The Anatomy of the Portal Vein

The portal vein is a blood vessel that delivers blood to the liver

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The portal vein is a blood vessel that delivers blood to the liver from the stomach, intestines, spleen, and pancreas. Most of the liver’s blood supply is delivered by the portal vein. Chronic liver diseases may disrupt portal vein blood flow, and many complications of cirrhosis are related to increased pressure in the portal vein system (portal hypertension).

Anatomy

The portal vein is formed by the confluence of the splenic vein, which brings blood from the spleen, and the superior mesenteric vein, which brings blood from the intestines. Smaller veins from the stomach and pancreas also contribute to portal vein blood flow.

The splenic vein and superior mesenteric vein join behind the neck of the pancreas to form the main portal vein. This then travels within the hepatoduodenal ligament toward the central portion of the liver, called the liver hilum.

There, it splits into the right and left portal vein branches, which enter the substance of the liver. The right and left portal veins then branch further to supply the different lobes of the liver.

Most veins in the body, called systemic veins, carry blood toward the heart. The portal vein and its contributing veins are different because they carry blood to the liver first.

Collectively, these veins are called the hepatic portal venous system and are an important source of complications in patients with chronic liver disease.

Anatomical Variations

About one in five people have variations in the branching pattern of the portal vein. These variants don’t usually cause symptoms or disease but become important if liver surgery is being planned.

Rarely, children may be born with an absent or underdeveloped portal vein. This condition, known as congenital agenesis of the portal vein, may be associated with abnormalities of the liver or cardiovascular system. Symptoms may be caused by blood flowing directly from the intestines and spleen into the systemic veins (portosystemic shunts).

Prognosis depends on the nature of the liver and cardiac disease, as well as the location of the shunts. These patients can sometimes be managed with medications or minimally invasive surgical procedures. In severe cases, liver transplantation may be necessary.

Function

Like any organ, the liver requires a constant flow of blood to maintain life. The liver has a dual blood supply derived from the portal vein and the hepatic artery. Most of the blood flow comes from the portal vein, which is responsible for providing much of the liver’s oxygen and nutrients.

The liver participates in the metabolism of ingested carbohydrates, proteins, and fats. It also detoxifies many harmful substances (drugs and toxins) which are absorbed by the gastrointestinal (GI) tract. Nutrients and other substances that are absorbed in the intestines travel via the portal vein to the liver, where they can be processed before being released to the rest of the body.

Clinical Significance

Liver cirrhosis and other chronic liver diseases may disrupt the flow in the portal vein. In cirrhosis, distortion of the liver architecture causes congestion of blood in the portal vein, raising the blood pressure. This state, called portal hypertension, is responsible for the major complications of cirrhosis (ascites, hepatic encephalopathy, and GI bleeding).

Portal hypertension can also be caused by clot formation in the portal vein (called portal vein thrombosis). In adults, thrombosis of the portal vein may result from genetic conditions that increase the likelihood of clot formation.

Inflammatory processes in the abdomen (such as pancreatitis or inflammatory bowel disease) may also cause portal vein thrombosis. Patients may also develop portal vein thrombosis as a result of underlying liver disease

Remember that the hepatic portal venous system is different from most veins in the body (systemic veins), which carry blood to the heart.

The portal vein and its tributaries carry blood to the liver first, allowing the liver to process nutrients and neutralize toxins before they pass on to the rest of the body.

In patients with portal hypertension, blood in the portal venous system attempts to bypass the liver as portal pressure increases. Abnormal connections (portosystemic collaterals) form between the portal venous system and the systemic veins. Large portosystemic collaterals around the stomach and esophagus (called varices) can cause gastrointestinal bleeding that may be life threatening.

Elevated portal venous pressures and sodium retention in cirrhosis can also cause seepage of fluid into the abdominal cavity. This fluid, called “ascites” can cause increased abdominal girth. Increasing ascites can push on the diaphragm, abdominal wall, and stomach, causing shortness of breath, abdominal pain, and early satiety.

Hepatic encephalopathy is a complication of cirrhosis characterized by problems with cognitive and motor function. In severe cases, patients may experience alterations in their level of consciousness. Hepatic encephalopathy results because elevated portal pressure forces blood away from the liver. Toxic substances—normally processed by the liver—are allowed to circulate throughout the body, affecting brain function.

Several different strategies exist to treat portal hypertension. Removing the cause of cirrhosis (such as alcohol or viruses) can significantly improve patient symptoms. Also, medications may reduce blood flow into portosystemic collaterals, or reduce resistance to blood flow within the liver.

Patients with refractory ascites or GI bleeding may benefit from the surgical placement of shunts between the portal and systemic circulation. For example, a transjugular intrahepatic portosystemic shunt (TIPS) is a shunt placed inside the liver that carries blood directly from the portal veins into the systemic circulation. 

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Additional Reading

  • Abdel-Misih SRZ, Bloomston M. Liver AnatomySurgical Clinics of North America. 2010;90(4):643-653. doi:10.1016/j.suc.2010.04.017

  • Costanzo LS. Physiology. Philadelphia, PA: Saunders/Elsevier; 2014.

  • Gallego C, Velasco M, Marcuello P, Tejedor D, Campo LD, Friera A. Congenital and Acquired Anomalies of the Portal Venous SystemRadioGraphics. 2002;22(1):141-159. doi:10.1148/radiographics.22.1.g02ja08141

  • Shen G-HHL-G, Jin Yang‚ Jin-Hua Mei‚ Yue-Feng Zhu. Insight into congenital absence of the portal vein: Is it rare? World Journal of Gastroenterology. 2008;14(39):5969. doi:10.3748/wjg.14.5969

  • Weissenborn K. (2012) Diagnosis of Overt Hepatic Encephalopathy. In: Mullen K., Prakash R. (eds) Hepatic Encephalopathy. Clinical Gastroenterology. Humana Press, Totowa, NJ.