Endocrine Abstracts

Background: Cerebral Salt Wasting Syndrome (CSWS) is a rare but serious cause of hyponatremia, characterized by hypovolemia and excessive urinary sodium loss, typically occurring in the context of acute neurological injury. Differentiating CSWS from other causes of hyponatremia, such as Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), is critical but often challenging.

Case Presentation: A 35-year-old male with chronic alcohol excess, previous seizures, and neuropsychiatric comorbidities presented following an alcohol-related fall. CT brain revealed large bilateral subdural hematomas requiring neurosurgical intervention. Postoperatively, he developed polyuria, hypovolemia, and severe hyponatremia (Na 114–123 mmol/l). Investigations showed markedly elevated urinary sodium (>200 mmol/l), fractional excretion of sodium >15%, preserved pituitary function, and no renal tubular injury.

Management and Outcome: The patient was managed with intravenous normal and hypertonic saline, fludrocortisone to reduce urinary sodium losses, and strict fluid-electrolyte monitoring. Sodium levels improved to 126–129 mmol/lwith resolution of polyuria and hypovolemia. Salt-sensitive hypertension developed transiently during hypertonic saline therapy and resolved upon cessation. He was discharged in stable condition after five weeks.

Discussion: This case underscores the diagnostic complexity of CSWS, particularly in patients with multifactorial neurological and systemic illness. Key differentiating features from SIADH included hypovolemia and persistently high urinary sodium excretion.

Conclusion: Prompt recognition and targeted management of CSWS are essential to prevent morbidity. Clinicians should maintain a high index of suspicion for CSWS in acute neurological patients with hyponatremia, as timely intervention can significantly improve outcomes.