Choroidal neovascular membrane (CNVM) is an abnormal vascular network originating in the choroid and breaching Bruch’s membrane into the sub-retinal pigment epithelium (sub-RPE), subretinal, or intraretinal space.[1] CNVM arise most commonly from retinal conditions such as neovascular age-related macular degeneration (AMD), polypoidal choroidal vasculopathy (PCV), myopic macular degeneration, central serous chorioretinopathy, macular telangiectasia, presumed ocular histoplasmosis syndrome (POHS) and other inflammatory chorioretinopathies, trauma, and angioid streaks. However, CNVMs may be idiopathic. CNVMs may result in visual disturbance, especially if there is exudation or hemorrhage from the CNVM.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10]
The retina is a multilayered tissue composed of neurons specialized in visual information processing. Photons of light traverse the entire thickness of the retina where they are received by the deepest (ie, outermost) retinal layer, comprised of photoreceptors. Photoreceptors convert photons of light into electrical impulses, which then are transmitted back inward through the retinal layers until reaching the inner layers comprised of ganglion cells, the axons of which comprise the innermost retinal layer, the nerve fiber layer (NFL). The NFL axons converge at the optic disc, where they continue onward towards the visual pathways of the brain.[11, 12, 13, 14, 15, 16, 17]
Beyond the photoreceptor layer lies the retinal pigment epithelium (RPE), a layer of epithelial cells that nourishes and maintains the overlying neurosensory retina, especially the photoreceptors. The RPE also functions as the outer blood-retinal barrier, preventing molecules >300kDa from passing into or out of the retina under physiologic conditions. In pathologic states such as CNVM, this barrier is disrupted, and due to the apical-to-apical arrangement of photoreceptors and RPE, fluid or hemorrhage may accumulate in the subretinal potential space. Bruch’s membrane separates the RPE from the highly vascular choroid and is comprised of 5 layers: RPE basement membrane, inner collagenous layer, elastin layer, outer collagenous layer, and basement membrane of the choriocapillaris.[11, 16, 17, 18]
CNVM occurs due to disruption in Bruch’s membrane which allow neovascular tufts to extend underneath the RPE (sub-RPE, ie, Type 1 CNVM). Because Type 1 CNVM is sub-RPE and thus not in contact with the overlying neurosensory retina, visual symptoms can be mild unless there is exudation, ie, leakage of fluid or hemorrhage into the subretinal or retinal spaces.[1, 17] In Type 2 CNVM, the neovascular membrane breeches the RPE and extends in the potential space between the neurosensory retina and RPE (ie, subretinal space).[1, 17] The pathophysiology of Type 3 CNVM, also known as retinal angiomatous proliferation (RAP), is not fully understood but may involve the development of intraretinal neovascularization as well as subretinal and choroidal neovascularization, leading ultimately to retino-choroidal anastomosis between these.[1, 17, 19, 20] CNVMs arising from wet AMD is more likely to Type 1 than are CNVMs from other causes.[21, 22]
Exudation from CNVMs may result in hemorrhage or fluid accumulating in the retina, subretinal, or sub-RPE spaces, resulting in impairment or damage to neurosensory retina and in turn, visual symptoms. Existing pharmacologic treatments of CNVM therefore center largely upon resolving exudation, as evidenced by resolution of fluid and/or hemorrhage on examination and imaging. Rarely, hemorrhage may break through the retina resulting in vitreous hemorrhage. Over time, CNVM may progress to a cicatricial stage with formation of disciform scars, resulting in destruction of the RPE and overlying outer retina over time.[1, 17, 21, 22]
There are no large studies evaluating the epidemiology of CNVM specifically, as CNVM is a sequela of a multitude of retinal diseases.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10] Thus, existing epidemiological studies focus upon the incidence of causative conditions for CNVM themselves.
The most common cause of CNVM is neovascular AMD.[1] In the United States, the prevalence of AMD (non-neovascular and neovascular AMD) is estimated to be 2% amongst patients aged 40-44 years, and the prevalence rises with age for those aged 45-49 (5.4%), 50-54 (7.8%), 55-59 (9.7%), 60-64 (11.5%), 65-69 (13.3%), 70-74 (18%), 75-79 (24%), 80-84 (32.4%), and 85-89 (42.2%) years. Approximately 10% of patients with AMD have neovascular AMD. Rates of AMD and neovascular AMD are higher amongst women than men and higher amongst those of European ancestry than amongst those of Asian or African ancestry. Other risk factors for neovascular AMD include smoking and genetic risk alleles.[23, 24] PCV is a variant of AMD that is more common in patients of African or Asian descent than those of European descent.[2]
CNVM and most related diseases are not characterized by increased mortality rates. Morbidity is limited to the loss of central vision; the peripheral vision is virtually always retained in cases of CNVM except in rare cases.
