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Endocrine Abstracts (2023) 90 P8 | DOI: 10.1530/endoabs.90.P8

ECE2023 Poster Presentations Adrenal and Cardiovascular Endocrinology (72 abstracts)

SARS-CoV-2 provoked acute adrenal crisis with severe hypovolaemic hyponatraemia

Naychi Kyaw Kyaw 1 , Kieran Mullins 1 , Aneliya Sirkova 2 & Gideon Mlawa 3


1Queen’s Hospital (Barking, Havering and Redbridge Universities NHS Foundation Trust), Respiratory Department, Romford, London, United Kingdom; 2Queen’s Hospital (Barking, Havering and Redbridge Universities NHS Foundation Trust), Specialty Doctor, Diabetes and Endocrinology, Romford, London, United Kingdom; 3Queen’s Hospital (Barking, Havering and Redbridge Universities NHS Foundation Trust), Diabetes and Endocrinology Department, Romford, London, United Kingdom


Hyponatraemia is the commonest electrolyte disturbance among inpatients. Prompt diagnosis and management of the underlying cause is important. A 49-year-old Caucasian male presented to the emergency department with a two-day history of fever, altered mental status, vomiting, diarrhoea and postural dizziness. A rapid point of care RT-PCR test resulted positive for the SARS-CoV-2. A provisional diagnosis was presented of COVID-19 encephalopathy. The patient was usually fit and well, worked as a heating engineer and had no known immunodeficiency. Medical history was notable for atypical polymyalgia rheumatica treated with oral glucocorticoids more than two years prior. Admission laboratory studies were significant for a serum sodium level of 130mmol/l. Despite supportive treatment and with normal saline his clinical condition deteriorated over the first seventy-two hours of admission culminating in orthostatic syncope during clinical examination on day three. Repeat laboratory testing revealed serum sodium had fallen to 118 mmol/l. Urine sodium and osmolality were high. Random cortisol was reported as 6 nmol/l. Following intravenous resuscitation with high dose glucocorticoids and hypertonic saline his condition improved with slow normalisation of serum sodium, restoration of extracellular fluid volume and abatement of orthostatic symptoms. A tetracosactide stimulation test was performed with t=0 min cortisol level of 9nmol/l and t=30 min 39 nmol with a pre-test serum ACTH level of 4ng/L. A t=60 min cortisol was not performed. The remainder of the pituitary profile including serum thyroid stimulating hormone was unremarkable. Magnetic resonance (MR) imaging of the Sella revealed no evidence of pituitary adenoma and subsequent MR adrenals showed bilateral adrenal atrophy. Lumbar puncture revealed quiet cerebrospinal fluid. Adrenal antibodies were not available at the time of writing. The patient was discharged on oral hydrocortisone and remains well at three months follow up. The presumptive diagnosis in this case is acute SARS-CoV-2 infection precipitating acute adrenal crisis in a predisposed individual. The unexpectedly low plasma ACTH was surmised to be due to acute illness. The patient awaits formal endocrinological evaluation. This case highlights the importance of prompt diagnosis and expedient management of hyponatraemia and particularly in high stakes cases where the underlying mechanism is adrenal failure. Although an uncommon cause of hyponatraemia it is critical to exclude adrenal insufficiency when approaching such patients. Timely recognition of adrenal crisis is associated with reduced complications and mortality associated with this disease.

Volume 90

25th European Congress of Endocrinology

Istanbul, Turkey
13 May 2023 - 16 May 2023

European Society of Endocrinology 

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