing, is required. Postoperatively the foot is splinted until there is radiographic evidence of fusion. Weekly splint changes with PROM or mobilization of the other distal joints may be beneficial.