Conditions of the Adult Canine Shoulder

Several conditions can affect the canine shoulder joint. Often the signalment of the animal helps to distinguish those diseases that typically occur in the juvenile patient, such as osteochondritis dissecans, from those that are more common in adult animals. This chapter discusses four disease conditions that are sources of shoulder lameness more commonly affecting the adult, large-breed dog.

The Rotator Cuff

Many of the conditions of the adult canine shoulder involve components of the rotator cuff. The term "rotator cuff" was initially used in reference to four muscles of the human shoulder that are responsible for the motion of the brachium and for providing active shoulder stability. The four muscles include the supraspinatus, infraspinatus, teres minor, and subscapularis. The canine shoulder differs in form and function from the human shoulder owing to the quadripedal nature of the dog, however the presence and importance of these four muscles persist. Whereas in the human, the cuff muscles are largely responsible for abduction and rotation of the brachium, these muscles serve predominantly to flex and extend the canine shoulder, in addition to providing active stability to the joint.

Calcification of the Supraspinatus

Calcification or mineralization of the supraspinatus tendon of the canine shoulder is a well-documented condition, yet it remains controversial with respect to its etiopathogenesis, relationship to clinical signs, and treatment. The supraspinatus muscle originates from the supraspinous fossa of the scapula and inserts on the greater tubercle of the humerus, extending to the medial aspect of the tubercle through a broad tendon. The muscle acts to extend the shoulder. Microangiographic studies have revealed an area of the central tendon of the insertion over the greater tubercle that is completely devoid of blood vessels [1].

Etiopathogenesis

Much of what is known about the etiopathogenesis of rotator cuff calcific tendinopathy must be extracted from the human literature. The two causative agents that are discussed most frequently are tissue hypoxia and localized pressure [2]. Most researchers concur with a theory describing the process of calcification to be reactive in nature rather than primarily degenerative [2]. Furthermore, it has been suggested that the disease evolves in various stages: precalcific, calcific, and postcalcific. During the precalcific stage, fibrocartilaginous metaplasia occurs in avascular areas of the tendon and the new chondroid cells produce glycosaminoglycan-rich extracellular matrix [2,3]. The calcific stage is subdivided into three phases: formative, resting, and resorptive [4]. The hallmark of the formative phase is the formation of chalky deposits of coalescing matrix vesicles containing calcium crystals [2]. Histopathologic analysis will reveal positive staining of the calcific clumps with Von Kossa’s stain. The resting phase of the calcific stage marks the cessation of calcium deposits that are surrounded by fibrocartilagenous tissue without evidence of inflammation. The resorptive phase may occur nonpredictably following the resting phase, and is so named for the presence of macrophages and multinucleated cells that begin to phagocytose the calcified deposit, resulting in a granulomatous appearance to the lesion [3]. The chalky clumps previously detected change into a toothpaste-like substance during the resorptive phase. The postcalcific stage is one of remodeling that occurs through the formation of granulation tissue, neovascularization, and deposition of type III collagen in an attempt to heal the void left after the resorption of calcium deposits [2].

Clinical Relevance

Several reports now document the occurrence of calcification of the supraspinatus tendon in dogs [5-8]. Adult Labrador retrievers, Rottweilers and German shepherd dogs are the most frequently reported affected animals, however this may indicate breed popularity rather than true prevalence [5-8]. Other than the speculation of localized tissue hypoxia within the avascular portion of the supraspinatus tendon, no definitive risk factors have been determined in reported canine populations. The relationship between clinical signs and the presence of calcific deposits in the supraspinatus is not clear. Supraspinatus calcifying tendinopathy may be an incidental finding and result in no clinical signs [6,8]. Interestingly, Bardet reports that 11% of dogs affected with shoulder instability concurrently possess supraspinatus calcification [9]. In another study assessing 13 dogs positively diagnosed with calcification of the supraspinatus that also underwent radiographic examination of the elbows, 69% had evidence of fragmented coronoid processes, elbow osteoarthritis, or both [6]. What cannot be determined from these studies is if the diagnosis of supraspinatus calcification is related to other orthopedic conditions within the same joint or limb, or if its incidence reflects coincidence. From reports of humans who are symptomatic from calcific tendinopathy of the supraspinatus alone and the successful resolution of clinical signs following calcific deposit dissolution or removal in some dogs, one may conclude that the presence of the disorder is responsible for lameness in a certain percentage of dogs. However, concurrent sources of forelimb pain should always be pursued and addressed appropriately.

