Syndrome of abnormal secretion of antidiuretic hormone (SIADH) is a group of clinical syndromes caused by abnormally increased or overactive secretion of antidiuretic hormone (ADH) in the body. SIADH was first reported by Scharte in 1957 and is thought to be caused by a variety of malignancies, such as lung cancer, pancreatic cancer, brain tumors and hematologic tumors, especially small cell lung cancer (SCLC). Improper management can be life-threatening. The etiology may be related to the following factors: 1. malignant tumors and infections to heterogenous ADH secretion disorder, 2. central nervous system lesions such as brain hemorrhage, brain trauma, brain tumors, brain infections, etc. 3. drugs that cause ADH release or enhance its effect, such as anticancer drugs, especially CTX, VCR, etc., analgesics such as morphine, diuretics such as thiazides, hypoglycemic drugs such as chlorosulfonylurea, antipsychotics, antidepressants, sedative-hypnotics, etc. Sedative-hypnotic drugs can stimulate the abnormal secretion of ADH. Clinical manifestations of SIADH: No clinical symptoms when serum sodium is 120 mmol/L. If there are no clinical symptoms at 120 mmol/L and water restriction is not effective, tachyphylaxis 1 mg/kg ivgtt should be used as a diuretic, and repeated if necessary. Because tachypnea can inhibit the reabsorption of sodium and chloride by renal tubular epithelial cells, impede the formation of renal medullary hyperosmolar state, so that renal tubular reabsorption is blocked, in order to achieve the effect of inhibiting ADH. Pay close attention to the change of serum potassium in the process of use to prevent the occurrence of hypokalemia. Special attention should not be paid to the use of sodium-excluding thiazide diuretics. C. If fluid intake cannot be corrected, 300mg of norethindrone can be used orally twice a day, and serum sodium can rise to 130mmol/L within 3–1 days. This drug can inhibit the effect of antidiuretic hormone on renal tubules, reduce the reabsorption of water by renal tubules and correct hyponatremia. Since the metabolites of this drug are mainly excreted from the kidney and bile, it should be avoided or reduced in the case of hepatic and renal insufficiency. D. Sodium replacement therapy: If the serum sodium is 120mmol/L with symptoms, 3% hypertonic saline 200-300mL ivgtt should be given immediately to raise the blood sodium to 120mmol/L, then change to slow drip, to raise the blood sodium 0,5-1,0mmol/L per hour is appropriate, in the first 24 hours. In the first 24 hours, the blood sodium should not exceed 12mmol/L, and in the following days, the rate of slow injection should not exceed 5-7mmol/L every 24 hours, and when the serum sodium rises to 130mmol/L, the diuretic can be used simultaneously. Too rapid or too adequate supplementation of serum sodium and concentration may reverse the osmotic pressure gradient inside and outside the cells, causing brain cell dehydration and atrophy, thus causing central pontine demyelination with dangerous manifestations such as altered mental status, convulsions, inadequate pulmonary ventilation, decreased blood pressure, eventual pseudomyelination, limb paresis, dysphagia, and other life-threatening manifestations. E. Inhibition of pituitary release of ADH treatment: phenytoin sodium 0, 1 2 – 3 times a day orally, can inhibit the release of ADH from the pituitary gland, can also control the symptoms of convulsions, can be used when appropriate, but the duration of action is short. Fludrocortisone 2-8mg/day. In recent years, the application of arginine pressor V2 receptor antagonist: SR121463 can directly counteract the effect of plasma ADH on the renal collecting duct, reduce renal collecting duct water permeability, and improve hyponatremia. 3, hyponatremia caused by peritoneal cavity fluid: after appropriate infusion of saline can be corrected, but also available urea 30g, magnesium lucate 15g, aluminum hydroxide 15g into a combination, once taken. Or oral mannitol and other methods will also be effective.