Bursitis is inflammation of a synovial bursa — a synovial membrane-lined fluid-filled sac that reduces friction between bone and soft tissue. Over 150 bursae exist in the body and the vast majority are clinically insignificant. Most commonly affected are subacromial/subdeltoid (shoulder), olecranon (elbow), prepatellar (knee), trochanteric (hip), and retrocalcaneal (heel) bursae. Bursitis etiology falls into three main categories: aseptic (mechanical irritation, trauma, overuse), septic (infectious — usually S. aureus, direct inoculation from skin abrasion), and crystal (gout, pseudogout). On MRI and US, distended fluid-filled bursa, synovial thickening, and surrounding peribursal edema constitute the diagnostic combination. Septic bursitis is an urgent subtype requiring emergent treatment — delayed treatment may progress to joint sepsis and osteomyelitis. Aseptic bursitis is managed conservatively with excellent prognosis.
Age Range
25-70
Peak Age
45
Gender
Equal
Prevalence
Very Common
Bursae are synovial membrane-lined sacs anatomically positioned to reduce friction between bony prominences and overlying tendons, muscles, or skin. Normal bursa contains minimal synovial fluid (1-3 mL) and bursal wall consists of thin synovial membrane and subsynovial connective tissue. Bursitis pathophysiology develops through different mechanisms depending on etiology: (1) Mechanical/traumatic bursitis — repetitive friction or direct trauma irritates the synovial membrane triggering the inflammatory cascade (IL-1, TNF-alpha, PGE2) → increased vascular permeability → plasma extravasation → increased fluid production → bursal distension. In chronic mechanical irritation, synovial membrane undergoes hypertrophy with villous proliferation and fibrosis. (2) Infectious (septic) bursitis — usually develops from direct inoculation through skin abrasion or superficial wound (hematogenous spread is rarer). S. aureus is the most common pathogen (80-90%). Bacterial invasion triggers acute neutrophilic inflammatory response → purulent fluid, cellular debris, fibrin mesh accumulate. Untreated septic bursitis may spread to surrounding tissues (cellulitis, osteomyelitis, septic arthritis). (3) Crystal bursitis — gout (monosodium urate) or pseudogout (calcium pyrophosphate dihydrate — CPPD) crystals deposit within the bursa → crystal-induced neutrophilic inflammation (NLRP3 inflammasome activation). The bright appearance of bursal fluid on T2 fat-sat MRI results from free water (synovial fluid) protons having long T2 relaxation time (~80-120 ms). Synovial thickening shows enhancement on contrast sequences — inflammatory neovascularization and increased capillary permeability lead to gadolinium extravasation. Peribursal edema reflects spread of the inflammatory process to surrounding tissues and increased vascular permeability in adjacent tissue.
Distended fluid-filled sac at anatomic bursa location with synovial thickening and surrounding peribursal edema on T2 fat-sat or STIR is the diagnostic triad for bursitis. Bursa localization determines the diagnosis — subacromial (shoulder), olecranon (elbow), prepatellar (knee), trochanteric (hip). Differentiation of septic from aseptic is made by clinical findings (erythema, warmth, fever) and imaging features (wall irregularity, debris, cellulitis).
On T2 fat-sat or STIR images, a distended fluid-filled sac at anatomic bursa location is seen. Fluid may be T2 hyperintense (simple fluid — homogeneous bright signal) or heterogeneous (hemorrhage, debris, infection). In simple (aseptic) bursitis, fluid is homogeneously hyperintense with thin wall; in septic bursitis, debris (irregular signal islands) and fluid-fluid levels may be seen — neutrophils and fibrin layer by gravity. In hemorrhagic bursitis, T1 fluid signal increase (methemoglobin) with heterogeneous T2 signal is seen. Bursa size, fluid volume, wall thickness, smoothness, and surrounding tissue reaction should be reported.
Report Sentence
Distended bursa with T2 hyperintense fluid is noted at the anatomic bursa location, consistent with bursitis.
