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General considerations
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Patients present with a shock out of proportion to the severity of the trigger, if a trigger is identified (see below) The shock is typically resistant to inotropes and fluid resuscitation if the adrenal crisis is not recognized and promptly treated with parenteral glucocorticoids Risk factors for adrenal crises include a history of previous adrenal crises, older age (>65 years), adolescence and transition from pediatric to adult care, and a higher comorbidity burden Glucocorticoid tapering down and discontinuation are crucial times, as glucocorticoid-induced adrenal insufficiency can become clinically apparent
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Diagnosis
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Hypotension or hypovolemic shock
plus at least one of the following:
Nausea or vomiting Severe fatigue Fever Impaired consciousness (incl. lethargy, confusion, somnolence, collapse, delirium, coma, and seizures)
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Possible laboratory abnormalities (not required for the diagnosis)
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Hyponatremia (typically with raised urinary sodium) Hyperkalemia Signs of volume depletion (eg, raised urea and creatinine) Hypoglycemia Lymphocytosis Eosinophilia
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Factors that can trigger an adrenal crisis or elicit symptoms of adrenal insufficiency
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Common to all patients with adrenal insufficiency:
Infections (including gastrointestinal, genitourinary, respiratory, and sepsis) Acute illness (including fever) Physical trauma Surgery or other procedures requiring general, regional, or local anesthesia Bowel procedures requiring laxatives/enema Labor and delivery Dental procedures Severe stress and pain (including severe anxiety and bereavement) Strenuous exercise
Specific to patients with glucocorticoid-induced adrenal insufficiency:
Abrupt glucocorticoid withdrawal in subjects on long-term treatment Glucocorticoid tapering below physiological replacement doses Switch between different types, formulations, and doses of inhaled glucocorticoids, which can lead to considerable variability of glucocorticoid systemic absorption Initiation of strong cytochrome P450 3A4 inducers, which leads to increased liver metabolism of several glucocorticoids. Strong inducers include apalutamide, carbamazepine, enzalutamide, fosphenytoin, lumacaftor, lumacaftor-ivacaftor, mitotane, phenobarbital, phenytoin, primidone, and rifampicin
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