Alcoholic hepatitis is an acute reaction to prolonged excessive alcohol consumption. Mild forms of the syndrome improve without intervention, but when severe there is nearly a 50% 1 month mortality without treatment. Histologically, alcoholic hepatitis is characterized by swollen hepatocytes that contain Mallory bodies (alcoholic hyaline), a neutrophilic infiltrate, and fibrosis between the hepatocyte and the endothelial cell. The pathophysiology includes direct and indirect toxicity from ethanol, oxidative stress, impaired gut barrier function, and immune dysregulation.

Alcoholic liver disease has a spectrum of pathologic findings, including fatty liver disease, alcoholic hepatitis and eventually cirrhosis. Alcoholic hepatitis increases the risk of progression to cirrhosis, and is frequently seen with cirrhosis on liver biopsy.

  • Acute jaundice with cholestatic liver findings in the setting of prolonged heavy alcohol use

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  • Imaging confirming no biliary obstruction

  • Alcohol intake may have ceased or decreased in the preceding weeks when the patient first became ill

Key symptoms of alcoholic hepatitis

  • Jaundice

  • Hepatomegaly

  • Right upper quadrant (RUQ) tenderness/mild pain (due to swelling of the liver capsule)

  • Ascites

  • Anorexia

  • Nausea

  • Encephalopathy

  • Fever

  • Ecchymoses

  • Hepatic bruit

  • Associated with: hepatorenal syndrome, gastrointestinal (GI) bleeding

Alcoholic hepatitis has 20% prevalence among individuals with alcoholism.

  • Older age (typical age is 40-60 years old)

  • Female gender (although more men have alcoholic hepatitis due to the increased risk of alcohol abuse among men

  • Amount of alcohol (often greater than 100g/day) (standard drink in the United States = 14g)

  • Viral hepatitis

  • Obesity

  • Genetic polymorphisms

  • Obstructive biliary processes, including hepatic abscess, Budd-Chiari syndrome, Mirizzi syndrome, pancreatic cancer, hepatocellular carcinoma, and cholangiocarcinoma.

  • Liver processes, such as chronic viral hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, hemochromatosis, Wilson’s disease, autoimmune hepatitis, non-alcoholic steatohepatitis, alpha-1-antitrypsin deficiency, and drug-induced liver disease

  • Elevated iron studies due to increased alcohol intake and acute liver injury can mimic hemochromatosis.

  • Jaundice

  • Hepatomegaly

  • RUQ tenderness/mild pain (due to swelling of the liver capsule)

  • Ascites

  • Hepatic bruit

  • Encephalopathy

  • Fever

  • Ecchymoses


  • Liver panel (total bilirubin, direct bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase)

  • – Elevated total and direct bilirubin

  • – Elevated AST/ALT (ratio often greater than 2, AST rarely greater than 400). If transaminases greater than1000, think of other etiologies.

  • – Mild elevation in alkaline phosphatase

  • Albumin (frequent hypoalbuminemia)

  • Prothrombin time/international normalized ratio (INR) (frequent coagulopathy)

  • Complete blood count (CBC) with differential (frequent leukocytosis with neutrophilia, often occult GI bleeding)

  • Chemistry 7 (frequent hyponatremia, risk of acute renal failure 2/2 hepatorenal syndrome, frequent acid/base abnormalities such as metabolic acidosis with renal failure or respiratory alkalosis due to liver failure)

  • Magnesium (rule out hypomagnesium with alcohol abuse)

  • If febrile, rule out infection:

  • – Blood cultures

  • – Urinalysis / urine culture to rule-out urinary tract infection

  • – Diagnostic paracentesis (if ascites is present) – to rule-out spontaneous bacterial peritonitis

  • Tests for specific liver diseases (if there is uncertainty in the diagnosis)

  • Liver biopsy – only when the diagnosis is uncertain, or if considering liver transplantation. Transjugular route preferred to decrease the bleeding risk.

Tests used to predict mortality and whether or not to treat:

  • Maddrey’s discriminant function (DF) = [4.6 x (prothrombin time – control prothrombin time)] + serum bilirubin

  • – (Prothrombin time is in seconds. Bilirubin is in milligrams per deciliter.)

