Author Response, “Do Intraocular Pressure Measurements Under Anesthesia Reflect the Awake Condition?”
We thank Mamata and colleagues for their interest in our study attempting to evaluate the relationship between intraocular pressure (IOP) measurements under general anesthesia (GA) compared with the awake condition.1 The authors raised several interesting questions to discuss.
First, they questioned the external validity of our results since we induced GA using propofol target-controlled infusion (TCI) system. They are correct when claiming that TCI is not commonly used to induce GA for IOP measurement. However, we used TCI in the study design in order to standardize propofol induction in an objective, verified manner. Our results show that the pure pharmacodynamic effects of propofol do not include reduction of IOP, and therefore, any observed changes in IOP during induction are caused by other factors. These could potentially include propofol overdose or aggressive bolusing, among other etiologies. It was also argued that TCI models were developed using healthy subjects and might not be appropriate for other populations. While we agree with this comment, we feel that the alternative study design, namely blousing propofol in a fixed dose (eg, 2 mg/kg) would not be more appropriate to answer the study question regarding the pharmacodynamic relationship of propofol and IOP. Furthermore, TCI use in morbid and critically ill populations is described for both anesthesia and sedation,2,3 which may be a relevant option for IOP measurements in certain noncooperative populations.
The authors also mentioned our use of several end-tidal concentrations of sevoflurane and raised concerns regarding comparing the effect of 0.5% to higher sevoflurane concentrations on IOP. It should be emphasized that we did not compare the effect of 0.5% to that of 2% or 5% sevoflurane, but rather showed that IOP did not differ in any of those concentrations when compared to the baseline, awake measurement. Furthermore, the 2 groups in our study only differed in the rapidity in which they achieved 5% end-tidal concentration, and our results show that even rapid rise in sevoflurane concentration does not alter the IOP in a clinically relevant manner.
We thank Mamata and colleagues for pointing out the important issue of use of muscle relaxants, since this was not properly described in our original article. Intubation was achieved in our study after administering rocuronium 0.6 mg/kg. Notably, even the use of this nondepolarizing muscle relaxant in its normal clinical dose did not cause a reduction of IOP in our cohort.
Lastly, they mention our measurement of IOP in both the operated and nonoperated eyes of our patients undergoing strabismus surgery, and raise the potential difference in IOP between the eyes due to extraocular tissue congestion as a result of the procedure. We wish to emphasize that all IOP measurements in our study were completed before the initiation of surgery.