Overview

FormationBehind neck of pancreas, ≈L1–L2

Length≈7–8 cm

Share of hepatic blood flow≈75%

Normal portal pressure≈5–10 mmHg

Course. The portal vein forms behind the neck of the pancreas, at about the L1–L2 level. It is about 7–8 cm long and about 1 cm wide. It runs up behind the first part of the duodenum and then in the free edge of the lesser omentum (the hepatoduodenal ligament). There it lies behind the common bile duct (on the right) and the proper hepatic artery (on the left), in front of the epiploic foramen. At the porta hepatis it divides into right and left branches. These branch repeatedly and run in the portal triads, ending in the hepatic sinusoids.

A portal system. The portal vein connects two capillary beds in series: the capillaries of the gut and the sinusoids of the liver. Absorbed nutrients, drugs and toxins therefore reach the liver before the rest of the body. This is the basis of first-pass metabolism.

Blood supply to the liver. The portal vein supplies about 75% of the liver's blood flow and about half of its oxygen. Normal portal pressure is about 5–10 mmHg. Like the rest of the portal system, it has no valves.

Anatomy

Tributaries: The superior mesenteric vein and the splenic vein (which forms it). The splenic vein usually receives the inferior mesenteric vein. The portal vein also receives the left and right gastric veins, the cystic veins, the paraumbilical veins and the posterior superior pancreaticoduodenal vein.
Development: The portal vein develops from the vitelline veins and the anastomoses between them around the duodenum. The left umbilical vein becomes the ligamentum teres, and the ductus venosus becomes the ligamentum venosum.

Function

Delivers absorbed nutrients and gut-derived substances to the liver for processing, storage and detoxification.
Supplies about 75% of hepatic blood flow.
Carries pancreatic hormones (insulin, glucagon) to the liver at high concentration.

Clinical significance

Portal hypertension

Portal hypertension is a hepatic venous pressure gradient above 5 mmHg. It becomes clinically significant at 10 mmHg or more, and varices can bleed at 12 mmHg or more. Causes are prehepatic (portal vein thrombosis), intrahepatic (cirrhosis, the commonest cause, and schistosomiasis) and posthepatic (Budd–Chiari syndrome, right heart failure).

Consequences include an enlarged, overactive spleen with low platelet counts, ascites, varices at the portosystemic anastomoses and hepatic encephalopathy. Treatment includes non-selective β-blockers, endoscopic band ligation of varices and TIPS.

Portal vein thrombosis

Portal vein thrombosis complicates cirrhosis, cancer, pancreatitis, clotting disorders and umbilical vein catheterisation in newborns. It is a cause of portal hypertension with a normal liver.

Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.