Lateral epicondylitis (tennis elbow), a familiar term used to described a myriad of symptoms about the lateral aspect of the elbow, occurs more frequently in nonathletes than athletes, with a peak incidence in the early fifth decade and a nearly equal gender incidence. Lateral epicondylitis can occur during activities that require repetitive supination and pronation of the forearm with the elbow in near full extension. Runge first described the clinical entity in 1873, and since then almost 30 different conditions have been proposed as etiologies. Although originally described as an inflammatory process, the current consensus is that lateral epicondylitis is initiated as a microtear most often within the origin of the extensor carpi radialis brevis. Microscopic findings demonstrate immature reparative tissue that resembles angiofibroblastic hyperplasia. The pathological process mainly involves the origin of the extensor carpi radialis brevis but can involve the tendons of the extensor carpi radialis longus and the extensor digitorum communis.
The diagnosis of tennis elbow is made by localizing discomfort to the origin of the extensor carpi radialis brevis. Tenderness is present over the lateral epicondyle approximately 5 mm distal and anterior to the midpoint of the condyle. Pain usually is exacerbated by resisted wrist dorsiflexion and forearm supination, and there is pain when grasping objects. Plain roentgenograms usually are negative; occasionally calcific tendinitis may be present. MRI demonstrates tendon thickening with increased T1 and T2 signals but generally is not indicated.
Other entities that can produce pain in this general vicinity are osteochondritis dissecans of the capitellum, lateral compartment arthrosis, varus instability, and perhaps most commonly, radial tunnel syndrome. Radial tunnel syndrome is a compressive neuropathy of the posterior interosseous nerve caused by any of four different anatomical structures in the radial tunnel, including a fibrous band near the anterior aspect of the radial head, a vascular leash of the recurrent radial artery, the distal extensor carpi radialis brevis tendon margin, or the supinator margin at the arcade of Frohse. The pain of radial tunnel syndrome is located 3 to 4 cm distal to the lateral epicondyle and may be reproduced with long finger extension against resistance. The latter finding is inconsistent, as are abnormalities on EMG. True lateral epicondylitis and radial tunnel syndrome may coexist in up to 5% of patients.
Regardless of the underlying cause, nonoperative treatment is successful in 95% of patients with tennis elbow. Initial non-operative treatment includes rest, ice, injections, and physical therapy centered around treatment such as ultrasound, iontophoresis, electrical stimulation, manipulation, soft tissue mobilization, friction massage, stretching and strengthening exercises, and counter-force bracing.
A few patients (5% to 10%) are unresponsive to conservative treatment. Patients who fail to respond to a nonoperative regimen should be scrutinized for possible sources of secondary gain, perhaps through the Minnesota Multiphasic Personality Inventory (MMPI) or psychological evaluation, if other maladies in the differential diagnosis have been excluded. In some patients, one or two local injections of a steroid preparation to the area of maximal tenderness are helpful. About 40% of patients obtain complete and permanent relief of symptoms after steroid injections. Other studies also have shown a high rate of success using early local corticosteroid injection. As an adjunct to local injection an attempt to “complete the lesion” by forcibly flexing the wrist after local anesthetic injection to initiate the inflammatory cascade and induce healing can be done. Preliminary data from studies reporting newer treatment methods such as low-level laser and extracorporeal shockwave therapy are promising, but further investigation is necessary.
If prolonged (6 to 12 months) nonoperative treatment is ineffective, operative treatment may be considered; it is effective in 90% of properly selected patients. Some have advocated manipulation under anesthesia, especially in patients with concomitant flexion contractures. The technique involves sudden, forcible, full extension of the elbow with the wrist and fingers flexed and the forearm pronated to place the extensor carpi radialis brevis and extensors under tension. An audible, palpable snap frequently can be elicited, and the results can be excellent.
A number of surgical procedures have been described for the treatment of tennis elbow. The technique popularized by Boyd and McLeod included excision of the proximal portion of the annular ligament, release of the entire extensor origin, excision of an adventitious bursa originally described by Osgood (if found), and resection of hypertrophic synovium in the radiocapitellar articulation, as originally described by Trethowan.
