Predictors of bacteraemia and mortality in patients with acute liver failure

Karvellas, Constantine J.; Pink, Fred; McPhail, Mark; Cross, Timothy J.S.; Auzinger, G.; Bernal, William; Sizer, Elizabeth; Kutsogiannis, Demetrios J.; Eltringham, Ian; Wendon, Julia

doi:10.1007/s00134-009-1472-x

Cited by 96 publications

(47 citation statements)

References 32 publications

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“…10,11 These infections are associated with increasing severity of complications, such as worsening hepatic encephalopathy but interestingly do not seem to adversely influence outcomes. 12,13 This may be due to increased surveillance and heightened alertness for bacterial infection as well as early (preemptive) therapy with effective antimicrobials. 14 Similarly, patients with liver failure awaiting transplantation are at increased risk of infections, and although infections before transplantation may not affect mortality, in the posttransplant period early bacterial infections are a major cause of mortality.…”

Section: Significance Of Infectious Insult In Liver Diseasementioning

confidence: 98%

Infections in Liver Disease

Nanchal

Ahmad

2016

Critical Care Clinics

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Section: Significance Of Infectious Insult In Liver Diseasementioning

confidence: 98%

Infections in Liver Disease

Nanchal

Ahmad

2016

Critical Care Clinics

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“…In more recent reports, the predominant organisms reported are Gram-negative. 10,11 Renal failure has been described in 40%-80% of patients in western series, and is associated with a poor prognosis. It occurs more frequently in acetaminophen induced ALF (70%) and less frequently in ALF due to other causes (30%) in western series, suggesting that there may be a toxic effect of acetaminophen on renal tubules.…”

mentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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Acute liver failure (ALF) is a rare, potentially fatal complication of severe hepatic illness resulting from various causes. In a clinical setting, severe hepatic injury is usually recognised by the appearance of jaundice, encephalopathy and coagulopathy. The central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique and multifactorial. Ammonia plays a central role in the pathogenesis. The role of newer ammonia lowering agents is still evolving. Liver transplant is the only effective therapy that has been identified to be of promise in those with poor prognostic factors, whereas in the others, aggressive intensive medical management has been documented to salvage a substantial proportion of patients. A small fraction of patients undergo liver transplant and the remaining are usually treated with medical therapy. Therefore, identification of the complications and causes of death in such patients, and use of appropriate prognostic models to identify those who need liver transplant and those who can be managed with medical treatment is a vital component of therapeutic strategy. In this review, we discuss the various pathogenetic mechanisms and treatment options available. ( J CLIN EXP HEPATOL 2015;5:S104-S115)A cute liver failure (ALF) can be a fatal complication of acute hepatic injury and occurs unpredictably. It is a rare clinical entity marked by the sudden loss of hepatic function and a severe life-threatening course in a person with no prior history of liver disease. ALF represents a syndrome rather than a specific disease, having multiple causes that vary in course and outcome. ALF is difficult to identify in its early stages, resulting in frequent delays in initiation of treatment. The causes of ALF include viral hepatitis, drug induced and toxin-induced liver damage, metabolic errors, ischemia, and miscellaneous rare causes.ALF is defined by three criteria: (1) rapid development of hepatocellular dysfunction (jaundice, coagulopathy), (2) encephalopathy, and (3) absence of a prior history of liver disease. 1 However, the interval between onset of acute hepatic injury (jaundice) and onset of liver failure (encephalopathy with or without coagulopathy) in such patients (icterus-encephalopathy interval; IEI) has been described to be between 4 weeks (Indian definition) 2-4 to 24 weeks (AASLD-ALF study group). 5 Further, due to the diverse natural course, ALF has been sub-classified as hyperacute (IEI # 7 day), acute (IEI # 4 weeks) and sub-acute ALF (IEI $ 5 week to #12 weeks) by British authors. 6 Despite these differences in definitions, the central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique an...

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“…In recent reports, the predominant organisms reported are Gram negative. 18,30 There are several non-hepatotropic viruses that can also lead to similar syndrome. One example is Yellow fever, which is caused by a virus carried by mosquitoes.…”

Section: Acute and Subacute Liver Failurementioning

confidence: 99%