What Is the Splenic Vein?

Portal vein, including hepatic portal vein and pituitary portal vein. The hepatic portal vein is formed by confluence of the splenic vein (inferior mesenteric vein into the splenic vein) and superior mesenteric vein, and blood from the abdominal organs is recovered. There is no valve in the portal vein, so when the portal vein is hypertensive, blood can flow through the branches.

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(A) on the mesentery

Portal of normal human liver

Portal vein portal vein disease types

Congenital abnormalities of the portal vein (such as atresia) are caused by abnormal atresia of the yolk vein and its ventral anastomotic branch. Multi-lumen-like changes in the portal vein generally occur shortly after birth, and are the result of new lumens formed due to thrombosis after birth. Portal vein hemangiomas are extremely rare.

Nodular regenerative hyperplasia is a rare disease. Hepatocellular hyperplasia can be seen everywhere in the liver and is related to the formation of portal hypertension. These hepatocyte nodules are thought to be caused by vasculitis, which can cause ischemic damage and compression of the central vein.

Portal vein portal vein thrombosis

Portal vein thrombosis (PVT) can occur in any segment of the portal vein. The etiology is unknown in more than half of the cases, but may be related to systemic or local infections (such as purulent portal phlebitis, cholecystitis, lymphadenitis in the vicinity, pancreatitis, and liver abscess). PVT can occur in 10% of patients with cirrhosis and is often complicated by hepatocellular carcinoma. PVT can also occur in pregnancy (especially in patients with eclampsia) and in patients with portal vein congestion (such as hepatic vein occlusion, chronic heart failure, constrictive pericarditis). PVT can also be caused by tumors of the pancreas, stomach or other parts of the portal vein. Similar to Budd-Chiari syndrome, thrombotic haematological conditions can also lead to PVT. It is also seen after hepatobiliary surgery or splenectomy.

Portal vein symptoms and signs

The clinical consequences of PVT depend on the location, extent, rate of progression, and nature of the primary liver disease. Portal vein thrombosis can lead to cirrhosis or segmental atrophy, and can cause acute death if combined with mesenteric venous thrombosis. In about 1/3 of patients, portal vein thrombosis is slow, can form collateral circulation, and the portal vein can reopen (portal multi-lumen transition), but eventually progress to portal hypertension. In newborns, dehydration and various inflammations can lead to PVT. However, depending on the collateral circulation, portal hypertension may not appear until later in childhood. Nodular regenerative hyperplasia is a rare disease. Hepatocellular proliferative lesions are everywhere in the liver and are associated with portal hypertension. These hepatocyte nodules are thought to be caused by vasculitis, causing ischemic damage and central vein compression.

The symptoms of primary disease (such as hepatocellular carcinoma) can be more obvious, and esophageal varices bleeding are more common. If liver function is normal, patients often can tolerate repeated small bleeding; splenomegaly is the main feature, especially in children. Generally no ascites.

Portal vein diagnosis and treatment

When portal hypertension is present and liver function is normal, the presence of PVT should be suspected. Ultrasound and CT are helpful for diagnosis, but the diagnosis depends on angiography (such as transsplenoportography, venous phase of superior mesenteric arteriography) or MRI.

In patients with acute PVT, anticoagulant treatment is too late because a blood clot has formed, but it prevents the spread of the blood clot. For chronic PVT patients, conservative treatment can be given. For esophageal varices bleeding, endoscopic esophageal venous embolization should be the first choice. Surgical decompression of the portal system has many problems because there are often no suitable veins for proper shunting. If the splenic vein is not blocked, it can be used as a distal splenorenal shunt. If this fails, a mesenteric-caval shunt is feasible. Since small veins are more prone to thrombosis, shunting in children should be delayed as much as possible.