SUN-422 Panhypopituitarism Secondary to Pituitary Macroadenoma with Optic Chiasm Compression and Possible Apoplexy

Learning Objective: To recognize profound hyponatremia as a presenting feature of pituitary adenoma. Ten percent of the population have undiagnosed pituitary adenomas; rarely leading to hypopituitarism and apoplexy. A 75 year old man presented to the hospital with severe headache, vomiting and double- vision. He reported decreased libido, axillary and pubic hair for the past year. Vital signs were stable and physical exam revealed diplopia but no bitemporal hemianopsia or other visual defects. Initial lab work showed a sodium level of 116. Testosterone was <7.0, LH 0.54 and FSH of 4.3, ACTH <5.0, TSH 0.772, free Thyroxine of 0.44 which raised concern for hypopituitarism. Brain MRI was contraindicated due to a pacemaker. CT head with contrast confirmed a pituitary macroadenoma measuring 2.6 cm by 2.0 cm by 1.2 cm with compression of the optic chiasm. There was increased attenuation diffusely in the pituitary and pituitary apoplexy could not be ruled out. Prompt therapy was initiated with dexamethasone, levothyroxine, and intravenous fluids. He underwent a successful transsphenoidal resection with development of diabetes insipidus post-operatively. Discharge medications included desmopressin, hydrocortisone and levothyroxine. Hypopituitarism can occur from direct pituitary dysfunction or hypothalamic damage and can be congenital or acquired. Most causes are acquired such as pituitary macroadenoma, transcranial surgery or apoplexy. The anterior pituitary gland is extremely well-vascularized and depends on this for release of hypothalamic factors to the pituitary cells and release of hormones into blood. Blood-supply lesions are caused by compression of the long portal blood vessels or apoplexy from a tumor or local hemorrhage. Apoplexy occurs only in 2-12% of adenomas, most commonly in nonfunctioning tumors. Recognition is crucial as it is life-threatening due to the corticotropic deficiency. Recent evidence suggests that pituitary tumors are at an increased risk of spontaneous infarct even without evident hemorrhage. This is due to the intrinsic features of the tumor, high demand for nutrients and limited blood supply. This makes the tumor vulnerable to infarction from surgery, hypotension, hypoglycemia from insulin or from given hypothalamic releasing factors which causes increased metabolic demand. We present a patient with panhypopituitarism from a pituitary adenoma and possible pituitary apoplexy. Hyponatremia is a unique presentation of an underlying pituitary adenoma and occurs due to cortisol deficiency. Recognition of such subtle clinical signs is key for the prompt treatment of an underlying pituitary dysfunction. Oldfield, EH & Merrill, MJ. (2015) Apoplexy of pituitary adenomas: the perfect storm. Journal of Neurosurgery. 122:1444-1449 Stieg, MR, Renner, U, Stalla, GR, Kopczak, A. (2017) Advances in understanding hypopituitarism. F1000Research. 6;178