Ann Thorac Surg 1996;62:1516-1517
© 1996 The Society of Thoracic Surgeons
Case Report
Acute Adrenal Insufficiency After Coronary Artery Bypass Grafting
Fraser W. H. Sutherland, FRCS,
Surendra K. Naik, FRCS
University Department of Cardiac Surgery, Glasgow Royal Infirmary University N.H.S. Trust, Glasgow, United Kingdom
Accepted for publication June 3, 1996.
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Abstract
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We report a case of acute adrenal insufficiency after elective coronary artery bypass grafting. This potentially fatal complication has been reported only once before in the cardiac surgical literature, more than 15 years ago. Unfortunately, adrenal insufficiency in this setting is easily confused with the clinical picture of septic shock or an acute abdominal pathology, and it is our belief that this condition could easily escape recognition and thus contribute to needless mortality.
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Introduction
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A 64-year-old man underwent elective coronary artery bypass grafting for chronic stable angina. Prior investigation had indicated triple-vessel disease with good left ventricular function. There was no past medical history of note. At operation, the left internal mammary artery was anastomosed to the left anterior descending artery and two aortocoronary saphenous vein grafts were anastomosed to the obtuse marginal and posterior descending vessels. The aorta was cross-clamped once for 30 minutes and the patient received one dose of 900 mL of St. Thomas' cardioplegia into the aortic root. Total cardiopulmonary bypass time was 63 minutes, during which the patient cooled to 28°C and rewarmed. The patient was heparinized with 400 mg/kg heparin, which was reversed with protamine at the end of the procedure.
The operation was straightforward without complication, and the patient was weaned easily from cardiopulmonary bypass in sinus rhythm, without support. He returned to the intensive care unit in a stable condition, the surgeon anticipating a full and rapid recovery. However, as the patient regained consciousness he became somewhat agitated and required sedation. During this period, the peripheral temperature rose to 39°C and the blood pressure became somewhat labile. At 12 hours postoperatively dopamine administration was commenced at a rate of 9 mg•kg-1•min-1. However, this condition failed to improve. Echocardiography indicated good left ventricular function and no evidence of valvular disease. A pulmonary artery floatation catheter was passed, which confirmed high cardiac output and low systemic vascular resistance. Accordingly, noradrenaline administration was commenced. The clinical picture was considered to be one of sepsis in view of the persistent pyrexia and the observed hemodynamics. However, repeated blood, urine, and sputum cultures over the ensuing 2
weeks failed to show any evidence of infection.
On the seventeenth postoperative day the question of adrenal insufficiency was raised and random cortisol assay confirmed an abnormally low cortisol level of 134 nmol/L (fluorescent polarization immunoassay; Abbott Laboratories Ltd, Maidenhead, Berks, UK). Hydrocortisone treatment was commenced at 100 mg every 8 hours, and he promptly improved to the extent that he could be weaned from all inotropes and vasopressor agents within 48 hours and extubated several days later. A stimulation test carried out 1 week later with tetracosactrin (Synacthen; CIBA Laboratories, Horsham, West Sussex, UK) showed an increase from a basal cortisol level of 128 nmol/L to 323 nmol/L at 30 minutes. He continued to receive maintenance steroids and was discharged from the hospital in good condition 7 weeks after the operation. Since discharge an attempt to wean him from steroids was met with the classic symptoms of anorexia, lethargy, and weight loss. Morning cortisol assay showed ongoing adrenal insufficiency, and his symptoms disappeared upon resumption of steroid replacement. It seems likely that he will require long-term maintenance therapy.
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Comment
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The effect of cardiopulmonary bypass on adrenocortical function has been widely studied. Serum cortisol, aldosterone, and adrenocorticotropic hormone levels diminish during hypothermic cardiopulmonary bypass and increase in the postoperative period, becoming maximal at 6 to 12 hours. No difference is seen in these hormone profiles between pulsatile and nonpulsatile cardiopulmonary bypass [1–4]. However, the practice of intraoperative administration of 1.0 to 1.5 g of methylprednisolone with the intention of diminishing reperfusion injury lowers serum cortisol and aldosterone levels in the early postoperative period [4].
