Portal Circulation.
(click to enlarge)

The Portal Circulation is an unusual circulatory system. Venous blood is brought from various organs, including the intestines (inferior and superior mesenteric veins), stomach (right, left, and short gastric veins), and spleen and pancreas (splenic vein), to the liver through the portal vein. The organs being drained include the spleen, the pancreas and other gastrointestinal organs. Investigate this from a lateral view and from the posterior.

The portal venous blood then goes to the liver sinusoids where it mixes with hepatic arterial blood. The blood then flows into the systemic venous system through the hepatic veins and inferior vena cava, and eventually returns to the right atrium.

Injuries to the liver lead to an obstruction in portal flow and result in elevation of the portal venous pressures. In addition, a decrease in portal flow leads to the release of endogenous vasodilators, resulting in an increase in hepatic arterial flow into the liver. This can lead to a further increase in portal venous pressure.

Normally the pressure difference between the portal circulation and the systemic circulation is 5-10 mm Hg. In some literature, portal hypertension exists when the portal-systemic venous gradient is greater than 12 mm Hg, with the portal pressure estimated by the hepatic vein wedge pressure. Other reports define portal hypertension as more than 5 mm Hg above the systemic pressures.

The most common cause of portal hypertension is cirrhosis of the liver, with a relative obstruction to flow. Other causes are increased flow in the portal circulation as seen with arterio-venous fistulae, obstruction to liver drainage (restrictive pericarditis, hepatic vein thrombosis) or obstruction below the liver (portal vein thrombosis, splenic vein thrombosis).

Portal hypertension leads to the development of and blood flow through collateral vessels. Clinically, the most important of these are related to the gastric veins and vessels surrounding the esophagus, which flow to portal systemic shunts in the proximal esophagus. The short gastric veins arise off of the splenic vein. A posterior view can better demonstrate the relationships when the stomach is superimposed. Finally, investigate the stomach and esophagus from a lateral view to better appreciate the splenic and gastric veins.

The spontaneous shunts and the resultant enlargement of vascular channels in the stomach and esophagus (esophagogastric varicies) are the most important clinical manifestation of portal hypertension. The resultant varicies frequently rupture leading to life-threatening hemorrhage. Rectal shunts with resultant rectal varicies can also develop. Below are video clips showing normal anatomy, as well as images from patients with varicies.

There are still other manifestations of portal hypertension. Fetal vascular structures in the falciform ligament (superior border shown), such as the residual umbilical vein, can dilate with resultant abdominal wall varicosities (anterior view), as well as splenic-renal vein anastomoses that can lead to retroperitoneal varicies.