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Author: Wang Mingming, Chief Physician, Jinan Infectious Disease Hospital, Shandong University.
This article is published by Yimaitong authorized by the author.
Please do not reprint without authorization.
The liver has its unique venous system.
The portal vein is upstream and the hepatic vein is downstream.
The liver is the wetland between the two.
The aquatic plants are luxuriant and full of vitality, fulfilling various complex metabolic functions.
It is precisely this sentence: Organ structure adapts to changes in function.
Understanding these two venous systems is helpful to our understanding and prevention of liver cirrhosis and its complications.
Portal vein and portal hypertension syndrome The portal vein contains blood from 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 the portal vein is 1200 ml/min.
Accompanying the portal vein is the hepatic artery, and the blood flow is 400 ml/min.
After entering the liver, the portal vein is gradually divided into interlobular veins, hepatic sinusoids, central hepatic veins and inferior hepatic veins.
The venous blood of the superior mesenteric vein and the inferior mesenteric vein 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 the liver cells further complete the metabolic process.
If liver fibrosis or cirrhosis is caused for some reasons (such as hepatitis B, alcoholic hepatitis, etc.
), these venous systems in the liver (mainly interlobular veins) are destroyed, which will inevitably cause the blood flow of the portal vein to be blocked.
The so-called portal hypertension spreads to the superior mesenteric vein, inferior mesenteric vein and splenic vein.
The blood flow of the superior mesenteric vein is blocked, and collateral circulation will be formed through the left gastric vein and azygos vein, leading to varicose veins in the lower end of the esophagus and the fundus of the stomach.
Varicose veins may rupture and bleeding due to improper diet or sudden increase in abdominal pressure.
Obstruction of blood flow in the inferior mesenteric vein can cause intestinal congestion and hemorrhoid formation.
Obstruction of the blood flow of the splenic vein can cause splenomegaly, which in turn causes 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 The hepatic veins are formed by the inferior hepatic lobule veins, and the hepatic venous blood flows back to the heart through the inferior vena cava and superior vena cava.
The blood flow of the hepatic vein is 1600 ml/min (portal blood volume of 1200 ml/min + hepatic artery blood volume of 400 ml/min), which maintains the balance of blood in and out of the liver.
If the blood flow of the hepatic veins is blocked due to some reasons (such as thrombosis caused by hypercoagulable state, cancer thrombus formed by the spread of cancer cells, vascular malformations, etc.
), hepatic venous hypertension can be caused, which in turn makes the entire liver blood flow obstructed and forms the liver Posterior portal hypertension, with hepatomegaly and severe ascites, is called hepatic vein obstruction syndrome, or Budd-Chiari syndrome.
Because the cause of Budd-Chiari syndrome is more secretive and difficult to be discovered, it is often mistaken for ordinary liver cirrhosis and portal hypertension in clinical practice.
The possibility of Budd-Chiari syndrome should be considered when there is no chronic liver disease, severe symptoms, unobvious liver damage, and unexplained portal hypertension.
Imaging examination of the hepatic veins is helpful for diagnosis.
Hepatic sinusoid and sinusoidal obstruction syndrome As mentioned above, the hepatic sinusoid is a continuation of the interlobular veins of the liver, a special capillary network, and an important place for material exchange between liver cells and blood, so it is also metabolized by liver cells.
Important place.
Damage to sinusoidal endothelial cells can also affect the outflow of portal vein blood, leading to increased intrahepatic portal pressure.
Because the pathological changes and clinical manifestations caused by hepatic sinusoid injury have their particularities, we call this disease sinusoidal obstruction syndrome.
Its clinical manifestations are mainly characterized by liver pain, hepatomegaly, hyperbilirubinemia, ascites, and weight gain.
The common cause of hepatic sinus obstruction syndrome is irrational use of drugs, the most common of which is the misuse of panax notoginseng.
Its toxic substance is pyrrolidine alkaloids, and there have been a large number of clinical reports.
Therefore, Chinese herbal medicines containing pyrrolidine alkaloids, such as Tusanqi, Senecio, Heliotrope, and daisy tea, should not be taken indiscriminately.
