Portal hypertensive enteropathy

Introduction to portal hypertensive enteropathy Portal hypertensive bowel disease (PHC) was proposed by Kozarek in 1991 to refer to intestinal submucosal telangiectasia, congestion, increased blood flow, arteriovenous shorts, and capillary endothelium and hemorrhage based on portal hypertension (PHT). Changes in the ultrastructure of the mucosal epithelium. PHC is mainly characterized by colorectal bleeding. Bleeding is mainly caused by submucosal varices, sudden increase in pressure in the portal vein, erosion or ulceration of the mucosal surface, obstacles in blood coagulation, and decreased quality or quantity of platelets. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: knot, rectal melanosis

Causes of portal hypertensive enteropathy

(1) Causes of the disease

The common cause of PHC is the presence of corresponding primary diseases such as hepatitis, cirrhosis, schistosomiasis liver fibrosis, primary portal hypertension, portal vein embolism, etc., based on long-term portal hypertension (PHT) damage.

(two) pathogenesis

1. PHC is a lesion characterized by intestinal vasodilation secondary to portal hypertension. The pathogenesis is basically the same as that of portal hypertensive gastropathy (PHG). It is also related to the portal vein hyperdynamic circulation. The measurement of pressure hepatic venous pressure gradient (HVPG) found that cirrhosis with PHC was significantly higher than those without PHC. Liver cirrhosis portal hypertension not only increased gastric blood flow by 1 time, but also increased blood flow in esophagus, small intestine and colon. %60%, Shanmen passed the laser Doppler method found that in addition to the cecum, the blood flow from the rectum to the ascending colon mucosa accompanied by PHC was significantly increased with PHC, and the change of mucosal blood flow was followed by severe PHC. Mild PHC? Without PHC, Tezuka et al. used organ reflectance spectroscopy to measure rectal mucosa in patients with cirrhotic portal hypertension, and found that the blood flow of the mucosa increased, indicating that the high power cycle prevalent in portal hypertension is involved in the occurrence of PHC. It has been reported that the width of the inner diameter of the portal vein is proportional to the vascular malformation of the colon. The colonic mucosal damage is more obvious in patients with a history of bleeding, and the viscosity of the colon in the chronic portal hypertension. The membrane, the submucosal arterioles dilate, and the blood flow to the colon increases, that is, "splanchnic hyperemia", which increases the blood flow in the portal vein and is one of the mechanisms for maintaining chronic high portal pressure.

Observing some vasodilator substances in patients with portal hypertension, such as nitric oxide, glucagon, prostaglandins, intestinal vasoactive peptides, calcitonin-related gene peptides, adenosine and carbon monoxide, may increase with synthesis, reduce inactivation Related to factors such as portal-body shunt, the peripheral arterial vasoconstrictor is decreased in patients with portal hypertension. It is known that the vasoconstrictor such as norepinephrine is higher than normal in portal hypertension, but the visceral blood vessels are expanded. The main, presenting a high power cycle, is associated with an increase in the patient's endogenous vasodilator mass, causing the peripheral arteries to dilate, which in turn leads to a high power cycle.

Nitric oxide is thought to be a key mediator of vasodilation, high-powered circulation, and PHC in many mediators. Nitric oxide is an inhibitory neurotransmitter that mediates mucosal vasoactive expansion and mucosal microcirculatory disorders. The pathogenesis of PHC, experimental observation of portal hypertension, increased gastrointestinal nitric oxide synthase levels, nitric oxide acts on vascular smooth muscle, causing blood vessels to dilate, nitric oxide also inhibits gastrointestinal smooth muscle function, causing obstructive congestion, intestinal The dysfunction of the motor is involved in the occurrence of PHC. In addition, glucagon plays an important role in causing high-intensity circulation of the portal hypertension. Glucagon can dilate the intestinal vasculature and make the intestinal blood vessels to the noradrenal gland. , the vasopressor's vasoconstrictor's reactivity decreases, which ultimately leads to visceral congestion, vasodilation, increased vascular permeability, plasma extravasation, extensive edema of the gastrointestinal mucosa, vascular distortion, liver dysfunction and liver Internal and external door-body shunt.

2. Intestinal mucosa and submucosal vasodilation and mucosal lamina propria edema thickening is a characteristic histological manifestation of PHC. Under the light microscope, colonic mucosal edema, congestion, massive telangiectasia, and occasional arteriovenous short circuit may be associated. Mucosal tissue is slightly inflamed, a small number of intestinal mucosa lamina propria lymphocytes slightly proliferate, mild lymphocytes and plasma cells infiltrate the mucosa lamina propria; mucosal epithelial cells fall off necrosis, forming erosion and bleeding; some cases submucosa or intermuscular plexus The edema and neuronal degeneration were observed. The ultrastructural changes of capillary endothelium and mucosal epithelial cells were observed under electron microscope.

