Pathogenesis

Septicaemic shock is thought to occur due to intravascular exposure to large amounts of endotoxin. Endotoxin is a lipopolysaccharide component of Gram negative bacterial cell walls. Similar substances from the wall of Gram positive bacteria may also act like endotoxin. (1,2)

Exposure to endotoxin is thought to trigger a number of processes. Monocytes are stimulated to produce cytokines such as tumour necrosis factor and interleukin-1. The complement system is directly activated and this in turn activates neutrophils which adhere to each other and to vascular endothelium. Factor XII is also stimulated, resulting in the promotion of coagulation and the release of hypotensive agents such as bradykinin.

These events cumulatively result in tissue damage, capillary leakage, fever, metabolic changes, vasodilation and disseminated intravascular coagulation.

This is clinically manifest as a sepsis syndrome, which in severe cases may lead to adult respiratory distress, multiple organ failure and death.

Reference

1. Nguyen HB et al. Emergency Department Sepsis Education Program and Strategies to Improve Survival (ED-SEPSIS) Working Group. Severe sepsis and septic shock: review of the literature and emergency department management guidelines. Ann Emerg Med. 2006 Jul;48(1):28-54.
2. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med. 2003 Jan 09;348(2):138-50