A high incidence of occurrence has been noted in the Bernese Mountain Dog, German Shepherd, Rottweiler, Golden Retriever, and Labrador Retriever. Other breeds affected are the Newfoundland, Saint Bernard, Mastiff, Springer Spaniel, Australian Shepherd, Chow Chow, Shar-Pei, Shetland Sheepdog, and some Terrier breeds. Typically, both elbows are affected. However, unilateral elbow dysplasia is also recognized.
Forelimb lameness is a relatively common presentation for the growing puppy with frequent presentation being the rule for some breeds. Although there are a number of developmental anomalies of the forelimb resulting in lameness, the focus of this presentation is restricted to those conditions most commonly referred to as elbow dysplasia. The developmental growth of the canine forelimb coupled with the potential for trauma in the active playful puppy set the stage for the developmental anomalies that lead to elbow dysplasia. Since considerable joint degeneration can occur over minimal time, it is critical to be aware of the predispositions to and early symptoms of all forms of this disease. Ununited anconeal process, osteochondritis of the medial condyle of the humerus, and fragmented coronoid process are three conditions that may occur independently or concurrently in the same animal. The pathophysiology, diagnosis, and treatment of these three manifestations of elbow dysplasia are the subject of this report.
The canine elbow joint allows flexion and extension as well as a limited degree of supination and pronation. A common feature of UAP, OCD, and FCP is the presence of some level of elbow incongruity. Each of these conditions may then precipitate the secondary changes associated with degenerative joint disease. The time of occurrence of UAP, OCD, and FCP is usually between the ages of four and six months. At that time, the bones and joints are incompletely formed. In the elbow joint, an abnormally small curvature of the trochlear notch could result in a FCP through weight bearing forces transmitted via the humerus on an immature coronoid process lying above the level of the adjoining radius. For the same reason, the result could be an OCD lesion, caused by pressure exerted via the medial coronoid process on the opposite immature articular humeral cartilage, interfering with normal endochondral ossification. In dogs with a separate center of ossification of the anconeal process, stresses caused by the abnormally tight fit between the anconeal process and the opposite humerus, and present before union (ie-between the ages of 4-6 months), could cause microscopic movement at the level of the cartilage plate between the separate center of ossification and the ulna and result in a UAP. This developmental elbow incongruity is responsible for joint injury, which is manifested by continual cartilaginous breakdown and subsequent degenerative joint disease.
In FCP, the incongruous growth of the radius and ulna results in misalignment of the bones such that a tremendous amount of pressure is placed on the coronoid process, making it highly susceptible to the development of fractures or fissures. In addition, the location of the coronoid process at the medial extent of the articulation of the humerus, radius, and ulna make it prone to mechanical damage because of a shearing effect between the radial head and the coronoid during rotation of the forelimb, resulting in fragmentation of the coronoid process and potentially the development of a loose body. The cartilage damage induced by the erosion of the incongruent articular surfaces is usually manifested as an OCD lesion on the more medial articular surface of the humeral condyle. As with FCP, UAP is a consequence of incongruent growth between the radius and ulna resulting in the anconeal process remaining ununited with the proximal ulna. Since the anconeal process can no longer provide support to the elbow joint because of its instability, articular instability and degenerative changes ensue.
The primary source of pain in elbow dysplasia is from the increased joint pressure, joint effusion, and loose cartilage fragments, which results from the destruction of the hyaline cartilage. These fragments induce synovitis, alterations in joint fluid consistency, and volume and joint instability, as the incongruent joint surfaces fail to properly bear weight. Characteristic of this degeneration is focal cartilage degeneration, proliferation of the synovial membrane, and formation of periarticular osteophytes. In advanced cases, erosion of the cartilage is so severe that subchondral bone becomes denuded and sclerotic. Chronicity causes capsular scarring and eventually a decreased range of motion in the joint with resultant gait changes.
