Primary hypopituitarism and peri‐operative steroid supplementation

Abstract

An elderly male was admitted for surgical repair of a fractured neck of femur. He was ASA grade 3, with a past medical history including angina, two previous myocardial infarctions and recent pneumonia. Recurrent transient ischaemic episodes had rendered him dysphasic and incapable of giving consent for surgery. He had primary hypopituitarism resulting from inoperable pituitary cysts, and was taking hydrocortisone 10 mg twice-daily (administered consistently throughout his hospital admission), but not fludrocortisone. Fifty-six hours after admission, he underwent an uneventful hip hemiarthroplasty under spinal anaesthesia, and returned to a general orthopaedic ward. Overnight, nursing observations were irregular, and the patient was found at 06.00 the next morning to be unresponsive, hypoglycaemic (blood glucose 2.2 mmol.l−1, treated with intravenous dextrose) and dehydrated (treated with intravenous crystalloids). Addisonian crisis was diagnosed by a medical specialist registrar 11 h later, whereupon steroids and fluid supplementation were administered. Despite treatment, the patient deteriorated, was managed according to a terminal care pathway and died 5 days later of multiple organ failure. The coroner recorded a verdict of accidental death secondary to his original fall. Hospital critical incident root cause analysis focused on the patient’s lack of peri-operative steroid supplementation, and the need to develop future Trust–wide guidelines. It has long been established that patients receiving steroid therapy require additional steroid administration during periods of pathophysiological stress [1]. Nicholson’s [2] excellent review of peri-operative steroid supplementation remains the most comprehensive guidance for anaesthetists, but fails to distinguish clearly between the peri-operative management of hypopituitarism secondary to exogenous steroid suppression of the hypothalamic-pituitary axis, and primary hypopituitarism, for example, caused by tumour/cysts (as in this patient’s case), surgery, radiotherapy, granulomatous disease or Sheehan’s syndrome [3]. Having read Nicholson’s review and The British National Formulary guidance, the anaesthetist in this case surmised that, because the patient’s daily dose of hydrocortisone was only 20 mg (equivalent to 5 mg prednisolone), further peri-operative supplementation was not required, as the patient would ‘have a normal response to hypothalamic-pituitary axis testing’. At later review, the Trust’s endocrinologists asserted that exogenous steroids were not suppressing the patient’s hypothalamic-pituitary axis, because the patient in fact had no pituitary function to suppress. As such, primary hypopituitarism is a condition that always requires peri-operative steroid supplementation, regardless of the normal daily dose taken. This is reflected in our new Trust guidelines with regards patients with hypothalamic-pituitary axis dysfunction – (i) minor procedures: double ‘daily’ dose of hydrocortisone on day of procedure; (ii) moderate procedures: usual dose pre-operatively, an extra 50 mg hydrocortisone intravenously at induction of anaesthesia, 200 mg intravenously over 24 h, tapering by 50% daily as patient recovers; and (iii) major surgery: usual dose pre-operatively, an extra 50 mg hydrocortisone intravenously at induction of anaesthesia, 200 mg/24 h intravenous for 48–72 h, tapering by 50% daily as patient recovers. In addition, a multidisciplinary medical management strategy is advocated, with specific peri-operative input from endocrinologists.