Fat Embolism Syndrome

Fat embolism and fat embolism syndrome (FES) are not interchangeable terms. Fat droplets commonly enter the circulation after a long-bone fracture or intramedullary procedure without causing illness. FES is the clinical syndrome that develops when embolic fat and its inflammatory effects produce organ dysfunction, classically in the lungs, brain and skin. Only a minority of patients with measurable fat embolisation develop the syndrome. Two mechanisms help explain the presentation. A fractured or instrumented femur can generate high intramedullary pressure, forcing marrow fat and other contents through torn venous sinusoids. Droplets approximately 7–10 micrometres in diameter lodge in pulmonary capillaries, creating mechanical obstruction, ventilation–perfusion mismatch and increased pulmonary vascular resistance. The biochemical mechanism explains why the patient may initially look well. Catecholamines and other stress hormones mobilise fat stores, while lipase and secretory phospholipase A2 break triglycerides into free fatty acids. These fatty acids injure pulmonary endothelium and pneumocytes and trigger arachidonic-acid and cytokine-mediated inflammation. The result can progress to diffuse alveolar injury and acute respiratory distress syndrome (ARDS). This delayed inflammatory injury accounts for the characteristic 12–72-hour interval between the...