Introduction

Despite major advances in critical care and surgery, the incidence of sepsis and the number of sepsis-related deaths are high and increasing. A recent epidemiology survey of severe sepsis in the United States reported 751,000 cases per year, with a mortality of 28.6 percent [1]. Sepsis is associated with prolonged stay both in the intensive care unit and in the hospital. Over the first year following an episode of sepsis, mortality remains high and an increased sepsis-associated risk of dying may persist for up to 5 years after hospitalization. Additionally, the long-term quality of life of sepsis survivors is reduced compared to age- and sex-matched controls. The economic burden associated with sepsis has recently been estimated at US$17 billion (€16.8 billion) each year in the United States alone [1].

Inflammatory cascading reactions that occur in sepsis induce increased microvascular permeability and microvas-cular leakage resulting in interstitial fluid accumulation, loss of protein, and tissue edema [2]. In this situation hypoalbu-minemia frequently occurs as a result of transcapillary loss and impaired hepatic synthesis of albumin leading to reduced intravascular colloid osmotic pressure, which, in turn, compromises the ability to preserve intravascular volume. Consequently, sepsis and septic shock are characterized by a relative as well as an absolute intravascular volume deficit. The absolute volume deficit is caused by fever, increased perspiration and increased insensible loss, vomiting, diarrhea, and volume loss by drains or sequestration. The relative volume deficit is due to vasodilatation, venous pooling, and alterations in the endothelial barrier. The functional disturbances during sepsis-induced micro-vascular leak are associated with impaired tissue perfusion and organ oxygenation causing organ dysfunction, which is reflected by increased blood lactate concentrations, oliguria, coagulation abnormalities, and altered mental state.

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