Abstract
Abstract Fat embolism, a distinct entity with definite clinical and laboratory manifestations, occurs to a significant degree in 50 to 60 per cent of persons who incur severe trauma. Approximately 5 to 10 per cent of these persons will die as a direct result of the fat emboli. Two recognizable phases, mechanical and chemical, constitute the pathophysiologic basis of traumatic lipemia. Respiratory distress and right heart strain initiated by acute massive pulmonary capillary plugging may compensate undetected during treatment of the primary injuries. Some twenty-four to forty-eight hours later, however, hydrolytic neutral fat breakdown occurs with release of free fatty acids. As a result of alveolar-capillary irritation copious amounts of blood-tinged sputum are produced. Simultaneous systemic toxicity results in pyrexia, irritability, disorientation, and cerebral depression. Treatment of fat embolization is directed at minimizing its magnitude and controlling its complications. Minimizing its magnitude is accomplished by early and proper handling of all fractures. Complications are controlled by intensive and persistent adherence to readily available regimens such as sedation, tracheal suction, and maintenance of normothermia. Sufficient laboratory and clinical evidence is now available, however, to warrant concomitant use of at least two fat-clearing substances. Heparin, lacking anticoagulant capability when administered orally, has been demonstrated to stimulate lipolytic lipase activity. Ethyl alcohol has been shown to regulate the rate of fat hydrolysis. These two relatively safe pharmacologic agents, when used in a specifically outlined manner, should help decrease the sequelae of capillary plugging and release of toxic fatty acids. If the morbidity and mortality associated with fat embolization are to be lowered, physicians who treat victims of trauma must be aware of this clinical entity, recognize its manifestations, and understand the rationale behind planned therapeutic regimens.
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