Updates in Immunonutrition in Sepsis

Abstract

Sepsis cause disruption of hemostasis through a currently cascade of excessive inflammation and coagulation. The pathophysiology of sepsis is complex and results from the effects of circulating bacterial products, mediated by cytokine release, occurring as a result of sustained bacteremia. Early in septic shock, the rise in cardiac output is often limited by hypovolemia and fall in preload because of low cardiac filling pressures. When intravascular volume is augmented, the cardiac output is usually elevated, but the performance of the heart reflected by stroke volume is usually depressed and the blood lactate level is elevated. Myocardial depression and peripheral vasodilatation and a reduced systemic vascular resistance are the characteristic hemodynamic features found in patients with sepsis. Fluid resuscitation is a fundamental aspect of the hemodynamic management of patients with septic shock and should actually be achieved before vasopressors are used, but it is frequently necessary to employ vasopressors early as an emergency measure in patients with septic shock. The goal resuscitation should achieve adequate levels of oxygen delivery to avoid flow dependent tissue hypoxia.