Ascites and intraabdominal infection.
OBJECTIVE
This review will give an overview of current trends in diagnosis, treatment, and pathogenesis of ascites and intraabdominal infection in cirrhotic and noncirrhotic critically ill patients.


RESULTS
Single clone-bacterial DNA has been found in sterile ascites and serum, proving the concept of direct translocation. Activation of mesenteric macrophages can be induced by splanchnic vasodilatation but also by hypoxia. Carbon monoxide, an end product of heme catabolism, promotes splanchnic vasodilatation, representing a possible link between gastrointestinal hemorrhage and circulatory dysfunction. Colorimetric test strips and automated counters accurately diagnose spontaneous bacterial peritonitis. Vasopressin V2-antagonists have been introduced as novel therapy for impaired water excretion in hyponatremia.


CONCLUSIONS
Emerging pathophysiological concepts have modified the conventional view of hydrostatic and Starling forces in the evolution of ascites. Current data indicate that the dynamic sequence of bacterial translocation, mesenteric inflammation, splanchnic vasodilatation and intrahepatic vasoconstriction determines occurrence, severity, and outcome of ascites and intraabdominal infection.
Kramer
Ludwig
L
Department of Medicine IV, Vienna University Medical School, A-1090 Vienna, Austria. L.Kramer@akh-wien.ac.at
Druml
Wilfred
W
D001201:Ascites / Q000150:complications* / Q000188:drug therapy / Q000628:therapy; D001424:Bacterial Infections / Q000150:complications* / Q000188:drug therapy / Q000628:therapy; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications; D010538:Peritonitis / Q000150:complications* / Q000188:drug therapy / Q000628:therapy; D011379:Prognosis