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Glucocorticoids are known to have an anti-insulin action on glucose metabolism, leading to increased lactate production . Alternatively, glucocorticoid-induced apoptosis is a well-recognized phenomenon initiated by mitochondrial dysfunction . Increased lactate production follows loss of mitochondrial membrane potential during apoptosis. Both mechanisms may lead to clinically relevant hyperlactatemia following glucocorticoid administration during cardiac surgery requiring cardiopulmonary bypass.
All adult patients undergoing cardiac surgery and cardiopulmonary bypass from 5 October through 21 November 2005 in a large academic teaching hospital in Rotterdam, the Netherlands were included in this study. Dexamethasone (60 to 80 mg) was given perioperatively at the discretion of the anesthetist. Lactate levels were measured within 1 hour postoperatively. The association between dexamethasone treatment, serum lactate levels and possible confounders was evaluated using ANOVA and linear regression.
A total of 82 patients 18 years and older underwent cardiopulmonary bypass for cardiac surgery in the above-mentioned period. Three patients undergoing heart or lung transplantation, who thus received methylprednisolone, were excluded; a further two patients who received hydrocortisone for allergic reactions were also excluded. Data were incomplete for one patient, leaving a total of 76 patients for analysis. The mean lactate level was 1.2 mmol/l in the 47 patients who did not receive steroids and 2.6 mmol/l in the 29 patients who received dexamethasone (P < 0.0001, Figure Figure1).1). When adjusting for potential confounders such as age, glucose level, duration of cardiopulmonary bypass and preoperative NYHA heart failure classification, this difference remained significant (P < 0.0001).
Administration of dexamethasone during cardiac surgery requiring cardiopulmonary bypass is associated with a significant hyperlactatemia.