Canine elbow dysplasia is an abnormal development of the elbow joint. The term is used to describe developmental diseases which include ununited anconeal process, fragmentation of the medial coronoid process and osteoarthritis secondary to joint incongruity. The pathophysiologic mechanism leading to elbow dysplasia is thought to be a lack of elbow congruity secondary to improper growth of the radius/ulna during maturation. For example, the axial length of the ulna is shorter in cases with ununited anconeal process as compared to breed matched cases without UAP. The hypothesis is that as growth proceeds the anconeal process of affected dogs presses against the humeral trochlea. This creates a shear force separating the anconeal process from the ulnar metaphysic. (Fig.1)
In cases with abnormal medial coronoid process of the ulna, CT has shown the articular surface of the radial head to be positioned below (distal) the joint line of the coronoid process. This finding leads one to speculate that the growth of the radius was retarded at some point during development (alternatively, ulnar growth could have been accelerated leading to a longer ulna). In either circumstance, with the coronoid positioned higher than the radial articular surface, increased weight bearing forces are directed onto the lateral region of the medial coronoid. Increased force could give rise to abnormal stresses which initiate fragmentation of the medial coronoid (Fig. 2) or result in an osteomalacia coronoid (similar to legg perthes of the femoral head (Fig. 3)
The degree of elbow incongruity will vary in severity (similar to hip dysplasia!!). Some dogs have severe incongruity which causes abrasion of the articular cartilage overlying the medial coronoid and under surface of the humerus. Clinical signs are variable and dependent upon the degree of incongruity. The worse the incongruity the more severe the clinical findings and the earlier the clinical signs are expressed. Moderate to severe joint effusion, pain on manipulation of the elbow, and loss of full range of motion are signs indicative of significant incongruity. (Fig.4 CT showing radioulnar incongruity).
Although the above clinical presentation is indicative of significant incongruity, clinical signs in the majority of younger dogs with FCP/incongruity are not debilitating. In most dogs, the presenting complaint is a periodic lameness associated activity. Gait observation may or may not show lameness; similarly effusion and pain are variable. The most consistent clinical finding is loss of normal flexion.
Dogs with minimal incongruity may present with lameness later in life (2-5 years of age); The clinical finding in these cases is often a discernable limp. No joint effusion, pain or loss of motion in elbow is seen. Radiographs often show no obvious signs of DJD. These cases are commonly misdiagnosed as having "soft tissue" injury or shoulder "instability." A nuclear bone scan will localize the problem to the elbow and a CT will be diagnostic of a fragmented coronoid or osteomalacic coronoid. Dogs with moderate to severe incongruity may present with a lameness which is non-responsive to rest and/or NSAIDs. Unfortunately, many of these cases have severe DJD and erosion of articular cartilage in the medial compartment. (Fig. 5&6)
Treatment and prognosis are controversial. Some studies have not shown a difference in outcome between non-operative or operative treatment. However, these studies did not classify the severity of incongruency making it difficult to judge accuracy. Our clinical experience suggests outcome is dependent upon the degree of incongruency and associated cartilage erosion. Surgical intervention is warranted in all cases and will improve clinical function. Dogs with minimal to no incongruency, no cartilage erosion, and a fragmented of osteomalacic coronoid a have a good long-term prognosis with arthroscopic intervention. Fragments or osteomalacic bone can be removed (arthroscopically) from both elbows at the same time without causing significant discomfort. Dogs presenting with severe incongruency and cartilage erosion will improve with surgical intervention. Removal of fragments and osteomalacic bone will improve limb function. Proximal ulnar ostectomy will improve function and may slow progressive OA.
Osteochondritis desiccans (OCD) is a manifestation of osteochondrosis. Osteochondrosis is a disturbance in endochondral ossification which effects the humeral epiphysis. Although the abnormal endochondral ossification is seen throughout the epiphysis on CT, the most apparent gross clinical finding is a section of cartilage lifted from the articular surface.. Despite unilateral lameness, this condition is often bilateral.
