I. Is portal hypertension a syndrome?
Symptoms of portal hypertension include.
1. splenomegaly.
2, hypersplenism.
3. bleeding esophagogastric fundic varices.
4, ascites.
5, spontaneous bacterial peritonitis.
6, hepatic encephalopathy, etc.
Second, the trunk of portal vein and blood flow direction?
1.The trunk of portal vein is 1cm-1.2cm in diameter and 7cm in length.
2.The blood of portal vein flows into liver, about 75% of blood and 50% of oxygen of liver is supplied by portal vein.
Third, the characteristics of portal vein?
1.Capillary network at both ends: one end is the capillary network of gastrointestinal, pancreas and spleen, and the other end is the capillary network in the liver.
2.No venous valves: blood is susceptible to reverse flow by pressure.
3.There are side branches open between with inferior vena cava.
Fourth, the most common cause of portal hypertension?
More than 80% are caused by cirrhosis of the liver.
1, post-hepatitis cirrhosis.
2.Alcoholic cirrhosis.
3, biliary cirrhosis.
4, schistosomal cirrhosis, etc.
V. Does esophagogastric fundic variceal bleeding occur?
1.The esophagogastric fundic vein is closest to the main trunk of portal vein and superior vena cava, with the largest pressure difference, and is the earliest and most heavily affected by portal hypertension.
2, esophagogastric fundic varices are prone to bleeding by friction of rough food and erosion of gastric acid reflux.
3, nausea and vomiting, coughing, defecation force can lead to variceal vein rupture and bleeding.
Sixth, the appearance of splenomegaly, hypersplenism?
1. obstruction of portal venous reflux, the spleen is bruised and enlarged.
2. Splenic reticuloendothelial cells proliferate and the spleen’s role in destroying blood cells is enhanced, resulting in hypersplenism – a decrease in whole blood cells, especially in white blood cells and platelets.
Seven, the emergence of hepatic encephalopathy?
1. changes in amino acid transmitters caused by portal hypertension: decrease in excitatory transmitters and increase in inhibitory transmitters (e.g. gamma aminobutyric acid).
2, poor liver function, some pseudo-neurotransmitters can not be cleared in the liver, resulting in central nervous system dysfunction.
VIII. Imaging examination of portal hypertension?
1.Ultrasound: portal vein trunk >1.5cm, splenic vein >1cm, splenomegaly.
2.X-ray barium meal imaging: finding esophagogastric fundic varices.
3, CT: reduced liver volume, atrophy of the liver lobe, uneven liver density, splenomegaly.
4.Fiber gastroscopy: discovering the degree of esophagogastric fundic varices.
9.Treatment of bleeding in portal hypertension?
1.Acute bleeding from esophagogastric fundic varices: by endoscopic (variceal ligation, etc.), pharmacological (posterior pituitary hormone, growth inhibitor, etc.), medical means such as three-chamber diathermy tube compression; by interventional bleeding vessel embolization, transjugular intrahepatic portosystemic shunt (TIPS), etc. to stop the bleeding.
2.Surgical treatment: for acute bleeding when medical treatment fails and bleeding cannot be controlled, or elective preventive surgery: the main purpose of surgery is to prevent ruptured esophagogastric fundic variceal bleeding by portal odd vein dissection surgery (most often used), or portal vein shunt surgery or a combination of both, and to eliminate hypersplenism by removing the spleen, but surgery should be strictly controlled for indications, and surgery is not to change the liver However, the indications for surgery should be strictly controlled, and surgery cannot change the damage caused by the disease itself (such as cirrhosis, hypoproteinemia, coagulation dysfunction).
X. What are the postoperative complications of portal hypertension?
1, intra-abdominal hemorrhage (1%)
2.Postoperative fever (15%)
3, hepatic encephalopathy (1-6%)
4, ascites, pleural fluid.
5, subphrenic infection, incisional dehiscence.
6, pancreatic fistula.
7, portal vein thrombosis, etc.