eMedicine Specialties > Ophthalmology > Choroid

Neovascularization, Choroidal

Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Teodoro Evans, MD, Retina Fellow, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica

Updated: Jul 25, 2007

Introduction

Background

This disorder 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.

Pathophysiology

Mechanisms of CNV are not understood. Virtually any pathologic process that involves the RPE and damages the Bruch membrane can be complicated by CNV. Recently, 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. 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 receptors in endothelial cells activating several signal transduction pathways that end with the formation of a network of 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.

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. 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.

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.
  
• 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.

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.

Clinical

History

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

Physical

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

Causes

Virtually any pathologic process that involves the RPE and damages the Bruch membrane can be complicated by CNV.

• Degenerative conditions
  
  
  • ARMD
  • Myopia
  • Angioid streaks
• Inflammatory or infectious conditions
  
  
  • Histoplasmosis
  • Sarcoidosis
  • Multifocal choroiditis
  • PIC
• Choroidal tumors
  
  
  • Nevi
  • Melanoma
  • Hemangioma
  • Osteoma
• Trauma
  
  
  • Choroidal rupture
  • Laser photocoagulation
• Idiopathic

Differential Diagnoses

Other Problems to Be Considered

Lacquer crack with adjacent hemorrhage secondary to myopic macular degeneration
Atrophic macular scar with adjacent hemorrhage

Workup

Laboratory Studies

• Laboratory studies may be indicated if certain underlying medical conditions, such as pseudoxanthoma elasticum (PXE), are present.

Imaging Studies

• Fluorescein angiography
  
  
  • Fluorescein angiography (FA) is an essential tool in diagnosing and managing CNV.
  • Several angiographic patterns have been described for CNV.
  • A lesion that hyperfluoresces in the early phases of the angiogram, maintains well-demarcated borders, and leaks late (obscuring its borders) is a classic CNV.
  • A lesion whose borders cannot be determined by FA is an occult CNV.
    
    
    • Fibrovascular pigment epithelial detachment (PED) and late leakage of undetermined source (LLUS) represent patterns of occult CNV.
    • A fibrovascular PED is a lesion that is elevated solidly and hyperfluoresces irregularly to different degrees.
    • The lesion may be well demarcated or poorly demarcated. LLUS is seen during FA as an irregular, indistinct, late, sub-RPE leakage.
  • According to its location relative to the center of the fovea, CNV has been classified as extrafoveal (200-1500 µm), juxtafoveal (1-199 µm), and subfoveal.
• Indocyanine green angiography
  
  
  • Indocyanine green (ICG) is a water-soluble tricarbocyanine dye that contains 5% sodium iodide; it rapidly binds almost completely to globulins after intravenous injection. ICG has a peak absorption and fluorescence in the near infrared range. This 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. A hot spot is a well-defined focal hyperfluorescent area that is less than one disc area in size. Hot spots usually fluoresce early. A plaque refers to a hyperfluorescent lesion that is larger than one disc area in size. A plaque usually does not fluoresce early, and its intensity diminishes late. Finally, some eyes harbor 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
  
  
  • CNV causes thickening and fragmentation of the highly reflective RPE-choriocapillaris band. If the CNV is well defined, it is seen as a fusiform thickening of the RPE-choriocapillaris band. In contrast, 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. Serous, hemorrhagic, or fibrovascular RPE detachments reveal focal RPE elevations with shadowing of the structures beneath the elevated areas. Serous detachments are characterized by complete shadowing of the underlying structures. A hemorrhagic RPE detachment shows a moderately reflective layer beneath the detached RPE. Fibrovascular RPE detachments demonstrate 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.
  • Rogers and coworkers have proposed an optical coherence tomography (OCT) classification scheme of CNV following photodynamic therapy (PDT).³⁰
    
    
    • Stage I occurs shortly after PDT and lasts for about a week. It is characterized by an inflammatory reaction that causes an increase in intraretinal fluid in a circular fashion that corresponds with the treatment spot.
    • Stage II represents the restoration of a near-normal foveal contour with diminished subretinal fluid occurring 1-4 weeks after treatment.
    • Stage III represents reperfusion and involution of CNV. It 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 contains a greater subretinal fluid to fibrosis ratio, indicating active CNV. Lesions in Stage IIIb have more prominent fibrosis with minimal intraretinal fluid, indicating inactive CNV.
    • Further involution of CNV may lead to cystoid macular edema, signifying Stage IV.
    • In Stage V, CNV and the subretinal fluid resolve, leading to fibrosis and retinal thinning.
  • Despite the many advantages of OCT, FA remains the imaging modality of choice in the management of CNV. Currently, OCT cannot replace FA in the management of CNV.

