Pulmonary Gas Exchange Impairment Following Tourniquet Deflation: A Prospective, Single-Blind Clinical Trial

Abstract

The tourniquet has been considered as a recognized cause of limb ischemia/reperfusion injury in orthopedic surgery resulting in a transient neutrophil, monocyte activation, and enhanced neutrophil transendothelial migration with potential remote tissue injury. This study investigated the effect of unilateral tourniquet application within a safe time limit on pulmonary function and the roles of lipid peroxidation and systemic inflammatory response. Thirty patients undergoing unilateral lower extremity surgery with or without tourniquet were equally divided into a control group with no tourniquet (Group C) and a tourniquet (Group T). Arterial partial pressure of oxygen (P(a)O(2)), arterial-alveolar oxygen tension ratio (a/A ratio), alveolar-arterial oxygen difference (A-aDO(2)) and respiratory index, plasma malondialdehyde, serum interleukin (IL) -6 and IL-8 levels were measured immediately before and 1 hour after tourniquet inflation/operation beginning, 0.5, 2, 6, and 24 hours after tourniquet deflation/operation ending. The results represented no significant changes in Group C with regard to either blood gas variables or levels of circulating mediators, while blood gas variable changes of greater A-aDO(2) and respiratory index and lower PaO2 and a/A ratio were shown at 6 hours following tourniquet deflation. The levels of malondialdehyde, IL-6, and IL-8 were increased over baseline values from 2 to 24 hours following tourniquet deflation in Group T. We concluded that tourniquet application within a safe time limit may cause pulmonary gas exchange impairment several hours after tourniquet deflation, where lipid peroxidation and systemic inflammatory response may be involved.