This Consensus represents the first attempt to create a universal language for diagnosing and treating sepsis. Sepsis

is defined as systemic inflammatory response syndrome (SIRS), resulting from infection. Identifying patients with severe sepsis early and correcting the underlying microvascular dysfunction may improve patient outcomes. If not corrected, microvascular dysfunction can lead to global tissue hypoxia, direct tissue damage, and ultimately, organ failure. Systemic inflammatory response syndrome (SIRS) SIRS is a reference for the complex findings that result from a systemic activation of the innate immune response, regardless of cause. It includes the presence of more than one of the following manifestations: Temperature > 100.4°F or < 96.8°F (> 38°C or < 36°C) Heart rate > 90 beats/min Tachypnea, as manifested by AZD1480 a respiratory rate > 20 breaths/min or hyperventilation, as indicated by a PaCO2 < 32 mm Hg Alteration of white blood cell count > 12,000 cells/mm3, < 4,000 cells/mm3, or the presence of > 10% immature neutrophils. Sepsis Sepsis is defined by the American College of Chest selleck Physicians/Society of Critical Care Medicine (ACCP/SCCM)

as SIRS resulting from infection. Severe sepsis Severe sepsis is sepsis associated with at least one acute organ dysfunction, hypoperfusion, or hypotension. Septic shock Septic shock occurs when sepsis-induced hypotension persists despite adequate fluid resuscitation. Multiple organ dysfunction syndrome (MODS) MODS includes altered functions of two or more organs Amino acid in an acutely ill patient. Pathophysiology Abdominal sepsis occurs as result of intra-abdominal infection. The pathophysiology of sepsis takes origin from the outer membrane components of both gram-negative Fedratinib concentration organisms (lipopolysaccharide [LPS], lipid A, endotoxin) and gram-positive organisms (lipoteichoic acid, peptidoglycan). These outer membrane components are able to bind to the CD14 receptor on the surface of monocytes. By virtue of the recently described toll-like receptors, a signal is then

transmitted to the cell, leading to the eventual production of the proinflammatory cytokines, including tumor necrosis factor (TNF), interleukin 1 (IL-1), IL-6, IL-8, and gamma interferon (IFN-), as well as other inflammatory mediators such as prostaglandins, leukotrienes, platelet activation factor, and nitrogen and oxygen intermediates. Most of these immunological mediators present multiple biologic effects, play a critical role in inflammation and immune responses, and have been recognized as key mediators in the pathogenesis of infectious diseases and, more particularly, the pathophysiologic alterations observed in endotoxic shock. As a result of the vicious cycle of inflammation, cardiovascular insufficiency and multiple organ failure occur and often lead to death [8–10].