From aquaresis to antidiuresis: urine output-guided management of extreme hypernatremia (> 180 mmol/L) in central diabetes insipidus with reduced intracranial compliance: a case report

Acute decompensation in central diabetes insipidus (CDI) is frequently misinterpreted as a disorder of serum sodium rather than real-time water balance. Reliance on sodium alone may delay recognition of ongoing aquaresis and result in inappropriate or unsafe correction strategies. In patients with intracranial pathology, reduced cerebral compliance further amplifies vulnerability to osmotic shifts, rendering both hypernatremia and its correction potentially injurious. We present a case of extreme hypernatremia developing within 24 h following desmopressin omission, highlighting urine output as the primary real-time marker of disease activity and redefining management priorities in acute CDI. A 15-year-old boy with pineal germinoma complicated by obstructive hydrocephalus and established CDI on desmopressin developed acute agitation and reduced consciousness following omission of a scheduled dose during chemotherapy. Within 24 h, serum sodium rose from 141 mmol/L to 189 mmol/L, with serum osmolality of 385 mOsm/kg. Urine osmolality remained inappropriately low (105 mOsm/kg), confirming ongoing aquaresis. Management prioritized restoration of AVP activity using intravenous desmopressin alongside hypotonic fluid replacement titrated to urine output rather than serum sodium. Following administration, urine osmolality increased to 647 mOsm/kg with abrupt reduction in urine output, representing transient desmopressin-induced antidiuresis before recurrence of dilute polyuria as pharmacological effect waned. Sodium correction was deliberately limited to < 10 mmol/L/day in view of ventricular dilatation and reduced intracranial reserve. The patient demonstrated progressive neurological recovery with stabilization of serum sodium. Subsequent evaluation revealed previously unrecognized panhypopituitarism, including central adrenal insufficiency and central hypothyroidism, necessitating sequential hormone replacement. This case demonstrates that acute CDI decompensation is fundamentally a disorder of dynamic water flux rather than isolated dysnatremia. Urine output provides the most immediate indicator of AVP activity, whereas serum sodium represents a delayed cumulative consequence. Intravenous desmopressin induces rapid shifts from uncontrolled aquaresis to transient antidiuresis, creating a narrow therapeutic window requiring careful titration. In the presence of reduced intracranial compliance, sodium correction strategies must be individualized beyond conventional time-based classifications. Structural CDI should also prompt systematic evaluation of anterior pituitary function, as global axis failure may remain clinically silent until physiological stress unmasks it. Management strategies that prioritize serum sodium over urine output risk both delayed intervention and iatrogenic overcorrection.