| Corneal neovascularization | |
|---|---|
| Classification and external resources | |
| ICD-10 | H16.4 |
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 |
Etiology [edit]
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-hydroxy-ethyl 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.
Treatment [edit]
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 [edit]
In advanced stages, corneal neovascularization can threaten eyesight, which is why eye routine (annual) exams are recommended for contact lens patients.
Research [edit]
Reduction of neovascularization has been achieved in rats by the topical instillation of commercially available triamcinolone and doxycycline.[1]
Some evidence exists to suggest that the Angiotensin II receptor blocker drug Telmisartan will prevent corneal neovascularization.[2]
References [edit]
- ^ Riazi-Esfahani, M; Peyman, GA; Aydin, E; Kazi, AA; Kivilcim, M; Sanders, DR (2006 Aug). "Prevention of corneal neovascularization: evaluation of various commercially available compounds in an experimental rat model.". Cornea 25 (7): 801–5. PMID 17068457.
- ^ Usui, T.; Sugisaki, K.; Iriyama, A.; Yokoo, S.; Yamagami, S.; Nagai, N.; Ishida, S.; Amano, S. (2008). "Inhibition of Corneal Neovascularization by Blocking the Angiotensin II Type 1 Receptor". Investigative Ophthalmology & Visual Science 49 (10): 4370–4376. doi:10.1167/iovs.07-0964. PMID 18829859.
External links [edit]
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