创伤性脑损伤后肺损伤的发病机制研究进展

背景 创伤性脑损伤(traumatic brain injury,TBI)患者可能发生肺损伤,严重时甚至发生肺功能障碍.脑与肺通过复杂途径相互联系.发生肺功能障碍的TBI患者病死率增加、 加强治疗病房住院时间延长且神经预后较差.目的 综述TBI后肺损伤的研究进展.内容 讨论TBI后肺损伤的发生特点并综述其潜在机制.趋向 根据具体情况评估TBI患者发生肺损伤的潜在风险,并在其临床症状出现前进行相应干预有助于降低发生TBI后肺损伤的风险.

Pathogenesis of acute lung injury after traumatic brain injury

Background Traumatic brain injury (TBI) may be accompanied by lung injury and pulmonary dysfunction. The TBI patients with pulmonary complications tend to have prolonged stay in intensive care unit, poorer prognosis, and increased risk of death. Objective To review the manifestations and potential pathophysiological basis of lung injury after TBI. Content Some TBI patients develop pulmonary injury, including acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema (NPE), and ventilator-associated pneumonia (VAP). Multiple processes that involve in the development of pulmonary injury following TBI include hyperactivity of sympathetic, but hypoactivity of parasympathetic nervous system, enhanced release of substance P, neuropeptide A, proinflammatory cytokines, and adhesion molecule-1, and activation of high-mobility group box-1-RAGE axis, etc. Reversal or blocking of these processes prevent or attenuate lung injury. Trend Further investigations are needed to determine the potential risk factors that affect the incidence of lung injury in TBI patients. The information is critical to develop appropriate intervention or prevention strategies to improve treatment for TBI.