Ophthalmic Surgery, Lasers and Imaging Retina

Clinical Science 

Management of Cystoid Macular Edema After Vitrectomy for Proliferative Vitreoretinopathy

Miguel A. Busquets, MD; Calvin T. Lutz, MA; Tailun Zhao, MD

Abstract

BACKGROUND AND OBJECTIVE:

To assess therapies for cystoid macular edema (CME) following pars plana vitrectomy for proliferative vitreoretinopathy (PVR).

PATIENTS AND METHODS:

Retrospective analysis of 42 eyes developing CME after PVR surgery. Treatments included topical therapy, sub-Tenon's triamcinolone acetonide (STTA), intravitreal bevacizumab and combinations thereof. Best-corrected visual acuity (BCVA) as well as central subfield thickness (CST) were tracked.

RESULTS:

Mean Snellen BCVA improved from 20/598 to 20/297 (logMAR change −0.21; confidence interval [CI], −0.39 to −0.03; P = .03). Mean CST improved from 448 µm to 260 µm (CI, −248.70 to −126.06; P < 0.01). There was no difference in efficacy between treatment subgroups (analysis of variance, P = 0.16, 0.43), but STTA yielded statistically significant improvement in both categories (CI, −0.79 to −0.11; P = 0.01; and CI, −333.74 to 166.51; P < .01).

CONCLUSIONS:

Treatment of CME following PVR surgery is possible with a variety of different options. STTA appears to yield anatomical and visual improvement.

[Ophthalmic Surg Lasers Imaging Retina. 2020;51:436–443.]

Abstract

BACKGROUND AND OBJECTIVE:

To assess therapies for cystoid macular edema (CME) following pars plana vitrectomy for proliferative vitreoretinopathy (PVR).

PATIENTS AND METHODS:

Retrospective analysis of 42 eyes developing CME after PVR surgery. Treatments included topical therapy, sub-Tenon's triamcinolone acetonide (STTA), intravitreal bevacizumab and combinations thereof. Best-corrected visual acuity (BCVA) as well as central subfield thickness (CST) were tracked.

RESULTS:

Mean Snellen BCVA improved from 20/598 to 20/297 (logMAR change −0.21; confidence interval [CI], −0.39 to −0.03; P = .03). Mean CST improved from 448 µm to 260 µm (CI, −248.70 to −126.06; P < 0.01). There was no difference in efficacy between treatment subgroups (analysis of variance, P = 0.16, 0.43), but STTA yielded statistically significant improvement in both categories (CI, −0.79 to −0.11; P = 0.01; and CI, −333.74 to 166.51; P < .01).

CONCLUSIONS:

Treatment of CME following PVR surgery is possible with a variety of different options. STTA appears to yield anatomical and visual improvement.

[Ophthalmic Surg Lasers Imaging Retina. 2020;51:436–443.]

Introduction

Proliferative vitreoretinopathy (PVR) is a significant obstacle to optimal outcomes for patients undergoing rhegmatogenous retinal detachment (RRD) repair. It is the principal cause of failure in retinal detachment surgery, as approximately 75% of all primary surgical failures are due to this entity.1 PVR develops in response to dedifferentiated retinal pigment epithelial cells and results from the action of multiple trophic factors (including epidermal and fibroblast growth factors, vascular endothelial growth factor [VEGF], platelet-derived growth factor, and tumor necrosis factor alpha and beta) and cytokines, together with macrophages and retinal glial cells.2–4 Cellular membranes that develop on the surfaces of the retina cause contraction that yields secondary tractional and RRDs.5 Numerous pharmacologic agents have been evaluated for the treatment and prevention of PVR with disappointing results.6–11 Surgical repair of PVR-related retinal detachments remains the standard of care. Multiple series have shown that a 180° to 360° retinectomy procedure can be effective in the treatment of anterior and posterior PVR-related retinal detachments, both anatomically and visually, with reattachment rates varying between 70% and 93%.12–15 Similarly, the Silicone Study Group16,17 demonstrated the relative benefit of longer-acting tamponade agents, such as silicone oil (SO).

Visual prognosis in patients with PVR may be compromised by the very nature of the condition, particularly after one or more macula-off events. A series by Pournaras et al.18 reported that only 29% of patients undergoing an average of four surgeries for recurrent retinal detachments often associated with PVR had a best-corrected visual acuity (BCVA) better than 20/40. In another series, De Silva et al. found that only 16% of patients undergoing retinectomy achieved a final visual acuity (VA) of 20/60 or better.19 Thus, postoperative development of CME would pose an unfortunate additional challenge to visual recovery in these patients.

