Choroidal neovascular membranes (CNVs) most commonly occur with age-related macular degeneration (ARMD). Features of ‘dry’ AMD include hard drusen, soft drusen, ­retinal pigment epithelial disruption and geographic atrophy. Patients with extensive small drusen, non-extensive intermediate size drusen or pigment abnormalities have only a 1.3 % 5-year probability of progression to advanced AMD according to the ARED Study (Age-Related Eye Disease Study Research Group 2001). Those with extensive intermediate size drusen, at least one large druse, noncentral geographic atrophy in one or both eyes, or advanced AMD or vision loss due to AMD in one eye, are at risk of vision loss from advanced AMD in up to 50 % (large drusen with pigmentary changes) after 5 years (Ferris et al. 2005).

Simplified AREDS scoring system:

This risk can be reduced by taking a cocktail of high-dose vitamins (commercially available in combination preparations) such as 500 mg vitamin C; 400 IU vitamin E; 15 mg beta-­carotene (to be avoided in smokers or ex-smokers of less than 10 years because of an increased risk of lung carcinoma); zinc, 80 mg, as zinc oxide and copper, 2 mg, as cupric oxide (Age-Related Eye Disease Study Research Group 2001). This cocktail has been shown to reduce the chance of advancement in patients with high-risk characteristics by approximately 30 %.

Patient’s CNVs already in one eye are at particular risk of progressing to ‘wet’ ARMD with CNV production. The CNVs cause distortion and loss of vision with serous elevation of the retina, subretinal haemorrhage and finally disciform scar formation.

The CNVs are usually classified on fluorescein angiography into:

The frequent bilaterality of the condition results in a high proportion of patients who are technically blind, with severe loss of central vision. For this reason, surgical approaches have been tried. However, these are much less commonly used since the effectivity of anti-VEGF treatments bevacizumab (Avery et al. 2006), pegaptanib (Chakravarthy et al. 2006) and ranibizumab (Rosenfeld et al. 2006a, b; Brown et al. 2006) has been proven. The last is now established as the therapy of choice for CNVs from AMD.

Vitreomacular traction is more common in eyes with exudative AMD (38 %) compared with nonexudative AMD (10 %) and PVD that are less common (21 and 68 %, respectively), suggesting to some investigators a role for the vitreous in exudative AMD (Robison et al. 2009).

There may be situations where the surgery can be of use:

A patient with sudden onset vitreous haemorrhage with evidence of a large subretinal craggy mass on ultrasound is very likely to have suffered a subretinal bleed from a CNV from AMD (Orth and Flood 1982). The subretinal haemorrhage is usually in the macular area but occasionally is due to a peripheral CNV, and the macula is clear of blood. Removing the vitreous haemorrhage is useful to restore peripheral vision. The haemorrhage is often very thick and may be altered to an ochre colour seen in severe bleeds. The vitreous may or may not be detached. If attached, separate it from the retina as in macular hole surgery. If there are large bullae of subretinal haemorrhage, there is a temptation to remove some of the subretinal blood via retinectomy; however, this is often not very effective in removing the blood as fibrinous mass has a ‘cottage cheese’ consistency and cannot be washed out. The retinectomies may allow fluid blood to egress in the postoperative period causing severe hyphaema and the potential for raised IOP and corneal staining. A larger 180° retinectomy will allow access to the blood for removal but runs the risk of postoperative PVR, and visual recovery is unlikely to be much improved after prolonged surgery. If the subretinal blood is localised, leave it in situ; in most circumstances, it will remain localised, allowing the patient to achieve vision from unaffected parts of the retina.

Often these patients are on antiplatelet or anticoagulation therapy (Kuhli-Hattenbach et al. 2010). Examine the other eye for evidence of AMD.

Preoperative injection of intravitreal tissue plasminogen ­activator can be used to try to liquefy the clot (Oshima et al. 2007).

A bleed from a CNV may spread under the macula, giving a rise to a large central scotoma. It is possible to facilitate resorption of the haemorrhage and perhaps to displace the bleed away from the fovea by performing a PPV and gas. The patient is required to posture upright to allow the gas bubble to act on the haemorrhage displacing it inferiorly. There is a debate whether either intravitreal tissue plasminogen activator (tPA, 0.05 ml, 50 μg) or subretinal tPA should be injected to facilitate the breakup of the clot (Gopalakrishan et al. 2007; Ohji et al. 1998; Hesse et al. 1996; Singh et al. 2006). The molecular size of tPA is similar to bevacizumab which is able to cross the retina in AMD. Any agent injected into the vitreous cavity in a vitrectomised eye however tends to have a shorter half-life because of more rapid clearance of the drug in the fluid-filled vitreous cavity in comparison to the gel-filled cavity. If injecting tPA into the subretinal space, the drug can be inserted using a 40-gauge needle to raise a bleb of fluid under the retina. As with any injection under the macula, take care that the pressure rise in the subretinal space does not ‘blow’ a hole in the fovea, the weakest point in the macula.