Authors: Shaikh N et al.
Cureus 17(11): e96136, November 2025. DOI: 10.7759/cureus.96136
Fat embolism syndrome (FES) remains uncommon but clinically important after long-bone and pelvic fractures and is increasingly recognized after body-contouring procedures. The review synthesizes historical and current perspectives, emphasizing two complementary mechanisms: a mechanical pathway (marrow fat entering torn venules with pulmonary trapping and potential systemic passage via shunts/AV channels) and a biochemical pathway (lipolysis to toxic free fatty acids driving inflammation and lung injury). Incidence estimates vary widely (≈0.9% clinically to ~20% at autopsy), with higher risk in young patients, bilateral femoral injuries, pathological fractures, delayed fixation, overzealous/pressurizing intramedullary reaming, and large-volume or combined cosmetic procedures.
Diagnosis has shifted from “exclusion” to integrated clinical–imaging strategies. Classic clinical tools include Gurd & Wilson (≥1 major + ≥4 minor), Schonfeld’s score (>5), and Lindeque’s respiratory criteria. Imaging adds specificity: chest radiograph (flake-like “snowstorm” opacities), CT (ground-glass ± septal thickening, small nodules), and brain MRI for cerebral FES—early “starfield” DWI pattern (days 1–4) evolving to confluent white-matter injury; SWI may show pontine microhemorrhages (“walnut-kernel”). Point-of-care ultrasound can visualize echogenic microemboli moving from IVC to right heart and assess right-sided strain. Differential diagnoses include PE (CTPA filling defects), aspiration, contusion, cardiogenic/noncardiogenic edema, and pneumonia.
Management is primarily supportive: oxygenation/ventilation, hemodynamic optimization, temperature control, thromboembolism prophylaxis, and albumin-containing fluids (binding free fatty acids). Pharmacologic disease-modifiers remain unproven overall, but a recent meta-analysis suggests steroids reduce FES risk after long-bone fractures without increasing infections or mortality. Orthopedic strategy influences risk: early fracture fixation (within 24–72 h) is favored. Standard reamer design changes have not reduced FES, whereas reamer–irrigator–aspirator (RIA) systems can decrease intramedullary fat embolic load. For cerebral FES, supportive neurocritical care and early fracture stabilization predominate; neurological deficits are often reversible, though early severe MRI grades correlate with worse outcomes. Ophthalmic involvement (Purtscher-like changes) is rare but may threaten vision.
Outcomes have improved with modern critical care; mortality typically ranges 5–15%, higher in elderly and non-orthopedic etiologies. Underdiagnosis is likely in aesthetic surgery; maintaining a high index of suspicion with early imaging shortens time to treatment.
What You Should Know
• Think “mechanical + biochemical”: marrow fat entry and toxic free-fatty-acid injury both matter.
• Diagnose early using clinical criteria plus imaging (CT chest, brain MRI “starfield”), and consider bedside POCUS for right-heart/IVC microemboli.
• Supportive care is the cornerstone; albumin-based resuscitation is reasonable.
• Steroids may reduce FES after long-bone fractures per recent meta-analysis; evidence for other drugs (heparin, ethanol, aspirin) is insufficient.
• Favor early definitive fixation; RIA systems can reduce embolic load during reaming.
• Watch special populations: bilateral femur trauma, cosmetic liposuction/fat grafting, and elderly (higher mortality).
• Cerebral and ophthalmic variants exist; many neurological deficits resolve with supportive care and early fracture management.
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