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Choroidal Neovascularization

  • Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Mar 08, 2016
 

Practice Essentials

Choroidal neovascularization (CNV) involves the growth of new blood vessels that originate from the choroid through a break in the Bruch membrane into the sub–retinal pigment epithelium (sub-RPE) or subretinal space. CNV is a major cause of visual loss.

Signs and symptoms

In the history, patients with CNV describe the following:

  • Painless loss of vision
  • Metamorphopsia
  • Paracentral or central scotoma
  • Apparent change in image size

Physical findings in patients with CNV include the following:

  • Subretinal blood
  • Subretinal fluid
  • Lipid exudation
  • Retinal pigment epithelial detachment
  • Subretinal fibrosis (disciform scar)

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies may be indicated if certain underlying medical conditions, such as pseudoxanthoma elasticum (PXE), are present. Imaging studies include the following:

  • Fluorescein angiography (FA)
  • Indocyanine green (ICG) angiography
  • Spectral domain optical coherence tomography (OCT) - The imaging modality of choice

Fluorescein angiography

FA was once an essential tool in diagnosing and managing CNV. Spectral domain OCT has largely replaced FA as the imaging modality of choice in the management of CNV. Angiographic patterns that have been described for CNV include the following:

  • A lesion that hyperfluoresces in the early phases of the angiogram, maintains well-demarcated borders, and leaks late (obscuring its borders) – Classic CNV
  • A lesion whose borders cannot be determined by FA – Occult CNV
  • A lesion, well demarcated or poorly demarcated, that is elevated solidly and hyperfluoresces irregularly to different degrees – Fibrovascular pigment epithelial detachment (PED); a form of occult CNV
  • A lesion that demonstrates irregular, indistinct, late, sub-RPE leakage – Late leakage of undetermined source (LLUS); a form of occult CNV

According to its location relative to the center of the fovea, CNV has been classified as follows:

  • Extrafoveal (200-1500 µm)
  • Juxtafoveal (1-199 µm)
  • Subfoveal

Indocyanine green angiography

ICG has a peak absorption and fluorescence in the near infrared range, which allows visualization of choroidal pathology through overlying serosanguineous fluid, pigment, or a thin layer of hemorrhage that usually blocks visualization during FA.

Because ICG is bound tightly to the plasma proteins, less dye escapes from the choroidal circulation, allowing better definition of choroidal vasculature.

Three types of ICG patterns that are assumed to represent CNV may be imaged, as follows:

  • Hot spot – A well-defined focal hyperfluorescent area that is less than one disc area in size; hot spots usually fluoresce early
  • Plaque – A hyperfluorescent lesion that is larger than one disc area in size; plaques usually do not fluoresce early, and their intensity diminishes late
  • A combination of plaques and hot spots – In these eyes, the hot spots may be at the edge of the plaque, may overlie the plaque, or may be far from the plaque

High-speed or dynamic ICG angiography uses a scanning laser ophthalmoscope that takes up to 32 frames per second. These images are recorded like a movie, and the flow in and out of the vessels can actually be seen. The main use of dynamic ICG angiography is in the identification of CNV feeder vessels that are located in the Sattler layer of the choroid.

Optical coherence tomography

With the advent of anti-VEGF therapy, OCT plays a major role in the management of CNV; despite its many advantages, however, OCT cannot replace FA in the management of CNV.

Well-defined CNV is seen as a fusiform thickening of the RPE-choriocapillaris band.

Poorly-defined CNV is seen as a diffuse area of choroidal hyperreflectivity that blends into the normal contour of the normal RPE band.

A normal boundary cannot be defined.

A subretinal hemorrhage is seen as a layer of moderate reflectivity that elevates the neurosensory retina and causes optical shadowing, resulting in a lower reflectivity of the underlying RPE and choroid.

A serous RPE detachment is characterized by complete shadowing of the underlying structures.

A hemorrhagic RPE detachment shows a moderately reflective layer beneath the detached RPE.

A fibrovascular RPE detachment demonstrates moderate reflectivity throughout the entire sub-RPE space under the elevation.

Detachments of the neurosensory retina appear as elevations of a moderately reflective band above the RPE band.