Diagnosis

Pain may or may not be elicited on palpation of the tendon of insertion of the supraspinatus over the greater tubercle and on shoulder flexion [5,7]. Because of the concurrence of supraspinatus calcification and other shoulder pathology, the biceps tendon should also be palpated for evidence of pain or inflammation, and the joint examined for signs of instability. Similarly, the elbow should be thoroughly palpated to examine for signs of pain, effusion, and decreased range of motion.

The most common diagnostic tool is radiography. However, mineralization of the supraspinatus may be indistinguishable from that of the biceps tendon if only mediolateral radiographs are taken. Therefore, a flexed cranioproximal-craniodistal tangential view of the intertubercular groove, or "skyline" view, should also be taken to distinguish the location of the calcific density (Fig. 101-1) [8]. Depending on the stage of the disease process, the affected area of the tendon may not be detectable with radiographs. Ultrasonography can be used successfully to detect disruption or inflammation within tendon fibers. Furthermore, if present, calcification is easily recognized as hyperechoic foci with distal acoustic shadowing.10 If magnetic resonance imaging is used, T1-weighted images will show calcifications as areas of decreased signal intensity and T2-weighted images may demonstrate a perifocal band of increased signal intensity associated with edema [2].

Figure 101-1. Lateral and craniproximal – craniodistal or "skyline" radiographic views showing two calcific deposits in the supraspinatus tendon. The skyline view allows localization of the pathology to the supraspinatus tendon versus the biceps tendon (photos courtesy of Dr. Loic Dejardin).

Treatment

Various treatments have been described for lameness attributable to calcification of the supraspinatus in the dog, including conservative management, surgical removal of the calcific deposits and extracorporeal shock-wave therapy. Surgery consists of accessing the deposits through longitudinal incisions in the tendon for their subsequent removal. Interestingly, in a long-term follow-up study of four operated cases, Laitinen noted that the calcific deposits had reoccurred in all the dogs after a mean follow-up time of 5.1 years after surgery [6]. However, despite the reformation of the calcium-based deposits, resolution of lameness has been reported following their surgical removal in the majority of cases [6-8]. In the human, conservative management is the favored initial treatment and surgery is indicated only if 1) clinical signs progress, 2) the pain appears to be consistent and interfering with quality of life, and 3) if conservative management fails [11]. Current opinions from veterinary orthopedic researchers have become similar, recommending a period of conservative management including rest, administration of nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy for 3 months from the time of diagnosis before attempting surgery [6]. Lameness attributable to calcification of the supraspinatus has been shown to resolve in some dogs with conservative management [6]. Another advantage of this approach is to allow other sources of underlying lameness to manifest and be appropriately diagnosed because the incidental occurrence of supraspinatus calcification appears to be high and may serve as the proverbial red herring.

Another treatment strategy that has been reported in the dog is extracorporeal shock-wave therapy, which employs low-frequency, high-pressure pneumatic impulses that are generated outside of the body but delivered to the affected area through a hand-held applicator in a noninvasive, but site-specific fashion [5]. Success with this technique in alleviating clinical signs has been demonstrated in a small population [5].

Other techniques described in the human literature include ultrasound-guided needle aspiration and lavage, and arthroscopic-assisted aspiration and debridement [2]. These authors have had success with using arthroscopy to assist in the debridement of focal calcium deposits in a small population of dogs. However, the use of needle aspiration has not been described in the dog to the knowledge of the authors.

Infraspinatus Contracture

The infraspinatus is a fusiform muscle of the shoulder rotator cuff that originates from the infraspinous fossa of the scapula and inserts on the lateral aspect of the greater tubercle over a small bursa. It can either flex or extend the shoulder depending on the joint’s position when the muscle contracts.

