Author: Wang Mingming, Chief Physician of Jinan Infectious Disease Hospital Affiliated to Shandong University
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Introduction
The liver has its own unique venous system. The portal vein is upstream, the hepatic vein is downstream, and the liver is the wetland between the two. The aquatic plants are lush and vigorous, completing various complex metabolic functions. It is exactly this sentence: organ structure adapts to changes in function. Knowing these two venous systems is helpful in our understanding and prevention of cirrhosis and its complications.
Portal vein and portal hypertension syndrome
The portal vein receives the superior mesenteric vein , inferior mesenteric vein and splenic vein, the blood flow of each vein is 400 ml/min, and the total flow of portal vein is 1200 ml/min.
The portal vein is accompanied by the hepatic artery with a blood flow of 400 ml/min. After entering the liver, the portal vein gradually divides into the hepatic interlobular vein, the hepatic (blood) sinus, the central hepatic vein and the sublobular vein.
The venous blood of the superior and inferior mesenteric veins contains a large amount of nutrients absorbed from the gastrointestinal tract , These large amounts of nutrients are transported to the liver through the portal vein, and further metabolic processes are completed by hepatocytes.
If liver fibrosis or cirrhosis is caused for some reasons (such as hepatitis B, alcoholic hepatitis, etc.) These venous systems (mainly the hepatic interlobular veins) inevitably lead to obstruction of portal blood flow, resulting in so-called portal hypertension, which affects the superior mesenteric, inferior mesenteric, and splenic veins.
The blood flow of the superior mesenteric vein is blocked, which will form collateral circulation through the left gastric vein and azygos vein, leading to the esophagus. Varicose veins in the lower end and fundus of the stomach, the varicose veins can rupture and bleed due to improper diet or sudden increase in abdominal pressure.
The obstruction of blood flow in the inferior mesenteric vein can cause intestinal congestion and hemorrhoids to form. Obstruction of blood flow to the splenic vein can cause splenomegaly, which in turn can lead to hypersplenism, which is manifested as a decrease in white blood cells, red blood cells, and platelets in the blood routine.
hepatic veins and Budd-Chiari syndrome
hepatic veins converge from sublobular veins The hepatic venous blood returns to the heart via the inferior vena cava and the superior vena cava. The blood flow of the hepatic vein is 1600 ml/min (the blood volume of the portal vein is 1200 ml/min + the blood volume of the hepatic artery is 400 ml/min), which maintains the balance of blood in and out of the liver.
If the hepatic vein is caused by some reasons (such as thrombosis caused by hypercoagulability, Tumor thrombus, vascular malformation, etc.) cause blood flow obstruction, which can cause hepatic venous hypertension, which in turn impairs the blood flow of the entire liver, resulting in post-hepatic portal hypertension, hepatomegaly and severe ascites. This is called hepatic venous occlusion syndrome. Also called Budd-Chiari syndrome.
Because the etiology of Budd-Chiari syndrome is more hidden and not easy to be found, it is often mistaken for ordinary liver in clinical practice Sclerosing portal hypertension. The possibility of Budd-Chiari syndrome should be considered in cases of unexplained portal hypertension without chronic liver disease, severe symptoms, and insignificant liver damage. Imaging of the hepatic veins can help in the diagnosis.
Sinusoidal and sinusoidal obstruction syndrome
As discussed above, sinusoidal It is the continuation of hepatic interlobular veins, a special capillary network, and an important place for material exchange between liver cells and blood, so it is also an important place for liver cell metabolism.
The damage of hepatic sinusoidal endothelial cells can also affect the outflow of portal blood and lead to the increase of intrahepatic portal pressure. high. Because the pathological changes and clinical manifestations of hepatic sinusoidal injury have their particularities, we call this condition hepatic sinusoidal obstruction syndrome. Its clinical manifestations are mainly characterized by liver pain, hepatomegaly, hyperbilirubinemia, ascites, and weight gain.
The common cause of hepatic sinusoidal obstruction syndrome is irrational drug use, among which The most common is the abuse of soil panax notoginseng, and its toxic substances are pyrrolizidine alkaloids, and there have been a large number of clinical reports. Therefore, Chinese herbal medicines containing pyrrolizidine alkaloids such as Tusanqi, Qianliguang, heliotrope, and daisy tea should not be taken indiscriminately.
Hematopoietic stem cell transplantation and some antitumor drugs can also cause hepatic sinusoidal obstruction syndrome, which has gradually been recognized and attracted the attention of the industry.
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