Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care cung cấp cho các bạn kiến thức về ngành y đề tài: Rescue therapy in septic shock – is terlipressin the last frontier? | Available online http content 10 2 131 Commentary Rescue therapy in septic shock - is terlipressin the last frontier Marc Leone and Claude Martin Intensive Care Unit and Trauma Center Nord University Hospital Marseilles School of Medicine Marseilles France Corresponding author Claude Martin Published 21 March 2006 This article is online at http content 10 2 131 2006 BioMed Central Ltd Critical Care 2006 10 131 doi cc4863 See related research by Rodriguez-Nunez et al. in issue http content 10 1 R20 Abstract Use of terlipressin an analogue of vasopressin can be considered in septic shock patients with intractable hypotension and high cardiac output in whom fluid resuscitation and high-dose conventional catecholamines have failed. The effects of this agent on organ function are poorly evaluated in humans. The limited number of patients evaluated precludes any analysis of adverse outcomes and prognosis. In the previous issue of Critical Care Rodriguez-Nunez and coworkers 1 report their experience with terlipressin in 16 children with refractory septic shock. Over the past few years there has been much interest in the use of terlipressin in such settings both in adults 2-6 and children 7-10 . Septic shock is a form of distributive shock characterized by arteriolar and venous vasodilatation. The objectives of treatment are twofold 11 to maintain oxygen delivery above a critical threshold and to increase mean arterial pressure MAP to a level that allows distribution of cardiac index CI sufficient for adequate organ perfusion. Among the catecholamines noradrenaline norepinephrine and dopamine are often favoured. However vascular responsiveness to catecholamines diminishes over time and patients may die in states of intractable shock 12 . The vascular hyporeactivity to catecholamines is caused among other mechanisms by excessive nitric oxide formation associated with an activation of ATP-sensitive
