This chapter reviews the most common lesions and antecedent events that lead to the development of retinal breaks and the subsequent mechanism of retinal detachment. After reading the chapter, the reader should be comfortable with the diagnosis and management of retinal detachment and its predisposing lesions.
Posterior Vitreous Detachment
The vitreous gel is attached most firmly at the vitreous base, a circumferential zone straddling the ora serrata that extends approximately 2 mm anterior and 4 mm posterior to the ora. Vitreous collagen fibers at this base are so firmly attached to the retina and pars plana epithelium that the vitreous cannot be separated without tearing these tissues. The vitreous is also firmly attached at the margin of the optic nerve head, at the macula, along major vessels, at the margins of lattice degeneration, and at chorioretinal scars.
Most retinal tears result from traction caused by spontaneous or traumatic posterior vitreous detachment (PVD) (Fig 16-1). The predisposing event is syneresis (collapse) of the central vitreous. There is increasing evidence that age-related PVD is insidious and slowly progressive over many years. A PVD typically begins with a shallow separation in the perifoveal cortical vitreous. Liquid vitreous enters through a cortical tear and detaches the macular vitreous cortex, causing a partial vitreous detachment. The early stages are usually asymptomatic and occult; in most eyes, the evolving PVD remains subclinical for years until separation from the optic nerve head margin (the area of Martegiani) occurs. This separation from the optic nerve head is often accompanied by symptoms associated with the appearance of a Weiss ring. The vitreous gel remains attached at the vitreous base. Vitreous traction on the retina can produce a retinal break, usually at the posterior edge of the vitreous base (Fig 16-2).
The prevalence of PVD increases with age. Other conditions associated with vitreous syneresis, synchysis (liquefaction), and PVD include aphakia, pseudophakia with open posterior capsule, inflammatory disease, trauma, vitreous hemorrhage, and axial myopia. Whether the vitreous is attached to or separated from the surface of the retina may be difficult to determine using biomicroscopy. Clinical studies typically reveal a low incidence of PVD in patients younger than 50 years. Autopsy studies demonstrate PVD in fewer than 10% of patients under age 50 years but in 63% of those over age 70 years.
Figure 16-1 Posterior vitreous detachment. Color fundus photograph (A) shows attached vitreous and (B) shows an acute Weiss ring over the fovea with obscuration (arrow) occurring several days later.
(Courtesy of Stephen J. Kim, MD.)
Figure 16-2 Schematic representations of mechanisms of retinal tear formation associated with posterior vitreous separation. A, Round or oval hole. B, Flap tear: posterior extension of vitreous base with firm vitreoretinal attachment.
(Illustration by Christine Gralapp, based on illustrations by Tim Hengst.)
Many patients do not report acute symptoms when a PVD occurs. Symptoms of PVD at the initial examination include the entoptic phenomena of photopsias (flashing lights), multiple floaters, and the appearance of a curtain or cloud across the visual field. Patients with these symptoms should be examined promptly, and office staff should be made aware of the urgency of these symptoms. Photopsias are caused by the physical stimulus of vitreoretinal traction on the retina. Floaters are caused by vitreous opacities such as blood, glial cells torn from the optic nerve head, or aggregated collagen fibers, all of which can cast shadows on the retina.
Vitreous hemorrhage may arise from avulsion of superficial retinal or prepapillary vessels or from rupture of retinal vessels that cross retinal tears. Important predictors of subsequent new retinal breaks are vitreous hemorrhage at the initial examination and an increase in the number of floaters after the initial examination. Overall, 7%–18% of all patients with acute symptomatic PVD have retinal tears. If vitreous hemorrhage is present, then 50%–70% have retinal tears, versus only 7%–12% without vitreous hemorrhage. Patients with an acute PVD complicated by a retinal tear are 7 times more likely to present with vitreous pigment or granules than are those without a tear.
van Overdam KA, Bettink-Remeijer MW, Klaver CC, Mulder PG, Moll AC, van Meurs JC. Symptoms and findings predictive for the development of new retinal breaks. Arch Ophthalmol. 2005;123(4):479–484.
Examination and Management of Posterior Vitreous Detachment
Indirect ophthalmoscopy with scleral depression or slit-lamp biomicroscopy with a 3-mirror lens or indirect contact lens are used to clinically diagnose PVD and rule out retinal breaks or detachment. In unclear cases, optical coherence tomography (OCT) can be employed to confirm the state of the vitreous gel on the optic nerve head and macula. Re-examination of the patient 2–4 weeks following presentation may be appropriate, because as the PVD evolves over time, new retinal breaks may occur. Additional risk factors to consider in follow-up determination include aphakia, myopia, fellow-eye history, family history of retinal detachment, and signs of Stickler syndrome. All patients should be instructed to return to the ophthalmologist immediately if they notice a change in symptoms, such as increasing numbers of floaters or the development of visual field loss.
If a large vitreous hemorrhage precludes a complete examination, bilateral ocular patching and bed rest, with the patient’s head elevated 45° or more for a few days, may allow the hemorrhage to settle sufficiently to permit detection of breaks in a superior location. Echography may be performed to find flap tears and rule out retinal detachment and other fundus lesions. If the cause of the hemorrhage cannot be found, the patient should be reexamined at frequent, regular intervals, and early vitrectomy should be considered to reduce the risk of retinal detachment.
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.