Corticosteroid therapy and adverse effects — formative SAQs

SAQ 1 — Dose, weaning and adverse-effect monitoring in a child on long-term prednisolone (10 marks, 15 minutes)

Stem: A seven-year-old on daily prednisolone for frequently relapsing nephrotic syndrome has been on 2 mg/kg per day for three months. The team asks you to describe the corticosteroid pharmacology, the safe-weaning plan, and the adverse-effect monitoring you would put in place. [1]

Model answer

Pharmacology and equivalence (2 marks). Prednisolone is a synthetic glucocorticoid about four times as potent as hydrocortisone, with slight mineralocorticoid activity. The equivalent-dose anchor is hydrocortisone 20 mg equals prednisolone 5 mg equals methylprednisolone 4 mg equals dexamethasone 0.75 mg. Because the course is well beyond two to three weeks, the hypothalamic-pituitary-adrenal axis is suppressed, and the child cannot mount a cortisol response to stress until the axis recovers over weeks to months. [9]

Safe-weaning plan (4 marks). Do not stop abruptly. Reduce the prednisolone to a physiological equivalent — about hydrocortisone 8 to 10 mg per square metre per day — then step the dose down every one to two weeks while the child remains well, watching for fatigue, hypotension, and hypoglycaemia. Before declaring recovery and stopping, test the axis with an early-morning cortisol and, if indicated, a short Synacthen test. The family must keep the sick-day rules and emergency hydrocortisone through the recovery window, because full adrenal responsiveness lags behind the wean. [9]

Sick-day rules and MedicAlert (2 marks). During a febrile illness the family doubles the oral dose for two to three days; if the child vomits and cannot absorb orally, they switch to parenteral hydrocortisone. The child carries a steroid card and wears a MedicAlert identifier, and the school is notified of the emergency plan. [9]

Adverse-effect monitoring (2 marks). At every visit measure and plot height (growth suppression is the earliest reversible sign), check blood pressure, examine for bruising and striae, ask about mood and behaviour, and review bone health with a low threshold for vitamin D and bone density assessment in this heavily exposed child. Introduce steroid-sparing agents early to lower cumulative exposure. [1] [9]

SAQ 2 — Adrenal crisis in a steroid-dependent child (10 marks, 15 minutes)

Stem: A six-year-old on long-term prednisolone for juvenile idiopathic arthritis presents to the emergency department with vomiting, drowsiness, and a fever. She is hypotensive, and the bedside glucose is 2.1 mmol/L. Outline the diagnosis, the immediate resuscitation, and the subsequent management. [9] [12]

Model answer

Diagnosis (2 marks). This is adrenal crisis until proven otherwise. The child has long-term corticosteroid exposure (HPA suppression), an intercurrent febrile illness (the precipitant), and the classic presentation — collapse, hypotension, and hypoglycaemia. Hypoglycaemia is particularly prominent in younger children because glycogen reserves are small. Sepsis is both a precipitant and a differential and must be assumed and treated in parallel. [9] [12]

Immediate resuscitation (4 marks). Give intravenous or intramuscular hydrocortisone immediately at the age-banded stress dose — 50 mg for this six-year-old — followed by a continuous infusion (around 2 to 3 mg/kg per 24 hours) or repeated intravenous doses every six hours. Hydrocortisone, not dexamethasone, is the crisis drug because at stress doses it carries the mineralocorticoid activity the child also needs. In parallel, give a 10 to 20 mL/kg isotonic saline bolus for shock, correct the hypoglycaemia with intravenous dextrose, take cultures and start broad-spectrum antibiotics, and draw a cortisol and ACTH sample for later interpretation without delaying the steroid. [9]

Why hydrocortisone and not dexamethasone (2 marks). Dexamethasone has negligible mineralocorticoid activity, so a child given dexamethasone alone may continue to salt-waste. Hydrocortisone at stress doses covers both the glucocorticoid and the mineralocorticoid deficit. The mineralocorticoid activity is independent of the glucocorticoid potency, which is the trap examiners test. [9]

Subsequent management and disposition (2 marks). Identify and treat the precipitant. Reassess blood pressure, capillary refill, and glucose within the first hour; escalate to PICU if there is no improvement. Once stable, step down to a ward, educate the family on hydrocortisone injection and sick-day rules, arrange endocrinology review, and discharge with a written emergency plan and MedicAlert identifier, because recurrence risk is high without a robust plan. [9] [12]