Etiopathogenesis

Contracture of the infraspinatus represents a chronic process by which initial injury to the muscle and tendon eventually results in severe fibrosis and adherence to the underlying joint capsule. The condition was first described in 1970 [12], and is a well-recognized disorder occurring in medium- to large-breed working dogs [13]. The initiation of the process can either be self-inflicted through vigorous activity or a result of a traumatic event. Most typically, affected dogs present with acute pain and swelling over the lateral aspect of the shoulder after a period of strenuous activity, although this phase of the disease frequently goes unnoticed. Palpation of the supraspinatus and infraspinatus muscle groups during this acute injury phase reveals swelling and elicits a painful response. During the ensuing weeks, the dog is typically reluctant to bear weight and flex or extend the affected limb at the level of the scapulohumeral joint. Over time, the tendon can undergo irreversible and severe contraction with marked concomitant muscle atrophy. The result is the adoption of a classic posture of the affected forelimb consisting of adduction of the elbow, abduction of the antebrachium, and external rotation of the limb with extension at the level of the shoulder (Fig. 101-2). Research has demonstrated that the suprascapular nerve is not involved in this process and that fibrous tissue eventually replaces the vast majority of affected normal muscle fibers [14,15]. The supraspinatus muscle can be simultaneously or independently involved in a similar process [16].

Figure 101-2. A dog affected by infraspinatus contracture with classic position of the limb (photos courtesy of Dr. James Tomlinson).

Diagnosis

A presumptive diagnosis can be made based on patient history, the characteristic positioning of the affected limb, and orthopedic examination. Dogs affected by this condition will carry the limb in a similarly characteristic fashion during ambulation in which the lower limb swings out in a circumducted fashion while advancing the foot forward. Careful palpation will reveal atrophy of the infraspinatus and possibly the supraspinatus muscles with subsequent prominence of the scapular spine and acromial process. Attempts to internally rotate or adduct the proximal humerus will result in noticeable scapular excursion away from the thoracic wall. Radiographs of the shoulder may be normal or reveal a narrowing of the scapulohumeral joint space, particularly evident on the craniocaudal view. Ultrasonographic examination of the infraspinatus muscle and tendon can be completed to substantiate the diagnosis, as findings associated with both the early and late stages of the disease have been described [17].

Treatment

If the disorder can be diagnosed in the early stages, in which the tendon has been strained prior to any secondary fibrotic response, conservative management consisting of rest and NSAIDs has been reported to be successful [17]. Ultrasound examination of these injuries will greatly assist with this early intervention [17]. However, if pursuing conservative management, owners should be advised about the risk for contracture to occur. Once the muscle and tendon have undergone fibrosis and contracture, only surgical release has been shown to be successful. The infraspinatus is released through tenotomy and partial excision of the tendon close to its insertion on the lateral aspect of the greater tubercle. Adhesions to the underlying joint capsule must be examined for and freed. A dramatic release and recession of the proximal myotendinous junction with immediate restoration of joint range of motion should be detected once the tendon is completely released. Prognosis with this treatment appears to be good to excellent.

Biceps Tendon Pathology

Pathologic conditions of the biceps tendon reported to occur in dogs include tenosynovitis, partial or complete rupture, avulsion, tendinitis, tendinosis, displacement, and bipartite tendon [18-25]. Most often, these conditions occur in middle-aged medium- and large-breed dogs that participate in athletic activities. No documented gender predisposition exists to the authors’ knowledge. Apart from rupture or avulsion, dogs with biceps tendon pathology are presented for unilateral forelimb lameness of insidious onset. Dogs typically bear weight on the affected limb. Rupture or avulsion may result in more acute and more severe lameness.

Etiopathogenesis

Bicipital tenosynovitis (also called tendinitis or tendinosis), with or without partial tearing, appears to be the most common pathologic condition of the biceps tendon in dogs [18-25]. The etiology likely involves chronic overuse with superimposed "micro" or "macro" traumatic episodes involving the tendon. The problem is chronic inflammation of the portion of the biceps tendon that crosses the shoulder joint. Histologically, synovial villous hypertrophy, hypervascularity, and lymphocytic-plasmacytic infiltration are noted [21,24]. Long-term, this condition can result in tendon fibrosis, necrosis, fibril disruption, collagenolysis, metaplasia, and calcification; enthesiophytosis; and secondary osteoarthritis [21,24].

