Zycortal Symposium Proceedings

Management of an acute Addisonian crisis

Eilidh Gunn BVMS DVMS DipECVIM-CA MRCVS

Hypoadrenocorticism is characterised by a deficiency of glucocorticoid +/- mineralocorticoid production and is usually caused by primary adrenal gland dysfunction. Although a potentially life threatening endocrine emergency, if diagnosed promptly and treated appropriately the majority of acute Addisonian crises represent rewarding cases to treat. An index of suspicion for an Addisonian crisis is usually prompted by a combination of historical signs, physical exam findings and clinicopathological abnormalities. These clinical signs can vary widely on a case to case basis but often reflect the deficiencies of each hormone: glucocorticoid deficiency is typically associated with signs referable to the gastrointestinal tract (e.g. anorexia, vomiting, diarrhoea, melena) and clinicopathological changes such as lymphocytosis, hypocholesterolaemia and hypoglycaemia. Mineralocorticoid deficiency can cause hyponatraemia and hyperkalaemia, which in turn can precipitate hypovolaemia, bradycardia and collapse.

In general the following features may prioritise an Addisonian crisis amongst other differentials for collapse:

• Bradycardia or ‘normal’ heart rate despite findings of clinical dehydration.

• More severe dehydration than would be expected from the fluid losses (usually gastrointestinal) reported.

• Poor body condition despite only a recent history of disease.

Confirming the Diagnosis

It is not appropriate for hypoadrenocorticism to be diagnosed on compatible clinical signs and electrolyte changes alone and confirmation of a diagnosis with an ACTH stimulation test is preferred prior to instigating treatment with corticosteroids. Unfortunately once steroid therapy has been initiated, it can be very difficult to obtain a diagnosis of hypoadrenocorticism due to cross reactivity of several steroid formulations with cortisol assays and the suppressive effect of many steroids on the hypothalamic-pituitary-adrenal axis. Steroid therapy is usually not required immediately for the emergency treatment of any collapsed patient, and therefore an ACTH stimulation test can always be performed before starting steroid therapy. Patients that genuinely have hypoadrenocorticism can be stabilised in the short term with fluid therapy and management of electrolyte levels. Steroid therapy should be withheld until pre- and post-ACTH serum blood samples have been obtained.

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