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Central diabetes insipidus unmasked by glucocorticoid replacement — ABIM Board MCQ

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HardEndocrinologyCentral diabetes insipidus unmasked by glucocorticoid replacementABIM Board

A 58-year-old man is hospitalized with progressive headache, fatigue, nausea, and postural dizziness. MRI shows a 2.4-cm sellar and suprasellar mass involving the pituitary stalk. Blood pressure is 82/50 mm Hg. Laboratory studies show sodium 126 mEq/L, serum osmolality 268 mOsm/kg, urine osmolality 510 mOsm/kg, morning cortisol 1.2 mcg/dL, low ACTH, and low free thyroxine with an inappropriately normal TSH. Intravenous hydrocortisone and 0.9% saline are administered. Eight hours later, his blood pressure is 118/72 mm Hg and he appears euvolemic, but urine output has increased to 700 mL/hour. Repeat studies show sodium 153 mEq/L, serum osmolality 318 mOsm/kg, and urine osmolality 108 mOsm/kg. Serum glucose and calcium are normal, and he has not received a diuretic. Which of the following is the most appropriate next management?

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Correct answer: C — Continue hydrocortisone, administer desmopressin, and replace the free-water deficit with 5% dextrose

This patient has central diabetes insipidus unmasked by treatment of central adrenal insufficiency. Cortisol deficiency increases vasopressin activity and impairs renal free-water clearance, explaining the initial hyponatremia and concentrated urine despite pituitary-stalk disease. Glucocorticoid replacement restores free-water clearance, revealing severe hypotonic polyuria. Hypernatremia with a markedly dilute urine establishes diabetes insipidus without requiring water deprivation testing; stalk involvement strongly favors central disease. Treatment must address both ongoing renal water loss and the accumulated free-water deficit: continue essential hydrocortisone, administer desmopressin, and provide hypotonic replacement such as 5% dextrose with close monitoring of sodium and urine output. A is inappropriate because isotonic saline does not replace free water and may worsen hypernatremia once circulation is restored. C removes lifesaving treatment for central adrenal insufficiency; glucocorticoids should not be withdrawn merely because they revealed diabetes insipidus. D uses a therapy more commonly employed for nephrogenic diabetes insipidus and does not provide prompt vasopressin replacement. E treats excess vasopressin action and would intensify water loss; tolvaptan and fluid restriction are used in selected hyponatremic states, not central diabetes insipidus with hypernatremia.

Reference: Syndrome of Inappropriate Antidiuresis: From Pathophysiology to Management (2023) — https://pmc.ncbi.nlm.nih.gov/articles/PMC10502587/ Diagnosis and Management of Central Diabetes Insipidus in Adults (2022) — https://pmc.ncbi.nlm.nih.gov/articles/PMC9516129/ Diagnosis and Management of Adrenal Insufficiency (August 20, 2018) — https://www.ncbi.nlm.nih.gov/books/NBK279122/