Infection, coagulation, and variceal bleeding in cirrhosis
- Liver Transplantation and Hepatobiliary Medicine Unit, Royal Free Hospital, London, UK
- Correspondence to:
Professor A K Burroughs
Liver Transplantation and Hepatobiliary, Medicine Unit, Royal Free Hospital, Pond St, London NW3 2QG, UK; Andrew.Burroughsroyalfree.nhs.uk
- Accepted 13 August 2004
- Revised 1 August 2004
- infection
- coagulation
- variceal bleeding
- cirrhosis
- antibiotics
- bacterial translocation
- endotoxin
- portal pressure
SUMMARY
Bacterial infections in cirrhotic patients are common. There is a predisposition to intestinal bacterial overgrowth, intestinal dysmotility, and increased intestinal permeability, all leading to an increase in bacterial translocation. Bacterial translocation is the probable mechanism for some of the most common infections in cirrhosis, such as spontaneous bacterial peritonitis, but is also the source of bacterial byproducts such as endotoxin which can cause an increase in portal pressure, impairment of liver function, and worsening of haemostasis.
The effects of bacterial infection and bacterial products on portal and systemic haemodynamics in cirrhosis and clinical data on infection, from both retrospective and prospective studies of variceal bleeding and other settings, demonstrate the importance of infection in pathophysiological mechanisms in cirrhosis. This has been followed by recent clinical evidence that antibiotic therapy reverses systemic vasodilation and prevents early variceal rebleeding.
INTRODUCTION
In cirrhotic patients there is an increased susceptibility to bacterial infection, related to the degree of liver dysfunction1 leading to several abnormalities of defence mechanisms, all of which increase the susceptibility to infection, including deficiency of bactericidal and opsonic activities, impaired monocyte function, depressed phagocytic activity of the reticuloendothelial system (RES), defective chemotaxis, and low levels of complement in serum.
A particularly important role is played by the reduced RES activity, due to the presence of extrahepatic and intrahepatic shunts through sinusoids without Kupffer cells, reduced number of Kupffer cells, and impaired Kupffer cell function. Thus cirrhotics with impaired RES phagocytic activity (as assessed by elimination of 99 m technetium-sulphur colloid) develop acute bacterial infections more frequently than cirrhotics with normal RES phagocytic activity.2
Both community and hospital acquired bacterial infections are frequently diagnosed in cirrhotics, most frequently spontaneous bacterial peritonitis (SBP), urinary tract infections, pneumonia, and skin infections.3 Their incidence rises with worsening liver function.3 Importantly, half of …
