Endotoxin release is a common feature of all Gram-negative bacteria, with the lipid A structure preserved across various species and serotypes. This substance activates the complement cascade, producing a chain of effects that can ultimately lead to ARDS. It can also activate factor XII and initiate another progression of events resulting in DIC.
Many of the effects of endotoxin are believed to be mediated through its stimulation of the release of the polypeptide hormone TNF, also known as cachectin. The pyrogen IL-1 and several of the prostaglandins are some of the endogenous substances that can be released through this septic cascade and that can stimulate effects such as hypotension, fever, and shock (Fig 2). The profound drop in blood pressure observed in septic shock appears to be related to indirect effects of endotoxin on the kinin system via other mediators. Because bacterial endotoxin can be released from the cell wall during and after the organisms are killed by antimicrobial agents, a great deal of recent research into the prevention and management of septic shock has focused on development of new modalities to specifically block or moderate the harmful effects of endotoxin.


Figure 2. The septic cascade: pathogenesis of septic shock. Adapted with permission.