Patients with advanced tumor with metastasis to bone, liver, lung and other systemic organs often have various metabolic abnormalities and disturbance of water-electrolyte balance due to multiple organ dysfunction, which may lead to a series of psychoneurological symptoms. Hyponatremia is common in patients with advanced tumors. Hyponatremia is classified into three categories according to the etiology: 1) low intake, sodium deficiency hyponatremia, where the total amount of sodium in the body is reduced; 2) dilutional hyponatremia, which is often caused by renal failure, hepatorenal syndrome, corticosteroid deficiency, and rare ADH secretion disorder; 3) idiopathic hyponatremia, which often occurs in patients with advanced malignant tumors, and in severe cases, psychoneurological symptoms. In addition, there are three special hyponatremia: 1. SIADH (such as lung infection, tuberculosis, tumor, etc. causing abnormal secretion of ADH; 2. morbid cell syndrome: chronic wasting and critically ill patients; 3. potassium deficiency hyponatremia. It is common for tumor patients to have hyponatremia clinically, which may be due to intracellular protein catabolism consumption, decreased intracellular osmotic pressure, and water transfer from intracellular to extracellular. However, tumor patients often have multiple organ dysfunction in advanced stages, so hyponatremia is not a single cause but the result of multifactorial multi-organ dysfunction. If not carefully analyzed it may lead to misdiagnosis and missed diagnosis. Hyponatremia in tumor patients should be considered first: 1. Paraneoplastic syndrome: Paraneoplastic syndrome refers to systemic manifestations other than symptoms caused by tumor compression, infiltration and metastasis, also called companion cancer syndrome. For lung cancer, it refers to the extra-pulmonary manifestations caused by lung cancer acting on other systems, including abnormal changes of endocrine, neurological, connective tissue, blood system and vascular system. As far as the endocrine system is concerned, gonadotropins, adrenocorticotropic hormone-like substances and antidiuretic hormone can be secreted, the latter of which can cause dilutional hyponatremia, i.e. SIADH manifestation. 2. SIADH antidiuretic hormone secretion disorder syndrome: It is a group of syndromes with abnormal increase of endogenous ADH secretion, which leads to water retention, increased urinary sodium excretion and dilutional hyponatremia and other related clinical manifestations. It can be caused by a variety of reasons. The most common cause is oat cell carcinoma of the lung, which is responsible for 80% of SIADH patients. The syndrome of abnormal secretion of antidiuretic hormone (SIADH) is characterized by excessive secretion of ADH and water retention in the body, causing dilutional hyponatremia and low blood osmolality. Increased extracellular fluid, suppressed secretion of aldosterone, and increased sodium excretion from the body further aggravate hyponatremia, leading to water retention in the body and worsening cerebral edema. At this time, the patient shows excessive body fluid despite the manifestation of urinary collapse. 3, Cerebral salt-wasting syndrome (CSWS). CSWS was first proposed by Peters et al. in 1950. He reported three cases of hyponatremia in patients with intracranial disorders due to a large loss of Na from the urine, and the detailed mechanism was unclear. In recent years, peptides with strong natriuretic effects, including cardiac natriuretic peptide (ANP) and brain natriuretic peptide (BNP), have been extracted from the hypothalamus and other sites. It has been found that in central hyponatremia secondary to acute and chronic central nervous system diseases (cerebral hemorrhage, traumatic brain injury, subarachnoid hemorrhage, hydrocephalus, brain tumor), patients have abnormally high plasma ANP and BNP values and a negative correlation with sodium balance. Therefore, it is believed that the cause of CSWS is related to hyponatremia caused by disorders in the renal regulation of ANP or BNP due to central nervous system pathology, resulting in impaired sodium reabsorption by the renal tubules and decreased sodium retention by the kidneys. It is manifested as increased urine volume, decreased blood sodium and increased urine sodium, decreased circulating blood volume, and may appear as anorexia, nausea, vomiting, weakness, upright hypotension, inelastic skin, sunken eyes, increased heart rate, etc. In addition blood volume and blood sodium changes cause changes in other hormones such as aldosterone, resulting in different manifestations of water-sodium imbalance. Tumor patients are usually mostly elderly people, often combined with cardiovascular and cerebrovascular diseases, so for patients with brain damage can occur neuroendocrine abnormalities, and the incidence is high, which has a significant impact on the recovery of patients. 5. Adrenal insufficiency in the elderly is a relatively common phenomenon, and even if the adrenocortical hormone measurement is normal, there may be a possibility of relative deficiency. Hypoadrenocorticism can also cause antidiuretic hormone secretion disorder syndrome. Some tumors cause hypoadrenocorticism, and blood cortisol level decreases, causing water and sodium cannot be stored, and a large amount of sodium is excreted through urine, which is loss hyponatremia. In this case, serum sodium concentration and osmolality decrease, urine volume increases, urine sodium concentration increases, urine specific gravity increases, and total urine sodium volume in 24h also increases. Therefore, adrenal function needs to be tested. The diagnostic criteria for SIADH are: (1) low blood sodium, serum sodium below 135 mmol/L. (2) low blood osmolality, serum osmolality below 270 mOsm/(kg.H2O). (3) High urinary sodium, urinary sodium concentration greater than 20mmol/L. Check 24h urinary sodium quantification. (4) Concentrated urine, urine osmolality greater than 300 mOsm/(kg.H2O). (5) Normal renal function, blood inosine less than 12ng/dl, urine protein quantification, renal function test. (6) Normal adrenal