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In patients with progressing severe sepsis or who have developed septic shock, an additional dose of endotoxin may be deleterious. In patients with uncomplicated gram –ve infections, antibiotic-induced endotoxin release is most probably of limited value. Ī number of in vitro and in vivo studies have shown an increase in endotoxin release after exposure to antibiotics. Ĭirculating endotoxin can induce an overwhelming inflammatory host response (= systemic inflammatory response or sepsis cascade ) Įndotoxin stimulates reactions such as the release of cytokines and arachidonic acid from monocytes, neutrophils, and vascular endothelial cells. It may be precipitated by insults such as pancreatitis, burns or trauma, in addition to many conditions which are less common. The term SIRS describes patients who exhibit a sepsis-like syndrome, but who are not infected. When hypotension persists despite adequate fluid resuscitation and hypo-perfusion or organ dysfunction is present the term septic shock is used. Severe sepsis is sepsis with signs of at least one acute organ dysfunction: Respiratory CVS Renal and hepatic Hematologic CNS Unexplained metabolic acidosis.
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Sepsis is severe inflammatory response syndrome (SIRS) with a presumed or confirmed infectious process. Sepsis is defined as a condition with fever, tachycardia, tachypnea and leukocytosis or leukopenia caused by infection. In sepsis there is an exaggerated stimulation of the normal host responses to the invading pathogen, leading to a widespread release of inflammatory mediators and vasodilatation. Sepsis has now come to be recognized as the systemic response to infection. Sepsis originally meant putrefaction, a decomposition of organic matter by bacteria and fungi. Highlight possible mechanisms of antibiotic induced sepsis. Objective Define sepsis and antibiotic induced sepsis. Antibiotic-induced Sepsis Amr Badreldin Hamdy MD FCCP