Cystoid macular edema (CME) can be a similarly confounding obstacle to achieving optimal post-surgical results after eye surgery. CME is defined as the presence of intraretinal and/or subretinal fluid (SRF) in macular tissue. Although multiple etiologies exist for this condition, including retinal vein occlusions and side effects from various medications, intraocular surgery is a known risk factor for its development. Postoperative inflammation associated with cytokine release disrupts the blood-retinal barrier. Increased perifoveal vascular permeability causes macular swelling and secondary visual disability.20–22 Its development during the postoperative period limits and delays optimal results, particularly in cases with heavy loads of proinflammatory mediators, as is the case with PVR.

Few articles exist to document the incidence, timing, and management of CME after vitreoretinal surgery. These reports vary in their findings, demonstrating post-vitrectomy CME rates between 10% and 87%.23,24 Relating to RRDs, the incidence of postoperative CME after vitrectomy ranges from 2.3% to 43%, regardless of the use of small-gauge vitrectomy, presence of scleral buckle, or types of adjuvant agents.25-28 A small number of series and case studies assessing treatment outcomes for CME after RRD have been reported. Lai et al.25 noted remission of CME after 2.8 sub-Tenon's triamcinolone acetonide (STTA) injections in 55% of patients. In a case of CME after scleral buckle for macula-off RD that only partially improved after STTA, Bonifiglio et al.29 reported resolution of CME with visual improvement following implantation of a sustained-release 0.7-mg dexamethasone implant after 6 months. To our knowledge, no studies exist that comparatively assess the efficacy of various treatments for postoperative CME following silicone oil removal post-vitrectomy surgery for PVR.

Patients and Methods

Data Acquisition

The course of therapy and outcomes of 42 consecutive eyes that developed CME after SO removal following vitrectomy surgery for grade CP or CA (1 to 12)30 PVR-associated macula-off retinal detachment (tractional or combined tractional/rhegmatogenous) were analyzed retrospectively. Informed consent for data acquisition was obtained from all participants. Analysis of all variables was performed using PROC GLM and PROC FREQ procedures in SAS/STAT software version 9.4 (SAS Institute, Cary, NC).

Subjects underwent all relevant surgeries by one of four surgeons in a single outpatient center and had received initial surgery for macula-off RRD repair with 25-gauge vitrectomy, laser retinopexy, and gas tamponade. A second small-gauge PPV for PVR involving membrane stripping, 180° to 360° retinectomy, perfluoro-n-octane (PFO) injection, and endolaser followed by PFO-1,000 centistoke SO exchange was performed (range: 6 to 16 weeks post initial procedure). A third small-gauge vitrectomy with SO removal and air-fluid exchange was performed between 12 and 16 weeks after injection of SO for all patients in this series. Patients received topical antibiotic and prednisolone acetate 1% drops four times per day for 1 week postoperatively. Inclusion in the study required onset of CME within 26 weeks of SO removal, central subfield thickness (CST) on optical coherence tomography (OCT) greater than 250 µm, and follow-up of at least 12 weeks from time of final surgery. The diagnosis of clinically significant CME was based on: (1) the presence of intraretinal edema, with or without SRF on OCT; (2) leakage on fluorescein angiography (FA) in the characteristic petalloid, hyperfluorescent pattern; and (3) clinical correlation via contact lens biomicroscopic examination. Patients were followed for 120 weeks or until resolution of CME. Subjects with prior history in the study eye of any of the following were excluded: CME, any vitrectomy prior to initial surgical study procedure or cataract surgery within 2 years of first study procedure, additional ocular surgery during follow-up, visually significant cataract, diabetic retinopathy, epiretinal membranes, retinal vein occlusions, uveitis, hypotony or pre-existing glaucoma. Primary outcomes of Snellen BCVA and CST were tracked. FA was also performed at each visit. Intraocular pressure (IOP) was monitored via Goldmann applanation tonometry to assess for secondary glaucoma. For the purposes of this study, IOP spikes were defined as IOP greater than 25 mm HG or an increase in IOP of greater than 10 mm HG during the follow-up period after initiation of therapy for CME.

Complete resolution of CME was defined as complete absence of fluid and leakage using the three aforementioned modalities. Clinical resolution of CME was defined as normalization of OCT findings with persistent leakage on FA regardless of VA. Any residual intraretinal or SRF contributing to retinal thickening constituted persistent CME. Time to onset (TTO) and time to clinical or complete resolution (TTR) of CME were also measured for all patients.

