Endocrinology, Diabetes, and Metabolism· Topic 4.8 Hypothalamic-pituitary axis and water homeostasis· 4.8.17

Central diabetes insipidus

Central diabetes insipidus is inability of the posterior pituitary to produce adequate antidiuretic hormone, causing free water loss, polyuria, and hypernatremia; common causes include pituitary/hypothalamic tumor, surgery, trauma, and infiltrative disease. Diagnosis is confirmed with a water deprivation test followed by a desmopressin challenge, and treatment is desmopressin (DDAVP) 10-40 mcg intranasally or 0.1-0.4 mg orally, dosed once nightly or twice daily and titrated to control polyuria while avoiding dilutional hyponatremia from over-replacement.

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What this article covers

  • Overview

    Definition: central diabetes insipidus (DI) is inability of the posterior pituitary gland to produce adequate antidiuretic hormone (ADH, vasopressin), preventing renal water reabsorption and causing polyuria and polydipsia.

  • Epidemiology

    Central DI can occur at any age and is most often acquired, related to a hypothalamic-pituitary tumor, pituitary or skull-base surgery, head trauma, or infiltrative/autoimmune disease.

  • Risk factors

    Pituitary or hypothalamic tumor, including craniopharyngioma and other suprasellar masses.

  • Pathophysiology

    The posterior pituitary normally stores and releases ADH synthesized in the hypothalamus; ADH acts on renal collecting duct aquaporin channels to promote water reabsorption.

  • Clinical features

    Polyuria, polydipsia, and persistent thirst with dilute urine are the hallmark presenting features.

  • Differential diagnosis

    Nephrogenic DI: polyuria and hypernatremia from renal ADH resistance (lithium, demeclocycline, amphotericin B, genetic causes) rather than ADH deficiency; distinguished by the absence of urine…

  • Diagnosis

    Central DI is diagnosed by demonstrating an inappropriately dilute urine in the setting of hypernatremia and elevated serum osmolality, then confirming ADH deficiency (rather than ADH resistance)…

  • Management

    First, correct the free water deficit and address any hemodynamic instability, replacing free water enterally or with hypotonic IV fluids while hormone replacement is arranged, and monitor serum sodium closely during correction.

  • Complications

    Severe hypernatremia with altered mental status, lethargy, seizures, or coma occurs if free water access is inadequate to compensate for ongoing water loss, most often in patients who cannot express thirst or access water independently.

  • Prognosis

    Postoperative central DI is often transient, particularly after pituitary surgery, and may resolve over days to weeks as posterior pituitary function recovers, though some patients progress through the triphasic pattern to permanent DI.

  • Prevention

    Check serum sodium at least daily for the first postoperative week after pituitary or hypothalamic surgery, since the SIADH phase of the triphasic response peaks around postoperative day 7-8, to…

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