RPE tears can be seen as thick elevated areas of high reflectivity; the underlying choroid is completely shadowed, whereas the adjacent choroid reveals a hyperreflective image because of the absence of RPE.

Retinal edema or thickness can be measured objectively by defining the anterior and posterior borders of the retina.

A proposed classification scheme of CNV following photodynamic therapy (PDT) is as follows[1] :

  • Stage I – Occurs shortly after PDT and lasts for about a week; characterized by an inflammatory reaction that causes an increase in intraretinal fluid in a circular fashion that corresponds with the treatment spot
  • Stage II – Restoration of a near-normal foveal contour with diminished subretinal fluid; occurs 1-4 weeks after treatment
  • Stage III – Represents reperfusion and involution of CNV; typically occurs 4-12 weeks following treatment and is subdivided into 2 categories based on the ratio of subretinal fibrosis to fluid present; stage IIIa is characterized by a higher subretinal fluid to fibrosis ratio, indicating active CNV; while lesions in Stage IIIb have more prominent fibrosis with minimal intraretinal fluid, indicating inactive CNV
  • Stage IV – Further involution of CNV leading to cystoid macular edema
  • Stage V – CNV and the subretinal fluid resolve, leading to fibrosis and retinal thinning

See Workup for more detail.

Management

Anti-VEGF treatment counters angiogenesis and increased vascular permeability; accumulation of subretinal fluid secondary to increased permeability is an important component of decreased vision in CNV.[2]

The major limitation of anti-VEGF treatment is the injection burden. Most patients require multiple injections. Therefore, a number of different protocols are looking at combining photodynamic therapy, corticosteroids, and anti-VEGF drugs.[3, 4, 5, 6, 7]

Currently, the treatment of choice for CNV secondary to exudative age-related macular degeneration (ARMD) is intravitreal anti-VEGF therapy.

Intravitreal ant-VEGF agents used for the treatment of CNV include the following:

  • Pegaptanib sodium [8]
  • Ranibizumab
  • Bevacizumab (off-label)
  • Aflibercept

Other treatment approaches

  • Laser photocoagulation
  • Photodynamic therapy – Uses light-activated drugs (eg, verteporfin) and nonthermal light to achieve selective destruction of CNV; may be combined with intravitreal agents
  • Surgical excision of subfoveal CNV via pars plana vitrectomy
  • Surgical translocation of the fovea, for subfoveal CNV; the resulting juxtafoveal or extrafoveal CNV can then be treated with standard laser photocoagulation or PDT
  • Low-dose radiation therapy

See Treatment and Medication for more detail.

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Background

Choroidal neovascularization describes the growth of new blood vessels that originate from the choroid through a break in the Bruch membrane into the sub–retinal pigment epithelium (sub-RPE) or subretinal space. Choroidal neovascularization (CNV) is a major cause of visual loss.

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Pathophysiology

Mechanisms of CNV are not well understood. Virtually any pathologic process that involves the RPE and damages the Bruch membrane can be complicated by CNV. CNV may be considered as a wound healing response to an insult of the RPE. A protein derived from the RPE, pigment epithelium derived factor (PEDF), was found to have an inhibitory effect on ocular neovascularization. Another peptide, vascular endothelium growth factor (VEGF), is a well-known ocular angiogenic factor.

The balance between antiangiogenic factors (eg, PEDF) and angiogenic factors (eg, VEGF) is speculated to determine the growth of CNV. The cause of VEGF upregulation in CNV remains unclear. VEGF upregulation is known to occur secondary to hypoxia, high glucose and protein kinase c activation, advanced glycation end products, reactive oxygen species, activated oncogenes, and a variety of cytokines.

VEGF has been temporally and spatially correlated with the development of CNV. Histopathologic specimens obtained from submacular surgery reveal the presence of VEGF in CNV. In addition, several researchers have induced CNV formation in animal models by overexpressing VEGF. Once secreted, VEGF binds to its tyrosine kinase receptors in endothelial cells activating several signal transduction pathways. Activation of VEGF induces vascular permeability, endothelial cell proliferation, and cell migration. The end product is the formation of a network of new vessels. These new vessels were previously thought to occur secondary to angiogenesis.

