investigation
Last edited 06/2020
Investigations include:
- biochemistry
- damage to adrenal cortex results in mineralocorticoid deficiency causing low serum sodium, and raised serum potassium and H+ (1)
- serum urea and albumin are raised because of dehydration
- serum renin is raised due to sodium depletion.
- in secondary hypoadrenalism, electrolytes are usually normal as aldosterone-secreting cells are normal
- serum cortisol level (ideally between 8-9 am)
- random measurements have a low sensitivity for Addison's disease due to the pulsatile nature and diurnal variation of cortisol secretion (2)
- if level of serum cortisol is
- <100 nanomol/L - adrenal insufficiency is highly likely ( if the patient is not on oral or inhaled steroids)
- >400 nanomol/L - adrenal insufficiency is unlikely (diagnosis is not excluded if the patient is acutely unwell at the time since cortisol values may increase during illness)
- between 100 and 400 nanomol/L - refer to a specialist for further investigations e.g. - synacthen test (1)
- blood glucose may be low - insulin-induced hypoglycaemia
- possible ECG findings are detailed - click here
Secondary care investigations carried out to confirm the diagnosis and to find the cause nclude:
- plasma rennin (1)
- markedly elevated plasma ACTH - greater than 80 ng per litre - with low or normal serum cortisol on presentation or in the morning after omitting replacement therapy is an early indication of primary hypoadrenalism
- synacthen test:
- short test may confirm suspected hypoadrenalism
- depot test may discriminate primary and secondary causes
- adreno-cortical antibodies - often present in autoimmune adrenalitis - more common in women - 80% - than men - 10%
- abdominal film - calcified adrenals of tuberculosis
- chest radiology - tuberculous lesions, areas of malignancy and calcification
- clinical or serological evidence of other organ specific autoimmune disease
Reference: