The liver is an important metabolic and defense organ of the body. During pregnancy, certain idiopathic liver diseases or complications of pregnancy can cause liver damage. The main idiopathic liver diseases include intrahepatic cholestasis during pregnancy and acute fatty liver during pregnancy; pregnancy complications include severe pregnancy vomiting, gestational diabetes, hyperemesis, and HELLP syndrome. Bleeding, infection and certain medications may also cause liver damage. Pregnancy combined with viral hepatitis is also one of the main causes of liver injury and maternal mortality. According to statistics, the incidence of liver disorders during pregnancy is about 3%. I. Changes in the liver during pregnancy During pregnancy, estrogen and aldosterone increase in the body, water increases by 30%-70% compared with the pre-pregnancy period, and total blood volume rises, but liver blood flow remains unchanged, so the relative blood flow in the liver decreases. On the other hand, the metabolic rate of the body increases during pregnancy, and fatigue, bleeding, and anesthesia during delivery all increase the burden on the liver. There are no significant histological abnormalities in the liver during pregnancy, and there are no changes in size or shape. In the second trimester, the liver cannot be palpated because the uterus enlarges and the liver is pushed to the right, up and back. If the liver is palpated under the ribs or measured by ultrasound at 7 months of gestation or more, it is considered hepatomegaly. Liver function remains essentially normal in normal pregnancy with slight variations, and returns to a non-pregnant state rapidly after delivery. The more obvious changes in each index of liver function test in normal pregnant women include: 1. alkaline phosphatase (ALP or AKP): ALP is pooled in the placenta during pregnancy and can rise exponentially, reaching 2-4 times that of non-pregnancy after 7 months of pregnancy. 2, lactate dehydrogenase (LDH): the isoenzymes LDH2 and LDH3 mainly reflect diseases of the liver and placenta, so they can be mildly elevated in late pregnancy. 3.Total bilirubin (TB): Serum bilirubin concentration rises in late pregnancy due to the decrease of bilirubin tolerance. 4.AFP: AFP is produced by human embryonic cells during pregnancy, so AFP is elevated. 5.Lipids: cholesterol (TC) increases from the 4th month of pregnancy and reaches a peak in the 8th month of pregnancy (7.8-10.4N/L); triglycerides (TG) can rise 2-4 times. 6.Serum total protein and albumin are mildly decreased due to hemodilution during pregnancy. 7. Indicators of coagulation and fibrinolytic function: normal pregnant women’s blood is in a hypercoagulable state, with shortened plasma prothrombin time (PT) and activated partial thromboplastin time (APTT), and a 40-50% increase in plasma fibrinogen (FIB), reaching an average of 4.5 g/L at the end of pregnancy; D-dimer (D-D) levels: progressive increase from early pregnancy to the end of labor. Second, direct obstetric problems cause liver damage. Hyperemesis is the most common cause of liver function abnormalities in early pregnancy, with an incidence of about 0.1-2%. The etiology is not very clear, but in recent years, some studies have found a close relationship between Helicobacter pylori infection and severe pregnancy vomiting. Hepatic impairment is seen in about 20% of cases of severe pregnancy vomiting, and nearly a quarter of patients present with mild liver function abnormalities. There is mild enlargement and pressure in the liver, elevated serum bilirubin (usually mildly elevated, no more than 4 times normal) and elevated alanine aminotransferase (ALT) (≤200 U/L, rarely more than 1000 U/L ). Alkaline phosphatase (ALP) is not more than 2-fold. Elevated unconjugated bilirubin is rare. Amylase may also be elevated and may cause a decrease in plasma protein and fibrinogen and a bleeding tendency. Liver damage from severe pregnancy vomiting usually improves rapidly after the vomiting is controlled and the systemic condition is stabilized. In severe cases, care should be taken to prevent hepatic encephalopathy when hepatic impairment is evident. If treatment is ineffective or if there is: persistent jaundice, persistent elevation of blood bilirubin, persistent proteinuria, temperature >38 degrees, heart rate >130 bpm, or psychiatric symptoms, pregnancy must be terminated. Pre-eclampsia or eclampsia and HELLP syndrome 1. Pre-eclampsia can occur in about 5-10% of pregnant women, of which 20-30% may have abnormal liver function; it is generally believed that the clinical symptoms of pre-eclampsia liver damage are related to the degree of endothelial dysfunction of the hepatic sinusoids. Due to increased perihepatic resistance and local ischemia in the liver, the hepatic blood sinusoids are obstructed by intravascular fibrin-like deposits, which in severe cases leads to blockage of blood flow. Further development of liver damage manifests as coagulation disorders; in severe cases, periportal necrosis, subperitoneal hematoma formation and liver rupture may also occur, endangering the life of mother and child. Histological examination of the liver shows fibrin deposition in the hepatic sinusoids, periportal hemorrhage, hepatocyte necrosis, and even infarction. Clinical manifestations include discomfort in the upper abdomen or right upper abdominal region, sometimes nausea and vomiting; early liver function tests show elevated serum transaminases, which may even reach ten times the normal high limit, but elevated bilirubin is rare. In severe cases, periportal necrosis and subperitoneal hematoma formation may occur, and liver rupture may also occur, endangering the life of mother and child. The combination of pre-eclampsia with liver damage indicates a serious condition and warrants a high degree of caution. Common complications of liver damage include renal failure, liver rupture or infarction, eclampsia, and increased perinatal morbidity and mortality. In patients with preeclampsia, blood pressure should be strictly controlled and the pregnancy should be terminated as soon as liver damage occurs. The biochemical indicators of the liver usually return to normal within a short time after delivery. 2. HELLP syndrome 5%-10% of patients with severe pre-eclampsia will develop HELLP syndrome. The syndrome is considered a specific subtype of pre-eclampsia/eclampsia, while some pregnant women do not have any symptoms of pre-eclampsia. Most HELLP syndromes occur in mid- and late pregnancy, and some occur in the postpartum period. Multiple births and maternal age >35 years are high risk factors. The etiology and pathogenesis of HELLP syndrome are not fully understood. Most scholarly studies consider vascular endothelial injury in pregnant women with hyperemesis as its main pathological alteration. Endothelial injury leads to fibrin deposition, vasospasm, platelet activation and increased local aggregation, resulting in systemic microvascular damage leading to microvascular hemolytic anemia, thrombocytopenia and periportal hepatocyte necrosis. The portal vein becomes engorged with blood, local hepatocytes are squeezed, and hepatocytes become necrotic after ischemia, resulting in liver damage. With the severity of tissue ischemia, hypoxia, dehydration and hemolysis, a large amount of lactic acid is produced. Lactic acid is competitively inhibited with uric acid when excreted by the kidneys, resulting in a relative decrease in uric acid and lactic acid excretion. LDH elevation is the earliest and is a sensitive indicator for early hemolysis diagnosis; AST and ALT elevation mostly appear before platelet drop, which is related to the degree of thrombocytopenia; PT prolongation indicates combined DIC, in which Tennessee diagnosis is divided into complete and partial, with all three indicators meeting the diagnosis as complete and any one or two abnormalities as partial.