Hematopoietic stem cell transplantation and certain anti-tumor drugs can also cause sinusoidal obstruction syndrome, which has gradually been recognized and attracted the attention of the industry.
References (slide down): [1] Zhong Jianping, editor in chief.
Clinical research on portal hypertension, Annals of Chinese Surgery, Second Military Medical University Press: 299-304.
[2] Wang Fei, Wang Bingyuan.
2010 European Cirrhosis Ascites clinical practice guidelines, Chinese Journal of Hepatology, 2010,18(12):951-958.
[3] Tran-Harding K, Winkler M, Raissi D.
Bleeding stomal varices in portal hypertension.
Radiol Case Rep.
2018;13( 2):356-360[4] Chen Dongfeng, Xiong Ji.
Progress in the mechanism and treatment of portal vein thrombosis in liver cirrhosis, Journal of Clinical Hepatobiliary Diseases, 2017, 33(3): 451-453.
[5] Zhang W, Wang QZ, Chen XW, et al.
Budd-Chiari syndrome in China: A 30-year retrospective study on survival from a single center.
World J Gastroenterol.
2018 Mar 14;24(10):1134-1143.
[6] Guo Chenghao.
Bujia Study on the etiology of the syndrome, Chinese Journal of Basic and Clinical Medicine, 2014,(12): 1469-1471.
[7] Du Hongtao, Xu Hao.
Research progress of sinusoidal obstruction syndrome, Contemporary Medicine, 2013,(10) : 20-21.
[8] Lu Junzhu, Zhan Jun.
Research progress of liver sinusoidal obstruction syndrome caused by medicine liver, New Medicine, 2017(12):833-838.
[9] Nishida M, Kahata K, Hayase E,et al.
Novel Ultrasonographic Scoring System of Sinusoidal Obstruction Syndrome after Hematopoietic Stem Cell Transplantation.
Biol Blood Marrow Transplant.
2018 May 24.
[10] Kernan NA,Grupp S, Smith AR, et al.
Final results from a defibrotide treatment-IND study for patients with hepatic veno-occlusive disease/sinusoidal obstruction syndrome.
Br J Haematol.
2018;181(6):816-827.
This article is published by Yimaitong authorized by the author.
Please do not reprint without authorization.
The liver has its unique venous system.
The portal vein is upstream and the hepatic vein is downstream.
The liver is the wetland between the two.
The aquatic plants are luxuriant and full of vitality, fulfilling various complex metabolic functions.
It is precisely this sentence: Organ structure adapts to changes in function.
Understanding these two venous systems is helpful to our understanding and prevention of liver cirrhosis and its complications.
Portal vein and portal hypertension syndrome The portal vein contains blood from 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 the portal vein is 1200 ml/min.
Accompanying the portal vein is the hepatic artery, and the blood flow is 400 ml/min.
After entering the liver, the portal vein is gradually divided into interlobular veins, hepatic sinusoids, central hepatic veins and inferior hepatic veins.
The venous blood of the superior mesenteric vein and the inferior mesenteric vein 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 the liver cells further complete the metabolic process.
If liver fibrosis or cirrhosis is caused for some reasons (such as hepatitis B, alcoholic hepatitis, etc.
), these venous systems in the liver (mainly interlobular veins) are destroyed, which will inevitably cause the blood flow of the portal vein to be blocked.
The so-called portal hypertension spreads to the superior mesenteric vein, inferior mesenteric vein and splenic vein.
The blood flow of the superior mesenteric vein is blocked, and collateral circulation will be formed through the left gastric vein and azygos vein, leading to varicose veins in the lower end of the esophagus and the fundus of the stomach.
Varicose veins may rupture and bleeding due to improper diet or sudden increase in abdominal pressure.
Obstruction of blood flow in the inferior mesenteric vein can cause intestinal congestion and hemorrhoid formation.
Obstruction of the blood flow of the splenic vein can cause splenomegaly, which in turn causes 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 The hepatic veins are formed by the inferior hepatic lobule veins, and the hepatic venous blood flows back to the heart through the inferior vena cava and superior vena cava.
The blood flow of the hepatic vein is 1600 ml/min (portal blood volume of 1200 ml/min + hepatic artery blood volume of 400 ml/min), which maintains the balance of blood in and out of the liver.
