42
QUESTION
WHAT RETINAL FINDINGS SHOULD BE TREATED BEFORE CATARACT SURGERY, REFRACTIVE SURGERY, OR YTTRIUM-ALUMINUM-GARNET LASER?
Franco M. Recchia, MD
The goal of prophylactic retinal treatment is to reduce the chance of postsurgical complications related to vitreoretinal disorders. These potential complications include rhegmatogenous retinal detachment (RRD), macular edema, and progression of vision-threatening retinopathy.
RRD typically arises from vitreous traction on the peripheral retina leading to peripheral retinal breaks. Peripheral vitreoretinal traction often occurs in the setting of posterior vitreous detachment. Posterior vitreous detachment formation can be accelerated by anterior movement of the vitreous following cataract extraction or following yttrium-aluminum-garnet (YAG) laser capsulotomy.1 It has been speculated that LASIK may also alter the vitreoretinal interface via compression/decompression changes in the anteroposterior axis induced during intraoperative suction. Retinal breaks are more likely to occur in areas of particularly adherent vitreous and/or retinal weakness.
Retinal or systemic conditions that may predispose to the development of a RRD include retinal break, lattice degeneration, vitreous hemorrhage, high myopia, RRD in the fellow eye, family history of RRD, premature birth, and systemic collagen disorders (specifically Stickler syndrome). Preoperative retinopexy with laser photocoagulation or cryotherapy should be applied to all symptomatic retinal breaks and all horseshoe retinal tears whether symptomatic or not. Retinopexy is strongly recommended to areas of lattice retinal degeneration in patients with a history of lattice-associated RRD in the fellow eye. Asymptomatic operculated holes and atrophic holes do not necessarily require treatment, but the option of treatment should be discussed with the patient. Prophylactic cryotherapy or laser cerclage (360° photocoagulation placed posterior to the vitreous base) is recommended in patients with genetic proof or high clinical suspicion of Stickler syndrome. This hereditary disorder of connective tissue (caused by mutations in Type II collagen) is characterized by high myopia, early cataract, cleft palate, mid-facial flattening, hearing loss, cardiac and joint abnormalities, and strong family history of these symptoms and carries a risk of bilateral RRD approaching 75%.2 Laser cerclage is also advisable in cases of high myopia (especially > 15 diopters) and in eyes of patients with poor visual acuity in the fellow eye, particularly for patients in whom postoperative follow-up or cooperation is limited.
Given the strong association (up to 70%) of peripheral retinal breaks in nondiabetic eyes with vitreous hemorrhage, these eyes must be examined especially carefully. Ultrasonography should be employed in cases in which complete visualization of the retinal periphery is precluded by media opacity. If removal of the hemorrhage is required for adequate fundus visualization to facilitate retinal treatment, then vitrectomy should be performed either prior to cataract surgery or, in cases of dense cataract, concomitant with or immediately following cataract surgery.
A special clinical scenario seen with growing frequency involves the patient born prematurely or who had retinopathy of prematurity (ROP). The syndrome of adult ROP includes early-onset cataracts and associated rhegmatogenic retinal pathology. Among these patients, the reported risk of RRD after cataract surgery approaches 25%. You should ask all patients if they were born early (< 32 weeks of gestational age) or if they were told that they were born with a low birth weight. Many patients with a history of premature birth or ROP have a myopic refraction, but may not necessarily have posterior cicatricial changes.
Macular edema following cataract surgery or YAG laser capsulotomy typically arises from leakage of fluid from hyperpermeable parafoveal capillaries.3 This hyperpermeability can be exacerbated by 2 mechanisms: (1) vitreomacular traction and (2) inflammation. Thus, treatment directed at retinal conditions that are associated with traction or inflammation should be helpful in reducing the chance of postoperative macular edema.
Retinal or systemic conditions that signal a high risk for postoperative macular edema include:
- Disorders of the vitreomacular interface (vitreomacular adhesion, posterior hyaloidal contraction, epiretinal membrane). Treatment with topical non-steroidal anti-inflammatory drugs (NSAIDs) beginning 3 to 7 days prior to cataract extraction may reduce the incidence of pseudophakic macular edema and optimize postoperative vision recovery.4,5 In certain cases of coexisting cataract and vitreomacular interface disease, it is unclear how much of the vision impairment is due to cataract and how much is due to macular disease. In such cases, it is advisable to remove the cataract first, allow complete recovery, and then reassess the extent of macula-related vision impairment.
- The incidence of macular edema following even uneventful cataract surgery is higher in a diabetic eye, even in the absence of diabetic retinopathy, than in nondiabetic eyes.6 Collective laboratory and clinical evidence suggests a pathoetiologic role for inflammation mediated by prostaglandins and inflammatory cytokines and for vascular permeability driven by vascular endothelial growth factor (VEGF). In 2 prospective, randomized, vehicle-controlled, comparative studies of patients with diabetic retinopathy, treatment with the topical NSAID nepafenac 0.1% (3 times daily, starting 1 day before cataract surgery) was associated with less postoperative macular edema and better visual acuity at 3 months (Table 42-1).7
The risk and severity of postoperative macular edema and the risk of exacerbating diabetic retinopathy are correlated with the severity of macular edema and diabetic retinopathy at the time of cataract surgery. While the conventional teaching has been to control diabetic retinopathy and eradicate macular edema (traditionally using laser photocoagulation) completely for several months prior to cataract surgery, this may not always be achievable, and the time required to do so may delay the time to vision improvement. Intravitreal administration of corticosteroid (typically in the form of triamcinolone or a Ozurdex implant [dexamethasone]) and/or anti-VEGF medications (eg, bevacizumab, ranibizumab, aflibercept) significantly reduce postoperative macular edema in diabetic eyes (see Table 42-1).8 A special situation involves the patient with longstanding (typically several decades) or chronically poorly controlled diabetes in whom minimal or no retinopathy is seen. In such cases of silent retinopathy or featureless retina, chronic retinal ischemia has damaged the native retinal vasculature so severely that the typical compensatory microaneurymal and neovascular changes cannot arise. Fluorescein angiography reveals massive peripheral capillary nonperfusion. When unrecognized and untreated, these eyes can progress rapidly to neovascular glaucoma within a short time following cataract surgery. Prophylactic treatment with anti-VEGF medication and/or panretinal laser photocoagulation is recommended in such cases.
- As in diabetic retinopathy, retinal ischemia arising from venous occlusion can lead to vision-threatening macular edema or vitreous hemorrhage due to posterior segment neovascularization. These complications are mediated primarily by increased VEGF levels driven by retinal ischemia. Perioperative treatment with anti-VEGF medications is recommended in eyes with macular edema or in eyes recently treated for macular edema (see Table 42-1). In eyes with vitreous hemorrhage due to neovascularization, preoperative peripheral scatter retinal laser photocoagulation to the affected area is recommended.
Table 42-1
Recommendations for Perioperative Pharmacologic Treatment in Patients With Retinal Vascular Disease Undergoing Cataract Surgery
| Topical NSAID |
|
| Intravitreal anti-VEGF and corticosteroid |
|
| Intravitreal anti-VEGF |
|
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