To the Editor:—
In the article by Cheng et al. 1on the effect of prone positioning on intraocular pressure (IOP) during spinal operations, they reported an increase in IOP from 19 ± 1 mmHg supine baseline to 40 ± 2 mmHg at the end of the procedure in the prone position. The range of IOPs at the end of the case in the prone position was 25 to 54 mmHg. Despite an approximate 47% reduction in ocular perfusion pressure (MAP − IOP) from baseline to the end of the case, and an average duration of 320 ± 107 min, no visual deficits were reported. The very high IOP in this study is difficult to accept at face value.
As the authors pointed out, Lam and Douthwaite 2reported that IOP increased in awake volunteers from 13.5 ± 2.01 mmHg baseline supine to 20.0 ± 3.27 mmHg in the prone position. Why was the initial prone value of IOP (27 mmHg) so much higher in the study of Cheng et al. with anesthetized patients compared to the study of Lam and Douthwaite with awake volunteers? Our studies have also shown lower initial prone values of 18.1 ± 0.8 mmHg, with peak prone IOP values of 24.6 ± 1.1 mmHg. 3It seems that that technical error might be responsible for this difference. One of the most important causes of spuriously high recordings of IOP is inadvertent pressure on the globe while retracting the eyelids. This problem can be difficult to avoid when there is significant periorbital/conjunctival swelling, particularly in the prone position. In addition, contact of the tonometer with the globe must be made at a 90° angle. Failure to perform IOP measurements with these guidelines will result in erroneous values.
Although the authors discuss the possibility that an increased arterial carbon dioxide tension (Paco2) may increase the IOPs, it is unlikely that this would result in IOPs up to 54 mmHg. We have found that the measurement of IOPs during emergence (unpublished data) results in greatly elevated IOPs, similar to normal awakening. 4,5In the study of Cheng et al. , although reportedly not statistically significant, there is a trend toward increasing mean arterial pressure (MAP) at the end of the case (“prone 2” MAP, 84 ± 11 mmHg, and “supine 2” MAP, 91 ± 11 mmHg) compared to the initial supine and prone MAP measurements (“supine 1” and “prone 1” MAPs of 72 ± 7 and 75 ± 9 mmHg, respectively). This is consistent with “lightening” of anesthesia and perhaps early emergence from anesthesia. It is plausible that partial emergence from anesthesia, in conjunction with the technical challenge of retracting edematous eyelids, contributed to the extremely high IOPs observed in this study at the end of the procedure in the prone position.
Another explanation for increased IOP is the effect of fluid administration. With increasing duration of surgery, one would expect greater fluid requirements. The significantly elevated IOP (31 mmHg, “supine 2”) even after return to supine at the conclusion of surgery, suggests this mechanism may be operative. Our studies also demonstrated a statistically significant increase in IOPs at the end of the case (average duration, 450 min) in the supine position (21 ± 1.1 mmHg, SEM), compared to baseline values (12 ± 0.7 mmHg), with very large average estimated blood loss and intravenous fluid administration. 3Unfortunately, this study lacks a control supine group to evaluate this possibility in isolation. Elective supine cases should be matched for duration, estimated blood loss, and quantity of intravenous fluid administration. Given that those cases are difficult to find, it may be acceptable to study IOP in either supine operations of long duration or with comparable estimated blood loss and large intravenous fluid administration. A control group would allow changes in IOP caused solely by position to be evaluated independently of the other factors. The study results, while interesting and relevant, must be interpreted in the absence of these necessary controls.