If the blood flow of the hepatic veins is blocked due to some reasons (such as thrombosis caused by hypercoagulable state, cancer thrombus formed by the spread of cancer cells, vascular malformations, etc.
), hepatic venous hypertension can be caused, which in turn makes the entire liver blood flow obstructed and forms the liver Posterior portal hypertension, with hepatomegaly and severe ascites, is called hepatic vein obstruction syndrome, or Budd-Chiari syndrome.
Because the cause of Budd-Chiari syndrome is more secretive and difficult to be discovered, it is often mistaken for ordinary liver cirrhosis and portal hypertension in clinical practice.
The possibility of Budd-Chiari syndrome should be considered when there is no chronic liver disease, severe symptoms, unobvious liver damage, and unexplained portal hypertension.
Imaging examination of the hepatic veins is helpful for diagnosis.
Hepatic sinusoid and sinusoidal obstruction syndrome As mentioned above, the hepatic sinusoid is a continuation of the interlobular veins of the liver, a special capillary network, and an important place for material exchange between liver cells and blood, so it is also metabolized by liver cells.
Important place.
Damage to sinusoidal endothelial cells can also affect the outflow of portal vein blood, leading to increased intrahepatic portal pressure.
Because the pathological changes and clinical manifestations caused by hepatic sinusoid injury have their particularities, we call this disease sinusoidal obstruction syndrome.
Its clinical manifestations are mainly characterized by liver pain, hepatomegaly, hyperbilirubinemia, ascites, and weight gain.
The common cause of hepatic sinus obstruction syndrome is irrational use of drugs, the most common of which is the misuse of panax notoginseng.
Its toxic substance is pyrrolidine alkaloids, and there have been a large number of clinical reports.
Therefore, Chinese herbal medicines containing pyrrolidine alkaloids, such as Tusanqi, Senecio, Heliotrope, and daisy tea, should not be taken indiscriminately.
Hematopoietic stem cell transplantation and certain anti-tumor drugs can also cause sinusoidal obstruction syndrome, which has gradually been recognized and attracted the attention of the industry.
References (slide down): [1] Zhong Jianping, editor in chief.
Clinical research on portal hypertension, Annals of Chinese Surgery, Second Military Medical University Press: 299-304.
[2] Wang Fei, Wang Bingyuan.
2010 European Cirrhosis Ascites clinical practice guidelines, Chinese Journal of Hepatology, 2010,18(12):951-958.
[3] Tran-Harding K, Winkler M, Raissi D.
Bleeding stomal varices in portal hypertension.
Radiol Case Rep.
2018;13( 2):356-360[4] Chen Dongfeng, Xiong Ji.
Progress in the mechanism and treatment of portal vein thrombosis in liver cirrhosis, Journal of Clinical Hepatobiliary Diseases, 2017, 33(3): 451-453.
[5] Zhang W, Wang QZ, Chen XW, et al.
Budd-Chiari syndrome in China: A 30-year retrospective study on survival from a single center.
World J Gastroenterol.
2018 Mar 14;24(10):1134-1143.
[6] Guo Chenghao.
Bujia Study on the etiology of the syndrome, Chinese Journal of Basic and Clinical Medicine, 2014,(12): 1469-1471.
[7] Du Hongtao, Xu Hao.
Research progress of sinusoidal obstruction syndrome, Contemporary Medicine, 2013,(10) : 20-21.
[8] Lu Junzhu, Zhan Jun.
Research progress of liver sinusoidal obstruction syndrome caused by medicine liver, New Medicine, 2017(12):833-838.
[9] Nishida M, Kahata K, Hayase E,et al.
Novel Ultrasonographic Scoring System of Sinusoidal Obstruction Syndrome after Hematopoietic Stem Cell Transplantation.
Biol Blood Marrow Transplant.
2018 May 24.
[10] Kernan NA,Grupp S, Smith AR, et al.
Final results from a defibrotide treatment-IND study for patients with hepatic veno-occlusive disease/sinusoidal obstruction syndrome.
Br J Haematol.
2018;181(6):816-827.