Histologic Findings

New capillaries and fibroblasts originate from the choroid and grow through a defect in the Bruch membrane into the subretinal space (type 2 CNV) or the sub-RPE space (type 1 CNV). Reactive hyperplastic RPE is present at the advancing edge of CNV.

Specimens obtained from surgical excision of CNV reveal that the most common cellular components are vascular endothelium and RPE. These were present in more than 85% of samples. Fibrocytes and macrophages also have been identified in more than 50% of specimens. Extracellular components include collagen and fibrin. VEGF has been identified in the specimens obtained during submacular surgery.

Treatment

Medical Care

Current knowledge of molecular events in the pathogenesis of CNV has allowed CNV to be targeted with very specific antiangiogenic factors. Targeting VEGF allows a two-hit strategy: antiangiogenesis and antipermeability. VEGF is 50,000 times more potent than histamine in inducing vascular permeability. An important component of decreased vision is the accumulation of subretinal fluid secondary to increased vascular permeability.

• Pegaptanib sodium
  
  
  • Pegaptanib sodium is an aptamer against VEGF165, the isoform identified with pathological angiogenesis. An aptamer is an oligonucleotide that acts like a high affinity antibody to VEGF, neutralizing it before it can contact its receptor.
  • Pegaptanib sodium is given as an intravitreal injection every 6 weeks.
  • Overall, pegaptanib sodium was able to decrease visual loss when compared to placebo in a similar fashion to that of PDT therapy with verteporfin. Only 6% of eyes were reported to have an improvement in visual acuity of 3 or more lines after 12 months of follow-up. Unlike therapy with verteporfin, all eyes with exudative ARMD benefited from treatment regardless of lesion composition. In addition, the trials using pegaptanib sodium included eyes with larger lesions than those eyes in the trials using verteporfin.
  • Complications associated with the intravitreal injection of pegaptanib sodium are few but include retinal detachment and endophthalmitis.
• Ranibizumab
  
  
  • Ranibizumab is a recombinant monoclonal antibody Fab fragment that neutralizes all active forms of VEGF-A.
  • Ranibizumab is delivered as a monthly intravitreal injection.
  • The US Food and Drug Administration approved the use of ranibizumab for the treatment of all angiographic subtypes of subfoveal neovascular ARMD.
  • Intravitreal ranibizumab is the first treatment that significantly improves visual acuity in up to 40% of eyes.
  • Although infrequent, complications associated with this treatment include endophthalmitis and severe uveitis.
• Bevacizumab
  
  
  • Bevacizumab is a humanized, recombinant monoclonal immunoglobulin G (IgG) antibody that binds and inhibits all VEGF isoforms and is currently approved for systemic use in metastatic colorectal cancer and non–small cell lung cancer.
  • Off-label use of intravitreal bevacizumab for CNV secondary to ARMD was first reported in 2005. Most of the reports of bevacizumab are uncontrolled, open-label case series that have proven functional and anatomical efficacy, short-term safety, and low cost.
  • Results from several studies suggest that bevacizumab may be useful in the treatment of CNV secondary to myopia, angioid streaks, and ARMD.
• Several other antiangiogenic compounds are currently in different stages of development. These agents include angiostatic steroids, such as anecortave acetate, squalamine, genetic therapy with an adenovector of PEDF, si (small interference) RNA-VEGF, and combretastatin A4.

Surgical Care

• The Macular Photocoagulation Study (MPS) proved the efficacy of laser photocoagulation in the treatment of CNV secondary to ARMD, POHS, and idiopathic causes.
• The goal is to completely obliterate CNV.
• Partial treatment of CNV is not beneficial when compared to observation.
  
