Low ADH production by the posterior pituitary can cause excessive urination, severe dehydration and high sodium measures. The natural response is increased thirst leading to additional water intake. Polyuria could be so advanced that drinking alone would not correct dehydration or sodium anomalies. Supplementation with ADH hormone is needed in these cases.
Please find below excerpts from Endocrine Society guidelines on central diabetes insipidus published in November 2016.
Central diabetes insipidus
Central DI occurs when the secretion of ADH (also called vasopressin) by the posterior pituitary is insufficient to meet urine concentration requirements. The prevalence of medically treated DI is about 100 per 1 million inhabitants. DI can be congenital or acquired; it can be secondary to a variety of pathological processes including tumors (mostly craniopharyngioma and germinomas), head trauma, and inflammatory, autoimmune, granulomatous, infectious diseases involving the hypothalamus and/or posterior pituitary. Sometimes the cause of DI is unknown (“idiopathic DI”) and is thought to be autoimmune in nature. In some of these cases, periodical follow-up imaging may unveil the cause, particularly in young patients. DI is very rarely encountered in nonoperated pituitary adenomas.
We recommend simultaneously measuring serum and urine osmolarity in patients with polyuria (>5 L/100 kg of body weight in 24 hours). In the presence of high serum osmolarity (>295 mOsmol/L), urine osmolarity should reach approximately 600 mOsmol/L (urine/plasma osmolality ratio should be ≥2), whereas urine dipstick should be negative for glucose.
When administering desmopressin (DDAVP) in diabetes insipidus (DI), we suggest individualized therapeutic schedules. Although clinicians should offer therapy to all patients, some patients with partial DI may not be bothered by polyuria and may prefer no treatment. To reduce the risk of hyponatremia, we recommend that clinicians educate all patients receiving DDAVP about the risk of overdosing. Periodically (at least weekly), patients should experience a phase of polyuria during which the effect of the medication has obviously worn off. (Ungraded Good Practice Statement)
In postpituitary surgery DI, we suggest that clinicians should make at least one attempt to discontinue DDAVP during the weeks/months after surgery to determine whether posterior pituitary function has recovered. (Ungraded Good Practice Statement)
We suggest that all patients with DI wear an emergency bracelet or necklace to inform clinicians of the patient’s health problem if incapacitated. (Ungraded Good Practice Statement)
Because adrenal insufficiency (relative hypovolemia) may mask the presence of partial DI, we suggest monitoring for the development of DI after starting GC replacement. Conversely, patients with improved DI without an adrenal insufficiency diagnosis should undergo AI testing.
We suggest that initial therapy for DI utilizes short-acting sc aqueous antidiuretic hormone (ADH), allowing for safer use in the vast majority of cases in whom DI resolves spontaneously.
We do not suggest prescheduled DDAVP dosages in the first week postsurgery because of the risk of hyponatremia after transient DI resolves and the risk of syndrome of inappropriate ADH secretion that may occur 7–10 days after surgery.
We suggest oral or intranasal DDAVP after discharge, with clear instructions that patients should only use the medication if significant polyuria occurs.
We suggest retesting all pituitary axes starting at 6 weeks after pituitary surgery and then periodically to monitor the development or resolution of pituitary deficiencies.
In pregnant women with pre-existing DI, we suggest continuing DDAVP during pregnancy and adjusting doses if required.