Infection. Another frequently advocated hypothesis is that MODS develops in
response to a systemic insult precipitated by an infectious process. This observation is
underscored by the work of Knaus et al. [6] that the development of MODS is frequently
associated with the diagnosis of sepsis or infection at the time of ICU admission. In this
scenario, bacteria and, in particular, lipopolysaccharide derived from the cell membrane
of the bacteria, activates complement and plasmin stimulating the release of kinins [20].
These substances, in turn, activate macrophages that release cytokines; cytokines, in conjunction
with kinins, stimulate granulocytes to adhere to the endothelium. In addition, the
coagulation cascade is activated, the net result of which is adhesion and microembolization
of platelets in organ capillary beds. These processes result in damage to endothelial
cells which, in turn, result in increased capillary permeability, interstitial edema, a further
decrease in tissue oxygen uptake, and organ dysfunction.