It seems portal vein thrombosis is caused by Virchow’s triad which includes: Reduced portal blood flow, hypercoagulable state, and vascular endothelial injury. There are two mechanisms that contribute in loss of portal vein blood flow to liver, arterial rescue and venous rescue. It is a rapid process and takes a few days to start and 3-5 weeks to complete after portal vein obstruction. Collateral vessel joins to form cavernoma which connects the proximal and distal part of thrombosed portal vein. Finally, the portal vein becomes a fibrosed and thin cord. All these events leads to low systemic vascular resistance and high. These are the characterstic findings of hyperkinetic circulation.

• Portal vein is formed by the union of the splenic vein and superior mesenteric vein and divides into a right and a left branch before entering the liver.

• The portal vein drains blood into the liver, not from the liver, the blood entering the liver from the portal vein, after being cleaned by the liver, flows into the inferior vena cava via the hepatic veins.
• The inferior mesenteric vein usually does not directly connect to the hepatic portal vein; it drains into the splenic vein.

• Portal vein branches into many generations of vessels that open into hepatic sinusoids. Blood is recollected into the hepatic vein and enters the inferior vena cava.

The tributaries of the hepatic portal vein include:

• Left gastric vein and right gastric vein
• Superior mesenteric vein
• Splenic vein

• It is thought that vein thrombosis is caused by Virchow’s triad which includes:^[1]
  • Reduced portal blood flow
  • Hypercoagulable state
  • Vascular endothelial injury

<figure-inline><figure-inline><figure-inline><figure-inline></figure-inline></figure-inline></figure-inline></figure-inline>

Shown below is a table depicting the elements of Virchow’s triad and their modern counterparts.

• There are two mechanisms that contribute in loss of portal vein blood flow to liver:^[6]
  • Arterial rescue:
    • Arterial rescue is the phenomenon that occurs after portal vein clamping during liver surgery.^[7]
    • It is a vascular reflex present in organs with both arterial and venous supply.
    • It has a role in preserving liver function in the acute stages of portal vein thrombosis.
  • Venous rescue:
    • Venous rescue is the phenomenon of neovascularization by forming collateral vessels.
    • It helps to bypass the obstruction.
    • It is a rapid process and takes a few days to start and 3-5 weeks to complete after portal vein obstruction.^[8]
    • Collateral vessel joins to form cavernoma which connects the proximal and distal part of thrombosed portal vein.
    • Finally, the portal vein becomes a fibrosed and thin cord.^[9]
• All these events leads to low systemic vascular resistance and high cardiac output. These are the characterstic findings of hyperkinetic circulation.^[10]

• The development of portal vein thrombosis is the result of G201210A mutations.

• Conditions associated with portal vein thrombosis include:^[1][11][12]
  • Cirrhosis
  • Hepatocellular carcinoma
  • Portal cavernoma
  • Gastric or esophageal varices/bleeding
  • Hepatic encephalopathy
  • Portal biliopathy or cholangiopathy
  • Peritonitis
  • Hypoxia or pulmonary artery hypertension
  • Portal hypertensive gastropathy

• There is no finding on gross pathology of portal vein thrombosis.

• There is no finding on microscopic histopathological analysis.