Experimentally induced fat embolism syndrome: shift from obstruction to toxic effects

Background Two hypothetical mechanisms have been proposed for fat embolism syndrome: mechanical obstruction and biochemical reactions. However, it has not been proven whether these mechanisms are correlated. This study aimed to demonstrate the relationship between these two hypothetical mechanisms by observing biochemical and histological changes in animals. Methods After a preliminary study, 700 mg/kg of triolein was injected via the ear vein into 25 rabbits and hemodynamic changes in triglycerides, lipases, free fatty acids, and albumin over time were observed. Necropsies were immediately conducted on all experimental animals, and the lungs were examined histologically. Results Eight rabbits died within 1 hour after the injection due to mechanical obstruction. Six rabbits died 7–60 hours after the injection due to diffuse hemorrhage of the lung induced by the toxic biochemical reactions of free fatty acids. Histological examinations of the lungs of the surviving rabbits showed petechiae on the surfaces and evidence of recovery from hemorrhage. Blood levels of free fatty acids increased immediately after the injection of triolein. Conclusions This study revealed that fat emboli primarily injure the lung via mechanical obstruction. The fat is hydrolyzed into fatty acids and causes secondary damage via biochemical reactions. The present study sheds light on the pathophysiology of fat embolism syndrome, with possible implications for its management and prevention.