Incidence of cystoid macular edema following secondary posterior chamber intraocular lens implantation

ARTICLE

Incidence of cystoid macular edema following secondary posterior chamber intraocular lens implantation Linda M. Meyer, MD, Sebastian Philipp, MD, Marie T. Fischer, MD, Peter Distelmaier, MD, Patrick Paquet, MD, Natascha E. Graf, MD, Christos Haritoglou, MD, Carl-Ludwig Sch€ onfeld, MD

PURPOSE: To investigate the incidence and risk factors for the occurrence of cystoid macular edema (CME) after secondary posterior chamber intraocular lens (PC IOL) fixation. SETTING: Eye Clinic Herzog Carl Theodor, Munich, Germany. DESIGN: Retrospective case series. METHODS: Eyes with secondary PC IOL implantation were included. Eyes in Group 1 were treated because of preexisting aphakia; eyes in Group 2 had reimplantation or refixation of a failed primary PC IOL (Group 2). Patients were followed for at least 12 months with measurement of corrected distance visual acuity (CDVA) and central retinal thickness with optical coherence tomography (OCT). Risk factors for CME occurrence were evaluated with standard statistical procedures. Cutoff points of sensitivity and specificity were calculated for the prediction of CME with the receiver operating characteristic (ROC) method. RESULTS: Forty-two eyes of 40 patients (16 men, 24 women; mean age 75.4 years G 13.7 [SD]) were included. There were 28 eyes in Group 1 and 14 eyes in Group 2. Seven eyes (16.7%) developed CME with significant impairment of CDVA and an increase in central retinal thickness on OCT. Five eyes in Group 1 and 2 eyes in Group 2 were affected, without a significant difference between groups. The CDVA after surgery had a significant influence, and there was a trend toward patient age as a risk factor. The ROC analysis yielded 83.9 years of age and a CDVA of 0.35 logMAR, respectively, as meaningful cutoff points. CONCLUSIONS: Secondary PC IOL fixation was performed with good results despite the inherent CME risk from the procedure. Advanced age and poor CDVA after surgery might predict CME occurrence. Financial Disclosure: No author has a financial or proprietary interest in any material or method mentioned. J Cataract Refract Surg 2015; 41:1860–1866 Q 2015 ASCRS and ESCRS

Phacoemulsification of the crystalline lens with implantation of a posterior chamber intraocular lens (PC IOL) is the most commonly performed surgical intervention in industrialized countries.1 Although the procedure as such is appropriately tested and proven effective, it is not free from risks and complications; in particular, the dislocation of the IOL into the vitreous cavity imposes major surgical and ophthalmologic hazards.2–5 In general, scleral fixation of a PC IOL is a technically demanding procedure that involves considerable manipulation and consequently causes a clinically 1860

Q 2015 ASCRS and ESCRS Published by Elsevier Inc.

relevant release of proinflammatory cytokines (ie, interleukins and tumor necrosis factor).6,7 To avoid a large tunnel incision, placement of the IOL in the ciliary sulcus following scleral fixation can be considered.3,4 In the present paper, secondary scleral IOL fixation is presented with 3 fixation eyelets in the haptics; the procedure allows for a torsion-free fixation to avoid postoperative lens astigmatism and has shown favorable preliminary results.A However, this method is not only technically demanding but also involves comparably severe trauma because the http://dx.doi.org/10.1016/j.jcrs.2015.10.024 0886-3350

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IOL has to be explanted and replaced; therefore, a certain amount of cytokine release has to be assumed. Previously, it has been demonstrated that even relatively uncomplicated ocular surgical procedures cause a release of proinflammatory mediators into the vitreous and that macular edema can evolve as a consequence8–10; therefore, the development of cystoid macular edema (CME) can be used as a marker of cytokine release after complex manipulations in the eye. Presently, the evidence base for the assessment of the CME risk in secondary PC IOL insertion and especially the clinically relevant predisposing factors is fragmentary, and little is known about the possibility of identifying populations at risk before damage to the macula actually occurs. In the present trial, we investigated the actual frequency of CME after secondary PC IOL fixation in a risk-conscious environment and attempted to identify the relevant risk factors. PATIENTS AND METHODS Patient Sample

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the frown incision was closed with cross-stitching under astigmatic control with a Placido disk device. Finally, the IOL was intrasclerally sutured with meandering zigzag sutures, and the scleral flap was fixated with 10-0 nylon single button sutures. After repeated bulbus adjustment, the conjunctiva was closed with 2 10-0 polyglactin (Vicryl) single button sutures. After surgery, all patients received a peribulbar injection of 4 mg dexamethasone and 75 mg cefuroxime.

