In recent years, there have been more studies on the pathogenesis, diagnosis, and treatment of cirrhotic ascites in China, but there is a big gap compared with the previous ones. The more stringent the sodium restriction, the stronger the RAAS activity. The RAAS activity is suppressed after correction of hyponatremia; (2) the hepatorenal syndrome (HRS) is not induced by hypovolemia due to vasoactive substance disorders in patients with cirrhotic ascites, but by hypovolemia due to sodium restriction and diuresis; (3) some provisions of foreign (US) guidelines for the diagnosis and treatment of cirrhotic ascites contradict each other. According to these outstanding problems, research on cirrhotic ascites should be emphasized. Yuan Gang, Department of Hepatology, Ningbo Second Hospital, Ningbo, China, has some questions about the treatment of cirrhotic ascites. 78 mmol/d”. This treatment is contradictory to the goal because the combination of spironolactone and furosemide increases urinary sodium by 158 mmol/d, causes a sodium deficit of 70 mmol at 24 h, which is about 10% of total plasma sodium, and decreases plasma sodium by 14.6 mmol/L at 24 h. Thus sodium restriction and oral diuretics are unlikely to maintain the plasma sodium concentration required for physiologic activity, much less maintain urinary sodium excretion > The concern is that during sodium restriction and oral diuretic therapy, plasma sodium decreases gradually and the diuretic effect is diminished or non-responsive. When urinary sodium excretion is reduced, the US guidelines for the diagnosis and treatment of cirrhotic ascites are called recalcitrant ascites and emphasize that liver transplantation should be performed as soon as possible. In this regard, we have every reason to believe and confirm that sodium restriction and diuretic treatment of cirrhotic ascites induces recalcitrant ascites and HRS, which is the result of the US guidelines for the diagnosis and treatment of cirrhotic ascites misjudging the pathogenesis of recalcitrant ascites and HRS, one-sidedly and solely pursuing the issue of RAAS activity, ignoring The physiological protective effect of feedback-induced RAAS activity enhancement during plasma hyponatremia was ignored. As a result, more stringent sodium restriction results in lower plasma sodium, stronger RAAS activity, and less urinary sodium excretion, at which point the diagnosis of intractable ascites is made, but associated with sodium restriction and diuretic therapy. The guidelines recommend the use of an extraordinary dose of aldosterone antagonist, with a maximum dose of spironolactone 400 mg/d. Why the use of such a dose still fails to antagonize aldosterone, or to inhibit RAAS activity before the patient loses the chance of survival, should attract our attention to this question, because so far no reports of RAAS activity inhibition by sodium restriction, diuresis and the use of aldosterone antagonists have been found. It indicates that the feedback activation of RAAS activity by plasma hyponatremia has a much greater effect than the antagonistic effect of spironolactone on aldosterone, and the inhibition of RAAS activity by correcting hyponatremia is in turn much greater than the antagonistic effect of spironolactone. Question 2: Tension ascites occurs in patients with cirrhotic ascites after excessive sodium restriction and use of diuretics during treatment, because of reduced plasma sodium and diminished or non-responsive diuretic effect. At present, there is a large gap between the prognosis judgment and treatment of tonic ascites in China compared with the US guidelines for the diagnosis and treatment of cirrhotic ascites. (1) “Chronic hyponatremia is common in patients with cirrhotic ascites, and death rarely occurs as a result. In this regard, we believe that the morbidity and mortality rate of patients with plasma sodium <125mmol/L is significantly higher, and the main cause of death is hypotonic encephalopathy and HRS induced by insufficient blood volume. The prognosis is extremely poor, or hyponatremia may lead to irreversible demyelination of nerve fibers. Correction of hyponatremia at this time can increase the effect of diuretics to prevent nerve fiber demyelination and induce hypo-osmolar encephalopathy and V. (2) "Patients with tonic ascites can be drained by laparotomy first, followed by sodium restriction and oral diuretics. Clinical observation confirms that hyponatremia already exists in patients before the formation of tonic ascites, and the discharge of ascites can further decrease plasma sodium, on the basis of which continued sodium restriction and oral diuretics will aggravate and accelerate electrolyte disorders, which will easily lead to a decrease in circulating blood volume and circulatory failure, and is the main cause of hypotonic encephalopathy and HRS. Sodium restriction and oral diuretics after ascites discharge are not conducive to ascites regression, which not only have no theoretical basis and clinical guidance, but also contribute to ascites recovery. The American guidelines for the diagnosis and treatment of cirrhotic ascites refer to hypotonic encephalopathy induced by electrolyte disorders as hepatic encephalopathy, because the pathogenesis and treatment of hepatic encephalopathy and hypotonic encephalopathy are completely different and should be a cause for concern. Hepatic encephalopathy occurs less frequently in patients with cirrhotic ascites treated with sodium restriction and diuresis, and is mostly hypotonic encephalopathy if there are no predisposing factors such as upper gastrointestinal bleeding. Hypotonic encephalopathy is caused by the decrease of plasma sodium and osmotic pressure. During sodium restriction and diuretic treatment, the lower the plasma sodium, the higher the chance of hypotonic encephalopathy, which often coexists with intractable ascites and HRS. If hypo-osmolar encephalopathy is misdiagnosed as hepatic encephalopathy, the treatment of hypoammonia and dehydration will not only be of no help, but also the patient will lose the chance of survival. Receive the ideal effect of dehydration, lowering intracranial pressure, expanding volume, preventing hypochlorhydria alkalosis and demyelination changes of nerve fibers. The US guidelines for the management of cirrhotic ascites state that "the prognosis for HRS is poor, and the aim of medical treatment is to control azotemia and maintain electrolyte balance before liver transplantation, including hemodialysis and vasoactive drugs such as dopamine. All these treatments cannot be explained by the causes and pathogenesis of HRS, and cannot solve the problem of HRS hypovolemia, let alone maintaining water-electrolyte balance, because hyponatremia is present before and after the formation of HRS, and obvious electrolyte disorders and hypotonic or isotonic dehydration have already occurred, which are the main causes of hypovolemia. In this case, correcting the electrolyte disorder can suppress the imbalance between RAAS activity and other vascular substances, resolve hypotonic dehydration and restore blood volume. Hemodialysis and the use of vasoactive substances can only aggravate the vasoactive substance disorder and further enhance RAAS activity, which will not help the recovery of patients with intractable ascites and HRS, and make it difficult to maintain patients' vital signs and avoid liver transplantation. Since intractable ascites, HRS and hypoosmolar encephalopathy are associated with hyponatremia, diuresis, discharge of ascites, catheterization and the use of vasoactive substances with a time limit of sodium are unlikely to resolve tonic and intractable ascites, let alone change the pathogenesis of HRS and liver transplantation. Clinical studies have found that correction of hyponatremia can receive inhibition of RAAS activity, enhanced diuretic sensitivity, increased urinary sodium excretion, decreased serum creatinine, prevention of hepatic encephalopathy, and relief of hypo-osmolar encephalopathy and HRS. We are very interested in the clinical observation of the problem of treatment of HRS given by the same people to correct hyponatremia. In conclusion, the phenomenon of hyponatremia in patients with cirrhotic ascites should be taken seriously because sodium and chloride are important substances to maintain the physiological activities of human body. It is one of the measures that cannot be ignored and should be given attention. Excerpted from: Journal of Clinical Hepatobiliary Diseases, Vol. 28, No. 9, 2012