Early diagnosis and immediate intervention are crucial to improving outcomes. The prognosis of all CNVMs is very good, especially if treatment is initiated before bleeding or scarring occurs. Many patients with CNVM, especially due to etiologies such as AMD, may require treatment for many years.
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. Office staff should be instructed that these patients should be seen within a few days and undergo OCT imaging and clinical examination.
Patients with choroidal neovascular membranes (CNVMs) may report the following:
Or less commonly, the following:
In some cases, especially with Type 1 CNVM without exudation, the patient may notice no visual disturbance.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10]
CNVM arise most commonly from retinal conditions such as neovascular age-related macular degeneration (AMD), polypoidal choroidal vasculopathy (PCV, myopic macular degeneration, central serous chorioretinopathy, macular telangiectasia, presumed ocular histoplasmosis syndrome (POHS) and other inflammatory chorioretinopathies, trauma, and angioid streaks. However, CNVMs may also be idiopathic.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10]
The clinician will perform an examination using a slit lamp biomicroscopy and a fundus contact lens or 78-or 90-diopter (D) lens. Optical coherence tomography (OCT) is standard-of-care for assessing the retinal microstructure to identify and characterize the CNVM. Fluorescein angiography (FA), indocyanine green angiography (ICG), and/or OCT-angiography are required in some cases.
CNVM typically appear as gray or greenish lesions and may occur in the macula or in the periphery. There may be secondary subretinal or intraretinal fluid or hemorrhage. Other clinical findings may be present which provide clues as to the etiology of the CNVM, such as: drusen and RPE changes (AMD), peripapillary atrophy, tilted nerve, staphyloma or myopic fundus (myopic degeneration), inflammatory uveitic lesions, choroidal rupture, angioid streaks, etc.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10]
OCT has become an essential imaging tool for the diagnosis of CNVM and its causes and complications, as well as evaluation of response to treatment. Fluorescein angiography (FA), indocyanine green angiography (ICG), and/or OCT-angiography (OCT-A) may be needed in some cases to diagnose CNVM and/or its causes, as well as to help guide treatments such as laser or photodynamic therapy (PDT) when indicated.[25, 26, 27, 28, 29, 30]
Typical findings of CNVM on OCT include highly reflective fibrovascular tissue with irregular borders between RPE and Bruch’s membrane (Type 1 CNVM) or above the RPE (Type 2 CNVM), or as a serous fibrovascular pigment epithelial detachment (PED). Type 3 CNVM manifests with sub-RPE hyperreflective tissue with intraretinal angiomatous changes and cystic changes. In the setting of exudation from CNVM, there may be intraretinal or subretinal fluid, visualized as cystic hyporeflective spaces within or under the retina, respectively, or hemorrhage visualized as mildly hyperreflective material underneath or within the retinal tissues. Late-stage cicatricial CNVM, ie, disciform scar, manifests with hyperreflective dense tissue with overlying atrophy of the outer retinal tissues.[28, 31, 32, 33]
FA features of CNVM include early hyperfluorescence with leakage characterized by increased hyperfluorescence with poorly defined edges in late stages for Type 2 CNVM. A lacy neovascular net may be noted. Type 1 CNVM often manifests with ill-defined, poorly demarcated hyperfluorescence or late leakage on FA. On ICG, CNVM show low-intensity hypercyanescence. ICG may be useful for highlighting Type 1 CNVMs in cases where FA is inconclusive. Retino-choroidal vascular communications may be visible on early phases of ICG.[34, 35, 36, 37, 38] On OCT-A, CNVM is visualized as a neovascular, higher flow, complex.[39, 40, 41]
PCV is a variant of AMD characterized by Type 1 CNVM with polypoid lesions and branching networks with feeder and draining vessels. FA may show features of Type 1 CNVM noted above, but typically is not ideal for diagnosing PCV. ICG is helpful for PCV because it demonstrates early hypercyanescence demonstrating branching vascular networks, with or without associated polypoid lesions. Rarely, pulsations may be noted in the polypoid lesions during early ICG phases. Features on OCT that suggest a PCV diagnosis rather than AMD include: sharp-peaked (inverted U-shaped) PED, en face OCT with complex RPE elevation, and ring-like lesion in the subretinal space (consistent with a polyp). Other features include presence of SRF more commonly than of intraretinal fluid. The PED may be notched such that a sharp-peaked PED is connected to a lower-lying PED. The polyps may be visualized under the sharp-peaked PED, whereas a double-layer sign signifying the branching vascular network may be seen in the low-lying PED. OCT-A demonstrates the branching vascular networks under the RPE and polyps.[2, 42, 43, 44, 45, 46]
No laboratory tests exist for most diseases associated with choroidal neovascular membranes (CNVMs).
