Ischemic hepatitis refers to acute, diffuse liver injury due to hypoperfusion. The most common causes of hepatic hypoperfusion are cardiopulmonary failure and shock. Clinical presentation varies and may be asymptomatic or involve abdominal pain, nausea, vomiting, and anorexia. Diagnosis is established based on medical history (e.g., history of heart failure) and severely elevated serum aminotransferase levels, elevated LDH, and bilirubin levels. Management consists of treating the underlying condition and hemodynamic support.
- Prevalence: approx. 2% of individuals admitted to the ICU develop ischemic hepatitis 
- Most common cause of severe acute liver injury in the United States 
- Approx. 80% of cases associated with underlying heart failure 
Epidemiological data refers to the US, unless otherwise specified.
- Impaired hepatic perfusion: heart failure, severe hypotension, cardiogenic shock, hypovolemic shock, thromboembolism, cardiac tamponade
- Hypoxemia: respiratory failure
- Increased metabolic demand: septic shock, extensive burns, surgery
Pathophysiology of hepatic tissue hypoxia and necrosis:
- Hepatic congestion due to an underlying condition (e.g., heart failure) → hepatic structural changes (e.g., sinusoidal centrilobular dilation, hepatocyte atrophy) and ↓ hepatic blood flow
- Low cardiac output, hypovolemic shock, or cardiac arrest → ↓ hepatic blood flow
- Septic shock: ↑ hepatic metabolic needs → ↓ O2 extraction capacity, circulating endotoxins, and inflammatory cytokines → ↓ ability of hepatocytes to extract and use oxygen→ ↓ hepatic blood flow
- Fatigue, weakness, altered mental status
- Hypotension, tachycardia
- Nausea, vomiting, anorexia, right upper quadrant tenderness, hepatomegaly
- Medical history and physical examination: cardiopulmonary disease, hypotension
Laboratory studies 
Severely elevated AST levels (> 1000 U/L)
- Serum levels peak 1–3 days
- Values return to normal within 7–10 days, once hepatic perfusion is restored.
- Elevated bilirubin levels
- Elevated LDH levels
- ALT:LDH ratio of < 1.5
- Elevated serum creatinine and BUN levels
- Normal alkaline phosphatase levels
- Severely elevated AST levels (> 1000 U/L)
- Coagulation studies: prothrombin time may be prolonged
- Imaging: to identify hepatic artery obstruction or portal vein thrombosis (e.g., with Doppler ultrasound, MRI, or arteriography)
- Other: : to rule out other causes of acute liver injury (e.g., acetaminophen intoxication, acute viral hepatitis)
- Diffuse hepatic injury
- Centrilobular necrosis (zone 3 of the hepatic acinus) with very few inflammatory cells
- Drug-induced liver injury; (due to acetaminophen or herbal supplement poisoning)
- Acute viral hepatitis
- Hepatic infarction
The differential diagnoses listed here are not exhaustive.
There is no specific treatment for ischemic hepatitis.
- Treat the underlying cause.
- Restore cardiac output and provide hemodynamic support (e.g., volume resuscitation, vasopressor, inotropes).
- Depends on the underlying condition, duration, and extent of the hemodynamic compromise
- Factors associated with higher mortality rates: 
- Necessity of vasopressor therapy
- Prolonged INR
- Septic shock
- Renal failure