Therapeutic Interventions

Therapeutic options included (1) topical therapy with a corticosteroid (prednisolone acetate 1% four times per day) and non-steroidal anti-inflammatory drug (NSAID) (bromfenac 0.07.% or 0.09% every day), (2) periocular corticosteroids (sub-Tenon's triamcinolone acetonide [STTA], 40 mg/1 mL, repeated PRN), (3) intravitreal anti-VEGF agent injection (bevacizumab [IVB] [Avastin; Genentech, South San Francisco, CA] 1.25 mg, once every 4 weeks, as needed), (4) combinations of all of these modalities, including “Triple” therapy with STTA, IVB, and topical NSAID. Patients in the STTA + Topical arm received a topical NSAID but no topical steroid, due to the administration of STTA. Subject and treatment counts within the treatment subgroups are summarized in Table 1.

Treatment Breakdown by Subgroup

Table 1:

Treatment Breakdown by Subgroup

Results

Mean age in the study was 65 years. The study sample was 36% female and 64% male. Complete resolution of CME resulted in 74% of cases (31/42), whereas 24% (10/42) demonstrated clinical resolution and 2% (1/42) demonstrated persistent CME. Mean BCVA and CST improved for all patients combined. Mean preoperative Snellen BCVA for the overall group was 20/1,247, whereas mean baseline (at time of onset of CME) and final Snellen BCVA were 20/598 and 20/297, respectively. This represented a mean change in baseline to final logMAR vision of −0.21 (confidence interval [CI], −0.39 to −0.03; P = .03). LogMAR improvement in vision from preoperative to final (−0.63) was also statistically significant (CI, −0.79 to −0.42; P < .0001). At final follow-up, 31% of eyes had BCVA greater than 20/40, 33.3% of eyes were between 20/40 and 20/80, 14.3% between 20/80 and 20/200, and 21.4% were less than 20/200. VA data breakdown by treatment subgroup is summarized in Table 2. Mean CST for all subjects combined also improved from 448 µm to 260 µm between baseline and final assessments (prism diopters = −188; CI, −248.70 to −126.06; P < .0001 < .01). CST data breakdown by treatment subgroup is summarized in Table 3. Figure 1 demonstrates the trend in BCVA improvement from preoperative to baseline to final assessments, as well as the trend CST reduction from baseline to final for all treatment subgroups and all subjects combined. Analysis of variance (ANOVA) testing and pairwise comparisons for primary outcomes of change in BCVA and CST across all treatment subgroups demonstrated no statistically significant difference between treatment types (P = .16 for logMAR BCVA; P = .43 for CST).

Visual Acuity Metrics

Table 2:

Visual Acuity Metrics

CST Metrics

Table 3:

CST Metrics

Visual acuity (VA) and central subfield thickness (CST) trends. Analysis of variance testing and pairwise comparisons demonstrated no significant difference between treatments relative to these variables. IVB = intravitreal bevacizumab; STTA = sub-Tenon's triamcinolone acetonide

Figure 1.

Visual acuity (VA) and central subfield thickness (CST) trends. Analysis of variance testing and pairwise comparisons demonstrated no significant difference between treatments relative to these variables. IVB = intravitreal bevacizumab; STTA = sub-Tenon's triamcinolone acetonide

TTO and TTR data are illustrated in Figure 2. Mean TTO combined for all treatment subgroups was 12.66 weeks (range: 4 to 26 weeks; standard deviation [SD]: 11.43; CI, 9.10–16.22), whereas mean TTR was 28.84 weeks (range: 4 to 120 weeks; SD: 37.54; CI, 17.14–40.54) from baseline. One patient in the series within the “Triple” therapy category did not achieve even clinical resolution of the CME and was categorized as having persistent CME. The mean TTR data for the “Triple” category was impacted by inclusion of this patient.

Time to onset (TTO) and time to clinical or complete resolution (TTR) by treatment group. Analysis of variance (ANOVA) testing demonstrated no significant difference between treatment groups regarding TTO (P = .99). ANOVA testing on TTR coupled with pairwise comparisons demonstrated the STTA/IVB subgroup had a significantly longer mean TTR (109.43 weeks; standard deviation: 82.63; confidence interval: −95.84 to 314.69; P < .01). IVB = intravitreal bevacizumab; STTA = sub-Tenon's triamcinolone acetonide; IVB = intravitreal bevacizumab

Figure 2.

