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Updated: Jan 24, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
[Sodium balance impairment in a child with severe traumatic brain injury]
Y S Aleksandrovich1, K V Pshenisnov1, A S Ustinova2
1Saint-Petersburg State Pediatric Medical University.
Insights
This case study details cerebral salt-wasting syndrome in a boy with traumatic brain injury. High-dose Fludrocortisone successfully managed persistent hyponatremia and polyuria, aiding recovery.
Area of Science:
- Neuroscience
- Endocrinology
- Neurosurgery
Background:
- Severe traumatic brain injury can lead to complex neuroendocrine complications.
- Cerebral salt-wasting syndrome is a rare but serious condition affecting sodium balance.
Observation:
- A 12-year-old boy with severe traumatic brain injury developed refractory intracranial hypertension and later presented with symptoms suggestive of central diabetes insipidus.
- Persistent hyponatremia emerged on day 17 post-injury, despite initial hypernatremia and hypovolemia.
- Treatment with Fludrocortisone was initiated and titrated to manage electrolyte and fluid imbalances.
Findings:
- High-dose Fludrocortisone (up to 600 µg/day) effectively normalized plasma sodium levels and reduced polyuria in a patient with cerebral salt-wasting syndrome.
- The patient's condition improved, allowing for gradual discontinuation of Fludrocortisone and transfer to rehabilitation.
Implications:
- This case highlights the potential efficacy of high-dose Fludrocortisone in managing refractory cerebral salt-wasting syndrome post-traumatic brain injury.
- Early recognition and aggressive management of neuroendocrine disturbances are crucial for improving outcomes in pediatric TBI patients.
Abstract:
We report a case of cerebral salt-wasting syndrome in a 12-year-old boy with severe traumatic brain injury. The child developed refractory intracranial hypertension at the time of injury, which required decompressive craniectomy on the 7th day after injury. Infusion of hypertonic sodium chloride solutions performed at the intensive care unit resulted in hypernatremia on the 5th day and polyuria and hypovolemia on the 11th day, which was regarded as manifestations of central diabetes insipidus. Persistent hyponatremia developed on the 17th day after injury; on the next day, the therapy was supplemented with Fludrocortisone at a dose of 100 µg/day, followed by an increase in the dose to 150 µg/day, which had no significant effect. Fludrocortisone was discontinued on the 30th day of therapy, but it was re-used at a dose of 400 µg/day from the 54th day. During this treatment, polyuria gradually decreased to 4 to 5 l/day, and the plasma sodium concentration remained within the reference values. The dose of Fludrocortisone was increased to 600 µg/day since the 66th day. The child was transferred to a specialized department on the 67th day after injury. At the Department of Neurosurgery, the dose of Cortineff was gradually reduced starting with the 94th day and completely discontinued on the 122nd day after injury. On day 132th of the post-traumatic period, the patient was transferred to another hospital for rehabilitation therapy.
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