Septicaemic Shock

Abstract

Sepsis is the body's response to invading microbes or their toxins; severe sepsis is sepsis accompanied by sepsis‐related organ dysfunction; and septic shock (the most severe form) is severe sepsis with hypotension that does not respond to fluid resuscitation. Septic shock is common and associated with high mortality and morbidity rates.

Keywords: sepsis; septic shock; inflammation; endotoxin; bacteraemia

Figure 1.

The activation of nuclear factor (NF)‐κB, an intracellular protein that regulates the transcription of many cytokine genes, is a multistep process that involves numerous upstream molecules. As shown in this simplified diagram, bacterial molecules such as lipopolysaccharide (LPS) are thought to interact, via CD14, with one or more Toll‐like receptors (TLRs) in the plasma membrane. LPS‐binding protein (LBP) facilitates this interaction. The kinase pathway from TLR to NF‐κB seems to be very similar to that used by the interleukin‐1 receptor (IL‐1R); this pathway converges with the tumour necrosis factor receptor (TNFR) pathway at the kinase called NF‐κB‐inducing kinase (NIK). IκB, inhibitory κB; IKK, IκB kinase; IRAK, interleukin‐1 receptor‐associated kinase; MyD, myeloid differentiation; TRADD, TNFR‐associated death domain; TRAF, TNFR‐associated factor.

Figure 2.

Overview of inflammation‐associated clotting. Intravascular fibrin formation is promoted when activated monocytes and endothelial cells express tissue factor, the key factor for initiating coagulation, and by decreases in the circulating levels of natural anticoagulant proteins (C and S antithrombin III). Fibrin removal is decreased by high blood levels of plasminogen activator inhibitor‐1 (PAI‐1). Fibrin, platelets and leucocytes accumulate in microvascular thrombi, which are thought to play an important role in multiorgan failure.

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References

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Further Reading

Annane D, Bellissant E and Cavaillon JM (2005) Septic shock. Lancet 365: 63–78.

Brown KA, Brain SD, Pearson JD et al. (2006) Neutrophils in development of multiple organ failure in sepsis. Lancet 368: 157–169.

Hopf HW (2003) Molecular diagnostics of injury and repair responses in critical illness: what is the future of ‘monitoring’ in the intensive care unit? Critical Care Medicine 31: S518–S523.

Vincent JL and Abraham E (2006) The last 100 years of sepsis. American Journal of Respiratory and Critical Care Medicine 173: 256–263.

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How to Cite close
Vincent, Jean‐Louis(Sep 2007) Septicaemic Shock. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0002223.pub2]