In the central macula, the retinal thickness in eyes with pathologic myopia is not that different from that in emmetropic eyes, particularly in younger individuals. In older subjects with marked thinning of the choroid, there may be loss of the outer retinal bands and apparent thinning of the central macula (Fig 10-1). Outside of the macula, the retinal thickness in eyes with pathologic myopia is thinner than that in emmetropic eyes. Lattice degeneration is more commonly found in myopic eyes. With increasing age, the vitreous starts to detach in all eyes, starting with smaller areas of detachment bordering areas of attachment; this is also true for myopic eyes. Vitreous traction in areas of persistent attachment can cause retinal tears and then detachment, or may even cause subretinal fluid to occur in association with small atrophic holes in lattice degeneration. The proportion of retinal detachment secondary to holes as compared with tears increases with more exaggerated amounts of myopia. Repairing retinal detachment may be more difficult in patients with high myopia because of the thinner retina, a higher prevalence of lattice degeneration, the thinner sclera (which can complicate buckle placement), the more posterior location of retinal breaks, and the possibility of multiple retinal defects.
Traction on the retina in eyes with larger amounts of myopia can affect broader areas of the retina, independent of vitreous attachment. The posterior portion of the retina can remain attached to the retinal pigment epithelium (RPE) despite broad areas of traction. Retinal thickness increases because of the fluid accumulation within the retina and distention of the cellular elements in the retina.
Figure 10-1 Swept-source optical coherence tomography (SS-OCT) image demonstrates some of the many abnormalities that can be present in a highly myopic eye. The magnitude and thickness of the reflection from the ellipsoid layer (arrowheads) shows a rough correlation to the thickness of the underlying choroid, but do vary with the location in the image because of a number of factors, including defocus of the illumination beam and astigmatism. The subfoveal choroid is 15 μm thick and the subfoveal sclera is 78 μm thick. Both measurements are less than 10% of their expected values. The layers of this eye are so thin that it is possible to image structures in the orbit behind the eye, including blood vessels. Note the unusual shape of the eye, which is due to the presence of a staphyloma.
(Courtesy of Richard F. Spaide, MD.)
Myopic macular schisis most commonly involves Henle fiber layer but can also involve the inner nuclear layer, the ganglion cell layer, and the region underneath the internal limiting membrane (ILM). The traction can be related to vitreous traction from attached vitreous, but eyes with myopic macular schisis can still have vitreous traction with posterior vitreous detachment (Fig 10-2). Myopic macular retinoschisis can occur in eyes with posterior vitreous detachment that, at the time of surgery, are found to have minimal amounts of adherent residual vitreous. After posterior vitreous detachment, a skim coat of vitreous remains on the surface of the retina and appears to cause traction. Varying amounts of epiretinal membrane may also contribute to the traction. Peeling of the ILM causes resolution of the schisis, typically near the area where the ILM was peeled, leading to the conclusion the ILM may be altered in eyes with myopic macular retinoschisis. An alternate possibility is that many of these eyes have progressive myopia with continued ocular expansion. The ILM may not necessarily be remodeled, and thus it may not expand like the outer retina.
More advanced tractional changes can lead to retinal detachment over staphylomas and to myopic macular holes. Macular holes in eyes with high myopia have a lower proportion of successful repair than in emmetropic eyes and frequently require the use of the inverted ILM technique in which the ILM is folded over the hole prior to fluid gas exchange. In addition, in eyes with high myopia macular holes may lead to extensive or complete retinal detachment (see Chapter 16, Fig 16-20 in this volume).
Traction appears to affect the retinal vessels in pathologic myopia. The retinal vessels can straighten, particularly the maculopapillary bundle, with occasional microaneurysm formation, and there can be a slight elevation of the arcade vessels. Paravascular cavitations and lamellar holes may also be found, but these defects do not appear to have any clinically meaningful effect.
Figure 10-2 Successive OCT examinations of a female patient with myopic macular schisis. At presentation, the patient had a perifoveal vitreous detachment (A) that separated (B). C, Four months later, a larger fovea cavitation developed. D, One month after that, a localized detachment of the fovea occurred. E, One month after the image in D was taken, the detachment was slightly larger (F). G, At 4-month follow-up, the macular detachment had increased in size. H, One month later, she returned with a substantial loss of central vision. Imaging revealed a large retinal detachment with edematous folding of the outer retina. I, A small macular hole caused the larger detachment (arrow). J, The macular hole was repaired by vitrectomy with internal limiting membrane removal, which resulted in resolution of the retinal detachment and the myopic macular schisis.
(Courtesy of Richard F. Spaide, MD.)
Located between the RPE and the choriocapillaris, Bruch membrane forms early in the development of the eye and appears to undergo varying amounts of remodeling over time. However, this may not be true in eyes with more advanced amounts of myopia. In these eyes, the Bruch membrane opening shifts so that the nasal portion of the optic nerve head is undermined by Bruch membrane. The nerve fibers must course around the nasal portion of the Bruch membrane opening; this has been referred to as “supertraction” or “supertraction crescent.” Corresponding temporal displacement of the posterior part of Bruch membrane opening is related to the myopic macular crescent typically located on the temporal side of the optic nerve. The lack of choroidal circulation in this region creates a white appearance due to the visualization of the sclera.
Ocular expansion puts stress on Bruch membrane, potentially leading to fine ruptures called lacquer cracks. The outer lamella of Bruch membrane is the basement membrane of the choriocapillaris. The cracks disrupt not only the avascular membrane, but may also rupture the capillaries in the choriocapillaris, resulting in subretinal hemorrhages. These hemorrhages can be difficult to differentiate from those caused by choroidal neovascularization (CNV), which is discussed in the following section. Lacquer cracks offer a region of ingress for CNV (Fig 10-3). Extension of lacquer cracks through the center of the fovea can cause distortion and loss of visual acuity. If many lacquer cracks develop, a region of pigmentary granularity can form. In late-stage myopic degeneration, large dehiscences in Bruch membrane may occur.
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.