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Chen, Hsi-Fu MD*; Yeung, Ling MD*; Yang, Ko-Jen MD; Sun, Chi-Chin MD, PhD*,‡

doi: 10.1097/IAE.0000000000000657
Original Study

Purpose: To investigate the incidence, risk factors, and clinical course of persistent corneal epithelial defects (PCED) after pars plana vitrectomy (PPV).

Methods: The charts of 426 consecutive patients (511 eyes) who received PPV from January 2008 to December 2011 were reviewed. Corneal complications were defined as the presence of corneal epithelial defects, corneal edema, or superficial punctate keratopathy at least 1 week after vitrectomy. The PCED was defined as corneal epithelial defects lasting longer than 2 weeks after vitrectomy despite conventional treatment. The demographic, preoperative, intraoperative, and postoperative data were compared between PCED and non-PCED corneal complication groups to evaluate the risk factors and clinical outcomes.

Results: Postoperative corneal complications developed in 103 of 460 (22.4%) eyes. Diabetes was associated with postoperative corneal epithelial defects (P = 0.021) and superficial punctate keratopathy (P = 0.022) but not corneal edema (P = 0.925). Among 103 eyes with corneal complications, 21 eyes developed PCED. The eyes with PCED had poor final visual acuity, with 23.8% (5/21) of the eyes in the PCED group having visual acuity of 20/200 or better compared with 51.2% (42/82) of the eyes in the non-PCED group (P = 0.024). Logistic regression analysis demonstrated that diabetes mellitus (P = 0.025), use of perfluoropropane (P = 0.001), and assistance of a first-year resident (P = 0.029) were statistically significant risk factors for PCED after PPV. There was also a high incidence of geographic herpes simplex virus epithelial keratitis among recalcitrant PCEDs lasting longer than 4 weeks (36%, 4/11 eyes).

Conclusion: The overall incidence of PCED after PPV was 4.8%. Diabetes mellitus, intravitreal tamponade with perfluoropropane, and assistance of a first-year resident were risk factors for PCED after PPV. Persistent corneal epithelial defects after PPV were correlated with poor postoperative visual outcomes. Early and aggressive management is necessary for patients presenting with corneal epithelial defects after vitrectomy to prevent poor outcomes.

Early identification and aggressive management is necessary for patients presenting with persistent corneal epithelial defects after vitrectomy to prevent poor visual outcomes.

*Department of Ophthalmology, Chang Gung Memorial Hospital, Keelung, Taiwan;

University Eye Center, Taipei, Taiwan; and

Department of Chinese Medicine, Chang Gung University, Kwei-shan, Taoyuan, Taiwan.

Reprint requests: Chi-Chin Sun, MD, PhD, Department of Ophthalmology, Chang Gung Memorial Hospital, Keelung, Taiwan, 222 Mai Chin Road, An Leh District, Keelung, Taiwan; e-mail:

None of the authors have any financial/conflicting interests to disclose.

H.-Fu Chen and L. Yeung have contributed equally to this work.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND), which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially.

Persistent corneal epithelial defects (PCED) after pars plana vitrectomy (PPV) are a challenging problem for ophthalmologists. They are associated with a variety of significant clinical morbidities, including infectious keratitis, endophthalmitis, corneal scarring, melting, and perforation, which can result in discomfort, compromised therapeutic effect of vitrectomy in visual recovery, and even visual loss or phthisis bulbi.1

The pathogenesis of PCED is unclear.2 Several etiologies have been proposed, including dry eye, corneal limbal stem cell deficiency, diabetes mellitus, and neurotrophic keratitis.3 Moreover, many contributing factors also have been reported to compromise corneal epithelial and endothelial cell layers after vitrectomy surgery, including the duration of surgery, intraoperative epithelial debridement, intraoperative lensectomy, a history of previous vitrectomy, contact viewing lens for vitrectomy, preoperative lens status, anterior capsule integrity, and the use of adjunctive intraocular long-acting expansile gas or silicone oil.4 The chronic lack of healing from PCED after PPV may therefore not only be caused by predisposing corneal comorbidity but also by a compromised cornea because of vitreoretinal surgery. However, little is known about the development of PCED after PPV in eyes with corneal complications. Therefore, we conducted this study to investigate the incidence, risk factors, and clinical course of PCED after PPV to elucidate their preoperative, intraoperative, and postoperative distinguishing characteristics.

