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A-Z Glossary

Table of Contents

Choroidal Neovascularization

Courtney Dryer, OD
Written byCourtney Dryer, OD
Courtney Dryer, OD
Courtney Dryer, ODOptometristCharlotte, NC

Bio

Dr. Courtney Dryer earned her doctorate from Southern College of Optometry, Memphis, Tennessee in 2011. She opened her own practice Autarchic Spec Shop in 2013 in Charlotte, NC. She has had the privilege of writing for numerous optometric publications and serving in various industry capacities. In 2015, Vision Monday named her a rising star and one of the most influential women in optometry. Her optometric passions include practice management, specialty contact lenses, and dry eye management.

  • Last updated November 3, 2022

What Is Choroidal Neovascularization?

Choroidal neovascularization (CNV) is the condition characterized by the growth of new, abnormal blood vessels from the choroid layer of the retina, through  Bruch’s membrane, and into the subretinal space (the space between the choroid and retina). These new blood vessels do not function properly, damage the retina and result in vision loss or blindness. In older adults, an advanced or wet form of macular degeneration indicates choroidal neovascularization. In younger individuals, the condition may occur in the lacquer cracks which are degenerative breaks in the retina associated with high myopia (nearsightedness).

Key Takeaways

  • Choroidal neovascularization is the growth of new, leaky blood vessels from the choroid layer of the eye into the subretinal space.
  • Ophthalmologists can detect the presence of choroidal neovascularization using a combination of techniques, including a dilated eye exam, Optical Coherence Tomography (OCT), and angiography.
  • Age-related macular degeneration (AMD) is the most prevalent cause of the development of choroidal neovascularization.
  • Anti-VEGF medications reduce new blood vessel growth and edema. 
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Understanding Choroidal Neovascularization 

The choroid is a dense network of blood vessels that supply oxygen and nutrients to the eye. The choroid layer is located underneath the retina. Choroidal neovascularization (CNV) is an abnormal growth of blood vessels from the choroidal vasculature through Bruch’s membrane to the space underneath the retina.

In patients with  age-related macular degeneration (AMD), significant amounts of vascular endothelial growth factor (VEGF) is produced by retinal pigment epithelial cells, neurons, glial cells, endothelial cells, ganglion cells, Müller cells, and smooth muscle cells in the posterior part of the eye. VEGF  stimulates the growth of new abnormal, leaky blood  vessels that  allow fluid to enter the retina. The fluid can disrupt vision by causing swelling in the otherwise flat-shaped retina. Over time, this swelling will damage the photoreceptors, the light-sensing cells in the retina, resulting in vision loss.

Symptoms of Choroidal Neovascularization

The symptoms of choroidal neovascularization may include

  • Gray/black/void spot in the central vision
  • Central area of distortion 
  • Bent or wavy lines 
  • Variations in color perception in each eye
  • Loss of vision
  • Paracentral or central scotoma (vision loss in the center or beside the center of vision)

Etiology of Choroidal Neovascularization

Choroidal neovascularization (CNV) is multifactorial and occurs due to the alterations in Bruch’s membrane, mitigation of macrophages, and secretion of vascular endothelial growth factor (VEGF), which has a critical role in the onset of the disease. CNV can develop in various conditions such as myopic degeneration, chronic central serous chorioretinopathy, macular telangiectasia type 2, various white dot syndromes, uveitic processes, and a few choroidal tumors. Visual acuity is affected by hemorrhages and  fluid leakage resulting in retinal edema. 

Pathophysiology of Choroidal Neovascularization

Despite much research, the pathogenesis of choroidal neovascularization is still poorly understood.

In age-related macular degeneration, the normal transport of metabolites, ions, and water molecules is altered through the Bruch’s membrane, which alters the stability and nutrition supply of the retinal pigment epithelium (RPE) and transport of waste out of the inner layers of the retina. 

Hypoxia (decreased oxygen supply) results in the release of vascular endothelial growth factor (VEGF) by the RPE, which initiates a cascade of angiogenic responses at the level of the choroidal endothelium and results in abnormal blood vessel growth. The damage to Bruch’s membrane is needed to allow the passage of abnormal vasculature from the choroid through the breaks in the membrane to the retina. 

Diagnostic Procedures

On a dilated exam, choroidal neovascularization (CNV) can appear as grayish macular lesions associated with the subretinal fluid, cystoid macular edema, hemorrhages, and exudation. Optical Coherence Tomography (OCT) is used to obtain a cross-section view of the retina to confirm the diagnosis. An OCT is able to detect even small amounts of fluid present in the retina due to CNV. 

In addition to OCT, fluorescein angiography (FA) utilizes injected dye and retinal imaging  to gain more data about the condition. The doctor is able to view the dye diffusing through retinal vasculature and identify aberrant vessels and fluid leakage.

Treatment

Since vascular endothelial growth factor (VEGF) is part of the pathogenesis of choroidal neovascularization, several treatments have been developed to block VEGF. Anti-VEGF treatments including aflibercept (EyeleaTM), bevacizumab (Avastin) and ranibizumab (LucentisTM) are used to treat choroidal neovascularization. An ophthalmologist will perform a series of injections into the back of the eye to stop the growth of new blood vessels.

Bibliography

  1. Rationale for combination therapies for choroidal neovascularization. Spaide RF. Am J Ophthalmol. 2006 Jan;141(1):149-56. doi: 10.1016/j.ajo.2005.07.025. PMID: 16386991
  2. W R Green, D J Wilson PMID: 2433662, DOI: 10.1016/s0161-6420(86)33609-1
  3. Hans E Grossniklaus , W Richard Green, DOI: 10.1016/j.ajo.2003.09.042
  4. Mitchell P, Liew G, Gopinath B, Wong TY. Age-related macular degeneration. Lancet.2018Sep29;392(10153):1147-1159.doi: 10.1016/S0140-6736(18)31550-2. PMID: 30303083.
  5. Stewart MW. The expanding role of vascular endothelial growth factor inhibitors inophthalmology.MayoClinProc.2012 Jan;87(1):77-88.doi: 10.1016/j.mayocp.2011.10.001. PMID: 22212972; PMCID: PMC3498409.
  6. Tadayoni R. Choroidal Neovascularization Induces Retinal Edema and its Treatment Addresses this Problem. J Ophthalmic Vis Res. 2014 Oct-Dec;9(4):405-6. doi: 10.4103/2008-322X.150799. PMID: 25709762; PMCID: PMC4329697.

Related Terms

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Episclera

is a fibroelastic structure consisting of two layers joined together loosely. It is the white of the eye

Asteroid Hyalosis

is a condition where small calcium particles float inside the vitreous, the jelly-like fluid that fills your eye

Epiretinal Membrane

is fibrous tissue (scar tissue) that forms on the top of the retina

Pars Plana

is the posterior part of the ciliary body, located in the middle of the eye

Drusen

is an accumulation of cellular debris underneath the retina

Enophthalmos

is when one eye is displaced deeper into the eye socket compared to the other eye

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