Septic Bursitis

Septic bursitis usually arises in chronically inflamed superficial bursae after skin inoculation, while deeper bursae are more often seeded hematogenously. The key bedside challenge is separating septic bursitis from aseptic bursitis and from septic arthritis, then deciding when aspiration actually helps.

Diagnosing and Managing Septic Bursitis

• Typical pathogens and hosts: Staphylococcus aureus causes about 80% of septic bursitis, usually in patients with chronic bursitis, repetitive microtrauma, diabetes, gout, rheumatoid arthritis, or immunocompromise.
• Superficial versus deep spread: Prepatellar and olecranon bursae are usually infected from the skin, whereas iliopsoas and subacromial bursae more often reflect hematogenous spread, a distinction that matters clinically.
• Bedside clues to infection: Redness and swelling alone do not prove infection, but fever, malaise, and a warmer bursa than surrounding skin raise concern; one study found a surface temperature difference over 2.2 C highly predictive.
• Separating bursa from joint: Pain with passive range of motion, axial loading, or tenderness through the full arc points toward septic arthritis rather than isolated bursitis; ultrasound helps localize the effusion. We get into the ultrasound distinctions in the episode.
• Aspiration through erythema: Unlike arthrocentesis, overlying erythema is not necessarily a contraindication to bursal aspiration if a fluid collection is present, and ultrasound guidance can support a safer longer-track approach.
• Fluid testing and treatment debate: Bursal WBC counts above 2000 cells/µL, PMN predominance, low glucose, and a positive Gram stain support septic bursitis, but whether uncomplicated cases need aspiration before antibiotics remains unsettled. We walk through that management controversy in the chapter.