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Subjects and Study Design

This is a retrospective review of 426 consecutive patients (511 eyes) who received PPV at Chang Gung Memorial Hospital, Keelung, Taiwan between January 1, 2008, and December 31, 2011. The Institutional Review Board of Chang Gung Memorial Hospital approved this study. The patients' demographic, preoperative, intraoperative, and postoperative data were recorded. To avoid the confounding effect of comorbid diseases of the cornea, 51 patients (51 eyes) were excluded because of 1) preexisting corneal edema or epithelial disturbance before vitrectomy (4 eyes), 2) infectious endophthalmitis (24 eyes), and 3) open-globe trauma (22 eyes). In total, 460 eyes were included in this study.

All patients received PPV with standard three-port 20-gauge or 23-gauge incisions using a contact viewing lens system with a handheld contact lens and viscoelastic lubricant. Balanced salt solution plus (Alcon Laboratories, Inc, Fort Worth, TX) was used as the intraocular irrigating solution in all patients. Scleral buckling for retinal detachment was performed with an encircling band. For the patients requiring air–fluid exchange or intraocular tamponade, either air, long-acting expansile gas mixtures, such as perfluoropropane (C3F8) gas or sulfur hexafluoride (SF6) gas, or silicone oil was used. The type of gas or silicone oil used was dependent on the individual clinical situation. Tobradex (0.3% tobramycin and 0.1% dexamethasone) ophthalmic ointment (Alcon Laboratories, Inc) was applied postoperatively two times daily for an average of 3 to 4 weeks.

We defined corneal complications using the criteria proposed by Hiraoka et al,5 that is, the presence of corneal epithelial defects (ED), corneal edema, or superficial punctate keratopathy lasting for at least 7 days after PPV. We divided these eyes into non-PCED and PCED groups for statistical analysis. We adopted the definition of PCED reported by Tsubota et al,3 as “a corneal ED persisting for more than 2 weeks without improvement despite conventional treatment such as artificial tears or extended wearing of soft contact lenses.”

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Statistical Analysis

SPSS statistical software version 18.0 was used for all statistical analyses (SPSS Inc, Chicago, IL). Pearson chi-square test or Fisher's exact test was used to compare categorical variables between the PCED and non-PCED corneal complication groups in terms of demographic characteristics, history of previous ophthalmic surgery, surgical indications, simultaneous surgical procedures, operative time, experience of the assisting residents, preoperative lens status, postoperative lens status, ocular hypertension receiving glaucoma medications within 2 weeks after PPV, preoperative visual acuities, and final documented postoperative visual acuities. Continuous variables were evaluated with the independent sample t-test. Multivariate logistic regression was used to adjust for potential confounding risk factors for the occurrence of PCED. A P value of less than 0.05 was considered to be statistically significant.

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We identified 103 eyes from 96 patients who had corneal complications after PPV. The overall incidence of corneal complications after PPV was 22.4% (103/460 eyes), with 82 eyes (75 patients) in the non-PCED group, and 21 eyes (21 patients) in the PCED group. The demographic data are shown in Table 1. The incidence of PCED after PPV was 4.6% (21/460 eyes). The clinical characteristics of each group are summarized in Table 2. Diabetes mellitus (P = 0.024), intravitreal tamponade with C3F8 (P = 0.001), assistance by a first-year resident (P = 0.037), and postoperative ocular hypertension for which glaucoma medication was given within 2 weeks after PPV (P = 0.040) were significantly associated with PCED. The above factors and the operative time were included in a multivariate logistic regression analysis. Only diabetes, intravitreal tamponade with C3F8, and assistance by a first-year resident were significantly associated with PCED (Table 3).

Table 1

Table 1

Table 2

Table 2

Table 3

Table 3

Among the 103 eyes with corneal complications, 29 had corneal ED. Corneal ED were either acute-onset or delay-onset in this study. Twenty-four eyes (83%) had acute-onset ED, which occurred on postoperative Day 1 in 23 eyes and was caused by intraoperative epithelial debridement to improve visualization in 1 eye. Five eyes (17%) had delayed-onset ED, which were preceded by persistent corneal edema and superficial punctate keratopathy from postoperative Day 1. The mean interval to having a diagnosis of delayed-onset corneal ED after PPV in these 5 eyes was 20.2 days (range, 6–33 days). Of the 29 patients with corneal ED after PPV, 8 eyes (27.6%) healed within 2 weeks with a mean duration of 8.8 days (range, 7–12 days), whereas the remaining 21 eyes (72.4%) experienced PCED in a mean duration of 41.24 days (range, 15–172 days).

