Characteristics and surgical outcomes of rhegmatogenous retinal detachment following myopic LASIK

To describe the clinical features and surgical outcomes of rhegmatogenous retinal detachment [RRD] following myopic laser in situ keratomileusis [LASIK]. In a retrospective, non-comparative case series, 46 eyes that had undergone vitreoretinal surgery for management of RRD following myopic LASIK were identified. Data was reviewed with emphasis on characteristics of the RRD, employed surgical techniques, and anatomic and visual outcomes. Mean pre-LASIK myopia was -9.7 +/- 3.9 [range -4.00 to -18.00] diopters [D]. Mean interval between LASIK and development of RRD was 11.6 +/- 11.2 months. Posterior vitreous detachment was present in 44 eyes [95.6%]. The retinal breaks included flap tears in 36 [78.3%] eyes, giant tears in 8 [17.4%] eyes and atrophic holes in 2 [4.3%] eyes. In eyes with flap tears, the breaks were multiple, large or posterior to the equator in 24 [66.7%] eyes. Retinal breaks were related to lattice degeneration in 20 [43.5%] eyes of which, three had history of prophylactic barrier laser photocoagulation. Scleral buckling was performed as the initial procedure in 32 [69.6%] eyes and primary vitrectomy was undertaken in 14 [30.4%] eyes. The initial surgical procedure failed in 14 [30.4%] eyes due to proliferative vitreoretinopathy [PVR]. Retinal reattachment was finally achieved in 43 [93.4%] eyes. Postoperative visual acuity >/= 20/40 and >/= 20/200 was achieved in 16 [34.8%] and 25 [54.3%] eyes, respectively. Post-LASIK retinal detachment has a complex nature in eyes with moderate to high myopia. The retinal detachment is complex in terms of size, number and location of retinal breaks, is associated with a high rate of PVR and entails unfavorable visual outcomes

Two different doses of intravitreal bevacizumab for treatment of choroidal neovascularization associated with age-related macular degeneration

To compare the efficacy and safety of 1.25 mg versus 2.5 mg intravitreal bevacizumab [IVB] for treatment of choroidal neovascularization [CNV] associated with age-related macular degeneration [AMD]. In this randomized clinical trial, consecutive patients with active CNV associated with AMD received 1.25 mg or 2.5 mg IVB. Best corrected visual acuity [BCVA], foveal thickness and side effects of therapy were evaluated one and three months after intervention. Overall 86 subjects were enrolled and completed the scheduled follow-up. Forty seven and 39 patients received 1.25 and 2.5 mg IVB respectively. The study groups were balanced in terms of baseline characteristics such as age, BCVA and foveal thickness. Mean improvement in BCVA was 0.06 +/- 0.3 logMAR in the 1.25 mg group and 0.07 +/- 0.34 logMAR in the 2.5 mg group [P=0.9]. Mean decrease in foveal thickness was 49 +/- 36 micro m in the 1.25 mg group and 65 +/- 31micro m in the 2.5 mg group [P=0.6]. Three cases of vitreous reaction and one case of massive subretinal hemorrhage were observed in the 2.5 mg group. Double dose [2.5 mg] IVB does not seem to be more effective than regular dose [1.25 mg] injections for treatment of CNV due to AMD and may lead to more complications

Vitreopapillary traction in nonarteritic anterior ischemic optic neuropathy

To describe the association between vitreous traction on the optic disc and nonarteritic anterior ischemic optic neuropathy [NAION]. Eighty three eyes of 83 patients with NAION were evaluated by optical coherence tomography [OCT] for detecting vitreous adhesion to the optic nerve head with separation from the adjacent retina [partial posterior vitreous detachment]. Eyes which were negative for such adhesion underwent ultrasonography to detect complete posterior vitreous detachment [PVD]. Fifty male and 33 female subjects with mean age of 51.9 +/- 10 years were studied. Partial PVD with optic nerve head adhesion was found in 54 patients [65.1%] using OCT. Ultrasonography detected complete PVD in all other eyes with optically empty spaces on OCT. Vitreous traction on the optic nerve head from partial PVD may play a causative role in some cases of NAION. This traction may impair vascular supply and/or axoplasmic flow leading to signs and symptoms of NAION