  • – If DF greater than or equal to 32, consider initiating prednisolone

  • – If DF greater than or equal to 32, mortality is 46.1% at 1 month

  • Model for end-stage liver disease (MELD) = 9.57 x log creatinine (in milligrams per deciliter) + 3.78 x log bilirubin (in milligrams per deciliter) + 11.20 x log INR + 6.43

  • – Increased MELD score portends a worse prognosis

  • – A MELD = 21 is associated with a 90 day mortality of 20%

  • Other scores are also used including Glasgow score, Child-Pugh score, age-bilirubin-INR-creatinine (ABIC) score

  • RUQ ultrasound with doppler.

  • Chest x-ray to rule out pneumonia (given fevers), and evaluate for sympathetic right sided pleural effusion.

  • Computed tomography (CT) head scan without contrast – (if mental status changes) to rule out subdural (or central nervous system (CNS) pathology otherwise) given increased fall risk with alcohol use and/or encephalopathy.

  • Ammonia level (level does not correlate with presence or severity of hepatic encephalopathy)

  • Ceruloplasmin is unreliable (low levels seen in liver diseases besides Wilson’s disease, including alcohol induced liver disease)


– If Maddrey’s discriminant function is greater than or equal to 32 (may alternatively use MELD score or Glasgow score), consider use of prednisolone and hepatology consultation.

  • Prednisolone 40mg per os (PO) daily for 28 days (and stopped or tapered over the next 2 months). Historically this has been the drug of choice for alcoholic hepatitis. Recent data favors use of prednisolone over pentoxifylline when not contraindicated.

  • – Avoid in the setting of upper GI bleed and active infection.

  • – Prednisolone is used primarily (instead of prednisone) because prednisone requires conversion to prednisolone in the liver.

  • – Lille score used to determine if prednisolone should be discontinued after 7 days of treatment due to insufficient response.

Lille Score = 3.19 – 0.101 x age in years + 0.147 x albumin in g/L on day 0 + 0.0165 x change in bilirubin in micromoles/L from day 0 to 7 – 0.206 x renal insufficiency (rated as 0 if absent and 1 if present) – 0.0065 x bilirubin in micromoles/L on day 0 – 0.0096 x prothrombin time in seconds.

A Lille score greater than 0.45 indicates a patient has not benefited from corticosteroids.

  • Pentoxifylline 400mg PO three times daily for 28 days (up to 3 months). A recent meta-analysis of 22 studies suggested pentoxifylline reduces short term mortality but was limited by poor-quality evidence.

  • – Renal dosing (CrCl < 30): 400 mg PO daily for 28 days (up to 3 months)

Additional therapies under study: N-acetylcysteine, granulocyte colony stimulating factor, metadoxine, enteral nutrition, early liver transplantation, and combination therapies.

  • Use short acting (e.g. lorazepam or oxazepam) rather than long acting (e.g. diazepam or chlordiazepoxide) benzodiazepines to lessen risk of over-sedation

  • A symptom-triggered approach, such as one based on the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA-Ar), is preferred in order to minimize the cumulative benzodiazepine exposure and shorten hospital stay

  • Regular oral diet (consider nutrition consult +/- enteral feeding if malnourished)

  • Thiamine 100mg daily (at least)

  • Folate 1mg daily (at least)

  • Multivitamin

  • Lactulose (titrate to 4 stools/day)

  • Rifaximin (if still encephalopathic with 4 stools/day on lactulose, and/or incontinence with lactulose)

  • Octreotide

  • Midodrine

  • Albumin intravenous (IV) (especially in the setting of spontaneous bacterial peritonitis)

  • Proton pump inhibitor

  • Octreotide

  • Emergent endoscopy

  • Sigmoidoscopy/colonoscopy

  • Vitamin K 5mg PO daily for 3 days (will treat concomitant nutritional deficiency of vitamin K)

  • Evaluate for jaundice (evaluate for scleral icterus, skin and sublingual jaundice).

