Pituitary Apoplexy With Marked Hyperprolactinemia in a 19-Year-Old Woman: A Case Report of Diagnostic Challenges and Surgical Management

Pituitary apoplexy is uncommon in adolescents and young adults and may present with subacute or evolving features rather than a fulminant endocrine emergency. Marked hyperprolactinemia in the setting of a hemorrhagic sellar mass can create diagnostic uncertainty between stalk effect and a prolactin-secreting tumor, with important implications for initial management. A 19-year-old woman presented with a one-month history of progressive headaches and photophobia. Magnetic resonance imaging demonstrated a 15-mm hemorrhagic cystic pituitary lesion with suprasellar extension and mild displacement of the optic chiasm. Formal ophthalmologic assessment identified bilateral superior visual field defects. Serum prolactin was markedly elevated at 4624.73 mIU/L, while other pituitary hormones were within reference ranges. She was initially managed conservatively with stress-dose hydrocortisone and low-dose cabergoline under close clinical and visual monitoring. On day 5, she developed clinical deterioration with worsening headache, orthostatic symptoms, and blood pressure instability, prompting urgent endoscopic transsphenoidal resection with multilayer skull-base reconstruction. Postoperatively, she developed cerebrospinal fluid rhinorrhea that resolved with lumbar drainage, as well as transient diabetes insipidus treated with desmopressin. Prolactin fell rapidly to 153.47 mIU/L within 24 hours of surgery and normalized by six weeks. Histopathology confirmed a pituitary neuroendocrine tumor (PitNET). Headaches resolved completely within two weeks, and she returned to university studies within four weeks. Pituitary apoplexy should be considered in young patients presenting with headache and visual disturbance, even with a subacute course. In hemorrhagic sellar lesions, markedly elevated prolactin may reflect either a prolactinoma or stalk effect; a rapid postoperative prolactin decline supports stalk compression as the dominant mechanism. Close observation during conservative management is essential, and clinical deterioration should prompt timely surgical decompression to optimize neurological and endocrine outcomes.