Theoretically, any factor that causes damage to the hypothalamic-pituitary system can affect the secretion of antidiuretic hormone (ADH) and produce central uremia. Therefore, postoperative polyuria after transsphenoidal pituitary adenoma is often simply diagnosed as central uremia and treated with antidiuretic drugs. However, the fact is that the pituitary gland is highly resistant to injury as far as ADH secretion is concerned. Experiments have shown that even surgical removal of the pituitary gland can only cause a transient impairment of ADH secretion. When the patient’s ADH stores are above 10% of normal levels, urine output is only mildly increased, and symptoms of excessive drinking and irritability are so mild that they are even ignored by the patient, manifesting as partial central dysuria, which does not require clinical intervention. Complete central enuresis occurs only after transsphenoidal pituitary adenoma surgery when ADH stores are below 10% of normal levels, and is often transient. Loss of more than 90% of large cell neurons in the supraoptic and paraventricular nuclei is required to cause permanent enuresis. In the neurosurgery department of Xuanwu Hospital, Capital Medical University, Guilin Li resects pituitary adenomas via the pterygoid sinus approach. Due to the protection of the saddle diaphragm, surgical interference with the hypothalamus is limited to traction and scratching and does not affect the blood supply to the hypothalamus. Moreover, with the advancement of surgical techniques and surgical instruments, the surgical field becomes clearer and clearer, and the method of segmental tumor resection can control the saddle diaphragm to descend gradually from posterior to anterior and from both sides to the center, which affects the pituitary gland and hypothalamus less and less. The single nostril-pyriform sinus approach is significantly less invasive than the classical transoral nasopalatine sinus approach. Patients can resume eating and bed activities soon after surgery. The role of hypothalamic thirst center threshold downregulation and psychogenic polyhydramnios due to postoperative stress in patients is becoming increasingly evident in postoperative enuresis after transsphenoidal-pterygoid sinus surgery. The thirst center is located in the hypothalamic endplate vascular apparatus. It is sensitive to changes in the internal environment due to the lack of a blood-brain barrier. Transsphenoidal approach to pituitary adenoma resection can affect the hypothalamic thirst center, resulting in a downregulation of the thirst threshold. The plasma osmolality threshold for inducing thirst in normal subjects is 289-307 mOsm, and postoperative patients with pituitary adenoma have a significant sensation of thirst and urge to drink at an effective plasma osmolality of 283-288 mOsm. Patients’ incomplete knowledge of increased postoperative urine output also in fact increases patients’ fear and need to drink actively. The postoperative transoral breathing due to nasal mucosal edema also increases the sensation of thirst. central uropyrosis due to impaired ADH secretion, hypothalamic downregulation of the central threshold of thirst and psychogenic polyhydramnios due to postoperative stress of the patient play a combined role in postoperative uropyrosis due to transsphenoidal-pituitary adenoma. But again, they have different characteristics and play different roles at different times after surgery. Central polyhydramnios due to impaired ADH secretion after surgery appears quickly, mostly within a few hours after surgery, and manifests as a complete polyhydramnios. The data from a 1994 study in our department showed that central uremia occurs from 1 to 22 h after surgery, with a mean of 11 h, and lasts from 4 to 12 h, with a mean of 37 h. The volume of urine increases gradually from 200 ml/h to a maximum of 1000 ml/h. The volume of urine is independent of the rate of infusion, wakefulness or sleep state, with a urine specific gravity <1.005 and a plasma osmolality >300 mOsm, which can reach a maximum of 340 mOsm. Posterior pituitary hormone drugs must be used to control urine output (4). The urine volume is closely related to the rate of infusion and the amount of water drunk, with urine specific gravity between 1.005 and 1.015 and plasma osmolality in the normal range. Patients have significant irritable thirst and drink a lot of water. Thus central dysuria due to impaired ADH secretion plays a major role in the 24h postoperative period, and once it occurs it is often complete. In contrast, uremia occurring after 24 h postoperatively is often the result of a hypothalamic thirst center threshold downregulation based on ADH secretion disorder and psychogenic excessive drinking due to postoperative stress in the patient, and the latter plays a major role. Inappropriate management can lead to prolongation and exacerbation of enuresis. Increased urine output after transsphenoidal-pituitary adenoma surgery is the result of a combination of thalamic thirst central threshold downregulation and psychogenic polyhydramnios due to postoperative stress on top of ADH secretion disorder. The management of postoperative enuresis after transsphenoidal-pituitary adenoma has its own specificity due to the simultaneous presence of ADH secretion disorder, down-regulation of thirst central threshold and psychogenic polyhydramnios. Under physiological conditions, after drinking large amounts of water, body fluids are diluted, plasma crystalloid osmotic pressure decreases, ADH secretion decreases, and urine output increases. Under physiological conditions, drinking 1 liter of clear water in 20 minutes can result in a urination rate of 15 ml/min after 1 h. Drinking saline does not result in hydrodiuresis, and the urination rate is stable at 2 ml/h. However, due to the presence of impaired ADH secretion, the results of drinking saline are similar to those of drinking clear water. Moreover, saline also decreases the secretion of aldosterone, which increases urine output. Since hypotonic urine is eliminated, the retention of salt ions increases thirst. Therefore, in the management of postoperative transsphenoidal-pituitary uremia caused by the combined effect of a lowered central threshold of thirst and psychogenic polyhydramnios on the basis of impaired ADH secretion, increasing the amount of water drunk and accelerating the rate of infusion not only fails to control uremia, but also aggravates irritable thirst and polyuria. Under the premise of close monitoring of vital signs, firstly, strictly control the infusion rate, control the drinking rate, and supplement plain water orally in small amounts and several times. Observe for 2~3h, no trend of reduction, and give 12.5~25mg of oral dihydrocortisone. we believe that dihydrocortisone reduces plasma osmolality to below the threshold of thirst mainly by increasing the elimination of NaCl, while causing negative sodium balance, increasing renal proximal tubular reabsorption and reducing urine output. In clinical practice, the urine volume firstly increases transiently after oral administration of dihydroketonuria, reaching 300~400ml/h for 1-2 hours, the feeling of thirst gradually decreases after 1h of administration, the urge to drink disappears, and the urine volume gradually decreases to 50~100ml/h after 1-2 hours of administration, which can be maintained for 6~12 hours. It also confirms our view. At the same time, once the patient develops urinary collapse, it often lasts for 1~2 d. Therefore, according to the frequency of the appearance of thirst, dihydrocotrimoxazole should be given orally regularly so that the organism can obtain a relatively stable internal environment to facilitate the recovery of ADH secretion regulation. We do not advocate the use of posterior pituitary hormones in patients with hypothalamic thirst center threshold downregulation and postoperative stressful polyhydramnios caused by urinary collapse on the basis of ADH secretion disorder. Because the patient’s ADH level is not reduced to the level of complete enuresis, enuresis is caused by hypothalamic thirst central threshold downregulation and the patient’s postoperative nervous polyhydramnios. Posterior pituitary hormones may interfere with the recovery of the hypothalamic-pituitary axis. In clinical practice, we often see a recurrence of enuresis in patients after discontinuation of posterior pituitary hormones, which also leads to complex electrolyte disturbances. It must be stated, however, that impaired ADH secretion is the main cause of uroemesis that occurs within 24 hours after surgery, and that the use of posterior pituitary hormones is necessary to control urine output.