The morbidity and mortality of cirrhosis is increasing in developed countries and has become the 14th leading cause of death worldwide, but the 4th leading cause of death in Central Europe. Cirrhosis is increasingly viewed not as a single disease, but as a group of systemic diseases staged with significant clinical signs. A recent review published in The Lancet reviewed recent studies on cirrhosis and summarized the pathophysiological mechanisms associated with cirrhosis, clinical diagnostic approaches, strategies for the management of important complications and clinical ideas for the comprehensive diagnosis and treatment of early cirrhosis. Decompensated liver function and portal hypertension are the two main outcomes of cirrhosis development. Portal vein pressure depends on portal blood flow and portal vein resistance. Increased portal vein resistance in cirrhosis is the initiating factor for the development of portal hypertension, while increased portal blood flow is an important factor in maintaining and exacerbating portal hypertension. The dysregulation of vasoactive substances, including decreased N0, increased thromboxane A2, and increased norepinephrine, angiotensin 2 and endothelin. The increased responsiveness to vasoconstrictor factors causes increasing hepatic vascular tension; 2. Increased portal blood flow: Due to the decreased liver function, the body’s ability to clear substances such as norepinephrine decreases, and sympathetic excitation, which in turn increases cardiac contraction and cardiac output. As the body exhibits an increase in NO, CO, endogenous cannabinoids or glucagon in an adaptive response, its vasodilating effect and damage to the G protein-dependent conduction pathway of the vasoconstrictor substances cause vascular hyporesponsiveness to the vasoconstrictor substances; together with angiogenesis driven by vascular endothelial growth factor (VEGF), which leads to the dilation of small visceral arteries, creating a visceral hyperdynamic in patients with cirrhosis circulation. At this time, the visceral vessels are congested, the portal blood flow increases, and the venous pressure continues to rise; 3. varices and formation of collateral circulation: local anatomical factors and VEGF-driven angiogenesis, together with the increasing portal pressure, lead to the formation of collateral circulation between the portal bodies to reduce portal pressure, and therefore many traffic branches are formed between the portal vein and the vena cava. After the opening of these traffic branches, there are changes in the direction of blood flow, venous dilatation and tortuosity; 4. Portal shunt encephalopathy: Due to the reduced first-pass effect and the decreased role of the reticuloendothelial system, the opening of the interportal collateral circulation allows portal blood not to pass through the liver but to return directly to the right heart through the side branches via the veins, eventually causing a rise in blood ammonia and accumulation of toxins in the body. Clinical diagnosis of liver cirrhosis The diagnostic model of liver fibrosis established by combining various serum indicators has become a hot research topic in recent years. Among a series of non-invasive diagnostic indexes of liver fibrosis proposed at home and abroad, the more representative ones are Fibro Test (FT), Forns Index, APRI Index and Hepascore. It must also be combined with ultrasound, CT, MRI and acoustic radiation force pulsed imaging techniques for a comprehensive assessment of the disease in patients with cirrhosis. Strategies for prevention and treatment of important complications Cirrhosis often leads to death due to serious complications, including portal hypertension, varices and bleeding from ruptured varices, ascites, infection, hepatic encephalopathy, and hepatocellular liver cancer. This article provides an in-depth analysis outlining the prevention and treatment strategies for the complications of cirrhosis. The following are the clinical response guidelines for portal hypertension and ascites, respectively: Prevention and treatment strategies for portal hypertension and esophagogastric fundic varices 1. It is necessary to treat the cause of the disease, change the lifestyle or apply statins and anticoagulants, etc.; 2, clinical symptoms of portal hypertension, i.e. HVPG >10mmHg, when the risk of cirrhosis decompensation or progression to hepatocellular liver cancer increases, which is likely to cause varices in the portal collateral circulation. The main measure is to prevent bleeding from variceal rupture by repeated endoscopic ligation until the variceal state is eradicated; at the same time, non-selective β-blockers can be applied to reduce HVPG by at least 20% within the maximum tolerable dose (controlled heart rate above 50 beats per minute and systolic blood pressure above 90 mmHg) or to keep HVPG below 12 mmHg, (if carvedilol is used If carvedilol is used, 6.25-12.5mg daily is recommended); 3. When HVPG R12mmHg, it is very easy to cause variceal rupture and bleeding. Once bleeding, blood should be transfused immediately until the hematocrit reaches 70-90g/L, intravenous vasoactive drugs, endoscopic ligature treatment within 12 hours, and broad-spectrum antibiotic treatment for 5 days. Consider emergency TIPS (transjugular intrahepatic portosystemic shunt) if the patient has a Child classification of C or B combined with active bleeding; 4. Secondary prevention of variceal rupture bleeding. Combined endoscopic skin ring ligation and non-selective β-blockers are performed, and if they fail, TIPS or liver transplantation is considered. Strategies for prevention and treatment of ascites 1. At the early stage of portal hypertension in cirrhosis, non-selective β-blockers can be applied to prevent further dilation of viscera and peripheral vessels; 2. When peripheral vasodilation causes decreased circulating blood volume, sodium retention, increased cardiac output and leads to ascites, sodium intake should be strictly limited, diuretics such as ambrisentin and tachyphylaxis should be applied, ACEI drugs should be stopped, and NSAIDs and aminoglycoside antibiotics should be avoided. At this time, consider whether liver transplantation is appropriate; 3. When renal vasoconstriction and reduced cardiac output evolve into refractory ascites (type 2 hepatorenal syndrome), a large amount of ascites must be released and TIPS should be considered; 4. When renal dysfunction progresses (type 1 hepatorenal syndrome), all diuretics should be stopped and terlipressin combined with albumin infusion can be applied. Consider liver transplantation if necessary. Clinical ideas for prevention and treatment of early cirrhosis 1. Identify risk factors, including obesity, alcohol abuse and patients born in the United States between 1945-1965. They should be screened using noninvasive fibrotic tests and hepatitis virus tests. The first consideration is to change the patient’s lifestyle, such as weight loss, smoking and alcohol cessation, which can be complemented by the use of antioxidants and appropriate antiviral therapy. 2. If cirrhosis persists, check the patient for the presence of esophagogastric fundic varices and perform primary screening for hepatocellular hepatocellular carcinoma. NSAIDs, PPIs and aminoglycosides; 3. If the patient has ascites, treatment with a low-salt diet, diuretics, and discontinuation of ACEI-like drugs can be considered for liver transplantation. For spontaneous bacterial peritonitis, quinolones can be applied for secondary prevention; 4. If the variceal vein ruptures and bleeds, endoscopic skin ring ligation and non-selective beta-blockers are feasible; 5. If there is hepatic encephalopathy, the primary treatment is to control and remove the causative factors and protect liver function from further damage, and patients with mild hepatic encephalopathy must be detected early. Early preventive interventions to prevent disease progression and avoid or delay the emergence of clinical decompensation complications are the goals of prevention and treatment of cirrhosis. A large number of clinical randomized controlled trials are still needed in the future to explore and validate new treatment options for the increasing number of patients with cirrhosis.