Diagnosis and management of acute liver failure

Larson, Anne M.

doi:10.1097/mog.0b013e32833847c5

Cited by 42 publications

(30 citation statements)

References 64 publications

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“…Clinical management includes discontinuation of sedative agents or, if necessary, use of short-acting benzodiazepines or propofol, as these can decrease intracranial pressure [55]. Symptomatic treatment of encephalopathy includes bowel decontamination with neomycin or rifaximin, and induction of diarrhea by administration of lactulose, thus reducing ammonia absorption, and treatment with branched-chain amino acids to improve peripheral ammonia metabolism, though large, randomized clinical trials have failed to show clinical improvement [56,57].…”

Section: Hepatic Encephalopathymentioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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Section: Hepatic Encephalopathymentioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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“…Acute liver failure was defined as the onset of coagulopathy (INR≥1.5) and any degree of hepatic encephalopathy within 26 weeks of the appearance of symptoms 10 .…”

Section: Methodsmentioning

confidence: 99%

Post-transplant withdrawal of lamivudine results in fatal hepatitis flares in kidney transplant recipients, under immune suppression, with inactive hepatitis B infection

2017

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Objective: To evaluate the consequences of lamivudine withdrawal in kidney transplant recipients, under immunosuppression, with inactive hepatitis B virus (HBV) infection. Introduction: HBV infection is more frequent in kidney transplant recipients than in the general population mainly due to the high risk of acquisition during dialysis, before kidney transplantation. Methods: The records of hepatitis B surface antigen (HBsAg)-positive, immunosuppressed kidney transplant recipients, where lamivudine was withdrawn after transplantation along with reduction in immunosuppressant dose, admitted to our hospital between 2005 and 2012, were retrospectively evaluated. Discussion: Three patients aged 33, 42 and 33, experienced hepatitis flares 2-3 months after lamivudine withdrawal. Serum HBV DNA levels were 2.5×10 7 , 3.4×10 4 and 4×10 3 IU/ml in cases 1, 2, and 3, respectively. Lamivudine was re-initiated in all cases which led to rapid viral suppression. However, liver function continued to deteriorate leading to severe jaundice, coagulopathy and encephalopathy. All patients died of acute liver failure within six months after the onset of withdrawal hepatitis. Conclusion: Lamivudine should be continued as long as immunosuppressive therapy lasts.

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“…While hepatitis viruses are among the most common causes of acute liver failure in developing countries, CAM/drug intoxication by kava, ephedra, skullcap, pennyroyal and acetaminophen etc. predominates in the USA and Europe [15][16][17] .…”

Section: Acute Liver Failurementioning

confidence: 99%