ESPE Abstracts (2015) 84 P-2-167

Hyponatraemia Secondary to Exudative Eczema

Irene Pilar Fernandez Viseras & Michal Ajzensztejn


The Evelina London Children’s Hospital, London, UK


Background: Classically adrenal insufficiency presents with hyponatraemia and hyperkalaemia, however the differential may be of alternative origin. Atopic dermatitis is a common inflammatory skin disease of infancy and childhood. In severe cases, the exudation from wet lesions can produce serious complications such as infection+very rarely electrolytes abnormalities as seen in this case.

Case report: A 6-month-old female infant was referred for endocrine review due to hyponatremia (129 mmol/l) and hyperkalaemia (6.6 mmol/l) with a suspected diagnosis of adrenal insufficiency and possible congenial adrenal hyperplasia (CAH). She was not virilised and blood pressure was normal. She had a background of severe eczema. Initial bloods showed normal glycaemia, no acidosis. Cortisol 183 nmol/l, ACTH 10 ng/l, 17-OH-progesterone 14.5 nmol/l (<6) with a highly elevated aldosterone >2.700 pmol/l and renin levels >500.00 mU/l with normal sodium level urine <10 mmol/l. She also underwent a synacthen test (peak cortisol 1975 nmol/l) and urine steroid profile both of which excluded CAH. Her eczema was infective with widespread exudate and was treated with oral flucloxacillin, topical emollients and steroids. The hyponatraemia was treated with sodium supplementation. The hyponatraemia and abnormal biochemistry completely resolved with improvement of the eczema on repeat testing.

Conclusion: The cause of this patient’s hyponatraemia, hyperkalaemia, hyperaldosteronemia and hyperreninemia were secondary to oozing exudation due to severe atopic dermatitis associated with loss of fluid and electrolytes, which resolved on appropriate dermatological treatment. The raised aldosterone and renin levels associated with hyponatraemia, led to consideration of both CAH and pseudohypoaldosteronism type I (PHAI-I). CAH was excluded as described above and PHA-1 which results from renal tubular unresponsiveness or resistance to the action of aldosterone resulting in elevated Aldosterone and Renin levels and a similar biochemical picture with renal salt losing was excluded due to an appropriately undetectable urinary sodium level; thus type I (PHAI-I) was ruled out.

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