Highlights & Basics
- Acute liver failure is a rare, life-threatening, potentially reversible condition defined by jaundice, coagulopathy, and hepatic encephalopathy.
- Occurs in patients with no preexisting liver disease and may result in severe liver impairment and rapid clinical deterioration.
- The etiology and the interval from onset of jaundice to the development of encephalopathy have a significant impact on prognosis.
- Etiology is established by history, serological assays, and exclusion of alternative causes, including acute presentations of chronic liver diseases.
- Treatment involves intensive care unit monitoring, specific therapies based on etiology, and management of known complications.
- All patients should be considered for possible liver transplantation.
- Prognostic models may be used to assess the probability of spontaneous recovery and are instrumental in selection of patients who should potentially undergo liver transplantation.
Quick Reference
History & Exam
Key Factors
hepatotoxic medication
chronic alcohol misuse
pregnancy
jaundice
coagulopathy
signs of hepatic encephalopathy
Other Factors
absence of history of chronic liver disease
abdominal pain
nausea
vomiting
malaise
signs of cerebral edema
right upper quadrant tenderness
hepatomegaly
absence of splenomegaly
absence of spider angiomata
absence of palmar erythema
absence of ascites
depression or suicidal ideation
Wilson disease
exposure to hepatotoxins
illicit drug use
absence of malignancy
Diagnostics Tests
1st Tests to Order
liver function tests
prothrombin time/INR
basic metabolic panel
CBC
blood type and screen
serum amylase and lipase
arterial blood gas
arterial blood lactate
acetaminophen level
urine toxicology screen
viral hepatitis serologies
autoimmune hepatitis markers
pregnancy test
chest x-ray
abdominal ultrasound with Doppler
Other Tests to consider
factor V level
viral hepatitis polymerase chain reaction (PCR) studies
serum ceruloplasmin
serum copper
24-hour urinary copper excretion
slit-lamp ophthalmologic examination
arterial ammonia
HIV test
urinalysis and urine sodium
surveillance cultures
Coombs test
biomarkers
liver biopsy
CT scan of head
CT/MR cholangiography
Transcranial Doppler
Treatment Options
acute
all patients
all patients
acetaminophen-related or with mild to moderate (grade 1 or 2) hepatic encephalopathy
with herpes simplex hepatitis
with acute fatty liver of pregnancy or the hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome
with suspected Amanita phalloides poisoning
with autoimmune hepatitis
with acute hepatitis B
with acute Budd-Chiari syndrome
with acute Wilson disease
with established UNOS Status 1A priority
Definition
Classifications
By interval from onset of jaundice to development of hepatic encephalopathy
- Hyperacute if occurring within 7 days
- Acute if occurring between 7 and 21 days
- Subacute if between 22 days and 26 weeks.
By interval from onset of hepatic illness to development of hepatic encephalopathy
Vignette
Common Vignette
Other Presentations
Epidemiology
Etiology
Pathophysiology
Diagnostic Approach
History and physical findings
Clinical evaluation of hepatic encephalopathy
- Grade 1: subtly impaired awareness, sleep alterations, shortened attention span, impaired addition or subtraction, heightened mood or anxiety, oriented in time and space.
- Grade 2: lethargy or apathy, disorientation for time, obvious personality change, inappropriate behavior, dyspraxia, asterixis.
- Grade 3: somnolence to semistupor, responsive to vocal stimuli, marked confusion, gross disorientation (disoriented in time and space), bizarre behavior. Physical findings may include hyperreflexia, nystagmus, clonus, and rigidity.
- Grade 4: coma.
