eMedicine Specialties > Ophthalmology > Choroid

Neovascularization, Choroidal: Treatment & Medication

Author: Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Coauthor(s): Teodoro Evans, MD, Retina Fellow, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Contributor Information and Disclosures

Updated: Jul 25, 2007

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.

Adult

0.3 mg injected intravitreal into affected eye q6wk

Pediatric

Not established

Ocular or periocular infections

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.

Adult

0.5 mg injected intravitreal into affected eye q4wk

Pediatric

Not established

Documented hypersensitivity; ocular or periocular infections

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.

Adult

1.25-2.5 mg have been reported in the literature

Pediatric

Not established

Documented hypersensitivity; recent thromboembolic events

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.

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

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

Documented hypersensitivity; porphyria

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

More on Neovascularization, Choroidal

Overview: Neovascularization, Choroidal
Differential Diagnoses & Workup: Neovascularization, Choroidal
Treatment & Medication: Neovascularization, Choroidal
Follow-up: Neovascularization, Choroidal
References
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References

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Further Reading

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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

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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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