Time to onset (TTO) and time to clinical or complete resolution (TTR) by treatment group. Analysis of variance (ANOVA) testing demonstrated no significant difference between treatment groups regarding TTO (P = .99). ANOVA testing on TTR coupled with pairwise comparisons demonstrated the STTA/IVB subgroup had a significantly longer mean TTR (109.43 weeks; standard deviation: 82.63; confidence interval: −95.84 to 314.69; P < .01). IVB = intravitreal bevacizumab; STTA = sub-Tenon's triamcinolone acetonide; IVB = intravitreal bevacizumab

(a) Postoperative cystoid macular edema prior to treatment, with cystic changes throughout the retinal layers and in the subretinal space. (b) Same patient 14 weeks after sub-Tenon's triamcinolone acetonide, demonstrating full resolution of edema and normalization of foveal contour.

Figure 3.

(a) Postoperative cystoid macular edema prior to treatment, with cystic changes throughout the retinal layers and in the subretinal space. (b) Same patient 14 weeks after sub-Tenon's triamcinolone acetonide, demonstrating full resolution of edema and normalization of foveal contour.

Incidence of secondary glaucoma based on the established criteria was 21% (nine of 42). Incidence of secondary glaucoma in the treatment cohorts receiving corticosteroid therapy was 22% (9/41). Fisher's Exact test revealed no predilection towards IOP spikes for any treatment subgroup (Fisher's P = .13).

Discussion

The subjects in this series are representative of a population that suffers from multiple obstacles to visual recovery. The presence of consecutive macula-off retinal detachments is only one such obstacle. Visual acuity better than 20/50 is reached in only 50% of macula-off RRD patients repaired within 9 days,31 largely due to photoreceptor apoptosis.32,33 Additionally, all patients in this study underwent three surgical procedures within a short, 6-month timeframe. Coupled with the development of PVR, an inherently pro-inflammatory condition,2,3 the eyes in this analysis were pathophysiologically prone to the resulting CME. Its development represents a final challenge in these patients. The cystoid spaces that develop in the inner nuclear and outer plexiform layers in cases of CME serve as evidence that vision-limiting morphologic changes at the neurosensory level take place in this condition.34 Residual intraretinal cystic and ellipsoid zone changes present in patients in this series with resolved CME point to this fact. Prompt diagnosis and effective treatment upon CME development could help eliminate an additional hurdle to complete visual recovery in these patients. In this series, there were no statistically significant differences regarding efficacy between individual treatment modalities pertaining to the overall improvement in primary outcomes. However, for all subjects combined, there was an anatomical and visual benefit to treatment, correlating with the fact that 98% of patients experienced at least clinical resolution of the macular edema.

Of the treatment subgroups, the STTA cohort was the only category that demonstrated statistically significant improvement in change in BCVA and CST. Although this subgroup contained the largest number of subjects, the small sample sizes of the other groups prevents the ability to draw conclusions about the correlation between the functional and anatomical parameters studied across treatments. This limitation in power is the primary weakness of this study, along with its retrospective nature. However, within the patient population contained in this study sample, STTA yielded statistically significant improvement in CME with minimal treatment burden. Furthermore, the mean treatment count of 1.3 injections for this subgroup was associated with a mean TTR of approximately 4 months (17.73 weeks), compared to almost 7 months (28.84 weeks) for the broader group.

Utilization of sub-Tenon's corticosteroid injections in vitrectomized eyes with macular edema has been studied in other case series, although the emphasis has largely been on diabetic patients.35,36 The surgeons in this study favored this modality over IVTA, as IVTA may have superior short-term performance but a faster decay than STTA in vitrectomized eyes.36,37 IVTA could thus be a potentially less favorable choice in cases of CME that are more chronic in nature, as the long mean, overall TTO and TTR in this study suggest the patients in this series may have had. A head-to-head comparison of these modalities would be informative.

The non-statistically significant P value for the TTO ANOVA suggests that TTO did not appear to influence treatment selection in this series. Further, the mean time to diagnosis of CME of 13 weeks, suggests that patients undergoing the surgical repairs represented by this analysis may require prolonged postoperative monitoring. Although Irvine-Gass syndrome following cataract surgery usually appears within 4 to 6 weeks,20–22 patients in this more complex context may be at risk for the development of CME for a longer period of time. Careful postoperative follow-up utilizing OCT and FA, when appropriate, in order to identify the CME, could make a difference in the final visual outcome by precipitating therapeutic intervention.

