Porto-systemic hypertension enteropathy

　　1. Etiology

　　The common cause of PHC is the existence of corresponding primary diseases, such as hepatitis, liver cirrhosis, schistosomal liver fibrosis, primary portal hypertension, portal vein thrombosis, etc., and the intestinal mucosal damage caused by long-term portal hypertension (PHT) on this basis.

　　2. Pathogenesis

　　1. PHC is a condition secondary to portal hypertension, characterized by intestinal vascular dilation.

　　The pathogenesis is basically the same as that of portal hypertension gastropathy (PHG), and is also related to portal hypertension hyperdynamic circulation. Through the measurement of hepatic venous pressure gradient (HVPG) reflecting portal pressure, Yamamoto et al. found that the incidence of liver cirrhosis with portal hypertension (PHC) was significantly higher than that without PHC. Portal hypertension in liver cirrhosis not only increases the blood flow of the stomach by a factor of 2, but also increases the blood flow of the esophagus, small intestine, and colon by 40% to 60%. Yamamoto's research using laser Doppler flowmetry found that except for the cecum, the blood flow of the mucosa from the rectum to the ascending colon in patients with PHC was significantly higher than that in patients without PHC, and the changes in mucosal blood flow were in the order of severe PHC, mild PHC, and no PHC. Tezuka et al. used organ reflectance spectroscopy to measure the mucosal blood flow of patients with liver cirrhosis and portal hypertension, and found that the mucosal blood flow increased. All this indicates that the hyperdynamic circulation commonly present in portal hypertension plays a role in the occurrence of PHC. There are reports that the width of the portal vein diameter is proportional to the formation of colonic vascular malformations, and patients with a history of bleeding have more obvious mucosal damage in the colon. In chronic portal hypertension, the small arteries in the mucosa and submucosa of the colon dilate, the blood flow of the colon increases, which is known as 'visceral polycythemia', increasing the blood flow into the portal vein, and is one of the mechanisms to maintain chronic high portal pressure.

　　Observing the increase of some vasodilators in patients with portal hypertension, such as nitric oxide, glucagon, prostaglandins, intestinal vasoactive peptide, calcitonin gene-related peptide, adenosine, and carbon monoxide, may be related to increased synthesis, decreased inactivation, and portal-systemic shunting. In patients with portal hypertension, the peripheral arteries show a decreased reactivity to vasoconstrictors, and it is known that vasoconstrictors such as norepinephrine are higher than normal during portal hypertension. However, the visceral vessels mainly show dilation, presenting a hyperdynamic circulation. This is related to the increase of endogenous vasodilators in patients, causing peripheral artery dilation, and subsequently leading to hyperdynamic circulation.

　　Among many mediators, nitric oxide is considered to be a key mediator causing vasodilation, hyperdynamic circulation, and PHC in patients with liver cirrhosis. Nitric oxide is an inhibitory neurotransmitter that participates in the pathogenesis of PHC by mediating the active dilation of mucosal blood vessels and the disturbance of mucosal microcirculation. Experimental observations show that the level of nitric oxide synthase in the gastrointestinal tract increases during portal hypertension, and nitric oxide acts on vascular smooth muscle to cause vasodilation. Nitric oxide also has an inhibitory effect on gastrointestinal smooth muscle, causing obstructive congestion and intestinal motility disorder, all of which participate in the occurrence of PHC. In addition, glucagon plays an important role in the hyperdynamic circulation of portal hypertension in the intestines, causing intestinal vascular dilation and reducing the responsiveness of intestinal blood vessels to norepinephrine and vasoconstrictor peptides. All these eventually lead to visceral congestion, vasodilation, increased vascular permeability, plasma leakage, extensive edema under the gastrointestinal mucosa, tortuous dilation of blood vessels, liver dysfunction, and intra-and extrahepatic portal-systemic shunts.

　　2. The expansion and thickening of the mucosal and submucosal blood vessels, and the edema and thickening of the mucosal固有层 are characteristic histological manifestations of PHC

　　Under light microscopy, the colon mucosa can be seen to be edematous, congested, with a large number of dilated capillaries, and occasionally arteriovenous shunts, which may be accompanied by mild inflammation of the mucosal tissue. A few intestinal mucosal固有层lymphocytes slightly increase, and there is mild infiltration of lymphocytes and plasma cells in the mucosal固有层. Mucosal epithelial cells fall off and necrotize, forming erosion and causing bleeding. In some cases, edema and nerve cell degeneration can be seen in the submucosal layer or intermuscular plexus. Under the electron microscope, ultrastructural changes can be seen in the capillary endothelium and mucosal epithelial cells.

　　The main manifestation is hemorrhoids in the rectum and colon. The intestinal mucosal blood vessels are dilated, there are spider-like changes and varices, etc. The pathogenesis is not yet clear, and it is generally believed to be closely related to the changes in intestinal hemodynamics caused by portal hypertension. In addition, endotoxemia, NO, prostaglandins, and other factors may also be involved in its occurrence. The capillary bed of the entire digestive tract mucosa from the stomach to the anus is almost dilated, and the diameter and cross-sectional area of the capillaries increase. In addition to the changes in submucosal blood vessels, other intestinal lesions lack specificity, including atrophy of the intestinal mucosa, mild inflammation, ulcers, and mucosal dot-like redness.

