Efstratios Mendrinos

Nonpenetrating Glaucoma Surgery

Nonpenetrating glaucoma surgeries have been developed in recent years in order to improve the safety of conventional filtering procedures. The goal of nonpenetrating filtering procedures is to reduce intraocular pressure by enhancing the natural aqueous outflow channels, while reducing outflow resistance located in the inner wall of the Schlemms canal and the juxtacanalicular trabecular meshwork. In the last few years viscocanalostomy and deep sclerectomy with external trabeculectomy have become the most popular nonpenetrating filtering procedures. Both involve removal of a deep scleral flap, the external wall of Schlemms canal and corneal stroma behind the anterior trabeculum and Descemets membrane, thus creating an intrascleral space. The aqueous humour leaves the anterior chamber through the intact trabeculo-Descemets membrane into the scleral space, from where it will egress into different pathways. The technique is associated with a long learning curve. Published clinical trials comparing nonpenetrating glaucoma surgery to full-thickness trabeculectomy have a consensus on the superior safety profile of nonpenetrating glaucoma surgery but are not in agreement when it comes to efficacy, where conflicting results have been found. This article reviews the nonpenetrating surgical techniques, mechanisms of action, indications, contraindications, complications, and results.

Intravitreal ranibizumab may induce retinal arteriolar vasoconstriction in patients with neovascular age-related macular degeneration.

OBJECTIVE To study the effect of intravitreal (IVT) ranibizumab (Lucentis; Genentech, Inc, San Francisco, CA) on the retinal arteriolar diameter in patients with neovascular age-related macular degeneration (AMD). DESIGN Prospective consecutive interventional case series. PARTICIPANTS Eleven eyes of eleven patients with previously untreated neovascular AMD. METHODS All eyes had 3 monthly IVT injections of ranibizumab. The diameter of the retinal arterioles was measured in vivo with a retinal vessel analyzer (RVA) before the first IVT injection and then 7 and 30 days after the first, second, and third injections. MAIN OUTCOME MEASURES Primary end points were changes in retinal arteriolar diameter and mean arterial pressure (MAP) after IVT ranibizumab. Secondary end points were changes in best-corrected visual acuity (BCVA), central retinal thickness, and intraocular pressure after IVT ranibizumab, and appearance of adverse events during the follow-up period. RESULTS A significant decrease of the retinal arteriolar diameter was observed after each IVT injection of ranibizumab. Thirty days after the first, second, and third injections, there was a mean decrease of 8.1+/-3.2%, 11.5+/-4.4%, and 17.6+/-7.4%, respectively, of the retinal arteriolar diameter compared with baseline values (P<0.01). There was no significant change in MAP during the period of follow-up (P>0.05). Thirty days after the third IVT injection of ranibizumab, mean BCVA improved by 6.5+/-4.9 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, and central retinal thickness decreased by 91+/-122 microm (P = 0.03). CONCLUSIONS These results suggest that IVT ranibizumab may induce retinal arteriolar vasoconstriction in patients with neovascular AMD after IVT ranibizumab. Further studies evaluating larger sample sizes are needed to confirm these results and potential adverse effects on the retinal circulation in patients with AMD and retinal vascular diseases. FINANCIAL DISCLOSURE(S) The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Ocular Ischemic Syndrome

Ocular ischemic syndrome encompasses a spectrum of clinical findings that result from chronic ocular hypoperfusion. It is relatively uncommon, and the diagnosis may be difficult to make because of its variable presentations. The presence of an ocular ischemic syndrome always implies underlying severe carotid occlusive disease and may be its sole clinical manifestation. It may also result from other causes of reduced blood flow to the eye and the orbit such as systemic vasculitis. Besides visual loss and ocular/orbital pain, affected patients are also at risk for developing cerebral and myocardial infarction. Establishing the diagnosis is therefore essential with respect not only to visual prognosis but also to patient survival. Ophthalmologists have an important role in early diagnosis and in coordinating the systemic evaluation of patients. Referral to the neuroradiologist and the neurovascular specialist is warranted. We present the current knowledge on the ocular ischemic syndrome.

Primary Vitrectomy without Scleral Buckling for Pseudophakic Rhegmatogenous Retinal Detachment

