Hypothalamic adipsia presenting as persistent hypernatremia after aneurysmal subarachnoid hemorrhage.

A woman in her 50s developed persistent hypernatremia after aneurysmal subarachnoid hemorrhage treated with surgical clipping. During the acute phase, she presented transient hypotonic polyuria requiring desmopressin, initially suggesting arginine vasopressin (AVP) deficiency (AVP-D). However, her subsequent course was characterized by recurrent hypernatremia without persistent polyuria and with complete absence of thirst. Urine output was low or inappropriately normal, with preserved urinary concentrating capacity, making persistent AVP-D unlikely. Neuroimaging showed ischemic changes close to hypothalamic regions involved in osmoregulation. The clinical pattern supported hypothalamic adipsia, with possible partial dysfunction of osmotically stimulated AVP release. Outpatient management focused on structured water intake, family supervision, digital reminder systems, and cautious low-dose desmopressin to minimize osmotic variability. This case emphasizes that hypernatremia following neurovascular injury should not be automatically attributed to AVP-D. Systematic assessment of thirst, urine output, and urine osmolality is key to identifying hypothalamic adipsia, facilitating early diagnosis and the implementation of structured hydration strategies to prevent recurrent severe hypernatremia and its complications.