Hereditary macular degeneration usually can be identified from clinical presentation, family history, angiography, electroretinogram (ERG),[42] electro-oculogram (EOG),[43] psychophysical testing (eg, color vision, perimetry, dark adaptation), and genetic testing.
The diagnosis of histoplasmosis is based on fundus findings not serologic or skin testing.
Angioid streaks usually are due to pseudoxanthoma elasticum (PXE), but they also have been reported in patients with sickle cell disease and Paget disease.
CNVM is a clinical and ocular-imaging-based diagnosis, and tissue diagnosis is not indicated.
In the Age-Related Eye Disease Study (AREDS and AREDS2), zinc combined with other antioxidants has been shown to reduce the progression rate of AMD to advanced stages such as wet AMD with CNVM, by approximately 25% in patients with intermediate stage AMD. No benefit has been demonstrated in eyes without AMD or early AMD.[47, 48, 49, 50, 51]
The standard treatment for most cases of CNVM includes intravitreal injection of anti-vascular endothelial growth factor (VEGF) medications. Upregulation of VEGF has been implicated in the pathogenesis of CNVM development and vascular permeability in CNVM leading to exudation.[52, 53, 54]
Most Phase II and III trials for medications for CNVM focus on wet AMD. There are limited studies in myopic CNVM. For all other indications for CNVM, smaller studies have demonstrated efficacy, and anti-VEGF agents are used off-label. Below is a summary of major trials for intravitreal injection therapies for CNVM with wet AMD.
Pegaptanib (Macugen, Bausch and Lomb) was the first anti-VEGF agent approved for wet AMD. Pegatabnib blocked VEGFA-165. Since then, a variety of anti-VEGF agents have been demonstrated to be more effective at safely improving vision by promoting resolution of exudation from and regression of CNVMs.[55, 56]
Bevacizumab 1.25mg (Avastin) is an off-label; full-length, humanized, recombinant monoclonal antibody against all isoforms of VEGF-A which was initially used off-label and found to promote resolution of exudation, regression of CNVM, and improvement in vision in patients with wet AMD.[57, 58]
Ranibizumab 0.5mg (Lucentis, Genentech) is FDA approved for wet AMD and myopic CNVM. Ranibizumab is a humanized, monoclonal antibody fragment against all isoforms of VEGFA. The ANCHOR and MARINA clinical trials established efficacy and safety of monthly intravitreal ranibizumab as compared to sham (MARINA) or PDT (ANCHOR) for minimally classic/occult CNVM (MARINA) or classic CNVM (ANCHOR). In the MARINA trials 95% of patients treated with ranibizumab, versus 62% of sham, lost fewer than 3 lines of vision; and 34% of ranibizumab-treated patients gained more than 3 lines of vision (versus 5% of sham-treated patients). On average, ranibizumab-treated patients gained 7 letters of vision at 24 months, as compared to 10 letters lost in the sham-treated patients. The ANCHOR study reported similar findings.[59, 60]
The HARBOR study compared monthly versus monthly as needed (PRN) intravitreal ranibizumab injection therapy in patients with wet AMD and found similar results at 24 months, with the PRN group achieving a mean gain of 7.9 letters with an average of 13.3 injections over 2 years (versus 24 injections in the monthly group).[61] However, significant clinical trial and real world data suggests that patients who receive more injections achieve superior visual outcomes and significant under treatment exists in clinical practice.[62, 63, 64] For example, the SEVEN-UP trial demonstrated that 7 years after ANCHOR or MARINA, 43% had stable or improved vision compared to the baseline upon entry into the ANCHOR/MARINA trials, while 34% had 3 or more lines of vision loss. In the 3.4 year interval of the SEVEN-UP study, eyes had a mean of 6.8 injections, but the subgroup of eyes who received 11 or more injections had significantly better vision gains. In addition, while 68% of eyes in the study had active exudation from wet AMD, only 46% were receiving ongoing injections.[63]
