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Abstract: PUB164

A Suspected Case of Cerebral Salt Wasting (CSW) Syndrome in a Patient with Traumatic Subdural Hematoma: Revisiting a Long Debated Topic

Session Information

Category: Trainee Case Report

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Attia, Karim T., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Greco, Jessica M., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
Introduction

It has long been debated whether CSW is a true entity causing hyponatremia in patients with central nervous system (CNS) pathology or whether the hyponatremia is actually secondary to SIADH while apparent salt wasting is due to underappreciated volume expansion. Literature agrees, for the most part, that CSW is a separate disease process and it has been mostly described in patients with aneurysmal subarachnoid hemorrhage. It has also been described in other forms of CNS pathology including traumatic brain injury, meningitis, and intracranial neoplasms. We present a unique case of symptomatic, severe hyponatremia and apparent renal salt wasting in a patient with subdural hematoma secondary to a traumatic head injury. It was transient and was successfully treated with hypertonic saline, mineralocorticoids, and salt tablets.

Case Description

A 30-year-old male with no significant past medical history presented to the hospital initially on 4/27/21 after a motorcycle accident that resulted in a subdural hematoma, minor cervical fractures, intraspinous ligaments strain, and lacerations. He was discharged on narcotic pain medications, gabapentin, and keppra for seizure prophylaxis. Serum sodium was 135mEq/L at the time of discharge. He returned on 5/5/21 after several days of feeling uncoordinated and having orthostatic symptoms. He was found to have evidence of volume depletion of physical examination. Computed tomography (CT) of the brain showed resolution of prior subdural hematoma. Serum sodium on admission was 115mEq/L. It later dropped to 112mEq/L post hydration with IV fluids composed of normal saline with 5% dextrose. Net sodium balance was calculated to be -60.4 mEq during that initial interval suggesting renal salt wasting. He eventually improved after several days of infusion with hypertonic saline, fludrocortisone, and salt tablets. His episode was transient as he maintained a normal serum sodium off hypertonic saline prior to discharge.

Discussion

We reexamined the proposed mechanisms behind CSW along with the different arguments for, and against it as a separate entity as they relate to this case. We also ecplored the key points of differentiation between CSW and SIADH while focusing on how they pertain to the management of these critically ill patients.