骨折后脂肪栓塞综合征的研究进展

Progressions in Pathogenesis of Fat Embolism Syndrome after Fractures

脂肪栓塞综合征(FES)多继发于骨折,发病原因至今未明。FES发病率较低,但死亡率很高。长期以来,机械阻塞学说和生化学说试图解释FES的发病机制,但这两种学说均不能满意的解释所有临床现象。近年来研究发现,FES与快速发展的急性肺内炎性反应(APIR)有较强的相关性,该领域成为FES研究的焦点。同时还发现许多脂肪栓子对患者的隐性损害。本文就此作一综述,以期为探明本病的病因及其防治作出提示。

Fat embolism syndrome（FES）often follows fractures,but its pathogenesis remains unclear. FES possesses a low incidence, but a high mortality, therefore arouses much attention during therapy of multiple fractures. There have been two major theories about the pathogenesis of FES, but either cannot explain the clinical findings of FES satisfactorily. Recent researches revealed that FES has a strong relationship with rapid-onset acute pulmonary inflammatory response（APIR）. And this area became the focus of FES research. Furthermore, there are many findings about the invisible lesions of fat emboli recently. This review is an attempt to make a summary of these progressions and problems, with an aim to present an indication of pathogenesis of FES, as well as clinical prophylaxis and therapy.