There is a lack of consensus on appropriate treatment regimens for wet AMD, with retinal physicians employing monthly or bi-monthly injections at fixed intervals, monthly as-needed injections in which an examination and imaging are performed monthly and injection given if there is active exudation, and/or treat-and-extend regimen. The treat-and-extend regimen aims to balance the need to limit treatment burden with the data demonstrating that undertreatment and persistent exudation are associated with worse long-term vision. In a treat-and-extend regimen, after one or more loading monthly intravitreal injections for wet AMD, the interval between injections is slowly extended by typically 2 weeks while the retina remains dry. If recurrent fluid is noted, the interval is reduced until resolution of exudation is achieved. The optimal treatment interval is identified and maintained for a period of time and then possibly extended again in the future. If patients achieve an every 12 week or longer regimen for a period of time (eg, 1 year) without exudative activity, some clinicians will stop treatment and monitor closely for re-activation.[65]
The CATT trial was a multicenter, single-blinded, randomized, controlled trial comparing bevacizumab monthly, bevacizumab monthly as needed, ranibizumab monthly, and ranibizumab monthly as needed for wet AMD. Patients in the monthly as needed groups were evaluated every month to determine whether treatment was indicated at that visit. At 2 years, the CATT trial found similar visual outcomes with bevacizumab versus ranibizumab. Of note, monthly treatment resulted in slightly better visual outcomes than monthly as needed treatment.[64]
Aflibercept 2mg (Eylea, Regeneron) and aflibercept 8mg (Eylea HD, Regeneron) are FDA approved for wet AMD. It is a recombinant fusion protein from human VEGF-receptor1/2 that targets VEGFA, VEGFB ,and platelet-derived growth factor (PGF). The VIEW1/2 clinical trials demonstrated that aflibercept 2mg monthly or every 2 months (after 3 initial monthly doses) was non-inferior to monthly ranibizumab for treatment of wet AMD.[66] In the PULSAR study, patients received 3 monthly aflibercept high dose (8mg) injections followed by treatment at q8-16 weeks (with more frequent retreatment as needed based on clinical evaluation). These studies found that 78% of patients maintained treatment intervals of 12 or more weeks over the 2 year study period. Eyes treated with aflibercept 8mg at these extended intervals achieved noninferior vision gains as compared to aflibercept 2mg given every 8 weeks, with fewer injections over 2 years (mean 8.2-9.7 injections versus 2.8 injections).[67]
Brolucizumab 6mg (Beovu, Novartis) is a single-chain antibody fragment that inhibits VEGFA. In the HAWK and HARRIER clinical trials, brolucizumab (3 or 6mg) given 3 times monthly followed by every 12 weeks (with reduction to every 8 weeks if disease activity was noted) was compared to aflibercept 2mg given every 8 weeks. At week 48, brolucizumab was non-inferior to aflibercept for change in vision. Anatomic outcomes were more favorable in the brolucizumab groups, as compared to aflibercept. There were no differences in adverse events in the trial.[68] Post-market reports reported cases of intraocular inflammation (IOI), including cases with occlusive retinal vasculitis with severe vision loss after brolucizumab injection.[69, 70, 71, 72]
An independent Safety Review Committee analyzed investigator re-viewed reports of intraocular inflammation, endophthalmitis, and retinal artery occlusion from the HAWK and HARRIER studies and identified 50 eyes with IOI, retinal vasculitis, and/or vascular occlusion. According to the committee, the incidence of IOI was 4.6%, including 3.3% with IOI with vasculitis and 2.1% with IOI with vasculitis and occlusion. The incidence of moderate vision loss (3 or more lines) was 0.74% and most of these cases involved IOI with vasculitis and occlusion.[73] In light of these adverse events and the existence of other safe, effective anti-VEGF agents, brolicizumab is infrequently employed in the treatment of wet AMD.
