Abstract
Patients with severe infections and major trauma often develop multiple organ dysfunction syndrome (MODS). Aggressive fluid resuscitation can be involved in such a process and several lines of evidence have demonstrated the detrimental effects of large crystalloid-based resuscitation strategies on MODS. Additionally, fluid-restrictive strategies have been associated with a decreased frequency of acute respiratory distress syndrome (and a shorter time to recover from it) and with trends toward a shorter length of hospital stay and lower mortality. Recent knowledge of the pathophysiology of septic shock and severe trauma indicates that a release of inflammatory mediators occurs early in the course of the disease. These mediators, especially pro-inflammatory cytokines as well as hypopituitary adrenal axis dysfunction, are involved in cardiac dysfunction and vasodilatation-induced hypotension. Taking into account this combination of severe inflammation and secondary changes in endocrine profile through an earlier use of vasopressors, inotropic drugs and/or hormones may help to achieve adequate hemodynamic goals without the need for aggressive fluid resuscitation. Studies are needed to integrate these new concepts into future guidelines regarding fluid resuscitation for hypotensive patients facing sepsis or severe trauma.