Intravitreal l-Arginine injection reverses the retinal arteriolar vasoconstriction that occurs after experimental acute branch retinal vein occlusion.

To investigate the effect of l-Arginine on the retinal arteriolar diameter following acute branch retinal vein occlusion (BRVO) in minipigs. Under general anesthesia, 10 eyes of 10 minipigs were evaluated. Two hours after BRVO, an intravitreal juxta-arteriolar micro-injection of 30 microl l-Arginine 1 mM (pH = 7.4) was performed in 7 eyes. Three eyes received a micro-injection of 30 microl of the solvent (pH = 7.4) that was used to prepare the solution of l-Arginine and served as controls. Retinal arteriolar diameter changes were measured using a Retinal Vessel Analyzer. Overall (n = 10), 2 h after BRVO there was a 10.5 +/- 1.9% decrease in the retinal arteriolar diameter in the affected territories compared to baseline (p < 0.001). An increase of 16.0 +/- 3.0% (p = 0.001) and 21.0 +/- 7.0% (p = 0.013) of the arteriolar diameter was evidenced 10 and 15 min respectively after l-Arginine injection (n = 7) compared to the diameter prior to l-Arginine injection. Thereafter, the vasodilatory effect of l-Arginine started to decrease but persisted and remained significant at the end of the study period (5.0 +/- 1.5% at 30 min, p = 0.007). Micro-injection of the solvent alone (n = 3) did not produce any significant effect on the retinal arterioles, which remained constricted at all time-points (p > 0.1). These findings demonstrate a significant arteriolar vasodilation after intravitreal juxta-arteriolar l-Arginine micro-injection in eyes with experimental BRVO in the affected territories. l-Arginine micro-injection can reverse the arteriolar vasoconstriction that occurs in acute experimental BRVO by stimulating nitric oxide production.

Retinal angiomatous proliferations: when should we suspect them and how should we detect them?

BACKGROUND: The aim of this study was to identify the clinical and angiographic features of retinal angiomatous proliferations (RAPs) in patients with age-related macular degeneration. PATIENTS AND METHODS: 26 eyes of 24 patients with RAPs were retrospectively reviewed. All patients had colour and red-free photographs, and fluorescein (FA) and indocyanine-green angiography (ICGA). The biomicroscopic and angiographic characteristics were evaluated and video-angiograms were analysed for staging the RAPs. RESULTS: The total number of RAPs was 29. Stage 1 was present in 3/29, stage 2 in 3/29 and stage 3 in 23/29 with a chorio-retinal anastomosis identified in 21 of these 23 eyes. The total number of retinal vessels involved were 83, 35 were arteries and 48 were veins. RAPs were seen in ICGA as hot spots in all but one case where it appeared as a plaque. A retinal pigment epithelial detachment (PED) was observed in 22/26 eyes. Cystoid macular oedema was observed in 13/26 eyes in FA and intraretinal ICG leakage in 6/26 eyes. Hard exudates were present in 21/26 eyes. Retinal haemorrhages were present in 23/26 eyes; all but one were intraretinal and had a size of less than half of the optic disc diameter. The RAP was bilateral in 2/24 patients. CONCLUSIONS: Clinicians should suspect the diagnosis of RAP when hard exudates, small intraretinal haemorrhages, PED or a hot spot in ICGA are present. Both fluorescein and ICG video-angiography provide adequate temporal resolution and vascular flow examination leading to easier RAP staging and identification of the anastomosis.

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

AIMS: To report corneal endothelial cell loss and in vivo visualization of the Ahmed glaucoma valve implant in eyes with refractory glaucoma. METHODS: Ten 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. RESULTS: Mean (+/-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. CONCLUSIONS: Corneal 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.

Bilateral multifocal retinal pigment epithelium detachments associated with systemic corticosteroids.

PURPOSE: To report an unusual case of central serous chorioretinopathy (CSC), presenting as bilateral and multifocal isolated serous retinal pigment epithelium detachments (RPEDs) following corticosteroid treatment. METHODS: An otherwise healthy 39-year-old man was evaluated for visual loss following blunt trauma of his right eye (RE). The patient underwent complete bilateral ophthalmologic examination, including optical coherence tomography and fluorescein (FA) and indocyanine green angiography (ICGA). RESULTS: At presentation, best-corrected visual acuity (BCVA) was 20/200 in the RE and 200/200 in the left eye (LE). Treatment included topical and oral corticosteroids. Three days later, the patient complained of metamorphopsia and further decrease in the VA of his RE. Fundus examination showed bilateral serous RPEDs. Optical coherence tomography, FA, and ICGA confirmed the diagnosis. Topical and oral corticosteroids were stopped and a follow-up examination 5 days later demonstrated marked resolution of the RPEDs in the RE. Five weeks later, RPEDs regressed in the RE while they persisted in the asymptomatic LE. Visual acuity in the RE further improved to 120/200. Nine months after the first visit, BCVA in the RE was 200/200. At that time, both eyes demonstrated retinal pigment epitheliopathy. CONCLUSIONS: Central serous chorioretinopathy is a known complication of corticosteroids. The classic variant of CSC consists of a shallow neuroretinal detachment located at the posterior pole of the fundus. Bilateral and multifocal isolated serous RPEDs represent an atypical form of CSC.