4/19/2023 0 Comments Time for change 2013![]() ![]() 5, 6 For example, high mobility group box 1 (HMGB1) is released during sterile injury and signals through TLR4 to mediate organ damage, even in the absence of infection. But the pattern recognition receptors used by the innate immune system to engage microbial ligands are the same receptors that recognise alarmins derived by host tissue and that are pathologically present in the extracellular environment. The receptors are activated by conserved microbial molecular structures, such as endotoxin or lipoteichoic acid. ![]() 6 Together these responses produce the phenotypic changes of sepsis. Work over the past few decades has shown that pattern recognition receptors, such as those of the Toll-like receptor (TLR) and the nucleotide-binding oligomerisation domain (NOD) protein families, initiate the distinct cellular responses. NOD=nucleotide-binding oligomerisation domain protein. Infectious and non-infectious stimuli that activate innate immunity and cytokine release and can cause sepsis 6 From a molecular perspective, the initial host response to infection does not differ appreciably from the host response to sterile inflammation from severe trauma, burns, ischaemic reperfusion injury, or other forms of tissue injury that are accompanied by cell necrosis. However, we know that sepsis arises through activation of an innate immune response to a stimulus that represents a danger to the host. 5 Whether this syndrome is mediated by endogenous endotoxin or by non-infectious stimuli can be very difficult to define. Several non-infectious processes that are associated with acute tissue injury and innate immune activation can induce a clinical syndrome analogous to sepsis ( figure), including multiple trauma, pancreatitis, transplant rejection, and autoimmune diseases. To reach a more precise definition of sepsis than the SIRS criteria provide, we need to establish whether sepsis is the same as sterile inflammation. Hence, the 1991 criteria for sepsis continue to be used. The delegates attempted to list major and minor criteria, as for endocarditis, but could not identify any meaningful criteria. By expanding the list of potential clinical criteria, the delegates risked making the definition less specific. Moreover, several such stressors might be present simultaneously in any patient.Ī second consensus conference in 2001 4 attempted to revisit the SIRS criteria but failed to come up with an easy-to-use list of variables to define sepsis. Third, deciphering the role of infection in the pathogenesis of SIRS has been difficult because sterile inflammation (present in, for example, severe trauma, burns, and pancreatitis) and infection can both elicit similar clinical signs of acute systemic inflammation. This host response has beneficial aspects, and a reduced or absent reaction could suggest that the individual is immunocompromised. Almost any infection-even a minor viral illness-is typically associated with fever and accompanying changes, including tachycardia, some hyperventilation, and an increased white cell count. Second, some degree of host response is actually inherent to the infection indeed, this is an important component of the difference between infection and mere colonisation. But, although all patients with sepsis have an infection, the reverse is not necessarily true-ie, not all patients with an infection have sepsis. ![]() If sepsis is defined by the presence of SIRS criteria plus an infection, and almost every acutely ill patient meets the SIRS criteria, then sepsis effectively equals infection. 2, 3 SIRS can be caused by many non-infectious clinical processes, such as severe trauma, burns, pancreatitis, and ischaemic reperfusion events. First, the SIRS criteria are so sensitive that up to 90% of patients admitted to an intensive care unit (ICU) meet the criteria. However, the SIRS approach has three major problems. ![]() These simple clinical criteria allowed researchers to identify patients to enrol in sepsis trials and were rapidly adopted. Only minor abnormalities in these variables are needed for a patient to meet the SIRS criteria. 1 For simplicity, the systemic inflammatory response syndrome (SIRS) was defined by four variables: temperature, heart rate, respiratory rate, and white blood cell count. In 1991, a North American consensus conference introduced the idea that sepsis is the host's inflammatory response to in fection. The modern concept of sepsis has focused on the human response to invading organisms. Galen and Celsus described the signs of inflammation as peripheral vasodilatation ( rubor), fever ( calor), pain ( dolor), increased capillary permeability ( tumor), and organ dysfunction ( functio laesa). For the Ancient Greeks, sepsis referred to rot, decay, or putrefaction. ![]()
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