Bursae are fluid-filled sac-like cavities or potential cavities that are located where friction occurs (eg, where tendons or muscles pass over bony prominences). Bursae minimize friction between moving parts and facilitate movement. Some communicate with joints.
Bursitis may occur in the shoulder (subacromial or subdeltoid bursitis), particularly in patients with rotator cuff tendinitis, which is usually the primary lesion in the shoulder. Other commonly affected bursae include olecranon (miner's or barfly’s elbow), prepatellar (housemaid’s knee), suprapatellar, retrocalcaneal, iliopectineal (iliopsoas), ischial (weaver’s bottom), greater trochanteric, pes anserine, and first metatarsal head (bunion) bursae. Occasionally, bursitis causes inflammation in a communicating joint.
Bursitis may be caused by the following:
Idiopathic and traumatic causes are by far the most common. Acute bursitis may follow unusual exercise or strain and usually causes bursal effusion. The olecranon and prepatellar bursae are the bursae most often involved when an infection is present.
Chronic bursitis may develop after previous attacks of bursitis or repeated trauma. The bursal wall is thickened, with proliferation of its synovial lining; bursal adhesions, villus formation, tags, and chalky deposits may develop.
Acute bursitis causes pain, particularly when the bursa is compressed or stretched during motion. Swelling, sometimes with other signs of inflammation (eg, erythema), is common if the bursa is superficial (eg, prepatellar, olecranon). Swelling may be more prominent than pain in olecranon bursitis. Crystal- or bacterial-induced bursitis is usually accompanied by erythema, pitting edema, pain, and warmth in the area over the bursa.
Chronic bursitis may last for several months and may recur frequently. Bouts may last a few days to several weeks. If inflammation persists near a joint, the joint’s range of motion may be limited. Prolonged limitation of motion may lead to muscle atrophy.
Superficial bursitis should be suspected in patients with swelling or signs of inflammation over bursae. Deep bursitis is suspected in patients with unexplained pain worsened by motion in a location compatible with bursitis. Usually, bursitis can be diagnosed clinically. Ultrasonography or MRI can help confirm the diagnosis when deep bursae are not readily accessible for inspection, palpation, or aspiration. These tests are done to confirm a suspected diagnosis or exclude other possibilities. These imaging techniques increase the accuracy of identifying the involved structures.
If bursal swelling is particularly painful, red, or warm or if the olecranon or prepatellar bursa is affected, infection and crystal-induced disease should be excluded by bursal aspiration. After a local anesthetic is injected, fluid is withdrawn from the bursa using sterile techniques; analysis includes cell count, Gram stain and culture, and microscopic search for crystals. Gram stain, although helpful, may not be specific, and white blood cell counts in infected bursae are usually lower than those in septic joints. Urate crystals are easily seen with polarized light microscopy, but the apatite crystals typical of calcific tendinitis appear only as shiny chunks that are not birefringent. Cholesterol plate crystals can be seen in chronic rheumatoid bursitis.
Acute bursitis should be distinguished from hemorrhage into a bursa, which should be considered particularly when a patient taking warfarin develops acute bursitis. Hemorrhagic bursitis can cause similar manifestations because blood is inflammatory. Fluid in traumatic bursitis is usually serosanguinous. Cellulitis can cause signs of inflammation but does not normally cause bursal effusion; cellulitis overlying the bursa is a relative contraindication to bursal puncture through the cellulitis, but if septic bursitis is strongly suspected, aspiration must be done.
For crystal-induced disease, see treatment of gout.
For suspected infection, empiric antibiotics effective against S. aureus should be given initially (see treatment of staphylococcal infection). Subsequent choice of antibiotic is determined by results of Gram stain and culture. Infectious bursitis requires drainage or occasionally excision in addition to antibiotics.
Acute nonseptic bursitis is treated with temporary rest or immobilization and high-dose NSAIDs and sometimes with other analgesics. Voluntary movement should be increased as pain subsides. Pendulum exercises are helpful for the shoulder joint.
If oral drugs and rest are inadequate, aspiration and intrabursal injection of depot corticosteroids 0.5 to 1 mL (eg, triamcinolone acetonide 40 mg/mL) is the treatment of choice. About 1 mL of local anesthetic (eg, 2% lidocaine) can be injected before the corticosteroid injection. The same needle is used; it is kept in place and the syringes are changed. Dose and volume of the corticosteroid may vary according to the size of the bursa. Infrequently, a flare-up occurs within several hours of injection of a depot corticosteroid; the flare-up is probably a synovitis in reaction to crystals in the injection or to needle disruption of calcium deposits. It usually lasts ≤ 24 hours and responds to cold compresses plus analgesics. Oral corticosteroids (eg, prednisone) can be used to treat the primary problem if a local injection is not feasible.
Chronic bursitis is treated the same as acute bursitis, except that splinting and rest are less likely to help, and range-of-motion exercises are especially important. Rarely, the bursa needs to be excised.
The usual causes of bursitis are injury and overuse, but infection and crystal-induced disease are possible.
Withdraw bursal fluid to diagnose bacterial or crystal-induced bursitis when the olecranon or prepatellar bursa is affected or when there is warmth, redness, tenderness, and pitting edema.
If no infection is present, treat most cases with rest, high-dose NSAIDs, and sometimes intrabursal corticosteroid injection.