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J Thorac Cardiovasc Surg 1994;107:621-0622
© 1994 Mosby, Inc.

Letters to the Editor

Routine dexamethasone therapy for cardiac operations?

Department of Cardiothoracic Surgery

P. D. MacNaughton, MRCP

Department of Intensive Care
Royal Brompton and National Heart and Lung Hospital
Sydney St.
London, SW3 6NP United Kingdom

To the Editor:

We read with interest the JOURNAL article by Jansen and colleagues. ¹ We agree that there are some interesting differences between the control and steroid-treated groups, both in level of inflammatory mediators and in cardiovascular response. However, we believe that there is a serious design error in this study, notably the use of an anesthetic protocol incorporating an infusion of etomidate, which is likely to produce adrenocortical suppression.

Etomidate has been shown to be a potent inhibitor of endogenous adrenal steroid synthesis, which has led to a decline in its use, particularly as a method for maintenance of anesthesia by prolonged infusion. Watt and Ledingham ² were the first to describe an increase in mortality rate associated with reduced plasma cortisol levels in patients receiving etomidate infusions. A number of studies have subsequently revealed that etomidate has a specific direct action on the adrenal cortex, inhibiting 11-ß hydroxylation. ³ The main effects are to decrease cortisol and aldosterone synthesis. These effects last for 6 to 8 hours after a single-induction dose and would be expected to last considerably longer after a prolonged infusion. A sigmoid relationship between cortisol suppression and etomidate concentration has been described, with a median effective dose of 20 ng/ml. ⁴ Because an infusion rate of 5µg/kg/per minute of etomidate results in a plasma level on the order of 200 ng/ml, ⁵ we suspect that even the lowest infusion rate used in this study (1.5 µg/kg/ per minute) caused significant suppression of endogenous steroid synthesis.

From the data presented in the article of Jansen and colleagues, ¹ one can infer that corticosteroid levels have an effect on cardiovascular function and circulating levels of inflammatory mediators. However, the observed differences between the two groups could be explained by an impaired adrenocortical response to surgery in the control group, with the supplemental steroid merely counteracting the effect of the etomidate. The conclusion in the article, "Prophylactic dexamethasone treatment . . . is recommended for routine use during [cardiopulmonary bypass] procedures," ¹ cannot be justified on the basis of this study. A more appropriate conclusion might be that patients anesthetised with infusions of etomidate require exogenous steroid supplements.

References

1. Jansen NJG, van Oeveren W, Broek L, et al. Inhibition by dexamethasone of the reperfusion phenomena in cardiopulmonary bypass. J THORAC CARDIOVASC SURG 1991;102:515-25.[Abstract]
   
2. Watt I, Ledingham IMA. Mortality amongst multiple trauma patients admitted to an intensive therapy unit. Anaesthesia 1984;39:973-81.[Medline]
   
3. Wagner RL, White PF, Kan PB, Rosenthal MH, Feldman D. Inhibition of adrenal steroid genesis by the anaesthetic etomidate. N Engl J Med 1984;310:1415-21.[Abstract]
   
4. Crozier TA, Beck D, Wattke W, Kettler D. In vivo suppression of steroid synthesis by etomidate is concentration dependant. Anaesthetist 1988;37:337-9.[Medline]
   
5. Birks RJS, Edbrooke DL, Mundy JVB. Etomidate as a sedative agent in patients undergoing hip surgery under epidural anaesthesia. Br J Anaesth 1983;55:289-96.[Abstract/Free Full Text]
   

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Moat, N. E. Articles by MacNaughton, P. D. Search for Related Content PubMed PubMed Citation Articles by Moat, N. E. Articles by MacNaughton, P. D.