Retinal Complications of Cataract and Refractive Surgery
Retinal detachment and macular pathology are most frequent side effects.
ERIC CHEN, MD & CARL D. REGILLO, MD
Over the last several years, there have been significant advances in cataract and refractive surgery. Clear-cornea phacoemulsification has produced more efficient and less traumatic cataract extractions, with improved patient comfort and quicker postoperative recovery. Refractive surgery has expanded its scope and indications, shifting from photorefractive keratectomy (PRK) to laser-assisted in situ keratomileusis (LASIK) for mild and moderate ametropias. More recently, phakic intraocular lens (IOL) implants have demonstrated superior visual outcomes over LASIK without the risk of corneal ectasia in patients with moderate and high myopia, particularly in the areas of visual quality and contrast sensitivity. Although retinal complications from these surgeries are infrequent, it is crucial to properly manage them to maximize visual outcome. The more common, significant complications are discussed here.
Figure 1. Retained lens fragments following cataract surgery.
Retained Lens Fragments
One of the most commonly encountered intraoperative complications of cataract surgery referred to vitreoretinal specialists is posteriorly dislocated or retained lens fragments (RLF), with an incidence inversely related to surgeon experience and an overall range of 0.3% to 1.1% (Figure 1).1 Risk factors include dense brunescent, hypermature or posterior polar cataracts, topical anesthesia, prior vitrectomy, zonular compromise, fellow eye with complicated cataract surgery, and floppy iris syndrome. In addition, any conditions predisposing to posterior capsule tear, such as pseudoexfoliation, diabetes, trauma, or persistent hyperplastic primary vitreous (PHPV), increase the risk of RLF. While very small amounts of retained cortical material sometimes may be well tolerated and dissolve spontaneously, larger amounts of lens material or any nuclear fragments often lead to a phacotoxic (lens protein) or phacoanaphylactic (antibody formation) uveitis or glaucoma secondary to trabeculitis or trabecular meshwork blockage. Furthermore, persistent inflammation leads to higher rates of postoperative cystoid macular edema (CME) and compromised visual outcomes. Retained lens fragments also increase the risk of subsequent retinal detachment to as high as 14.5%.2
|Eric Chen, MD, is a second-year vitreoretinal fellow at Wills Eye Hospital in Philadelphia. Carl D. Regillo, MD, is the director of the Wills Clinical Retina Research Unit. He is also professor of ophthalmology at Thomas Jefferson University School of Medicine in Philadelphia. He can be reached at (215) 233-4300. Neither author has any financial interest in any products or devices mentioned in this article.
Optimal timing for pars plana vitrectomy (PPV) is somewhat controversial, but most would agree that it is best to proceed with vitrectomy within 3 weeks, especially if there are large amounts of retained material, persistent inflammation, or elevated intraocular pressure (IOP) despite adequate medical management. Chronic glaucoma and poor visual outcomes have been associated with delays of 3 weeks or more.3 Just as it is important for the anterior segment surgeon to avoid aggressive maneuvers to retrieve posteriorly dislocated lens particles, during vitrectomy the vitreoretinal surgeon must limit vitreous traction to avoid retinal injury. A complete vitrectomy should be performed before attempting to remove lens material with the posterior phacofragmatome. The vitreous cutter can remove cortical material and smaller nuclear pieces, while the phacofragmatome is used to emulsify and aspirate larger nuclear lens material. The visual prognosis in patients undergoing PPV for RLF is relatively good, with 44% to 83% achieving 20/40 or better vision, but clearly not as good as uncomplicated cataract extraction. Leading causes of poor outcomes include CME, corneal edema, and retinal detachment.4
Acute Postoperative Endophthalmitis
The rate of endophthalmitis after cataract surgery is 0.05% to 0.3%.5 Patients typically present within 6 to 8 weeks of cataract surgery with symptoms and signs of decreased vision, pain, conjunctival injection, corneal edema or infiltrate, hypopyon, anterior chamber fibrin, and/or vitreous inflammation (Figure 2). Other signs include vasculitis, periphlebitis, and midperipheral retinal hemorrhages. Seventy percent of isolates in the Endophthalmitis Vitrectomy Study (EVS) were coagulase-negative, gram-positive organisms such as Staphylococcus epidermidis while patients presenting within 2 days or with more significant clinical signs were more likely to be infected with a gram-negative species or a more virulent gram-positive organism.6 Ocular surface and adnexal flora are the source in most cases, and 5% topical povidone-iodine at the time of cataract extraction is the only proven modality for decreasing the rate of endophthalmitis.7
Patients with hand-motions vision or better are given intravitreal vancomycin 1 mg/0.1 mL and ceftazidime 2.25 mg/0.1 mL, along with frequent topical broad-spectrum or fortified antibiotics and corticosteroids, while those patients presenting with light-perception vision should undergo immediate vitrectomy with intravitreal antibiotics at the time of surgery. Repeat injections or PPV can be considered at 48 to 72 hours if there is no clinical improvement. Systemic antibiotics are not typically used, and intravitreal or oral steroids remain controversial. Initial vision is the best predictor of final visual outcome, and in the EVS, 53% of patients achieved 20/40 vision, and 74% 20/100 at 9 to 12 months. Poor outcomes were related to complications that occur in 6% to 8% of patients, such as dislocated IOLs, macular infarction, expulsive hemorrhage, or retinal detachment.8
Figure 2 appears courtesy of William Benson, MD.
