Cause

Repeated strain injury appears to be the primary cause of BT in the performance dog. This includes two-on/two-off contacts, landing vertically on the forelimbs from a misjudged jump, overstretching of the muscle, quick turns, and repetitive contractions of the muscle with the shoulder flexed and/or the elbow extended. Injury to the tendon can occur in a number of ways, including strain from overloading, degeneration, or disruption.²³ A single less than maximum load may injure some of the fibers without complete failure of the tendon, but the blood supply to the tendon proper is poor, leading to a longer healing time.²¹ Repetitive strain injury may initiate actual degeneration of the tendon.²¹ As the area continues to be reinjured, the tendon may weaken sufficiently for inflammation or microtears (tendinopathies) in the connective tissue in or around other tendons to form, ultimately leading to shoulder joint instability.²⁴

Diagnosis

Performance dogs with BT commonly have difficulty with quick turning to the affected side and are reluctant to jump. Agility dogs may also have issues performing two-on/two-off contacts and knocking bars with their forelimbs. On gait analysis of dogs with BT often have a shortened stride and a weight-bearing lameness (subtle to severe) that becomes worse with activity. Pain may be elicited by direct palpation over the biceps tendon. Pain and spasm may be noted when flexing the shoulder while at the same time extending the elbow (Figure 33-3).³ Radiographs are of minimal assistance when the injury is in its acute phase, but may reveal mineralization of the tendon when the condition is chronic.²⁴ Magnetic resonance imaging (MRI) and ultrasound may be used to identify the condition in acute and chronic situations.^23,24 Shoulder arthroscopy is recognized as superior to other diagnostic procedures for diagnosis of bicipital tenosynovitis (Figures 33-4 and 33-5).²³

Treatment

Acute cases of bicipital tenosynovitis may be treated by conservative medical management and rehabilitation therapy. Components of conservative medical management should include controlled activity, nonsteroidal antiinflammatory drugs (NSAIDs), and cryotherapy. Intraarticular injections of hyaluronic acid or steroids, or intra-tendinous injections of platelet rich plasma (PRP), stem cell therapy (SCT) or a combination of these may be considered.20,23–25 Regenerative medicine therapy should be considered if a core lesion is present. To promote healing and decrease adhesion formation, laser therapy or pulsed ultrasound may be of use to assist healing to (Figure 33-6).²⁰ Initiating low-load, pain-free, high-repetition exercise and range of motion (ROM) movements early in the healing process is important. Pain relief may be achieved with transcutaneous electrical nerve stimulation.²⁰ Acute tendon injuries should not be stretched because of the potential for producing more microtears caused by the chemical changes in the tissue.^1,20 Pain-free, passive ROM movements (flexion and extension of the limb while the dog is not weight bearing) and gentle wobble board activities (all directions, front to back and side to side), and alternating leg lifts are recommended first, with progression to active ROM exercises (weight-bearing exercises that cause flexion and extension of the limb). All exercises in the acute stage are aimed at increasing the strength of the shoulder and scapular stabilizers. Balance and proprioceptive exercises are required and are imperative to the healing process. An active dog requires stabilization of this region and strength of the slow twitch muscle fibers before resuming activity. Deep friction massage is used at this stage if it is not too painful.^25,26 Deep friction massage involves a sweeping motion made across the bicipital tendon (perpendicular to the fibers) for 5 minutes, daily if possible. The goal is to prevent adhesion formation and help realign the fibers of the inflamed tendon. After the cross-friction massage, cryotherapy and laser therapy are recommended before further treatment. A strengthening program consisting of controlled leash walking, stepping over cavaletti rails, wobble board use, and stabilizing exercises should follow. Examples of stabilization exercises include balancing on a well-controlled rocker board, standing on a therapy ball, weight shifting exercises, wheel-barrowing the dog so its weight is on the forelimbs, walking in figure eights, and walking in circles. Leash walks of increasing duration and end-stage eccentric exercises, such as walking and trotting down hills may then be introduced. Short periods of off-lead activity are allowed after leash walks have substantially increased without the return of lameness. In the acute stages, it is imperative to reinforce the owner or handler not to perform any activity that produces lameness. Many owners of performance dogs are eager to return to sports and often push their dogs too quickly.

