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The role of glucocorticoid supplementation in children with secondary adrenal insufficiency undergoing anaesthesia for imaging examinations

We read with great interest the guidelines by Woodcock et al. [1]. The authors have performed a remarkable job summarising existing literature and providing treatment recommendations for a prevalent and potentially dangerous condition. Evidence-based recommendations for the perioperative management of children with adrenal insufficiency are lacking. The authors note that the recommendations provided in the guidelines are based on hospital protocols rather than published data. These recommendations are reasonable, and reflect sound clinical judgement and practice; however, some are contradictory to published findings from our centre [2]. Through the retrospective review of anaesthesia records of 32 patients with secondary adrenal insufficiency (undergoing a total of 216 anaesthetics) for imaging examinations, we found that there was no difference in the incidence of hypotension, bradycardia, hypoglycaemia or suspected adrenal crisis episodes when patients were given stress dose glucocorticoid compared with when stress dose glucocorticoid was withheld. Studies examining the role of cortisol and the stress response in paediatric patients undergoing general anaesthesia have been limited to healthy children [3–5] and have contributed to the belief that stress dose glucocorticoids are necessary for general anaesthesia alone. A common response to concerns raised by these data is presented byWoodcock et al., “If in doubt about the need for glucocorticoids, they should be given as there are no long-term adverse consequences of short-term glucocorticoid administration” [1]. Whereas this approach may be true of limited stress dose glucocorticoid exposure, this concept discounts the fact that a subset of patients with secondary adrenal insufficiency require frequent anaesthetics. For instance, children undergoing cranial irradiation may require daily sedation before each radiotherapy session over several weeks. Our study, utilising craniopharyngioma as a model for secondary adrenal insufficiency, suggests that a prudent strategy for the peri-operative management of secondary adrenal insufficiency for patients undergoing anaesthesia for non-invasive indications, is to continue basal hydrocortisone replacement therapy and to remain vigilant throughout the peri-operative period. Intravenous hydrocortisone should be immediately available, and the patient/family should be educated in the early signs and symptoms of adrenal crisis. Each patient included in our study received more than 40 general anaesthetics (for line placement/removal, radiation therapy, imaging examinations, etc.) during a 2-year period. We determined that a stress dose glucocorticoid given for each of these anaesthetics would have raised their glucocorticoid exposure over this period by more than 30%. This substantial dose elevation carries the potential for increasing the risk of glucocorticoid-related adverse effects, which negatively skews the risk/benefit balance, particularly if our study suggests that the benefit (prevention of adrenal crisis) has historically been overestimated. It is important that we emphasise that our data pertain to the management of children with known secondary adrenal insufficiency undergoing anaesthetics for non-invasive procedures and do not apply to children with primary adrenal insufficiency and/or those undergoing invasive procedures. As we congratulate the authors on a superb publication, which provides much needed guidance and insight on the peri-operative management of adrenal insufficiency, we challenge commonly held perceptions in the interest of academic advancement and improved patient care.