Mechanism of increased susceptibility to infection following hemorrhage

Abstract

Although hemorrhage is known to cause increased susceptibility to infection, the precise mechanism remains unknown. Regional hypoxia due to reduced blood flow following hemorrhage appears to be a primary mediator that initiates the cascade of events leading to immunodepression and increased susceptibility to infection. This was evident from depression of lymphocyte functions, production of various lymphokines, macrophage expression of receptors involved in opsonin-mediated phagocytosis, and antigen presentation function of peritoneal, splenic, and Kupffer cells following hemorrhage. The depression in various immune functions is apparent immediately after hemorrhage and persists for a prolonged period of time, despite volume resuscitation. Furthermore, it appears that the increased release of systemic mediators, such as interleukin-1 (IL-1), IL-6, tumor necrosis factor, transforming growth factor type beta, and prostaglandin E2 is associated with marked depression in immune responses and increased susceptibility to infection following hemorrhage.