portal vein

The portal vein forms posterior to the neck of the pancreas via confluence of the splenic vein and superior mesenteric vein (the inferior mesenteric vein typically drains into the splenic vein). It ascends within the hepatoduodenal ligament, situated posterior to the hepatic artery proper and common bile duct (mnemonic: CBD is anterolateral, hepatic artery anteromedial, portal vein posterior), and enters the liver at the porta hepatis, branching into right and left portal veins to supply hepatocytes via sinusoids alongside hepatic arterioles.

Functionally, the portal vein carries blood from the stomach, intestines, spleen, and pancreas—rich in absorbed nutrients but low in oxygen—into the liver for metabolic processing, detoxification, and filtration before entering systemic circulation via hepatic veins into the IVC. This first-pass metabolism is critical for pharmacology (oral drug bioavailability) and toxin clearance.

Clinical significance centers on portal hypertension, most commonly caused by cirrhosis (increased resistance to flow), which raises portal venous pressure and causes blood to divert through portosystemic anastomoses, leading to esophageal varices (left gastric vein to azygos system), caput medusae (paraumbilical veins to superficial abdominal veins), and internal hemorrhoids (superior rectal to middle/inferior rectal veins). Other complications include ascites, splenomegaly, and hepatic encephalopathy due to shunting of ammonia-rich blood past the liver. Portal vein thrombosis can occur with hypercoagulable states, cirrhosis, or pancreatitis, causing variceal bleeding without cirrhosis. The Child-Pugh and MELD scores help assess severity of liver disease and portal hypertension complications. TIPS (transjugular intrahepatic portosystemic shunt) is a treatment for refractory variceal bleeding or ascites, creating a direct connection between the portal vein and hepatic vein to decompress the portal system.