Fat embolism syndrome (FES) develops through two mechanisms: mechanical theory (fat globules from fractured bone marrow physically enter the venous circulation and lodge in pulmonary capillaries, then pass to systemic circulation via patent foramen ovale or transpulmonary passage) and biochemical theory (circulating fat globules are hydrolyzed by pulmonary lipase into free fatty acids that cause direct endothelial damage, increased capillary permeability, inflammatory mediator release, and ARDS-like pathology). The combination produces pulmonary injury (V/Q mismatch, non-cardiogenic pulmonary edema), cerebral dysfunction (microinfarcts from fat emboli), and dermal petechiae (capillary fragility from fatty acid damage). The nurse must perform comprehensive respiratory and neurological monitoring, recognize early signs, manage oxygenation, coordinate with the multidisciplinary team, and prepare for possible mechanical ventilation.