SUN-079 When Fluid Management Obscures the Diagnosis: Diagnosing Polyuria in a Patient with SAH

Abstract Disclosure: J. Naz: None. K.B. Huynh: None. S. Mahmud: None. T.B. Vaughan: None. Introduction: Alterations in water metabolism are common after subarachnoid hemorrhage (SAH), including cerebral salt wasting (CSW), syndrome of inappropriate antidiuretic hormone secretion (SIADH), and central diabetes insipidus (CDI). Aggressive fluid therapy can lead to natriuresis and polyuria, which may mimic these conditions, complicating the diagnosis. Case presentation A 37-year-old male presented with severe headache and neck pain. CTA head revealed SAH secondary to a ruptured anterior communicating artery aneurysm, for which he underwent surgical clipping after an endovascular coiling attempt. His postoperative course was complicated by aspiration pneumonia and surgical evacuation of subdural hemorrhage. On day 7, coil embolization of a residual aneurysm was performed but he developed right eye deviation and left-sided weakness. CT confirmed vasospasm, treated with aggressive hydration by neurosurgery.Over the next several weeks he had polyuria (30-35 liters/day). To maintain euvolemia, his UOP was matched with NS. Sodium levels were normal to mildly low. An initial trial of desmopressin to stop the polyuria was unsuccessful. The endocrinology team was consulted. At the time of the evaluation, the differential diagnosis included CDI, sodium natriuresis, and CSW. A variety of other agents had been utilized including hypertonic saline and salt tablets.Fluid supplementation was slowly adjusted downward to stop potential natriuresis. His polyuria improved and sodium levels stabilized. He was gradually weaned off saline, urea, salt tablets, and vasopressin. At that point, his sodium increased to 145-155 mEq/L with dilute urine suggesting partial CDI. Natriuresis was no longer in the differential diagnosis. Desmopressin alone improved sodium levels and diminished urine output. He was later switched to a stable nightly dose of desmopressin. Discussion: This case highlights that several entities may explain polyuria in a patient with intracranial pathology. Sodium natriuresis is a common cause of polyuria and alternate diagnoses can be obscured when patients are receiving large volumes of saline. The patient’s initial hyponatremia and polyuria were attributed to CSW. A diagnosis of CDI was later entertained but did not respond initially to vasopressin. Iatrogenic natriuresis from exuberant fluid administration delayed a definitive diagnosis, which could not be made until fluid replacement was diminished to more physiologic amounts. Presentation: Sunday, July 13, 2025