With chronic BT the inflammatory process must be reinitiated to break down scar tissue and remodel the tendon fibers into the proper orientation, which increases the tendon’s load capacity. Because of the need to reinitiate the inflammatory response, NSAIDs or intraarticular corticosteroids are not recommended for chronic tendinopathies. Appropriate therapy for chronic tendinopathies includes deep cross-friction massage, heat, ultrasound therapy, and pain-free ROM/stretching. At this stage cross-friction massage is applied for approximately 10 minutes, two to three times per week. Acupuncture and laser to increase circulation and for pain control may be beneficial as well. The exercise progression is similar to that recommended for acute tendinopathies, but stretching after treatment is advised. Active ROM exercise such as walking for longer periods also is recommended. End-stage eccentric exercises, such as walking and trotting down hills, should be added followed by short periods of off-lead activity provided lameness is completely resolved.

Because of the chronic nature of the tendon changes, the dog usually takes longer to recover and progress through the healing and exercise stages. It is again imperative to convey to the owner and handler that the progression of conservative management of BT may be lengthy and nothing should be done to aggravate the condition. The dog should be pain free and not exhibit any lameness.

Regenerative medicine therapy may also be considered in the treatment of chronic BT, however, modification of the rehabilitative therapy protocol is necessary to promote healing and prevent damage to the injected cells.

Surgical treatment is recommended for biceps avulsion-tears and chronic cases of BT that are not responsive to medical management or rehabilitation therapy. Surgical options include tenodesis (releasing and reattaching the tendon at a distal location on the proximal humerus) or an arthroscopic tendon release.²⁷ Controlled activity is an important component during the postoperative period and should include leash walks of increasing duration and end-stage eccentric exercises, such as walking and trotting down hills. Short periods of off-lead activity are allowed after the lameness has resolved. Nonsteroidal antiinflammatory drugs may be used to decrease pain and inflammation following surgery. Modalities as described for the acute treatment of BT may be used postoperatively to improve comfort and function and facilitate progression to the retraining phase of recovery.

Toward the end of rehabilitation therapy sport-specific retraining should begin. Examples of retraining techniques for BT may include starting with low, straight-line jumps with very wide sweeping turns that progress over time to higher jumps with tighter angles. Do not include the A-frame and weave poles until late in the retraining period. Alterations in contact controls from a two on/two off to running or four on the floor may be necessary. Be sure to start with turns toward the injured limb and progress to turns toward the uninjured limb.

Dogs that will be returning to jumping activities should start with low-level activities before returning to the sport.4,26 In jumping activities, the biceps muscle and tendon act eccentrically to control the landing of the body. After cavaletti work has been employed, low-level jumping can be initiated. The jump heights should be set lower than the dog’s normal jump height. For example, if the dog normally jumps 22 inches in competition, the jump height should be set at 16 inches. Three or four jumps should be set up and the surface should be padded or the exercise should be performed in sand. Three to five repetitions should be performed of the jump sequence—the dog going over the jumps—and then the dog should be reevaluated. The jump sequencing should not cause any lameness and should only be performed three times per week with at least a 48-hour break in between. Plyometrics should be progressed by increasing the jump height and the number of repetitions. Once the dog is up to its normal jump height on a controlled surface, additional training surfaces can be added.

Following a warm-up, make sure to perform active stretching techniques. Following agility work, use an appropriate cool down with cryotherapy and passive stretching techniques (including shoulder flexion with elbow extension). Treadmill walking and the use of an underwater treadmill are also useful for the rehabilitation of BT. In acute stages exert caution with swimming because the shortened position of the biceps tendon with rapid joint motions may aggravate the condition.

Cause

The cause of this injury in performance dogs appears to be related to repeated strain injury. This includes hitting the ground or agility contacts on an outstretched forelimb, slipping, overstretching, or overuse of the muscle, quick turns and repetitive eccentric contractions (contractions during lengthening of the muscle), as well as concentric contractions (contractions with shortening of the muscle) with the muscle in a lengthened state.

