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Objective. – To evaluate recent data provided on new treatments of patients with septic shock.Data extraction. – A Medline search was performed to identify pertinent literature on the pathophysiology of septic shock and treatment strategies from 1990 to 2003. Keywords were “septic shock”, “sepsis”, “inflammation” and “management”.Data synthesis. – Advances were performed in our current understanding of pathophysiology of sepsis. The loss of homeostatic balance among the systemic inflammatory response and the disturbance of coagulation with generalized coagulopathy lead to organ failures and death. The administration of activated protein C (drotrecogin alfa) reducing this coagulopathy can decrease the mortality of septic shock patients. The modulation of inflammation did not make it possible to improve survival of septic shock patients until now. The efficacy of low doses of steroid has been recently shown in septic shock patients. In addition, new data highlighted the interest of an early goal therapy in patients with sepsis who are admitted to emergency.Conclusion. – The improvement of survival in septic syndrome patients is a difficult challenge. The uses of different new therapeutic options like protein C reactive, steroids, or early goal therapy in association should make it possible to reduce the mortality in septic patients. [Copyright &y& Elsevier]

Objective. – To analyze the pattern of adhesion molecules in patients with septic shock.Data sources. – References obtained from Pubmed® databank.Data extraction. – Models of inflammation linking endothelial dysfunction, adhesion molecules and septic states were analyzed.Data synthesis. – The endothelium has been identified as the central effector in the inflammatory response. Adhesion molecules are strongly involved in the inflammatory process by modulating the leukocyte trafficking. The most important adhesion molecules are the selectins (E–, L–, and P–selectins) and members of the immunoglobulin superfamily (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1). Plasma levels of these molecules are increased in septic shock patients, which may be related to a marked activation of the endothelium. However, a dichotomous profile is observed between plasma and tissue expression. The inhibition of adhesive molecule actions could make it possible to control the inflammatory response. [Copyright &y& Elsevier]

Objective. – Vasopressin (antidiuretic hormone) is emerging as a potentially major advancement in the treatment of septic shock. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has haemostatic, gastrointestinal, and thermoregulatory effects. This article reviews the physiology of vasopressin and all the relevant clinical literature on its use in the treatment of septic shock.Data sources and extraction. – Extraction from Pubmed database of French and English articles on the physiology and clinical use of vasopressin. The following key words were selected: vasodilatory shock, vasopressin, septic shock, catecholamines, norepinephrine, renal function, diuresis, mesenteric haemodynamic. The collected articles were reviewed and selected according to their quality and originality.Data synthesis. – Vasopressin mediates vasoconstriction via V1–receptor activation on vascular smooth muscle. Septic shock causes first a transient early increase in blood vasopressin concentrations that decreases later to very low concentrations compared to other causes of hypotension. Vasopressin infusion of 0.01–0.04 U min–1 in septic shock patients increases plasma vasopressin concentrations. This increase is associated with a lesser need for other vasopressors. Vasopressin has been shown to produce greater blood flow diversion from non-vital to vital organ beds than does adrenaline. A large randomized clinical trial should be performed to assess its place as a therapeutic agent of septic shock patient. [Copyright &y& Elsevier]