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脂肪栓塞发病机制与治疗的基础研究。I.骨折机制与脂肪栓塞

[Basic studies on the pathogenesis and treatment of fat embolism. I. Fracture mechanism and fat embolism].

作者信息

Parzer R, Kolarik B, Schnabel P, Gottlob R

出版信息

Z Exp Chir. 1979;12(5):277-85.

PMID:547530
Abstract

We examined the amount of fat that can be forced into the circulation by compression of femora and of heads of the tibia in the very moment of injury. By fractures of diaphyses no considerable reduction of the intraosseous space was achieved and no fat was expelled through the foramina nutritia before the hard cortical bone was splintered. However, considerable amounts of fat were expelled into veins, when the epiphyses of the femora or when the head of the tibia was compressed from medially and from laterally. Even by a purely manual compression some fat was forced to leave the spongiosa by the foramina nutritia. This is explained by the higher elasticity of the spongious bone, permitting a marked space reduction by compression even before a fracture sets in. The mechanism resembles the procedure of opacification of veins by contrast media, injected into the bone cavity under pressure. The significance of these findings for the pathogenesis of clinical fat embolism is discussed.

摘要

我们研究了在损伤瞬间通过挤压股骨和胫骨头部能被挤入循环系统的脂肪量。骨干骨折时,在坚硬的皮质骨破碎之前,骨髓腔空间没有明显减小,也没有脂肪通过滋养孔排出。然而,当从内侧和外侧挤压股骨骨骺或胫骨头部时,大量脂肪被排入静脉。即使是单纯的手动挤压,也会有一些脂肪通过滋养孔被迫离开松质骨。这是因为松质骨具有较高的弹性,即使在骨折发生之前,通过挤压也能使空间显著减小。该机制类似于通过在压力下将造影剂注入骨腔来使静脉显影的过程。本文讨论了这些发现对临床脂肪栓塞发病机制的意义。

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[Basic studies on the pathogenesis and treatment of fat embolism. I. Fracture mechanism and fat embolism].脂肪栓塞发病机制与治疗的基础研究。I.骨折机制与脂肪栓塞
Z Exp Chir. 1979;12(5):277-85.
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