Posterior Vitreous Detachment
Posterior vitreous detachment (PVD) occurs when a dehiscence in the vitreous cortex allows fluid from a syneretic cavity to enter the potential subhyaloid space, causing the remaining hyaloid face to be stripped from the internal limiting membrane (ILM) of the retina (Fig 10-7). As fluid drains out of the syneretic cavities under the newly formed posterior hyaloid, the vitreous body collapses anteriorly, remaining attached at its base. Vitreous detachment generally occurs rapidly over the course of a few hours to days. Occasionally, traction may occur on the peripheral retina, perifoveal macula, or retinal blood vessels as a PVD occurs.
Figure 10-6 Gross photograph demonstrates vitreous condensations outlining syneretic cavities.
(Courtesy of Hans E. Grossniklaus, MD.)
Figure 10-7 Gross photograph showing a posterior vitreous detachment. Retraction of the vitreous from the posterior retina is seen.
(Courtesy of Hans E. Grossniklaus, MD.)
An age-related weakening of the adherence of the cortical vitreous to the ILM also plays a role in PVDs. The prevalence of PVD in individuals aged 70 years and older has been reported as 50% or higher in clinical and pathologic studies. The incidence of PVD is increased in persons with intraocular inflammation, aphakia or pseudophakia, trauma, myopia, or vitreoretinal diseases. PVD is important in the pathogenesis of many conditions, including retinal tears and detachment, macular hole formation, and vitreous hemorrhage. See BCSC Section 12, Retina and Vitreous, for additional discussion of these conditions.
Retinal tears and potential sequelae
Retinal tears (breaks) are often the result of vitreous traction on the retina during or after a PVD or secondary to ocular trauma. Tears are most likely to occur at sites of greatest vitreoretinal adhesion, such as the vitreous base (Fig 10-8) or the margin of lattice degeneration. The vitreous base extends anteriorly from the ora serrata (approximately 2 mm) over the ciliary body, and posteriorly (about 4 mm) over the peripheral retina. Histologic examination of retinal tears reveals that the vitreous adheres to the retina along the flap of the tear. In the area of retina separated from the underlying retinal pigment epithelium (RPE), there is loss of photoreceptors.
Rhegmatogenous retinal detachment (RRD) occurs when vitreous traction and fluid currents resulting from eye movements combine to overcome the forces maintaining retinal adhesion to the RPE. With an RRD, cellular membranes may form on either surface (anterior or posterior) of the retina (Fig 10-9). Clinically, this process is referred to as proliferative vitreoretinopathy (PVR). These membranes, which often have a contractile component, form as a result of proliferation of RPE cells and other cellular elements, including glial cells (Müller cells, fibrous astrocytes), histiocytes, fibroblasts, myofibroblasts, and possibly hyalocytes. The cell biology of PVR is complex and involves the interaction of various growth factors and integrins, as well as cellular proliferation. Studies have shown a significant association between clinical grades of PVR and the expression levels of specific cytokines and/or growth factors in the vitreous fluid.
Figure 10-8 Peripheral retinal tears. A, The gross photograph shows several retinal tears at the vitreous base. B, The photomicrograph demonstrates condensed vitreous (arrow) attached to the anterior flap of the retinal tear.
(Courtesy of W. Richard Green, MD.)
Figure 10-9 Preretinal membrane (area between arrows) on the surface of the retina, secondary to proliferative vitreoretinopathy.
(Courtesy of David J. Wilson, MD.)
Idiopathic macular holes most likely form as the result of degenerative changes in the vitreous. Optical coherence tomography (OCT) has greatly advanced our understanding of the anatomical features of full-thickness macular holes and early macular hole formation. The results of these studies are most consistent with a focal vitreomacular traction mechanism. Localized perifoveal vitreous detachment (an early stage of age-related PVD) appears to be the primary pathogenetic event in idiopathic macular hole formation (Fig 10-10). Detachment of the posterior hyaloid from the pericentral retina exerts anterior traction on the foveola and localizes the dynamic vitreous traction associated with ocular rotations into the perifoveolar region.
OCT has clarified the pathogenesis of macular holes, particularly the early stages: a foveal pseudocyst (stage 1A) is typically followed by disruption of the outer retina (stage 1B) before progressing to a full-thickness dehiscence (stage 2). Histologically, full-thickness macular holes are similar to holes in other locations. A full-thickness retinal defect with rounded tissue margins (stage 3) is accompanied by loss of the photoreceptor outer segments in adjacent retina, which is separated from the RPE by subretinal fluid (see Fig 10-10C). An epiretinal membrane composed of Müller cells, fibrous astrocytes, and myofibroblasts is often present on the surface of the retina adjacent to the macular hole. Cystoid macular edema in the parafoveal retina adjacent to the full-thickness macular hole is relatively common. Following surgical repair of macular holes, closer apposition of the remaining photoreceptors and variable glial scarring close the macular defect. See BCSC Section 12, Retina and Vitreous, for further discussion.
Smiddy WE, Flynn HW Jr. Pathogenesis of macular holes and therapeutic implications. Am J Ophthalmol. 2004;137(3):525–537.
Steel DHW, Lotery AJ. Idiopathic vitreomacular traction and macular hole: a comprehensive review of pathophysiology, diagnosis, and treatment. Eye. 2013;27(Suppl 1):S1–S21.
Excerpted from BCSC 2020-2021 series: Section 4 - Ophthalmic Pathology and Intraocular Tumors. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.