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      Drugs & Diseases > Ophthalmology

      Choroidal Neovascular Membranes

      Updated: Mar 01, 2017
      • Author: Steve Charles, MD; Chief Editor: Andrew A Dahl, MD, FACS  more...
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      Overview

      Background

      Choroidal neovascular membranes (CNVMs) are associated with many diseases. The most common causes are age-related macular degeneration (AMD), [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26] presumed ocular histoplasmosis syndrome (POHS), [27] myopic macular degeneration, [28] trauma, and angioid streaks; however, many cases are idiopathic.

      The natural history of patients with AMD should not be overlooked when pilot studies of new therapies are reported. In a randomized trial (of 481 patients) of interferon alpha-2, 62% of the placebo group stabilized at 1 year, losing less than 3 lines of vision. Randomized clinical trials are necessary in assessing treatment efficacy in cases of CNVM secondary to AMD as well as other causes. Submacular surgery, photodynamic therapy, translocation, and transpupillary thermotherapy (TTT) were once advocated as a means of stabilizing vision, where stable is defined a modest reduction in the rate of vision loss. True stabilization should be defined as no visual loss. A therapy that purports to stabilize vision requires large numbers of patients in a randomized trial with long-term follow-up to prove stabilization.

      Clinical trials of ranibizumab not only showed true stabilization in approximately 75% of cases (ie, avoidance of 3 lines [15 ETDRS letters] of visual loss [defined as moderate visual loss]) but also 30-40% of patients had visual improvement.

      Subfoveal CNVMs do not result in a loss of ambulatory vision if untreated. The natural history of subfoveal CNVMs never results in total blindness, while this outcome is all too frequent with macular translocation and occasionally with submacular surgery. [29]

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      Pathophysiology

      CNVMs may be thought of as the initial phase of a choroidal scar. Because these structures angiographically demonstrate a network of vessels, they are often referred to as "nets." The early phase of these lesions is termed exudative, while the later phase is termed cicatricial. Increased permeability of new vessels to fluorescein and indocyanine green (ICG) creates the familiar angiographic appearance referred to as "leakage."

      Vascular endothelial growth factor (VEGF) is present during the neovascularization phase. Because the scars are often circular in nature, they are called disciform scars when they enter the cicatricial phase. CNVMs, like all scarring disorders, seem to be a repair process with tissue loss or damage initiating the repair activity. The cause of tissue destruction in AMD is probably apoptosis, programmed cellular death. POHS, trauma, laser therapy, and angioid streaks all have in common a defect in the retinal pigment epithelium (RPE) and/or choriocapillaris. [30, 11, 31, 32, 33] Genetic abnormalities, specifically single polynucleotide polymorphism in the alternative complement pathway and reactive oxygen species, play a specific role in AMD.

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      Epidemiology

      Frequency

      United States

      The overall prevalence of neovascular AMD in people older than 40 years is estimated to be 1.47%. The prevalence increases with advancing age. Patients in their 70s are more likely to have AMD than patients in their 60s, and patients in their 80s are more likely to have wet AMD than patients in their 70s. [34, 35]

      International

      Polypoidal choroidal vasculopathy, which is a risk factor for CNVMs, is more common in Asian patients than in white patients. [36]

      Myopia, which is also a risk factor for CNVMs, is more common in Asian patients than in white patients or black patients.

      Mortality/Morbidity

      CNVM and most related diseases are not characterized by increased mortality rates. Smoking increases the progression rate of AMD by 350-500%, and, of course, smoking dramatically increases cancer and cardiovascular death rates. Morbidity is limited to the loss of central vision; the peripheral vision is virtually always retained in cases of CNVM unless complications of surgical therapy occur.

      Race

      The incidence rate of AMD is less in blacks than in whites (see Age).

      Other causes of CNVMs are not associated with differences in racial incidence, except for angioid streaks associated with sickle cell disease and ethnic differences in the incidence of myopia.

      Sex

      Ocular trauma is more common in men than in women and is a known cause of CNVMs. AMD is slightly more common in women than in men. No known significant sexual predilection exists for other causes of CNVMs.

      Age

      The prevalence of AMD increases rapidly with age. [22]

      AMD is more common after age 60 years, with the frequency increasing for patients in their 70s and an even greater frequency for patients in their 80s. The frequency of AMD is 11.90% in white men older than 80 years and 16.39% in white women older than 80 years.

      Histoplasmosis typically occurs in the 30s or 40s.

      Angioid streaks occur in individuals aged 30-60 years.

      Myopic macular degeneration typically occurs after age 25 years.

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      Prognosis

      Early diagnosis and immediate intervention with anti-VEGF therapy are crucial to improving outcomes. The prognosis of all CNVMs is very good, regardless of cause, if anti-VEGF therapy is initiated before bleeding or scarring occurs. Many patients with AMD require treatment for many years. In general, patients who receive more injections have better outcomes. No known adverse events are associated with anti-VEGF therapy.

      Patients treated with a monthly (31-42 days, no longer) regimen or treat-and-extend approach (preferred practice pattern) have a better prognosis than patients treated using a PRN strategy (ie, treatment administered only when subretinal fluid or intraretinal fluid is noted on optical coherence tomography [OCT] imaging).

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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; it should not be limited to a scripted definition of "distortion." 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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