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      Drugs & Diseases > Ophthalmology

      Choroidal Neovascular Membranes

      Updated: Sep 21, 2023
      • Author: Mrinali Gupta, MD; Chief Editor: Andrew A Dahl, MD, FACS  more...
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      Overview

      Background

      Choroidal neovascular membrane (CNVM) is an abnormal vascular network originating in the choroid and breaching Bruch’s membrane into the sub-retinal pigment epithelium (sub-RPE), subretinal, or intraretinal space. [1]  CNVM arise most commonly from retinal conditions such as neovascular age-related macular degeneration (AMD), polypoidal choroidal vasculopathy (PCV), myopic macular degeneration, central serous chorioretinopathy, macular telangiectasia, presumed ocular histoplasmosis syndrome (POHS) and other inflammatory chorioretinopathies, trauma, and angioid streaks. However, CNVMs may be idiopathic. CNVMs may result in visual disturbance, especially if there is exudation or hemorrhage from the CNVM. [1, 2, 3, 4, 5, 6, 7, 8, 9, 10]

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      Pathophysiology

      The retina is a multilayered tissue composed of neurons specialized in visual information processing. Photons of light traverse the entire thickness of the retina where they are received by the deepest (ie, outermost) retinal layer, comprised of photoreceptors. Photoreceptors convert photons of light into electrical impulses, which then are transmitted back inward through the retinal layers until reaching the inner layers comprised of ganglion cells, the axons of which comprise the innermost retinal layer, the nerve fiber layer (NFL). The NFL axons converge at the optic disc, where they continue onward towards the visual pathways of the brain. [11, 12, 13, 14, 15, 16, 17]

      Beyond the photoreceptor layer lies the retinal pigment epithelium (RPE), a layer of epithelial cells that nourishes and maintains the overlying neurosensory retina, especially the photoreceptors. The RPE also functions as the outer blood-retinal barrier, preventing molecules >300kDa from passing into or out of the retina under physiologic conditions. In pathologic states such as CNVM, this barrier is disrupted, and due to the apical-to-apical arrangement of photoreceptors and RPE, fluid or hemorrhage may accumulate in the subretinal potential space. Bruch’s membrane separates the RPE from the highly vascular choroid and is comprised of 5 layers: RPE basement membrane, inner collagenous layer, elastin layer, outer collagenous layer, and basement membrane of the choriocapillaris. [11, 16, 17, 18]  

      CNVM occurs due to disruption in Bruch’s membrane which allow neovascular tufts to extend underneath the RPE (sub-RPE, ie, Type 1 CNVM). Because Type 1 CNVM is sub-RPE and thus not in contact with the overlying neurosensory retina, visual symptoms can be mild unless there is exudation, ie, leakage of fluid or hemorrhage into the subretinal or retinal spaces. [1, 17]  In Type 2 CNVM, the neovascular membrane breeches the RPE and extends in the potential space between the neurosensory retina and RPE (ie, subretinal space). [1, 17]  The pathophysiology of Type 3 CNVM, also known as retinal angiomatous proliferation (RAP), is not fully understood but may involve the development of intraretinal neovascularization as well as subretinal and choroidal neovascularization, leading ultimately to retino-choroidal anastomosis between these. [1, 17, 19, 20]  CNVMs arising from wet AMD is more likely to Type 1 than are CNVMs from other causes. [21, 22]

      Exudation from CNVMs may result in hemorrhage or fluid accumulating in the retina, subretinal, or sub-RPE spaces, resulting in impairment or damage to neurosensory retina and in turn, visual symptoms. Existing pharmacologic treatments of CNVM therefore center largely upon resolving exudation, as evidenced by resolution of fluid and/or hemorrhage on examination and imaging. Rarely, hemorrhage may break through the retina resulting in vitreous hemorrhage. Over time, CNVM may progress to a cicatricial stage with formation of disciform scars, resulting in destruction of the RPE and overlying outer retina over time. [1, 17, 21, 22]

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      Epidemiology

      There are no large studies evaluating the epidemiology of CNVM specifically, as CNVM is a sequela of a multitude of retinal diseases. [1, 2, 3, 4, 5, 6, 7, 8, 9, 10]  Thus, existing epidemiological studies focus upon the incidence of causative conditions for CNVM themselves. 

      The most common cause of CNVM is neovascular AMD. [1]  In the United States, the prevalence of AMD (non-neovascular and neovascular AMD) is estimated to be 2% amongst patients aged 40-44 years, and the prevalence rises with age for those aged 45-49 (5.4%), 50-54 (7.8%), 55-59 (9.7%), 60-64 (11.5%), 65-69 (13.3%), 70-74 (18%), 75-79 (24%), 80-84 (32.4%), and 85-89 (42.2%) years. Approximately 10% of patients with AMD have neovascular AMD. Rates of AMD and neovascular AMD are higher amongst women than men and higher amongst those of European ancestry than amongst those of Asian or African ancestry. Other risk factors for neovascular AMD include smoking and genetic risk alleles. [23, 24]  PCV is a variant of AMD that is more common in patients of African or Asian descent than those of European descent. [2]

      Mortality/Morbidity

      CNVM and most related diseases are not characterized by increased mortality rates. Morbidity is limited to the loss of central vision; the peripheral vision is virtually always retained in cases of CNVM except in rare cases.

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      Prognosis

      Early diagnosis and immediate intervention are crucial to improving outcomes. The prognosis of all CNVMs is very good, especially if treatment is initiated before bleeding or scarring occurs. Many patients with CNVM, especially due to etiologies such as AMD, may require treatment for many years.

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      Patient Education

      Teaching patients to use the Amsler grid, reading text and other home testing schemes daily, is essential to improving outcomes. Patients should be instructed to contact their eye physician immediately if any visual disturbance occurs. Office staff should be instructed that these patients should be seen within a few days and undergo OCT imaging and clinical examination.

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