Abstract: FR-PO0608
Cerebral Salt Wasting vs. Syndrome of Inappropriate Antidiuretic Hormone Secretion? Another Case for Debate
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Nawaz, Shaizore, Swedish Hospital, Chicago, Illinois, United States
- Pandya, Shan, Swedish Hospital, Chicago, Illinois, United States
- Batarseh, Tamara Ruth, Swedish Hospital, Chicago, Illinois, United States
- Shetty, Ashwin R., Swedish Hospital, Chicago, Illinois, United States
Introduction
Traumatic brain injuries (TBI) have long been associated with hyponatremia, with two possible mechanisms being Syndrome of Inappropriate Antidiuretic Hormone (SIADH) and Cerebral Salt Wasting Syndrome (CSW). Hypertonic saline is often used to treat severe hyponatremia. We present a case of TBI-associated hyponatremia refractory to hypertonic saline.
Case Description
55 year old male with history of Alcohol Abuse, Type 2 DM, and HTN was brought to the ER after being found down on the street. He was not on any medications. Initial labs were remarkable for Na 133 mEq/L, glucose 163 mg/dL, Cr 0.6 mg/dL, EtOH 402 mg/dL. CT Head revealed holohemispheric right subdural hematoma (SDH) causing significant mass effect and SDH evacuation was performed. Over 3 days, his Na decreased to 122 mEq/L. At this time, urine Na was 18 mEq/L, urine osm 865 mosm/kg, and serum osm 265 mosm/kg. He was alert and oriented, but did have headaches. His systolic BP ranged 107 to 127 mmHg, eventually rising above that. He was given 0.9% NaCl at 84cc/hr, but his Na dropped and repeat urine Na was 92 mEq/L. He was started on 3% saline at 20cc/hr. Na again dropped to 116 mEq and 3% saline was increased to 50cc/hr. His Na improved to 121 mEq/L, however decreased once discontinued. Repeat urine Na was 146 mEq/L, urine osm 394 mosm/kg, and uric acid 1.5 mg/dL. He urinated 2-3L per day. Despite receiving 3% saline for 3 days, his Na did not improve and one dose of tolvaptan 15 mg was given. His Na improved to 129 mEq/L and his headaches improved. After 2 days, his Na dropped again to 122 meq/L and he was given a second dose of tolvaptan 15 mg with Na stabilizing to above 127 meq/L.
Discussion
This case highlights the difficulty in differentiating between SIADH and CSW as well as the benefits of vaptans in this setting. His uric acid and lack of overt hypotension may suggest SIADH, however his rising urinary excretion of sodium and large volume urine output suggests possible CSW. Hypertonic saline did not improve this patient’s sodium, however tolvaptan significantly improved his sodium after two doses. Differentiating SIADH vs CSW remains very difficult and more research is warranted. Furthermore, vaptans can be an effective tool and should be worthy of consideration in the setting of TBI and severe hyponatremia.