Currently, many surgeons favor a more limited approach, which consists of exposure of the diseased extensor carpi radialis brevis origin, resection of degenerative tissue, and direct repair to bone.
Only a few patients with lateral epicondylitis (1% to 2%) cannot be treated successfully by either nonoperative or operative methods. Morrey divided these failures into two groups based on postoperative symptoms. Patients in the first group had symptoms similar to those experienced before surgery, whereas patients in the second group reported a different symptom complex after surgery. Treatment failed in patients in the first group because of inadequate release or incorrect initial diagnosis, most often related to radial tunnel syndrome; in the second group, treatment failed because of capsular or ligamentous insufficiency that resulted in either a capsular fistula or posterolateral instability. Elbow instability can occur in patients in either group (especially those with traumatic origins for their lateral elbow pain) after overzealous release that includes the anterior band of the lateral collateral ligament. Of 13 patients with failed primary lateral release in Morrey’s study, reoperation was successful in 11 after the correct diagnosis was made. Morrey emphasized the importance of obtaining a thorough history to determine if the patient’s symptoms have changed and a careful physical examination to identify instability, pain in the region of the epicondyle, or radial tunnel syndrome. These should be supplemented with arthrograms to detect synovial fistula and capsular insufficiency or with arthroscopy and examination with the use of anesthesia to detect instability or arthrosis.
According to most authors, patients who will improve after surgery do so within 3 to 4 months. Repeat intervention may be considered in one year if symptoms do not improve.
Medial epicondylitis is similar to lateral epicondylitis although much less common and more difficult to treat. The origin of the flexor carpi radialis and pronator teres (flexor pronator mass) are commonly involved and less typically, the flexor digitorum superficialis and flexor carpi ulnaris. This entity must be differentiated from ulnar nerve neuropathy and medial collateral ligament instability. Ulnar neurapraxia exists in about 60% of his patients with medial epicondylar symptoms, but in our experience this is much less common.
Medial epicondylitis frequently occurs in overhead athletes, including those involved in racket sports and others who participate in activities that create a valgus force at the elbow. Physical examination usually reveals pain along the medial elbow that becomes worse on resisted forearm pronation or wrist flexion. The area of maximal tenderness is approximately 5 mm distal and anterior to the midpoint of the medial epicondyle. Loss of range of motion and a flexion contracture may be present.
Roentgenograms usually are normal, but medial ulnar traction spurs and medial collateral ligament calcifications may be seen and may be associated with a chronic ulnar collateral ligament injury.
Conservative treatment is the mainstay of management. NSAIDs, splinting, and an occasional steroid injection provide sustained relief in most patients. If nonoperative treatment fails, excision of the diseased tendon origin and reattachment usually are successful. Techniques range from a percutaneous release to open debridement with or without release of the flexor pronator origin. Vangsness and Jobe described release of the flexor pronator origin, excision of the pathological tissue, and reattachment of the flexor pronator origin to bleeding bone. Nirschl preferred excising the pathological tissue of the flexor-pronator origin in a manner that leaves normal tissue intact and repairing the subsequent defect. The ulnar nerve should be decompressed and transposed in patients who have ulnar nerve symptoms preoperatively. Epicondylectomy also can be done, but no more than 20% of the ulnar collateral ligament. Overall, the results are not as successful as with lateral epicondylar procedures.
Acute or chronic irritation may result in swelling and pain in the olecranon bursae. Aspiration often relieves the pain and swelling, but care should be taken to use proper sterile technique. When the aspirate is not bloody, cell counts and cultures should be obtained. Gout, rheumatoid arthritis, and infection must be excluded. After aspiration, a compressive wrap is applied and is usually sufficient to prevent reaccumulation of the fluid. Elbow pads may be needed to prevent further injury and recurrences. Chronic cases of recurrent olecranon bursitis with fibrosis of the bursae may require surgical excision.