Angiogenesis can be defined as the growth of new vessels from preexisting vessels. Recent evidence suggests that CNV forms from both angiogenesis and vasculogenesis.[9] Vasculogenesis may be defined as the de novo growth of new blood vessels.

In an experimental model of CNV, it has been estimated that up to 20% of endothelial cells are bone marrow–derived progenitor cells that have been mobilized from the bone marrow.[10] These endothelial progenitor cells join the activated endothelial resident cells and incorporate into the nascent vascular tubular structure. The inhibition of endothelial progenitor cells mobilization from the bone marrow significantly reduced the size of the CNV lesion.[11, 12] Migration of endothelial cells requires remodelling of the extracellular matrix. Integrins and metalloproteinases play an important role at this stage. With time, vascular maturation and stability is achieved. Vascular maturation is intimately associated with platelet-derived growth factor (PDGF)-BB, which recruits pericytes to the new vessels.

As new choroidal blood vessels grow, they may extend into the sub-RPE space (Gass type 1) or into the subretinal space (Gass type 2). The location, growth pattern, and type (1 or 2) of CNV depend on the patient's age and the underlying disease. Bleeding and exudation occur with further growth, accounting for the visual symptoms. Alternatively, abnormal blood vessels may originate from an intraretinal location and grow into the subretinal space. This pattern of growth has been named retinal angiomatous proliferation (RAP), or type 3 neovascularization.[13]

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Frequency

United States

In the Wisconsin Beaver Dam Study, prevalence of CNV associated with age-related macular degeneration (ARMD) was 1.2% in adults aged 43-86 years.[14] Myopia is the second most common cause of CNV in the United States and Europe. CNV is estimated to occur in 5-10% of myopes; 60-75% of these are subfoveal.

Disciform scars secondary to CNV from presumed ocular histoplasmosis syndrome (POHS) were present in 0.1% of people living in endemic areas. In multiple evanescent white dot syndrome (MEWDS), development of CNV is rare. In multifocal choroiditis, estimates of CNV range from 25-40% of patients. In punctate inner choroidopathy (PIC), 33% of patients develop CNV. Of these, 50% are subfoveal and result in visual acuities between 20/80 and 20/200.

CNV occurs in 5% of patients with birdshot chorioretinopathy. CNV occurs in virtually all choroidal ruptures during the healing phase; most involute spontaneously. In 15-30% of patients, CNV may recur and lead to a hemorrhagic or serous macular detachment with concomitant visual loss.

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Mortality/Morbidity

ARMD is the most common cause of visual loss in people older than 50 years in the developed world. Up to 90% of visual loss in ARMD is secondary to CNV.

Myopia is the seventh greatest cause of registered blindness in the United States and Europe. CNV is responsible for most of this visual loss.[15, 16]

POHS is an uncommon cause of visual loss. Incidence and prevalence in the blind of Tennessee, an area endemic for histoplasmosis, were reported to be 2.8% and 0.5%, respectively.[17]

Sex

No gender predilection exists.

Certain diseases (ie, choroidal ruptures, angioid streaks, myopic macular degeneration, multifocal choroiditis, PIC, MEWDS) that may be complicated by CNV have gender proclivity.

Age

CNV is associated with multiple ocular conditions, so the age distribution of CNV reflects the underlying condition.

For instance, younger patients are affected with POHS, multifocal choroiditis, MEWDS, and PIC.

Older patients will be affected by CNV secondary to ARMD.

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Contributor Information and Disclosures
Author

Lihteh Wu, MD Asociados de Macula Vitreo y Retina de Costa Rica

Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Club Jules Gonin, Macula Society, Pan-American Association of Ophthalmology, Retina Society

Disclosure: Received income in an amount equal to or greater than $250 from: Bayer Health; Quantel Medical; Heidelberg Engineering.

Coauthor(s)

Dhariana Acón, MD Ophthalmologist, Caja Costarricense Seguro Social, Hospital de Guapiles, Costa Rica

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Brian A Phillpotts, MD, MD 

Brian A Phillpotts, MD, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, National Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Teodoro Evans, MD Consulting Surgeon, Vitreo-Retinal Section, Clinica de Ojos, Costa Rica

Disclosure: Nothing to disclose.

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