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Adrenal Disorders — Written Clinical Reasoning
DCE long-case preparation: structured written reasoning for adrenal disorders — Addison's disease presenting as adrenal crisis, the three-step Cushing diagnostic algorithm, primary aldosteronism workup, and phaeochromocytoma preoperative preparation — with problem-list synthesis, investigation interpretation, and integrated management planning.
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SAQ 1 — Adrenal Crisis: Emergency Management and Diagnostic Reasoning (20 marks, 30 minutes)
Prompt: This patient is in adrenal crisis. Outline your immediate emergency management (with drug doses and route), the diagnostic reasoning that confirms primary adrenal insufficiency, and the long-term management and patient education plan. Justify each decision with reference to the Endocrine Society guideline. [1]
Model Answer
Step 1 — Immediate emergency management (the first 30 minutes) (6 marks): [1]
This is a life-threatening adrenal crisis. I do NOT delay treatment for further tests — the mortality of untreated crisis is significant. My immediate actions: [1]
- Secure the airway and give high-flow oxygen (she is drowsy and hypoxic risk). Establish IV access (two large-bore cannulae).
- Take blood FIRST (within 1-2 minutes, before hydrocortisone if possible, but do NOT delay hydrocortisone beyond this): cortisol (already low at 45 — confirms), ACTH (already high at 520 — confirms primary), renin, aldosterone, electrolytes, glucose (already low at 2.1), FBC, blood cultures. The cortisol and ACTH results are already available and are diagnostic.
- IV hydrocortisone 100 mg stat, then 100 mg every 6-8 hours (or a continuous infusion of 200 mg over 24 hours). At these doses hydrocortisone provides sufficient mineralocorticoid activity — fludrocortisone is not needed acutely. The Bornstein 2016 Endocrine Society guideline (PMID 26760044) is explicit: treat first if the patient is sick.
- Aggressive IV fluid resuscitation: 1 litre of 0.9% saline stat, then 1 litre over 1 hour, then guided by clinical response. Add dextrose (e.g. 1 litre of 5% dextrose alternating with saline) — she is hypoglycaemic at 2.1 mmol/L, which is dangerous. Treat the hypoglycaemia directly: 50 mL of 50% dextrose IV (or 100 mL of 10% dextrose if central access is unavailable).
- Correct electrolytes: The hyperkalaemia (6.4) is from aldosterone deficiency and will resolve with hydrocortisone and fluids over the next few hours. I do NOT give insulin-dextrose or calcium resonium routinely unless there are ECG changes of severe hyperkalaemia (wide QRS) — those would be treated with the standard hyperkalaemia protocol. Check an ECG now.
- Identify and treat the precipitant: Blood and urine cultures, chest X-ray. Start broad-spectrum antibiotics (e.g. ceftriaxone 2g IV) once cultures are taken — she is febrile (38.5) and infection (likely gastroenteritis) is the commonest precipitant. [1]
Step 2 — Diagnostic reasoning — why this is primary adrenal insufficiency (3 marks): [1]
The diagnosis is confirmed by:
- Cortisol 45 nmol/L (markedly low — a stressed patient should have cortisol above 500 nmol/L; a value below 200 in an unwell patient is strongly suggestive of adrenal insufficiency).
- ACTH 520 pg/mL (markedly elevated, over 8 times the upper limit) — this is the key finding: the ACTH is HIGH, confirming the problem is at the ADRENAL level (primary). In secondary adrenal insufficiency (pituitary), ACTH would be low or inappropriately normal.
- Hyperpigmentation (palmar creases, buccal mucosa, scars) — pathognomonic: high ACTH/MSH cross-stimulates melanocytes. This is ABSENT in secondary adrenal insufficiency.
- Hyponatraemia (119) with hyperkalaemia (6.4) — the hallmark of aldosterone deficiency (primary). In secondary, the RAAS is intact, aldosterone is preserved, and potassium is NORMAL. This is the single best biochemical discriminator.
- Hypoglycaemia — cortisol is needed for gluconeogenesis; deficiency causes fasting hypoglycaemia.
