tailieunhanh - Báo cáo y học: " Reducing ventilator-induced lung injury and other organ injury by the prone position"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care cung cấp cho các bạn kiến thức về ngành y đề tài: Reducing ventilator-induced lung injury and other organ injury by the prone position. | Available online http content 10 2 139 Commentary Reducing ventilator-induced lung injury and other organ injury by the prone position Peter M Suter Vice-Rector University of Geneva Corresponding author Peter M Suter Published 6 April 2006 Critical Care 2006 10 139 doi cc4898 This article is online at http content 10 2 139 2006 BioMed Central Ltd See related research by Nakos et al. in issue http content 10 1 R38 Abstract Mechanical ventilation can cause structural and functional disturbances in the lung as well as other vital organ dysfunctions. Apoptosis is thought to be a histological sign of distant organ damage in ventilator-induced lung injury VILI . Nakos and colleagues observed a protective effect of prone positioning against VILI in normal sheep. Less alteration in the lung architecture and function and in liver transaminases and lower indices for apoptosis in the liver the diaphragm and the lung were noted in the prone position compared with the supine position. If confirmed these data open a new hypothesis for pathogenesis and prevention of VILI and its extrapulmonary complications. In the previous issue of Critical Care Nakos and colleagues presented interesting experimental research in sheep reporting beneficial effects of the prone position on the damage of mechanical ventilation MV on lung tissue and apoptosis in several vital organs 1 . These observations are an interesting addition to a number of experimental and clinical studies showing that MV can initiate as well as exacerbate lung injury and can worsen other vital organ function 2 3 . Ventilator-induced injury VILI can thereby contribute to an unfavourable outcome. At least two different basic mechanisms are involved in VILI and peripheral organ dysfunction direct mechanical lung damage and enhancement of inflammatory changes in pulmonary tissue 4 . As a result subsequent pathophysiological pathways contribute to .