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That is, our increased understanding of the pathogenesis of the disease has generally failed to substantially improve outcomes. However, research has also revealed that the progression of sepsis is much more complex than just inflammation or microbial or host pattern recognition sepsis also involves effects on endothelial tissues and microcirculation, primary and secondary immune tissues, coagulation, parenchymal tissues and neurological disturbances that directly affect microglial cells and neurons 9– 12.ĭespite a dramatic increase in our understanding of sepsis, its origins, progression and resolution (recovery or death), our ability to intervene and alter the trajectory of the disease has been only partially successful. The danger hypothesis purports that the innate immune system recognizes microbial patterns and unique host cellular products as ‘danger signals’ or ‘alarmins’ of microbial invasion or tissue injury. 8) have dramatic ally improved our understanding of sepsis and its pathogenesis. The discovery of how the host distinguishes self and non-self and the introduction of the ‘danger hypothesis’ (REF. In the 1980s, with the implementation of molecular cloning and the sequencing of human inflammatory genes, research in sepsis turned towards investigations that focused less on the pathogenicity of the microorganism and more on the host response to an invading pathogen 5– 7. Early research focused on the microorganism and its pathogenicity. The study of sepsis treatment reflects progress in our understanding of human pathophysiology and host– microorganism interactions. Operationally defined as requiring vasopressor therapy to maintain a mean arterial blood pressure of >65 mmHg and an increased plasma lactate level of >2 mmol per l Septic shock remains defined as a subset of sepsis in which the risk of mortality is substantially increased, and is characterized by hypotension that persists during volume resuscitation and requires the use of vasopressors.Ī subset of sepsis in which underlying circulatory and cellular–metabolic abnormalities are profound enough to substantially increase mortality In its place, sepsis is now defined as an infection associated with organ injury distant from the site of infection. Efforts have recently focused on eliminating the SIRS requirement entirely 4 ( BOX 2) because fever, tachycardia, tachypnoea and white blood cell changes reflect infection only and have proven to be too broadly applied in critically ill patients to be useful in the definition of sepsis. Since 1991, the consensus definition of sepsis has been the ‘systemic inflammatory response (SIRS) to a microbial infection’ (REFS 2, 3) ( BOX 1), with SIRS defined as at least two of the following: tachypnoea (rapid breathing), tachycardia (rapid heartbeat), pyrexia (fever) or hypothermia, and leukocytosis, leukopaenia or neutrophilia. Further described by Boerhaave, von Liebig, Semmelweis, Pasteur, Lister, Lennhartz and, most recently, Bone, sepsis and its treatment have confounded investigators for nearly 3,000 years. Sepsis has been recognized in some form or another since at least 1,000 BC - when it was first described by the Islamist philosopher Ibn Sīnā (also known as Avicenna) as putrefaction of blood and tissues with fever 1. Because of its complexity, improvements in sepsis outcomes are likely to continue to be slow and incremental. Similarly, no biomarker can definitely diagnose sepsis or predict its clinical outcome.
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Earlier recognition and improved implementation of best practices have reduced in-hospital mortality, but results from the use of immunomodulatory agents to date have been disappointing. Furthermore, patients who survive sepsis have continuing risk of mortality after discharge, as well as long-term cognitive and functional deficits. With earlier recognition and more compliance to best practices, sepsis has become less of an immediate life-threatening disorder and more of a long-term chronic critical illness, often associated with prolonged inflammation, immune suppression, organ injury and lean tissue wasting. Septic shock remains defined as sepsis with hyperlactataemia and concurrent hypotension requiring vasopressor therapy, with in-hospital mortality rates approaching 30–50%. Sepsis is now increasingly being considered a dysregulated systemic inflammatory and immune response to microbial invasion that produces organ injury for which mortality rates are declining to 15–25%. For more than two decades, sepsis was defined as a microbial infection that produces fever (or hypothermia), tachycardia, tachypnoea and blood leukocyte changes.