Alcoholic Hepatitis
Acute hepatic inflammatory injury from heavy alcohol; spectrum from mild to severe (MDF ≥32 or MELD >20)
Symptoms / Associated Sx
Rapid-onset jaundice (days to weeks), fever (low-grade)
Tender hepatomegaly, anorexia, nausea, vomiting, weight loss
Ascites, peripheral edema; stigmata of CLD if underlying cirrhosis
Denies
NSAID or new medication use (rules out DILI as primary)
IV drug use, high-risk sexual behavior (rules out acute viral hepatitis)
RUQ pain radiating to right shoulder (rules out acute cholecystitis)
Social History (SHx)
Heavy alcohol use (>40 g/day women, >60 g/day men for weeks-months); duration and pattern; prior episodes of alcoholic hepatitis; nutritional status; smoking.
Main Etiology
Heavy sustained alcohol → direct hepatocyte toxicity + innate immune activation (TLR4, cytokine storm)
Underlying cirrhosis in ~50%; nutritional deficiency invariably present
Most Common DDx
Acute viral hepatitis (HAV/HBV/HCV — check serology; no heavy alcohol history required; AST:ALT ratio typically <1 vs. >2 in AH; serology confirms)
Drug-induced liver injury (DILI) (new medication or supplement within 3 months; no heavy alcohol; liver biopsy distinguishes; RUCAM score)
Acute cholangitis (fever + jaundice + RUQ pain = Charcot's triad; CBD dilation on imaging; CBD stone or stent occlusion; ERCP is treatment)
Ischemic hepatitis / shock liver (preceding hypotension or cardiac event; transaminases >1000–10,000; rapid fall with resuscitation; no alcohol history needed)
Autoimmune hepatitis (young to middle-aged women; ANA/anti-smooth muscle Ab elevated; IgG elevated; responds to steroids; liver biopsy confirms)
Decompensated cirrhosis without acute alcoholic hepatitis (no acute jaundice; slower course; portal hypertensive signs; biopsy shows fibrosis without active steatohepatitis)
DATA
LFTs: AST >2:1 ratio over ALT (classic); bilirubin elevated; GGT elevated
PT/INR, albumin (synthetic function); CBC (leukocytosis, thrombocytopenia)
BMP (glucose — hypoglycemia risk); MDF calculation; MELD score
Hepatitis A/B/C serologies; ANA, anti-smooth muscle Ab (exclude AIH)
Blood cultures; diagnostic paracentesis if ascites; RUQ ultrasound; ± liver biopsy
Home Meds
All hepatotoxic medications (hold); NSAIDs (hold); diuretics (hold if AKI)
Thiamine, multivitamin, folate (ensure supplemented)
Plan
Complete alcohol cessation; addiction medicine referral
Nutrition: 35–40 kcal/kg/day; 1.2–1.5 g/kg/day protein; NG feeds if unable to take PO; Thiamine 100–200 mg IV/IM daily × 3–5 days before any dextrose; folate 1 mg daily; zinc 220 mg BID
Severe AH (MDF ≥32 or MELD >20) — rule out infection first:
Prednisolone 40 mg PO daily × 28 days (not prednisone)
Lille score at Day 7: >0.45 → stop steroids (non-responder); ≤0.45 → complete course
Pentoxifylline not recommended (STOPAH trial — no benefit)
NAC adjunct: 150 mg/kg IV × 1h → 50 mg/kg × 4h → 100 mg/kg × 16h (modest short-term benefit)
Alcohol withdrawal monitoring (CIWA scale; benzos if withdrawal — careful dosing)
Daily CBC, CMP, INR, glucose; trend bilirubin (response marker); hepatology consult; transplant evaluation
PT/OT; nutritional support team
Discharge: Complete steroid taper; alcohol cessation support (naltrexone once LFTs improving); thiamine/folate ongoing; hepatology 1–2 weeks; transplant evaluation if severe disease
Red Flags
MDF ≥32 or MELD >20 → 30–50% 30-day mortality without steroids
Lille >0.45 at Day 7 → non-responder; 6-month mortality ~75% → stop steroids; palliative + transplant
Active infection + AH → absolute contraindication to steroids; treat infection first
AKI + AH → HRS → hold diuretics; terlipressin + albumin; nephrology
Senior IM Resident Pearls
AST:ALT >2:1 — alcohol depletes pyridoxal-5-phosphate (ALT requires more); ALT rarely >300 in pure AH
MDF: 4.6 × (PT − 12) + total bilirubin (mg/dL); MDF ≥32 = severe; consider steroids
Lille score at Day 7: >0.45 = non-responder → stop steroids; ≤0.16 = complete response
STOPAH (2015): Prednisolone improved 28-day mortality; pentoxifylline no benefit — never use pentoxifylline
Common mistake: Using prednisone instead of prednisolone — prednisolone is active form; prednisone requires hepatic conversion (impaired in severe liver disease)
Common mistake: Starting steroids without ruling out SBP/infection — dramatically increases mortality