Large and giant-breed dogs are commonly affected and males are more often affected than females. Clinical signs often develop between 4 and 8 months of age; however, some dogs may not be presented for veterinary evaluation until they are mature or middle-aged. Affected animals are usually presented for examination because of unilateral forelimb lameness. Owners usually report a gradual onset of lameness that improves after rest and worsens after exercise. On physical examination, the shoulder should be palpated and moved through a complete range of motion. Crepitation or palpable swelling of the joint is seldom evident, but affected animals usually exhibit pain when the shoulder is moved into hyper-extension or extreme flexion. Often the examiner can detect muscle atrophy of the forelimb by loss of muscle mass adjacent to the spine of the scapula. Differential diagnoses include osteochondrosis, bicipital tenosynovitis, shoulder instability.
Despite apparent lameness in only one limb, both shoulders should be radiographed because this condition is often bilateral. Sedation may be required for quality radiographs particularly in large hyper-active dogs. The earliest radiographic sign of OCD is flattening of the caudal humeral head. This is due to thickening of the articular cartilage and deviation of the subchondral bone line. As the disease progresses, a saucer-shaped radiolucent area in the caudal humeral head may be visualized. Calcification of the flap may allow visualization of the flap either in situ or within the joint if it has detached from the underlying bone
Surgery is the treatment of choice in cases of OCD. Surgery can be accomplished via open arthrotomy or arthroscopically. We prefer to manage OCD arthroscopically; mobidity is decreased such that both shoulders can be operated (if bilateral). Details of the technique for open arthrotomy or arthroscopy can be reviewed in detail within textbooks related to canine surgery.
Hip dysplasia is an abnormal development of the coxofemoral joint. The syndrome is characterized by subluxation or complete luxation of the femoral head in the younger patient while in the older patient mild to severe degenerative joint disease is present. Laxity in the hip joint is responsible for the early clinical signs and joint changes. Subluxation stretches the fibrous joint capsule, producing pain and lameness. When the surface area of articulation is decreased, this concentrates the stress of weight bearing over a small area through the hip joint. Subsequently, fractures of the trabecular cancellous bone of the acetabulum can occur, causing pain and lameness. The cancellous bone of the acetabulum is easily deformed by the continual dorsal subluxation of the femoral head. This piston-like action causes a wearing of the acetabular articular surface from a horizontal plane to a more vertical plane causing subluxation to worsen. The physiologic response to joint laxity is proliferative fibroplasia of the joint capsule and increased thickness of the trabecular bone. This relieves the pain associated with capsular sprain and trabecular fractures. However, the surface area of articulation is still decreased causing premature wear of articular cartilage, exposure of subchondral pain fibers and lameness. (Fig.1 arthroscopic view of moderate DJD). There are two general recognizable clinical syndromes associated with hip dysplasia: (1) patients 5 to 16 months of age, (2) patients with chronic degenerative joint disease. Patients in group 1 present with lameness between 5 to 8 months of age. Symptoms include difficulty when rising after periods of rest, exercise intolerance and intermittent or continual lameness. The majority of young patients will spontaneously improve clinically around 15 to 18 months of age. This clinical improvement is due to pain relief as proliferative fibrous tissue prevents further capsular sprain, and increased thickness of the subchondral bone prevents trabecular fractures. If symptoms occur later in life, they may include difficulty in rising, exercise intolerance, lameness following exercise, atrophy of the pelvic muscle mass, and a waddling gait with the rear quarters. Physical findings in the younger group of patients include pain during external rotation and abduction of the hip joint, poorly developed pelvic muscle mass, and exercise intolerance. Hip exam performed under general anesthesia will reveal abnormal angles of reduction and subluxation reflecting excessive joint laxity.. Physical findings in the older group of patients include pain during extension of the hip joint, reduced range of motion, atrophy of the pelvic musculature, and exercise intolerance. Treatment is dependent upon the age of the patient, the degree of patient discomfort, physical and radiographic findings, client expectations of patient performance, and financial capability of the client. Conservative treatment is beneficial to a large number of patients in both the young and older patient groups. Conservative management is divided into acute management and long term management. When a dog exhibiting signs of hip dysplasia enters the clinic, it is generally because they have sprained the hip joint. The dysplastic joint is either hyperlax (young dog) or has a limited range of motion (mature dog). In either case, the joint is easily sprained and the dog that is presented with symptoms has overused (sprained) the hip joint. Rest, physical therapy, and non-steroidal analgesics will relieve signs in the majority of patients. Surgical intervention in the mature patient may be total hip replacement or femoral head ostectomy. Surgical intervention in the mature patient may be total hip replacement or femoral head ostectomy.