Ninety percent of all cases of fat embolism syndrome occur after blunt trauma. Other causes include acute pancreatitis, diabetes mellitus, burns, joint reconstruction, liposuction, cardiopulmonary bypass, decompression sickness, sickle cell crisis, and pathologic fractures.

The bone marrow from a fractured bone or other injured adipose tissue releases fatty globules that enter the systemic circulation through torn veins at the injury site. These fatty globules travel to the lungs, where they form an embolus that blocks pulmonary circulation. Lipase breaks down the trapped fat emboli into free fatty acids.

This process causes a local toxic effect that damages the epithelium, increases capillary permeability, and inactivates lung surfactant. The increased capillary permeability allows protein-rich fluid to leak into the interstitial space and alveoli, increasing workload of the right side of the heart and causing pulmonary edema. The decreased surfactant causes alveolar collapse, a decrease in functional reserve capacity, and ventilation-perfusion mismatch, leading to hypoxemia. Platelet aggregation on fat, normal injury-related platelet consumption, and platelet dilution through I.V. crystalloid administration all contribute to thrombocytopenia, petechiae and, possibly, disseminated intravascular coagulation. (See How fat embolism threatens pulmonary circulation, page 80.)