Abstract
In the last decade it has become clear that the acutely injured brain has profound interrelations with other failing organs in critically ill patients. In fact, non-neurologic organ dysfunction in patients with severe traumatic brain injury is independently associated with worse outcome. Moreover, the brain itself can be considered an initiator of multiple organ dysfunction syndrome (MODS). The intrinsic mechanisms behind these interactions are not well known but several recent animal and clinical studies have provided important information about the mechanisms underlying brain injury-induced MODS. Catecholamines, neurokinins, and cytokines are potentially injurious substances secreted secondary to brain injury. As acute brain injury is accompanied by neuroinflammation, it is natural to speculate that circulating inflammatory factor(s) originating in the brain may enter the circulation, pass through the disrupted blood–brain barrier, and mediate the inflammatory and cytotoxic effects in other organs. A better understanding of the role of inflammation and its potential for modulation could have profound implications for the treatment of patients after acute brain injury. In the near future, additional strategies that target inflammation in the very early phase of brain injury could offer exciting new tools to prevent or reduce secondary MODS and mortality.