  
  • Extrapolate these results to other conditions that are complicated by CNV on a case-by-case basis. Many patients and their physicians choose not to elect immediate loss or several lines of vision in an attempt to have a very modest visual improvement in 18 months.
  • Extrapolation of MPS results to CNV secondary to myopia probably is not indicated in juxtafoveal CNV.
  • Cases of enlargement of laser scars through the fovea with subsequent visual loss have been reported.
• PDT uses light-activated drugs and nonthermal light to achieve selective destruction of CNV with minimal effects on the surrounding normal tissues.
  
  
  • Randomized clinical trials have shown that PDT with verteporfin is effective in reducing visual loss in certain eyes with CNV secondary to ARMD.
  • In eyes with at least some classic CNV, treatment with verteporfin reduced visual loss. Subgroup analysis revealed that eyes with a classic component of greater than 50% fared much better than those eyes with a classic component of less than 50%. In eyes with a classic component of less than 50%, no difference existed in visual loss between the eyes treated with placebo and the eyes treated with verteporfin.
  • Another study reported that therapy with verteporfin for occult CNV secondary to ARMD was effective in slowing the progression of visual loss. However, such benefit was only seen after the second year of follow-up. Subgroup analysis revealed that eyes with a visual acuity of 20/50 or worse or eyes with lesions smaller than 4 disc areas in size had a better outcome. Further analysis of the data revealed that lesion size rather than lesion composition is a strong predictor of visual benefit following PDT with verteporfin.
  • Despite all the encouraging initial results, PDT provides marginal benefit. Most eyes will continue losing vision, though at a slower rate, and only 15% of eyes will manifest some visual improvement.
  • PDT in combination with intravitreal triamcinolone, bevacizumab, or ranibizumab may have better visual outcomes than PDT alone in patients with ARMD.
• High-speed ICG confocal angiography guided laser photocoagulation of feeder vessels is reportedly beneficial in selected patients with exudative ARMD but remains unproven.
• Uncontrolled studies have recommended surgical excision of subfoveal CNV via pars plana vitrectomy. The goal is to remove CNV but to leave the underlying RPE and choriocapillaris intact.
  
  
  • Surgical excision of type 2 CNV would be more beneficial than type 1 CNV.
  • Pilot studies resulted in substantial numbers of patients with worse vision, many with unchanged vision, and a small number with apparent improved vision. The current rhetoric is that stabilization may occur with surgery.
  • The Submacular Surgery Trial (SST), a randomized multicenter prospective trial sponsored by the National Eye Institute (NEI), confirmed that submacular surgery in eyes with CNV secondary to ARMD generally does not have a good visual outcome. In addition, with CNV secondary to idiopathic causes and POHS, submacular surgery offers a modest benefit in eyes with a baseline visual acuity of 20/100 or worse.
• Two surgical methods to translocate the fovea have been developed to treat subfoveal CNV. The previously subfoveal CNV is now juxtafoveal or extrafoveal; then, standard laser photocoagulation or PDT can be performed without damaging the fovea. Caution is warranted because high rates of retinal detachment, proliferative vitreoretinopathy (PVR), macular holes, recurrent CNV, cystoid macular edema (CME), and hemorrhage have been reported.
• Low-dose radiation therapy has been effective in inhibiting neovascularization in different tissues.
  
  
  • A randomized clinical trial reported better visual outcomes in eyes with exudative ARMD receiving radiation therapy of 24 Gy given in 6 fractions of 4 Gy each compared to observation.
  • However, other trials do not support radiation therapy as a treatment alternative in eyes with CNV secondary to ARMD. Long-term effects are unknown, and radiation retinopathy is definitely a concern.

Consultations

Diagnosis and treatment is often difficult. Consider referring to a retinal specialist who is experienced with these conditions.

Medication

Anti-VEGF therapy

Reduces risk of visual loss similar to that seen with PDT.

Pegaptanib (Macugen)

Selective VEGF antagonist that promotes vision stability and reduces visual acuity loss and progression to legal blindness. VEGF causes angiogenesis and increases vascular permeability and inflammation, all of which contribute to neovascularization in age-related wet macular degeneration.

Dosing

Adult

0.3 mg injected intravitreal into affected eye q6wk

Pediatric

Not established

Interactions

None reported

Contraindications

Ocular or periocular infections

Precautions

Pregnancy

B - Usually safe but benefits must outweigh the risks.

