Diagnosis and Management of Acute Liver Failure

Anne M. Larson

Curr Opin Gastroenterol. 2010;26(3):214-221.

Abstract and Introduction

Abstract

Purpose of review Acute liver failure (ALF) is a devastating syndrome afflicting previously healthy individuals. Early recognition of the illness is crucial, as aggressive treatment may improve outcomes. Despite significant advances in care, however, the mortality remains high (30–100%). This brief review will focus on the causes and overall management of the complications of ALF.
Recent findings Our knowledge of the causes of ALF has expanded significantly in the last decade. The mechanism of hepatic encephalopathy and cerebral edema in this setting continues to be elucidated and is discussed here.
Summary Improved outcomes can be achieved with the early recognition and aggressive management of ALF.

Introduction

Acute liver failure (ALF) is a catastrophic multiorgan syndrome occurring in previously healthy individuals that is characterized by severe hepatocellular dysfunction and may swiftly progress to death. ALF affects about 2000–2800 persons annually (3.5 deaths per million population) and accounts for 5–6% of liver transplants in the United States.^[1,2] The clinical syndrome is the same, regardless of the cause. Improved medical management and emergent orthotopic liver transplantation (OLT) have improved overall patient survival, yet mortality ranges from 30 to 100%. This review will briefly outline the causes, diagnosis, and up-to-date management of this devastating illness.

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Table 1. Laboratory evaluation in acute liver failure
Serum chemistries	Sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphate, glucose, blood urea nitrogen, and creatinine
Hepatic panel	AST, ALT, alkaline phosphatase, total bilirubin, and albumin
Prothrombin time/INR
Complete blood count	White blood cells, hemoglobin, hematocrit, and platelets
Arterial blood gas and lactate
Acetaminophen level
Toxicology screen
Viral hepatitis serologies	Anti-HAV IgM, hepatitis B surface antigen, anti-hepatitis B core IgM, anti-HCV^a, anti-HEV (as indicated)
Autoimmune markers	Antinuclear antibody, antismooth muscle antibody, and IgG levels
Pregnancy test
Ceruloplasmin level	If Wilson's disease is suspected

ALT, alanine aminotransferase; AST, aspartate aminotransferase; HAV, hepatitis A virus; HCV, hepatitis C virus; HEV, hepatitis E virus; IgG or IgM, immunoglobulin G or M; INR, international normalized ratio.
Data from Larson.^[17]
^a To identify underlying infection.

Table 2. Hepatic encephalopathy
Grade	Mental status	Reflexes
I	Subtle personality changes	Normal
	Slowed mentation	Apraxia
	Lethargy	Slight tremor
	Mild disorientation	Incoordination
	Sleep disturbances
II	More lethargic or apathetic	Brisk reflexes
	Mild confusion	Asterixis
	Disorientation for time	Ataxia
	Inappropriate behavior
	Answers appropriately
III	Somnolent but rousable	Ataxia
	Semistuporous	Asterixis
	Lack of focus	Unsustained clonus
	Inappropriate answers	Up-going toes
	Marked confusion
IVa	Coma	Sustained clonus
	Responsive to pain	Decerebration
IVb	Coma	Becoming flaccid
	Unresponsive to pain
Brain death	Unresponsive	Flaccid
		Absent reflexes

Data from ^[17,32–34].

Table 3. King's College criteria ^[66] for predicting death or need for transplantation in acute liver failure
Acetaminophen	Non-acetaminophen
Strongly consider OLT listing if arterial lactate >3.5 mmol/l after early fluid resuscitation	List for OLT if INR >6.5 irrespective of degree of hepatic encephalopathy
List for OLT if
pH<7.3 Arterial lactate >3.0 mmol/l after adequate fluid resuscitation	or any three: Age <10 or >40 years Jaundice for >7 days before encephalopathy
List for OLT if all three occur within a 24-h period	INR >3.5
Presence of grade 3 or 4 hepatic encephalopathy	Bilirubin >17 mg/dl
INR >6.5 Creatinine >3.4 mg/dl	Unfavorable cause such as Wilson's disease Idiosyncratic drug reaction Halothane Seronegative hepatitis