Prospective study of bacterial infection in acute liver failure: An analysis of fifty patients

Abstract

Fifty consecutive patients admitted with acute liver failure, minimal grade II encephalopathy, were studied prospectively to determine the incidence, timing and cause of bacterial infection, the relationship to clinical criteria for infection; and the influence of early microbiological diagnosis on clinical outcome. There were 53 proven bacterial infections in 40 patients, whereas in 5 of the remaining 10 patients infection was suspected on clinical grounds in the absence of significant cultures. Seven patients (14%) had more than one bacterial infection, and four patients had simultaneous infections caused by different organisms at each site. Fourteen infections (26.4%) were associated with bacteremia, and in six of these no source was found. Twenty-five infections (47.1%) arose from the respiratory tract, 12 (22.6%) from the urinary tract and 2 (3.7%) from central venous cannulas. Thirty-seven (69.8%) of the 53 infections were due to gram-positive bacteria; Staphylococcus aureus accounted for 19 (35.8%) of all the infections. Thirty patients died (60%), 28 of whom had bacterial infection at some time; in 24 of these the infection was diagnosed less than 24 hr before death. All nine deaths that occurred more than 7 days after admission were directly attributable to microbial infection. Clinical features such as elevated temperature and elevated peripheral white blood cell count were poor indicators of bacterial infection because these were absent in 30.2% of cases. These data show that there is a high incidence of bacterial infection early in the course of acute liver failure and suggest that prophylactic antimicrobial therapy, although unproven, might be justified.

Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver failure

“…1,21 This involved continuous intravenous dextrose infusion to prevent hypoglycemia; broadspectrum prophylactic antimicrobials to prevent bacterial and fungal infections, [22][23][24][25] and ranitidine and/or sucralfate to prevent acute gastrointestinal bleeding. 26 Children were admitted to the pediatric intensive care unit if they developed encephalopathy grade Ͼ2, became hypoxic, or needed sedation.…”

Hepatocyte growth factor prevents endotoxin-induced lethal hepatic failure in mice

“…[1][2][3] In particular, sepsis and endotoxemia are frequent complications, and bacteriologically proven infection occurs in up to 80% patients with fulminant hepatic failure. 4 Endotoxin is a gram-negative bacterial lipopolysaccharide (LPS) and releases a wide variety of inflammatory mediators, which are considered to be related to the development of fulminant hepatic failure as well as to multiple organ failure. [5][6][7] In mice injected with a high dose of LPS, multiple organ failure occurred, as characterized by circulatory failure, thereby reflecting a systemic inflammatory response syndrome and septic shock, rather than endotoxin-induced hepatic failure.…”

Acute Liver Failure : Management Update

“…Glucose infusion rates of 10 to 15 mg/kg/minute may be required to achieve stable serum glucose levels. 18 Hypokalemia Hypokalemia may be caused by dilution from volume overload, ascites, or renal wasting and correction depends upon aetiology. Judicious use of fluid, salt and if needed intravenous administration of potassium is the treatment of choice for hypokalamia.…”