On post-contrast T1 fat-sat images, synovial thickening and enhancement of the bursal wall are seen. Thickening may be smooth (aseptic — uniform thin wall enhancement) or irregular/nodular (septic, chronic — irregular thick wall, focal nodular areas). Enhancement reflects active inflammation and is used to assess treatment response. In septic bursitis, wall is markedly thickened (>3 mm) with irregular enhancement and accompanying cellulitis findings. In crystal bursitis, intraluminal crystal deposits may be seen as low-signal nodules in addition to wall enhancement.
Report Sentence
Synovial thickening and enhancement of the bursal wall are noted on post-contrast images, consistent with active bursitis.
On B-mode US, anechoic/hypoechoic fluid accumulation and synovial thickening are seen at anatomic bursa location. Simple fluid is anechoic (homogeneous black — no acoustic impedance difference); fluid with debris is hypoechoic and heterogeneous (irregular internal echoes). Synovial thickening is seen as hypoechoic or heterogeneous villous proliferation — normal bursal wall <1 mm, pathologic thickening >2 mm. In septic bursitis, wall is markedly thickened, fluid is heterogeneous, and surrounding cellulitis findings (diffuse hypoechoic soft tissue swelling) accompany. US provides guidance for bursa aspiration enabling real-time needle placement. Evaluation should be performed in both transverse and longitudinal planes with contralateral comparison.
Report Sentence
Bursal distension, fluid accumulation, and synovial thickening are noted at the anatomic bursa location on US, consistent with bursitis.
On STIR or T2 fat-sat images, soft tissue edema around the bursa is seen as hyperintense signal increase. Peribursal edema indicates acute or subacute bursitis process reflecting inflammation extending beyond bursa boundaries. In septic bursitis, surrounding cellulitis findings (diffuse soft tissue edema, skin thickening, subcutaneous fluid) may accompany — these findings are important in differentiating septic from aseptic bursitis. In olecranon bursitis prominent peribursal edema at dorsal elbow, in prepatellar bursitis at anterior patella is typical. In chronic bursitis, peribursal edema may be minimal or absent — active inflammation has subsided.
Report Sentence
Peribursal soft tissue edema is noted around the bursa, consistent with acute bursitis.
Increased vascularity in the bursal wall and synovial membrane is seen on power Doppler or color Doppler — indicating active inflammation. Normal bursal wall shows minimal vascularity or no Doppler signal is detected. In septic bursitis, vascularity is markedly increased and increased perfusion is also observed in surrounding cellulitis area. In crystal bursitis, vascularity is increased during acute flare and decreased in intermittent period. Doppler findings are valuable for treatment response monitoring — decreased vascularity after corticosteroid injection correlates with clinical improvement. Microbubble contrast US can increase low-flow sensitivity but is rarely used in routine practice.
Report Sentence
Increased synovial vascularity is noted in the bursal wall on power Doppler, consistent with active inflammation.
Higher than normal signal of bursal fluid on T1-weighted images suggests hemorrhagic bursitis. Methemoglobin, a subacute blood product, shows high signal on both T1 and T2 — this feature allows differentiation from simple fluid (T1 low, T2 high). Hemorrhagic bursitis usually develops in the setting of direct trauma, anticoagulant therapy, or hemophilia. Fluid-fluid levels may be seen — blood products layer by gravity. In chronic hemorrhagic bursitis, hemosiderin deposition may produce blooming artifact on T2* gradient-echo sequences — this finding should be distinguished from PVNS.
Report Sentence
Bursal fluid shows increased signal on T1, consistent with subacute hemorrhagic bursitis.
Criteria
Develops from mechanical irritation or trauma without infection signs. Aspirate is clear synovial fluid, Gram stain and culture negative.
Distinct Features
MRI: clear fluid (homogeneous T2 hyperintense), smooth thin wall, minimal peribursal edema. Conservative treatment sufficient — ice, NSAIDs, activity modification. US-guided corticosteroid injection for refractory cases. Excellent prognosis, recurrence possible if underlying cause persists.
Criteria
Infectious etiology. S. aureus most common (80-90%). Acute onset, erythema, warmth, fever, leukocytosis. Aspirate purulent, Gram stain and culture positive.