Diagnosis

Performance dogs with supraspinatous tendinopathy (ST) commonly have weight-bearing lameness on one side that becomes worse with activity and often is resistant to treatment. The supraspinatus muscle may be atrophied and direct palpation over the tendon and flexion of the shoulder may cause pain (Figure 33-8). Concurrent BT or shoulder instability may be present, so a thorough shoulder examination is required. Magnetic resonance imaging readily demonstrates the condition in the acute phase (Figure 33-9). Plain radiographs and computed axial tomography (CT), which reveals a cross-section of an internal body structure) may reveal mineralization in chronic cases. Musculoskeletal ultrasound is this author’s preferred diagnostic tool for this condition. This technique provides a non-invasive definitive diagnosis of ST and allows for serial evaluations to assess response to treatment. Arthroscopic exploration is recommended and may demonstrate impingement of the biceps tendon secondary to supraspinatus tendon swelling as well as concurrent pathologies, including medial shoulder instability in severe cases.

Treatment

Controlled activity, retraining, and preventive techniques for acute and chronic ST is similar to that used for bicipital tenosynovitis. Similar to the rehabilitation of BT, rehabilitation should be initially aimed at reducing the inflammation and increasing the strength of the shoulder and scapular stabilizers.⁴ After the inflammation has decreased and the core strength of the shoulder complex has improved, more dynamic activities may be initiated.

Treatment for acute cases consists of conservative medical management (controlled activity and NSAIDs) and rehabilitation therapy (manual therapy, modalities, ROM with progression to stretching and strengthening exercises), and acupuncture as described for BT.²⁰ Cross-friction massage may be performed to the supraspinatus tendon in the acute phases for 5 minutes daily and 10 to 15 minutes in chronic cases.

As with BT the inflammatory process should be reinitiated in chronic cases and follow a similar rehabilitation protocol. Shockwave and ultrasound therapy have also been described as valuable modalities for the treatment of chronic calcified supraspinatus tendinopathies.³¹

Regenerative medicine therapy should be considered, especially in cases in which a core lesion has been identified. Under ultrasound guidance, cells can be directly injected into the affected tendon. In more severe cases a second injection may be needed. This therapy can be used as the primary treatment of ST, however, arthroscopic evaluation of the shoulder is recommended as concurrent pathologies of the joint are common. In these cases, arthroscopic treatment of concurrent pathologies can be combined with intraarticular regenerative medicine therapy to promote healing and speed recovery. Appropriate modification of the rehabilitative therapy protocol is necessary to prevent damage to the injected cells.

Results of a pilot study of 185 dogs with a confirmed diagnosis of supraspinatus tendinopathy (ST) by ultrasound or MRI performed by one of the authors (SC) provides support of regenerative medicine therapy for treatment of ST. Performance and sporting dogs accounted for just over one third (67) of the population, while companion animals accounted for the remaining two thirds (118). Of the performance/sporting dog population, 48% participated in agility. At presentation, a majority of dogs had a history of failed response (unresolved discomfort or lameness) to rest and NSAID therapy (134). Seventy-five failed to respond to rehabilitation therapy and 6 received intra-articular injections (hyaluronic acid – 2; prednisolone sodium succinate – 4), which also did not resolve lameness. A unilateral forelimb lameness presentation was more common than bilateral (124 and 61, respectively). Lameness was graded from 0 (sound) to 6 (non-weight bearing lame). The average lameness score was 2.9 (median 3). Duration of lameness ranged from one week to greater than a year. 29.7% of dogs had a chronic (>1 year) lameness. Of those with lameness less than one year, the average duration was 15.2 weeks (median 13 weeks). Pain on direct palpation of the supraspinatus was found in 59% of dogs. Pain or spasm on shoulder extension and abduction was noted in 63.1% and 71.3%, respectively. Pain or spasm on flexion was recorded in 74.6% of dogs and pain on biceps stretch (shoulder flexion with elbow extension) was recorded in 47.5% of dogs. Shoulder radiographs were performed on 161 dogs. Of these, mineralization was noted in 35 cases. Of dogs diagnosed with bilateral disease on presentation (61), mineralization was noted in 8 cases. MRI of the shoulder was performed in 30 cases. Findings indicative of a supraspinatus tendinopathy on MRI include hyperintensity of signal on T1 and STIR sequences of the ST at its insertion on the greater tubercle. Diagnostic ultrasound was performed in 140 cases. In most cases the supraspinatus appeared enlarged (44.3%) with irregular fiber pattern (46.4%) and mixed echogenecity (80.7%). Shoulder arthroscopy was performed in 131 cases. A supraspinatus bulge was noted in 90.8% of dogs. Of these, impingement of the biceps tendon was noted in 59.5% of dogs. While 43.5% of dogs had bicipital tenosynovitis, only 13% had actual pathology of the biceps tendon. Pathology of the subscapularis was observed in 91.6% of dogs. MGL pathology was present in 51.1% of dogs. A tear of the labrum was noted in 29.8%, cartilage defects were noted in 32.8% and bone lesions in 8.3% of dogs. Seventy-four cases were treated with regenerative medicine therapy. Final evaluations were performed on 64 dogs. Of these, lameness resolved in 90% of cases and improvement was noted in the remaining 10%.

