lattice degeneration risk of retinal detachment

The goal of treatment is to create a chorioretinal adhesion surrounding a break so that no communication exists between the vitreous cavity and the subretinal space. 2,6 Symptomatic operculated breaks typically do not progress to RD unless residual vitreous remains adherent to retinal vessels adjacent to the break 2 however, most retinal specialists treat these lesions regardless of the status of the vitreous. Acute symptomatic horseshoe tears require prompt treatment in an attempt to prevent RD.2,5 Thirty to 50 percent of acute symptomatic horseshoe tears have been found to result in RD, and prophylactic treatment reduces the frequency of RD to 5 percent. The same patient with a superior peripheral retinal tear.Īcute symptomatic retinal breaks resulting from a PVD may result in RD. Hemorrhage at inferior vitreous base in a patient with floaters and an acute PVD. 2 All patients are counseled and instructed to return immediately if they have a significant change in their symptoms, such as an increase in photopsias and/or floaters, which might indicate progression of PVD with a retinal tear, or a 'shade' over their vision, which may indicate RD. The development of RD is unlikely if no retinal tears are present at four to six weeks follow-up. Patients with acute symptomatic PVD without peripheral retinal breaks require no immediate treatment but may be examined in one to two weeks, since some retinal breaks appear to develop days to weeks after the onset of symptoms. Weiss ring in a patient presenting with floaters and an acute posterior vitreous detachment. If a RD is also present, patients may complain of a 'curtain,' 'shade,' or 'shadow' obscuring their peripheral vision.įigure 1. There are no symptoms that can distinguish a PVD alone from a PVD with an associated retinal break. They are caused by vitreous opacities, such as epipapillary glial tissue torn from the optic disc, condensations of vitreous collagen, and/or blood. Floaters are described as 'cobwebs,' 'spots,' or 'hair' in the field of vision. Typical symptoms of PVD are 'flashes and floaters.' Photopsia, the subjective impression of flashing lights, is caused by vitreous traction on the peripheral retina. With still further traction, the flap may separate from the surrounding retina, leaving a round or oval hole with an overlying operculum. With additional traction, a horseshoe tear (flap tear) develops. Mild traction causes tenting of the retina. The PVD may produce retinal breaks in areas of firm vitreoretinal attachments and on narrow posterior extensions of the vitreous base. However, when the separating vitreous remains firmly adherent to an area of the retina, localized vitreoretinal traction results. This event is the result of vitreous syneresis (liquefaction). PVD occurs when the posterior vitreous separates from the retina and collapses anteriorly toward the vitreous base. Posterior vitreous detachment is the critical event leading to the development of retinal tears and retinal detachment. In this article, we will examine some of the conditions that put patients at risk for retinal detachment and the indications and potential benefits of prophylactic treatment. The management of these lesions is based on an increased understanding of their natural history and the potential for complications associated with treatment. Precursors to RD include posterior vitreous detachment, symptomatic retinal breaks, asymptomatic retinal breaks, lattice degeneration, and other less common vitreoretinal abnormalities.

Retinal detachment occurs with a frequency of 1/10,000 people per year, 1 and patients at risk for RD include those with myopia, aphakia, trauma, RD in the fellow eye, a family history of RD, certain systemic syndromes, and a variety of peripheral retinal lesions. RETINAL SURGEONS DIFFER IN THEIR APPROACH to prophylactic treatment of vitreoretinal abnormalities.

Lattice degeneration risk of retinal detachment