外傷後の肺微小塞栓症

骨折時のウサギ肺における骨髄および脂肪塞栓症特にその初期病変について

抄録

Post-traumatic pulmonary microembolism comprises pulmonary bone marrow and fat embolism and seems to be a major cause of death in patients dying of traumatic bone fracture. The authors examined the morphological changes of 21 rabbit lungs produced 30 minutes to 48 hours after mechanical fracture and discussed the pathogenesis of the initial lesions.
Thirty minutes after fracture, the embolized bone marrow and thrombi were found in the small arteries and arterioles, measuring 100μ to 500μ in diameter. Fat droplets were also demonstrated in the arteriole and capillary. At the same time, vacuolation of endothelial cells and smooth muscle cells, swelling of the media of small arteries as well as alteration of pneumocytes were observed. At 48 hours, there was a slight degeneration of the hematopoietic cells in the embolized bone marrow, invasion of fibroblastic cells into the thrombi and proliferation of modified smooth muscle cells in the arterial wall.
As early as 30 minutes, “vascular leukostasis” namely sticking (or plugging) of leukocytes to the endothelium or in the lumen of small artery and capillary was observed. A large proportion of leukocytes were neutrophils and eosinophils. In addition, they gathered in the subendothelial portion of the arterial wall. Ten hours after fracture, the degree of vascular leukostasis reached a maximum and monocytes relatively increased in number. As a result of the endothelial injury of capillary due to the action of neutrophils, vascular leukostasis caused remarkable edema and lymphangiectasia in the perivascular connective tissue.
From these observations, it seems probable that the complement-induced vascular leukostasis may be of etiologic importance in the pathogenesis of initial lesions of post-traumatic pulmonary microembolism and also in the progression of adult respiratory distress syndrome (ARDS).