Alterations in Pulmonary Function, Coagulation and Fat Metabolism in Patients with Fractures of the Lower Limbs

Abstract

If the underlying pathology of the syndrome of fat embolism is the presence of circulating emboli of neutral fat with adherent platelets and red blood cells, then one could expect certain changes in normal vascular cellular elements and fat metabolism, with resultant alterations in pulmonary function. In our series of 118 patients with fractures of the lower limbs we found that more than half of them exhibited hypoxemia as well as a decrease in the hematocrit and platelet counts with a concomitant increase in platelet adhesiveness. In addition, those patients with hypoxemia showed increased fibrinogen degenerative product levels indicating an increased fibrinolysis. We found only a slight temporary rise in the serum triglycerides, but the nonesterified fatty acid levels rose sharply over the first three days following trauma associated with an increase in serum lipase. Our study demonstrated that this increase in serum lipase occurred slightly before the peaking tendency observed in the nonesterified fatty acids. Following trauma, fat emboli with adherent platelets and other vascular cellular elements are formed; we would expect that these emboli would lodge in the capillaries and small vessels of the lung, thereby producing a physiological shunt. An increase in the A-aDo2 confirmed this hypothesis and was associated with a decrease in the arterial oxygen level in over half the patients studied. Although 58 of our patients showed evidence of hypoxemia associated with a fall in hematocrit and platelet count, not one of them showed clinical signs and symptoms of the fat embolus syndrome. This study suggests that a subclinical form of fat embolism does exist. What causes a small percentage of those patients with subclinical fat embolism to progress to a clinical fat embolism is still unknown. The majority of our patients spontaneously returned to normal within 5 days. Reviewing the results of those patients who developed hypoxemia and the two patients who developed clinical fat embolism, there seems to be no indication of what causes the progression. Hypotension and shock do not seem to be relevant to the progression of the subclinical condition. Not one of 110 reviewed had evidence of shock or persistent hypotension, yet 58 of these patients developed changes in arterial saturation, vascular elements, and evidence of disseminated intravascular coagulation.