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Polypoidal Choroidal Vasculopathy
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
In both criteria, ICGA is an indispensable tool to diagnose PCV. Single or multiple polyps can be clearly seen in the early phase of ICGA, but polyps may be obscured due to fluorescent blocking by dense bleeding or PED in some cases. Additionally, ICGA gives clinically useful information other than diagnosis. For example, a pulsatile polyp and cluster of grape-like polypoidal dilations of the vessels confer a high risk for massive bleeding. ICGA is also useful because it is the only imaging modality that can detect choroidal vascular hyperpermeability (CVH). CVH was first reported in eyes with central serous chorioretinopathy (CSC), but subsequent studies showed CVH is also observed in PCV. It has been reported that photodynamic therapy (PDT) is more effective in PCV with CVH compared to those without.5 Therefore, detecting CVH by ICGA is important in deciding treatment. Regarding diagnostics, there is adebate as to whether we still need to use ICGA to diagnose PCV or other imaging modalities, such as optical coherence tomography (OCT) and OCT angiography (OCTA), can replace ICGA, as discussed in the last section of this chapter.
Wavy Lines, Distorted Vision and Blur
Published in Amy-lee Shirodkar, Gwyn Samuel Williams, Bushra Thajudeen, Practical Emergency Ophthalmology Handbook, 2019
CSR: Patients with central serous chorioretinopathy should be reassured that the majority of cases resolve spontaneously in 3–6 months. Risk factors including exogenous steroids used should be avoided if possible and avoidance of stress factors (where possible). If there is evidence of scarring from previous episodes or no resolution after 6 months, photodynamic therapy is sometimes used.
Intravitreal triamcinolone acetonide in macular edema
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
In a previous report on a patient who showed longstanding central serous chorioretinopathy continuously recurring for 6 years, intravitreal injection of triamcinolone acetonide did not result in resolution of the subfoveal accumulation of fluid, suggesting that for this type of macular disorder, intravitreal injection of triamcinolone acetonide may not have a therapeutically positive effect.121 Our findings agree with those of a study on patients with central serous chorioretinopathy, for which preceding steroid therapy has been detected to be a risk factor.122,123
Intravitreal injections with anti-VEGF agent aflibercept versus subthreshold micropulse laser for chronic central serous chorioretinopathy: the alternative treatment regimens for verteporfin-shortage in China
Published in Annals of Medicine, 2023
Tantai Zhao, Jiani Li, Yanbin Wang, Xiaojian Guo, Yun Sun
Central serous chorioretinopathy (CSC), the fourth most common retinopathy, can lead to visual complaints such as decreased visual acuity, metamorphopsia, dyschromatopsia, micropsia, macropsia, relative central scotoma, and disturbed contrast vision [1–3]. CSC is characterized by the presence of serous subretinal fluid (SRF, defined as the accumulation of fluid beneath the neurosensory retina), retinal pigment epithelial (RPE) damage, as well as choroidal dysfunctions such as increased choroidal thickness, hyperpermeability, and congestion of choroidal vessels [4]. CSC can be further categorized as acute CSC, if the SRF resolves spontaneously within 4 months and chronic CSC (cCSC) if the SRF persists longer than 4 months [1]. A prolonged presence of SRF with persistent leakage can lead to RPE impairment with pigmentary changes, indicating a more aggressive form of this condition [5,6]. Patients with cCSC are more prone to developing choroidal neovascularization (CNV), with an estimated incidence of 4% to 8% [7,8]. The time of detection of CNV after the initial diagnosis of CSC varies from 1.65 ± 2.30 years to 17.0 ± 10.4 years [9,10]. Treatment is often advised for cases with persistent SRF [1,11]. Various forms of treatment have been reported for CSC, including conventional suprathreshold argon laser photocoagulation, subthreshold micropulse laser (SML), oral administration with mineralocorticoid antagonists eplerenone, intravitreal injection (IVI) with anti-vascular endothelial growth factor (VEGF) agents and photodynamic therapy (PDT).
One-year follow-up of choroidal and macular thickness in acute non-treated central serous chorioretinopathy
Published in Clinical and Experimental Optometry, 2023
Javier Orduña-Azcona, Elia Pérez-Fernández, Laura Modamio, Sofía De Manuel-Triantafilo, Carmen Fátima Rodríguez-Hernández, Pablo Gili
Central serous chorioretinopathy is a disorder characterised by serous macular detachment and retinal pigment epithelial changes. The pathogenesis of central serous chorioretinopathy is attributed to choroid hypermeability.1 Recent optical coherence tomography (OCT) modalities, such as enhanced depth imaging OCT (EDI-OCT) and swept-source OCT, have allowed the choroid to be studied due to their greater tissue penetrance and higher definition. Previous studies reported a greater choroidal thickness in eyes with central serous chorioretinopathy2–6 and fellow eyes4,7,8 as compared to normal controls, supporting a role for choroidal pathophysiology in this disease. Other studies reported a reduction in the choroidal thickness in eyes with central serous chorioretinopathy.9,10
Adult-onset bestrophinopathy mistaken as central serous chorioretinopathy
Published in Ophthalmic Genetics, 2022
Central serous chorioretinopathy (CSCR) is a common retinal cause of decreased vision in young and middle-aged men (1). CSCR is characterized by localized neurosensory detachment of the posterior pole in the setting of a thick choroid with or without an associated retinal pigment epithelium (RPE) detachment and in the absence of secondary cause (e.g., inflammation, infection, malignancy, choroidal neovascularization) (1). Middle-aged men are most commonly affected. Both corticosteroid use and endogenous hypercortisolism are risk factors. Visual complaints occur when subretinal serous fluid accumulates near the fovea. CSCR can be self-limited, recurrent, multifocal, or chronic. Management options include observation, focal laser treatment, and photodynamic therapy (1). Oral mineralcorticoid antagonists have been suggested to be of benefit but were not superior to placebo in a randomized controlled trial (2). Chronic CSCR can be complicated by choroidal neovascularization, for which intravitreal injection of pharmacologic anti-angiogenic therapy may be indicated. CSCR is not considered a Mendelian genetic eye disease, although certain variants may be more associated with the phenotype (1).