The goal of this program is to improve the management of lattice degeneration. After hearing and assimilating this program, the clinician will be better able to:
Lattice degeneration (LD): defined as an abnormal thinning of the peripheral retina with overlying vitreous liquefaction and firm vitreoretinal adhesions at the margins; increases the risk for retinal tears and retinal detachment (RD); retinal defects occur as round holes or horseshoe tears; LD occurs in 6% to 8% of the general population and up to one-third of individuals with myopia; most cases of LD are asymptomatic; symptomatic cases are usually associated with retinal tear or RD
Clinical features: not all cases of LD have lattice lines; Byer defines LD as any lesion with borders that show an abrupt, discrete irregularity of the otherwise smooth surface of the retina; appearance of LD has high interindividual and intraindividual variability; clinical features include pigmentation, thinning of the retina, and branching white lines; most lesions are ovoid with a long axis running parallel to the ora serrata; widefield imaging is helpful for diagnosis and documentation of LD; typical LD is characterized by color change (indicative of retinal thinning), pigment clumps, and crosshatching of sclerotic vessels; snail track degeneration is a form of LD with frosted yellow-white flecks; perivascular LD occurs in a radial configuration adjacent to retinal vessels and is associated with a higher risk for RD compared with circumferential LD
Etiology: theories include anastomosis of embryonic vasculature, localized retinal ischemia, and developmental anomalies of the internal limiting membrane; histologic studies show retinal thinning, vitreous liquefaction, and firm vitreoretinal adhesions at the margins
Differential diagnosis: includes cobblestone degeneration, retinoschisis, atrophic retinal holes, chorioretinal scarring, white without pressure, and congenital hypertrophy of the retinal pigment epithelium
Risk factors: include myopia, connective tissue disorders (eg, Marfan syndrome), and hereditary vitreoretinopathies (eg, Stickler syndrome); Marfan syndrome is associated with excessive LD, with RD occurring in ≤25% of patients; radial perivascular LD is often associated with Stickler syndrome; hereditary vitreoretinopathies are congenital abnormalities of the vitreous with severe degeneration, early onset of cataracts, and predisposition to RD; because RD occurs in two-thirds of patients with Stickler syndrome (which is inherited in an autosomal dominant pattern), prophylactic treatment may be considered
Risk for RD: 20% to 30% of patients with RD have LD; conversely, LD has a risk for RD of 0.3% to 0.7%; RDs develop from atrophic retinal holes with a cuff of subretinal fluid that develops from the overlying liquefied vitreous; LD associated with an atrophic retinal hole has risk for RD of <0.3%; retinal tears may not occur adjacent to the lattice lesion; study by Byer found that the risk for retinal tears adjacent to a lattice lesion was 1% after 10 yr; most patients have stable or slowly progressive LD; a natural history study by Byer reported that atrophic holes occurred in one-third of eyes over a mean follow-up of ≈11 yr; of these eyes, 6.7% had subclinical RD, 1.9% of eyes had tractional tears, and <1% had clinical RD; risk for RD in eyes with LD is highest immediately following a posterior vitreous detachment (PVD)
Treatment: goal is to reduce rate of RD; a Cochrane review found no evidence to support prophylactic treatment of LD without symptoms, holes, tears, or detachments; breaks that lead to RD during or after a PVD occur in areas that appear normal prior to the PVD; educate patients on symptoms of PVD and RD and the need for regular follow-up examinations; atrophic round holes within LD that have minimal subretinal fluid and no PVD do not require treatment; treatment should be considered in subclinical RDs if they become symptomatic or progress; young patients with myopia who have LD with holes should be followed routinely to monitor for subclinical RD; horseshoe tears induced by PVD should be treated with laser demarcation; in patients with LD and a history of RD, the fellow eye has an incidence of RD of 2% to 5% over 7 yr; no prophylactic treatment is required if the fellow eye has a PVD without a break; risk for RD in the fellow eye is 17% if a tractional tear is present, and treatment is appropriate; there are currently no guidelines for treatment of the fellow eye without a PVD; other risk factors for RD should be considered when weighing the risks and benefits of treatment
Cataract surgery: one study found that the rate of RD was 21% in eyes with LD and postoperative PVD, whereas eyes without LD had a rate of <1%; evidence is insufficient to support prophylactic laser treatment of LD prior to anterior segment surgery; patients should be evaluated by a retina specialist prior to surgery
Flaxel CJ, Adelman RA, Bailey ST, et al. Posterior vitreous detachment, retinal breaks, and lattice degeneration Preferred Practice Pattern [published correction appears in Ophthalmology. 2020 Sep;127(9):1279]. Ophthalmology. 2020 Jan;127(1):P146-P181; Manjunath V, Taha M, Fujimoto JG, et al. Posterior lattice degeneration characterized by spectral domain optical coherence tomography. Retina. 2011 Mar;31(3):492-496; Parma ES, Körkkö J, Hagler WS, et al. Radial perivascular retinal degeneration: a key to the clinical diagnosis of an ocular variant of Stickler syndrome with minimal or no systemic manifestations. Am J Ophthalmol. 2002 Nov;134(5):728-734; Wilkinson CP. Interventions for asymptomatic retinal breaks and lattice degeneration for preventing retinal detachment. Cochrane Database Syst Rev. 2012 Mar;3(3):CD003170; Zhang C, He F, Li B, et al. Development of a deep-learning system for detection of lattice degeneration, retinal breaks, and retinal detachment in tessellated eyes using ultra-wide-field fundus images: a pilot study. Graefes Arch Clin Exp Ophthalmol. 2021 Aug;259(8):2225-2234.
For this program, members of the faculty and planning committee reported nothing relevant to disclose.
Dr. Gill was recorded virtually at the 14th Annual Retina Symposium: Improving Clinical Outcomes, held March 26, 2021, and presented by the Illinois Eye and Ear Infirmary. For information about upcoming CME conferences from this presenter, please visit chicago.medicine.uic.edu. Audio Digest thanks the speakers and the Illinois Eye and Ear Infirmary for their cooperation in the production of this program.
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OP600801
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