It is unknown why sepsis progresses to MODS in only
certain individuals, or what the exact pathway is that leads
to this. If the inflammatory process that characterises
the systemic response to infectious pathogens becomes
self-sustaining and progressive, organ dysfunction ensues.
An extraordinarily complex and intricate cascade of
inflammatory mediators, extra- and intracellular cell signalling
pathways is activated. Prevailing wisdom suggests
that these result in either microvascular dysregulation
and/or mitochondrial dysfunction (so-called cytopathic
hypoxia). These processes result in tissue hypoperfusion,
and a further cascade of biochemico-physical alterations
culminating in MODS [12].