Avulsion or rupture of the biceps tendon can occur at the tendon’s origin at the supraglenoid tubercle or can include avulsion of the tubercle from the scapula [18,19,26,27] Avulsion of the tubercle can occur as a Salter-Harris fracture at the supraglenoid ossification center in immature dogs [26,27]. Rupture of the tendon can also occur at mid-substance or the musculotendinous junction. Avulsion and ruptures of all types are most often associated with trauma from jumping, falling, or blunt impact (i.e., vehicular trauma).

The etiology and significance of displaced and bipartite biceps tendons are not known [18,19]. These conditions may involve genetically based anatomic variations and appear to have a variety of manifestations from incidental findings to overt pain and lameness.

Diagnosis

Physical examination of dogs with biceps tendon pathology is similar regardless of specific cause. The most consistent examination findings reported include lameness, mild to moderate atrophy of the affected spinatus muscles, pain on shoulder flexion (especially with the elbow extended), and pain on direct palpation of the biceps tendon, and/or manual tensioning of the biceps muscle [18-25,28,29].

Definitive diagnosis and characterization of the type of pathology of the biceps tendon typically requires more advanced imaging modalities such as contrast arthrography, ultrasonographic evaluation, and/or arthroscopic visualization [18-25,28,29] Plain radiographic views of the affected shoulder joint provide relevant information regarding secondary bone and soft tissue changes and should be included in the diagnostic database. "Skyline" radiographic views may aid in evaluating the biceps groove [20,23]. In cases of bicipital tenosynovitis, radiographs may show evidence of osteophytosis and enthesiophytosis associated with the biceps tendon and groove (Fig. 101-3). Contrast arthrography provides additional information regarding the anatomy and integrity of the biceps tendon. Contrast arthrography is reported to be sensitive for identifying biceps tenosynovitis [23], but generally does not delineate type or extent of the pathology or give information regarding changes within the tendon tissue [18-25]. Ultrasonography of the biceps tendon, performed by an experienced individual, provides for assessment of intratendinous pathology, associated effusion, and pathologic changes of the biceps groove (Fig. 101-4) [23,25,29]. Ultrasonography is helpful for determining the type and severity of the pathology in the majority of cases.25,29 Arthroscopic evaluation of the shoulder joint allows for visualization and assessment of all intra-articular structures, providing definitive evidence of visible biceps pathology as well as involvement of other tissues (Fig. 101-5). More advanced imaging techniques such as computed tomography and magnetic resonance imaging are currently being investigated for their usefulness for diagnosis of shoulder joint pathology in dogs.

Figure 101-3. "Skyline" radiographic view showing reactive osseus proliferation within the intertubercular groove commonly seen with biceps tenosynovitis.

Figure 101-4. Ultrasonographic image showing a transverse view of a biceps tendon with disruption of normal tendon architecture and associated effusion indicating biceps tenosynovitis from a partial tear.

Figure 101-5. Arthroscopic views of a biceps tendon with tenosynovitis and partial avulsion.

It is critical to perform a comprehensive diagnostic evaluation of dogs suspected, or even confirmed, to have biceps tendon pathology. Biceps tendon pathology can be a secondary or incidental finding. Many dogs with biceps tendon problems also have elbow pathology, neurologic dysfunction, or neoplasia. It is vital to look for other pathology in every dog diagnosed with biceps tendon disorders as these other problems are often more clinically important and will greatly affect treatment and prognosis. The authors recommend performing a complete neurologic examination and obtaining radiographs of the elbows in all cases.

