Excerpt from Neovascularization, Corneal, CL-related

Synonyms, Key Words, and Related Terms: corneal neovascularization, contact lens-related corneal neovascularization, CL-induced corneal NV, NV, corneal NV, contact lens, contact lenses, CL, contact lens wear, CL wear, corneal insults, corneal trauma

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Background: The normal cornea is transparent and maintains itself as an immune privileged site, in part because it is avascular. Neovascularization (NV) of the cornea always represents a state of disease secondary to a variety of corneal insults, including contact lens (CL) wear.

Superficial NV is more common with CL wear 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 extended wear, poor compliance, and poor follow-up care. 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. Hydrogel, hard, and rigid gas permeable CLs stimulate NV by either mechanically irritating the limbal sulcus or by creating corneal hypoxia (stimulating limbal inflammation, epithelial erosion, or hypertrophy).

Epithelial trauma and/or hypoxia may stimulate production of angiogenic factors by local epithelial cells, keratocytes, and infiltrating leukocytes (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 factors 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.

Frequency:

In the US: Prevalence among CL wearers is between 1-20%. The following patients are at increased risk: those with high myopia (nearsightedness), those who have dry eyes or ocular surface disease (eg, idiopathic or associated with other diseases, such as acne rosacea, Sjögren syndrome, and immune dysfunction), those who use extended wear hydrogel CLs, and 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, 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.

Race: No ethnic predilection exists.

Sex: No gender predilection exists.

Age: NV can occur and progress at any age.