As a cause of clinical shock, sepsis is surpassed in frequency only by hemorrhage and myocardial infarction. The most common offending organisms are gram-negative bacteria, although septic shock may occasionally occur after infection with fungi, rickettsiae, viruses, and gram-positive bacteria. Infections with gram-negative bacilli are increasing in frequency and at present constitute the most commonly encountered life-threatening infections in patients in general hospitals. The mortality in large accumulated series of patients with gram-negative bacteremia approximates 40%. In patients in whom shock develops as a consequence of the bacteremia, the death rate ranges from 50% to 80%.
The pathophysiology of bacterial shock is incompletely understood. It is believed, however, that endotoxin, a complex lipopolysaccharide common to the cell wall of all gram-negative bacteria, plays a major role in initiating the hemodynamic events.1 Most experimental evidence supports the view that endotoxin effects a redistribution of blood within the vascular bed