Olecranon And Prepatellar Bursitis

Clinical appearance

Olecranon bursitis causes an easily detectable saccular swelling at the tip of the elbow. The sac may or may not be tender, warm, or red. Surrounding edema may be present, and pitting edema may extend down the back of the forearm distally to the dorsum of the hand. In acute cases elbow flexion is limited by pain over the bursa. Passive extension, however, is always full and pain free. This differentiates acute olecranon bursitis from acute elbow synovitis which results in semiflexion of the elbow. Olecranon bursitis may be caused by trauma, bacterial infection, gout, rheumatoid arthritis, and many other conditions. Traumatic bursitis usually results from recurrent microtrauma, such as undue leaning on the elbow, but rarely by a memorable trauma. Septic bursitis is caused by direct penetration of skin bacteria, with only the occasional case resulting from hematogenous spread. Hence, the etiology is predominantly staphylococcal (80%) or streptococcal (17%). In the United States, the staphylococci grown from bursal fluid are almost always resistant to penicillin. Bursal gout occasionally occurs before articular gout, and some gout patients have recurrent gouty bursitis rather than arthritis. Rheumatoid involvement of the olecranon bursa usually occurs because of intrabursal discharge of necrotic nodules from the bursal wall, a common site for rheumatoid nodules.

Differential diagnosis

It is usually not difficult to distinguish olecranon bursitis from other processes that affect the posterior elbow. Occasionally, surrounding cellulitis from bursal rupture or infection may be so intense that confusion with septic arthritis is possible. The physical finding of an unrestricted passive joint extension strongly supports a diagnosis of bursitis. Although these cases are almost always septic, similar findings may occur with gouty or traumatic bursitis. Superficial bursae have only a limited capability to respond to inflammatory stimuli, and it is not unusual for the leukocyte count in cases of septic bursitis to be in the range of 5-10,000/mm3, especially in early cases. Thus, a relatively clear fluid in no way rules out bacterial infection or gout. Samples should be routinely sent for leukocyte count and differential, polarizing microscopy, Gram stain, and aerobic culture. Additional studies such as anaerobic, fungal, and mycobacterial cultures should be obtained in immunosuppressed patients. Septic bursitis can be tentatively diagnosed and empirically treated pending culture results (Table 6). Rapid improvement with antibiotics, even with negative cultures, points to a bacterial etiology. A bacterial etiology can be proven only by culture; however, Gram stains are negative in over 50% of cases, and bacterial growth is often sparse and may be delayed several days because of low bacterial counts.

Treatment

Traumatic olecranon bursitis is unsightly but harmless. Protecting the bursa from further pressure results in spontaneous recovery within 3 months. Once infection has been excluded by a negative bursal fluid culture, the bursa may be injected with 20 mg of methylprednisolone acetate (14). Methylprednisolone acetate is preferable to triamcinolone hexacetonide, as skin atrophy and secondary infection have been described with the use of the latter (15). The bursal fluid is usually resorbed within a week. Septic bursitis in the olecranon bursa in a nonimmunocompromised patient may be treated with daily aspiration and 500 mg of oral dicloxacillin every 6 hours or 500 mg of cephalexin every 6 hours until the fluid culture reverts to negative, usually within 7-10 days. In patients with penicillin or cephalosporin allergy, vancomycin or another antibiotic that is bactericidal to staphylococcal and streptococcal species may be used. Older and immunocompromised patients as well as patients with prepatellar septic bursitis are best treated with parenteral antibiotics initially, and duration of treatment should be at least 2 weeks. Sterile bursal effusions occur in approximately 30% of patients who have completed antibiotic therapy. They do not signify recurrence of infection and are best left untreated. Gouty bursitis is treated in the same manner as acute gouty arthritis.

Role of the primary care physician

The key steps to diagnosis are aspiration and submission of the bursal fluid for cell count, differential, polarizing microscopy, and culture. Primary care physicians can treat traumatic and gouty bursitis. Septic bursitis, especially of the prepatellar bursa, is more complicated, and patients should be referred for specialist care.

Key issues

It is important to watch for infection. Intrabursal corticosteroids should not be administered unless the bursal fluid culture report is negative. Corticosteroid infiltration will expedite recovery in traumatic bursitis, a self-resolving condition.