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骨髓炎的发病机制

Authors
Jason Calhoun, MD
Madhuri M Sopirala, MD, MPH
Section Editor
Daniel J Sexton, MD
Deputy Editor
Elinor L Baron, MD, DTMH
Translators
杨大威, 主任医师

引言

骨髓炎是可导致炎症破坏后新骨形成的一种进行性骨感染，可根据感染的病理学机制分为三大类[1]：

●继发于邻近感染灶(例如，创伤后、外科手术后或关节假体植入术后)的骨髓炎

●继发于与血供不充分相关的邻近感染灶的骨髓炎，主要见于糖尿病和/或周围血管疾病的患者

●因感染的血行播散造成的骨髓炎，这是儿童脊椎骨髓炎的主要发病机制。以前认为，感染播散可能是通过椎静脉(称为Batson静脉丛)发生的，尤其是来自肠道或泌尿道的感染部位。播散在椎体终板的下方后，感染将累及椎间盘和其他相邻椎骨。小儿脊柱的血管止于椎间盘内，使得感染可直接蔓延[2]。目前有许多专家认为，螺旋迂曲的椎动脉血供可导致菌血症患者出现脊椎骨髓炎。

急性骨髓炎在数日至数周内进展，并可发展为慢性感染[1]。慢性骨髓炎的标志是存在死骨。慢性骨髓炎的其他常见特征还包括包壳(死骨的反应性骨包壳)、局部骨量减少，以及如果蔓延突破皮质骨时形成的窦道。

        

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Literature review current through: 2017-06 . | This topic last updated: 2017-05-02.
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