In 1979, Alport and associates [5] reported 5 cases of acute adrenal insufficiency after cardiopulmonary bypass. No other cases have since been reported in relation to cardiac operations. Nevertheless, there have been scattered cases reported in the critical care literature of acute adrenal insufficiency complicating other nonadrenal illness. The classic association with meningococcal septicemia (Waterhouse-Friedrichsen syndrome) is well known. A proportion of patients with nonmeningococcal septic shock, however, have also been shown to exhibit a degree of adrenal insufficiency at presentation. These patients respond to exogenous steroids in the short term but have higher overall mortality than patients presenting with septic shock and normal adrenal function [6, 7]. Adrenal insufficiency has also been reported in patients admitted to critical care units with extensive burns [8]. The cause of adrenal insufficiency in these different situations is unclear. A proportion of cases are shown to have sustained adrenal hemorrhage or infarction on computed tomography or at autopsy. However, others, including the case described here, show no such evidence. These reports would suggest, somewhat reassuringly, that cardiopulmonary bypass per se is not the underlying cause.
Each of the reported cases exhibits a striking similarity in pattern of presentation, the same symptoms and signs emerging into a seemingly hopeless clinical situation. The diagnosis is eventually considered, whereupon steroids are administered and an astonishingly rapid recovery ensues. It is somewhat surprising that there have been no other cases of adrenal insufficiency described in relation to cardiac operations since 1979 [5]. This suggests that some cases may have gone unnoticed. As the condition is readily and rapidly reversible with administration of steroids yet fatal if untreated, we suggest that one must be suspicious of any patient whose postoperative course is unexpectedly poor, especially in the face of an uncomplicated surgical procedure. The clinical features of cortisol deficiency include hypotension, diminished response to vasopressors, and a myriad of poorly understood systemic effects such as fever, delirium, and ileus with abdominal distention or abdominal pain. Indeed, the clinical picture has often been confused with that of septic shock or an acute abdominal pathology. Deficiency of mineralocorticoid, on the other hand, produces the well-known biochemical profile on hyponatremia and hyperkalemia; however, these abnormalities are frequently absent in the critical care setting where fluids and electrolytes are being monitored and replaced daily. Diagnosis is confirmed by low serum cortisol level and subsequently diminished response to administration of exogenous adrenocorticotropic hormone. Treatment is begun with 100 mg of hydrocortisone every 8 hours and gradually weaned as the patient recovers to 25 mg daily, which can be administered enterally. If further mineralocorticoid is needed then fludrocortisone can be administered orally at doses of 0.05 to 0.2 mg daily [8]. Repeated stimulation tests in the convalescent period enable one to determine whether or not damage is permanent, in which case long-term replacement therapy is required.
We hope that this will raise awareness of adrenal insufficiency as a potentially fatal complication of cardiac operations but one that is eminently treatable. Diagnosis requires a high index of clinical suspicion in any patient whose hemodynamic parameters relentlessly deteriorate after a seemingly uncomplicated surgical procedure.
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Footnotes
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Address reprint requests to Mr Sutherland, Cardiothoracic Unit, King's College Hospital, Denmark Hill, London, SE5 9RS UK.
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References
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- Taylor KM, Jones JV, Walker MS, Rao S, Bain WH. The cortisol response during heart-lung bypass. Circulation 1976;54:20–5.[Abstract/Free Full Text]
- Kono K, Philbin DM, Coggins CH, et al. Adrenocortical levels during cardiopulmonary bypass with and without pulsatile flow. J Thorac Cardiovasc Surg 1983;85:129–33.[Abstract]
- Chambers DJ, Karimzandi N, Baimbridge MV, et al. Hormonal and electrolyte responses during and after open heart surgery. Thorac Cardiovasc Surg 1984;32:358–64.[Medline]
- Weiskopf M, Braunstein GD, Bateman TM, et al. Adrenal function following bypass surgery. Am Heart J 1985;110:71–6.[Medline]
- Alport CA, Clifton KM, Mihalevich J, et al. Acute adrenal insufficiency following cardiac surgical procedures. J Thorac Cardiovasc Surg 1979;78:489–93.[Medline]
- Soni A, Pepper GM, Wyrwinski PM, et al. Adrenal insufficiency occurring during septic shock: incidence, outcome and relationship to peripheral cytokine levels. Am J Med 1995;98:266–71.[Medline]
- Moran JL, Chapman MJ, O'Fathartaigh MS, et al. Hypocortisolaemia and adrenocortical responsiveness at onset of septic shock. Intensive Care Med 1994;20:489–95.[Medline]
- Sheridan RL, Ryan CM, Tompkins RG. Acute adrenal insufficiency in the burn intensive care unit. Burns 1993;19:63–6.[Medline]
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D. Fink, S. Silberman, O. Merin, D. Bitran, and F. W. H. Sutherland
Acute Adrenal Insufficiency After Coronary Artery Bypass Grafting
Ann. Thorac. Surg.,
August 1, 1997;
64(2):
589 - 590.
[Full Text]
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Abstract
Introduction