Distinct Features
MRI: thickened irregular wall (>3 mm), debris and fluid-fluid levels, prominent peribursal cellulitis (diffuse soft tissue edema, skin thickening). US: heterogeneous fluid, septa, thick wall. URGENT treatment: bursa aspiration (culture + Gram stain) → IV antibiotics (empiric: flucloxacillin/cefazolin) → surgical drainage or bursectomy if needed. Life-threatening complications may develop if untreated (septic arthritis, osteomyelitis, sepsis).
Criteria
Intrabursal hemorrhage. Develops in setting of trauma, anticoagulant therapy, or hemophilia. Aspirate bloody, color varies with stage of blood products.
Distinct Features
MRI: T1 fluid signal increase (methemoglobin — subacute blood), heterogeneous T2 signal. Fluid-fluid level (gravity-dependent layering of blood products). In chronic hemorrhagic bursitis, hemosiderin deposition blooming on T2* GRE — must distinguish from PVNS (PVNS has solid synovial mass, hemorrhagic bursitis is predominantly fluid). US: heterogeneous echoes and internal debris.
Criteria
Gout (monosodium urate) or pseudogout (CPPD) crystal deposition. Crystals detected on polarized microscopy of aspirate.
Distinct Features
MRI: synovial thickening, enhancement, intraluminal low-signal nodules (crystal aggregations). Calcified deposits visible on CT (CPPD). US: hyperechoic deposits in bursal wall or fluid (crystal deposits), double contour sign (gout). Treatment: colchicine, NSAIDs, aspiration + corticosteroid injection in acute flare. Treatment of underlying metabolic disease (urate-lowering agents).
Distinguishing Feature
Ganglion cyst is a discrete cystic lesion with stalk connection to joint or tendon sheath, independent of anatomic bursa location — ganglion most commonly originates from dorsal wrist adjacent to scapholunate ligament. Bursitis shows distended bursa at specific anatomic bursa location. Synovial thickening and peribursal edema are typically absent in ganglion cyst, with thin smooth wall.
Distinguishing Feature
PVNS shows prominent blooming artifact on T2* GRE from hemosiderin deposition and lobulated solid synovial mass with low signal on T1/T2. Bursitis shows fluid-filled bursa without blooming artifact and without solid synovial mass component. In hemorrhagic bursitis, minor hemosiderin may deposit but not as prominent and extensive as in PVNS.
Distinguishing Feature
Synovial chondromatosis shows multiple calcified intra-articular loose bodies with ring-and-arc calcification pattern on CT, which is pathognomonic. Bursitis has no calcified bodies with fluid-filled distended bursa. Rarely, bursal chondromatosis may occur but much rarer than intra-articular form and usually in large bursae (subacromial).
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
3-monthBursitis treatment is planned by etiology and correct subtype diagnosis determines the treatment strategy. Aseptic bursitis is managed conservatively: ice (first 48 hours), NSAIDs (ibuprofen, naproxen — 7-14 day course), activity modification (avoid predisposing movement), compression bandage, and elevation. For cases not responding to conservative treatment, US-guided bursa aspiration and corticosteroid injection is applied for diagnostic (aspirate analysis) and therapeutic purposes. Septic bursitis requires URGENT treatment and is a medical emergency: bursa aspiration (Gram stain + culture + crystal analysis + cell count), empiric IV antibiotics (covering S. aureus — flucloxacillin, cefazolin, or vancomycin if MRSA risk), surgical drainage (for cases not responding to aspiration or complicated), and bursectomy (refractory or recurrent septic bursitis). Crystal bursitis: acute flare treatment (colchicine, NSAIDs, corticosteroid) and underlying metabolic disease management (urate-lowering agents — allopurinol, febuxostat). Bursectomy is considered as last resort in chronic refractory aseptic bursitis. Investigating underlying cause is critically important: repetitive occupational trauma, crystal arthropathy, rheumatoid arthritis, systemic inflammatory diseases.
Simple bursitis resolves with conservative treatment (rest, ice, NSAIDs). Infectious bursitis requires aspiration and antibiotics — aspirate culture is diagnostic. Corticosteroid injection is effective in chronic bursitis. Surgical bursectomy is performed in resistant cases. Surgical drainage may be needed for septic bursitis.