SUN-425 Pituitary Apoplexy, an Unexpected Cause of Syncope: Case Report

Background Pituitary apoplexy is a rare complication in 2-12% of pituitary adenomas (1). The most common presentation is headache and visual disturbance. Syncope has been noted in 7.8 -10% of apoplexy (2) and its etiology is typically adrenal insufficiency (AI). Clinical Case A 74 year old male presented to the ER with a 3 month history of syncope and loss of peripheral vision. He had a PMH of pituitary macroadenoma with GH and testosterone deficiency for 12 years, but he declined GH and testosterone treatment. In 2017, MRI showed a slight mass increment (2.4 x 2.7 x 3.8 cm from 2.4 x 2.7 x 3.5 cm). He also had a history of primary hypothyroidism on Levothyroxine 25 mcg for 3 years. In the ER, BP was 113/66 mmHg, no orthostatic BP recorded, HR 54 bpm, RR 14 and BT 35.8 °C. Physical exam showed only bradycardia. ECG revealed sinus bradycardia. The Initial concern was a cardiogenic syncope. CT brain found enlargement of suprasellar (1.8 cm from 1.2cm). Lab showed Na 128 mmol/L (serum osmol 296 mOsm/kg, urine osmol 271 mOsm/kg, urine Na 57 mmol/L). Serum cortisol (6 AM) was 2.2 (3.0-27.0 ug/dL), IGF-1 < 10 (32-200 ng/mL), total testosterone 15 (240-950 ng/dL), prolactin 18(male <18 ng/mL), TSH 3.51 (0.34-3.0 uIU/mL) and free T4 0.7 (0.6-1.6 ng/dL). MRI brain showed enlargement of pituitary mass (2.9x3.5x4.4 cm) with suprasellar extension into the clivus and cavernous sinus with new fluid level hinting hemorrhage. Bitemporal hemianopia was confirmed by visual field exam. The patient continued with a diagnosis of partial hypopituitarism, but with the addition of a new diagnosis: AI. He was stabilized on prednisone 10 mg daily and underwent transphenoidal decompression. Syncopal episodes resolved. He was discharged with hydrocortisone 20 mg in the morning and 10 mg in the evening as well as Levothyroxine 25 mcg. On Endocrine clinic follow up, the patient had permanent AI. Bitemporal hemianopia resolved. Conclusion Our patient presented with an uncommon endocrine problem, pituitary adenoma. He then developed a rare complication, pituitary apoplexy, presenting with an atypical symptom, syncope from secondary AI. Important, is that the diagnosis was delayed because of concern for bradycardia. However, once the PMH of pituitary adenoma was recognized, lab studies demonstrated AI and evidence of apoplexy from MRI. Treatment of AI has permanently corrected syncope. Also, of interest, despite a pituitary macroadenoma, the developed primary hypothyroidism. He was on Levothyroxine for 3 years prior to presentation; it’s unlikely that replacement was responsible for precipitating AI. Reference 1. Briet C, et al. Pituitary apoplexy. Endocrinology and metabolism clinics of North America. 2015;44(1):199-209. 2. Grzywotz A, et al. Pituitary apoplexy - A single center retrospective study from the neurosurgical perspective and review of the literature. Clinical neurology and neurosurgery. 2017;163:39-45.