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Decompression retinopathy is a dramatic clinical finding after IOPlowering surgery. Characterized by multiple intraretinal hemorrhage (some with white centers) and sometimes preretinal hemorrhage, it usually resolves itself without lasting effects unless there is bleeding in the macula. We initially hypothesized that one possible explanation for this event might be compromised autoregulation. The report by Bansal and Ramanathan (914) expands our understanding. In their case, they used both intravenous acetazolamide and slow decompression through a paracentesis to try to prevent a sudden drop in intraocular pressure. It is notable that their patients, like many others, had very high intraoperative pressure preoperatively. Even with these maneuvers, the patient had decompression retinopathy. This case points out that slow decompression in the operating room is not always preventive and our understanding of decompression retinopathy is incomplete. If it does represent a breakdown of autoregulation as suggested, does slow decompression help? How slowly must the eye be decompressed and to how low a level? Is the brief drop in IOP to 0 mmHg at the instant of creation of the sclerostomy enough to cause this retinopathy in a susceptible eye? At present, I still believe slow decompression of the eye to low IOP is not harmful and might be helpful in preventing some cases of this clinical event. Still missing from the literature is a case report of good quality fluorescein angiogram early in the course of decompression retinopathy. Such a case might further explain the vascular basis for at least some cases of decompression retinopathy.