eMedicine Specialties > Ophthalmology > Cornea

Neovascularization, Corneal, CL-related

Author: Barry A Weissman, OD, PhD, FAAO, Chief of Contact Lens Service, Professor, Department of Ophthalmology, Jules Stein Eye Institute, University of California at Los Angeles
Coauthor(s): Karen K Yeung, OD, FAAO, Director of Optometry, Arthur Ashe Student Health and Wellness Center, University of California at Los Angeles
Contributor Information and Disclosures

Updated: Apr 10, 2009

Introduction

Background

The normal cornea is transparent and maintains itself as an immune privileged site, in part because it is avascular. Ocular insult, including infectious keratitis, immunological conditions, corneal trauma, alkali injury, and contact lens wear (CL),1,2 can encourage new blood vessels to grow from the limbus and, hence, neovascularization (NV). NV is generally accompanied with an inflammatory response and always represents a state of disease. 

With CL wear, superficial NV is more common than deep stromal vessels. It is speculated that deep stromal NV may reflect a more profound insult (hypoxia) compared to that which generates only superficial NV. Both superficial and deep stromal NV are reported with the use of hydrogel, hard (polymethyl methacrylate [PMMA]), and rigid gas permeable CLs, especially with a history of aphakia, extended wear, poor compliance, and poor follow-up care.3 Deep stromal NV is serious, possibly leading to loss of optical transparency of the tissue through stromal hemorrhage, scarring, and lipid deposition.

Pathophysiology

NV is believed to result from an inflammatory or hypoxic disruption of an exquisitely balanced corneal immune system.4,5,6 Hydrogel, hard, and rigid gas permeable CLs stimulate NV by either mechanically irritating the limbal sulcus or by creating corneal hypoxia, which leads to limbal inflammation, epithelial erosion, or hypertrophy, and, hence, angiogenic mediator release.7

Epithelial trauma8 and/or hypoxia9 may stimulate production of angiogenic factors by local epithelial cells, keratocytes, and infiltrating leukocytes10,11 (eg, macrophages, neutrophils). Some of these factors (ie, acidic and basic fibroblast growth factors, interleukin 1 [IL-1], and vascular endothelial growth factor [VEGF]) have been identified and isolated from cornea and tears. Angiogenic factors12 stimulate a localized enzymatic degradation of the basement membrane of perilimbal vessels at the apex of a vascular loop. Vascular endothelial cells migrate and proliferate to form new blood vessels.13

Frequency

United States

Prevalence among CL wearers is 1-30%; prevalence is lower in those who wear gas permeable lenses than in soft CL wearers.14 There is an increased risk for patients who have high myopia, dry eyes, or ocular surface disease (eg, idiopathic or associated with other diseases, such as acne rosacea, Sjögren syndrome, and immune dysfunction). There is also an increased risk in those who use extended wear hydrogel CLs and in those who use aphakic or therapeutic CLs.

Silicone hydrogel CLs with oxygen permeabilities approaching 100-200 Fatt Dk units have decreased the incidence of corneal NV among CL users.

Mortality/Morbidity

  • This condition is not associated with mortality. Symptoms can range from asymptomatic and mild to severe with loss of vision. NV in the cornea's visual axis can threaten visual function directly or through secondary hemorrhage,15 scarring, or lipid deposition.
  • Incidence of subsequent corneal graft rejection is estimated by one study to be 1.7 times higher in a setting of vascularized rather than nonvascularized host corneas. Risk and severity of a graft rejection is believed to depend upon the depth and extent of NV; hence, deep stromal vessels incur more risk than superficial pannus, and the more quadrants involved, the higher the risk of rejection.16

Race

No ethnic predilection exists.

Sex

No gender predilection exists.

Age

NV can occur and progress at any age.

Clinical

History

  • Patients are almost always asymptomatic unless the central visual axis is involved.
  • Patients with CL-induced NV are often aphakic or report a history of sleeping or napping with their CLs on their eyes in an extended wear modality.
  • Often, a history of poor compliance with proper CL wear and care is present. The CLs may be tight.

Physical

  • NV can be observed in the cornea via slit lamp biomicroscopy. It can be seen in direct illumination or in retroillumination as a continuum of the limbal peripheral vessel arcades. Measuring both the extent and the depth of the corneal NV is important.
    • Superficial vessels emerge in the anterior stroma and appear as single or multiple (pannus) tortuous vessels under low magnification.
    • Deeper stromal vessels emerge through the cornea as straight vessels that arborize, occasionally accompanied by nerve fibers.
    • Active engorged vessels, occasionally surrounded by lipid exudates and exceeding 1-2 millimeters in length from the limbus, should raise concern.
    • Lipid deposition appears as yellow-white opacities at the leading edge or surrounding the stromal vessels.
    • Careful gonioscopy in eyes with deep NV rules out an iris angle choroidal tumor.
    • NV also should be differentiated at clinical examination from a conjunctival carcinoma extending onto the corneal epithelium.
  • Measurement of corneal sensation can be helpful in differentiating CL-related NV from a herpes simplex virus (HSV) keratitis (typically reduced sensation with HSV).

Causes

  • All CLs, including extended-wear hydrogel, daily-wear hydrogel, hard, and rigid gas permeable CLs, can cause corneal NV. NV primarily is related to corneal hypoxia from CL wear and chronic corneal desiccation associated with the edges or rigid lenses.

More on Neovascularization, Corneal, CL-related

Overview: Neovascularization, Corneal, CL-related
Differential Diagnoses & Workup: Neovascularization, Corneal, CL-related
Treatment & Medication: Neovascularization, Corneal, CL-related
Follow-up: Neovascularization, Corneal, CL-related
References
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References

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Further Reading

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Keywords

cornea, contact lens, neovascularization, corneal trauma

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Contributor Information and Disclosures

Author

Barry A Weissman, OD, PhD, FAAO, Chief of Contact Lens Service, Professor, Department of Ophthalmology, Jules Stein Eye Institute, University of California at Los Angeles
Barry A Weissman, OD, PhD, FAAO is a member of the following medical societies: American Academy of Optometry, American Optometric Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Karen K Yeung, OD, FAAO, Director of Optometry, Arthur Ashe Student Health and Wellness Center, University of California at Los Angeles
Karen K Yeung, OD, FAAO is a member of the following medical societies: American Academy of Optometry
Disclosure: Nothing to disclose.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Christopher J Rapuano, MD, Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Co-Chairman of the Cornea Service, Co-Chairman of Refractive Surgery Department, Wills Eye Institute
Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, International Society of Refractive Surgery, and Pan-American Association of Ophthalmology
Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; Inspire Honoraria Speaking and teaching; RPS Ownership interest Other; Vistakon Honoraria Speaking and teaching

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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