Sumeer Thinda

Phase-Variance Optical Coherence Tomographic Angiography Imaging of Choroidal Perfusion Changes Associated With Acute Posterior Multifocal Placoid Pigment Epitheliopathy.

Letters OBSERVATION Phase-Variance Optical Coherence Tomographic Angiography Imaging of Choroidal Perfusion Changes Associated With Acute Posterior Multifocal Placoid Pigment Epitheliopathy Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is characterized by bilateral multiple placoid white-gray lesions of the posterior pole at the level of the retinal pigment epithelium (RPE) and/or choriocapillaris, which self-resolve with recovery of vision. 1,2 The etiology is unknown, but APMPPE has been associated with viral pro- dromes and vasculitis. The placoid lesions are thought to represent focal RPE inflammation or choriocapillaris ische- mia based on fluorescein angiogram findings of early hypo- fluorescence and late hyperfluorescence. Phase-variance optical coherence tomographic angiogra- phy (pv-OCTA) allows noninvasive visualization of the cho- roidal blood flow in 3 dimensions in vivo. 3,4 A custom-built OCT system (125-kHz line rate, 855-nm central wavelength, and 4.5-μm axial resolution) was used to image choroidal perfu- sion over a 1.5 × 1.5-mm 2 area (equally spaced 350 A-scans in both x- and y-axes) in acute APMPPE. Report of a Case | A woman in her mid to late 20s with viral pro- drome presented with blurry vision in the left eye for 1 week. Visual acuity was 20/20 OD and 20/400 OS. The right eye was normal, and the left eye had normal anterior segment and vit- reous, but fundus showed multiple white-gray placoid lesions posteriorly with early hypofluorescence and late hyperfluores- cence on fluorescein angiogram (Figure 1). Patchy hypoperfu- sion of the choriocapillaris and Sattler layer was noted on pv-OCTA corresponding to focal areas of photoreceptor and RPE irregularity on OCT B-scans (Figure 2A-C). Serology test results were negative for syphilis, sarcoidosis, and tuberculosis. After 2 weeks, similar placoid lesions were noted in the right eye. After 6 weeks, placoid lesions resolved bilaterally to de- velop pigment clumping (Figure 1D) and choroidal perfusion mostly normalized on pv-OCTA. Visual acuity and photorecep- tor irregularity on OCT minimally improved (Figure 2D-F). By the 6-month follow-up, visual acuity was 20/20 OD and 20/30 OS, with almost normalized photoreceptor layer on OCT (Figure 2G). This study conforms to the World Medical Association Dec- laration of Helsinki 5 and subsequent amendments. The re- search protocol was approved by the University of California, Davis Office of Human Research. Figure 1. Fundus Photograph and Fluorescein Angiogram of the Left Eye A White-gray placoid lesions D Changes at 6 wk B C Early hypofluorescence E Late hyperfluorescence Changes at 6 wk At presentation, white-gray placoid lesions are seen (A), with early hypofluorescence (B) and late hyperfluorescence (C) on angiography; pigmentary changes developed by 6 weeks’ follow-up (D and E). jamaophthalmology.com (Reprinted) JAMA Ophthalmology August 2016 Volume 134, Number 8 Copyright 2016 American Medical Association. All rights reserved. Downloaded From: http://archopht.jamanetwork.com/ by a University of California - Davis User on 09/13/2016

Hypertensive retinopathy, choroidopathy, and optic neuropathy

Role of the Funder/Sponsor: Research to Prevent Blindness had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Additional Information: Our study conforms to the World Medical Association Declaration of Helsinki (June 1964) and subsequent amendments. The research protocol did not require approval per the University of California, Davis Institutional Review Board. Figure. Fundus photograph of the left eye shows optic nerve head edema, neovascularization of the disc, macular edema, scattered exudates and hemorrhages, Elschnig spots (white arrowhead), and Siegrist streaks (black arrowhead). Clinical Review & Education

Subthreshold micropulse laser reduces anti-VEGF injection burden in patients with diabetic macular edema

Purpose: To evaluate the efficacy of micropulse laser in the early treatment of diabetic macular edema (DME) and its associated burden of anti-vascular endothelial growth factor (VEGF) injections. Methods: This retrospective comparative study compared a group of 19 eyes with DME treated with micropulse laser to a matched control group of 19 eyes with DME treated with ranibizumab injections without micropulse laser. Recorded parameters included previous medical and ocular history, previous and subsequent ranibizumab injections administered for DME, visual acuity (VA), central macular thickness throughout the follow-up period, and the occurrence of any complications. Results: The improvement in VA was comparable in both groups, at 12 months and at the final follow-up. Patients treated with micropulse laser required significantly fewer ranibizumab injections than their controls, both at 12 months (1.7 ± 2.3 vs 5.6 ± 2.1) and by the end of the follow-up (2.6 ± 3.3 vs 9.3 ± 5.1) (p<0.001 for both). No complications related to the micropulse laser were encountered. Conclusions: Micropulse laser is a safe and effective treatment for DME, which may achieve comparable improvement in VA along with a significant reduction in the burden of anti-VEGF injections. We suggest a treatment approach for its inclusion in the early stages of DME.

Acute Retinal Necrosis Presenting in Developmentally-delayed Patients with Neonatal Encephalitis: A Case Series and Literature Review

ABSTRACT We report three cases of patients with developmental-delay from neonatal herpetic encephalitis and/or meningitis who presented years later with acute retinal necrosis due to herpes simplex virus. The diagnosis was delayed in all cases due to the patients’ inability to verbalize their ocular complaints and cooperate with eye examinations. This case series documents the clinical course, pathophysiologic mechanism, and treatment of acute retinal necrosis in this patient population. Clinicians should understand the importance of prudent consideration of acute retinal necrosis in patients with a history of neonatal herpetic encephalitis and/or meningitis presenting with a red eye.

OPHTHALMIC ARTERY OCCLUSION AFTER COCAINE USE

Sudden-onset, unilateral, painless, total vision loss is an alarming complaint of many patients that present to the emergency department (ED). After confirmation that the vision loss is indeed monocular, the differential diagnoses that should be considered include central retinal artery occlusion, ischemic central retinal vein occlusion, ophthalmic artery occlusion, vitreous hemorrhage, and retinal detachment (1). Most of the patients that present with these symptoms will have underlying vasculopathic diseases including hypertension, diabetes mellitus, and hyperlipidemia. Here we present an interesting case of a patient who sustained ophthalmic artery occlusion after cocaine use. This case serves to highlight the importance of considering illicit drug use as a risk factor for ischemic arterial occlusion, especially in young patients with no history of vasculopathic disease. In the BaltimoreYoung Stroke Study, illicit drug use was found to be the source of ischemic stroke in almost 40% of cases reviewed, as no other cause was apparent (2). Suggested mechanisms of illicit drug-induced ischemic stroke include prolonged vasoconstriction (e.g., cocaine) with or without intraluminal clot formation, embolism (e.g., cardiogenic vs. talc that is often used as filler in intravenous drugs), and increased coagulability (3,4). In addition to inducing vasoconstriction, cocaine has been reported to enhance platelet aggregation (5,6).