LAUSR

In Reply: Rajurkar and colleagues1 suggest that central mechanisms related to the supraoptic pathway and central nervous system–mediated reflective increase in aqueous flow do not play any role in the contralateral rise of intraocular pressure (IOP) in the initial weeks after Aurolab Aqueous Drainage Implant (AADI) implantation. The hypothesis put forth by Rajurkar and colleagues is that the central mechanisms act only when the AADI implantation results in lowering of IOP after dissolution of the ligatures. In contrast, the surgical procedure of AADI implantation consists of a number of steps such as anterior chamber paracentesis, and the peritubal leakage in the early postoperative period may itself activate various central nervous system pathways. The exact mechanism responsible for changes in IOP cannot be ascertained from our results as this was not the goal of our analyses. More insights into the pathophysiology of IOP change in the contralateral eye after surgical intervention can be best demonstrated by future animal studies. IOP in the medically uncontrolled glaucoma in the other eye was compared with the baseline IOP in that eye before surgery. Any fluctuations would have shown up then as well. We wish to highlight how dangerous it may be to operate upon such patients, and it will be worthwhile to plan both eyes one after the other to minimize the deleterious effects of a dangerous postoperative rise in the fellow eye An IOP difference of 6 to 8mm Hg is considered significant for diurnal variation in various tests such as the water-drinking test and the prone dark-room test. It must be noted that the standard of 6mm Hg has been applied for these tests, which are used for aiding the diagnosis of glaucoma, as a measure of the outflow facility, but not to study the variation of IOP among patients already on antiglaucoma therapy. An IOP difference of 4mm Hg was used in our study as the minimum error of the Goldmann Applanation Tonometer is 2mm.2 Thus, we considered twice the error to be clinically significant. Moreover, the mean change in IOP (which was often >4mm Hg) has been provided in the results of our paper in addition to the proportion of patients showing a ‘clinically significant’ rise of IOPZ4 mm Hg. All the fellow eyes of primary angle closure glaucoma were scheduled to undergo yttrium aluminum garnet peripheral iridotomy (PI). Yttrium aluminum garnet PI itself could cause a transient rise in IOP, and that is the reason patients who had undergone PI were excluded. We wished to study the natural course of the IOP change following surgery in the fellow eye rather than in one altered by any intervention. Our exclusion criteria mention those conditions in either eye. We concede that it should have read the “other eye.” As clarified above, we wanted to exclude other causes of raised IOP and therefore excluded neovascular glaucoma (NVG) as well. The NVG patients we included did not have NVG in the other eye. We may not have added the calculation of sample size in the paper. However, our study had adequate power. Taking a minimum value of 7.68% change in the fellow eye on the fourth day as significant, the calculated sample size with a 90% power is 37.3 We included twice that number. We appreciate Rajurkar and colleagues for sharing their experience and adding to our observations regarding changes in the contralateral eye IOP after glaucoma surgery.