An important pathologic change common to eyes with pathologic myopia is the development of CNV. Early manifestations of CNV in pathologic myopia include decreased or distorted vision. The clinical findings include subretinal hemorrhage, elevation and infiltration of the outer retina by vascular invasion, accumulation of subretinal fluid, and a localized area of pigmentary change. It is easy to overlook the findings of CNV in highly myopic eyes using ophthalmoscopy alone.
Figure 10-3 Myopic choroidal neovascularization (CNV) emanating from a lacquer crack. A, A patient with –16 diopter myopia developed a small scotoma near the center of the visual field. Note the lacquer cracks (arrow) and associated pigmentary changes (arrowhead). B, Fluorescein angiography image shows a hyperfluorescent lesion consistent with CNV. C, OCT scan shows a small elevated lesion (arrow) and also nonassociated macular schisis.
(Used with permission from Spaide RF. Choroidal Neovascularization. In: Spaide RF, Ohno-Matsui K, Yannuzzi LA, eds. Pathologic Myopia. New York: Springer-Verlag; 2014: 211–230.)
The size and apparent exudation of CNV appears to vary inversely with the amount of myopia. Myopic CNV does not cause retinal edema as commonly as age-related macular degeneration does. Myopic CNV is often seen in close association with lacquer cracks, or it may occur as an extension from a region of chorioretinal atrophy. In the United States, it is not uncommon to find CNV in young myopic women who show signs of multifocal choroiditis and panuveitis, either at the time or later. These eyes may develop damage from the CNV, from inflammation, or from both; each component requires careful treatment. Myopic CNV was first treated with thermal laser photocoagulation and then later treated with photodynamic therapy, but both approaches were suboptimal. The advent of injections of anti–vascular endothelial growth factor (anti-VEGF) agents was a major advance; this treatment caused regression of the neovascularization without causing immediate collateral damage (Fig 10-4). To control the CNV, episodic reinjection of medications may be necessary. Some patients may need frequent reinjections, including patients with CNV developing at the edge of a staphyloma or with untreated multifocal choroiditis and panuveitis. With or without treatment, CNV in pathologic myopia may become hyperpigmented; this lesion is called a Fuchs spot. With longer follow-up, areas of atrophy often develop at or adjacent to the pigmented lesions, and the atrophy eventually encompasses the central macula.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.