Patients treated for critical illness in the intensive care unit have underlying causes such as infection, trauma, major surgery, hemorrhagic shock, pancreatitis and other major insults. In this review we describe this signalling system, giving special attention to what is known about it in critically ill patients and its potential as a target for therapy.Ĭritical illness is a life-threatening disease by definition.

An important regulator of these systems is the angiopoietin/Tie2 signalling system. It functions at the intersection of several systems, including inflammation, coagulation, haemodynamics, fluid and electrolyte balance, and cell migration. The endothelium certainly plays an active role in MODS. We clearly need to understand better the mechanisms that underlie MODS. Unfortunately, only a few interventions, usually those targeting multiple mechanisms at the same time, have appeared to be beneficial. Overwhelming inflammation, immunoparesis, occult oxygen debt and other mechanisms have been investigated, and – despite many unanswered questions – therapies targeting these mechanisms have been developed.

The pathophysiological mechanism underlying MODS are not entirely clear, although several have been proposed. The mortality rate is high despite intensive supportive care. Multiple organ dysfunction syndrome (MODS) occurs in response to major insults such as sepsis, severe haemorrhage, trauma, major surgery and pancreatitis.

Betsid review