Contact lens-induced deep corneal
neovascularization with secondary lipid deposition

ICD-10 Diagnosis Codes:

H16.431–Localized vascularization of cornea, right eye
H16.432–Localized vascularization of cornea, left eye
H16.433–Localized vascularization of cornea, bilateral
H16.441–Deep vascularization of cornea, right eye
H16.442–Deep vascularization of cornea, left eye
H16.443–Deep vascularization of cornea, bilateral

Localized Vascularization of Cornea




Corneal neovascularization is the growth of new blood vessels into the cornea.

Corneal neovascularization is a known complication of wearing contact lenses and both superficial and deep corneal neovascularization are reported with the use of hydrogel, PMMA, and rigid gas-permeable contact lenses.

DG37061ABxxx Contact Lens-Induced Corneal Neovascularization

  • Initiating insult can be mechanical in nature, with the contact lens causing irritation to the blood vessels at the limbus
  • Initiating insult can be hypoxic in nature, with the contact lens producing a low oxygen environment tha negatively affects the corneal endothelium and the corneal stroma

Associated Findings

  • A history of overnight contact lens wear
  • Poor compliance with proper contact lens hygiene
  • Poor follow-up care with an eye doctor while wearing contact lenses

 The following clinical circumstances are also associated with the development of corneal neovascularization:

  • Ocular injury
  • Chemical burn to the eye
  • Corneal degenerations
  • Uveitis
  • Glaucoma
  • Total retinal detachment
  • Pthisis bulbi

The histopathological changes needed to produce corneal neovascularization begin when epithelial trauma or chronic hypoxia causes stimulation of angiogenic factors by local epithelial cells, keratocytes and infiltrating leukocytes.  

Contact Lens-Induced Corneal Neovascularization

These angiogenic factors stimulate a localized degradation of the basement membrane of the peri-limbal blood vessels as they abut the cornea.  At the the apex of the vascular loop, the vascular endothelial cells start to migrate and proliferate to form new blood vessels that proliferate into the cornea.

1a (1) 2a 3a
CT_ICD9_370-60_Pic11_062109 Structural Damage to the Eye

  • New blood vessels disrupt the regularity of the collagen lamellae in the corneal stroma
  • Loss of structural regularity in the corneal stroma may produce a loss of corneal transparency
  • Severe presentations may produce corneal scarring
Functional Damage to the Eye

  • Decreased visual acuity secondary to a loss of corneal transparency can occur if the new blood vessels proliferate in to the axial region of the cornea
  • Lipid deposition secondary to deep corneal neovascularization encroaches into the pupillary zone

The main goal of the diagnostic evaluation is a patient with corneal neovascularization is to accomplish the following:

  • Determine the underlying etiology of the corneal neovascularization
  • Classify the disease
  • Prescribe a treatment program to eliminate or reduce to neovascularization
  • Prescribe a treatment program to prevent future occurrences

Patient History

Patients with corneal neovascularization may present with any of the following clinical signs and symptoms:

  • None
  • Chronic eye redness
  • Contact lens intolerance
  • Decreased vision
CT_ICD9_370-60_Pic04_041209 Clinical Appearance of the Bulbar Conjuctiva

  • Contact lens-induced blood vessel engorgement at the limbus may be present
  • Common cause is a contact lens fitting relationship that is too tight
  • Chronic vascular engorgement at the limbus can result in corneal neovascularization
Clinical Appearance of the Bulbar Conjuctiva

  • Blepharoconjunctivitis may produce increased conjunctival redness and corneal neovascularization
  • Patients may ask “Why are my eyes red all the time?”
CT_ICD9_370-60_Pic04_062109 Clinical Appearance of the Cornea

  • Deep corneal neovascularization secondary to contact lens-induced hypoxia
  • New blood vessel encroaches 2-3 mm into the cornea and then loops back towards the limbus

Corneal neovascularization is classified as superficial or deep based on its location in the corneal stroma.

CT_ICD9_370-60_Pic17_062109 Superficial Corneal Neovascularization

  • May occur in a circular pattern around the entire cornea
  • May be isolated to a specific sector
  • Affects the anterior stroma
  • Usually no permanent loss of vision
  • Fan-shaped lesions are common
Deep Corneal Neovascularization

  • Contact lenses are a common cause
  • Stromal scarring can occur secondary to lipid keratopathy
  • Patient is a 24-year-old white male wearing a hybrid contact lens to treat keratoconus
  • 20/40 visual acuity secondary to stromal scarring in the central region of the cornea

This would include any other eye diseases where corneal neovascularization is a clinical sign of the disease but is a manifestation of the primary eye disease.

  • Interstitial keratitis
  • Herpes simplex keratitis
  • Herpes zoster

The key to treating corneal neovascularization is to address the underlying condition that causes the stimulation of angiogenic factors in the cornea.

Phamacologic Treatment

  • Topical steroids can be used for active neovascularization

Mechanical Treatment

  • Discontinue contact lens wear
  • Change cornea-contact lens relationship
CT_ICD9_370-60_Pic15_062109 Look for sources of irritation to the cornea or conjunctiva in contact lens-induced neovascularization

  • Poor contact lens fitting relationship
  • Pinguecula or pterygium affecting contact lens fit
  • Compression ring on conjunctiva after lens removal

Treatment options for contact lens-induced neovascularization

  • Change to silicone-hydrogel contact lenses
  • Change to smaller diameter contact lens
  • Change to looser fitting contact lens
  • Decrease wearing time of contact lenses
  • Decrease or discontinue overnight lens wear if applicable

Surgical Treatment

  • Diathermy of large feeder vessels and corneal laser photocoagulation are surgical options to treat pannus
  • Limbal grafting is a treatment option for severe chemical injuries and limbal epithelial loss 

1.  Bowling EL.  Vital stains in cornea and contact lens practice.  Review of Cornea and Contact Lenses.  2005 Jan/Feb:  25-28.
2.  Silbert JA.  Is it an ulcer or an infiltrate?  RevOptom.  2007 June 15; (6): 91-101.
3.  Edwards K, Brian G, Stretton S, Stapleton F, Willcox MD, Sankaridurg PR, Sweeney DF, Holden BA.  Microbial Keratitis and Silicone Hydrogel Lenses.  Contact Lens Spectrum.  2004 Jan:  38-42.
4.  Snyder C.  Solution Interaction with the Ocular Surface:  The Significance in Making the Grade.  Clinical & Refractive Optometry.  2005; 16(5): 134-140.
5.  Raizman M.  Maintaining Corneal Barrier Integrity.  2007 Oct 15; (10): 5-6.
6.  Karpecki PM.  Much Ado About Staining.  RevOptom.  2006 Nov 15; (11): 135-136.
7.  Bowling E.  Russell GE.  Shovlin JP.  Sindt CW.  Corneal neovascularization.  RevOptom: The Corneal Atlas.  
2009 Jan. 10.

Localized vascularization of cornea

Deep vascularization of cornea

External ocular photography

Specular endothelial microscopy


  • The prevalence of corneal neovascularization is 1% – 20% of the population


  • Corneal neovascularization is distributed evenly throughout the population

Risk Factors

  • Contact lens wear
  • Overnight contact lens wear
  • Low oxygen transmission contact lenses
  • High myopia
  • Ocular surface disease
  • Ocular injury
  • Systemic conditions that affect the ocular surface (i.e., acne rosacea, Sjogren syndrome, immune system dysfunctions)