Corneal neovascularization

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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.

Pathogenesis[edit]

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.

Etiology[edit]

Corneal neovascularization can be elicited by a variety of causes, such as, Corneal infections. Corneal infections may be Bacterial, Viral, Fungal or Protozoal. Corneal neovascularization can also result from corneal inflammation (Keratitis) and chemical and physical trauma. 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. Veteran contact lens wearers can be relieved within a few days simply by removing their lenses if the condition is not too severe.

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] Subconjunctival injection of bevacizumab can regress corneal neovascularization.[3]

References[edit]

  1. ^ Riazi-Esfahani, M; Peyman, GA; Aydin, E; Kazi, AA; Kivilcim, M; Sanders, DR (August 2006). "Prevention of corneal neovascularization: evaluation of various commercially available compounds in an experimental rat model.". Cornea 25 (7): 801–5. doi:10.1097/01.ico.0000220768.11778.60. PMID 17068457. 
  2. ^ 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.  edit
  3. ^ Zeynep Ozbek, Rukiye Aydin, Ozlem Barut Selver, et al. Can Subconjunctival Bevacizumab Injection Regress Corneal Neovascularization? Pak J Ophthalmol 2013, Vol. 29 No. 1

External links[edit]