NV is believed to result from an inflammatory or hypoxic disruption of an exquisitely balanced corneal immune system. Angiogenic factors stimulate a localized enzymatic degradation of the basement membrane of perilimbal vessels at the apex of a vascular loop. Vascular endothelial cells then migrate and proliferate to form new blood vessels. Any NV of 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 non-vascularized host corneas.
Patients are almost always asymptomatic unless the central visual axis is involved.
There is often a history of poor compliance with proper contact lens wear and care. The contact lenses may be tight. It can be seen in direst illumination or in retroillumination as a continuum of the limbal peripheral vessel arcades. Deeper stromal vessels emerge through the cornea as straight vessels which arborize, occasionally accompanied by nerve fibers. Lipid deposition appears as yellow-white opacities at the leading edge, or surrounding, the stromal vessels.