Corneal neovascularization

Corneal neovascularization
Classification and external resources
Specialty ophthalmology
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.


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]


Chemical theory

There may be presence of vasostimulatory factor (VSF) or the breakdown (destruction) of previously existing vasoinhibitory factor (VIF).[2]

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 theory

Both release of some vasostimulatory factor (VSF) and structural loosening of compact corneal stroma by oedema are necessary for the neovascularization to occur.[3]


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.


In advanced stages, corneal neovascularization can threaten eyesight, which is why eye routine (annual) exams are recommended for contact lens patients.


Reduction of neovascularization has been achieved in rats by the topical instillation of commercially available triamcinolone and doxycycline.[4]

Some evidence exists to suggest that the Angiotensin II receptor blocker drug telmisartan will prevent corneal neovascularization.[5]

Recent treatment developments include, topical application of bevacizumab, an anti-VEGF.[6]


  1. Abdelfattah, NS; Amgad, M; Zayed, AA; Salem, H; Elkhanany, AE; Hussein, H; Abd El-Baky, N (2015). "Clinical correlates of common corneal neovascular diseases: a literature review.". International journal of ophthalmology. 8 (1): 182–93. doi:10.3980/j.issn.2222-3959.2015.01.32. PMID 25709930.
  2. Abdelfattah NS, Amgad M, Zayed AA, Hussein H, Abd El-Baky N. Molecular underpinnings of corneal angiogenesis: advances over the past decade. Int J Ophthalmol. 2016 May 18;9(5):768-79
  3. Abdelfattah NS, Amgad M, Zayed AA. Host immune cellular reactions in corneal neovascularization. Int J Ophthalmol. 2016 Apr 18;9(4):625-33.
  4. 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.
  5. 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.
  6. Cheng, Sheng-Fu; Dastjerdi, Mohammad H.; Ferrari, Giulio; Okanobo, Andre; Bower, Kraig S.; Ryan, Denise S.; Amparo, Francisco; Stevenson, William; Hamrah, Pedram; Nallasamy, Nambi; Dana, Reza (December 2012). "Short-Term Topical Bevacizumab in the Treatment of Stable Corneal Neovascularization". American Journal of Ophthalmology. 154 (6): 940–948.e1. doi:10.1016/j.ajo.2012.06.007.
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