What is the etiology of liver infarction and where does the clot originate from?

Etiology of Liver Infarction: Origin of Clots

Liver infarction is primarily caused by dual occlusion of both hepatic arterial and portal venous blood supply, as the liver's dual blood supply system typically protects it from infarction when only one vascular system is compromised.

Pathophysiology of Liver Infarction

Liver infarction is relatively rare due to the liver's unique dual blood supply system:

• Dual Blood Supply Protection: The liver receives approximately 75% of its blood from the portal vein and 25% from the hepatic artery 1
• Collateral Circulation: The hepatic arterial blood comes through three different routes, making simultaneous obstruction difficult 1

Common Sources of Clots Leading to Liver Infarction

1. Hepatic Artery Thrombosis:

   • Infected emboli
   • Polyarteritis nodosa (affecting both main and collateral arterial supply) 1
   • Post-liver transplantation complications (particularly with donors >60 years) 2
   • Surgical complications (ligation of main hepatic artery)

2. Portal Vein Thrombosis:

   • Cirrhosis (major risk factor) 3, 4
   • Prothrombotic conditions:
     • Factor V Leiden
     • Prothrombin gene mutations
     • Antiphospholipid syndrome 3
   • Chronic pancreatitis 4
   • Endoscopic treatments for esophageal varices (trigger for thrombosis) 4

3. Combined Vascular Occlusion:

   • Trauma with subsequent therapeutic transcatheter arterial embolization (TAE) 5
   • Budd-Chiari syndrome with concurrent portal vein thrombosis (found in about 15% of BCS patients) 3
   • Advanced liver disease with hypercoagulable features 3

Risk Factors for Thrombosis Leading to Liver Infarction

Cirrhosis-Related Factors

• Advanced portal hypertension 3
• Rebalanced but unstable hemostatic system in cirrhosis 3
• Hypercoagulable features despite prolonged standard coagulation tests 3
• Endotoxin absorption from intestines triggering platelet and coagulation activation 3

Vascular Factors

• Splenic vein occlusion or thrombosis 6
• Sinistral portal hypertension 6
• Low-flow portal system with incomplete clearance of activated coagulation factors 3
• Large endothelial surface in dilated collateral circulation 3

Procedural Factors

• Liver transplantation complications:
  • Donor age >60 years
  • Bench reconstruction of hepatic artery variants
  • Use of interpositional grafts (iliac conduits)
  • Previous transplantation 2
• Endoscopic procedures for varices (EVL, EIS) 4

Clinical Implications

1. Diagnostic Approach:

   • Sudden elevation of serum transaminases
   • Right hypochondralgia and flank pain
   • Multiple small nodular lesions on CT imaging 4
   • Combined imaging with contrast-enhanced CT/MRI and Doppler ultrasound 6

2. Management Considerations:

   • Anticoagulation therapy for at least 6 months in cases of thrombosis 3
   • Careful monitoring for heparin-induced thrombocytopenia, especially with unfractionated heparin 3
   • Thrombolysis coupled with angioplasty or stenting for recently thrombosed veins 3
   • TIPS (transjugular intrahepatic portosystemic shunt) may be effective in selected cases 3

Important Caveats

• Liver infarction can progress rapidly to hepatic failure 4
• The presence of both portal vein thrombosis and hepatic venous outflow obstruction typically results in more severe disease 3
• Patients with cirrhosis may appear to have normal or even hypercoagulable states despite abnormal standard coagulation tests 3
• The bleeding risk in critically ill patients with liver disease is often attributed to portal hypertension rather than hemostatic failure 3

Understanding the dual vascular occlusion requirement for liver infarction is crucial for early diagnosis and management to prevent progression to irreversible liver damage and failure.