Editorial Advanced Approaches for Management of Retinal Detachment

Vitrectomy without scleral buckling1 for rhegmatogenous retinal detachment is often referred to as “primary vitrectomy”2; a term which at least initially implied that scleral buckling was the standard of care and should be tried before resorting to vitrectomy. This “rescue therapy ” approach is considered to be “conservative ” and applied in many specialties and disease processes but can produce the unintended consequence of delaying adoption of improved therapies and putting the patient through an unnecessary procedure. Anterior segment surgeons do not try intracapsular cataract extraction before resorting to phaco or RK before LASIK. Long bone fractures were not randomized to sham therapy after casts were developed. There are no high quality clinical trials comparing vitrectomy3,4, scleral buckling, and combined vit-buckle procedures for rhegmatogenous retinal detachment surgery because there are a high number of clinical variables and many treatment options which are often used in combination. Pre-operative variables include type of breaks, size of breaks, number of breaks, lens status, refractive error, vitreous hemorrhage, vitreous traction, family history, status of the other eye, medical status, and many others. Variables in scleral buckling include: hard silicone versus sponges, subretinal fluid drainage versus non-drainage, radial versus circumferential elements, encircling versus segmental buckles, use of air or gas, paracentesis and many others. Variables in vitrectomy include air, SF6, C3F8 or silicone oil, laser versus cryo, 20, 23, 25 or 27 gauge5, use of liquid perfluorocarbons, combined lensectomy6 or phacoemulsification, post-operative positioning, and many others. Scleral buckle advocates7 have stated that pneumatic retinopexy often causes PVR but they manage “fish-mouthing ” in scleral buckling with gas injection; this is not rational. Some surgeons use vitrectomy only for pseudophakic eyes believing incorrectly that vitrectomy causes de novo nuclear sclerosis when, in fact, it only causes progression of pre-existing nuclear sclerosis because a permanent increase in the partial pressure of oxygen (12 mmHg)