The inflammatory response is a central component of sepsis as it drives the physiological alterations that are recognized as systemic inflammatory response syndrome (SIRS). In contrast to the hypothesis of exuberant inflammatory response in sepsis is the finding that septic patients may have a relative anti-inflammatory environment. Cellular death may be a key factor in sepsis and its related mortality. Cells that are destined to die can do so by two mechanisms: apoptosis and necrosis. In sepsis, cytokine-induced coagulopathy triggers increased activity of tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) and decreased levels of the natural anticoagulant protein C on mononuclear and endothelial cells. Critical illness related corticosteroid insufficiency (CIRCI) occurs as a result of either a decrease in adrenal steroid production. In patients with severe sepsis, a strategy of glycaemic control using intravenous insulin should include a nutritional protocol with preferential use of the enteral route.