Background: The underpinning pathophysiology, prevalence, and clinical relevance particular to hemorrhagic shock-induced liver damage have been explored only recently. Importantly, several investigators have revealed that an aberrant periportal endothelial response, characterized by the early release of oxidizing mediators, perpetuates and eventually amplifies the extent of hepatic reperfusion injury.
Case: We present a case that illustrates the clinical impact of hepatic ischemia-reperfusion injury and a potential means of ameliorating the attendant self-propagating hepatic destruction.
Conclusion: Reversal of hemorrhagic shock may lead to the induction of a hepatic oxidation response with a resultant furthering of liver injury. Antioxidants such as N-acetylcysteine may represent a tolerable and logical means of attenuating the aberrant oxidant cascade and stabilizing or reversing ischemic-reperfusion hepatopathy.