Current treatment options for elbow disease (Proceedings)
Traumatic Fragmented Medial Coronoid Process
Traumatic fragmented medial coronoid process (TFMCP) is a condition in the elbow joint of dogs that appears to occur commonly in performance dogs. Unlike the classic condition of fragmented medial coronoid process (FMCP) affecting the elbow joints of skeletally immature large to giant breed dogs, jump down syndrome (TFMCP) appears to have no age or size limitations.
CauseThe cause and pathogenesis of TFMCP are poorly understood. It is possible that abnormal repetitive loading, such as landing from a jump, hitting contacts or a flyball box, and so on, may lead to microfractures of the bone underneath the cartilage (subchondral fractures). Additionally, increased repetitive loading can arise from contraction of the biceps/ brachialis muscle complex. When the biceps/brachialis contracts, a force is generated that rotates the medial coronoid into the radius. These microcracks disturb the mechanical properties of bone, and if not repaired properly through normal body mechanisms, fatigue fractures develop. Additionally, loss of osteocytes (bone cells), indicated by decreased osteocyte densities, has been strongly associated with the presence of microdamage after fatigue loading. These studies imply that excess load may lead to fatigue microdamage of the subchondral trabecular bone and eventual fracture, which we believe may play an important role in the pathogenesis of TFMCP. Dogs may be further predisposed to this condition if they have elbow dysplasia. Dogs with elbow dysplasia had asymmetric growth of the radius and ulna during development, resulting in elbow joint incongruity. Elbow incongruity such as radioulnar step defects, humeroulnar incongruence/conflict, and varus deformity of the humerus causes abnormal contact patterns in the elbow, specifically at the coronoid trochlear articulation, which is theorized to increase the load on the medial coronoid process (MCP). Regardless of the etiology, if left untreated as a continual lameness, secondary osteoarthritis may progress as noted by damage to the cartilage such as softening, fibrillation, fissuring, and erosions as well as additional subchondral bone microcracks and fragmentation. The free fragments contribute to frictional abrasion ("kissing lesions") of the opposing surface including the medial aspect of the humeral condyle and radial head.
History and Clinical Signs
Dogs with TFMCP may present with a history ranging from a subtle intermittent offloading of the forelimb to significant unilateral or bilateral forelimb lameness. This lameness is typically exacerbated with exercise and heavy activity. The onset of lameness is insidious. As lameness persists, it may increase in severity. Affected dogs often place the carpus in an exaggerated valgus position (turned out) when sitting or standing, and circle the foreleg outward and move the elbow away from the midline (circumduct the antebrachium and abduct the elbow) during the swing phase of the stride. The history of dogs with TFMCP typically includes a lack of response to rest and non-steroidal anti-inflammatory drugs (NSAIDs). Many dogs with TFMCP are mistakenly treated for shoulder pathology because the attending veterinarian elicits a pain response when the shoulder is extended. The authors believe the pain response actually arises from the elbow because when the veterinarian performs an extension maneuver of the shoulder, the elbow is usually simultaneously extended. Extension of the shoulder and elbow causes tension in the biceps/brachialis muscle complex. Tension in the biceps/brachialis exerts pressure on the medial coronoid and overlying inflamed joint capsule causing the pain response.
On physical examination discomfort is usually noted on direct palpation of the medial compartment of the elbow joint, specifically the medial coronoid process. Discomfort may also be noted on hyperflexion of the elbow. Most dogs with TFMCP are reluctant to allow for full endrange flexion. In chronic cases, full flexion may not be obtained. Crepitus may be noted when placing the elbow through range of motion. Some investigators suggest that the carpus should be placed in a flexed, externally rotated position while the elbow is extended. Joint effusion may be detected as a fluctuant swelling beneath the lateral or medial epicondyle of the humerus. Depending on the chronicity, atrophy may be noted in the affected forelimb.
In addition to history, gait analysis, physical examination, orthopedic and neurologic examinations, further diagnostic tests used to differentiate causes of elbow pathology currently consist of hematology, biochemical profile, urinalysis, arthrocentesis, imaging modalities, and arthroscopy. Unfortunately, radiographs have been shown to be of little value because of difficulty identifying the fragment or line of separation using standard radiography. In some chronic cases, however, radiographs may reveal secondary evidence of bony remodeling consistent with osteoarthritis. These changes may include sclerosis within the ulnar notch, and remodeling along the anconeal process and MCP. Advanced diagnostic imaging modalities such as CT scans, MRI, nuclear scans, and arthroscopy may allow confirmation of the condition. Arthroscopic evaluation of the elbow joint allows direct observation of all major intra-articular structures with magnification, "dynamic" evaluation of tissues during elbow range-of-motion tests, and "palpation" of intra-articular tissues using arthroscopic instrumentation. Arthroscopic exploration of the elbow provides a definitive diagnosis of TFMCP when a fragment or cartilage fissure. In a small percentage of cases, advanced imaging (nuclear scan, CT, MRI) indicates fragmentation of the coronoid but arthroscopic observation does not reveal a fissure or fragment. In such cases, the fissures (microcracks) are believed to be within the coronoid bone beneath the cartilage surface.