PURPOSE To report the anatomic and functional results of primary vitrectomy without scleral buckling for the treatment of pseudophakic rhegmatogenous retinal detachment (PsRD). DESIGN Prospective, nonrandomized surgical technique study. METHODS One hundred eyes of 98 patients with PsRD were operated by vitrectomy alone. Internal subretinal fluid drainage, cryocoagulation and/or endolaser and fluid-air exchange with sulfur hexafluoride 20% was applied in all cases. The preoperative and postoperative characteristics were analyzed. Main outcome measures were anatomic success rates after initial surgical intervention and after reoperation for primary failures, visual outcome at the last follow-up visit, and complications. RESULTS Mean follow-up +/- standard deviation (SD) was 12 +/- 6.3 months (range, seven to 36 months). Mean final visual acuity +/- SD was 0.42 +/- 0.45 logarithm of the minimum angle of resolution (logMAR) compared with 0.95 +/- 0.73 logMAR before surgery (P < .01). Mean number +/- SD of retinal breaks found before surgery was 1.36 +/- 1.12 (range, zero to five), and an additional 1.58 +/- 2.26 (range, zero to 15) retinal breaks were found during surgery. The retina was reattached successfully after a single surgery in 92 eyes (92%). Recurrence of retinal detachment occurred in eight eyes (8%), caused by proliferative vitreoretinopathy in six eyes (75%) and by new breaks in two eyes (25%). Final anatomic reattachment was obtained in these cases after a mean of 1.75 subsequent operations. Three eyes required permanent silicone oil tamponade so that final anatomic success was achieved in 97 eyes (97%). The most common postoperative complication was ocular hypertonia of more than 21 mm Hg, observed in 36 (36%) eyes, which was managed successfully. CONCLUSIONS Primary vitrectomy without scleral buckling provides a high anatomic success rate in eyes with PsRD and is associated with few complications.

Coupling of HRT II and AS-OCT to evaluate corneal endothelial cell loss and in vivo visualization of the Ahmed glaucoma valve implant.

AimsTo report corneal endothelial cell loss and in vivo visualization of the Ahmed glaucoma valve implant in eyes with refractory glaucoma.MethodsTen eyes underwent Ahmed valve implant surgery and were followed-up for 12 months. Data collected included intraocular pressure (IOP), number of antiglaucoma medications and surgery-related complications. At 6 and 12 months postoperatively, the intracameral length of the drainage tube (ICL) and the distance between the tube and the cornea (T–C distance), and the iris (T–I distance) were assessed using anterior segment optical coherence tomography (AS-OCT). Heidelberg cornea tomograph II (HRT II) was used to measure the corneal endothelial cell density.ResultsMean (±SEM) preoperative IOP was 29.5±4 mmHg. Mean postoperative IOP was 11.6±2 at 12 months (P<0.01). Over a 6-month period, mean corneal endothelial loss was 7.9%±2.5 in the central and 7.5%±2.4 in the peripheral cornea (P<0.01). There was no correlation between central or peripheral corneal endothelial cell loss and the T–C, T–I distance or the ICL of the tube.ConclusionsCorneal endothelial cell loss occurs following Ahmed valve implant surgery, this appears to be multifactorial. AS-OCT and HRT II are promising methods for the follow-up of patients with a glaucoma drainage device.

Long‐term results of the effect of intravitreal ranibizumab on the retinal arteriolar diameter in patients with neovascular age‐related macular degeneration

Purpose:  To study the effect of intravitreal (IVT) ranibizumab on the retinal arteriolar diameter in patients with neovascular age‐related macular degeneration (AMD).

Postoperative IOP is related to intrascleral bleb height in eyes with clinically flat blebs following deep sclerectomy with collagen implant and mitomycin

Aim To investigate the relationship between intrascleral bleb height and intraocular pressure (IOP) following deep sclerectomy with collagen implant (DSCI) and mitomycin C (MMC) in eyes with clinically flat blebs. Methods The records of 25 eyes of 22 consecutive patients presenting with clinically flat blebs following DSCI with MMC for primary or secondary open angle glaucoma were reviewed. Anterior segment optical coherence tomography (AS-OCT) scans were used to evaluate postoperative intrascleral bleb height and its relation to IOP control. Eyes requiring postoperative bleb manipulations, needling or goniopunctures were excluded. Results The mean age of the patients was 71.9±12.6 years, and the mean preoperative IOP was 25.3±5.6 mm Hg. The mean time of the AS-OCT examination from the operation was 8±4.9 months, and the mean IOP at that time was 13.8±4.2 mm Hg (p<0.001). All operated eyes manifested an intrascleral bleb with AS-OCT. The mean intrascleral bleb height was 0.58±0.16 mm. IOP and intrascleral bleb height were found to be inversely correlated (p<0.001, r=−0.626). None of the eyes had subconjuctival blebs, and 17/25 eyes showed microscopic conjuctival fluid collections. Conclusion The authors report a positive inverse correlation between intrascleral bleb height and postoperative IOP in eyes presenting clinically flat blebs following DSCI with MMC, suggesting an important role for intrascleral filtration in lowering IOP. Further studies are warranted to evaluate this relationship at different postoperative time points and possibly with different types of implants.

