The pathophysiologic mechanism of fat embolism syndrome (FES) has been thought to depend on mechanical blockage of capillaries by fat emboli or on the toxic effect of free fatty acids on the capillary endothelium. Aggregation of platelets, microembolism, disseminated intravascular coagulation, and vasoactive amines are considered to be involved. The question of why some patients develop fat embolism while other patients with similar injuries do not remains to be solved.Blood tests in ten patients who developed FES and their reaction to stress were compared to the same tests in ten patients with similar injuries without FES at least 1 year after trauma. The following were measured: blood Hb, leucocytes, platelets, protein and lipid electrophoresis, ACTH, cortisol, TSH, GH, insulin, glucose, NEFA, certain coagulation and fibrinolytic studies, alpha, antitrypsin, and antithrombin III. The platelet values, especially after stress, and P+P values were higher in the FES-patients. The alpha-beta lipoprotein ratio was lower and the blood glucose values were higher in half of those FES-patients in whom a diabetic heredity was discovered. The U-catecholamines were also somewhat higher in the FES-patients. Disturbances of the lipid and carbohydrate metabolism as well as a high platelet count and high P+P values may predispose to thrombosis and DIC. More numerous petechiae in Rumpel-Leede's stasis test in fat embolism patients suggest increased capillary fragility. Low growth hormone values in FES-patients and a different cortisol reaction to stress compared to control patients suggests a disturbed neurohumoral regulation in FES.