Pulmonary fat embolism.

Recovery of an injured patient depends on several factors, among them, the severity of the injury itself, the primary treatment, and the management of posttrauma complications. Fifty years ago, the severely injured patient died of shock or sepsis; thirty years ago, he died of shock or renal failure. Today, if death is not immediate due to hopeless damage. effective resuscitation from the initial shock state and proper treatment of the injury may allow the patient to survive only to later develop a complex post-traumatic syndrome. This syndrome often encompasses endocrinologic, metabolic. nutritional, blood rheologic and clotting disturbances, as well as renal and respiratory insufficiency. The pulmonary damage results from fluid overload, bacterial toxins. shock, oxygen toxicity. blood cell aggregates and tissue and fat emboli. It is this last complication which shall concern us here. When body homeostasis is altered, blood rheology disturbances are induced and changes in serum fat emulsification occur. More important, however, is the mobilization of depot fat which leads to the commonly found post-traumatic condition of lipemia. The boundaries between the mobilization of microand macroglobules of fat is the important factor here. Fat embolism from large aggregates of fat is the pathologic event. It is found in a large percentage and variety of trauma conditions, especially after damage to fat-containing soft tissues and bone has occurred. These fat macroglobuli adhere to blood cells and fibrin and have the potential to produce embolism in the arteriolar tree. The clinical entity. fat embolism syndrome, is characterized by symptoms exhibited by the affected organ systems. The fat embolus particularly affects the vulnerable pulmonary respiratory function and also the brain, which is so sensitive to low oxygen tension.