TTR data are significant for two reasons. First, the mean overall TTR of 29 weeks alludes to the potential chronicity of CME following vitrectomy for PVR. Second, the pairwise comparisons show that the STTA plus IVB subgroup had significantly longer time to resolution than all other categories. Because of small subgroup sample sizes, it is unclear whether this outcome reflects poor therapeutic efficacy for this modality, or if the patients in this category represented a subset that is prone to CME of an ultra-chronic nature. It is noteworthy that of the 10 patients with clinical resolution of CME in this series, three were in this group (representing 100% of the group), and normalization of the OCT was delayed in all three of these cases. Other series have demonstrated poor response to IVB as a treatment for CME. In vitrectomized eyes with recalcitrant CME, Alam et al.38 demonstrated no benefit to IVB and Chen et al.39 found similar results after epimacular membrane surgery.

Based on this analysis, CME arising after vitrectomy surgery with retinectomy and silicone oil tamponade for CP/CA PVR, can be effectively treated using a variety of modalities, resulting in improvements in both VA and CST. Sub-Tenon's triamcinolone acetonide injection was the only treatment group to yield statistically significant improvement both anatomically and visually. Studies comparing the groups herein to the application of standard and extended-duration intravitreal corticosteroids are indicated. Randomized, prospective clinical trials with larger sample sizes, identifying risk factors for development and recurrence of CME after PVR surgery, and correlating severity stratification with outcomes associated with different therapeutic options, would likely be of benefit to this population.

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Treatment Breakdown by Subgroup

Treatment Subject Number Average Number of Treatments
Topical 7 N/A
IVB 1 1.0
IVB + Topical 4 1.8
STTA 13 1.3
STTA + Topical 9 1.6
STTA + IVB 3 7.3 (3 STTA, 4.3 IVB)
Triple 5 5.2 (1.6 STTA, 3.6 IVB)
All 42 2.1

Visual Acuity Metrics

Treatment Preoperative BCVA Baseline BCVA Final BCVA CHANGE in logMAR (Final Minus Baseline)
Snellen (20/x) logMAR Snellen (20/x) logMAR Snellen (20/x) logMAR logMAR Δ P Value (logMAR) 95% CI (logMAR)
Topical 970 1.25 420 0.88 388 0.96 0.08 .70 (−0.33 to 0.49)
IVB 4000 2.30 800 1.60 60 0.48 1.12 .04 (−2.21 to −0.04)
IVB+Topical 300 1.15 110 0.69 138 0.72 0.02 .93 (−0.52 to 0.56)
STTA 1,567 1.65 711 1.29 193 0.79 0.45 .01 (−0.79 to −0.11)
STTA+Topical 1,064 1.28 668 0.92 576 0.90 −0 .02 .90 (−0.38 to 0.34)
STTA+IVB 1,911 1.81 1423 1.28 103 0.77 −0.51 .10 (−1.14 to 0.11)
Triple 1,000 1.52 280 0.85 232 0.59 −0.26 .28 (−0.74 to 0.22)
All 1,247 1.46 598 1.04 297 0.80 0.21 .03 (−0.39 to −0.03)

CST Metrics

Treatment Baseline CST Final CST Change in CST (Final Minus Baseline)
Mean P Value 95% CI
Topical 275.60 228.20 −47.40 .57 (−215.12 to 120.32)
IVB 367.00 300.00 −67.00 .72 (−442.03 to 308.03)
IVB+Topical 350.25 251.50 −98.75 .29 (−286.27 to 88.77)
STTA 522.46 277.62 −244.85 < .01 (−348.86 to −140.83)
STTA+Topical 460.38 255.38 −205.00 < .01 (−337.59 to −72.41)
STTA+IVB 424.00 226.33 −203.00 .13 (−468.19 to 62.19)
Triple 524.25 273.00 −251.25 .01 (−438.77 to −63.73)
All 447.73 259.74 −187.38 < .01 (−248.7 to −126.1)
Authors

From Retina Associates of Kentucky, Lexington, Kentucky (MAB); the Department of Statistics, University of Pittsburgh, Pittsburgh, Pennsylvania (CTL); and Vitreoretinal Service, Associates in Ophthalmology, Pittsburgh, Pennsylvania (TZ).

The authors report no relevant financial disclosures.

Address correspondence to Miguel A. Busquets, MD, 120 N. Eagle Creek Drive, Suite 500, Lexington, KY 40509; email: mbusquets@retinaky.com.

Received: January 13, 2020
Accepted: July 01, 2020

10.3928/23258160-20200804-03

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