　　In addition to the clinical manifestations of portal hypertension due to liver cirrhosis, there are few detailed reports on the natural history of PHC. The main manifestations of PHC are hemorrhoids in the rectum and colon, mainly due to submucosal varices. Sudden increase in portal vein pressure, friction of feces in the intestines, erosion or ulceration of the mucosal surface, decreased tolerance and repair ability of the mucosa to injury, coagulation disorder, decreased platelet quality or quantity, and other factors are all causes of bleeding. Varices hemorrhage has been reported in all parts of the rectum and colon, among which the incidence of rectal varices is the highest, but it is much lower than that of esophageal and gastric varices hemorrhage. The amount of bleeding is also less, and it is light and self-limiting, with few cases requiring hospitalization or blood transfusion. Any fresh stool with portal hypertension should consider rectal varices, and it needs to be differentiated from hemorrhoids. Active bleeding caused by colonic vascular dilation is less common than that of PHG.

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　　5What kind of laboratory tests need to be done for portal hypertension enteropathy

　　1. Coagulation mechanism disorder:2. Long-term chronic bleeding:

　　Hemoglobin and hemoglobin levels may decrease.

　　3. Positive fecal occult blood

　　4. Colonoscopy: The colonoscopic examination of PHC mainly shows the following:

　　(1) Vasodilation (vasularectasias, VE): It is a characteristic change of PHC, manifested as spider-like, coil-like, elevated or flat red small patch lesions of intestinal mucosal blood vessels, with an incidence rate of 28.6% to 93%. The mucosal biopsy of PHC can show capillary dilation and mucosal atrophy.

　　(2) Varices: The mucosa of the rectum and sigmoid colon can be seen with tortuous and significantly thickened veins. In severe cases, they can expand into cystic shape, with an incidence rate of 16% to 45.7%. In a few special cases, extremely expanded rectal varices may be misdiagnosed as colon tumors by colonoscopy, and biopsy may cause massive hemorrhage.

　　5. Endoscopic ultrasonography:Endoscopic ultrasonography (EUS) is generally inserted through the anus, and can also be detected through the vagina to examine rectal and perirectal varices. On the ultrasound image, varices are manifested as cystic anechoic areas. The positive rate of detecting rectal varices is higher than that of endoscopy.

　　What kind of food is good for portal hypertension enteropathy patients:

　　In terms of diet, it is advisable to consume foods rich in protein, such as lean meat, beef, mushrooms, jujube, sesame seeds. In addition, food for the prevention and treatment of deficiency syndrome includes black fungus, yam, coriander, chive, eggplant, euryale, lotus root, fennel, litchi, chicken, mutton, figs, etc.

　　I. Treatment

　　1. Life guidance

　　(1) Diet: It is recommended to consume a diet rich in vitamins, low in residue, and low in fiber, to ensure an adequate intake of high-quality protein, 50-100g/d.

　　(2) Abstain from alcohol: Alcohol can dilate intestinal blood vessels, increase portal vein blood flow and pressure, and can also damage the gastrointestinal mucosa, which is an important precipitating factor for gastrointestinal bleeding. It should be strictly abstained from.

　　2. Prevention of gastrointestinal bleeding

　　(1) Prevention of recurrent gastrointestinal bleeding: If there is no gastrointestinal bleeding, PHC generally does not require treatment. For those with a history of bleeding, the main treatment for preventing recurrent gastrointestinal bleeding is to reduce portal vein pressure. Propranolol can significantly reduce portal vein pressure, alleviate intestinal mucosal congestion, and improve intestinal microcirculation during PHC by blocking the β2 receptors of intestinal blood vessels. The usage is the same as that of PHG. Other calcium channel blockers such as nifedipine (nifedipine), verapamil (isoptin), and nitroglycerin drugs can be used in combination with propranolol to enhance efficacy.

　　(2) Hemostasis: The treatment method for active bleeding is similar to that for esophageal and gastric fundus variceal bleeding. Terlipressin, somatostatin, or its analog octreotide are commonly used for hemostasis.

　　3. Endoscopic treatment

　　(1) Hemorrhage from colonic varices: Treatment with sclerotherapy or ligation can be performed.

　　(2) Treatment of vascular dilation: Literature reports that thermal probe coagulation therapy and laser irradiation therapy are effective in eliminating VE, and argon plasma coagulation is also effective. APC is a new non-contact coagulation method, where energy is conducted to the colon mucosa through ionized argon gas, causing the dilated vessels to coagulate.

　　4. Interventional therapy:Transjugular intrahepatic portosystemic shunt (TIPS) is a radiological interventional method for treating portal hypertension, and due to its ability to significantly reduce portal vein pressure, it has become a method for treating complications related to portal hypertension. In recent years, there have been increasing reports of the disappearance of vascular dilation after TIPS treatment for PHC.

　　5. Surgery:There are few reports on the treatment of gastrointestinal bleeding caused by PHC by portosystemic shunt surgery, because PHC is far less aggressive than esophageal and gastric fundus variceal bleeding. In most cases, bleeding is less and is easy to stop spontaneously.

　　II. Prognosis

　　Endoscopic ligation treatment of rectal variceal bleeding or ligation treatment, with a low recurrence rate, is a safe and effective new method worth recommending. Kaiz et al. successfully treated recurrent rectal and anal variceal bleeding with transjugular intrahepatic portosystemic shunt (TIPS), with satisfactory results.