Examination Patients were routinely evaluated on 1 day and 3, 4, 12, and 52 weeks after surgery. The postoperative examination included the corrected distance visual acuity (CDVA) and spectral-domain optical coherence tomography (SD-OCT) (Spectralis, software version 5, Heidelberg Engineering GmbH). Cystoid macular edema was considered when fluid-filled cysts of any size were apparent with or without an increase in central retinal thickness; the spatial resolution of SD-OCT allows for detection of cysts of 10 mm or more in diameter. Slitlamp examination was performed to exclude anterior segment irritation. The anterior chamber was examined for the presence of cells or the Tyndall phenomenon.

Statistical Analysis

Consecutive patients who had secondary PC IOL implantation in our clinic between January 10, 2008, and March 1, 2012, were retrospectively included in the study. Patients with preexisting macular edema (detected by means of fundus biomicroscopy with a 90.0 diopter lens) had surgery but were excluded from the evaluation. Patients were followed over a postoperative observation period of at least 12 months.

Surgical Technique Access to the anterior chamber was gained by a conjunctival incision over 3 quadrants, a 7.0 mm frown incision, and a bilateral 45-degree paracentesis. In cases of dislocated PC IOLs, the old IOL was extracted with Eckardt tweezers and a meticulous anterior vitrectomy was performed (especially behind the iris) to avoid the placement of vitreous between haptics and sulcus. A 10-0 polypropylene (Prolene) suture was threaded through the center eyelet of the secondary IOL (Type 81B with 3 eyelets, Morcher GmbH) and subsequently, the curved needle was lanced through the frown incision and the sulcus to the exterior of the eye. After hydration of each paracentesis with a balanced salt solution,

Submitted: October 2, 2014. Final revision submitted: December 23, 2014. Accepted: January 26, 2015. From the Eye Clinic Herzog Carl Theodor, Munich, Germany. Presented in part at the 111th annual meeting of the Deutsche Ophthalmologische Gesellschaft, Berlin, Germany, September 2013. Corresponding author: Carl-Ludwig Sch€onfeld, MD, Department of Ophthalmology, Ludwig Maximilians-University, 80336 Munich, Germany. E-mail: [email protected].

Data were analyzed with the Statistica (release 9.1, Statsoft, Inc.) and BiAS for Windows (release 10.11, Epsilon) software packages. Group comparisons were performed with Fisher exact test and Mann-Whitney U test, and the correlation between potential confounders and the CME diagnosis was analyzed according to the receiver operating characteristic (ROC) method.11 This method allows for the definition of rationally based cutoff points for the risk assessment in defined samples and therefore was chosen to indicate rational stratifying criteria in case any statistically significant influences on the occurrence of CME were found.

RESULTS The study included 42 eyes of 40 patients. Twentyeight eyes received secondary PC IOL implantation due to preexisting aphakia (Group 1), and 14 eyes had explantation of PC IOLs with consecutive secondary scleral PC IOL implantation or refixation of a dislocated IOL in the sulcus ciliaris (Group 2). The clinical features of the patient sample are shown in Table 1. Patients were predominantly women. Twelve percent of patients had diabetes, but none had diabetic retinopathy. Prevalent concomitant ocular diseases were pseudoexfoliation (PXF) syndrome, a history of vitrectomy, age-related exudative macular degeneration, and epiretinal membrane formation. All patients received an anterior vitrectomy during the secondary IOL implantation and/or refixation of a dislocated IOL. A subgroup of patients had a history of full pars plana vitrectomy due to concomitant retinal diseases (Table 1). None of the included patients had received intravitreal therapy and/or local treatment with nonsteroidal antiinflammatory drugs