Tests
- Blood tests: prothrombin time and international normalized ratio (INR) and liver function tests, viral serologies, autoimmune markers, toxicology screening, and parameters to assess overall clinical status, such as hematology, acid-base balance, and renal dysfunction.[4] Serum amylase and lipase levels should be assessed to exclude pancreatitis, which may develop as a complication of ALF; however, hyperamylasemia may also develop as a result of renal dysfunction and multiorgan failure.[51] [52] [53] [54] [55] Although hyperamylasemia is associated with an increased risk of mortality, it is not an independent predictor of mortality in ALF.[55]
- All at-risk female patients of childbearing age should have a pregnancy test.[4]
- Serum acetaminophen levels should be measured in all patients.[4] Acetaminophen levels can be useful when elevated; however, low acetaminophen levels do not rule out acetaminophen hepatotoxicity, and suspected cases should be managed accordingly. Over 50% of patients with acute liver injury or ALF attributed to acetaminophen may have undetectable levels of plasma acetaminophen levels.[56]
- Initial imaging should include a chest x-ray to confirm possible aspiration pneumonia or to rule out other pulmonary abnormalities, and abdominal Doppler imaging to assess hepatic vein thrombosis associated with Budd-Chiari syndrome.[4] Liver imaging is also appropriate if drug-induced liver injury is suspected to assess whether there may be a competing etiology. Abdominal ultrasound is first-line to assess whether cirrhosis, biliary obstruction or other focal liver changes are present. CT and MR cholangiography may also be useful to assess whether vascular abnormalities or pancreatobiliary disease are present.[29]
- Polymerase chain reaction studies for hepatitis B, hepatitis C, and herpes simplex virus DFNA may establish the diagnosis before serology studies become positive.
- HIV test.
- Serum ceruloplasmin, serum and hepatic copper levels, 24-hour urinary copper excretion, and slit-lamp ophthalmologic evaluation for the presence of Kayser-Fleischer rings if Wilson disease is suspected.[8]
- Coombs test: in the presence of hemolysis, a negative Coombs test may further differentiate between Wilson disease and autoimmune hemolysis, which is typically Coombs-positive.
- Arterial ammonia levels are characteristically elevated if hepatic encephalopathy is present, although it is a nonspecific test. High levels may predict an increased risk of developing intracranial hypertension.
- Head computed tomography is useful for further evaluation of cerebral edema or other underlying pathology in advanced encephalopathy.[4]
- A transcranial Doppler, with estimation of cerebral perfusion pressure and intracranial pressure, may be considered in patients with grade 3 to 4 hepatic encephalopathy who are at risk of intracranial hypertension or for those in whom developing cerebral edema is expected.[57]
- Surveillance cultures: blood, urine, and sputum cultures should be obtained at regular intervals once advanced grade of encephalopathy develops.
- Urinalysis and urine sodium should be obtained if renal dysfunction is present.
- Liver biopsy: although a liver biopsy may provide additional information to suggest potential etiologies of ALF in indeterminate cases, it is not a required test to confirm a diagnosis and generally does not have an impact on clinical management, outcome, or assessment of prognosis. For these reasons, liver biopsies in the setting of ALF are not usually performed.[58] An exception to this may include circumstances in which there is suspicion for infiltrative malignancy such as lymphoma or metastatic liver disease.[4] [59] A liver biopsy may also be helpful in the diagnosis of conditions such as suspected autoimmune hepatitis or acute herpes simplex virus hepatitis.[4] [60] [61] If a drug-induced liver injury is suspected, liver biopsy may help to identify the hepatotoxic drug, based on the histological pattern(s), or determine the mechanism of injury, and it may also provide useful prognostic information.[29] If a liver biopsy is considered, a transjugular approach is preferable given the increased risk of bleeding associated with coagulopathy during ALF.[4] Type and screen of blood units should be performed in case a transfusion is needed.
Prognosis assessment
Risk Factors
History & Exam
Tests
Differential Diagnosis
Severe acute hepatitis
Differentiating Signs/Symptoms
- Patients may present with jaundice and coagulopathy. However, this would not be considered ALF in the absence of hepatic encephalopathy. Severe acute hepatitis should be followed very closely as this may potentially develop into ALF or subacute liver failure, depending on the time course and development of hepatic encephalopathy.
Differentiating Tests
- Grade 1: subtly impaired awareness, sleep alterations, shortened attention span, impaired addition or subtraction, heightened mood or anxiety, oriented in time and space.
- Grade 2: lethargy or apathy, disorientation for time, obvious personality change, inappropriate behavior, dyspraxia, asterixis.
- Grade 3: somnolence to semistupor, responsive to vocal stimuli, marked confusion, gross disorientation (disoriented in time and space), bizarre behavior. Physical findings may include hyperreflexia, nystagmus, clonus, and rigidity.
- Grade 4: coma.
