Clinically, we often encounter patients with cirrhotic decompensation who have severe hyponatremia and even electrolyte disorders. The main reason for this is that the patient is ordered by the physician to limit salt. This is because the patient has water and sodium retention and it is believed that the patient is hyponatremic not because of low sodium, but because of dilutional hyponatremia and therefore cannot be supplemented with sodium. This view should be corrected. Patients with cirrhotic decompensation often need to use diuretics, and the common diuretics currently used in clinical practice are sodium-excluding diuretics. If a patient has low sodium, the body itself will stop sodium excretion, and in severe hyponatremia, the use of diuretics will not be able to eliminate sodium, and if sodium cannot be excreted, the diuretic effect cannot be produced. The results of studies in clinical practice also suggest that the diuretic effect is best when the blood sodium is maintained at the low limit of normal in patients with cirrhotic decompensation. In addition, the body needs a stable internal environment. The stabilization of blood sodium in the normal range is necessary to reduce the possibility of other complications. Therefore, it is recommended that patients do not need to strictly restrict salt intake in their diet. A normal diet is possible, and water intake can be appropriately reduced in the presence of ascites.