  • Do a thorough abdominal exam, evaluating for hepatomegaly and/or splenomegaly, hepatic bruit, RUQ tenderness suggesting swelling of liver capsule, ascites.

  • Evaluate for encephalopathy, looking for sleep/wake cycle changes, asterixis, lack of orientation, history from family regarding confusion.

Every day:

  • CBC +/- differential – evaluate for occult bleeding, infection

  • Chemistry 7 (frequent hyponatremia, risk of acute renal failure 2/2 hepatorenal syndrome, acid/base changes

  • Magnesium and phosphorus – monitor for re-feeding syndrome daily with resumption of full enteral nutrition

Every day or every other day:

  • Liver panel (total bilirubin, direct bilirubin, AST, ALT, alkaline phosphatase)

Every few days:

  • Albumin (frequent hypoalbuminemia)

  • Prothrombin time/INR

  • Treatment of alcohol (+/- drug) abuse/addiction

  • Evaluation for liver transplantation if fulminant liver failure and/or cirrhosis

  • Stop prednisolone if upper GI bleeding or infection

  • Maximum dose of acetaminophen in 24 hours is 2000mg


Avoid non-steroidal anti-inflammatory drugs (NSAIDS) and angiotensin-converting enzyme inhibitors (ACE-inhibitors).

(See the chapter “Hepatorenal syndrome”)

No change in standard management.

Check echo to evaluate for cardiomyopathy due to alcohol. Avoid ACE-inhibitors, as they may increase the risk of hepatorenal syndrome.

Caution with aspirin if risk of bleeding.

Follow for hypoglycemia if fulminant hepatic liver failure.

No change in standard management.

Consider converting prednisone to prednisolone. If the patient is on chronic steroids at baseline, pentoxifylline could be used if treatment of the alcoholic hepatitis is necessary. Ultimately there is no evidence to guide management in the setting of baseline chronic steroids.

No change in standard management with human immunodeficiency virus (HIV).

No change in standard management.

  • In the setting of coagulopathy, treat with vitamin K 5mg PO daily for 3 days due to frequent vitamin K deficiency due to malnutrition, although coagulopathy is usually mainly due to liver failure.

  • Check vitamin B12 and folate levels in patients with macrocytosis.

  • Regular oral diet (consider enteral feeding if malnourished or unable to eat by mouth)

In the setting of coagulopathy, treat with vitamin K 5mg PO daily for 3 days due to frequent vitamin K deficiency due to malnutrition, although coagulopathy is usually mainly due to liver failure.

Check vitamin B12 levels. Consider CNS imaging due to trauma risk with alcohol abuse/addiction.

  • Avoid sleep agents (zolpidem, diphenhydramine) that could worsen encephalopathy; use trazadone 25mg-50mg PO before bedtime if necessary

  • Avoid benzodiazepines (unless for alcohol withdrawal) due to risk of encephalopathy

  • Caution with narcotics due to risk of worsening encephalopathy

  • Avoid NSAIDS due to risk of hepatorenal syndrome

  • Avoid ACE-inhibitors for hypertension due to risk of hepatorenal syndrome

  • Maximum dose of acetaminophen in 24 hours is 2000mg

Length of stay is expected to be less than 7 days if mild and more than 7 or longer if severe.

The patient is ready to be discharged when liver tests and coagulation factors are stable, kidney function is normal or stable, and there is no evidence of GI bleeding, dropping hemoglobin (Hgb)/hematocrit (Hct) and no encephalopathy.


Follow-up should be arranged with a primary care physician and a hepatologist – to investigate liver transplantation if necessary.


  • Liver panel (total bilirubin, direct bilirubin, AST, ALT, alkaline phosphatase)

  • Albumin

  • Prothrombin time/INR

  • CBC with differential

  • Chemistry 7

  • Alcohol (and/or drug) rehabilitation

  • Short term skilled nursing home and/or rehab if debilitated

  • Hospice depending on prognosis and patient wishes

When alcoholic hepatitis is severe there is nearly a 50% 1 month mortality without treatment. Abstinence improves survival.


Avoid deep vein thrombosis prophylaxis if GI bleeding.

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