The onset of gradual and variable clinical signs makes elbow dysplasia difficult to diagnose at an early stage in all cases. A combination of physical examination, gait analysis, palpation, radiography, nuclear scintigraphy (bone scans), or arthroscopy may be needed to adequately diagnose the syndrome. The most common symptoms associated with elbow dysplasia include limping or short striding steps in the forelimbs, difficulty lying down or rising, lying down with elbows abducted, warming out of lameness after minimal exercise, increased lameness after heavy exercise, and frequent shifting of weight with a noticeable head bob during ambulation.
Pain, crepitus, and swelling of the joint due to excess synovial fluid and capsule thickening may be elicited on palpation. A lateral deviation of the elbow when standing or walking may be observed, and the elbow usually exhibits a decreased range of articular motion. Although palpation and gait analysis are important means of detecting elbow dysplasia, any suspicion of joint disease should be confirmed by radiography. It is important to remember, however, that a decreased range of motion, lameness, and joint pain/effusion may be present before radiographic changes are evident.
Radiography of the affected joint should include standard anterior-posterior, medial to lateral, flexed lateral, and anterior-posterior medial to lateral oblique views to completely evaluate the joint. Initial osteophyte formation may be seen on the proximal anconeal process, medial epicondyle, medial humeral condyle, and medial aspect of the proximal ulna. High quality radiographs are essential for diagnosis, but it should be pointed out that even excellent radiographic technique might fail to adequately disclose signs of the disease being present. Mild cases are difficult to diagnose by radiography alone; lesions that do not appear through conventional radiography may be discerned through nuclear scintigraphy, MRI or CT scanning, arthroscopy, and/or standard arthrotomy.
Inadequate treatment of elbow dysplasia usually will lead to considerable degeneration of the elbow joint as well as the potential development of orthopedic problems in other joints due to resultant abnormal weight transfer during ambulation. Depending upon the degree and nature of the case and the physical expectations for the dog, elbow dysplasia may be treated with a multi-pronged approach including diet and exercise restriction, medical therapy and surgery via standard arthrotomy or arthroscopy. Because it is inexpensive and non-invasive, medical therapy may be an effective method of treating minor elbow dysplasia cases, which exhibit mild or intermittent pain. Medical therapy is also indicated for those patients who, for any number or variety of reasons, may not be considered surgical candidates. Medical therapy involves the administration of nutritional chondroprotectants (glucosamine, chondroitin, creatine, MSM), injectable chondroprotectants (Adequan), the utilization of steroidal and nonsteroidal anti-inflammatory drugs, pain management, acupuncture, physical therapy, platelet rich plasma injections, and Class IV laser therapy. While medical therapy has limited applications by itself in those patients in obvious need of surgical intervention (since it does not eliminate either the original joint incongruity or the resulting histological trauma), medical therapy is a critical adjunct to arthrotomy and arthroscopy.
Several surgical approaches to the medial aspect of the elbow joint for the treatment of FCP and OCD have been described, requiring osteotomy, tenotomy, or transection of muscle. Although each technique provides good exposure of the medial coronoid process and medial humeral condyle, exposure is gained at the expense of additional surgical time and tissue manipulation. Longitudinal myotomy of the flexor carpi radialis provides rapid atraumatic access to the medial aspect of the elbow. The FCP is identified, dissected free, and removed. The medial humeral condyle is inspected for the presence of an OCD, and the lesion is curetted if present. In addition, gentle subchondral bone abrasion with microfracture of the involved surface may help liberate pluripotential stem cells, which serve to allow formation of an improved fibrocartilaginous weight bearing surface. Treatment options for UAP include a lateral approach to the joint via a myotomy of the anconeal muscle and removal of the anconeus. There is evidence that proximal transverse osteotomy of the ulna may improve joint congruity and allow for the effective treatment of early UAP and FCP cases in young dogs. Ulnar osteotomy in young UAP cases may allow for the realignment of the ulna with the humeral condyle and the consequent reattachment of the anconeal process. Treatment of FCP by ulnar osteotomy must also involve the removal of the loose and degenerated bony fragments.
