Fat embolism syndrome: traumatic coagulopathy with respiratory distress

Abstract

Fractures and other types of trauma can cause severe metabolic, platelet, coagulative, and pulmonary changes. These changes are variable but tend to increase with the severity of the trauma and may result in the clinical findings often referred to as the fat embolism syndrome. The role in pathogenesis of increased liberation of lipids into the bloodstream, either from the marrow at the fracture site or because of physiochemical changes in the blood and mobilization of fat stores, has received a great deal of attention. These changes, however, may not be as important as the platelet activation and intravascular coagulation that occurs simultaneously. All of these phenomena appear to impair pulmonary function and cause hypoxemia. The results of treatment of the fat embolism syndrome should improve if there is a realization that even relatively uncomplicated fractures of the extremities cause significant metabolic, platelet, coagulation and pulmonary changes. These asymptomatic or subclinical forms of fat embolism are far more frequent than generally appreciated. Evidence of increasing platelet, coagulation or blood gas changes should alert the physician to begin aggressive therapy. Particular emphasis must be placed on maintaining optimal ventilation, using ventilatory assistance early if needed. Aspirin or massive steroids may also be quite helpful, particularly if they are given before the fat embolism syndrome has become fully established.