portal collateral circulation
Introduction
Introduction There is a wide communication branch between the portal vein and the body vein. In the case of cirrhotic portal hypertension, in order to stagnant blood in the portal system, these traffic branches are largely open, and the dilated or varicose veins are matched with the veins of the systemic circulation. The collateral circulation, so the portal vein blood can go straight back to the right heart without the liver. In cirrhosis, the portal pressure increases. When the water exceeds 200 mm, the blood flow to the normal digestive organs and spleen is blocked by the liver, resulting in a portal-body collateral circulation between many parts of the portal system and the vena cava. Due to the portal hypertension of cirrhosis, the normal hepatic portal vein obstruction, the blood through the two anastomosis into the vena cava system, due to the small veins in the anastomosis, the blood flow will be varicose, once ruptured can lead to major bleeding, such as hematemesis, blood in the stool, around the umbilicus You will see the veins of the varicose veins.
Cause
Cause
Various pathogenic factors cause severe damage to liver parenchyma cells and Kupffer cells.
Its main collateral circulation has the following ways:
(1) At the bottom of the stomach, the gastric coronary veins of the portal vein are anastomosed with the intercostal veins, septal veins, esophageal veins, and semi-singular veins of the vena cava, forming the lower esophagus and gastric varices. These varicose veins are supported by weak submucosal tissue, which is often eroded by food friction and reflux of the whole esophagus acidic gastric juice, which is prone to rupture and bleeding. In severe cases, it can be fatal. Traditionally, the two hypotheses of gastric acid reflux erosion of esophageal mucosa and portal pressure increase explain the rupture of esophageal and gastric varices. Increased portal pressure, large varicose vein volume, and thin wall can cause the varicose vein wall pressure to rise above the elastic limit and cause rupture. Determination of varicose vein wall pressure has important clinical significance for predicting variceal hemorrhage.
(2) The subcutaneous vein around the umbilicus communicates with the umbilical vein during the fetal period, and the umbilical vein is occluded after birth. Subcutaneous varices are visible around the umbilicus and in the upper abdomen as the umbilical vein reopens and expands during portal hypertension.
(3) The superior iliac vein of the portal vein is anastomosed to the middle and lower iliac veins of the intestinal venous system to form the nucleus.
(4) The establishment of collateral circulation in all the abdominal organs and the retroperitoneal tissue or in the site of adhesion to the abdominal wall, including the umbilical vein of the liver to the septum, the spleen and renal ligament and the vein in the omentum, the lumbar vein or the posterior The abdominal wall vein, and the vein formed in the scar tissue of the laparotomy staff.
Examine
an examination
Related inspection
Liver disease ultrasound diagnosis of hepatobiliary dynamic imaging liver, gallbladder, pancreas, spleen MRI examination liver, gallbladder, spleen CT examination liver dynamic blood pool imaging
symptom:
The onset and progression of cirrhosis are generally slow, and can be concealed for 3-5 years or more than ten years. The clinical manifestations can be divided into liver function compensation and decompensation period, but the two-stage boundary is not obvious or There are overlaps and should not be applied mechanically.
First, the liver function compensation period is mild, often lacks specificity, mainly fatigue, loss of appetite and dyspepsia. Can have nausea, oil, abdominal flatulence, upper abdominal discomfort, dull pain and diarrhea. These symptoms are mostly caused by gastrointestinal congestion, secretion and absorption dysfunction. Symptoms appear intermittently, aggravated by fatigue or associated disease, and can be relieved after rest or appropriate treatment. The spleen was mild or moderately enlarged, and the liver function test results were normal or mildly abnormal.
Some cases were occult, only during physical examination, surgery for other diseases, and even at autopsy.
Second, the liver function decompensation symptoms are significant, mainly due to two major clinical manifestations of liver dysfunction and portal hypertension, and may have systemic multi-system symptoms.
1. The general condition and nutritional status of the systemic symptoms are poor, thin and weak, lack of energy, and the severely ill are weak and bedridden. The skin is dry and rough, and the complexion is dark and dark. Often have anemia, glossitis, angular cheilitis, night blindness, polyneuritis and edema. There may be irregular hypothermia, possibly due to hepatocyte necrosis; liver detoxification function reduces intestinal absorption of toxins into the systemic circulation; portal vein thrombosis or endometritis; secondary infection.
