Pediatric osmotic demyelination syndrome triggered by post-traumatic pituitary stalk injury: a case report

TL;DR

A 13-year-old Chinese girl with traumatic brain injury developed osmotic demyelination syndrome after severe hyponatremia and post-traumatic pituitary stalk injury, with MRI showing extrapontine lesions and no pontine involvement. She improved after sodium correction, desmopressin, B-complex vitamins, and hyperbaric oxygen therapy, with central diabetes insipidus remitting by 3 months.

Key findings

• The patient’s serum sodium was 113 mmol/L; during correction with intermittent 150 mL 3% hypertonic saline, levels were 117, 120, and 128 mmol/L in the first 24 h and subsequent measurements were 130, 135, and 144 mmol/L. Total NaCl supplementation was 17.2 g in the first 24 h and an additional 19.6 g over the next 24 h.
• Initial MRI showed T2/FLAIR-hyperintense and T1-hypointense lesions with focal restricted diffusion in the bilateral caudate nuclei, putamen, and insulae; repeat contrast-enhanced MRI showed progression plus an absent T1-weighted posterior pituitary bright spot and an ill-defined pituitary stalk, without pontine T2-hyperintense lesions or abnormal enhancement.
• After treatment with B-complex vitamins (vitamin B1 10 mg TID, vitamin B2 5 mg TID, vitamin B6 10 mg once daily, and vitamin B12 0.5 mg TID for 1 month), rehabilitation, and hyperbaric oxygen therapy, follow-up MRI on hospital day 18 showed partial resolution; at 3-month telephone follow-up, dysarthria and dysphagia had lessened, left-sided hypertonia had resolved, and central diabetes insipidus had completely remitted.
• The paper states no prior case reports have documented ODS secondary to hyponatremia caused by post-traumatic pituitary stalk injury; pediatric ODS is rare, with 106 pediatric cases noted in a cited review from 1960–2018.

Methods

• Single case report of a 13-year-old Chinese girl with traumatic brain injury transferred after seizures; the clinical course, laboratory tests, hormone measurements, CT, and serial brain MRI were described.
• Diagnostic evaluation included serum sodium and osmolality, hormone levels (T3, fT3, T4, fT4, TSH, cortisol, ACTH), contrast-enhanced pituitary MRI, and multidisciplinary exclusion of hypoglycemic encephalopathy and CO poisoning; ODS was diagnosed from clinical history, hyponatremia, and neuroimaging.
• No controlled comparison or formal statistical analysis was performed; management included hypertonic saline, desmopressin, neuroprotective agents, muscle relaxants, analgesics, B-complex vitamins, and hyperbaric oxygen therapy.

Limitations

• Stated: no standardized treatment protocol for ODS has been established, clinical outcomes remain inconsistent, and the mechanisms—especially those pertaining to B-complex vitamin supplementation—remain to be elucidated.
• Evident: this is a single pediatric case report with no control group; the causal link between pituitary stalk injury, hyponatremia correction, and ODS is inferred from the clinical timeline and imaging rather than experimentally established.
• Evident: follow-up was limited to a 3-month telephone assessment, and some laboratory data (e.g., urine sodium and osmolality on day 1) were not available.