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Published on: April 25, 2016
Fatal and near-fatal encephalopathy with hyponatraemia in two siblings with fluticasone-induced adrenal suppression
M D C Donaldson1, C Morrison, C Lees
1Division of Developmental Medicine, University of Glasgow, UK. mdcd1t@clinmed.gla.ac.uk
Insights
High-dose inhaled fluticasone propionate (FP) can cause acute adrenal insufficiency, leading to hyponatremia and cerebral edema. This rare but serious side effect requires careful monitoring in children.
Area of Science:
- Pediatric Endocrinology
- Pharmacology
- Neurology
Background:
- Inhaled corticosteroids are widely used for pediatric respiratory conditions.
- Prolonged high-dose use of inhaled fluticasone propionate (FP) may lead to systemic absorption and adverse effects.
- Acute adrenal insufficiency is a rare but potentially life-threatening condition.
Observation:
- Two siblings presented with acute symptoms including vomiting, headache, visual impairment, seizures, and hyponatremia.
- One sibling died, with post-mortem findings of adrenal hypoplasia and cerebral edema.
- The surviving sibling also showed hyponatremia and cerebral edema, responding to intensive care.
Findings:
- Retrospective diagnosis of adrenal insufficiency in both siblings.
- Causal link between prolonged high-dose inhaled FP (up to 2000 mcg/day) and acute adrenal insufficiency.
- Hyponatremia and cerebral edema attributed to cortisol deficiency and impaired water excretion.
Implications:
- Highlights previously unreported acute effects of high-dose inhaled FP.
- Emphasizes the need for vigilance and careful cerebral monitoring in pediatric patients with acute adrenal insufficiency.
- Underscores the importance of considering endocrine side effects with long-term high-dose inhaled corticosteroid therapy.
Aim:
To document previously unreported acute effects of adrenal insufficiency.
Methods:
We describe two siblings who presented acutely with hyponatraemia and cerebral oedema following prolonged treatment with high dose inhaled fluticasone.
Results:
A girl aged 5.5 years presented with vomiting, headache, visual impairment and seizures. She was hyponatraemic but not hypoglycaemic. Her conscious level continued to deteriorate and she died, post mortem examination showing small adrenal glands and cerebral oedema. Four weeks later her 7-year-old brother presented with similar symptoms. Assessment showed hyponatraemia with cerebral oedema. His illness responded to intensive care. A diagnosis of adrenal insufficiency was made retrospectively in both cases. The siblings had been receiving Fluticasone propionate (FP) in doses of up to 2000 microg/day for several years.
Conclusion:
We believe that the hyponatraemia and cerebral oedema was related to cortisol deficiency, leading to impaired excretion of water. We emphasize the need for careful cerebral monitoring in acute adrenal insufficiency presenting with impaired consciousness.
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