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Table 1. Clinical data of patients with and without CME. Parameter No. of patients Age at surgery (y)* Mean G SD Range Sex, n (%) Female Male Indication, n (%) Preexisting aphakia Reimplantation/refixation Diabetes mellitus (no retinopathy), n (%) Previous or concomitant ocular diseases, n (%) Pseudoexfoliation syndrome Age-related macular degeneration Previous vitrectomy Epiretinal membrane CDVA (logMAR) before surgery Mean G SD Range CDVA (logMAR) after surgery† Mean G SD Range Time between surgery and CME diagnosis (d) Mean G SD Range CDVA (logMAR) on occurrence of CME Mean G SD Range

Total Sample

No CME

CME

42

35

7

75.4 G 13.7 25.6, 89.8

74.0 G 14.5 25.6, 89.8

82.5 G 5.4 73.8, 89.1

26 (61.9) 16 (38.1)

20 (57.1) 15 (42.9)

6 (85.7) 1 (14.3)

28 (66.7) 14 (33.3) 5 (11.9)

23 (65.7) 12 (34.3) 4 (11.4)

5 (71.4) 2 (18.6) 1 (14.3)

14 (33.3) 5 (11.9) 13 (31.0) 1 (2.4)

11 (31.4) 4 (11.4) 12 (34.3) 1 (2.9)

3 (42.9) 1 (14.3) 1 (14.3) 0

0.54 G 0.44 0.00, 2.00

0.53 G 0.47 0.00, 2.00

0.59 G 0.26 0.22, 1.00

0.40 G 0.36 0.00, 1.70

0.35 G 0.34 0.00, 1.70

0.65 G 0.40 0.10, 1.18 17.7 G 87.9 49, 283 0.84 C 0.38 0.30, 1.30

CDVA Z corrected distance visual acuity; CME Z cystoid macular edema *P Z .06 † P ! .05 for the comparison of patients with and without CME

(NSAIDs) prior to the secondary IOL implantation/ refixation. According to the chosen diagnostic criteria (any retinal fluid-filled cysts R10 mm with or without central thickening), 7 patients (16.7%) developed CME during the course of observation. The edema was treated with intravitreal corticosteroid injections (0.8 mg dexamethasone in 0.2 mL injected through the pars plana, 5 eyes) or topical NSAID treatment (1 eye); 1 eye with CME received no intervention due to the patient's refusal of treatment. Age and sex showed some, albeit not a significant, correlation with CME incidence. Patients who developed CME were older (P Z .06) and more often women (P Z .222) (Table 1). None of the preexisting and/or concomitant ocular diseases showed an appreciable (and/or statistically significant) relationship with the occurrence of CME, and previously performed vitrectomies did not increase the risk for CME development after PC IOL (Table 1).

There was no difference in the incidence between the 2 indication groups (Group 1: 5 of 28 eyes [17.9%]; Group 2: 2 of 14 eyes [14.3%]). In both groups, the

Figure 1. Kaplan-Meier diagram of CME occurrence in patients receiving secondary PC IOL because of preexisting aphakia and failed primary IOL (CME Z cystoid macular edema).

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Figure 2. Receiver operating characteristic diagram for the sensitivity/specificity of CME prediction by patient age.

Figure 3. Receiver operating characteristic diagram for the sensitivity/specificity of CME prediction by postoperative CDVA.