Differentiating Signs/Symptoms
- Jaundice may result from intra- or extrahepatic biliary obstruction as well as from intrahepatic cholestasis due to conditions such as drug-induced liver injury or a chronic cholestatic liver disease. In the setting of an acute biliary obstruction, a patient may present with shock associated with cholangitis. Key features that distinguish these presentations from ALF include absence of coagulopathy and of hepatic encephalopathy, both of which are present during ALF.
Differentiating Tests
- Normal prothrombin time (PT)/INR, absence of hepatic encephalopathy (according to the West Haven Criteria as mentioned above).[49] [69] [70] In the presence of coagulopathy associated with cholestatic disorders and vitamin K deficiency, administration of subcutaneous vitamin K would improve PT/INR and may also be considered as a differentiating test.
Hemolysis
Differentiating Signs/Symptoms
- May present with jaundice characterized by an elevated unconjugated (indirect) serum bilirubin.
- Typically occurs in the absence of liver dysfunction; therefore, coagulopathy and hepatic encephalopathy would not be present. Exceptions to this include ALF secondary to Wilson disease, which may be associated with a Coombs-negative hemolytic anemia.[42] ALF secondary to autoimmune hepatitis may coincide with an acute autoimmune hemolytic anemia.[42] [78] Sickle cell disease may also present acutely with jaundice, hemolysis, and liver dysfunction as a result of a sickle cell hepatopathy.[79]
Criteria
- pH <7.30, or
- INR >6.5 (PT >100 seconds) and serum creatinine >3.4 mg/dL (>300 micromol/L) in patients with grade 3 or 4 hepatic encephalopathy.
- INR >6.5 (PT >100 seconds), or
- any 3 of the following: age <10 or >40 years; etiology non-A, non-B hepatitis, or idiosyncratic drug reaction; duration of jaundice before hepatic encephalopathy >7 days; INR >3.5 (PT >50 seconds); serum bilirubin >17.6 mg/dL (>300 micromol/L).
- <20% of normal in patients ages <30 years, or
- <30% of normal in patients ages >30 years.
- Laboratory studies required for the model: creatinine, total bilirubin, and INR.
- MELD =9.57×log^e(creatinine)+3.78× log^e(bilirubin)+11.2×log^e(INR)+6.43
- Grade 1: subtly impaired awareness, sleep alterations, shortened attention span, impaired addition or subtraction, heightened mood or anxiety, oriented in time and space.
- Grade 2: lethargy or apathy, disorientation for time, obvious personality change, inappropriate behavior, dyspraxia, asterixis.
- Grade 3: somnolence to semistupor, responsive to vocal stimuli, marked confusion, gross disorientation (disoriented in time and space), bizarre behavior. Physical findings may include hyperreflexia, nystagmus, clonus, and rigidity.
- Grade 4: coma.
Treatment Approach
Intensive care management
- Grade 1: subtly impaired awareness, sleep alterations, shortened attention span, impaired addition or subtraction, heightened mood or anxiety, oriented in time and space.
- Grade 2: lethargy or apathy, disorientation for time, obvious personality change, inappropriate behavior, dyspraxia, asterixis.
- Grade 3: somnolence to semistupor, responsive to vocal stimuli, marked confusion, gross disorientation (disoriented in time and space), bizarre behavior. Physical findings may include hyperreflexia, nystagmus, clonus, and rigidity.
- Grade 4: coma.
Acetaminophen overdose or mild to moderate (grade 1 or 2) encephalopathy
Other disease-specific therapies
Liver transplantation
- Age >18 years, life expectancy without a liver transplant of <7 days, onset of encephalopathy within 8 weeks of the first symptoms of liver disease, absence of preexisting liver disease, admission to an intensive care unit, and 1 of the following:
- Ventilator dependence, requirement of renal replacement therapy, or INR >2.0.
Treatment Options
all patients
intensive care management
Comments
- Patients with ALF with grade 2 or higher hepatic encephalopathy should be admitted to an intensive care unit (ICU).[4] The natural history of ALF may be characterized by a rapid deterioration in neurologic status, high risk of complications including sepsis and cerebral edema, hemodynamic instability, and renal failure. Intensive care unit monitoring is critical in providing optimal care of the patient and to prevent and treat known complications of ALF.
