Neovascularization, Corneal, CL-related Clinical Presentation
- Author: Barry A Weissman, OD, PhD, FAAO; Chief Editor: Hampton Roy Sr, MD more...
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 (eg, wear extended intentionally or unintentionally through multiple sleep cycles) and care is present. Alternatively, the CLs may be "tight" (eg, restrict tear exchange).
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/or chronic corneal desiccation associated with the edges or rigid lenses.
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