Treatment

When biceps tendon pathology is determined to be a significant cause of pain, lameness, and/or dysfunction in dogs, treatment is indicated. Nonsurgical management of biceps tendon pathology consisting of activity modification, nonsteroidal anti-inflammatory drugs, analgesics, and/or intra-articular injections may be effective in many cases [18-20,22,25]. Exercise restriction appears to be a critical component of successful nonsurgical management. Success rates for nonsurgical treatment of biceps tenosynovitis range from 41% to 73% [20,25]. This variability in outcome is likely due in part to the inability to fully assess the cause and severity of tendon pathology preoperatively. Optimizing comprehensiveness and consistency in diagnosis and characterization of biceps tendon pathology in dogs may lead to more definitive algorithms for decision-making regarding indications for various treatments in these patients.

Surgical management is deemed necessary in a significant number of dogs with biceps tendon pathology [18-20,22-26,28-30]. The reported surgical treatment options for biceps tendon disease include tenodesis, tenotomy, primary repair, debridement, transposition, and lavage [18-20,22-26,28-30]. In the authors’ experience, primary repair, debridement, and transposition are rarely indicated for primary lesions of the biceps tendon. However, these treatment options have been reported to result in successful outcomes, and may warrant consideration in selected cases. Avulsions that include an adequate portion of supraglenoid tubercle can be successfully treated using open or closed reduction techniques and stabilized with internal fixation, such as pin and tension band wiring, divergent pinning, and/or lag screw fixation (Fig. 101-6) [26,27].

Figure 101-6. Postoperative radiographic views of a dog with avulsion of the biceps tendon origin at the supraglenoid tubercle treated by lag screw fixation after arthroscopically and fluoroscopically guided and performed reduction

For surgical treatment of biceps tenosynovitis with or without partial tears, biceps tenodesis via an open approach and open or arthroscopic biceps tendon release (tenotomy) are the most common surgical procedures used to treat biceps tendon problems in dogs [18-20,22,25,28-30]. Each of these techniques has been reported to be a successful means of treatment for biceps disorders in dogs. Arthroscopic biceps tenotomy was reported to result in good to excellent results in 5 dogs in a series based on subjective measures over a 6-month follow-up period [28]. Open tenodesis has been be associated with good and excellent outcomes in more than 90% of dogs treated [20,22]. Six dogs treated by arthroscopic tenodesis were judged to have good or excellent outcomes in another reported series [29].

The published literature regarding surgical treatment of biceps tendon pathology suggests that postoperative protection of the repair or treatment, weight management, and physical rehabilitation are critical for a successful outcome when treating biceps tendon problems using any modality [18-20,25,28-30]. It is important to counsel owners that maximal function may not be reached until 6 months following surgery in the majority of cases, and that these are typically chronic problems requiring compliance in treatment, careful monitoring, and most of all, patience. However, when these factors are addressed, the prognosis for the vast majority of biceps tendon disorders is good to excellent for pain-free, "pet-level" function, and guarded to good for high-level athletic function.

Shoulder Instability

Shoulder instability owing to periarticular soft-tissue pathology is a commonly diagnosed problem in humans. Bardet has described a shoulder instability syndrome in dogs [9]. Although lateral and multidirectional shoulder instabilities have been described [9,31], medial shoulder instability (MSI) appears to be the predominant type of shoulder instability seen in dogs [9,32,33]. Characterization of epidemiology, pathology, diagnosis, indications for treatment, treatment options, outcomes, and prognosis for MSI are currently a major focus in veterinary medicine. Dogs diagnosed with MSI are most commonly middle-aged, large-breed dogs with a history of chronic unilateral forelimb lameness [32,33]. Dogs with MSI typically have an intended purpose of work, performance, or active pet-level function [32,33].

Etiopathogenesis

The etiology of MSI is not known, but available data suggest that this problem occurs as a result of chronic overuse injury with episodes of "micro" trauma to the shoulder occurring during the development of disease. The pathology associated with MSI includes lameness, shoulder joint laxity, pain on manipulation of the shoulder, and abnormalities of the medial joint capsule, subscapularis tendon, and medial glenohumeral ligament observed via arthroscopy [9,32-34].

Diagnosis

Signalment, complete history, complete orthopedic and neurologic examination, blood work, radiographs, and ultrasonography are integral to the comprehensive diagnostic approach. Ultrasonographic evaluation is recommended for all potential MSI patients to rule out primary or concurrent musculotendinous pathology. Definitive diagnosis of MSI is based primarily on palpation and exploratory arthroscopy.