Increasingly, arthroscopic surgery is being utilized to treat elbow dysplasia. Loose coronoid fragments and OCD lesions may be effectively removed and curettaged less traumatically than standard arthrotomy. While the choice of surgical technique (arthroscopy or traditional surgery) may vary, the results are similar. Effective treatment of UAP, however, must still involve a standard arthrotomy.
While early surgical therapy is recommended, it should be mentioned that osteoarthritis may persist and progress despite appropriate surgical intervention and adjunctive medical therapy. The recent utilization of platelet rich plasma and Class IV laser therapy exhibit great promise in breaking this progressive cycle of degenerative joint disease. Because many of the degenerative changes that occur in elbow dysplasia are the result of joint incongruity, a few patients may progress to intractable disease, which may require the replacement or fusion of the joint. Total elbow replacement or arthrodesis of the elbow joint should be reserved for those cases that have progressed to massive cartilage damage and pain non-responsive to appropriate medical therapy. Most surgeons agree that the functional outcome after arthrodesis of the elbow is quite poor although pain in the joint was alleviated. A mechanical lameness results in almost all of these patients. In cases receiving total elbow replacement, each dog considered a surgical candidate had severe, daily lameness from chronic elbow osteoarthritis that was unresponsive to medical management. In many cases, surgery resulted in significantly improved limb function. The greatest disadvantage to elbow replacement, however, is that a serious complication can result in a second surgery that requires removal of the implant system. In the elbow, this leaves the surgeon with few options— generally arthrodesis, but amputation has also occurred following severe complications (neurogenic injury or untreatable infection). In lieu of amputation, some clients may elect for euthanasia because of the lack of medical or surgical therapy to return the pet to a comfortable, ambulatory gait.
Sliding Humeral Osteotomy (SHO) is a relatively new procedure that was developed specifically as a treatment for dogs with severe cases of elbow dysplasia with resultant medial compartment disease (severe cartilage loss in the medial aspect of the elbow joint). In many dogs with elbow dysplasia, the damage to the cartilage is confined to the medial (inside) half of the joint. The procedure begins by making a precise osteotomy through the humerus. A specially engineered SHO plate is applied onto the upper section of the humerus. As screws are applied to the plate and bone, the lower section of the humerus moves medially. This slide shifts weight-bearing forces off the medial compartment and over to the healthy cartilage of the lateral compartment of the elbow joint, thus relieving the pain on the inside of the joint. This would give the damaged medial compartment an opportunity to heal with a layer of fibrocartilage. While stem cell therapy has been universally disappointing in stimulating this healing process, the utilization of Class IV laser therapy and platelet rich plasma may prove more rewarding. While numerous studies have confirmed that the SHO effectively shifts the weight bearing forces to the lateral compartment, the overall decrease in joint surface contact area suggests that these procedures may induce focal increases in pressure that may cause iatrogenic cartilage damage and continued lameness. Nonetheless, good to excellent results have been reported with this procedure, with the majority of dogs undergoing SHO having demonstrated a decrease in clinical lameness postoperatively while requiring less anti-inflammatory medication to remain comfortable. Considering the alternatives (total elbow replacement or fusion), SHO may prove quite useful in helping to manage carefully selected patients with intractable pain and discomfort.
While the presence of multiple modalities of therapeutic options allow for a reasonable return to function, it is critical to determine the presence of elbow dysplasia before the joint deteriorates beyond repair in order to achieve the best possible prognosis. Ununited anconeal process, fragmented coronoid process, and osteochondritis all respond favorably if medical and surgical intervention is initiated early in the course of development and prior to severe degenerative changes.
Click here for a computed tomography report of elbow dysplasia
CT Scan of FCP Elbow Dysplasia CT Scan of FCP Elbow Dysplasia
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