We appreciate the correspondence from Yolcu and associates and are pleased to respond to their concerns about the effects of sub-Tenon local anesthetic on the results of our recently published study. As noted in our Methods section, we performed an injection of 3 mL of 2% lidocaine and 0.375% bupivacaine in a 50:50 solution, using a blunt cannula through a small incision in the inferior fornix. In fact, not all patients received the full amount of anesthetic at the time of the measurement prior to initiation of the surgical procedure, as many received additional anesthetic in the superior conjunctiva in cases of glaucoma surgery. We did not record the precise volume/location received by each patient. Perhaps we should have stated “up to 3 mL” of anesthetic injection to better describe our technique. As they correctly noted, retrobulbar local anesthetic, especially with added epinephrine, significantly alters ocular hemodynamics. However, our technique of sub-Tenon/subconjunctival anesthetic injection without epinephrine has not been shown to have a significant effect on ocular hemodynamics. We have also documented pO ₂ measurements on patients receiving only topical anesthetic of lidocaine gel 1% with no differences at any intraocular location (unpublished data).

Additionally, our group performed studies in a rabbit model, specifically evaluating effects of general and local anesthesia, as well as the oxygen saturation of hemoglobin (SaO ₂ ), on intraocular oxygen measurements. Shui and associates noted that injections of sub-Tenon/subconjunctival local anesthesia did not significantly alter oxygen measurements (unpublished data), yet hypoxia decreased oxygen levels in the anterior chamber angle, but not underneath the central cornea. This suggested that the source of oxygen in the anterior chamber of the eye is derived from diffusion of surface air across the central cornea, notably in contrast to oxygen in the angle, hypothesized to be derived from the ciliary vasculature. Thus, oxygen in the anterior chamber angle may be influenced by blood flow in the ciliary arteries, not the central retinal artery. A potential decrease in this circulation from local anesthetic would decrease, not increase, pO ₂ in the angle as measured in our study. In contrast, increased SaO ₂ as seen with general anesthesia (an exclusion criterion for our studies) increases pO ₂ at all locations in the rabbit eye and in humans (unpublished data).

Finally, the last sentence in their correspondence misquotes our findings. Central corneal thickness (CCT) does not correlate with pO ₂ under the central cornea. The only location measured that correlates with CCT is in the anterior chamber angle.