Hepatic venule occlusion

Introduction to hepatic venular occlusive disease Hepatic venous occlusion (HVOD) refers to swelling and fibrosis of the hepatic lobular vein and hepatic venule branch, which causes stenosis or even occlusion of the lumen, followed by hepatocyte atrophy, diffuse liver fibrosis, and clinical hepatomegaly. Pain, ascites, etc., more than half of patients can recover, 20% of patients die of liver failure, and a small number of patients develop cirrhotic portal hypertension. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific population Mode of infection: non-infectious Complications: pulmonary hypertension

Causes of hepatic venular occlusive disease

Causes:

Some biological toxins, chemical drugs and other factors lead to hepatic venous edema, thickening followed by stenosis, occlusion, accompanied by corresponding lesions in the intrahepatic portal vein. The most reported most of this disease is the intake of toxic alkaloids - wild lily. Caused by herbs, such as ragwort, pig kidney bean, heliotrope, earth sap, etc., chemical drugs such as urethane, vincristine, azathioprine, etc., can also be aflatoxin, dimethyl nitrosamine, Caused by radiation, treatment, etc. Other factors that cause HOVD may be: 1 arsenic, mercury, sub-toxic substances; 2 congenital or acquired immunodeficiency syndrome; 3 estrogen.

Pathogenesis:

In the acute phase, the liver is enlarged and the surface is smooth. The lymphatic vessels are dilated and the signs of "hepatic crying" are visible. Under the light microscope, the central vein and the inferior venous intima are obviously swollen, the lumen is narrow or occluded, the blood flow is blocked, and the hepatic sinus is obviously expanded. , congestion, accompanied by varying degrees of hepatocyte opacity, degeneration and necrosis, hepatocytes disappeared in severe areas of necrosis, residual reticular fiber scaffold, red blood cells infiltrated into the hepatic sinus and Disse's space, showing typical hemorrhagic necrosis . In the subacute stage, the surface of the liver is reticular regional contraction, the central vein and the subvalvular vein endothelium proliferate, thicken, form fibrosis and stenosis, occlusion, and there may still be hepatic sinus expansion, congestion and hemorrhagic hepatocyte necrosis. There is fibrosis in the central vein, and no false leaflets are formed. Chronic liver further cirrhosis, liver cell atrophy in the central area of hepatic lobules, reticular scaffold collapse and fibrous tissue hyperplasia, pseudo-lobular formation, and finally formation of small nodular cirrhosis, some cases may be associated with portal fibrosis and thrombosis, but The main hepatic vein is rarely affected.

Prevention of hepatic venous occlusion

There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease. Develop good habits. First of all, try to stay up late and let the liver get enough rest. Second, eat less greasy food and eat more fresh fruits and vegetables. Recommended vegetables, water spinach, leeks, cabbage, mushrooms, fungus, carrots, tomatoes, melon, cucumber and so on. In addition, it is best not to drink alcohol or abuse drugs.

Hepatic venous occlusion complications Complications pulmonary hypertension

Wild lily alkaloid poisoning is often not limited to the liver, but can also cause similar lesions of the pulmonary venules, which can be manifested as pulmonary hypertension, pulmonary congestion and right ventricular hypertrophy, which should cause clinical attention.

Symptoms of hepatic venular occlusion symptoms Common symptoms Liver dysfunction Sinusoidal dilatation Hepatic vein disease Nausea bloating Appetite loss Portal hypertension Ascites Liver enlargement Gallbladder volume reduction

Most patients may have gastrointestinal tract, respiratory tract and systemic symptoms before onset, acute onset of acute disease, severe pain in the upper abdomen, abdominal distension, rapid swelling of the liver, tenderness, ascites, may be associated with loss of appetite, nausea, vomiting, etc. Lower extremity edema is rare, often with abnormal liver function. The subacute phase is characterized by persistent hepatic enlargement and repeated occurrence of ascites. The chronic phase is characterized by portal hypertension, which is the same as other types of cirrhosis.

Examination of hepatic venular occlusive disease

Laboratory examinations and imaging examinations are not characteristic. Therefore, for suspicious cases, the medical history should be carefully inquired and analyzed, and necessary auxiliary examinations should be carried out. The most decisive factor is liver biopsy under laparoscopic direct vision, which is not only reliable but also safe. (The bleeding can be observed at the site of the material, and effective hemostasis is applied at the same time.) However, because the understanding of the disease is not deep enough, and the patients and doctors are afraid of complications such as bleeding, it is rare to perform this test. And inferior vena cava angiography has limited diagnostic value for this disease, but can be used for the identification of Budd-Chiari syndrome.

Diagnosis and differential diagnosis of hepatic venular occlusion

The diagnosis of HVOD is difficult. Patients with typical symptoms mentioned above should be carefully searched for related causes or incentives. Because of the characteristic liver tissue pathology, the diagnosis of HVOD mainly depends on liver biopsy.

The most easily confused with HOVD is Budd-Chiari syndrome (B-CS), the following points help to identify:

Differential diagnosis

1 The cause of the two is different: the most common cause of B-CS is increased blood coagulation, such as trauma, dehydration, women's perinatal period, infection, abdominal tumor and after heavy labor; and HOVD and taking herbs, shrub tea and herbal tea Plants containing wild lily, related to radiotherapy, chemotherapy or immunosuppressive drugs.

Although the acute phase of 2B-CS may also have symptoms such as abdominal distension and pain in the liver area, there are few symptoms such as fever, vomiting and diarrhea. More than half of the acute phase is accompanied by inferior vena cava syndrome, such as chest and abdominal wall venous engorgement. Lower extremity edema, superficial varicose veins of the perineum and lower extremities, ulceration of the ankle and foot, etc., but no HOVD.

3 Inferior vena cava, hepatic venography can confirm the obstruction of the main hepatic vein and inferior vena cava in B-CS, degree, extent and formation of collateral circulation, etc., HOVD has no positive findings.

4B super can be found in the B-CS when the inferior vena cava is stenosis, occlusion, obstruction, presence or absence of thrombosis and formation of the medial branch of the liver, while HOVD only shows hepatomegaly, acute phase sound enhancement, chronic phase echo enhancement, increase Thick, uneven distribution of light spots, enhanced mesh echo, no difference with B-CS.

5 liver biopsy has the most discriminative significance for B-CS and HOVD. B-CS may have thrombosis in the hepatic vein, and most of them are involved in the outlet of the main hepatic vein. HOVD has no hepatic vein thrombosis, and the lesion mainly involves the central vein and Inferior lobular veins, with edematous stenosis or fibrous stenosis, acute HOVD should also be differentiated from acute hepatitis and acute severe hepatitis.

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