Septic Shock: Mechanism and Signaling

Shock is defined as a state where the organs and tissues of the body are not receiving adequate blood perfusion and ultimately, enough oxygen. When this state of hypoperfusion occurs in the context of infection, it is termed “septic shock”.

The mechanism of septic shock becomes problematic due to its widespread nature within the body. When bacteria are degraded, free LPS is released which binds to LPS-binding protein intravascularly. CD14, located on monocytes and macrophages, then binds this LPS-LPS binding protein complex and subsequently recruits and activates monocytes via the Toll-like receptor (TLR). As macrophages become activated, they release interleukin-1 (IL-1) and tumour necrosis factor (TNF). The widespread nature of this reaction causes systemic vasodilation, leading to hypotension and inadequate end organ perfusion, decreased myocardial contractility, diffuse endothelial injury, and disseminated intravascular coagulation.

REFERENCES:

1. Kemp, W. L., Burns, D. K., & Brown, T. G. (2008). Pathology: The big picture. New York: McGraw-Hill Medical.
2. King, E. G., Bauzá, G. J., Mella, J. R., & Remick, D. G. (2013, September 23). Pathophysiologic mechanisms in septic shock. Retrieved from https://www.nature.com/articles/labinvest2013110