- Efforts should be made to minimize elevations of intracranial pressure. The head of the patient's bed should be raised to approximately 30 degrees and surrounding stimuli reduced to a minimum.[51] Once advanced encephalopathy develops (grades 3 or 4), tracheal intubation should be performed for airway protection.[4] Propofol and fentanyl are preferred agents for analgesia and sedation due to their short half-lives. Intravenous fluids should be administered with caution to prevent depletion or volume overload; central venous pressure and pulmonary arterial monitoring as well as renal replacement therapy should be considered early to ensure optimal fluid management, particularly if there is evidence of renal or circulatory dysfunction.[8] [99]
- Enteral nutrition is generally a concern in the setting of encephalopathy, in which the patient is unable to obtain adequate nutrition due to an altered mental status. Therefore, enteral nutritional support with calorie-dense feeds should also be initiated early during the hospital course.
- Prophylactic antimicrobial therapy does not appear to influence outcome and is not recommended.[4] [103] However, empirical antimicrobials are recommended if a patient develops positive surveillance cultures, refractory hypotension, progression to grade 3 to 4 hepatic encephalopathy, evidence of Systemic Inflammatory Response Syndrome; and in all patients who are listed for liver transplantation.[99]
- Proton-pump inhibitors or H2 antagonists should be administered as prophylaxis of gastrointestinal bleeding secondary to coagulopathy.[8]
liver transplantation assessment
Comments
- Criteria for United Network for Organ Sharing (UNOS) Status 1A designation include: age >18 years, life expectancy without a liver transplant of <7 days, onset of encephalopathy within 8 weeks of the first symptoms of liver disease, absence of preexisting liver disease, admission to an intensive care unit, and 1 of the following: ventilator dependence, requirement of renal replacement therapy, or INR >2.0. UNOS status 1A patients are listed with top priority for liver allocation. Wilson disease may also be given Status 1A priority.
- Contraindications to liver transplantation for ALF include severe cardiac or pulmonary disease, AIDS, extrahepatic malignancy, metastatic hepatocellular carcinoma, intrahepatic cholangiocarcinoma, uncontrolled sepsis, irreversible neurologic complications (e.g., brain death, intracerebral hemorrhage, intractable sustained raised intracranial pressure), ongoing alcohol or illicit substance misuse, and lack of an adequate social support system.[48]
neurologic status monitoring for advanced encephalopathy
Comments
- Neurologic status should be monitored carefully and regularly for the development of advanced encephalopathy (grade 3 to 4), which is associated with a greater risk of cerebral edema and intracranial hypertension.
- Head of the patient's bed should be raised to 30 degrees and surrounding stimuli reduced. Tracheal intubation and sedation with intravenous propofol or fentanyl should be performed once advanced encephalopathy develops. Central venous pressure monitoring, pulmonary arterial monitoring, and renal replacement therapy should be considered early.
monitoring of blood glucose, electrolytes, and cultures
Comments
- Blood glucose levels should be monitored every 1 to 2 hours by finger stick to assess for hypoglycemia. Hypoglycemia should be corrected with intravenous glucose infusion, with a glycemic target of 140 mg/dL.[51]
- Serum electrolytes, including sodium, phosphate, potassium, and magnesium, should be monitored at least twice daily and corrected aggressively.
- In patients with advanced encephalopathy (grade 3 or 4), surveillance cultures from blood, urine, and sputum should be obtained periodically given the high risk of bacterial and fungal infection; however, no clear impact of prophylactic antimicrobials has been shown.
- Other routine laboratory studies such as coagulation activity, blood cell counts, and liver enzymes should also be monitored closely at regular intervals.
acetaminophen-related or with mild to moderate (grade 1 or 2) hepatic encephalopathy
acetylcysteine
Primary Options
- acetylcysteine
consult specialist for guidance on dose
- acetylcysteine
Comments
- Acetylcysteine therapy should be given in all cases of acetaminophen overdose regardless of the dose or timing of acetaminophen ingestion. See Acetaminophen overdose .
