Posterior Vitreous Detachment

The vitreous is a transparent connective tissue composed of collagen and hyaluronan that is attached to the basal lamina of the lens, optic nerve, and retina, and fills the vitreous cavity of the eye. A posterior vitreous detachment (PVD) is the separation of the posterior cortical gel from the retinal surface, including its adhesions at the optic nerve head (the area of Martegiani), the macula, and blood vessels. At its base, the vitreous remains firmly attached to the retina—even after severe trauma—sometimes resulting in vitreous base avulsion. Because of this firm attachment, the basal cortical vitreous collagen cannot be peeled off the retina; instead, the vitreous must be “shaved” during vitrectomy, instead of being removed. See Chapter 16 in this volume for more on PVD.

With advancing age, the vitreous gel undergoes both liquefaction (synchysis) and collapse (syneresis). The viscous hyaluronan accumulates in lacunae, which are surrounded by displaced collagen fibers. The gel can then contract, possibly because of electrostatic attraction and crosslinking of adjacent collagen fibers in the absence of hyaluronan. With this contraction, the posterior cortical gel detaches toward the firmly attached vitreous base. The prevalence of PVD is increased in patients who have had cataract extractions, particularly if the posterior capsule’s integrity has been violated. Prevalence is also increased in individuals with a history of vitritis because of the loss or alteration of hyaluronan. Localized regions of the posterior cortical gel can separate slowly, over the course of many years, with few if any symptoms, compared with the more acute, symptomatic event.

The diagnosis of PVD is often made with indirect ophthalmoscopy or slit-lamp biomicroscopy, with which the posterior vitreous face may be observed a few millimeters in front of the retinal surface. In eyes with a PVD, a translucent ring of fibroglial tissue (the “Weiss” or “Vogt” ring) is frequently torn loose from the surface of the optic nerve head, and its observation helps the clinician make the diagnosis. Although a shallow detachment of the posterior cortical gel may be difficult or impossible to observe with biomicroscopy, this type of detachment may be revealed on contact B-scan ultrasonography as a thin, hyperreflective line bounding the posterior vitreous. Optical coherence tomography (OCT) has shown that PVDs often start as a localized detachment of the vitreous over the perifovea, called a posterior perifoveal vitreous detachment, later spreading anteriorly to involve larger areas.

Figure 17-1 A 3-dimensional rendering of spectral-domain optical coherence tomography (SD-OCT) imaging of vitreomacular traction (VMT) syndrome. The cone of vitreous is attached to and elevates the central fovea.

(Courtesy of Richard F. Spaide, MD.)

Persistent focal attachment of the vitreous to the retina can cause a number of pathologic conditions. Vitreous contraction as well as traction caused by ocular saccades may lead to breaks, particularly at the posterior edge of the vitreous base. Persistent attachment to the macula may lead to vitreomacular traction syndrome. Focal attachment to the foveola can induce foveal cavitation and macular hole formation (Fig 17-1). Remnants of the vitreous often remain on the internal limiting membrane (ILM) after a posterior vitreous “detachment.” For this reason, some authorities state that a presumed PVD often is actually posterior vitreoschisis that is internal or external to the layer of hyalocytes. These vitreous remnants may have a role in epiretinal membrane or macular hole formation and can contribute to tractional detachments in patients with pathologic myopia and to macular edema in patients with diabetes mellitus. Plaques of these adherent remnants of cortical vitreous can often be highlighted during vitreous surgery by applying triamcinolone (Fig 17-2).

• Gupta P, Yee KM, Garcia P, et al. Vitreoschisis in macular diseases. Br J Ophthalmol. 2011;95(3):376–380.

• Sakamoto T, Ishibashi T. Hyalocytes: essential cells of the vitreous cavity in vitreoretinal pathophysiology? Retina. 2011;31(2):222–228.

Epiretinal Membranes

An epiretinal membrane (ERM) is a transparent, avascular, fibrocellular membrane on the inner retinal surface that adheres to and covers the ILM of the retina. Proliferation of glia, retinal pigment epithelium (RPE), or hyalocytes at the vitreoretinal interface, especially at the posterior pole, results in ERM formation.

Figure 17-2 Visualization of a thin layer of adherent vitreous during vitrectomy with the use of triamcinolone. This patient appeared to have a posterior vitreous detachment (PVD) and underwent a vitrectomy. A, A small amount of triamcinolone was injected into the vitreous cavity; the excess was aspirated from the surface of the retina, leaving a fine distribution of triamcinolone sticking to the adherent vitreous. B, The vitreous membrane was elevated using a diamond-dusted silicone scraper. Note that the vitreous is difficult to see; the sheet of triamcinolone is the clue to its presence. C, A wide-angle viewing system then was used to visualize the elevation of the adherent vitreous, and the vitrector was set to suction only. D, Note the extent of the adherent vitreous sheet, which was removed with the vitrector set to cut.

(Courtesy of Richard F. Spaide, MD.)

