Neovascularization, Corneal, CL-related Treatment & Management
- Author: Barry A Weissman, OD, PhD, FAAO; Chief Editor: Hampton Roy, Sr, MD more...
The primary treatment of NV is eliminating the underlying cause. Ghost vessels remain even after NV is treated. Details are as follows:
For patients who wear CLs, NV can be minimized by decreasing CL wear time, discontinuing extended or all CL wear, refitting RGP CLs with improved edge designs and/or less tight (looser) fitting lenses, or refitting into higher oxygen permeable (Dk) CLs, such as high oxygen permeable (Dk) rigid gas permeable or soft silicone hydrogel lenses.
Since CL-induced NV is most common in patients who are highly nearsighted, have dry eyes, and use extended wear hydrogel CLs, these patients, depending on severity, should be refitted into daily wear, higher oxygen permeable silicone CLs  or daily wear rigid gas permeable CLs when NV is diagnosed.
For those patients with severe corneal NV, CL wear may be contraindicated.
Other coinciding injurious factors, such as acne rosacea, blepharitis, dry eye, and Staphylococcus hypersensitivity, should be addressed if present.
Topical corticosteroids can be used for active neovascularization. Discontinuation of CL wear is of essence during the recovery period for these patients. Corticosteroids can increase the risk of infection during CL wear, as well as glaucoma and cataracts.
More recently, topical and subconjunctival bevacizumab[24, 25, 26, 27] in combination with superficial keratectomy on ocular surface NV has shown promise as a new treatment option. Bevacizumab prevents the receptor binding of the soluble form of VEGF and, hence, prevents the process of the angiogenic pathway on superficial vessels. Bevacizumab alone is ineffective against existing blood vessels and is most effective in earlier than later stages of NV.
Because angiogenesis is a multistep process, many treatments in animal models are being tested to inhibit the migration, proliferation, and differentiation of endothelial cells. Some authors have discussed treatment in animal models with angiostatic steroids, heparin,[29, 30] systemic amiloride, cyclosporine A, thalidomide, arachidonic acid inhibitors, flurbiprofen, curcumin, and systemic suppression medications (cytotoxic agents).
Severe corneal NV may result in central corneal scarring, and permanent reduction in vision. In that case, and if medical management does not recover visual acuity, corneal transplantation may be indicated. Depending of the amount of neovascularization present (especially deep NV) such cornea grafts may be considered high risk.
Investigators have treated corneal NV with photodynamic therapy[36, 37, 38] and argon laser obliteration of the vessel lumen. This can be achieved in the corneal part of the vessels (accessible to be lasered) but usually has a short-term effect, as the vessel lumen invariably reopens. Argon laser pannus obliteration is mainly a temporizing measure.
Hyperbaric oxygen treatment has been used with limited success. This treatment modality aims to suppress angiogenesis by supplying the corneal tissue with redundant oxygen supply.
Amniotic membrane transplantation regenerates the ocular surface and thereby prevents neovascularization.
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