- Acetylcysteine therapy is also recommended for patients with mild to moderate hepatic encephalopathy, even when acetaminophen has not been ingested.[104] Based on available evidence, the American College of Gastroenterology recommends using intravenous acetylcysteine in patients with non-acetaminophen ALF.[4] In particular, a short course of intravenous acetylcysteine may be of benefit for hospitalized adult patients with ALF secondary to a drug-induced liver injury, but it is not recommended in children.[29]
- Oral acetylcysteine may be given in patients with up to grade 1 hepatic encephalopathy. Intravenous acetylcysteine is preferred for higher grades of hepatic encephalopathy or if the patient is intolerant of oral intake, has ileus or is pregnant, and should be accompanied by telemetry monitoring.[4] [29]
activated charcoal
Primary Options
- charcoal, activated
25-100 g orally as a single dose
- charcoal, activated
Comments
- In patients with acetaminophen overdose in whom ingestion is known to have occurred within 4 hours, a single-dose of activated charcoal can be given.[4]
with herpes simplex hepatitis
with acute fatty liver of pregnancy or the hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome
expedient delivery of the fetus
with suspected Amanita phalloides poisoning
intravenous fluids + gastric lavage + activated charcoal
Primary Options
- charcoal, activated
25-100 g as a single dose, repeat every 4-6 hours if required
- charcoal, activated
Comments
- Contact the poison control center for guidance. Continued supportive management includes intravenous fluids.[4]
penicillin-G
Primary Options
penicillin G sodium
300,000 to 1,000,000 units/kg/day intravenously once daily
Comments
- Amatoxins inhibit hepatocyte RNA polymerase II, leading to cell necrosis. Beta-lactam antibiotics are thought to be hepatoprotective in the setting of amanita toxicity. This has been reported through in vitro experiments, studies with animal models, and in the clinical setting following Amanita phalloides ingestion by humans, in which intravenous penicillin has been associated with clinical recovery and improved survival. The exact mechanism has not been well defined; however, it may be associated with blocking of amatoxin uptake by hepatocytes.[4] [29] [99] [122] [123]
acetylcysteine
Primary Options
- acetylcysteine
consult specialist for guidance on dose
- acetylcysteine
Comments
- Oral acetylcysteine may be given in patients with up to grade 1 hepatic encephalopathy. Intravenous acetylcysteine is preferred for higher grades of hepatic encephalopathy, or if the patient is intolerant to oral intake, has ileus or is pregnant; telemetry monitoring is recommended for intravenous dosing.
with autoimmune hepatitis
methylprednisolone
with acute hepatitis B
oral nucleoside or nucleotide analog
Primary Options
- entecavir
0.5 mg orally/nasogastrically once daily
- entecavir
- tenofovir disoproxil
300 mg orally/nasogastrically once daily
- tenofovir disoproxil
Comments
- Studies are limited, although antiviral therapy may have benefit and should be considered. Entecavir or tenofovir are the preferred agents.
with acute Budd-Chiari syndrome
anticoagulation
Comments
- Patients should be assessed for an underlying hypercoagulable disorder or myeloproliferative disease. Anticoagulation therapy (e.g., low molecular weight heparin) should be initiated in all patients.[4]
- Budd-Chiari syndrome is defined by hepatic outflow obstruction secondary to thrombosis at the level of the hepatic veins or suprahepatic inferior vena cava in the absence of cardiac disease. A key factor in the pathogenesis of Budd-Chiari syndrome is the presence of an underlying prothrombotic condition, which can be identified in the majority of cases. Thus, all patients presenting with Budd-Chiari syndrome should be considered for immediate anticoagulation therapy.
transjugular intrahepatic portosystemic shunt (TIPS)
Comments
- Hepatic vein angioplasty with stent or TIPS placement may be considered in patients not responding to anticoagulation.[4] However, some may ultimately require liver transplantation.
with acute Wilson disease
measures to decrease serum copper
Comments
- Acute Wilson disease with ALF is associated with high mortality despite measures to decrease serum copper levels, including plasmapheresis, continuous veno-venous hemofiltration, albumin dialysis, or plasma exchange. Chelation therapy for Wilson disease in the setting of ALF is generally ineffective, may be associated with hypersensitivity, and is not recommended.
with established UNOS Status 1A priority
liver transplant
Comments
- Wilson disease should be suspected in any patient presenting with ALF with nonimmune hemolytic anemia including acute intravascular hemolysis. These patients should be urgently evaluated for liver transplantation.[42]
- Patients with ALF who fulfill listing criteria, according to the United Network for Organ Sharing (UNOS), may be assigned category Status 1A and listed with top priority for liver allocation. Criteria for UNOS Status 1A designation include: age >18 years, life expectancy without a liver transplant of <7 days, onset of encephalopathy within 8 weeks of the first symptoms of liver disease, absence of preexisting liver disease, admission to an intensive care unit, and 1 of the following: ventilator dependence, requirement of renal replacement therapy, or INR >2.0. Patients with acute fulminant Wilson disease may also be given Status 1A priority.
