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Severe sepsis in cirrhosis†
Article first published online: 31 AUG 2009
Copyright © 2009 American Association for the Study of Liver Diseases
Volume 50, Issue 6, pages 2022–2033, December 2009
How to Cite
Gustot, T., Durand, F., Lebrec, D., Vincent, J.-L. and Moreau, R. (2009), Severe sepsis in cirrhosis. Hepatology, 50: 2022–2033. doi: 10.1002/hep.23264
Potential conflict of interest: Nothing to report.
- Issue published online: 20 NOV 2009
- Article first published online: 31 AUG 2009
- Accepted manuscript online: 31 AUG 2009 12:00AM EST
- Manuscript Accepted: 24 AUG 2009
- Manuscript Received: 22 JUN 2009
- Postdoctoral researcher of Belgian Fonds de la Recherche Scentifique–FNRS
- Interface INSERM–AP-HP fellowship
Sepsis is physiologically viewed as a proinflammatory and procoagulant response to invading pathogens. There are three recognized stages in the inflammatory response with progressively increased risk of end-organ failure and death: sepsis, severe sepsis, and septic shock. Patients with cirrhosis are prone to develop sepsis, sepsis-induced organ failure, and death. There is evidence that in cirrhosis, sepsis is accompanied by a markedly imbalanced cytokine response (“cytokine storm”), which converts responses that are normally beneficial for fighting infections into excessive, damaging inflammation. Molecular mechanisms for this excessive proinflammatory response are poorly understood. In patients with cirrhosis and severe sepsis, high production of proinflammatory cytokines seems to play a role in the worsening of liver function and the development of organ/system failures such as shock, renal failure, acute lung injury or acute respiratory distress syndrome, coagulopathy, or hepatic encephalopathy. In addition, these patients may have sepsis-induced hyperglycemia, defective arginine-vasopressin secretion, adrenal insufficiency, or compartmental syndrome. In patients with cirrhosis and spontaneous bacterial peritonitis (SBP), early use of antibiotics and intravenous albumin administration decreases the risk for developing renal failure and improves survival. There are no randomized studies that have been specifically performed in patients with cirrhosis and severe sepsis to evaluate treatments that have been shown to improve outcome in patients without cirrhosis who have severe sepsis or septic shock. These treatments include recombinant human activated C protein and protective-ventilation strategy for respiratory failure. Other treatments should be evaluated in the cirrhotic population with severe sepsis including the early use of antibiotics in “non-SBP” infections, vasopressor therapy, hydrocortisone, renal-replacement therapy and liver support systems, and selective decontamination of the digestive tract or oropharynx. (HEPATOLOGY 2009.)