Endocrine Abstracts

JOINT1034

Introduction: Pituitary apoplexy is a rare clinical syndrome that occurs as a result of acute haemorrhage and/or infarction within a pituitary tumour. Classical presentation includes sudden onset headache, vomiting, visual impairment and possible partial or panhypopituitarism. Pituitary apoplexy is frequently spontaneous, but predisposing factors can be identified in 10–40% of cases. As the clinical syndrome overlaps with other presentations, recognition of pituitary apoplexy is challenging, which delay diagnosis and management. We describe the case of a pre-existing history of migraines leading to a late diagnosis of pituitary apoplexy.

Clinical case: A 34-year-old man presented to the hospital with sudden onset throbbing headache and several episodes of vomiting without fever, rash or neck stiffness. He had a background of chronic migrainous headache requiring hospital admission previously. Past medical history also included type 1 diabetes mellitus, and a 12mm non-functioning pituitary macroadenoma. Initial CT head imaging did not reveal any pathology and both an MRI and lumbar puncture were planned to exclude SAH. During admission, he developed hyperglycaemia with ketosis, which was managed by an intravenous insulin infusion. His headache did not demonstrate improvement and lumbar puncture was positive for xanthochromia. On the sixth day of admission, his sodium level dropped from 133mmol/lto 108mmol/L. The medical team assessed the patient to be hypovolemic and administered intravenous fluids. The possibility of pseudohyponatraemia secondary to hyperglycaemia was also raised. On the same day, the patient reported new visual deterioration. An urgent pituitary MRI was performed and intravenous Hydrocortisone was commenced. Anterior pituitary profile showed a cortisol of 19nmol/l, FSH 1.1IU/l, LH <1.0IU/l, testosterone 0.5nmol/l, prolactin 40mIU/l, free T4 12.5pmol/l, free T3 2.2pmol/land TSH 0.08mIU/L. MRI showed signs of apoplexy. Severe hyponatremia was managed in Intensive Care and he was commenced on hydrocortisone, levothyroxine and testosterone, and surgery done after that. Interval surveillance pituitary MRI showed significant reduction in the size of the lesion without mass effect on the chiasm. The patient remains on replacement therapy with Hydrocortisone, Levothyroxine and Testosterone.

Discussion: This case highlights the importance of considering apoplexy early within the differential of a patient with a pituitary adenoma presenting with sudden onset headache. Delayed diagnosis of pituitary apoplexy is common in the case of undiagnosed pituitary adenoma, but can be avoided in a patient with a known diagnosis. Hyponatraemia may occur secondary to cortisol insufficiency. Therefore, when apoplexy is suspected, the management should include administration of intravenous glucocorticoid therapy.