sinusoidal dilatation
Introduction
Introduction Pathogenesis of hepatic venous occlusion: Hepatic sinus expansion symptoms occur in both the acute and subacute phases. In the acute phase, the liver is enlarged and the surface is smooth, and lymphatic vessel expansion and "liver crying" signs are seen. Under the light microscope, the central vein and the inferior venous intima were significantly swollen, the lumen was narrowed or occluded, the blood flow was blocked, and the hepatic sinus was obviously dilated and congested with varying degrees of hepatocyte turbidity, swelling and necrosis. Hepatocytes disappeared in the area of necrosis, residual reticular fiber scaffolds, red blood cells infiltrated into the hepatic sinus and Dissel's space, and typical hemorrhagic necrosis changes.
Cause
Cause
(1) Causes of the disease
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 cases of this disease are caused by the ingestion of herbs containing toxic alkaloids, monocrotaline, such as ragwort, pig kidney bean, helminth mustard, soil, etc., chemical drugs such as urethane, vincristine, sulfur Azathioprine, etc., can also be caused by aflatoxin, dimethyl nitrosamine, radiation, treatment, and the like.
Other factors that cause HOVD may be:
1 arsenic, mercury, sub-toxic substances;
2 congenital or acquired immunodeficiency syndrome;
3 estrogen and so on.
(two) pathogenesis
In the acute phase, the liver is enlarged and the surface is smooth, and lymphatic vessel expansion and "liver crying" signs are seen. Under the light microscope, the central vein and the inferior venous intima were significantly swollen, the lumen was narrowed or occluded, the blood flow was blocked, the hepatic sinus was obviously dilated and congested, accompanied by varying degrees of hepatocyte turbid swelling, degeneration and necrosis. Hepatocytes disappeared in the severely necrotic area, residual reticular fiber scaffolds, red blood cells infiltrated into the hepatic sinus and Dissel's space, and typical hemorrhagic necrosis changes.
In the subacute stage, the surface of the liver is reticulated, and the central vein and the inferior venous endothelium are hyperplasia and thickening, forming fibrosis and stenosis and occlusion. In this period, there may still be hepatic sinus expansion, hemorrhage and hemorrhagic hepatocyte necrosis, fibrosis in the central vein, and no false leaflet formation.
In the chronic phase, the liver is further hardened, the hepatocyte atrophy in the central region of the hepatic lobules, the collapse of the reticular scaffold and the proliferation of fibrous tissue, and the formation of pseudolobules is observed, and finally small nodular cirrhosis is formed. Some cases may be associated with portal fibrosis and thrombosis, but the main hepatic vein is rarely affected.
Examine
an examination
Related inspection
MRI examination of liver, gallbladder, pancreas and spleen by liver, gallbladder and spleen
Most patients may have gastrointestinal, respiratory 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 liver enlargement and repeated ascites. The chronic phase is characterized by portal hypertension, which is the same as other types of cirrhosis.
The diagnosis of HVOD is difficult. Patients with typical symptoms mentioned above should be carefully searched for the cause or cause. Because of the characteristic liver tissue pathology of this disease, the diagnosis of HVOD mainly depends on liver biopsy.
Diagnosis
Differential diagnosis
The most easily confused with HOVD is Budd-Chiari syndrome (B-CS), the following points help to identify:
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 tumors and heavy labor; and HOVD and taking herbal medicine, shrub tea and herbal tea It is related to plants containing wild lily, receiving 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 accompanying symptoms such as fever, vomiting and diarrhea. More than half of the acute phase is associated with inferior vena cava syndrome, such as chest and abdominal wall venous engorgement, lower extremity edema, perineal and lower extremity superficial varices, and foot and ankle ulcer formation, while HOVD is absent.
3 Inferior vena cava and hepatic venography can confirm the obstruction, extent, extent and collateral circulation of the main hepatic vein and inferior vena cava during B-CS. No positive findings were found in HOVD.
4B super can detect the presence or absence of stenosis, occlusion, obstruction, presence or absence of thrombosis and formation of medial branch of the inferior vena cava in B-CS, while HOVD only shows hepatomegaly, enhanced acute sound transmission, and increased echo in chronic phase. 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 vein, and edematous stenosis or fibrous stenosis. Acute HOVD should also be differentiated from acute hepatitis and acute severe hepatitis.
diagnosis:
Most patients may have gastrointestinal, respiratory 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 liver enlargement and repeated ascites. The chronic phase is characterized by portal hypertension, which is the same as other types of cirrhosis.
The diagnosis of HVOD is difficult. Patients with typical symptoms mentioned above should be carefully searched for the cause or cause. Because of the characteristic liver tissue pathology of this disease, the diagnosis of HVOD mainly depends on liver biopsy.
