慢性硬膜下血腫の成因 : 皮膜の光顕および電顕像よりみた血腫増大機序について

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The authors report the role of local inflammatory mechanisms in outer membranes to define the physiopathogenesis of the chronic subdural hematoma enlargement. The outer membranes in 20 adult patients of chronic subdural hematoma were investigated by means of light and electron microscopy. Microscopically, perivascular small hemorrhage and hemosiderin as well as fibroblasts, hemosiderin-laden macrophages, eosinophiles and plasma cells were found around the sinusoidal channels. Perisinusoidal hemorrhage, especially red blood cells were, usually, separated from the hematoma cavity by the fibrous layer. Several sinusoids could be seen coalesced to form multiple small cavities in outer membranes, with a fibroblast like lining. Such small hemorrhagic cavities, although not often, may rupture to communicate with the hematoma cavity. Ultrastructurally, the endothelial cells of sinusoids were rich in organelles, especially rough E.R., free ribosomes, mitochondrias, pinocytotic vesicles, and endothelial specific bodies. The site of vascular leakage was identified in several sinusoids as an endothelial gap, in the range of 1-8 ﾎｼ in diameter, presumably formed by separation at intercellular junctions. Perivascular exudation of plasma lead to destruct the extracellular matrix of the sinusoidal layer. Extensive accumulations of endogenous amorphous material and irregularly arranged thin collagen fibers showed interstitial edema. Fibroblasts manufacture tropocollagen molecules within the activated rough E.R., which are then secreted onto the cell surface and gradually polymerized into visible microfibrils and collagen fibers. Interstitial edema, ultimately, disappears in the fibrous layer. The fibrous layer is generally characterized by numerous collagen fibers, fibroblasts, serum proteins and only a few capillaries, some of which show direct openings into the hematoma cavity. Some perivascular edematous fluid in the sinusoidal layer may pass through the fibrous layer into the hematoma cavity. Under scanning electron microscopy, red blood cells and fibrin strands or sheets were seen especially around the outlets of the fibrous layer capillaries. The results indicate that outer membranes, once developed, enlarge chronic subdural hematoma by ruptures of small hemorrhagic cavities formed in outer membranes, direct hemorrhage from the fibrous layer capillaries, and exudation of perisinusoidal edematous fluid into the hematoma cavity.
日本脳神経外科学会の論文
1978-11-15

慢性硬膜下血腫の成因 : 皮膜の光顕および電顕像よりみた血腫増大機序について

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