Faricimab 6mg (Vabysmo, Genentech) is FDA approved for the treatment of wet AMD. Faricimab is a bispecfic antibody that dually inhibits both VEGFA and angiopoietin-2 (Ang2). Ang2 is a molecule in the angiogenisin1/Tie2 signaling axis that is implicated in angiogenesis and found to be elevated in eyes with wet AMD.[74, 75] Studies in animal models demonstrate that Ang2 inhibition reduces vascular permeability and that dual inhibition of both Ang2 and VEGF results in greater reduction in vascular permeability than inhibition of either alone.[76] Thus, dual inhibition of both of these pathways is thought to offer the potential of more potent clinical impact and in turn, longer durability.
The TENAYA and LUCERNE clinical trials compared faricimab given every 16 weeks (with the option of reducing intervals to 8 or 12 weeks based on disease activity) to aflibercent 2mg given every 8 weeks. Visual acuity at 48 weeks was non-inferior in faricimab compared to aflibercept, with fewer injections. Approximately 78% of patients maintained treatment intervals of every 12 weeks or longer with faricimab. There were no differences in adverse events.[77]
Biosimilars are reverse-engineered from the reference anti-VEGF biologic to mimic the reference drug’s pharmokinetic endpoints and thus have similar efficacy and safety. The FDA approval pipeline for biosimilars is shorter than for new drugs, and costs of biosimilars are lower, offering the potential to significantly reduce the cost of treating wet AMD.[78, 79] Biosimilars approved by the FDA for both wet AMD and myopic CNVM include: Byoovix (ranibizumab-nuna, Samsung Bioepis/Biogen)[78] and Cimerli (ranibizumab-eqrn, Coherence Biosciences).[79] Additional biosimilars are in the clinical trial and FDA approval pipeline.
Adverse effects after intravitreal injection include minor and common adverse events including conjunctival hyperemia or subconjunctival hemorrhage and post-injection, temporary ocular irritation/dryness.[80, 81, 82] Vision threatening ocular adverse events include: iatrogenic cataract, retinal tear/detachment (0-0.67%),[81, 82] and endophthalmitis (0.02-0.05%),[80, 81, 83, 84, 85] and intraocular inflammation (variable).[57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 76, 77, 78, 79, 80, 81, 83, 84, 85]
Laser photocoagulation promotes regression of CNVM, but the laser itself creates a chorioretinal scar, resulting in a scotoma. Thus, laser is rarely employed for the treatment of most CNVMs, especially in light of effective pharmacologic therapy as outlined above. It is largely reserved in some cases of non-central or peripheral CNVMs.
Verteporfin-photodynamic therapy (PDT) involves intravenous injection of photosensitive dye (verteporfin) followed by application of laser, which activates the verteporfin to create free radicals that impact the endothelial cell membranes on choroidal neovascular membranes, resulting in their regression. The efficacy of verteporfin-PDT for CNVM in wet AMD was established in two large clinical trials, VIP and TAP.[86, 87] However, the relative higher efficacy and better safety profile of pharmacologic agents has resulted in intravitreal injection therapy supplanting verteporfin-PDT for CNVM in wet AMD and most other conditions. Verteporfin-PDT may have a role, either alone or in combination with anti-VEGF therapy for CNVM due to PCV.[88, 89, 90]
In the EVEREST II trial, patients treated with intravitreal ranibizumab plus verteporfin-PDT achieved superior vision gains, better polypoid lesion regression, and fewer overall treatments than those treated with ranibizumab alone.[89] Other studies have found similar visual results, but better polyp regression with anti-VEGF versus antiVEGF combined with PDT.[90] PDT is also useful in wet AMD cases with inadequate response to anti-VEGF injecitons or to reduce anti-VEGF treatment burden in wet AMD.[91, 92, 93]
Most CNVM do not require surgical care. Prior to the advent of effective pharmacologic and office-based therapies, surgery was performed in some cases to remove subfoveal CNVMs. However, results of studies such as the Submacular Surgery Trial demonstrated that submacular surgery is ineffective CNVM from AMD and POHS and often resulted in vision loss.[94, 95, 96, 97, 98] Macular translocation surgery employed vitrectomy with 360-degree retinectomy to rotate the retina and in turn, change the position of the fovea away from the area of subfoveal CNVM. Visual outcomes were poor with macular translocation surgery, and there were significant complications such as bleeding, retinal detachment, proliferative vitreoretinopathy, macular holes, etc. There was also significant aniseikonia, high astigmatism, diplopia, enophthalmos, and cycloversion with retinal rotation procedures. Shortly after the advent of macular translocation surgery, anti-VEGF therapies became available for AMD. Thus, these surgeries are not employed currently for CNVM.[99, 100, 101, 102, 103, 104, 105, 106, 107]