2. Digestive symptoms The appetite is obviously reduced. After eating, the upper abdominal discomfort and fullness, nausea and even vomiting are poor, and the tolerance to fat and protein is poor. It is easy to cause diarrhea. The patient feels unbearable bloating due to ascites and gastrointestinal gas accumulation, and a toxic jejunum may appear in the advanced stage. The above symptoms are related to gastrointestinal congestion, edema, inflammation, digestive dysfunction and intestinal flora imbalance. More than half of the patients had mild jaundice, and a few had moderate or severe jaundice, the latter suggesting progressive or extensive necrosis of the liver cells.
3. bleeding tendency and anemia often have nasal discharge, gum bleeding, skin ecchymosis and gastrointestinal mucosal erosion bleeding. The tendency to hemorrhage is mainly due to the decreased function of the liver synthesis clotting factor, thrombocytopenia caused by hypersplenism, and increased capillary fragility. Patients also have varying degrees of anemia, mostly caused by factors such as lack of nutrition, poor intestinal absorption, spleen hyperactivity and gastrointestinal bleeding.
4. Endocrine disorders Endocrine disorders have increased estrogen, aldosterone and vasopressin. The main cause of liver function is weakened, but it is accumulated in the body and excreted in the urine. When estrogen increases, the anterior pituitary is inhibited by feedback mechanism. Function, which affects the function of the pituitary gland - the gonadal axis and the pituitary - adrenal axis, resulting in a decrease in androgen and a decrease in adrenocortical hormone.
Due to the imbalance between estrogen and androgen, male patients often have loss of libido, testicular atrophy, hair loss and breast development; female patients have irregular menstruation, amenorrhea, infertility and so on. In addition, some patients may have spider mites and/or telangiectasia in the vena cava drainage area such as the face, neck, upper chest, back, shoulders and upper limbs; redness in the palm of the hand, small intermuscular muscles and fingertips Liver palm. It is generally believed that the appearance of spider mites and liver palms is associated with increased estrogen, and some vasodilating active substances that are not destroyed by the liver also play a role. When liver function damage is severe, the number of spider mites can increase and the liver function can be reduced, reduced or disappeared.
When aldosterone increases, it acts on the distal renal tubules, which increases sodium reabsorption; when anti-diuretic hormone increases, it acts on the collecting tube, which increases the absorption of water. Sodium and water retention reduce the urine volume and edema, and the formation and aggravation of ascites Play an important role in promoting. If the adrenal function is impaired, skin pigmentation may occur on the face and other exposed areas.
diagnosis:
Decompensated cirrhosis can often be diagnosed based on clinical manifestations and related tests. The main diagnostic basis for cirrhosis is:
1 There are related medical history such as viral hepatitis, schistosomiasis, and long-term drinking;
2 The liver can be slightly larger, often shrinking in the late stage, hardening the texture, and uneven surface.
3 liver function damage.
Clinical manifestations of 4 portal hypertension.
5 liver biopsy has pseudolobule formation.
Diagnosis
Differential diagnosis
Portal hypertension is a group of syndromes caused by a persistent increase in portal pressure. The vast majority of patients are caused by cirrhosis, and a small number of patients are secondary to portal vein or hepatic vein obstruction and some unexplained factors. When the portal vein blood does not flow smoothly through the liver into the inferior vena cava, it will cause an increase in portal pressure. The performance of the portal-to-venous communication is open. A large amount of portal vein blood enters the systemic circulation directly through the traffic branch before entering the liver, resulting in abdominal wall and esophageal vein dilatation; splenomegaly and hypersplenism; liver function decompensation and ascites .
Portal venous gas (PVG) refers to the imaging signs of abnormal accumulation of gas in the portal vein and its intrahepatic portal vein due to various reasons, usually diagnosed by abdominal X-ray film. Common in neonatal necrotizing enterocolitis. Neonatal necrotic enterocolitis is the main clinical manifestation of abdominal distension, vomiting and blood in the stool. The cystic gas in the intestinal wall is a serious disease characterized by X-ray.
Portal vein thrombosis (PVT) is the leading cause of extrahepatic portal hypertension. Thrombotic obstruction of portal vein is often secondary to chronic liver disease and tumor disease. Simple extrahepatic portal vein obstruction is more common in adolescents and children. The most prominent and most common symptom is hemorrhage of the esophagogastric varices. Acute onset patients have symptoms such as abdominal pain, vomiting, and bloating, but rarely cause liver infarction.
