Corneal neovascularization
| Corneal neovascularization | |
|---|---|
| Classification and external resources | |
| Specialty | Lua error in Module:Wikidata at line 446: attempt to index field 'wikibase' (a nil value). |
| ICD-10 | H16.4 |
| Patient UK | Corneal neovascularization |
Corneal neovascularization is the excessive ingrowth of blood vessels from the limbal vascular plexus into the cornea, caused by deprivation of oxygen from the air.
Contents
Pathogenesis
Chemical theory: There may be presence of vasostimulatory factor (VSF) or the breakdown (destruction) of previously existing vasoinhibitory factor (VIF).
Mechanical theory: Blood vessels cannot invade normal cornea because of its compactness and loosening of the compactness of corneal tissue due to oedema was mandatory for neovascularization.
Combined chemical and mechanical theory: Both release of some vasostimulatory factor (VSF) and structural loosening of compact corneal stroma by oedema are necessary for the neovascularization to occur.
Cause
One of the most common cause of corneal neovascularization is contact lens wear, especially those made with older hydrogel contact lens materials such as HEMA (2-hydroxyethyl methacrylate) for both daily and extended wear. Such older hydrogel materials have a relatively low oxygen transmissibility so the cornea ends up being starved of oxygen hence the response of the ingress of blood capillaries into the clear cornea to satisfy that oxygen demand. Also, there has been multiple causes proved to be involved with corneal neovascularization, including herpes simplex and corneal ulcers.[1]
Treatment
Modern rigid gas permeable and silicon hydrogel contact lenses have a much higher level of oxygen transmissibility, making them effective alternatives to help prevent corneal neovascularization.
Complications
In advanced stages, corneal neovascularization can threaten eyesight, which is why eye routine (annual) exams are recommended for contact lens patients.
Research
Reduction of neovascularization has been achieved in rats by the topical instillation of commercially available triamcinolone and doxycycline.[2]
Some evidence exists to suggest that the Angiotensin II receptor blocker drug telmisartan will prevent corneal neovascularization.[3]
Recent treatment developments include, topical application of bevacizumab, an anti-VEGF.[4]
