Addison's disease: too little cortisol and aldosterone
Primary adrenal insufficiency destroys the adrenal cortex, most often through autoimmune disease, so both cortisol and aldosterone fall. Without aldosterone the kidney wastes sodium and water and retains potassium, producing hyponatraemia, hyperkalaemia, hypovolaemia and orthostatic hypotension. Without cortisol the client loses glucose regulation and stress tolerance, giving hypoglycaemia, fatigue, anorexia, weight loss, nausea, vomiting and muscle weakness.
The classic clue is hyperpigmentation — a bronze or tanned appearance over sun-exposed areas, knuckles, elbows, scars and buccal mucosa. It occurs because low cortisol releases the pituitary from feedback inhibition, raising ACTH and the melanocyte-stimulating fragment along with it. Because secondary insufficiency from pituitary disease leaves aldosterone intact, those clients have neither hyperpigmentation nor severe hyperkalaemia.
Management is lifelong replacement with hydrocortisone, often with fludrocortisone for mineralocorticoid effect. Nursing care includes daily weights, orthostatic blood pressures, monitoring for hyperkalaemic dysrhythmias, adequate sodium intake especially in hot weather or with vomiting, and teaching the client to carry emergency injectable hydrocortisone and wear medical identification.
Cushing's syndrome: too much cortisol
Cushing's syndrome results from prolonged glucocorticoid excess, most commonly exogenous steroid therapy, and less often from a pituitary adenoma, adrenal tumour or ectopic ACTH production. Excess cortisol produces truncal obesity with thin extremities, a rounded moon face, a supraclavicular and dorsocervical fat pad, purple striae over the abdomen, thin fragile skin that bruises easily, poor wound healing, hirsutism, mood lability and proximal muscle wasting.
The metabolic picture mirrors Addison's: sodium and water retention give hypertension and oedema, potassium is lost giving hypokalaemia, glucose rises giving hyperglycaemia and sometimes frank diabetes, and bone density falls giving osteoporosis and pathological fracture risk. Immune suppression masks infection, so a low-grade temperature or subtle change in condition is significant.
Nursing priorities are infection prevention, skin and fall protection, glucose monitoring, a diet high in protein, calcium and vitamin D but low in sodium and simple carbohydrate, and emotional support for body image change. Surgical management may involve hypophysectomy or adrenalectomy, after which the client needs cortisol replacement and close monitoring for adrenal insufficiency.
| Parameter | Addison's disease | Cushing's syndrome |
|---|---|---|
| Cortisol | Deficient | Excess |
| Sodium | Low | High |
| Potassium | High | Low |
| Glucose | Low | High |
| Blood pressure | Hypotension | Hypertension |
| Weight | Loss | Central gain |
| Skin | Bronze pigmentation | Thin, striae, bruising |
| Priority risk | Adrenal crisis and shock | Infection and fracture |
Adrenal crisis is the emergency to recognize
Acute adrenal insufficiency, or Addisonian crisis, is precipitated by infection, trauma, surgery, dehydration or abrupt withdrawal of steroid therapy. The presentation is profound weakness, severe hypotension progressing to shock, tachycardia, abdominal and flank pain, vomiting, fever, confusion and hyperkalaemia with dysrhythmias.
Treatment is immediate: intravenous hydrocortisone, aggressive isotonic fluid resuscitation with normal saline often containing dextrose to correct hypoglycaemia, and treatment of hyperkalaemia. Continuous cardiac monitoring is required, and the precipitating cause is identified and treated. The nurse minimizes physiological and psychological stress, clusters care, keeps the room quiet and does not allow the client to sit up abruptly.
The prevention question appears just as often as the treatment question. A client on long-term corticosteroids who stops the drug because they feel better, runs out of tablets on holiday, or is nil by mouth before surgery without a plan is being set up for crisis. The correct teaching is that the dose is tapered under supervision and increased during illness, injury or surgery.
- •Never discontinue corticosteroids abruptly
- •Increase the dose for fever, infection, surgery or major stress
- •Take oral steroids with food, and larger doses in the morning
- •Carry medical identification and emergency injectable hydrocortisone
- •Report weight change over 2 kg in a week, oedema, or persistent vomiting
- •Monitor glucose, blood pressure and potassium at follow-up visits
Phaeochromocytoma and other adrenal medulla content
Phaeochromocytoma is a catecholamine-secreting tumour of the adrenal medulla producing paroxysms of severe hypertension, pounding headache, palpitations and profuse diaphoresis — the classic triad. Diagnosis uses plasma free metanephrines or a twenty-four-hour urine collection for metanephrines and vanillylmandelic acid, and the nurse teaches which foods and drugs to avoid before collection and how to keep the specimen on ice.
The critical nursing rule is not to palpate the abdomen, because pressure on the tumour can release a surge of catecholamines and trigger a hypertensive crisis. Blood pressure is monitored closely, the environment is kept calm, and stimulants including caffeine are avoided. Alpha-adrenergic blockade is started before beta blockade preoperatively; giving a beta blocker first leaves unopposed alpha stimulation and worsens hypertension.
After adrenalectomy the client is monitored for haemorrhage, hypotension as catecholamine levels fall, and adrenal insufficiency when the procedure is bilateral. Steroid replacement, vital sign trends and fluid balance dominate the postoperative plan, and the same crisis prevention teaching applies.