How is the portal collateral circulation examined? The establishment and opening of the portal collateral circulation is a unique manifestation of portal hypertension, which is not only an important basis for the diagnosis of portal hypertension, but also has important clinical significance. The clinical manifestations of cirrhosis can be divided into hepatic function compensated and decompensated phases, but the boundary between the two phases is not obvious or there is overlap, and should not be applied mechanically. 1, liver function compensated stage symptoms are mild, often lack of specificity, mainly fatigue, loss of appetite and indigestion. There may be nausea, aversion to oil, abdominal flatulence, epigastric discomfort, vague pain and diarrhea. These symptoms are mostly due to gastrointestinal stasis, secretion and absorption dysfunction. Symptoms tend to appear intermittently, aggravated by exertion or concomitant morbidity, and may be relieved by rest or appropriate treatment. The spleen is mildly or moderately enlarged, and liver function test results may be normal or mildly abnormal. Some cases show insidious passage and are only discovered during physical examination, surgery for other diseases, or even at autopsy. 2. The symptoms of hepatic decompensation stage are significant, mainly the two main types of clinical manifestations due to hepatic decompensation and portal hypertension, and there can be systemic multi-systemic symptoms. 1, systemic symptoms general condition and poor nutritional status, emaciation and weakness, mental weakness, severe cases debilitated and bedridden. The skin is dry and rough, and the face is gray and dark. There are often anemia, tongue inflammation, stomatitis, night blindness, polyneuritis and swelling. There may be irregular low-grade fever. Possible causes are hepatocyte necrosis, decompensated liver detoxification toxins absorbed by the intestine into the body circulation, portal thrombosis or endocarditis, secondary infection, etc. 2, gastrointestinal symptoms significantly decreased appetite, after eating that the epigastric discomfort and fullness, nausea, and even vomiting, poor tolerance of fat and protein, into the greasy food, easy to cause diarrhea. Patients feel bloated due to ascites and pneumoperitoneum, and toxic bullae may appear in the late stage. These symptoms are associated with gastrointestinal bruising, edema, inflammation, impaired digestion and absorption, and dysbiosis of the intestinal flora. More than half of the patients have mild jaundice, and a few have moderate or severe jaundice, the latter suggesting progressive or extensive necrosis of hepatocytes. 3. Bleeding tendency and anemia often include epistaxis, gingival bleeding, skin bruising and bleeding from gastrointestinal mucosal erosions. The hemorrhagic tendency is mainly due to the decreased function of the liver in synthesizing coagulation factors, reduced platelets due to hypersplenism, and increased capillary fragility. Patients also have varying degrees of anemia, mostly caused by nutritional deficiencies, low intestinal absorption, hypersplenism and gastrointestinal blood loss. 4.Endocrine disorders include increased estrogen, aldosterone and antidiuretic hormone, mainly due to the weakening of their inactivating effect by the declining liver function, and their accumulation in the body and increased excretion in the urine, and when estrogen increases, it inhibits the anterior pituitary function through the feedback mechanism, thus affecting the pituitary-gonadal axis and pituitary-adrenocortical axis. –When estrogen increases, it inhibits the function of the anterior pituitary gland through a feedback mechanism, thus affecting the function of the pituitary-gonadal axis and pituitary-adrenocortical axis, resulting in a decrease in androgens and sometimes in adrenocorticotropic hormones. As a result of the imbalance between estrogen and androgen, male patients often suffer from loss of libido, testicular atrophy, hair loss and breast development, while female patients suffer from irregular menstruation, amenorrhea and infertility. In addition, some patients may have spider nevus and/or capillary dilatation in areas with vena cava drainage, such as the face, neck, upper chest, back, both shoulders and upper limbs, and redness in the large and small interphalangeal muscles and fingertips of the palm, called hepatic palm. It is believed that the appearance of spider nevi and hepatopalatine palms is associated with an increase in estrogen, as well as the role of vasodilatory substances that are not inactivated by the liver. When liver function is severely impaired, the number of spider nevi may increase and increase, while when liver function improves, they may decrease, shrink or disappear. When aldosterone is increased, it acts on the distal renal tubules to increase sodium reabsorption, and when antidiuretic hormone is increased, it acts on the collecting ducts to increase water absorption, and sodium and water retention to reduce urine output and swelling, which also plays an important role in promoting the formation and aggravation of ascites. If there is impaired adrenocortical function, skin pigmentation may occur on the face and other exposed areas.