We thank Parekh and associates for their thoughtful comments and interesting description of a case of blood reflux during cataract surgery 2 years after previous Trabectome surgery. The authors raised several plausible mechanisms for intraoperative blood reflux in patients who undergo intraocular surgery after Trabectome surgery. However, these mechanisms may not apply to cases of repetitive spontaneous hyphemas that occur in the absence of subsequent surgery, as represented by our series.

Although processes analogous to Swan syndrome potentially may lead to repetitive spontaneous hyphema after Trabectome surgery, we believe that it is unlikely because we have not identified by gonioscopy any neovascularization of the angle, either shortly before development of hyphema or after resolution of hyphema. Parekh and associates also raised the possibility that a membrane could have developed in the area of prior Trabectome ablation and bleeding might have occurred when the cleft was abruptly reopened. Although this may result because of mechanical changes that occur in the angle during surgery (related to fluid flow during cataract surgery and use of viscoelastic), it again does not explain why patients would experience spontaneous repetitive hyphemas after Trabectome surgery in the absence of trauma.

We believe that the more likely mechanism for spontaneous repetitive hyphemas after Trabectome surgery is the reduction of intraocular pressure to a level less than the episcleral venous pressure, or elevation of episcleral venous pressure to a level higher than intraocular pressure. This reversal of pressure gradient often is seen during gonioscopy as congestion of Schlemm’s canal. However, in the presence of an open blood-aqueous barrier, as created by the Trabectome, there can be reflux of blood into the anterior chamber through the open cleft.

The case that Parekh and associates described is similar to the case reported by Knape and Smith, in which the authors described anterior chamber blood reflux during trabeculectomy several months after previous Trabectome surgery. Of note, similar blood reflux is seen when cataract extraction is performed immediately after Trabectome surgery in a combined procedure. During viscoelastic removal, often there is prompt bleeding into the anterior chamber, long before any neovascularization or membrane formation can occur. Because the tissue ablated in Trabectome surgery (trabecular meshwork and inner wall of Schlemm’s canal) is avascular, the only source of blood is reflux from the episcleral veins when the anterior chamber pressure is decreased to less than the episcleral venous pressure. We believe that this single mechanism is sufficient to explain all hyphemas after Trabectome, whether it is immediately after the procedure or years after surgery. However, we fully agree with Parekh and associates that the pathophysiologic changes in the trabecular meshwork, Schlemm’s canal, and the distal outflow system after Trabectome surgery are poorly understood and warrant further investigation.