Pseudophakic Rhegmatogenous Retinal Detachment
The rate of rhegmatogenous retinal detachment (RRD) after cataract extraction is about 1%, with a risk 5 times greater at 10 years compared to patients who have not had cataract surgery.9 Possible mechanisms include partial liquefaction of the vitreous base with disturbance of anterior retinal holes, changes in hyaluronic acid content in vitreous, loss of crystalline lens protuberance and increased traction on the peripheral retina during saccades, and acceleration of posterior vitreous detachment. Other risk factors include axial length of greater than 25 mm, lattice, prior retinal detachment, younger age, male sex, Caucasian race, intraoperative posterior capsulotomy with or without vitreous loss, neodymium-doped yttrium aluminium garnet (Nd:YAG) capsulotomy, or postcataract trauma. Causative breaks may be difficult to locate because of their small size, multiple locations, anterior position near the ora serrata, and capsular opacification or related optical issues.
Over 50% of pseudophakic RRD occurs within 1 year of cataract surgery, with most presenting with the macula already detached. Due to a higher number of missed breaks and an increased rate of proliferative vitreoretinopathy (PVR), pseudophakic RRD has a lower reattachment rate compared to phakic RRD when repaired with pneumatic retinopexy or scleral buckling. PPV (with or without a scleral buckle) is also utilized to repair pseudophakic RRD. Some surgeons prefer this approach because it allows for better identification and treatment of the causative breaks. Success rates of 88% to 100% have been reported with this approach, with 62% to 82% of cases achieving a postoperative vision of 20/50 or better. Anatomical and functional recovery depend on several factors, including preoperative macula status, size and location of the breaks and of the detachment, presence (or development) of PVR, presenting vision, duration of symptoms, and presence of vitreous or intraoperative hemorrhage.
Cystoid Macular Edema
Following uncomplicated cataract surgery, CME is the most common cause of suboptimal vision. It typically presents 4 to 16 weeks after surgery, peaking around the 4th postoperative week. Angiographic CME seen on fluorescein angiography that is not visually significant can occur in 20% to 30% of patients,10 while clinical CME with vision below 20/40 occurs in 1% to 7% of uncomplicated cataract extractions.11 Risk factors include older age, diabetes, uveitis, retinitis pigmentosa, history of CME in the fellow eye, vitreous loss, secondary IOL implantation or IOL exchange, posterior capsulotomy, and RLF. Clinical findings may include vitreous wick to the wound or iris, an irregular pupil, anterior chamber cell and flare, blunting of the foveal light reflex, yellowish discoloration in the fovea, or frank cysts.
CME is thought to result from activation of the prostaglandin pathway with a breakdown in the blood-aqueous barrier and increased permeability of perifoveal capillaries. Although many cases spontaneously resolve within 6 to 12 weeks, a combination of ketorolac and prednisolone improves visual outcomes, with 89% of patients achieving vision of 20/40 or better.12 If no improvement occurs after at least 2 months of topical treatment, other comorbidities, such as vitreomacular traction or epiretinal membrane, can be ruled out before considering subtenon (40 mg) or intravitreal triamcinolone (IVT) (4 mg). These steroid injections produce a longer effect, although elevated IOP is a concern in 30% to 50% of eyes treated with IVT and may require drops or even glaucoma surgery. Other complications of IVT include cataract progression and endophthalmitis of both the noninfectious and infectious types. Vitrectomy with internal membrane peeling can be considered in certain cases of refractory chronic CME.
