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Aims: To compare the outcomes of neovascular glaucoma (NVG) treated with and without intravitreal bevacizumab in a large case comparison study., Methods: The study is a retrospective, comparative, case series of 163 eyes of 151 patients with NVG, including 99 treated without and 64 treated with intravitreal bevacizumab. Medical and surgical treatments for NVG were assessed. The main outcome measures were visual acuity (VA) and intraocular pressure (IOP)., Results: At the time of NVG diagnosis, the median VA was count fingers (CF) in the non-bevacizumab group and 2/300 in the bevacizumab group. IOP (mean±SD) was 43.1±13.0 mm Hg in the non-bevacizumab group and 40.8±11.5 mm Hg in the bevacizumab group. IOP (mean±SD) decreased to 18.3±13.8 mm Hg in the non-bevacizumab group and 15.3±8.0 mm Hg in the bevacizumab group, and the median VA was CF in both treatment groups at a mean follow-up of 12 months. Panretinal photocoagulation (PRP) substantially reduced the need for glaucoma surgery (P<0.001) in bevacizumab treated NVG eyes., Conclusions: Although bevacizumab delayed the need for glaucoma surgery, PRP was the most important factor that reduced the need for surgery. Vision and IOP in eyes with NVG treated with bevacizumab showed no long-term differences when compared with eyes that were not treated with bevacizumab. Thus, intravitreal bevacizumab serves as an effective temporizing treatment, but is not a replacement for close monitoring and definitive treatment of NVG. PRP remains the treatment modality that affects the course of NVG in terms of decreasing the need for surgery to control IOP.

Background/aims: To evaluate the course of treatment and outcomes of neovascular glaucoma (NVG) treated with intravitreal bevacizumab., Methods: The study is a retrospective, non-comparative, consecutive, interventional case series. Demographic data, past ocular history, cause of NVG and anterior chamber angle status were recorded. Visual acuity (VA), intraocular pressure (IOP), number of IOP-lowering medications and type of treatment administered were recorded at the time of NVG diagnosis and at follow-up intervals. Treatment-related complications and reasons for vision loss were recorded., Results: The study included 56 eyes of 52 patients. At the time of NVG diagnosis, the median VA was count fingers, and the mean IOP (SD) was 40 (11) mm Hg. At 6 months after initial bevacizumab injection, the median VA was 1/200, and the mean IOP (SD) was 18 (15) mm Hg. Seventy-one per cent of eyes underwent panretinal photocoagulation after NVG diagnosis. Sixty-one per cent of eyes received a glaucoma drainage implant (GDI). The Kaplan-Meier cumulative proportion of eyes with open angles receiving a GDI after initial bevacizumab injection was not statistically significantly different from that of eyes with closed angles. Forty-six per cent of eyes received repeat bevacizumab injections. Eleven eyes had hyphaema after both bevacizumab injection and GDI surgery, while three eyes had hyphaema after GDI surgery but prior to initial bevacizumab injection., Conclusions: Intravitreal bevacizumab is now a frequently used adjunct for the treatment of NVG. Eyes must be monitored closely after initial injection of intravitreal bevacizumab, regardless of initial angle status, as many may still require surgery to lower IOP or repeat injections of intravitreal bevacizumab.

Purpose: To investigate the anatomic and visual outcomes in patients with initial anatomic success after macular hole surgery and with at least 5 years of follow-up., Design: Retrospective, noncomparative, consecutive case series., Methods: Medical records of all patients who underwent surgery for idiopathic full-thickness macular holes by two surgeons (W.E.S., H.W.F.) at the Bascom Palmer Eye Institute between January 1, 1991, and December 31, 1996, were reviewed. All patients who had initial anatomic success with macular hole surgery and who had 5 years or more of follow-up postoperatively were included in the study. Main outcome measures included the rate of macular hole reopening and visual acuity outcomes., Results: Seventy-four eyes of 66 patients with a median age of 68.0 years (range, 45.0-86.8 years) were identified. The median duration of macular hole was 6.0 months (range, 1.1-93.8 months), and the median duration of follow-up after macular hole surgery was 91.0 months (range, 60.0 to 114.8 months). The hole reopened in 9 eyes (12%) during the follow-up interval; 6 of these eyes underwent reoperation, and the hole closed in 4 of 6 (67%). Preoperative visual acuity ranged from 20/50 to 20/400 (mean, 20/129; median, 20/100). In the 62 eyes that underwent cataract extraction (CE) after macular hole surgery, CE was performed at a median of 13.9 months after macular hole surgery. Patients achieved their best postoperative visual acuity at a median of 28.5 months after macular hole surgery. Best postoperative visual acuity ranged from 20/20 to 20/400 (mean, 20/36; median, 20/30). Visual acuity at last follow-up ranged from 20/25 to counting fingers (mean, 20/56; median, 20/40). At last follow-up, 43 eyes (58%) had a visual acuity of 20/40 or better, and 57 (77%) had an improvement in visual acuity of 3 or more Snellen lines compared with their preoperative acuity., Conclusions: Macular hole closure and visual acuity improvement after initially successful macular hole surgery persist at follow-up of 5 years and longer in the majority of patients; delayed visual acuity improvement is not attributable to cataract surgery alone.

In chloroform solution, the syn/anti rotamer ratios for N-(2-pyridyl)carbamates, 3, and N-phenylcarbamates, 4, are close to 0.05. Addition of the double hydrogen bonding acetic acid moderately stabilizes the syn rotamer of 4, but has no measurable effect on the syn/anti ratio for 3. Conversely, the hydrogen bond donor-acceptor-donor triad in 2,6-bis(octylamido)pyridine, 1, strongly stabilizes the syn rotamer of 3, but has no effect on the syn/anti ratio for 4. The K(a) for syn-3:1 is 10(3)-10(4) times higher than the K(a) for anti-3:1. This implies that the alkoxy oxygen in anti-3 is a much poorer hydrogen bond acceptor than the carbonyl oxygen in syn-3, most likely because of a combination of steric and electrostatic factors.