CME occurred evenly distributed over the observation period (Figure 1). Patients who developed CME during the course of observation had by trend (albeit not statistically significant) worse CDVA before surgery than patients who did not develop CME. Moreover, patients who developed CME had significantly worse CDVA after surgery (P Z .049). For all episodes of CME occurrence, possible predisposing factors were carefully analyzed. Because CDVA after surgery had a significant influence and age showed a marked trend, both criteria were included in an ROC analysis. According to these analyses, patients who had secondary PC IOL implantation were especially prone to develop CME with significant visual impairment when they were of advanced age or had a poor early postoperative visual acuity. The best cutoff point for age was 83.9 years. The prediction of CME occurrence according to this threshold had a sensitivity of 57.1% and a specificity of 82.6%, and 30% of cases would have been misclassified (Figure 2). The visual acuity immediately after IOL insertion allowed an even more accurate prediction, with a sensitivity of 85.7% and a specificity of 62.9% (25.7% misclassifications) for the cutoff point of 0.35 logMAR (Figure 3).

support) and moreover, the dislocation of a previously correctly placed IOL may require secondary procedures. If the primary IOL implantation is not feasible or an IOL is dislocated, the restoration of visual function is possible with a secondary procedure; there is a multitude of surgical techniques with specific advantages and disadvantages,4,12 and there are no general recommendations regarding the most favorable surgical approach. Basically, there are 4 approaches to the fixation of a posteriorly dislocated IOL: an anterior chamber IOL, a scleral-sutured PC IOL, an iris-sutured PC IOL, and a sutureless irisfixated IOL.3–5,13 Because of considerable intraoperative manipulation, the incidence of CME is higher after secondary PC IOL implantation than in standard cataract surgery. However, published reports of the CME incidence after PC IOL implantation is fragmentary, and SD-OCT, generally accepted as the gold standard for CME diagnosis,14–16 is not a standardized part of the postoperative evaluation of patients after PC IOL implantation. Moreover, there is no generally accepted standard diagnostic criteria for CME. Whereas a correlation between retinal thickness and visual acuity impairment, the clinical hallmark of CME, is undeniable, retinal thickness is no longer acceptable as the main criterion because SD-OCT offers much more sensitive methods of CME detection in cases in which the thickness is still normal.15 On the other hand, retinal thickness is still used in many pertinent studies,17–19 and in other trials the exact diagnostic criteria for CME are not stated.20,21 Because the incidence of clinically apparent CME after invasive ocular procedures is reportedly rather low (up to 2.5%),19,22 the

DISCUSSION The occurrence of CME is a serious complication after traumatizing intraocular procedures. Under favorable circumstances, the replacement of the opaque natural lens by an artificial lens in cataract surgery is performed in a single session that results in a stable placement of the IOL in the native lens capsule. However, this is not always attainable as a consequence of the anatomical situation (eg, insufficient capsule

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paramount importance of well-defined OCT criteria is obvious, and indeed much higher figures are observed when more sensitive signs of CME are considered.23 First, the present study found that CME can be avoided in many cases with a risk-conscious atraumatic surgical proceeding. According to our (admittedly limited) results, patient age and CDVA immediately after surgery allow for a simple and fairly accurate risk stratification. Cystoid macular edema occurred in 70% of eyes in patients who were 84 years or older and in 74% of eyes with a postoperative CDVA of more than 0.35 logMAR, and we would recommend a rigorous observation and metaphylaxis in patients who fulfill 1, and especially both, risk criteria. There is no established riskadjusted strategy so far, so we recommend to err on the side of caution. Patients at an increased risk should have frequent OCT examinations (eg, every 2 weeks) and when signs of incipient CME are detected they should receive immediate antiinflammatory treatment. The most appropriate agent for this intervention should be determined in further trials; for now, evidence does not support any strategy other than externally applied NSAIDs/corticosteroids and possibly short-acting intravitreal corticosteroids (ie, dexamethasone or triamcinolone).24–29 Long-acting steroid formulations and/or monoclonal antibodies may evolve as 2 interesting alternatives in the future, and their application should mainly take place in prospective study settings to gather pertinent evidence as soon as possible. There is an extremely broad spread of published data concerning the incidence of CME after ocular surgery. Whereas CME is not uniformly stated as a postoperative complication in the first place, there are series with no or few pertinent events13,30 as well as studies in which almost 50% of patients develop CME.23 Although a part of the observed differences is certainly attributable to differences in surgical procedures and concomitant disease, a greater percentage is most likely due to methodological issues. In many studies, an exact description of the diagnostic proceeding is notably absent, and it obviously makes a difference if an OCT examination is only performed on clinical suspicion of CME or as part of the routine follow-up. Moreover, the “traditional” diagnostic parameter, retinal thickness, should be replaced by the SD-OCT–derived presence of fluid-filled microcysts as the earliest sign of CME. It is important to point out that impairment of visual acuity does not occur in subclinical CME17; as the present study clearly demonstrates that CME can develop months (and probably even years) after surgery, cross-sectional assessments, and especially

