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Evaluating forelimb lameness in juvenile dogs


Find out which conditions are most likely and get general guidance on their diagnosis and treatment. (Part 1 of a 2-part series)

Lameness is a common malady in young dogs. Numerous differential diagnoses exist for lameness, but when you're looking for "horses rather than zebras," the list becomes quite short.

The first step in diagnosing any lameness is localization. Observe the animal's gait at a walk and run. Palpate the limbs in standing (weight-bearing allows for better assessment of joint effusion) and recumbent positions.

This article, the first in a two-part series reviewing lameness in juvenile dogs, reviews common conditions of the forelimb. See Table 1 for an overview of assessing juvenile dogs exhibiting forelimb lameness. (And see the Related Links below for Part 2 of the series.)

Table 1 Keys to identifying the cause of lameness in juvenile dogs


Lameness localized to the limb in general could be panosteitis, which affects the long bones of large- and giant-breed dogs at 5 to 18 months of age. It results in acute lameness and pain on palpation of the long bones. Its cause is largely unknown.

Panosteitis is characterized by endosteal new-bone formation, giving affected long bones the radiographic appearance of an increased and blotchy density of the medullary canal. The condition can affect multiple bones concurrently or sequentially. Treatment includes supportive care, analgesics and time. Panosteitis tends to be self-limiting but can recur, although it is unlikely to do so in the same limb.

Hypertrophic osteodystrophy

Localization to the distal metaphysis of the long bone in large- and giant-breed dogs that are 3 to 5 months old should lead you to consider hypertrophic osteodystrophy (HOD), an uncommon disease of unknown etiology characterized by marked necrosis, inflammation and hemorrhage in the metaphysis adjacent to the physis. These changes lead to the radiographic appearance of a pseudo or double physis seen at the distal aspect of the long bones and are pathognomonic for HOD (Figure 1).

Figure 1: A radiograph of the antebrachium in a young dog with hypertrophic osteodystrophy (HOD). Note the arrows pointing to the double or pseudo physis of the distal radius and ulna that is pathognomonic for this condition.

Affected dogs exhibit acute onset of swelling over the distal limbs, severe pain, anorexia and fever. The standard treatment for HOD includes supportive care, nutritional support and analgesics. Peracute and severe cases may benefit from a short course of corticosteroids. Antibiotics may be used to treat secondary infections (a specific infectious cause for HOD has not been identified, nor has a specific pathogen been isolated in these cases). Mild cases often spontaneously resolve. HOD is a self-limiting disease, and recurrence is rare.

Keep in mind that, as with panosteitis, it is unlikely HOD will recur in a single limb. So if recurrent single-limb lameness is noted in a young dog, further evaluation for other possible causes of the lameness is warranted.

Elbow dysplasia

Lameness localized to the elbow joint is usually the result of elbow dysplasia. The term dysplasia is used to define osteoarthrosis of the elbow resulting from one or more of the following: incongruence, ununited anconeal process, fragmented coronoid process or osteochondritis dissecans (OCD) of the humeral condyle. Elbow dysplasia is a polygenetic heritable disease in which one proposed pathogenesis includes incomplete ossification or bony fusion of the anconeus or medial coronoid process to the rest of the ulna. Premature distal antebrachial growth plate closure also can lead to joint incongruence and abnormal wear on articular surfaces.

Elbow dysplasia is common in rottweilers, Bernese mountain dogs, German shepherds, Labrador and golden retrievers and Newfoundlands 5 to 10 months old. Signs include intermittent or persistent weight-bearing forelimb lameness, a head-bobbing gait, decreased range of motion and joint effusion. Affected dogs often have an elbows-out stance. Most dysplastic dogs have bilateral disease. Radiography and computed tomography are used for diagnosis (Figure 2).

Figure 2: Radiographs of a young dog with elbow dysplasia-lateral (top left), cranio­caudal (top right) and hyperflexed lateral (immediately above) views are recommend­ed. Note the osteophytes associated with the head of the radius and along the anco­neal process, the sclerosis of the ulnar notch and incongruence present and the small osteochondritis dissecans (OCD) lesion on the medial humeral condyle indicated by the arrow.

Treatment can be medical or surgical but often involves both. Medical management consists of weight control, controlled exercise and administration of NSAIDs, analgesics and chondroprotectives. Surgical management includes either open or arthroscopic exploration of the joint, removal of fragments and débridement of fibrillated or malacic cartilage. It is imperative that surgical treatment be followed with good medical management.

All dogs with elbow dysplasia develop arthritis over time and eventually demonstrate some degree of lameness. All will require medical arthritic management for their lifetimes. Surgery is most helpful when dogs are young and still growing and have minimal or no arthritis. Arthroscopy provides a minimally invasive means to explore the joint and treat several components of elbow dysplasia with generally greater success than conventional surgical techniques.

Osteochondritis dissecans

The most common cause of forelimb lameness localized to the shoulder is OCD, which results from a disturbance of articular or epiphyseal cartilage growth characterized by slow ossification of deep zone cartilage, leading to thickened, poorly nourished articular cartilage susceptible to trauma experienced with normal weight-bearing. A dissection lesion develops between the subchondral bone and articular cartilage, resulting in the characteristic flap.

Figure 3: A lateral radiograph of the shoulder in a young dog demonstrating flattening of the caudal humeral head consistent with shoulder OCD (arrow). This view is best obtained under sedation to facilitate positioning so that the shoulder is not superimposed over the thorax and sternum.

OCD affects large-breed dogs, including Labradors and golden retrievers, rottweilers, Saint Bernards, German shepherds and Bernese mountain dogs, that are 5 to 10 months old. Most dogs with shoulder OCD have bilateral disease. Signs include forelimb lameness, adduction of the elbow, muscle atrophy over the scapula and pain with flexion and extension of the shoulder. The typical radiographic appearance is that of flattening and sclerosis of the caudal humeral head (Figure 3).

Figure 4: An arthroscopic image of the caudal humeral head with large OCD flap.

Treatment involves débridement of the cartilage flap and fragmented, malacic cartilage, followed by débridement of the lesion to the subchondral, bleeding bone via an open arthrotomy or arthroscopy (Figure 4). Arthroscopy provides a minimally invasive means to explore the entire shoulder joint, remove the cartilage flap and débride the cartilage defect with generally more rapid recovery than conventional surgical techniques. The prognosis for a dog with an appropriately treated shoulder OCD is good, and clinically significant osteoarthritis in the future is uncommon.

In part two of this series, I will review common causes of lameness in the hindlimb.

Dr. Janice Buback is a surgeon with Lakeshore Veterinary Specialists in Port Washington, Glendale and Oak Creek, Wis. She and her family, including Angus and Pinot (a.k.a. "Steak and Wine"), enjoy working and playing in southeast Wisconsin.

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