Septic bursitis is defined as an infection with the accumulation of pus within the sac-like structures which lie between the skin and bone or between the tendons, ligaments, and bone. It may be primary due to direct bacterial inoculation through a cutaneous wound or spread of local cellulitis or secondary to hematogenous spread of infection.
Bursae are sac-like structures which either lie superficially between the skin and bone or are located deeply between the tendons, ligaments, and bone. Inflammation of bursae could be septic (with the formation of pus) or non-septic. Septic bursitis (SB) is commonly encountered in the superficial bursae e.g. olecranon and prepatellar bursae. In a majority of the cases, SB follows direct inoculation of traumatic superficial cutaneous wounds or contiguous spread of infection from local cellulitis  . Rarely, deep bursae e.g. subacromial and iliopsoas bursae may get infected secondary to hematogenous spread of micro-organisms e.g. in septic arthritis, bacteremia, bacterial endocarditis. Micro-organisms implicated in SB are Staphylococcus aureus in a majority of the cases followed by streptococci, mycobacteria (both tuberculous and nontuberculous strains), fungi (Candida), and algae (Prototheca wickerhamii) . The incidence of SB is reported to be higher in men . Risk factors for SB include loss of skin integrity, impaired response to infection (eg, diabetes mellitus, alcohol abuse), and autoimmune conditions that lead to an increased amount of bursal fluid or tissue (such as rheumatoid arthritis or tophaceous gout)   .
Clinical presentation may help to differentiate between septic from nonseptic bursitis. SB is almost always associated with symptoms of pain, swelling, and fever  while non-septic bursitis is associated with only swelling . Erythema is present in both SB and non-SB . Other symptoms include local tenderness and a history of repeated trauma or movement. Concomitant symptoms of systemic comorbid conditions like syphilis or pulmonary tuberculosis, bacterial endocarditis may also be present.
Although the diagnosis of SB is not based on the clinical presentation, it may be suspected in presence of fever, and bursal inflammation as these symptoms are less severe in non-SB. Also, joint mobility is usually preserved in SB while it is limited in other types of bursitis. A detailed history to exclude trauma, occupation injury, comorbid medical conditions (rheumatoid arthritis, gout, diabetes mellitus, syphilis, HIV) should be obtained. A thorough physical examination needs to be performed to look for signs of inflammation locally as well as to exclude bacteremia. Routine laboratory blood work may reveal leukocytosis, elevated inflammatory markers (erythrocyte sedimentation rate, C-reactive protein) while blood culture is indicated if SB in the deep bursae is suspected. Rheumatoid factor (RF), and anti–citric citrullinated peptide (anti-CCP) tests should also be ordered to exclude autoimmune diseases. Aspiration and analysis of the bursal fluid form the mainstay of diagnosing SB as it is likely to show cell counts exceeding 70,000/µL, with a predominance of polymorphonuclear leukocytes (PMNs). Microbiological analysis of the aspirated fluid demonstrates Staphylococcus aureus and other gram-positive organisms in a majority of the cases .
Plain radiography will only reveal joint effusion or soft tissue swelling but does not help to detect SB. Although computed tomography (CT) is not required magnetic resonance imaging (MRI) can help to identify local joint anatomy, soft tissue abscesses as well as the bursal fluid . Ultrasonography is useful when the diagnosis is uncertain and to perform ultrasound guided aspiration of the bursa. Ultrasonography can also differentiate between solid and cystic masses and detect popliteal bursitis in presence of extensive joint deformities  .