Palpation under sedation is a key component of preoperative diagnosis of MSI. Range of motion in flexion, extension, and rotation, the "shoulder drawer sign" as described by Bardet [9], and the shoulder abduction test [32,33] should be assessed in each limb. Shoulder abduction angles measured under sedation have been reported to provide objective data for diagnosis of MSI in dogs [32,33]. Shoulders with clinical and arthroscopic evidence of MSI have significantly higher angles (53.7 ± 4.7°) compared with shoulders considered normal (32.6 ± 2.0°) [33].

Currently, arthroscopic exploration provides the most definitive diagnosis of MSI and allows assessment of cartilage damage and other key structures in the shoulder joint. Arthroscopic identification of tearing and laxity of the subscapularis tendon, medial glenohumeral ligament, and joint capsule are consistent findings in reported cases of MSI (Fig. 101-7) [32,33].

Figure 101-7. Arthroscopic view of the pathology of the medial joint capsule (A), subscapularis tendon (B), and medial glenohumeral ligament (C) typically seen in dogs diagnosed with medial shoulder instability. The distance between glenoid (D) and humeral head (E) also appears excessive.

It is vitally important to rule out separate or concurrent causes of shoulder lameness. Dogs with MSI may also have elbow pathology, neurologic dysfunction, or neoplasia. It is vital to look for other pathology in every dog presumptively diagnosed with MSI as these other problems are often more clinically important and will greatly affect treatment and prognosis. The authors recommend performing a complete neurologic examination and obtaining radiographs of the elbows in all cases.

Treatment

Few data are available regarding indications for treatment, treatment options, and prognosis for shoulder MSI in dogs. Treatment recommendations are based on extent and severity of instability, concurrent shoulder pathology, concurrent orthopedic problems, the overall health of the patient, the intended use of the patient, and the commitment of the owner [9].,31-35 The use of radiofrequency-induced thermal capsulorrhaphy (RITC) for treatment of MSI in dogs has been reported to be successful [32,34]. RITC treatment resulted in improved clinical function in 93% of cases, with 79% considered to have excellent outcomes and 7% considered to be failures [32]. Appropriate postoperative care appears to be a critical factor in realizing success in these cases. It is imperative that the dogs be kept in a non-weight bearing sling for 3 to 4 weeks after RITC treatment in order to protect the treated tissue. It is vital that careful attention to sling and limb management is employed during this period. Severe complications, primarily skin wounds and carpus and elbow contracture, can occur if the sling is not properly cared for and range of motion exercises are not performed at the time of sling change (at least once weekly). For the subsequent 6 weeks, strict exercise restriction with physical rehabilitation is recommended, followed by a progressive return to full function. Dogs do not reach improved function until 12 to 16 weeks after treatment and do not reach full post-treatment function until 5 to 6 months after treatment [32]. Bilateral shoulder instability, complete tears of the MGL, a single major traumatic episode as the cause of the MSI, concurrent forelimb orthopedic pathology, neurologic dysfunction, and shoulder osteoarthritis are reported to be contraindications for RITC treatment of MSI [32]. For complete tears of the MGL, ST, or MJC, open or arthroscopic reconstruction of the medial compartment by direct tissue reapposition and tissue anchor and suture or imbrication suture reinforcement is recommended [35]. Excision arthroplasty and arthrodesis may also be viable options in a subset of patients with severe MSI. For those cases that do not fit the inclusion criteria for any surgical treatment, non-surgical treatment consisting of weight management, activity modification, and medical therapy is recommended. No study in which any of these treatments for MSI were compared has been reported to date.

Shoulder instability appears to be a documented problem in dogs that can result in pain and lameness. However, our understanding of etiopathogenesis, clinical versus subclinical pathology, optimal diagnostic tools, indications for treatment, surgical decision-making, and prognostication for shoulder instability in dogs is lacking, and a significant amount of work needs to be done to further characterize and make definitive recommendations regarding this entity.