- Contraindications to liver transplantation for ALF include severe cardiac or pulmonary disease, AIDS, extrahepatic malignancy, metastatic hepatocellular carcinoma, intrahepatic cholangiocarcinoma, uncontrolled sepsis, irreversible neurologic complications (e.g., brain death, intracerebral hemorrhage, intractable sustained raised intracranial pressure), ongoing alcohol or illicit substance misuse, and lack of an adequate social support system.[48]
Emerging Tx
Nonbiologic hepatic assist devices
Bioartificial hepatic assist devices
Liver tissue engineering and hepatocyte transplantation
Auxiliary transplantation
Prevention
Primary Prevention
Secondary Prevention
Follow-Up Overview
Prognosis
Survival and outcomes
Monitoring
Complications
Citations
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Key Articles
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Guidelines
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Summary
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American College of Gastroenterology
Published
2023
Summary
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American Academy for the Study of Liver Disease
Published
2023
Summary
A comprehensive group of guidelines on the diagnosis and management of ALF. These guidelines are based on a thorough review and analysis of existing data on the topic.Published by
American Association for the Study of Liver Diseases
Published
2011
Summary
An overview and update on the epidemiology, natural history, etiology, pathophysiology, and treatment of ALF. The content is based on data presented at a workshop supported by the National Institutes of Health. Areas emphasized in this manuscript include new trends in the epidemiology and management of ALF, as well as recommendations for future research.Published by
National Institute of Diabetes and Digestive and Kidney Diseases; National Institute of Biomedical Imaging and Bioengineering; Office of Rare Diseases of the National Institutes of Health
Published
2008
Summary
Recommendations on the features (clinical, laboratory, and histologic) seen in patients with drug-induced liver injury. Includes expert opinion-based recommendations on patient management.Published by
American Association for the Study of Liver Diseases
Published
2022
Summary
A comprehensive guideline on the diagnosis of ALF.Published by
European Association for the Study of the Liver
Published
2017
Treatment
Summary
Practice recommendations for the treatment of ALF.Published by
American College of Gastroenterology
Published
2023
Summary
Provides guidance on the treatment of Wilson disease.Published by
American Academy for the Study of Liver Disease
Published
2023
Summary
A comprehensive group of guidelines on the diagnosis and management of ALF. Recommendations include disease-specific therapies and management approach of additional clinical features such as encephalopathy, infection, coagulopathy, gastrointestinal bleeding.Published by
American Association for the Study of Liver Diseases
Published
2011
Summary
These recommendations provide a detailed, evidence-based protocol on the intensive care management of patients with ALF. This consensus was designed as a guide for providers involved in the care of patients with ALF, including intensive care specialists.Published by
US Acute Liver Failure Study Group; National Institutes of Health; Food and Drug Administration
Published
2007
Summary
Recommendations on the features (clinical, laboratory, and histologic) seen in patients with drug-induced liver injury. Includes expert opinion-based recommendations on patient management.Published by
American Association for the Study of Liver Diseases
Published
2022
Summary
Evidence-based recommendations addressing common clinical questions surrounding the unique manifestations of liver failure in the critically ill patient to aid best practice. Includes recommendations for patients with acute liver failure.Published by
Society of Critical Care Medicine
Published
2020
Summary
Evidence-based recommendations addressing common clinical questions surrounding the unique manifestations of liver failure in the critically sick patient to aid best practice. Includes recommendations for patients with ALF.Published by
Society of Critical Care Medicine
Published
2023
Summary
A comprehensive group of guidelines on the management of ALF. Recommendations include disease-specific therapies and the management approach of additional clinical features such as encephalopathy, infection, coagulopathy, and gastrointestinal bleeding.Published by
European Association for the Study of the Liver
Published
2017
Summary
Guidance on the management of hepatic encephalopathy.Published by
European Association for the Study of the Liver
Published
2023