Portal hypertensive intestinal disease prevention

For the cause, actively and effectively treat the primary disease and avoid PHT. Eat less irritating things, smoke, alcohol, spicy and sweet and sour things; try to eat less, too oily, too greasy things to eat less. Some cold medicines (such as aspirin non-steroidal anti-inflammatory drugs) have to be very careful, take caution when eating cold medicine, try not to eat. Because these drugs are likely to induce an increase in the condition.

Complications of portal hypertensive enteropathy Complications , rectal melanosis

Mainly for colorectal bleeding. Intestinal mucosal vasodilation, spider-like changes and varicose veins. The pathogenesis is still unclear, and it is thought to be closely related to intestinal hemodynamic changes caused by portal hypertension. In addition, endotoxemia, NO, prostaglandins, etc. may also participate in its occurrence. The capillary bed of the entire digestive tract mucosa from the stomach to the anus is almost always dilated, and the diameter and cross-sectional area of the capillaries are increased. In addition to submucosal vascular changes, other lesions in the intestine lack features, including intestinal mucosal atrophy, mild inflammation, ulcers, and red spots on the mucosa.

Portal hypertensive enteropathy symptoms common symptoms intestinal bleeding variceal vein embolization liver fibrosis portal hypertension

In addition to the clinical manifestations of basal cirrhosis and portal hypertension, the detailed report of the natural history of PHC has been reported so far. The PHC is mainly characterized by colorectal hemorrhage. The bleeding is mainly due to submucosal varices, and the pressure in the portal vein is suddenly increased. Fecal friction, mucosal surface erosion or ulceration, mucosal tolerance to injury and repair, decreased blood coagulation mechanism, decreased platelet mass or quantity, etc., are all causes of bleeding, varicose veins are reported in various parts of the colorectal, including the rectum The incidence of varicose veins is the highest, but it is much lower than the incidence of esophageal varices bleeding, and the amount of bleeding is small, and it is light and self-limited. There are few patients who need hospitalization or blood transfusion. Anyone with blood with portal hypertension should consider rectal varices. And need to be differentiated from hemorrhoids, active oozing due to colonic vasodilation is less common than PHG.

Portal hypertensive bowel disease examination

1. Coagulation mechanism disorder, platelet quality or quantity decreased.

2. Long-term chronic bleeding, red blood cells and hemoglobin may decrease.

3. Fecal occult blood is positive.

4. Colonoscopy PHC colonoscopy mainly has the following performance:

(1) Vascular ectasias (VE): a characteristic change of PHC, which is characterized by a spider-like, coil-like, bulging or flat red piece of lesion in the intestinal mucosa, with an incidence of 28.6% to 93%, PHC. Mucosal biopsy showed telangiectasia and mucosal atrophy.

(2) Varicose veins: The thickened veins of the colorectal mucosa can be seen to be significantly thickened. In severe cases, the cysts can be dilated and the incidence is 16% to 45.7%. In a few special cases, the extremely dilated rectal varices can be colonized. The mirror is misdiagnosed as a colon tumor, and a biopsy can cause major bleeding.

(3) Others: Intestinal mucosal blood vessels can also be seen in curved shape, frontal spherical shape, distorted snakes and other irregular forms, and submucosal hemorrhage such as diffuse or isolated red spots or erythema. PHC has intestinal mucosal edema, Shanmen et al. PHC is divided into severe and mild type, severe: VE number 5, from the cecum to the rectum in the large intestine, the lesion spreads over 3 fields, multi-field vascular irregularities and venous distortion, mucosal red spots or erythema Frequent, mild: VE number less than 4, other vascular lesions scattered, by the measurement of hepatic venous pressure gradient (HVPG), the results were significantly higher than mild.

5. Endoscopic ultrasonography (EUS) is usually inserted through the anus. It can also be used to detect varicose veins around the rectum and rectum. The varicose veins on the ultrasound image show a cystic anechoic dark area and rectal varices are found. The positive rate is higher than the endoscope.

Diagnosis and diagnosis of portal hypertensive enteropathy

diagnosis

1. There are portal hypertension and corresponding primary diseases that cause portal hypertension, such as hepatitis, cirrhosis, schistosomiasis liver fibrosis, primary portal hypertension, portal vein embolism, mesenteric arteriovenous fistula.

2. Endoscopic findings of intestinal mucosa VE and varicose veins.

Differential diagnosis

1. Isolated small blood vessel dilatation is the cause of lower gastrointestinal bleeding, more common in elderly patients, mostly confined to the right colon, the general number is small, limited to a few.

2. hereditary telangiectasia (hereditary telangiectasia) occurs in the jejunum, but also in the colon.

3. Henoch-Schonlein purpura is more common in young people, and sometimes it can be seen like vasodilatation.

4. Vascular dysplasia (angiodysplasia) is seen in patients with aortic stenosis, and the incidence is mostly confined to the right colon.

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