function, blood cortisone concentration greater than 6 μg/dl. Check cortisol rhythm, blood and urine ACTH, etc. In response to the diagnostic criteria, accurately record the patient’s 24h in and out volume under the state of normal diet. Diagnostic criteria for CSWS: (1) Low blood sodium with polyuria. (2) Elevated urine sodium, increased urine volume and normal urine specific gravity. (3) Hyponatremia is not corrected by water restriction but worsens the condition. Experimental water restriction treatment can be identified. (4) Hyponatremia is accompanied by a decrease in central venous pressure. The patient must be noted for signs of decreased blood volume. Treatment: SIADH treatment: treatment of the primary disease, water restriction and sodium supplementation and ADH secretion inhibitors and their antagonists, (a) treatment of the cause of the disease and early diagnosis and treatment of the primary disease, drug-induced need to immediately stop. (B) correction of water overload and hyponatremia 1, restrict water intake is very important to control symptoms, for the general mild SIADH, strict restriction of water intake (about 800-1000ml of water daily), can make the symptoms eliminate. 2. When there are already severe water intoxication symptoms, tachypnea or diuretic (medullary loop diuretics drain more than urine) and hypertonic saline drip (0.1ml/kg?min) can be used to correct blood sodium concentration and plasma osmolality and control central nervous system symptoms (pay attention to prevent pulmonary edema and maintain electrolyte balance, not to apply 5% glucose solution drip). 3. 20% mannitol 250ml every 4-6 hours to facilitate water drainage, can be applied as appropriate. (C) ADH secretion inhibition or activity antagonism drugs norethindrone antagonizes the role of ADH on adenylate cyclase in renal tubular epithelial cell receptors, can be used for carcinoma and other heterologous ADH secretion, 600-1200mg/d, divided into 3 oral doses, can relieve hyponatremia in 1-2 weeks, but there is nephrotoxicity, can induce azotemia and secondary infection, can also try to have a similar effect of lithium carbonate treatment. However, the effect is not long-lasting and has serious side effects. Phenytoin sodium and other drugs can inhibit hypothalamic secretion of ADH, but the effect is short-lived and has no practical value. Treatment of CSWS: The principles of treatment of CSWS and SIADH are completely different. The main treatment is to maintain normal water and salt balance and to give rehydration therapy. Isotonic or hypertonic saline solutions can be administered intravenously or orally, either alone or in combination, depending on the severity of hyponatremia and the patient’s tolerance level. In mildly symptomatic patients, the rate of Na rise should not exceed 0.5 mmol/L per hour until Na rises to 120 mmol/L, and the patient can be removed from danger. For patients with severe neurological symptoms, firstly, inject 3% hypertonic saline intravenously at a rate of 1-1.5 mmol/L per hour to raise plasma Na by 5-10 mmol/L, and then continue to inject 3% hypertonic saline at a rate of no more than 0.5 mmol/L per hour. Thereafter, the plasma Na concentration should be increased gradually over several days. The general principle is to maintain the balance of water and salt and to maintain the plasma volume. In the presence of increased urine output, posterior pituitary hormone therapy is indicated. In the case of hyperalgesia, the antidiuretic hormone secretion disorder syndrome should be treated with sodium supplementation and glucocorticoid supplementation to reduce dilutional hyponatremia. In addition, we have found that in patients with tumors with blood in the blood or blood in the urine, after treatment with posterior pituitary hormone, the blood in the blood or blood in the urine is stopped, but hyponatremia that is difficult to correct occurs. Posterior pituitary hormone is extracted from the posterior pituitary gland of animals and contains two kinds of components: oxytocin and pressor hormone, which mainly use pressor hormone to act on smooth muscle of blood vessels to make small pulmonary arteries or bronchial arteries contract, which helps to clot and stop bleeding in ruptured blood vessels. Therefore, in the clinical application of posterior pituitary hemostasis should pay attention to prevent the occurrence of hyponatremia. It is also believed that intravenous potassium-magnesium menthylate and magnesium salts can help activate the sodium pump, raise blood pressure and correct hyponatremia. Others have treated idiopathic hyponatremia with plasma supplementation and achieved satisfactory results. Our department has handled a case of hepatocellular carcinoma patient with nausea and vomiting, mild ascites, bilateral lower limb edema, and abnormal mental status, which was diagnosed as dilutional hyponatremia and hyponatremic encephalopathy, which could easily be misdiagnosed as hepatic encephalopathy if not sufficiently recognized. The symptoms were rapidly relieved and the blood sodium was normal after the above treatment. Attention:When the brain tissue is in hypotonic state in hyponatremia, too rapid supplementation of hypertonic saline and correction of hyponatremia make the plasma osmolality rise rapidly, causing dehydration of brain tissue and destruction of blood-brain barrier, and harmful substances cross the blood-brain barrier leading to acute demyelination of neuromyelin. Its clinical manifestations are often sudden onset of flaccid paralysis of the limbs, mastication, swallowing and speech disorders, nystagmus and eye gaze disorders, etc. It may present as muteness and complete or incomplete atresia syndrome. MRI may reveal characteristic batwing-like lesions at the base of the pons, with symmetrical distribution of T1 low signal and T2 high signal, without enhancement effect. Also known as central pontocerebral myelinolysis and pontocerebral extramedullary myelinolysis (CPM), it is closely related to the overcorrection of hyponatremia and may essentially be an osmotic encephalopathy, which needs to be noticed in the clinic.