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Table 9. Signs and Symptoms of Adrenal Crisis and
Potential Precipitating Factors
General
considerations
• 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.
Diagnosis Hypotension or hypovolemic shock, plus at least one of the following :
• Nausea or vomiting
• Severe fatigue
• Fever
• Impaired consciousness (incl. letharg y, confusion, somnolence,
collapse, delirium, coma, and seizures)
Possible
laboratory
abnormalities
(not required
for the
diagnosis)
• Hyponatremia (typically with raised urinary sodium)
• Hyperkalemia
• Signs of volume depletion (e.g., raised urea and creatinine)
• Hypoglycemia
• Lymphocytosis
• Eosinophilia
Factors that
can trigger
an adrenal
crisis or elicit
symptoms
of adrenal
insufficiency
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.
Tables
