Cavernous change of portal vein

Introduction to portal vein sponge Cavernous transformation of the portal vein (CTPV) refers to the chronic partial or complete obstruction of the portal or intrahepatic portal vein, resulting in obstruction of portal vein blood flow, resulting in increased portal pressure, to reduce portal hypertension, forming a side around the portal vein Recirculation after circulation or blockage. basic knowledge The proportion of illness: 0.008% Susceptible people: no special people Mode of infection: non-infectious Complications: portal hypertension, esophageal and gastric varices, and rupture of bleeding

Cause of portal vein spongiformation

Congenital factors (45%):

Children's CTPV is mostly primary, mainly due to the absence of venous lumen in the hilar and its branches, structural congenital dysplasia, stenosis or atresia. It is currently believed that the following conditions can lead to CTPV in children:

1. Portal vein congenital malformation, dysplasia of the venous plexus between the umbilical mesenteric and hepatic veins after occlusion of the venous catheter, in place of the occluded portal vein.

2. CTPV itself is a hemangiomas of the portal vein.

3. The outcome of portal vein thrombosis, neonatal sepsis, umbilical infection and abdominal infection, inflammatory lesions involving the portal system, eventually leading to portal vein occlusion and the formation of collateral veins around the portal vein.

Abnormal portal blood flow (40%):

Adult portal vein sponge-like changes are secondary, characterized by the luminal structure of the original normal portal system, due to portal inflammation, perihepatic fibrosis, thrombosis, coagulopathy (erythrocytosis), tumor invasion, pancreas Inflammation and other causes portal blood flow is blocked, blood stasis or blood flow increases, pressure increases, in order to reduce pressure, collateral circulation is established around the portal vein, portal vein widening changes, and small and tortuous blood vessels are seen around the portal vein. Most of them were accompanied by cirrhosis, liver cancer, Xie Yinong reported 10 cases of portal vein cavernous degeneration, including 7 cases of liver cirrhosis, 2 cases of liver cancer, 1 case of portal vein embolization after splenectomy, other long-term oral contraceptives such as splenectomy, Umbilical vein catheterization, dehydration and hypovolemic shock can cause cavernous changes in the portal vein. However, despite detailed medical history collection and thorough examination, 50% to 60% of CTPV is difficult to ascertain the cause. .

Pathogenesis

The main pathological changes of this disease are: hyperplasia of small veins in the portal vein, ie portal vein cavernous sinusoidal changes, complete or partial thrombosis of the portal vein or thrombosis of the portal vein causes portal vein occlusion, resulting in extrahepatic portal hypertension, hepatic hilum A large number of collateral circulation vascular plexus is formed between the area or the portal. The collateral vessels of CTPV are derived from the venules and neovascular small vessels associated with lymphatic vessels, bile ducts, and blood vessels. Since the lesion is in the extrahepatic portal vein, the liver itself is often normal or The lesion is very mild, due to insufficient hepatic perfusion, liver function may also have different degrees of abnormalities. After the formation of portal hypertension, one of the most important pathological changes is the establishment of many traffic branches between the portal vein and the body vein and significant expansion, blood Increased flow rate, to some extent relieve portal pressure, when the scope of portal vein obstruction is more limited, such as only the main block, the collateral vein of the portal vein sponge can cross the obstruction site and open the portal vein branch of the liver, so that the portal vein of the liver Perfusion remains normal, and the portal vein is splendy despite a wide range of portal vein obstruction The collateral veins are involved in the portal vein, but insufficient collateral vein compensation can still lead to portal hypertension.

Portal vein sponge prevention

The essential element of liver protection, vitamin A, can fight liver cancer. The liver is the "warehouse" for the body to store vitamins. When the liver is damaged, the ability of the warehouse to store vitamins will also decrease. Studies have shown that vitamin A can protect the liver, prevent and inhibit the proliferation of cancer cells in the liver, and restore normal tissues. Adults should have a normal sleep time of 8 hours. Normally, they should go to bed from around 23 o'clock. When they are 1 to 3 o'clock in the morning, they will enter deep sleep. This is the best time to raise liver and blood. Will raise blood. Therefore, we call for not staying up late as much as possible. If you have to become a day and night, you should take more nutrients to protect yourself and minimize the damage to your body.

Portal vein sponge-like complications Complications , portal hypertension, esophagogastric varices, and rupture and bleeding

For portal hypertension and secondary esophageal varices and/or portal hypertensive gastropathy, occasional cavernous degeneration of the collateral vessels can compress the common bile duct, causing obstructive jaundice.

