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Anesth Analg 1999;89:1328
© 1999 International Anesthesia Research Society


LETTERS TO THE EDITOR

Remifentanil and Intraocular Pressure

Ratan Alexander, FRCA

Shackleton Department of Anaesthetics Southampton General Hospital Southampton SO16 6YD, England

I read the article by Artru and Momota (1) with interest. They stated in the introduction that "there are no reports of the effects of remifentanil on intraocular pressure." They are, however, mistaken. We published a study showing that remifentanil decreased intraocular pressure response to succinylcholine and endotracheal intubation after induction of anaesthesia with propofol (2). We also presented the preliminary data at the 7th annual meeting of the European Society of Anaesthesiology in Barcelona, Spain, April, 1998 (3).

References

  1. Artru AA, Momota Y. Trabecular outflow facility and formulation rate of aqueous humor during anesthesia with sevoflurane-nitrous oxide or sevoflurane-remifentanil in rabbits. Anesth Analg 1999;88:781–6.[Abstract/Free Full Text]
  2. Alexander R, Hill R, Lipham WJ, et al. Remifentanil prevents a rise in intraocular pressure following suxamethonium and endotracheal intubation. Br J Anaesth 1998;81:606–7.[Abstract/Free Full Text]
  3. Alexander R, Hill R, Lipham WJ, et al. Use of remifentanil to prevent a rise in intraocular pressure following use of suxamethonium and intubation [abstract]. Br J Anaesth 1998;S1:446.

 

Response

Alan A. Artru, MD

Department of Anesthesiology University of Washington School of Medicine Seattle, WA 98195-6540

We thank Dr. Alexander for his interest in our article (1). Our statement, "there are no reports of the effects of remifentanil on intraocular pressure," was correct in the sense that, at the time we composed our article, no such reports were listed in the literature search programs available to us. Our article (1) was composed before the article by Alexander et al. (2) was published in the October 1998 issue of British Journal of Anaesthesia. We have read the article of Alexander et al. (2) and wish to make two comments.

Our first comment considers the correct conclusion to draw from the data of Alexander et al. (2). They examined intraocular pressure (IOP) in two groups of patients. Both received midazolam 0.03 mg/kg 10 min before the induction of anesthesia, propofol 2 mg/kg at an infusion rate of 40 mg every 10 s for the induction of anesthesia, and succinylcholine 1 mg/kg after the loss of consciousness. In both groups, laryngoscopy and tracheal intubation (L/I) were performed 60 s after the initiation of the propofol infusion. Group S received saline immediately after succinylcholine, whereas Group R received remifentanil 1 µg/kg immediately after succinylcholine. In Group S, mean arterial blood pressure (MAP) and IOP increased after L/I, and in Group R, MAP and IOP decreased after L/I. We believe the following conclusion is supported by these data: giving an anesthetic dose before L/I that is large enough to decrease MAP after L/I decreases IOP after L/I, whereas, when the anesthetic dose given before L/I does not prevent the hypertensive response to L/I, IOP increases after L/I. In other words, the study design used by Alexander et al. (2) cannot prove that the decrease of IOP after L/I, seen when remifentanil was given, would not also have been seen with any other anesthetic dose sufficient to decrease MAP after L/I.

Our second comment relates to the abstract of Sung et al. (3) cited by Alexander et al. (2). Sung et al. (3) gave patients remifentanil 0.05 µg · kg-1 · min-1. Six minutes later, intermittent boluses of remifentanil 0.5 µg/kg were given for 15–20 s at 1-min intervals, until patients were adequately sedated (eyes closed, but rousable to command). IOP at the time of adequate sedation was not different from that at baseline, but IOP at 6 min and before the surgery decreased by 1.5 and 1.2 mm Hg, respectively. The decrease was statistically significant but was considered by Sung et al. (3) not to be clinically meaningful.

We hope that the data in our article (1) and those of Alexander et al. (2) and Sung et al. (3) are helpful to those interested in the intraocular effects of remifentanil.

References

  1. Artru AA, Momota Y. Trabecular outflow facility and formation rate of aqueous humor during anesthesia with sevoflurane-nitrous oxide or sevoflurane-remifentanil in rabbits. Anesth Analg 1999;88:781–6.
  2. Alexander R, Hill R, Lipham WJ, et al. Remifentanil prevents a rise in intraocular pressure following suxamethonium and endotracheal intubation. Br J Anaesth 1998;81:606–7.
  3. Sung YF, Stulting RD, Beatie CD, et al. Intraocular pressure (IOP) effects of remifentanil (R) (GI87084B) and alfentanil (A) [abstract]. Anesthesiology 1994;81:A35.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 1999 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press