A 2-year-old boy with global developmental delay presented with severe sodium fluctuations following debulking surgery for a progressive suprasellar glioma involving the thalamus, hypothalamus, and optic pathways. Born at term via normal delivery, he began experiencing seizures on day three of life. At 6 months, MRI revealed the expanding hypothalamic mass, for which he underwent ventriculoperitoneal (VP) shunting followed by chemotherapy. Preoperative labs showed normal pituitary function: TSH 5.3 mIU/L, free T4 17.2 pmol/L, ACTH 4.7 pmol/L, cortisol 427 nmol/L, GH 44 mIU/L, IGF-1 7.6 nmol/L, LH <0.5 IU/L, FSH 0.12 IU/L, prolactin 6.7 ng/mL, plasma osmolality 278 mOsm/kg, and urine osmolality 323 mOsm/kg. Initial weight was below the 5th percentile, but attributed to chronic illness. After craniotomy and suprasellar tumour debulking, he developed hypernatremia (serum Na peaked at 170 mEq/L), polyuria (>20 mL/kg/hr), and urine sodium >300 mmol/L with fluctuating serum osmolality up to 355 mOsm/kg. Notably, despite high serum sodium, he exhibited no thirst—a key sign of hypothalamic thirst center dysfunction.
 

Physical exam revealed dry mucous membranes, reduced skin turgor, and failure to request water orally, even during periods of dehydration. He cycled through hypernatremia (central diabetes insipidus phase), hyponatremia (CSW/SIADH overlap), and again hypernatremia, requiring sequential IV vasopressin, sodium replacement, and fluid restriction. Ultimately, a diagnosis of adipsic central diabetes insipidus was confirmed.