Septicaemic Shock


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 (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.



Angus DC, Linde‐Zwirble WT, Lidicker J et al. (2001) Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Critical Care Medicine 29: 1303–1310.

Annane D, Sebille V, Charpentier C et al. (2002) Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. Journal of the American Medical Association 288: 862–871.

Bernard GR, Vincent JL, Laterre PF et al. (2001) Efficacy and safety of recombinant human activated protein C for severe sepsis. New England Journal of Medicine 344: 699–709.

Dellinger RP, Carlet JM, Masur H et al. (2004) Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Critical Care Medicine 32: 858–873.

Levy MM, Fink MP, Marshall JC et al. (2003) 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Critical Care Medicine 31: 1250–1256.

Levy MM, Pronovost PJ, Dellinger RP et al. (2004) Sepsis change bundles: converting guidelines into meaningful change in behavior and clinical outcome. Critical Care Medicine 32(Suppl.): S595–S597.

Macias WL, Yan SB, Williams MD et al. (2005) New insights into the protein C pathway: potential implications for the biological activities of drotrecogin alfa (activated). Critical Care Medicine 9(4): S38–S45.

Martin GS, Mannino DM, Eaton S et al. (2003) The epidemiology of sepsis in the United States from 1979 through 2000. New England Journal of Medicine 348: 1546–1554.

Quartin AA, Schein RMH, Kett DH and Peduzzi PN (1997) Magnitude and duration of the effect of sepsis on survival. Journal of the American Medical Association 277: 1058–1063.

Rivers E, Nguyen B, Havstad S et al. (2001) Early goal‐directed therapy in the treatment of severe sepsis and septic shock. New England Journal of Medicine 345: 1368–1377.

Van den Berghe G, Wouters P, Weekers F et al. (2001) Intensive insulin therapy in the critically ill patient. New England Journal of Medicine 345: 1359–1367.

Verdant C and De Backer D (2005) How monitoring of the microcirculation may help us at the bedside. Current Opinion in Critical Care 11: 240–244.

Vincent JL, Moreno R, Takala J et al. (1996) The SOFA (Sepsis‐related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis‐Related Problems of the European Society of Intensive Care Medicine. Intensive Care Medicine 22: 707–710.

Vincent JL (2005) Give your patient a fast hug (at least) once a day. Critical Care Medicine 33: 1225–1229.

Vincent JL (2006) Is the current management of severe sepsis and septic shock really evidence based? PLoS Medicine 3: e346.

Vincent JL, Sakr Y, Sprung C et al. (2006) Sepsis in European intensive care units: results of the SOAP study. Critical Care Medicine 34: 344–353.

Vincent JL and Weil MH (2006) Fluid challenge revisited. Critical Care Medicine 34: 1333–1337.

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.

Contact Editor close
Submit a note to the editor about this article by filling in the form below.

* Required Field

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