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Submitted by: Nathan Wei
Before the days of antibiotics, septic bursitis was a potentially life-threatening problem.
Nowadays, because of higher index of suspicion as well as the presence of antibiotics, it should be, in most case, readily treatable. This article discusses this problem.
A bursa (plural=bursae) is a sack containing a small amount of fluid that serves as a protective cushion between bones and overlying muscles or between bones and tendons. Bursitis is inflammation of a bursa caused by repetitive use, trauma, infection, or a systemic inflammatory disease.
These sacks are lined with the synovium the same tissue that lines the inside of joints. Humans have approximately 160 bursae.
Bursitis most commonly affects the shoulder, elbow, hip, and knee. Symptoms of bursitis may include localized tenderness, edema, redness, heat, and limited ability to move the affected area.
When a bursa becomes infected, the condition is referred to as septic bursitis. In septic bursitis, trauma is the usual culprit. Trauma causes inoculation of bacteria into the bursa, which triggers an inflammatory response.
The two most commonly infected bursae are the olecrenon bursa at the elbow and the prepatellar bursa in the knee. The reason these two bursae get infected more easily is because of their location.
The olecranon bursa lies at the tip of the elbow. Because of its superficial location, it is easily traumatized from acute trauma or repetitive stress.
Trauma to the skin makes the olecranon a frequent location for infectious bursitis. The risk of septic bursitis increases in those who have a history of another chronic disease.
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Chronic repetitive stress from pressure on the elbows is seen in hemodialysis patients, computer users, and chronic lung disease patients.
When inflamed, the olecrenon bursa at the tip of the elbow becomes swollen, red, and painful. Bending the elbow makes the pain worse. Low grade fever and chills may also be present.
The prepatellar bursa lies in front of the knee between the patella (kneecap) and the skin.
Infection can develop due to either trauma or constant friction between the skin and the patella, most commonly when frequent kneeling is involved. It can be seen in carpet-layers, coal miners, roofers, gardeners, electricians, and plumbers. Actually any activity involving a lot of kneeling and friction can lead to septic prepatellar bursitis.
The superficial location of the prepatellar bursa allows for rather easy introduction of bacteria. This is similar to the situation involving the olecrenon bursa.
Prepatellar bursitis presents with swelling, redness, heat, and pain involving the front of the knee. Bending the knee causes increased pressure over the bursa and increases pain.
(A quick note: there is also another bursa called the infrapatellar bursa. It is located below the knee cap and may be confused with the prepatellar bursa).
As mentioned earlier, septic bursitis occurs from the introduction of bacteria through trauma. It can also occur from the spread of infection from the skin adjacent to a bursa. Skin infection is called cellulitis.
It is less likely for deeper bursae to become infected because of their location. This can occur as a result of spread from septic arthritis (an infected joint) or from bacteria carried to the bursa from the blood.
Predisposing factors include diabetes, alcoholism, steroid therapy, kidney disease, trauma, and skin disease. A history of noninfectious inflammation of the bursa (as seen in rheumatoid arthritis, gout, and pseudogout) also increases the risk of septic bursitis.
Signs that favor the diagnosis of septic over simple inflammatory bursitis include: severe tenderness, extreme redness, heat, fever, and chills.
Laboratory tests may show an increase in white blood cell count and erythrocyte sedimentation rate. Blood cultures should be obtained if deep bursal infection is suspected.
Aspiration and analysis of bursal fluid from a suspected infected bursa should be performed when possible. Certainly, the most frequently infected bursae, such as the olecranon and prepatellar bursae should undergo this procedure. The use of ultrasound makes aspiration much more accurate.
Bursal fluid culture is the most important test for diagnosis.
Fluid should also be examined for crystals. Monosodium urate crystals can be seen in gout and calcium pyrophosphate crystals can be seen in pseudogout; however, the presence of crystals does not exclude concomitant infection.
All fluid should be cultured.
Patients with suspected septic bursitis should be treated with antibiotics while awaiting culture results. Superficial septic bursitis can be treated with oral antibiotics.
Deep bursal infection will generally require intravenous antibiotics.
Staph aureus is the most common bacteria, causing more than 80% of cases. Streptococcal species account for 5-20% of cases. Other organisms are less common.
An appropriate antistaph antibiotic should be started. This should be a penicillinase-resistant penicillin, such as oxacillin sodium (Bactosill), or a first-generation cephalosporin, such as cefaclor (Ceclor). Penicillin allergic patients can be treated with erythromycin.
The length of antibiotic treatment varies with the patient and the clinical situation. Uncomplicated septic bursitis presenting within a week of infection should be treated with a 10-14 day course. Aspiration should be repeated every 1-3 days while antibiotics are being administered. Antibiotics should be continued for 5 days past sterilization of bursal fluid as seen by aspiration. Again, the use of ultrasound can help with fluid detection since aspiration of a bursa without fluid may yield very little valuable material.
Patients who are immunosuppressed require a longer course of treatment of at least 15 days.
Deep bursal infections require prolonged antibiotic therapy and surgery is often required.
Surgical intervention, such as incision and drainage is needed in complicated cases.
About the Author: Nathan Wei, MD FACP FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland. He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine. For more info:
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