Craniopharyngiomas are rare benign epithelial tumors of the sellar–suprasellar region, accounting for approximately 2–5% of all intracranial tumors. Despite their benign histology, they often lead to significant long-term morbidity due to local invasion and endocrine dysfunction secondary to surgical or radiotherapeutic intervention. Panhypopituitarism is one of the most common sequelae and may present with life-threatening adrenal crisis and severe hyponatremia. This report describes a patient who developed recurrent hyponatremia and Addison’s crisis after craniopharyngioma excision, complicated by steroid-induced psychosis and transient central diabetes insipidus, emphasizing the need for lifelong endocrine monitoring and patient education.

A 28-year-old man with a history of bifrontal craniotomy and excision of a sellar–suprasellar mass in 2010 presented with irritability, drowsiness, and poor appetite for two days. He had been non-adherent to hormone replacement therapy and had a history of recurrent hospitalizations for hyponatremia. On examination, he was confused and irritable, with left-sided second and third cranial nerve palsy and bilateral optic atrophy. Laboratory evaluation revealed severe hyponatremia (Na⁺ 113 mmol/L) and panhypopituitarism: cortisol <0.50 µg/dL, free T4 0.46 ng/dL with inappropriately normal TSH, GH <0.05 ng/mL, IGF-1 <15 ng/mL, and normal gonadotropins and testosterone. CT brain demonstrated postoperative changes with a small hypodense lesion in the sellar–suprasellar region, suggesting residual disease.

The patient was managed with intravenous hydrocortisone, levothyroxine, isotonic saline, and thiamine prophylaxis. Serum sodium improved to 125–127 mmol/L within 48 hours. On day two, he developed agitation, hallucinations, and aggressive behavior consistent with steroid-induced psychosis, which resolved after tapering hydrocortisone, switching to oral prednisolone, and initiating quetiapine. Subsequently, the patient developed polyuria and low urine osmolality (88 mmol/kg), indicating central diabetes insipidus, which responded to three doses of desmopressin and resolved after steroid stabilization. He was discharged in stable condition on oral prednisolone and levothyroxine, with detailed stress-dose steroid counseling and referral to neurosurgery for residual disease evaluation. Family members were educated on lifelong hormone replacement adherence and early recognition of adrenal crisis symptoms.

Craniopharyngioma survivors remain at lifelong risk for residual tumor and chronic hypopituitarism. This case illustrates how inadequate follow-up can lead to Addison’s crisis, severe hyponatremia, steroid-induced psychosis, and transient diabetes insipidus. Comprehensive endocrine replacement, structured patient education, and long-term multidisciplinary follow-up are essential to prevent recurrent crises and improve quality of life.