Surgical treatment is warranted for chronic cases that do not respond to conservative medical management and rehabilitation therapy. Surgical treatment should include arthroscopic exploration to identify and treat possible concurrent BT or shoulder instability, or removal of abnormal tissue through an open approach.³⁰ Surgery has been considered the treatment of last resort in humans with tendinosis because of the small reported difference in treatment success between surgical intervention and conservative management. Rehabilitation therapy, as described for BT, following surgical intervention is essential in returning the canine athlete to performance.

The retraining protocol for this condition mirrors that of retraining following rehabilitation of BT.

Cause

Causes reported include repetitive microtrauma, blunt trauma, and osteofascial compartment syndrome.41,42 Compartment syndrome is a disease process seen in people; however, it can also occur in dogs and horses.⁴³ The pathology to muscle tissue is caused by an increase in pressure in a confined, inelastic space that leads to muscle inflammation with no room to expand.⁴³ Muscle necrosis occurs when the pressure rises to greater than 30 mm Hg (normal, −2 to 8 mm Hg) in a single compartment with no relief.⁴³ A compartmental pressure greater than 120 mm Hg may lead to complete and irreversible nerve block.⁴⁴ Causes for an increased pressure within a compartment include hemorrhage, postischemic tissue swelling, external pressure (bandage), or intramuscular injection.³² In elastic barriers that predispose to compartment syndrome there are structures such as fascia and bone.⁴³ Four different compartments have been described in the dog: femoral, craniolateral crus, caudal crus, and caudal antebrachial.^43,44

It may be possible that compartment syndrome may play a role in the contracture of the muscles of the shoulder joint. If an injury is sustained to the infraspinatus muscle that leads to moderate cellular inflammation, the muscle begins to swell and has no room to expand. Inflammation within the boundaries of the deltoids, scapula, and surrounding fascia increase the compartmental pressure and inhibit venous blood flow, initially causing congestion. Then arterial blood flow and innervation are affected, as well as diminished cellular response to damaged tissue. It is the unforgiving pressure that leads to further cellular damage. Cellular swelling caused by pressures rising to greater than 30 mm Hg is what seems to lead to necrosis and/or fibrosis of the affected muscles. Early treatment is focused on surgical decompression by fasciotomy; however, if contraction has already occurred, tenectomy or myectomy may be necessary.⁴⁵

Electrophysiologic studies of affected dogs indicate that infraspinatus contracture is a primary muscle disorder rather than a neuropathy. Histologically, affected tissues demonstrate degeneration and atrophy of skeletal muscle with fibrous tissue replacement. These findings support the hypothesis that acute traumatic events caused incomplete rupture of the infraspinatus muscle, leading to fibrosis and contracture.

Diagnosis

After an acute onset of a painful non–weight-bearing lameness, the initial pain and lameness improve over a period of 1 to 4 weeks, after which a characteristic circumducted gait abnormality develops in the forelimb. The initial injury to the infraspinatus muscle is not fully recognized or correctly interpreted in most cases, at least not with regard to its potential as a precursor of myopathy. Affected dogs most often present with mature contractures and adhesions of the tendon of insertion of the infraspinatus muscle to the adjacent joint capsule. As a consequence most or all of the internal rotation of the humerus in relation to the scapula is lost. This lack of rotation is a reliable clinical sign for diagnosis of the disorder. The humerus may also be held in slight abduction and external rotation.