- Autoimmune context (type 1 diabetes, autoimmune thyroid disease) — this is autoimmune polyglandular syndrome type 2 (Schmidt syndrome), the commonest cause of Addison's in developed countries. [1]
The short Synacthen test (250 mcg cosyntropin, cortisol at 0, 30, 60 min) would confirm a peak cortisol below 500 nmol/L, but in this acute setting it is unnecessary — the cortisol is already critically low with a high ACTH, and treatment should not wait. The Synacthen test can be done after recovery to document the baseline deficit formally. [1]
Step 3 — Finding the cause (2 marks): [1]
After stabilisation:
- 21-hydroxylase antibodies — to confirm autoimmune Addison's (positive in 80-90% of autoimmune cases). This is the expected cause given her autoimmune history.
- Adrenal CT — small/atrophic adrenals confirm autoimmune disease; enlarged adrenals suggest infiltrative/malignant causes; calcified adrenals suggest old TB.
- Screen for and manage associated autoimmune conditions (thyroid, B12/pernicious anaemia, premature ovarian failure) — she already has type 1 diabetes and thyroid disease. [1]
Step 4 — Long-term replacement therapy (4 marks): [1]
Once stable and able to take oral medications:
- Hydrocortisone 15-25 mg/day in divided doses — e.g. 10 mg on waking, 5 mg at midday, 5 mg at 4-5 pm. The largest dose is in the morning (mimicking the circadian peak); the smallest dose is latest (to avoid insomnia). Titrate to well-being, with a day curve (serial cortisol measurements through the day) if symptoms persist.
- Fludrocortisone 50-200 mcg/day (typically 100 mcg) — ESSENTIAL in primary adrenal insufficiency, because the adrenal cannot produce aldosterone. Monitor with blood pressure (including postural), serum sodium, and plasma renin (aim for high-normal renin).
- Continue treatment for any precipitating cause (e.g. infection).
- Address bone health (DEXA — she is at risk of osteoporosis from chronic illness, not from the hydrocortisone replacement at physiological doses, but she may have other risk factors). [1]
Step 5 — Patient education and prevention of future crises (3 marks): [1]
This is the most important long-term intervention. Hahner et al. (PMID 25419882) showed that adrenal crises still occur in 8.3 per 100 patient-years in EDUCATED patients, with a 6% mortality per crisis — so education must be comprehensive and reinforced:
- Sick-day rules: double oral hydrocortisone for minor illness (fever, infection); triple or give IM hydrocortisone 100 mg for severe illness, vomiting, or surgery. Provide WRITTEN instructions.
- Emergency hydrocortisone injection kit (100 mg vial, syringes, instructions) — teach the patient and at least one family member to give IM hydrocortisone. She carries this at all times.
- MedicAlert bracelet stating "Adrenal insufficiency — requires hydrocortisone."
- Steroid card with diagnosis, medications, and emergency instructions.
- Education on never omitting steroids, recognizing early crisis symptoms (nausea, vomiting, weakness, dizziness), and when to seek urgent medical attention. [1]
Step 6 — Communication and shared decision-making (2 marks):
- Explain the diagnosis in plain language: "Your adrenal glands, which sit above your kidneys, have been destroyed by your immune system. They cannot make the hormones you need to stay alive — cortisol and aldosterone. We will replace these hormones for life."
- Discuss the autoimmune context and screen family members if there is a family history of autoimmune endocrinopathy.
- Address the psychological impact of a lifelong diagnosis requiring daily medication and emergency preparedness. [1]
References6ShowHide
- [1]Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline J Clin Endocrinol Metab, 2016.PMID 26760044
- [2]Nieman LK, Biller BMK, Findling JW, et al. The diagnosis of Cushing's syndrome: an Endocrine Society Clinical Practice Guideline J Clin Endocrinol Metab, 2008.PMID 18334580
- [3]Esteves LF, Rey NA, Dos Santos HF, et al. Theoretical Proposal for the Whole Phosphate Diester Hydrolysis Mechanism Promoted by a Catalytic Promiscuous Dinuclear Copper(II) Complex Inorg Chem, 2016.PMID 26934384
- [4]Lenders JWM, Duh QY, Eisenhofer G, et al. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline J Clin Endocrinol Metab, 2014.PMID 24893135
- [5]Hahner S, Spinnler C, Fassnacht M, et al. High incidence of adrenal crisis in educated patients with chronic adrenal insufficiency: a prospective study J Clin Endocrinol Metab, 2015.PMID 25419882
- [6]Oldfield EH, Doppman JL, Nieman LK, et al. Petrosal sinus sampling with and without corticotropin-releasing hormone for the differential diagnosis of Cushing's syndrome N Engl J Med, 1991.PMID 1652686