1986 Volume 17 Issue 4 Pages 515-529
In order to study the pathogenesis of pulmonary fat embolism (PFE), the author investigated the temporal sequence of morphological changes using 92 rabbits divided into three groups : In the first group, triolein (300mg/kg) was infused into the marginal ear vein and in the second group both the triolein (300mg/kg) and tissue thromboplastin (1 mg/kg) were injected simultaneously into the separate ear veins. In the third group, oleic acid (100mg/kg) was used in the similar way. In the first group, fat emboli appeared in the interalveolar capillaries and pulmonary leukostasis occurred in the lumen of small arteries with edema in the perivascular connective tissue. In the second group, fatty acid was histochemically demonstrated in the capillary, essentially with the similar findings as seen in the first group. Furthermore, "intra-alveolitis" and thrombi in small arteries were also manifested. Although neither fat embolism nor pulmonary leukostasis was found in pulmonary vessels in the third group, intense hemorrhagic "intra-alveolitis" with necrosis of the interalveolar septum occurred at first. Then, the intraalveolar lesions were replaced by granulomas with calcium deposits and foreign body giant cells, resulting in formation of the localized fibrous foci. So far, the fatty acid has been considered playing an important role upon the pathogenesis of PFE. From this series of study, the author has realized that the pulmonary leukostasis caused by embolization of fat droplets and the thrombi induced by tissue thromboplastin should not be disregarded as the important factors for the occurrence of PFE.
