Hepatic infarction

Hepatic infarction is an ischemic injury affecting two or more liver lobules. It is extremely rare due to the protective effect of the dual blood supply in the liver. For hepatic infarction to occur, blood flow is typically impaired in both the hepatic artery and portal vein. Etiologies include local causes (e.g., portal vein thrombosis, trauma, liver transplantation) and systemic conditions (e.g., sepsis, HELLP syndrome, sickle cell disease). Clinical features include sudden upper abdominal pain, fever, and jaundice. Elevated liver enzymes and an elevated white blood cell count support the diagnosis. Abdominal imaging (e.g., duplex US, CT abdomen) shows a wedge-shaped abnormal area and impaired blood vessel flow. Management focuses on treating the underlying cause. Complications can be severe and include liver failure, ascites, infection, and bile duct necrosis.

For hepatic injury due to hypoperfusion, see "Ischemic hepatitis."

Hepatic infarction typically occurs due to impaired blood flow in both the hepatic artery and portal vein. ^[1]

Local causes ^[1][2][3]

• Portal vein thrombosis
• Hepatic artery thromboembolism
• Abdominal trauma
• Iatrogenic causes
  • Chemoembolization
  • Liver transplantation
  • Abdominal surgery
  • Transjugular intrahepatic portosystemic shunt

Systemic causes

• Sepsis, shock ^[3]
• Diabetic ketoacidosis ^[3]
• Vasculitis ^[2]
• Splanchnic vasoconstrictors (e.g., glyburide) ^[1]
• Hypercoagulable states, e.g., due to: ^[1]
  • Antiphospholipid syndrome
  • Protein C deficiency
  • Sickle cell disease ^[4]
  • HELLP syndrome ^[5]
  • Hypereosinophilic syndrome ^[6]

The dual blood supply in the liver (hepatic artery and portal vein) typically protects against hepatic infarction. ^[2]

• Very rare ^[1]
• Occurs in 3% of adult liver transplant recipients ^[2]

Epidemiological data refers to the US, unless otherwise specified.

Clinical features are nonspecific. ^[5]

• Sudden-onset upper abdominal pain
• Fever
• Jaundice

Initial studies ^[3]

Laboratory studies

• LFTs
  • Severely elevated transaminases
  • ↑ Bilirubin
• CBC
  • ↑ WBC count
  • Features of an underlying cause (e.g., thrombocytopenia in HELLP syndrome) ^[5]

Imaging

• Duplex ultrasound abdomen ^[1]
  • Heterogeneous area in the liver
  • Abnormal flow in the hepatic artery and/or portal vein
  • Features of portal vein thrombosis (e.g., portal cavernoma)
• Contrast-enhanced CT abdomen ^[2]
  • Wedge-shaped area of low attenuation
  • Lack of enhancement in collateral vessels
• MRI abdomen with contrast: wedge-shaped area of edema (hypointense on T1-weighting and hyperintense on T2-weighting) ^[2]

Further studies ^[1]

Consider further studies to evaluate for an underlying cause and to rule out alternative diagnoses (e.g., malignancy).

• Thombophilia testing (see "Hypercoagulable states")
• Cardiovascular screen for thromboembolic disease (e.g., ECG, TTE)
• Liver biopsy ^[3][5]
  • Rule out alternative diagnoses (e.g., hepatocellular carcinoma)
  • Identify hepatic cell necrosis

• Liver abscess
• Liver hematoma
• Biloma
• Hepatic carcinoma
• Cholangiocarcinoma

The differential diagnoses listed here are not exhaustive.

• There are no standardized management guidelines.
• Treat the underlying cause (e.g., portal vein thrombosis, sickle cell disease). ^[2]
• Consider therapeutic anticoagulation. ^[1]
  • Aims to prevent infarction extension and/or recurrence
  • May facilitate recanalization and reperfusion
• Manage complications; see, e.g.:
  • "Treatment of acute liver failure"
  • "Treatment of ascites"

• Acute liver failure
• Ascites
• Infection
• Biloma due to bile duct necrosis

We list the most important complications. The selection is not exhaustive.