Treatment and prevention of decreased secretion of antidiuretic hormone (adh)

  Reduced secretion of antidiuretic hormone (adh) is one of the symptoms of syndrome of inappropriateantidiuretic hormone secretion (SIADH), a 9-peptide hormone secreted by nerve cells in the supraoptic and paraventricular nuclei of the hypothalamus. hormone, which is released after reaching the pituitary gland via the hypothalamic-pituitary bundle. Its main role is to increase the water permeability of the distal convoluted tubules and collecting ducts, promote water absorption, and is a key regulatory hormone for urine concentration and dilution. In addition, the hormone also enhances the permeability of the collecting ducts of the inner medulla to urea. After drinking large amounts of water, the blood is diluted, the crystal osmolarity decreases, and the secretion of antidiuretic hormone is reduced.  Treatment of the primary disease: Those caused by malignant tumors should have early surgery, radiotherapy or chemotherapy. Those caused by drugs should stop this medicine immediately. Some brain disorders such as acute subdural or subarachnoid hemorrhage caused by brain infection are sometimes transient and disappear with the improvement of the primary disease.  In mild cases, hyponatremia can be corrected by limiting water intake and discontinuing drugs that hinder water excretion.  Drug treatment (1) demeclocycline (demeclocycline, demeclocycline): can antagonize the role of AVP on adenylate cyclase in renal tubular epithelial cell receptors inhibit the role of AVP on renal tubular reabsorption of water, can also inhibit ectopic AVP secretion common dose of 600-1200mg/d divided into 3 oral doses, cause isotonic or hypotonic diuresis, can be within 1 to 2 weeks This drug can be nephrotoxic and can induce chlorosis and secondary infection, so it is prohibited for people with liver and kidney failure.  (2) Furosemide (furosemide, tachyphylaxis) 40~80mg/d orally, with NaCl3g/d to supplement sodium loss.  (3) Phenytoin sodium: it can inhibit the secretion of AVP from the hypothalamus is effective in some patients, but the effect is transient.  Treatment of severe hyponatremia Severe hyponatremia with confusion, convulsions or coma should be treated urgently. Furosemide 1mg/kg can be administered by sedation and repeated if necessary, but care must be taken: it may cause hypokalemia, hypomagnesemia and other water-electrolyte disorders. Replace the sodium loss with 3% NaCl solution 1~2ml/(kg-h) according to the urinary sodium excretion. Once the blood sodium rises to a safe level (125 mmol/L), the rate of sodium administration should be slowed down and controlled within the range of 0.5-1.0 ml/(kg-h) of 3% NaCl solution. In the first 24h blood sodium elevation should not exceed 12mmol/L to avoid the occurrence of cerebral bridge demyelination lesion which is a serious neurological complication caused by the correction of hyponatremia too fast, its clinical manifestations are the deterioration of neurological symptoms, mental changes, convulsions, pulmonary hyperventilation hypotension, and finally pseudomyelitis, tetraplegia, swallowing difficulties, etc. after the correction of hyponatremia.  Prevention: 1. Limit water intake to prevent recurrence of SIADH.  2, Children should not take Demeclocycline (desmethylgentamicin) because it affects bone development. It can induce azotemia, and renal function should be reviewed regularly.  Prognosis: Diagnosis of SIADH must pay attention to prevent electrolyte disorders and congestive heart failure, but also must pay attention to over-correction of hyponatremia caused by central (especially cerebral bridge) myelin breakdown, which can be avoided if the rate of sodium rise <2mmol/L. Symptoms are relieved by proper treatment and the prognosis is good.