Elbow Tendinopathies: Triceps Tendon Rupture and Snapping

Anatomy

The anatomy of the attachment of the triceps has not been thoroughly studied. Confluence of the three heads forms a common tendon that inserts at the olecranon with a footprint that is about 2 cm in diameter ( Fig. 65.1 ). Medial and, more importantly, lateral expansion in the form of the anconeus provide some active extension, which makes the diagnosis somewhat difficult due to the residual extension strength that exists, even with complete rupture of the central tendon.

Demographics and Pathology

Triceps tendon rupture is a rare situation, representing less than 1% of all tendon injuries. Hence a high index of suspicion is required to make an early diagnosis. The male-to-female ratio is 7 : 1, and the dominant extremity is affected approximately 60% of the time. In the largest series to date, the average age of injury was 47 years old, but rupture has also been reported in a large spectrum of age, ranging from children and adolescents in whom the olecranon physis has just closed to individuals in the eighth decade of life. Injury to the extensor mechanism may be in one of three locations. The typical injury pattern is avulsion of the tendon, and though greater than 90% of the injuries occur at the olecranon, the entire mechanism is rarely disrupted. Detachment of the central third of the tendon is the most common lesion. Failure at the musculotendinous junction has occasionally been reported.

History

Triceps tendon injuries usually occur in the fourth to fifth decades of life and may be associated with predisposing conditions. These include chronic olecranon bursitis, systemic disease, such as renal osteodystrophy or secondary hyperparathyroidism, systemic lupus erythematosus, chronic acidosis, Marfan syndrome, and osteogenesis imperfect tarda. Medications such as steroids and fluoroquinolone can cause tendinopathy and thus increase the risk of tendon rupture. Musculotendinous junction injuries are associated with diabetes. With underlying or predisposing pathology, these patients may report minimal trauma but with some prodromal symptoms.

The mechanism of injury is typically an eccentric load applied to the triceps tendon; blunt or penetrating trauma to the posterior elbow is less commonly reported.

The athletic population is also at risk for triceps injuries, especially in powerlifters/bodybuilders and handball players. The injury in the athletic population is commonly due to overuse. Anabolic steroid abuse, errors in technique, and skeletal immaturity place the bodybuilder at an increased risk of rupture. The injury in the powerlifter population may be associated with a hematoma and can cause ulnar nerve compression. Overuse injuries can also be seen in patients who are wheelchair or transfer dependent.

Triceps rupture is less commonly reported after fractures, often related to exposure of fixation. Finally, deficiency or rupture of the triceps mechanism after total elbow replacement, especially after infection, is common and is discussed elsewhere in this book (see Chapter 102 ).

Pathology

Greater than 90% of the injuries occur at the olecranon, and the entire mechanism is rarely disrupted. Detachment of the central third of the tendon is the most common lesion. Failure at the musculotendinous junction has occasionally been reported.

Associated injuries have also been reported. Several instances of concurrent fracture of the radial head have been noted, and a report of six such injuries suggests that the association may be more common than is appreciated. One of the authors (RvR) has treated a case of triceps tendon rupture with a concomitant capitellar injury, and a report of a distal radius fracture along with fracture of the radial head supports one mechanism of injury being a fall on the outstretched hand.

Diagnosis of Acute Ruptures

In the acute rupture, a history of acute pain and weakness in extension with swelling, bruising, or ecchymosis seen on inspection is the most reliable method of making this diagnosis. Patients usually report a mechanism consistent with an eccentric load suddenly placed on the triceps, though with certain predisposing conditions a low-energy mechanism may precipitate the rupture. Typically there is no deformity evident from gross inspection because the medial and lateral extensions of the extensor mechanism usually remain intact. Occasionally a defect will be observed at the site of attachment ( Fig. 65.2 ). The pain from a partial rupture usually does not cause major functional limitations. Hence the presentation may be delayed for days, weeks, or months, and occasionally after the partial rupture progresses to a complete rupture.

Palpation focuses on the central tendinous attachment and will reveal a deficiency with full ruptures. In the acute setting this will be variably painful so it must be done gently. If the rupture is partial thickness a defect may not be present. Further examination usually demonstrates a full arc with minimal pain, especially with passive motion. However, full flexion usually does elicit pain. In a full-thickness rupture, extension against gravity or resistance will be very difficult or impossible and is painful. If weakness is not obvious, resisted extension with the elbow flexed past 90 degrees and comparison with the opposite extremity is helpful to define the deficiency. Finally, a modified Thompson test used for Achilles tears can be performed by squeezing the triceps muscle with the forearm supported. Lack of extension is suggestive of the diagnosis.