Lactate-Induced Retinal Arteriolar Vasodilation Implicates Neuronal Nitric Oxide Synthesis in Minipigs

PURPOSE To investigate the role of neuronal nitric oxide (NO) synthesis in the retinal vasodilatory response to lactate in minipigs. METHODS Thirteen eyes of 13 minipigs were evaluated. Ten eyes received an intravenous infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME). After 1 hour, the same eyes received an intravitreous juxta-arteriolar microinjection of 30 microL of L-lactate 0.5 M (pH 7.4) through a micropipette. Ten minutes later, 9 of 10 eyes received an intravitreous juxta-arteriolar microinjection of 30 microL of L-NAME 0.01 M (pH 7.4), and 1 received physiologic saline solution (PSS). The remaining three eyes received a microinjection of 30 microL of L-lactate 0.5 M (pH 7.4), without intravenous or intravitreous L-NAME. RESULTS The three eyes that received juxta-arteriolar injection of L-lactate only showed a reproducible increase in retinal arteriolar diameter that persisted during the entire study period (maximum effect at 20 minutes, 40.9% +/- 3.2%). Retinal arteriolar diameter decreased by 4.1% 1 hour after intravenous L-NAME when compared with baseline but the difference did not reach significance. The juxta-arteriolar injection of L-lactate induced a significant increase in retinal arteriolar diameter (22.7% and 28.7% at 5 and 10 minutes, respectively; P < 0.01), followed by a significant decrease (8.6%; P < 0.01) 10 minutes after juxta-arteriolar injection of L-NAME. Injection of PSS had no effect on retinal arteriolar diameter. CONCLUSIONS Juxta-arteriolar administration of L-lactate induced vasodilation, which was also observed with continuous intravenous infusion of L-NAME. Moreover, juxta-arteriolar L-NAME microinjection significantly suppressed the vasodilatory effect of L-lactate. These data suggest that neuronal-derived NO is an important mediator of lactate-induced vasodilation in minipigs.

Rapid and persistent regression of severe new vessels on the disc in proliferative diabetic retinopathy after a single intravitreal injection of pegaptanib

Editor, P egaptanib sodium is an aptamer directed against vascular endothelial growth factor (VEGF) isoform 165, which is responsible for pathological ocular neovascularization and vascular permeability. It is the first anti-angiogenic agent developed for intraocular administration and has been approved for the treatment of subfoveal neovascular age-related macular degeneration (Gragoudas et al. 2004). A phase II clinical trial has demonstrated its benefit in reducing diabetic macular oedema; it has also been noted to induce regression of small areas of retinal neovascularization (Cunningham et al. 2005; Adamis et al. 2006). We report a case of rapid and persistent regression of severe new vessels on the disc in proliferative diabetic retinopathy after a single intravitreal injection of pegaptanib. A 29-year-old woman with juvenile insulin-dependent diabetes presented with decreased vision in her left eye (LE). One year earlier, she underwent panretinal photocoagulation for severe non-proliferative diabetic retinopathy in both eyes. Three months before presentation, she had also undergone pars plana vitrectomy for massive preretinal and non-clearing vitreous haemorrhage in her right eye (RE). At the time of examination, visual acuity was 30 ⁄200 LE and 60 ⁄ 200 RE. Slitlamp examination was without any abnormal findings and intraocular pressure was within the normal limits. Severe optic disc neovascularization (NVD) was noted in the RE. Changes of non-proliferative diabetic retinopathy were present in the RE. Fundus fluorescein angiography (FA) revealed high-risk proliferative diabetic retinopathy (PDR) with profuse late leakage from the NVD and diffuse macular leakage (Fig. 1). Glycosylated haemoglobin (Hb) A1C was < 7%, indicating good control of diabetes, but laboratory work-up revealed anaemia; Hb concentration was 9 g ⁄dl. The patient elected to be treated with intravitreal pegaptanib after providing informed consent. Treatment of anaemia consisted of biweekly injections of erythropoietin. A single intravitreal injection of pegaptanib (Macugen; Pfizer Inc., New York, USA) 0.3 mg was performed in the LE. Three weeks after the injection, there was complete regression of NVD and VA improved to 80 ⁄ 200 LE. Visual acuity further improved to 120 ⁄200 LE at the 6 month follow-up visit. FA performed at that time confirmed the sustained complete regression of NVD and also showed reduced macular leakage (Fig. 2). Hb concentration was now 12.3 g ⁄dl. At the 15 month follow-up visit, fundus examination showed no signs of new vessel recurrence. Visual acuity was now 180 ⁄ 200 LE. Hb concentration was always within the normal range. VEGF has a key role in the development of retinal neovascularization, which represents an important risk factor for severe visual loss in patients with diabetes mellitus (Aiello et al. 1994). A phase II randomized clinical study in patients with diabetic macular oedema found that pegaptanib resulted in better VA outcomes, reduced central retinal thickness and reduced need for additional photocoagulation compared to sham injections (Cunningham et al. 2005). A retrospective data analysis of 16 eyes with PDR suggested a possible beneficial effect, with 62% of these eyes showing regression or absent neovascularization at the 6 month follow-up visit. However, mean number of injections was five (range 3–6) and only one patient had high-risk PDR. Moreover, this patient had no NVD,

Topographic variation of the choroidal watershed zone and its relationship to neovascularization in patients with age-related macular degeneration

Purpose:  To evaluate the patterns of choroidal watershed zones (WZs) in exudative age‐related macular degeneration (AMD) and to describe their relationship with choroidal neovascularization (CNV).