Precautions

Intravitreous injections have been associated with endophthalmitis; use proper aseptic technique; may increase intraocular pressure; most frequent adverse effects reported in 10-40% of patients over 24 mo include anterior chamber inflammation, blurred vision, cataract, conjunctival hemorrhage, corneal edema, eye discharge, eye irritation, eye pain, hypertension, ocular discomfort, punctate keratitis, reduced visual acuity, visual disturbance, vitreous floaters, and vitreous opacities

Ranibizumab (Lucentis)

Ranibizumab is a recombinant monoclonal antibody Fab designed to bind and inhibit VEGF-A, a protein that is believed to play a critical role in the formation of new blood vessels of exudative ARMD. First approved treatment with visual improvement for exudative ARMD.

Dosing

Adult

0.5 mg injected intravitreal into affected eye q4wk

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; ocular or periocular infections

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established

Precautions

Always use proper aseptic injection technique, as intravitreal injections, including those with ranibizumab, have been associated with endophthalmitis and retinal detachments; monitor intraocular pressure and perfusion of the optic nerve head, as increases in intraocular pressure have been noted within 60 min of intravitreal injection with ranibizumab; although there was a low rate (<4%) of arterial thromboembolic events observed in the ranibizumab clinical trials, there is a theoretical risk of arterial thromboembolic events following intravitreal use of VEGF inhibitors

Bevacizumab (Avastin)

A nonspecific monoclonal anti-VEGF. Off-label drug with apparent similar efficacy of ranibizumab.

Dosing

Adult

1.25-2.5 mg have been reported in the literature

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; recent thromboembolic events

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established

Precautions

Informed consent is critical because of off-label use; systemic anti-VEGF therapy can cause systemic hypertension, proteinuria, and thromboembolic events

Photosensitizers for photodynamic therapy

Reduction of leakage from abnormal, neovascular vessels, resulting in reduced visual loss.

Verteporfin (Visudyne)

A benzoporphyrin derivative monoacid (BPD-MA), consists of equally active isomers BPD-MAC and BPD-MAD, which can be activated by low-intensity, nonthermal light of 689-nm wavelength. After activation with light and in presence of oxygen, verteporfin forms cytotoxic oxygen free radicals and singlet oxygen. Singlet oxygen causes damage to biological structures within range of diffusion. This leads to local vascular occlusion, cell damage, and cell death. In plasma, verteporfin is transported primarily by low-density lipoproteins (LDL). Tumor and neovascular endothelial cells have increased specificity and uptake of verteporfin because of their high expression of LDL receptors. Effect can be enhanced by use of liposomal formulation.

Dosing

Adult

6 mg/m² (dissolved in 30 mL of solution) IV for 10 min
Second part of treatment consists of activation of drug: Recommended light intensity of 600 mW/cm², takes 83 s to apply necessary light dose of 50 J/cm²

Pediatric

Not established

Interactions

None reported; many drugs can influence effect; theoretical examples include concomitant use of other photosensitizer (eg, tetracycline, sulphonamide, phenothiazine, sulphonylurea, hypoglycemic substances, thiazide diuretics, griseofulvin) could increase photosensitivity; compounds that scavenge active oxygen species or radicals (eg, dimethylsulphoxide, beta-carotene, ethanol, formate, mannitol) could reduce activity; calcium channel blockers, polymyxin B, or radiation therapy can increase rate of uptake by vascular endothelium; anticoagulants, vasoconstrictors, or platelet-aggregation inhibitors (eg, thromboxane-A2 inhibitors) can reduce effectiveness

Contraindications

Documented hypersensitivity; porphyria

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Patients remain photosensitive to sunlight and strong artificial light for 48 h after infusion with verteporfin; wearing sunglasses and long-sleeved clothing highly recommended to avoid serious skin and eye burns; indoor lighting is safe in general and recommended over complete darkness because accelerates breakdown of active drug; caution in advanced liver disease; extravasation can cause severe pain, inflammation, swelling, and discoloration at injection site; cold compresses and analgesia help reduce pain and complications of extravasation

Follow-up

Further Outpatient Care

• Two weeks following laser photocoagulation, a patient should be observed and have a fluorescein angiogram.
  
