Cerebral Salt-Wasting Syndrome Masquerading as Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) in a Patient with Subdural Hemorrhage

Introduction: Cerebral salt wasting syndrome (CSWS) is characterized by hyponatremia, high urine sodium, and hypovolemia. It is important to distinguish CSWS from SIADH, as these are treated differently. Case Description: Our patient is an 82-year-old male who presented for rehabilitation after a hospital admission for acute subdural hemorrhage, frontal lobe contusions, and skull fracture with acute onset of dizziness and confusion. He was found to have hyponatremia with sodium in the range of 106 and was treated with hypertonic saline and urea tablets, which improved sodium to 130 over 6 days. He had a history of diabetes mellitus, hypertension, and benign prostatic hyperplasia. His home medications included insulin, losartan, mirtazapine, and doxazosin. On current admission, his serum sodium was 113 with worsening confusion and altered mental state, and he had dry mucus membranes. He denied excessive water intake. He did not have hematuria, or desire for excessive water intake, or thirst. He was transferred to the ICU for further care. Overnight, 3% hypertonic saline was given. The following day, his serum sodium was 117, and 4 hours later, serum sodium was 115. His urine output was 150 milliliters/hour, suggesting high free water clearance. Serum sodium 112, urine sodium 164, urine potassium 19, and polyuria, likely suggestive of CSWS. The patient was given hypertonic saline at 60 ml/hour. He had a urine output of 2.9 liters in 24 hours. Serum sodium was 125 on the morning of the 3rd day, after which 3% saline was stopped. Within 4 hours of stopping, sodium dropped to 121. To prevent worsening hyponatremia with ongoing natriuresis, he was started on sodium tablets, urea tablets, and fludrocortisone. His serum sodium on discharge was 132, improved over 7 days, and close nephrology follow-up was advised. Discussion: CSWS is characterized by hypovolemic hyponatremia with elevated urine sodium and urine osmolality, while SIADH is associated with euvolemic to hypervolemic states. CSWS is treated with fluid repletion, and SIADH usually with fluid restriction. The common etiologies of CSWS include central nervous system pathologies, the most common being aneurysmal subarachnoid hemorrhage. This case underscores the importance of monitoring volume status and electrolytes in neurologically injured patients with hyponatremia.