PubMed · 7757670
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H Rakugi, T Ogihara. 1993. [Partial Addison's disease].. https://pubmed.ncbi.nlm.nih.gov/7757670/
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Most symptoms and signs of adrenocortical insufficiency are aspecific. For a definitive diagnosis a stimulation test is often needed. In case of secondary adrenocortical insufficiency glucocorticoid substitution nearly always suffices. Patients with primary adrenocortical insufficiency need substitution not only with glucocorticoids but also with mineralocorticoids. A standard daily dose of 30 mg hydrocortisone as glucocorticoid substitution is too high for many patients, while for some a standard daily dose of 0.1 mg fludrocortisone as mineralocorticoid substitution is too low. Patients with adrenocortical insufficiency need adequate instructions about what to do in case of stress, such as a (febrile) illness or trauma. Duration and severity of the suppression of the pituitary-adrenal axis by the use of pharmacological amounts of glucocorticoids are highly variable. When pharmacological amounts of glucocorticoids (> 7.5 mg prednisone daily) are used for 3 weeks or longer, a clinically relevant suppression of the pituitary-adrenal axis is possible, and this may persist for one year after discontinuing the use of glucocorticoids.
We describe the case of a 55 year old patient with acute adrenal insufficiency who suffered from abdominal pain, recurrent syncope and cardiac arrest. 32 hours after the successful cardio-pulmonal resuscitation, the patient developed a catecholamine resistant hyperdynamic shock. With the initiation of prednisolone therapy, because of suspected acute adrenal insufficiency, catecholamines became effective and led to a hemodynamic stabilisation and a general amelioration of the patient. Glucocorticoids have a permissive function for catecholamines and therefore are essential in these situations. After fluid replacement acute adrenal insufficiency may present as hyperdynamic shock which can be confounded with septic shock. Cardiac arrest however is an unusual complication of Addison's disease and the responsible pathological mechanism is unknown.