Cushing’s syndrome
Cushing’s syndrome is the clinical state resulting from chronic exposure to excess glucocorticoids (endogenous or exogenous). Severity ranges from subtle biochemical hypercortisolism to fulminant multisystem disease.
In emergency care the priorities are recognition, treatment of life‑threatening complications, identification of exogenous steroid exposure, and prompt referral for specialist endocrine assessment and definitive management.
Classification and pathophysiology
Cortisol excess may be endogenous (overproduction by the hypothalamic-pituitary-adrenal axis or adrenal glands) or exogenous (therapeutic/iatrogenic glucocorticoids). A practical classification is:
- ACTH‑dependent
- Pituitary corticotroph adenoma (Cushing’s disease) - the commonest endogenous cause.
- Ectopic ACTH secretion (for example, bronchial carcinoids, small‑cell lung cancer).
- Exogenous ACTH administration (rare).
- ACTH‑independent
- Adrenal cortisol‑secreting adenoma or carcinoma.
- Bilateral adrenal hyperplasia.
- Exogenous glucocorticoid administration - the commonest overall cause of a cushingoid phenotype.
Chronic glucocorticoid excess causes protein catabolism (muscle wasting, thin skin, poor wound healing), central adiposity, insulin resistance and hyperglycaemia, hypertension, osteoporosis, immune suppression, psychiatric disturbance and a prothrombotic state.
When to suspect Cushing’s syndrome (red flags)
Typical features usually develop over months but may be rapid with ectopic ACTH or exogenous steroids. Consider Cushing’s syndrome when you see any of the following: