No abstract

Nine cases of septic bursitis are presented, and the literature on the subject comprehensively reviewed, with an emphasis on the clinical manifestations of septic bursitis in various anatomic locations. Physical activities associated with increased susceptibility to septic bursitis and systemic conditions that increase the severity of septic bursitis are catalogued. Analysis of the microbiology of cases reported in the literature demonstrates that greater than 80% of cases of septic bursitis are caused by Staphylococcus aureus and other gram-positive organisms. However, a wide variety of gram-negative microorganisms, fungi, and other infectious agents have been reported to cause septic bursitis and may lead to complications in diagnosis and treatment. The nine cases reported here demonstrate the potential severity of septic bursitis and emphasize that significant systemic complications may result from this common musculoskeletal infection. Indications for hospitalization and/or intravenous antibiotic therapy for septic bursitis include the presence of fulminant local infection, evidence for systemic toxicity, or infection in an immunocompromised patient. Patients who fail to respond to intravenous antibiotics and percutaneous aspiration of the bursa may require surgical drainage or bursectomy by one of several methods that have been proposed. There is some recent evidence that intrabursal corticosteroid injection for therapy of nonseptic subcutaneous bursitis may be more effective than systemic antiinflammatory medication or simple bursa aspiration.

Five cases of septic prepatellar and 20 cases of septic olecranon bursitis are reported. All were men, with a mean age of 47 years. Seventeen had a history of recent trauma to the affected limb or sustained pressure on knees or elbows, or both, required by certain occupations. Septic bursitis was not associated with septic arthritis and could be easily distinguished from it by the characteristic bursal swelling and joint examination. Septic bursitis was misdiagnosed as nonseptic bursitis in eight cases despite characterstic bursal fluid leukocytosis (greater than 1000 cells/mm3) and recovery of bacteria on culture. Staphylococcus aureus was identified in 22 cases; 76% were resistant to penicillin. Intravenous antibiotics and bursal fluid drainage were uniformly succesful. Oral antibiotic ttherapy was also successful unless the infection was extensive or there was underlying bursal disease. Early recognition, prompt therapy, and preventive measures are necessary to reduce the morbidity of septic bursitis.

To investigate the impact of synovial fluid volume on oxygen tension (Po,) and other metabolic correlates, 24 specimens of synovial fluid from the knees of 22 patients were analyzed for volume, number of leukocytes (WBC), pH, PO,, Pco,, glucose, protein, and complement (CH50) levels. Concurrent arterial blood samples were obtained in 21 instances. Synovial fluid Po, values varied inversely with volumes of synovial fluid (r = -0.54, P < 0.01), but when patients with rheumatoid arthritis were excluded, the correlation was more significant (r = -0.76, P c 0.001). When synovial fluid Po, dropped below 45 mm Hg, intraarticular acidosis resulted. The decrease in pH (r = 0.93, P < 0.001), the lowering of glucose values (r = 0.89, P < 0.001), and the rise in PCO, (r = -0.79, P < 0.01) can be explained by a shift toward anaerobic metabolism coupled with the impaired elimination of its products. Systemic acidosis and hypoxia were not found. Intraarticular hypoxia most likely represents circulatory imbalance at the level of the synovial membrane, although an inverse relationship of synovial fluid PO, and WBC was also noted. Complement and protein levels had no correlation with volume, pH, or respiratory gas tensions of synovial fluids. Our data support the importance of the effective blood Address reprint requests to George Ho, Jr., MD, Veterans Administration Medical Center, Davis Park, Providence, Rhode Island 02908.Submitted for publication July 8, 1980; accepted in revised form November 25, 1980 flow to the joint in maintaining homeostasis. The volume of synovial effusion and the compliance of the joint c a p sule appear to be important determinants of the articular blood supply.The study of synovial fluid respiratory gases began when easily reproducible measurements of pH, Po,, Pco2, and HCO, by blood gas analyzers became available. Several studies examined the diagnostic specificity of synovial fluid respiratory gases and their metabolic and histologic correlates (1-3). Most have shown that progressive hypoxia was associated with increased glucose consumption leading to lactate accumulation, bicarbonate consumption, acidosis, and hypercapnia. The lowest PO, and pH levels with the highest Pco2 and lactate levels were usually found in synovial fluids from adults with rheumatoid arthritis who had the most advanced histopathologic changes (2). The precise mechanism of intraarticular hypoxia is unknown, but a "circulatory-metabolic" imbalance was proposed and investigated by Goetzl et a1 in 1971 (4). The present study was undertaken to confirm the profound metabolic consequences of intraarticular hypoxia and to examine the influence of synovial fluid volume on respiratory gases in joint effusions of various causes. MATERIALS AND METHODSTwenty-four specimens of synovial fluid from 23 knee joints of 22 patients were obtained during diagnostic or therapeutic arthrocentesis. All patients were supine with the knee in maximal extension. The initial 2-3 ml were aspirated into a heparinized syringe and the remainder was remove...