Several large series suggest that refractive surgery does not appear to be an additional risk factor for RRD. In most studies, retinal breaks and lattice with vitreous traction were treated with barrier laser photocoagulation prior to surgery. Asymptomatic tears and lattice alone do not always warrant treatment, as treatment is not innocuous, the majority of RRD are thought to occur in normal areas, and most areas of retinal pathology do not evolve into retinal detachments.
A 5-year follow-up of 38 823 eyes after LASIK13 reported a frequency of RRD after LASIK of 0.08%, and another mean 31-month follow-up of 59 424 eyes after LASIK14 recorded an cumulative incidence of 0.08% and yearly incidence of 0.03% of RRD. RRD following phakic anterior chamber IOLs have an incidence of 0.6% to 4.8%,15,16 while the largest series of RRD following posterior chamber phakic (PCP) IOL implantation documented a RRD incidence of 2.07% in a mean 64-month follow-up of 771 eyes.17 These figures are consistent with the overall incidence of retinal detachment of 0.03% per year18 and fall within the lower reported numbers for incidence of RRD in myopic patients, which range from 0.7% to 3.2%.19
Myopic eyes are predisposed to RRD due to premature vitreous liquefaction and posterior vitreous detachment (PVD), increased axial length, and an increased prevalence of lattice degeneration. Manipulation during LASIK has been hypothesized to increase the risk of RRD through several mechanisms. The pneumatic suction ring can increase IOP to great than 65 mm Hg, leading to compression and decompression of anterior and, consequently, posterior segment structures, producing a closed-eye type injury. This could lead to vitreous deformation and traction, aggravating pre-existing peripheral retinal pathology, as well as exacerbating macular pathology in an already fragile Bruchs membrane.20 Excimer-laser-induced shock waves may also contribute to PVD formation and mechanical stress on the vitreous base. Phakic IOL implantation may induce traction on the anterior and/or posterior margin of the vitreous base. Transient alterations in IOP may also destabilize the vitreous, promoting PVD or chronic alteration of the vitreous.21
Retinal detachment in these patients has similar characteristics as primary RRD, and surgical management with pneumatic retinopexy, scleral buckling, or vitrectomy is successful, although there are special considerations. Visualization with phakic IOLs may be more difficult, and PPV may be preferred for undetected breaks, posterior breaks, or PVR. Unstable IOLs or anterior PVR may require explantation at the time of retinal detachment repair. However, in the setting of young phakic patients, a major drawback of vitrectomy is the risk of nuclear sclerosis. Despite a myopic shift in the spherical equivalent with scleral buckling surgery, there do not appear to be significantly different best-corrected visual acuity outcomes when compared to myopic patients without refractive surgery undergoing RRD repair.
Another possible association exists between myopic maculopathy and refractive surgery. There have been scattered reports on the progression of degenerative myopia, macular or posterior pole hemorrhages, lacquer cracks, Fuchs spots, macular hole formation, branch retinal vein occlusion, retinal nerve fiber layer defects, and the progression of choroidal neovascularization (CNV) following LASIK surgery. One series of 294 eyes with anterior chamber phakic IOL placement reported CNV in 7 eyes (2.38%) and epiretinal membrane formation in another patient.22,23 Proposed etiologies in LASIK include mechanical forces from the sudden change in IOP during corneal-flap formation with the suction ring and microkeratome or from shockwaves produced by the excimer laser. In eyes more susceptible to mechanical forces because of pre-existing lacquer cracks and myopic changes, ruptures in Bruchs membrane, enlargement of lacquer cracks, or hemorrhagic CNV, complications can occur more frequently.24 Surgery for phakic lens placement can cause complications related to hypotony or inflammation from intraocular surgery. Macrophage recruitment may contribute to angiogenesis and development of CNV, especially in eyes with pre-existing pathology such as drusen or altered Bruchs membranes.
Overall, serious retinal complications following refractive surgery do not appear to happen at significantly higher rates than in the general myopic population, which is inherently predisposed to retinal pathology. Although there is no clear cause-and-effect relationship, patients should be reminded that refractive surgery corrects refraction alone and does not lower any risks inherent to the underlying myopia. Retinal complications following refractive surgery may be unrelated and purely coincidental. RP
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Retinal Physician, Issue: April 2007