Symptoms of portal vein spongiform symptoms Common symptoms Repeated vomiting of blood stasis, ascites, upper gastrointestinal bleeding, obstructive jaundice, tar varicose veins

In the absence of portal hypertension, patients with primary CTPV may have no discomfort. Secondary CTPV patients are mainly primary manifestations. After portal hypertension, the main manifestations are portal hypertension and secondary esophageal varices rupture and (or) accompanied by portal hypertensive gastropathy, patients can repeatedly hematemesis and tar, accompanied by mild to moderate splenomegaly, hypersplenism, so the liver function of patients is good, so rarely occur ascites, jaundice and liver Encephalopathy, occasionally cavernous degeneration of the collateral vessels can compress the common bile duct, causing obstructive jaundice.

Portal vein sponge examination

1. Abdominal B-ultrasound normal portal vein structure disappears, replaced by irregular curved vascular shadow, or honeycomb, seeing blood flow inside, blood flow direction is irregular; blood vessel wall thickening echo is enhanced, visible intravascular thrombus, Ueno divides CTPV into 3 types according to color Doppler imaging: Type I shows that the normal structure of the portal vein is unclear, only the portal vein is honeycomb structure, and the primary CTPV belongs to this type; the type II is the portal vein. It can be shown, but the internal embolization is filled, and the collateral vein can be seen around it; type III is characterized by the presence of a lump echo near the portal vein, the portal vein is formed by the portal vein, and the type II and III are secondary CTPV.

2. Abdominal CT blood flow direction is irregular, visible intravascular thrombosis.

(1) The structure of the portal vein is disordered, and the structure of the normal portal vein disappears. In the direction of the portal vein, a network of similar agglomerate soft tissue formed by entangled collateral veins can be seen, and the boundary between them is unclear, and the portal vein is enhanced after scanning. Significantly enhanced interwoven into the net, sinus-like or tube-like soft tissue structure, in the hilar part of the liver can be seen to extend the thin strip density around the intrahepatic portal vein.

(2) Abnormal liver parenchymal perfusion. In the arterial phase, the contrast agent accumulates in the peripheral part of the liver parenchyma, forming a high-density band-like shadow, sometimes showing the proximal dilated arterial shadow, while the entire liver is uniformly equi-density in the portal vein phase. Shadow.

(3) Patients with portal hypertension can see collateral vessels in the coronal vein, umbilical vein, retroperitoneal cavity, hepatic and gastroduodenal ligament and the fundus esophageal junction. The distortion was a mass, and the enhanced scan showed significant enhancement during the portal vein.

3. Digital subtraction angiography (DSA) is mainly manifested by the unclear structure of the normal portal vein in the portal vein. The normal portal vein is replaced by a disproportionately distorted, cavernous vessel with a tumor-like dilation, which is shown to be parallel to the portal vein trunk. The varicose veins (Fig. 3), the splenic veins dilate, the gastric coronary veins and the esophageal veins are distorted.

4. Upper gastrointestinal angiography found esophageal varices or irregular and nodular gastric folds.

5. Gastroscopic examination showed varicose veins of the esophagus.

Diagnosis and diagnosis of portal vein sponge

diagnosis

For repeated upper gastrointestinal bleeding, mild or moderate spleen, and patients with normal liver function should consider the possibility of CTPV, diagnosed with B-ultrasound or color Doppler combined with portal angiography.

Differential diagnosis

Hepatic cirrhosis of portal hypertension: examination revealed that the portal vein branches into the subfoliate vein and the interlobular vein in the portal area, and branches further to the hepatic sinus. The hepatic sinus blood is gradually returned to the hepatic vein, inferior vena cava, and heart through the central lobular vein. Under normal circumstances, there are very few small branches of the portal vein and the central vein of the hepatic lobules. There is basically no circulation, but in the case of cirrhosis, these traffic branches are open to a large extent, and new traffic branches are formed. These traffic branches form an abnormal or pathological collateral circulation, including: 1 portal vein-hepatic vein shunt; 2 hepatic artery-portal shunt; 3 hepatic artery-hepatic vein shunt.

Idiopathic portal hypertension: clinical manifestations of portal hypertension. Liver function is normal or mildly abnormal. Isotope scanning showed liver and spleen development and bone marrow was not developed. Laparoscopy showed uneven liver surface but not cirrhosis. Liver histology revealed fibrosis in the portal area and portal vessel wall but no diffuse nodules in the parenchyma. Portal venography showed a decrease in small branches in the portal vein, and the model vessels were reduced or disappeared.

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