Rhegmatogenous retinal detachment: a reappraisal of its pathophysiology and treatment.

This article represents a synthesis of an extensive literature review and the authors' decades-long personal experience with both scleral buckling (SB) and vitrectomy for rhegmatogenous retinal detachment (RD). Presenting a coherent understanding of the pathophysiology and treatment of RD, the authors confirm numerous findings described in earlier publications but also challenge certain long-standing dogmas. The key argument made here is that it is extremely rare for the chain of events leading to an RD to start with a retinal pathology. Rather, the initial pathology is syneresis of the vitreous, which then allows gel movement (intraocular currents). At the point of vitreoretinal adhesion, dynamic traction is exerted on the retina, which may be sufficient to tear it. If the tear is operculated and the dynamic traction overcomes the forces keeping the neuroretina and retinal pigment epithelium (RPE) together, the heretofore virtual subretinal space becomes accessible through the retinal tear. The intraocular currents allow the free (nonbound) intravitreal fluid to enter the subretinal space, and once the amount of the incoming fluid overwhelms the draining capacity of the RPE, an RD ensues. Detachment of the posterior cortical vitreous (PVD) is not a necessary prerequisite to RD development; furthermore, PVD cannot be diagnosed preoperatively with adequate certainty with current technology such as biomicroscopy, ultrasonography or optical coherence tomography. The surgeon should expect no or only partial (anomalous) PVD at the time of surgical repair in over half of eyes. The treatment's primary goal must thus be weakening (pneumatic retinopexy, SB) or eliminating (vitrectomy) this dynamic traction. If vitrectomy is employed, it must be a truly complete vitreous removal. This includes a surgically induced PVD if one is not present, close shaving at the periphery, and removing the vitreous immediately behind the lens. The vitrectomy is followed by the creation of a chorioretinal scar around the tear and aided by some form of intraocular tamponade. The main function of the tamponade is not to temporarily cover the break but to significantly reduce the intraocular currents and thus prevent fluid entry through the break until the chorioretinal adhesion will have become sufficiently strong to seal the retinal edge around the tear; postoperative positioning is therefore not as important as currently assumed.