Acutely the shoulder is swollen and very painful. The initial trauma usually resolves with rest and supportive treatment. However, the affected limb begins to show signs of contracture several days to weeks after the initial trauma.⁴⁰ Physical examination of a chronic case usually indicates a bright, alert dog, without signs of any systemic illness. There is usually a weight-bearing lameness of the affected forelimb and a characteristic gait. Palpation and manipulation of the contracted limb does not usually elicit a pain response.^38,40 The remaining shoulder muscles, mainly the supraspinatus⁴⁰ and deltoid muscles, may show signs of disuse atrophy or be contracted as well.^33,34,39,40 A substantial decrease in range of motion of the shoulder joint is appreciated.⁴⁰ The affected forelimb is usually held with the shoulder in abduction and the elbow in adduction against the thoracic wall³⁸ (Figure 33-10). The distal forelimb and carpus are externally rotated and held in abduction.^36,40 Gait abnormalities usually consist of weight-bearing lameness and circumduction^33,38–40 of the affected forelimb with a characteristic fliplike action of the paw when placing the foot.^36,40 When the patient is placed in lateral recumbency with the affected limb up, a true infraspinatus contracture will cause the distal forelimb to remain in an abducted and externally rotated position off the floor and away from the body.

Siems et al. reported a series of ultrasonographic findings of two concurrently traumatized infraspinatus muscles in the same dog; one resolved without complications, and the other resulted in contracture.³⁹ The primary ultrasonographic description of a contracted infraspinatus muscle is increased echogenicity when compared with a normal supraspinatus muscle.^36,39 Magnetic resonance imaging is another diagnostic modality that may be useful for diagnosing the condition in both the acute and chronic phases.

Treatment

Physical rehabilitation of acute or subacute infraspinatus tendinopathies may be used to maintain joint motion and prevent contracture. Continuous ultrasound and stretching exercises may help maintain the length and mobility of the affected tissues. Mature contractures most likely require surgical release. Mature contractures are treated with a tenotomy of the tendon of insertion of the infraspinatus muscle and release of capsular adhesions of the tendon. Infraspinatus muscle contracture carries an excellent prognosis with tenectomy of the infraspinatus tendon.40,46 Lateral or craniolateral approaches to the shoulder both provide good exposure of the infraspinatus tendon.^33,40,41 Complete transection of the infraspinatus tendon with removal of a length of the tendon is required to restore motion in the affected limb and most often proves curative with an immediate release of contracture and return to function of the shoulder joint.^36,40 It is common to find adhesions to the infraspinatus tendon and joint capsule during surgery; however, after they are dissected away they seldom cause further problems.^40,41 Postoperative bandages need not be applied, and rehabilitation therapy should start when sutures are removed to prevent the formation of further adhesions.⁴⁰

The postoperative management after adhesion release includes full weight bearing and gentle, pain-free passive ROM, massage, and stretching exercises of the shoulder, elbow, and carpus two to three times daily to maintain ROM and promote normal alignment of the healing tissues. Cryotherapy may be used after exercise. Excessive activity such as unrestricted running or playing should be avoided in the first several weeks to avoid tissue damage and recurrence of fibrous tissue. If the contracture has been present for more than a few weeks before the surgery is performed, atrophy of other forelimb muscles may be present. General conditioning exercises for the limb, such as progressive walking, wheel-barrowing, and aquatic therapy, should be used to gradually return these muscles to normal size and strength. The use of neuromuscular electrical stimulation may also be considered if the atrophy is severe and the dog is having difficulty using the limb because of weakness.