those that only apply OCT after the occurrence of visual impairment, tend to underestimate the “true” incidence of CME after ocular surgery. From the present study's viewpoint, routine examinations with SD-OCT should be used as part of the standard follow-up after major eye surgery, and only if such data are more readily available will a reasonable assessment of CME incidence be possible. At this point, a rational benchmarking as part of a quality assurance strategy is not possible. In the present series, patient age and the CDVA immediately after surgery were the only identified risk factors for CME. The complete absence of any quantitative trends for diabetes and concomitant eye diseases makes it rather unlikely that those will play a major role in larger patient samples. In general, diabetes mellitus predisposes to CME,19 but the operative factor is diabetic retinopathy and not poor glycemic control; as such, the absence of an influence of diabetes in our sample, taken together with the fact that our diabetic patients had no retinopathy, verifies this. However, the availability of prospective data from larger studies may reveal other risk markers of interest. We found no indication of a risk difference between patients who had primary refixation of a luxated PC IOL in the ciliary sulcus and those with preexisting aphakia. This observation is of relevance because of the assumption that the trauma might be more pronounced in procedures in which the IOL implantation was postponed. In contrast, patients with dislocated artificial lenses mostly had a long stable period. A possible reason for this dislocation is PXF syndrome, but there was no relationship between PXF and CME in the present series to corroborate this assumption. As stated above, there is no sufficient evidence to recommend any specific intravitreal medication for postoperative CME. However, in patients with a preexisting glaucoma or an increased risk for secondary glaucoma, vascular endothelial growth factor inhibitors should be considered as an alternative to shortacting corticosteroids. As described in the Methods section, we took great care to avoid incarcerations of the vitreous because these can cause traction on the iris and subsequent prostaglandin-induced acute edema. In technically complex and demanding procedures, the consultation of a vitreoretinal surgeon should be considered to minimize this risk; the higher short-term staff demand is probably far outweighed by a subsequent reduction due to avoidance of complications. In conclusion, CME is a serious complication of ocular surgery and difficult to treat. It is, however,

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anything but inevitable, even after major procedures, and patients at an increased risk should be closely monitored with frequent OCT examinations. Swift and forceful intervention in preclinical CME can limit the retinal damage and preserve visual acuity. Further studies are required for the evidence-based assessment of the CME risk after PC IOL implantation and the most appropriate treatment strategy. WHAT WAS KNOWN  Secondary PC IOL implantation is a mandatory procedure in IOL dislocation and provides a significant improvement in aphakic eyes; however, the procedure is burdened with a substantial risk of CME development. WHAT THIS PAPER ADDS  The risk for CME development was equivalent in PC IOL insertion for aphakia and dislocated primary PC IOLs. Poor visual acuity immediately after the procedure was a significant risk factor for CME development, and advanced age showed a marked trend; both parameters might serve as stratification criteria for aggressive metaphylaxis.  Aggressive metaphylaxis should include intravitreal application of short-acting corticosteroids, but the possible benefit of alternatives (long-acting corticosteroids and/ or vascular endothelial growth factor inhibitors) should be investigated systematically.

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OTHER CITED MATERIAL A. Philipp S, Meyer LM, Distelmaier P, Fischer MT, Mammen A, € nfeld C-L, “Incidence of Cystoid MacuPaquet P, Haller K, Scho lar Edema (CME) Following Secondary Posterior Chamber Intraocular Lens Implantation (PC-IOL),” presented at the 111th annual meeting of the Deutsche Ophthalmologische Gesellschaft, Berlin, Germany, September 2013. Abstract available in: Ophthalmologe 2013; 110:(suppl 1):141

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First author: Linda M. Meyer, MD Augenklinik Herzog Carl Theodor, Munich, Germany