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Войти в исследования Neuro endocrinology letters · 2025
Cerebral Salt Wasting Syndrome in an Elderly Patient With Traumatic Brain Injury: Diagnostic Challenges. A case report.
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Gumuscubuk Yagmur Kinaci, Cakmak Nuray Yilmaz
Аннотация
OBJECTIVE: Cerebral salt-wasting syndrome (CSWS) is an underdiagnosed cause of hyponatremia following intracranial injuries. This case highlights the diagnostic challenges of CSWS in elderly patients, particularly when typical volume depletion signs are absent.
CASE: We report an 80-year-old male with multiple comorbidities who developed CSWS following motor vehicle accident-related subarachnoid hemorrhage. The patient was confused, with a Glasgow Coma Scale (GCS) score ranging from eight to ten. Serum sodium declined significantly from 145 to 117 mmol/L approximately 20 days. The patient remained euvolemic with normal urine output and did not respond to fluid restriction. Elevated 24-hour urine sodium (563 mEq), and brain natriuretic peptide (154 pg/mL) confirmed CSWS. The patient initially responded to treatment; however, on the seventh day after discharge, he presented to the emergency department with a seizure. The patient died with a serum sodium level of 109 mmol/L.
CONCLUSIONS: CSWS can present without volume depletion signs. Differentiation from SIADH is pivotal, as the therapeutic approaches vary considerably. In this group of patients with intracranial trauma, the prognosis may be worse due to the risk of recurrent severe hyponatremia. Despite treatment, fatal recurrence highlights the need for intensive outpatient follow-up and frequent sodium monitoring.
CASE: We report an 80-year-old male with multiple comorbidities who developed CSWS following motor vehicle accident-related subarachnoid hemorrhage. The patient was confused, with a Glasgow Coma Scale (GCS) score ranging from eight to ten. Serum sodium declined significantly from 145 to 117 mmol/L approximately 20 days. The patient remained euvolemic with normal urine output and did not respond to fluid restriction. Elevated 24-hour urine sodium (563 mEq), and brain natriuretic peptide (154 pg/mL) confirmed CSWS. The patient initially responded to treatment; however, on the seventh day after discharge, he presented to the emergency department with a seizure. The patient died with a serum sodium level of 109 mmol/L.
CONCLUSIONS: CSWS can present without volume depletion signs. Differentiation from SIADH is pivotal, as the therapeutic approaches vary considerably. In this group of patients with intracranial trauma, the prognosis may be worse due to the risk of recurrent severe hyponatremia. Despite treatment, fatal recurrence highlights the need for intensive outpatient follow-up and frequent sodium monitoring.