Surgery may be indicated for complications related to the CNVM such as vitreous hemorrhage or subretinal hemorrhage. Vitreous hemorrhage is a rare complication of massive hemorrhage from CNVM and, if not clearing spontaneously, may be removed via pars plana vitrectomy. Surgery may also be considered to displace large-subfoveal hemorrhage from CNVM, as such hemorrhage can be toxic to the outer retina. Such surgery involves vitrectomy, possible injection of subretinal tissue plasminogen activator (tPa), and placement of a partial gas bubble. The gas bubble, with appropriate head positioning, enables displacement of the hemorrhage inferiorly and out of the foveal region.[108, 109, 110, 111, 112] Some clinicians attempt a similar approach without surgery involving in-office gas injection for pneumatic displacement, with or without intravitreal tPa injection.[113, 114, 115]
Generally, patients undergoing surgery or in-office displacement also receive anti-VEGF therapy. These displacement approaches have been demonstrated effective at displacing fluid and in some cases, improving vision. However, there is also a risk of procedure-related complications such as retinal detachment, macular hole, and vitreous hemorrhage,[108, 109, 110, 111, 112, 113, 114, 115] and vision improvement has also been noted with pharmacologic therapy with anti-VEGF alone.[116, 117] There are no large trials comparing antiVEGF therapy alone versus in combination with displacement approaches. Displacement may be considered for larger hemorrhages that can be taken to the operating room promptly, ie, before the hemorrhage begins to organize.
Patients with CNVM should be referred to a retinal specialist for appropriate diagnosis, treatment, and monitoring of the condition.
Higher dietary intake of lutein/zeaxanthin (found in nuts, oily fish, etc), carotenoids (found in dark green, leafy vegetables such as kale, spinach, arugula, mustard greens, collard greens, etc), as well as lower dietary intake of fats and high-glycemic index foods have been shown to be associated with reduced risk of advanced AMD (including CNVM).[118, 119, 120, 121] In the Age-Related Eye Disease Study (AREDS and AREDS2), zinc combined with other antioxidants has been shown to reduce the progression rate of AMD to advanced stages such as wet AMD with CNVM, by approximately 25% in patients with intermediate stage AMD. No benefit has been demonstrated in eyes without AMD or early AMD.[47, 48, 49, 50, 51]
Smoking significantly increases the risk of CNVM development in patients with wet AMD and thus, smoking cessation should be encouraged.[122, 123, 124, 125]
Clinical Context: A 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. Macugen is much less effective than bevacizumab, aflibercept, or ranibizumab.
As outlined above, treatment for CNVM often is ongoing. Even in those patients who achieve quiescence of CNVM and stop therapy, regular evaluations are required to assess for recurrent activity of the CNVM. In addition, patients are advised to monitor their vision, including with aides such as Amsler grid or home monitoring systems, and to report any changes in vision immediately.
All medical and surgical treatments for choroidal neovascular membranes (CNVMs) can be performed in an outpatient setting.
Patients with CNVM should be referred to a retinal specialist for appropriate diagnosis, treatment, and monitoring of the condition.
CNVM or the exudation resulting from CNVM may result in damage to the RPE or outer retinal tissues, resulting in vision loss. RPE rips with associated vision loss may also occur in the setting of large PEDs with underlying CNVM, and this risk may be potentiated by rapid regression of the fibrovascular PED after treatment. Treatment is highly effective at mitigating damage and thus vision loss from CNVM. See above regarding potential complications of various CNVM treatments themselves.
The prognosis of CNVM is generally excellent when diagnosed and treated promptly. However, visual outcomes from long-term real world data suggests vision loss over time even in the era of anti-VEGF therapy, whereas clinical trials typically demonstrated visual acuity gains in the shorter term (1-2 years). Potential causes for long term vision loss include undertreatment and/or development of macular atrophy. Prognosis is worse in cases that present with significant subretinal hemorrhage or those diagnosed late due to presence of RPE and outer retinal damage.[57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 76, 77, 78, 79, 80, 81, 83, 84, 85]
Patients should be educated about their diagnosis of CNVM, the cause, natural history, and treatment course. They should be instructed to monitor their vision, including with aides such as Amsler grid or home monitoring systems, and to report any changes in vision immediately.