Frontiers in medicine · 2026
Cerebral salt wasting syndrome in an elderly patient with traumatic brain injury: a case report.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Li Pengpeng, Gao Yangyang, Li Junfeng, Lin Shaohua, Zhang Zehong, Luo Lei, Liu Wei
Аннотация
BACKGROUND: Cerebral Salt Wasting Syndrome (CSWS) represents a diagnostically challenging and potentially fatal complication of traumatic brain injury (TBI). It is defined by renal sodium excretion-induced hyponatremia accompanied by hypovolemia, yet its clinical signature-worsening consciousness-frequently mimics intracranial hypertension or Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH). Misdiagnosis, particularly the imposition of fluid restriction, may precipitate catastrophic deterioration.
CASE PRESENTATION: An 83-year-old male with pre-existing hypertension and atrial fibrillation presented with moderate-to-severe TBI (GCS 8) following a fall, with imaging revealing cerebral contusions, subarachnoid hemorrhage, and subdural hematoma. Initial conservative management yielded progressive neurologic recovery (GCS 13 by day 7). On day 8, however, he abruptly lapsed into coma. Urgent cranial CT demonstrated interval resolution of hemorrhagic lesions without new mass effect or hydrocephalus. Biochemical analysis uncovered severe hyponatremia (123.5 mmol/L). CSWS was diagnosed based on clinical trajectory, volume status assessment, laboratory parameters, and exclusion of SIADH. Prompt intervention with hypertonic saline and intravascular volume repletion produced rapid neurologic recovery.
CONCLUSION: This case illuminates CSWS as an insidious mimic of primary neurologic deterioration in TBI patients, particularly the elderly with cardiovascular comorbidities. Hyponatremia must be investigated as a reversible cause of unexplained coma in this population. Accurate differentiation from SIADH is critical to avert iatrogenic harm, and timely, monitored sodium correction can achieve dramatic reversal of life-threatening neurologic deficits.
CASE PRESENTATION: An 83-year-old male with pre-existing hypertension and atrial fibrillation presented with moderate-to-severe TBI (GCS 8) following a fall, with imaging revealing cerebral contusions, subarachnoid hemorrhage, and subdural hematoma. Initial conservative management yielded progressive neurologic recovery (GCS 13 by day 7). On day 8, however, he abruptly lapsed into coma. Urgent cranial CT demonstrated interval resolution of hemorrhagic lesions without new mass effect or hydrocephalus. Biochemical analysis uncovered severe hyponatremia (123.5 mmol/L). CSWS was diagnosed based on clinical trajectory, volume status assessment, laboratory parameters, and exclusion of SIADH. Prompt intervention with hypertonic saline and intravascular volume repletion produced rapid neurologic recovery.
CONCLUSION: This case illuminates CSWS as an insidious mimic of primary neurologic deterioration in TBI patients, particularly the elderly with cardiovascular comorbidities. Hyponatremia must be investigated as a reversible cause of unexplained coma in this population. Accurate differentiation from SIADH is critical to avert iatrogenic harm, and timely, monitored sodium correction can achieve dramatic reversal of life-threatening neurologic deficits.