ABSTRACT

Septic shock, regardless of its aetiology, is defined as sepsis (systemic response to infection) with hypotension resulting in impaired tissue perfusion and oxygen extraction (Parrillo, 1990). The definition of septic shock is independent of the presence or absence of a multiple organ dysfunction syndrome (MODS), which is defined as impaired organ function such that homeostasis cannot be maintained without intervention (Baue, 1993). MODS may either occur as is a direct result of a well-defined insult to a specific organ (e.g. primary MODS) or as a consequence of an exaggerated host response (secondary MODS). This enhanced host response termed systemic inflammatory response syndrome (SIRS) may occur in response to infection, multiple trauma, haemorrhage, ischaemia and immune-mediated organ injury (Baue, 1993). Current therapeutic approaches for septic shock include antimicrobial chemotherapy, volume replacement, inotropic and vasopressor support, oxygen therapy and mechanical ventilation as well as haemodialysis and haemofiltration. These have, however, failed to make a substantial impact on the high mortality associated with septic shock (Nathanson et al., 1994) and, hence, septic shock remains the major cause of death in noncoronary intensive care units with an estimated mortality ranging between 50 and 80%. As shock is also by far the most common cause of prolonged admission to an intensive care unit, the clinical and socioeconomic importance of this illness is substantial.