Peri‐operative steroid supplementation

‘The need for patients on long-term steroid treatment to increase their dose of glucocorticoids when under stress is a principle that rests in one of the most tranquil corners of medical dogma’ [1]. Two case reports published in the early 1950s described cardiovascular collapse and death in young patients undergoing routine orthopaedic surgery. A 34-year-old man died after the withdrawal of steroids (25 mg cortisone bd) 48 h pre-operatively. Although the case was complicated by possible transfusion reactions and pre-existing cardiomegaly, the cause of death was ascribed to acute adrenal insufficiency precipitated by withdrawal of steroid therapy [2]. The second patient was a 20-year-old woman who had taken 62.5–100 mg cortisone daily for 4 months; she became hyperpyrexic and died less than 6 h after surgery [3]. Autopsy findings revealed gross bilateral adrenal haemorrhage and histological changes of complete, adrenal cortical atrophy. These reports are considered the initial clinical recognition of iatrogenic adrenal insufficiency resulting from exogenous glucocorticoid administration. Subsequently, it has been assumed that the administration of steroids to patients frequently results in suppression and atrophy of the hypothalamic–pituitary–adrenal (HPA) axis through feedback inhibition of both hypothalamic and pituitary function. Adrenocorticotrophic hormone (ACTH) is necessary for normal adrenal gland growth and function and, in its absence, the adrenal glands become atrophic and unable to respond during periods of stress by secreting glucocorticoids. Further studies supported the contention that patients with suppression of the HPA axis required significant glucocorticoid supplementation during physiological stress. However, many of the case reports lacked conclusive biochemical evidence of adrenal insufficiency and Cope pointed out that ‘the vast majority of such incidents seem to be associated with medical diagnostic and not adrenal failure’ [4]. Nevertheless, the case report in 1953 concluded with a list of recommendations for peri-operative glucocorticoid treatment, which have become standard practice [3]. These recommendations amount to approximately a four-fold increase in the dose of glucocorticoid and there now appears to be an ingrained consensus that patients, currently or recently taking exogenous steroids, require additional large doses of steroids when subjected to surgery. Excessive, or prolonged, glucocorticoid administration can result in adverse clinical sequelae, including immunosuppression, delayed wound healing, decreased glucose tolerance, fluid and electrolyte imbalance and psychological effects. In two influential studies in 1969, Plumpton, Besser and Cole attempted to clarify the issue of steroid cover in a prospective study of 100 patients undergoing surgery who had either never received steroids (40 patients), recently stopped taking steroids (40 patients) or who were currently still receiving steroids (20 patients) [5]. Of the 20 patients currently receiving long-term steroid therapy, 10 patients were receiving replacement therapy for Addison’s disease, hypopituitarism or following adrenalectomy and the remaining 10 patients were receiving immunosuppressive therapy for unspecified conditions [6]. The patients treated previously had received prednisolone, or equivalent, in doses ranging from 5 to 50 mg.day for between 6 days and 10 years; the interval since treatment varied from 3 days to 24 months. The patients currently receiving treatment had taken prednisolone, or equivalent, in doses ranging from 5 to 50 mg.day for between 8 days and 15 years [5]. The first two groups of patients did not receive any peri-operative steroids. Steroid-treated patients were assessed pre-operatively using an insulin tolerance test; Anaesthesia, 1998, 53, pages 1091–1104