Fat embolism syndrome (FES) results from both mechanical embolization and biochemical inflammatory cascade. Mechanically, intramedullary fat and marrow particles enter the venous circulation through torn medullary venous sinusoids after long bone fracture or intramedullary instrumentation. These particles lodge in pulmonary capillaries, causing V/Q mismatch. Particles <20 micrometers can traverse the pulmonary capillary bed to reach the systemic circulation (paradoxical embolization through pulmonary microvasculature or patent foramen ovale), causing cerebral and cutaneous manifestations. Biochemically, pulmonary lipase hydrolyzes neutral fat into free fatty acids that are directly cytotoxic to capillary endothelium, activating the complement cascade, causing platelet aggregation and consumption (thrombocytopenia), increasing capillary permeability (non-cardiogenic pulmonary edema), and triggering DIC. The clinician must apply Gurd's diagnostic criteria, manage respiratory failure, order advanced diagnostics, prescribe supportive therapy, and coordinate surgical fixation to prevent further embolization.