Septic Shock

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Abstract
Among the different therapeutic approaches that could affect the outcome of septic shock, three are reviewed in this article: modulation of the inflammatory response, organ-specific hemodynamic management, and the role of nitric oxide in patients with septic shock. Septic shock is characterized by an exaggerated inflammatory response. Clinical trials designed to block this response have failed to show any outcome improvement. It is now realized that the inflammatory response is required by the host to build up adequate defense mechanisms against an infectious challenge. Future efforts will be directed at identifying patients that have in fact an excessive and deleterious mediator release, because they are most likely to benefit from therapeutic strategies aimed at decreasing the intensity of the inflammatory response. Hemodynamic monitoring should ideally be regional rather than systemic to detect signs of organ hypoperfusion before systemic variables indicate global damage. Recent studies have shown that intramucosal gastric pH is a physiologic variable related to the balance between energy supply and demand in the intestine. It is related to prognosis in critically ill patients, and its use as a therapeutic tool in critically ill patients could improve survival. An excessive release of nitric oxide leads to vascular hyporeac-tivity in septic shock and is toxic to the cells. The inhibition of the inducible isoform of nitric oxide synthase, so that the constitutive release of nitric oxide necessary to maintain organ perfusion is not suppressed, could lead to an improved outcome in septic shock. Studies to define the effects on organ function and on mortality associated with the administration of nitric oxide synthase inhibitors should be performed.

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