  
  • Pay special attention to the borders, especially the foveal border, of the laser treatment zone to detect any persistence.
  • If no leakage is detected, the patient should have another fluorescein angiogram 4 weeks later or if there are new changes on the Amsler grid.
  • If no leakage is detected again, another angiogram should possibly be obtained 4-6 weeks later.
• Clinical examination cannot replace FA during the first 18 months after laser treatment, because most persistent and recurrent leakage occurs during this period.

Complications

• After 5 years of follow-up study, the MPS reported that 55% of patients with exudative ARMD, 33% of patients with POHS, and 34% of patients with idiopathic CNV had a recurrent or persistent CNV after laser photocoagulation.
• • These recurrences, regardless of etiology, tended to be toward the foveal side and were associated with visual loss.
  • In most cases, photocoagulation of these recurrent CNV is indicated.
  • Laser treatment of peripapillary CNV may be complicated by thermal damage to the papillomacular bundle.
• Surgical excision of CNV may be complicated by retinal detachment, postvitrectomy cataract, choroidal hemorrhage, epimacular membrane, and macular hole.
• • CNV recurrence following excision occurred in up to 44% of cases.
  • How to effectively manage these recurrences is unclear.

Prognosis

• Location, growth pattern, type (1 or 2) of CNV, and underlying condition determines the prognosis.
• • The 5-year follow-up of the MPS ARMD study showed that 46% of eyes with extrafoveal CNV that were photocoagulated had severe visual loss (loss of 6 lines or more from baseline) compared to 42% of eyes that were followed. In the juxtafoveal study, 49% of treated eyes compared to 58% of observed eyes had severe visual loss. In the subfoveal study, 22% of treated eyes and 47% of observed eyes had severe visual loss.
  • The 5-year follow-up of the MPS POHS study has shown that 12% of eyes with extrafoveal CNV that were photocoagulated had severe visual loss compared to 42% of eyes that were followed.
    • In the juxtafoveal study, 12% of treated eyes also had severe visual loss compared to 28% of eyes that were followed.
    • The natural history of untreated subfoveal CNV secondary to POHS shows that 14-23% of patients retain 20/40 or better visual acuity.
    • Pilot studies of photocoagulation of subfoveal CNV secondary to POHS were inconclusive.
    • Photocoagulation of peripapillary CNV secondary to POHS reduced severe visual loss from 26% of control eyes to 14% of treated eyes.
  • The 5-year follow-up of the MPS idiopathic CNV study showed that 27% of eyes with extrafoveal CNV that were photocoagulated had severe visual loss compared to 44% of eyes that were followed.
    • Few eyes were entered in the juxtafoveal study; at the 3-year follow-up, 10% of treated eyes versus 27% of observed eyes had severe visual loss.
    • The natural history for idiopathic subfoveal CNV is not necessarily associated with profound loss of vision.
    • Size of CNV seemed to be an important prognostic factor. If the CNV was smaller than 1 disc area at initial examination, prognosis was better.
    • In the MPS, the median visual acuity for untreated extrafoveal and juxtafoveal idiopathic CNV was 20/80.
  • CNV in myopia does not necessarily imply bad prognosis.
    • Up to 50% of patients can expect spontaneous improvement or stabilization of vision.
    • About 25% of extrafoveal CNV becomes subfoveal, but up to 25% of subfoveal CNV involutes spontaneously.

Patient Education

• Once diagnosed with maculopathy secondary to POHS, the patient is asked to self-monitor each eye with a near card and an Amsler grid.
• If a disturbance is detected, prompt examination is encouraged.

Miscellaneous

Medicolegal Pitfalls

• Early detection and treatment may help to reduce the chance of visual loss.

References

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Keywords

choroidal neovascularization, choroidal NV, CNV, subretinal neovascularization, Bruch's membrane, subretinal space, retinal pigment epithelium, RPE, visual loss, vision loss, vascular endothelium growth factor, VEGF, pigment epithelium derived factor, PEDF

Contributor Information and Disclosures

Author

Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, 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, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Teodoro Evans, MD, Retina Fellow, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Disclosure: Nothing to disclose.

Medical Editor

Brian A Phillpotts, MD, Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine
Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

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, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

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, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

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