Septic shock, multiple organ failure, and acute respiratory distress syndrome

Abstract

In 1914, Schottmueller wrote “Septicemia is a state of microbial invasion from a portal of entry into the blood stream which causes signs of illness.” In the last few decades, the evidence that sepsis results from an exaggerated systemic inflammatory host response induced by infecting organisms is compelling; inflammatory mediators are the key players in the pathogenesis of septic shock and multiorgan failure. Sepsis and its sequelae represent a continuum of clinical syndrome encompassing systemic inflammation, coagulopathy, and hemodynamic abnormalities. Severe sepsis and septic shock continue to be the major causes of morbidity and mortality in the United States; sepsis deaths currently match mortality from myocardial infarction. Despite significant advances in our understanding of the pathophysiology and technological innovations in the supportive management, mortality from septic shock remains excessive. After many disappointments with strategies to manipulate the inflammatory response, modulation of coagulation cascade to decrease sepsis mortality has become a clinical reality. This review will highlight and discuss recent advances in the pathophysiology and management of sepsis.