Ischemic Hepatitis (Shock Liver)

Definition

Ischemic hepatitis (IH)—also called shock liver or hypoxic hepatitis—is an acute, usually reversible liver injury caused by severe reduction in hepatic oxygen delivery, leading to centrilobular (zone 3) hepatocyte necrosis, typically occurring in the setting of systemic hypotension, hypoxia, or low cardiac output.

Key concept:
Ischemic hepatitis reflects global circulatory failure, not primary liver disease.

Why the Liver Is Vulnerable

The liver has a dual blood supply:

• Portal vein (≈75%) – nutrient-rich, relatively hypoxic
• Hepatic artery (≈25%) – oxygen-rich

Hepatic Acinar Zones 

→ Zone 3 hepatocytes are first to undergo necrosis during hypoperfusion

Etiology / Precipitating Factors

1. Cardiac Causes (Most common)

• Cardiogenic shock
• Acute MI
• Acute decompensated heart failure
• Arrhythmias
• Cardiac tamponade
• Pulmonary embolism with RV failure

2. Circulatory Shock

• Septic shock
• Hypovolemic shock
• Anaphylactic shock

3. Respiratory Failure

• Severe hypoxemia (ARDS)
• Acute exacerbation of COPD
• Massive pulmonary embolism

4. Others

• Major surgery (especially cardiac surgery)
• Severe anemia
• Cardiac arrest and resuscitation
• Budd–Chiari syndrome (rare differential)

Important exam point:
Up to 50% of patients do NOT have documented hypotension → low hepatic oxygen extraction & congestion also contribute.

Pathophysiology

Core Mechanisms

1. Reduced hepatic blood flow
2. Reduced arterial oxygen content
3. Impaired hepatic oxygen extraction

Additional Contributors

• Passive hepatic congestion (right heart failure)
• Microcirculatory dysfunction (sepsis)
• Mitochondrial dysfunction
• Reperfusion injury

Key insight:
Ischemic hepatitis often represents “hepatic manifestation of multiorgan failure.”

Clinical Presentation

Symptoms

• Often asymptomatic
• May have:
• Fatigue
• Nausea
• Right upper quadrant discomfort

Signs

• Features of shock or heart failure
• Hepatomegaly (congestive component)
• Jaundice is uncommon initially

Laboratory Features (Hallmark)

Transaminases (Defining Feature)

• AST & ALT rise abruptly
• Typically >1000 IU/L
• Often AST > ALT
• Peak within 24–72 hours
• Rapid decline if perfusion restored

Other Labs

High-yield exam pearl:
AST/ALT >1000 + very high LDH = ischemic hepatitis until proven otherwise

Diagnostic Criteria (Commonly Used)

All three should be present:

1. Clinical setting of hypoxia or hypoperfusion
2. Massive, transient rise in aminotransferases
3. Exclusion of other causes of acute liver injury

Differential Diagnosis 

Imaging

• Not diagnostic
• Used to exclude:
• Biliary obstruction
• Hepatic vein thrombosis
• Doppler may show reduced hepatic flow

Histopathology (Rarely Needed)

• Centrilobular (zone 3) necrosis
• Minimal inflammation
• Sinusoids congested

Management

No Specific Liver-Directed Therapy

Core Principles

Treat the underlying cause

1. Hemodynamic Optimization

• Restore MAP
• Optimize cardiac output
• Vasopressors/inotropes as needed

2. Oxygenation

• Correct hypoxia
• Mechanical ventilation if needed

3. Treat Precipitating Cause

• Revascularization (MI)
• Treat sepsis
• Control arrhythmias
• Treat heart failure

4. Supportive Care

• Avoid hepatotoxic drugs
• Monitor:
• LFTs
• INR
• Lactate
• Renal function

N-acetylcysteine:
Not routinely recommended unless acetaminophen toxicity or selected acute liver failure cases.

Prognosis

Liver Recovery

• Excellent if hemodynamics corrected
• LFTs normalize within 7–10 days

Mortality

• High overall mortality (30–70%)
• Death usually due to underlying shock or cardiac disease, not liver failure