Anatomy

Anatomically, the shoulder joint is one of the least stable joints in the dog, relying on soft tissue structures for stability and function (Figure 33-11).⁴⁶ In dogs the glenohumeral (shoulder) joint has the widest ROM and is capable of movements in any direction, but its primary movements during ambulation are flexion and extension.⁴⁶ The glenohumeral joint relies heavily on capsuloligamentous support to provide stability because its anatomic conformation does not provide a stable socket.⁴⁶ The humeral head and glenoid cavity of the scapula make up the ball and socket of the shoulder joint. The glenoid provides little coverage of the humeral head. The joint capsule, ligaments, and surrounding muscles and tendons all contribute to the stability of the shoulder. Insult or injury to any portion of the capsuloligamentous support structures can potentially cause shoulder joint pathology resulting in pain and dysfunction.⁴⁷ The components that are most commonly affected by MSS and MSI include the craniomedial joint capsule, medial glenohumeral ligament, subscapularis tendon, supraspinatus tendon, labrum, and less commonly the biceps tendon (shown in Figures 33-12 and 33-13). Depending on the severity and chronicity of the condition, the cartilage may also be affected.

Cause

Currently, the exact cause of MSS in dogs is unknown, although it is suspected to be related to chronic repetitive activity or overuse rather than trauma. Overuse of the shoulder support structures leads to degeneration of the tissues, lowering the tensile strength of the tissues and predisposing them to fraying, disruption, and eventually complete breakdown.1,20 Sporting athletes that participate in activities such as agility undergo extreme stresses on their muscles, ligaments, and tendons. Repetitive activities such as jump-turn combinations and weave poles performed regularly during practice and at weekend trials place the shoulder near its end range of abduction (as shown in Figure 33-14), and stress the soft tissues of the medial shoulder complex. Additionally, events such as slipping on wet surfaces, mishaps on the dog walk, teeter, or A-frame may also contribute to the trauma inflicted on the shoulder while participating in agility. Over time there may be a cumulative effect of the microtrauma occurring to the ligaments, tendons, and joint capsule, leading to a decrease in performance.

Diagnosis

Orthopedic Examination.

Findings from gait evaluation may range from a mildly shortened stride in the affected forelimb at a walk and a trot to significant weight-bearing lameness. Depending on chronicity, atrophy may be noted in the affected shoulder muscle(s) on physical examination. Forelimb circumference may be decreased in the affected forelimb when compared with the contralateral unaffected forelimb. Dogs with MSS typically have restriction and decreased range of motion in shoulder extension. The most consistent physical exam findings in dogs with MSS are shoulder spasm and discomfort on abduction of the affected shoulder. If a concurrent supraspinatus tendinopathy is present, pain may be noted when placing the shoulder into flexion (direct stretch of the supraspinatus) or on direct palpation of its point of insertion.

Because preoperative diagnosis of MSS is critical for clinical decision making, a palpation technique has been developed known as the shoulder abduction test.⁴⁸ Although this test was originally described in dogs under sedation in lateral recumbency, it is noted by the author that this test may be performed with similar consistent results on dogs awake and standing. To appropriately engage the components of the craniomedial shoulder, the elbow and shoulder must be placed in full extension with concurrent abduction of the forelimb. The scapula at the level of the acromion process must be stabilized with the evaluator’s opposite hand to achieve a passive stretch of the craniomedial shoulder components. A goniometer is held such that one arm of the goniometer runs parallel to the spine of the scapula so that the center of rotation of the goniometer is centered over the shoulder joint and the free arm of the goniometer extends over the axis of the humerus in contact with the skin. With the elbow and shoulder held in extension, the forelimb is abducted to its physiologic limit and the measurement obtained as shown in Figure 33-15. In severe cases, which clinically appear to be much less common, a slight “thud” or subluxation may be felt when abducting the shoulder. The procedure should then be performed on the contralateral shoulder for comparison. Using this palpation technique, it has been reported that a normal mean shoulder abduction angle is approximately 30 degrees.⁴⁸ Although this report revealed that dogs with medial shoulder instability had abduction angles significantly larger than 30 degrees,⁴⁸ a more recent study showed an inconsistent correlation between abduction angles and medial compartment pathology identified arthroscopically.⁴⁹ This is also the author’s clinical observation. Dogs with MSS rarely show evidence of “instability,” but rather show signs of dysfunction and pain associated with craniomedial pathology, including varying degrees of subscapular tendinopathy; medial glenohumeral ligament (MGL) disruption; craniomedial capsular lesions; and labral tears. Because MSS is usually a unilateral problem, the contralateral shoulder usually does not show signs of dysfunction, pain, or spasm on abduction.

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