ERMs are relatively common; at autopsy, they are discovered in 2% of patients older than 50 years and in 20% older than 75 years. ERMs are most common in persons over age 50 years, and both sexes are equally affected. The incidence of bilaterality is approximately 10%–20%, and severity is usually asymmetric. Detachment or separation of the posterior vitreous is present in almost all eyes with idiopathic epiretinal membranes, and may be a requisite for ERM development. Schisis of the posterior vitreous may leave variable portions of the posterior cortical vitreous attached to the macula, allowing glial cells from the retina to proliferate along the retinal surface and hyalocytes to proliferate on posterior cortical vitreous remnants on the retinal surface. Secondary ERMs occur regardless of age or sex in association with abnormal vitreoretinal adhesions and areas of inflammation, as well as following retinal detachment or retinal bleeding.

Figure 17-3 Epiretinal membrane (ERM). A, Scanning laser ophthalmoscope 30° fundus reflectance multicolor image reveals an ERM in the central macula with radiating striae of the internal limiting membrane (ILM) in the superior, temporal, and inferior macula. The colors in reflectance multicolor images are not exactly true to life. B, OCT scan through the fovea shows increased retinal thickening and cystoid edema with a large central cyst. The ERM is distorting the retinal surface temporally, which appears as several small optical voids between the ERM and the retina.

(Courtesy of Colin A. McCannel, MD.)

Signs and symptoms

Epiretinal proliferation is generally located in the central macula—over, surrounding, or eccentric to the fovea (Fig 17-3). The membranes usually appear as a mild sheen or glint on the retinal surface. Over time, ERMs become more extensive, increasing retinal distortion and thickening (Figs 17-4 and 17-5; Activities 17-1 and 17-2). However, their rate of progression and severity vary greatly. In some cases, the ERM may become opaque, obscuring underlying retinal details. A “pseudohole” appearance is produced when this preretinal membrane contracts to the edge of the clivus, steepening the gentle slope around the fovea into a cylindrical depression. Occasionally, intraretinal hemorrhages or whitened patches of superficial retina representing delayed axoplasmic flow in the nerve fiber layer (NFL) and edema may be present. The cellular origin of ERMs is still under debate. Histologic examination reveals mainly RPE cells and retinal glial cells (astrocytes and Müller cells); however, myofibroblasts, fibroblasts, hyalocytes, and macrophages have also been identified.

Figure 17-4 SD-OCT line cube scan of the right macula of a 61-year-old woman with ERM. The visual acuity at the time of the scan was 20/30. A loss of foveal depression can be appreciated. The outer nuclear layer is thickened and peaks toward the retinal surface. The infrared reflectance image (left) shows the surface wrinkling with striae radiating outward from the central macula with the ERM. See also Activity 17-1.

(Courtesy of Colin A. McCannel, MD.)

Figure 17-5 ERM progression. SD-OCT image of a patient’s right macula with ERM that has developed over the previous 5 years. The ERM expanded and eventually covered the fovea with a secondary complete loss of foveal depression. In this patient, the ERM and retinal thickness did not change much after the fovea was covered. Visual acuity was initially 20/20, but declined slightly to 20/25 at the time the foveal contour was lost and has remained stable during follow-up. See also Activity 17-2.

(Courtesy of Colin A. McCannel, MD.)

ACTIVITY 17-1 OCT Activity: Epiretinal membrane.

Courtesy of Colin A. McCannel, MD.

Access all Section 12 activities at www.aao.org/bcscactivity_section12.

ACTIVITY 17-2 OCT Activity: Epiretinal membrane progression.

Courtesy of Colin A. McCannel, MD.

Contracture of ERMs produces distortion and wrinkling of the inner surface of the retina, called cellophane maculopathy or preretinal macular fibrosis. It can range from mild to severe, with wrinkling or striae to severe macular puckering. Increased traction may cause shallow macular detachment, diffuse thickening, or cystic changes. Furthermore, traction on retinal vessels results in increased vascular tortuosity and straightening of the perimacular vessels. Fluorescein angiography (FA) may show staining of the optic nerve and capillary leakage in the central macula. The most common OCT findings are a highly reflective epiretinal reflective layer, loss of the normal retinal contour, and retinal thickening. Additional findings include irregularities of the inner retinal surface and cystic edema.

Treatment

When ERMs are asymptomatic and visual acuity is good, intervention is not indicated. Asymptomatic ERMs should be monitored periodically, because they will often worsen, sometimes over a relatively short period of time, after being stable. In rare cases, an ERM may spontaneously detach from the inner retinal surface, with concomitant improvement or resolution of the retinal distortion and improvement in symptoms and vision. If the patient is bothered by reduced visual acuity or metamorphopsia, vitrectomy should be considered (see also Chapter 20). The goal of surgery is to optimize visual acuity, reduce metamorphopsia, and restore binocularity if it was affected preoperatively.

• Johnson TM, Johnson MW. Epiretinal membrane. In: Yanoff M, Duker JS. Ophthalmology. 4th ed. St Louis: Elsevier; 2014:614–619.

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.