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Minerva Anestesiologica 2013 August;79(8):884-90


language: English

Ammonia plasma concentration and prolonged infusion of remifentanil in patients with acute kidney injury

Roquilly A. 1, Perbet S. 2, Simonneau F. 1, Cinotti R. 3, Sebille V. 4, Volteau C. 4, Gratas C. 5, Minet-Quinard R. 6, Loutrel O. 1, Rozec B. 4, Lejus C. 1, Constantin J. M. 2, Asehnoune K. 1

1 CHU Nantes, Pôle Anesthésie Réanimations, Service d’Anesthésie Réanimation Chirurgicale, Hôtel Dieu-HME, Nantes, France; 2 CHU Clermont Ferrand, Service de Réanimation Adultes, CHU Estaing, Clermont-Ferrand, France; 3 CHU Nantes, Pôle anesthésie réanimations, Service d’Anesthésie Réanimation chirurgicale, HGRL, Nantes, France; 4 Cellule de Biostatistique – Plateforme de Biométrie, CHU de Nantes, Nantes, France; 5 CHU Nantes, Service de Biochimie, Pôle de Biologie, Nantes, France; 6 CHU Clermont-Ferrand, Service de Biochimie, Pôle de biologie, Clermont-Ferrand, France


Background: Glycine is an excipient of remifentanil and may induce side effects. To investigate glycine and ammonia concentration with the use of remifentanil in Intensive Care Unit patients with acute kidney injury (AKI) defined by a decrease in creatinine clearance above 50%.
Methods: Prospective open-label cohort study in three surgical Intensive Care Units. Thirty-three patients with AKI and requiring sedation for at least 72 hours. Sedation with remifentanil and midazolam or propofol was adapted every six hours according to ATICE. Glycine and ammonia plasma concentrations were measured at H0 (start of infusion) and every 12 hours during a continuous intravenous 72 hours remifentanil infusion, and 24 hours after the end of the infusion. Clinical and biological glycine or ammonia toxicity were evaluated.
Results: Fifteen patients required continuous veno-venous hemodiafiltration (CVVHDF). Glycine and ammonia plasma concentrations exceeded the normal value respectively for 11 (33%) and 15 (45%) patients before remifentanil infusion (H0). Accumulation of glycine or ammonia was observed neither for patients with or without CVVHDF. For patients without CVVHDF, the plasma ammonia concentration at the end of remifentanil infusion was significantly correlated with the creatinine clearance at H72 (P=0.03) and with the mean rate of remifentanil infusion (P=0.002). No side effect was reported.
Conclusion: Remifentanil was not associated with an accumulation of glycine or ammonia in patients with AKI. Plasma ammonia concentration was correlated with the mean rate of remifentanil and creatinine clearance. A 72-hours remifentanil infusion appeared safe for sedation of patients with AKI.

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