The clinical course of the PCED group is shown in Table 4. The ED of 10 eyes (47.6%) healed within 4 weeks. Another 11 eyes (52.4%) failed medical therapy within 4 weeks and had a mean time to healing of 61.9 days (range, 29–172 days). Of these 11 eyes, 5 (45.5%) developed infectious keratitis, 7 (63.6%) developed corneal opacity after complete re-epithelialization, and 1 (9.1%) developed infectious endophthalmitis. The progression of recalcitrant PCED to sight-threatening complications was common. Our results demonstrated that the eyes with PCED for more than 4 weeks were associated with higher risks of infectious keratitis (P = 0.045) and corneal opacity (P = 0.005). Of the five eyes that developed infectious keratitis, one progressed to endophthalmitis, which eventually became phthisical, and the remaining four developed geographic corneal ulcers with impaired corneal sensation detected by a Cochet–Bonnet esthesiometer, which was compatible with herpes simplex virus (HSV) keratitis. The time to diagnose geographic HSV epithelial keratitis after the occurrence of ED after PPV ranged from 15 to 83 days. Oral (4 of 4 patients) or topical (1 of 4 patients) acyclovir therapy was initiated immediately in all patients, 3 of whom healed in 27 days (range, 22–27 days), and the remaining eye with severe corneal melting because of a delayed diagnosis was eventually healed in 88 days after adjunctive treatment of amniotic membrane transplantation and topical autologous serum (Figure 1).

Table 4

Table 4

Fig. 1

Fig. 1

Table 5 summarizes the preoperative and the postoperative visual acuity. There was no significant difference in preoperative visual acuity between the groups. However, compared with the non-PCED group, the PCED group had a higher incidence of a final visual acuity worse than 20/200 (76.2% vs. 48.8%, P = 0.024).

Table 5

Table 5

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Pars plana vitrectomy may offer the opportunity for visual recovery in many vitreoretinal diseases that threaten vision. However, corneal complications, such as corneal ED, corneal edema, and superficial punctate keratopathy, are major early morbidities after PPV. The overall rate of corneal complication was 22.4% in our study. In most of the cases, early corneal complications can usually be reversed if recognized early and properly treated; however, 4.6% of the eyes developed PCED in this study. In multivariate analysis, the risk factors associated with PCED were diabetes, assistance by a first-year resident, and intravitreal tamponade with C3F8.

The reported incidence of PCED after PPV using a contact viewing lens ranges from 5.1% to 11.3%,1,6,7 which is slightly higher than in this study (4.6%). A possible explanation is that there was a lower rate of intraoperative epithelial debridement in this study. In previous reports, 2.3% to 32% of patients needed intraoperative epithelial debridement to improve visualization during PPV.1,6–8 However, Virata et al7 found that 6 of 14 (42.9%) of corneal ED due to epithelial debridement progressed to PCED without healing within 2 weeks. Because of the awareness of our surgeons and improvements in instrumentation and surgical techniques, we rarely perform intraoperative epithelial debridement.

Assistance by a first-year resident was associated with a higher risk of PCED in this study. This may be because the junior residents had less experience in holding or manipulating the contact viewing lens, which may have caused more corneal trauma during surgery. In our department, one resident or one fellow would be assigned to the vitreoretinal team every month. This resident or fellow was responsible for holding the contact lens viewing system in all of the vitreoretinal surgeries within this month, regardless the duration of the surgery. Neither nurse nor other vitreoretinal specialist would help to hold the contact lens viewing system. A noncontact lens viewing system is not available in our hospital. Furthermore, we also performed a statistic analysis comparing the operative time between first-year-resident assisting cases and non–first-year-resident assisting cases. There was no significant difference found (mean operative time: 128.80 minutes vs. 121.55 minutes, P = 0.552). Thus, the association between first-year-resident assistant and PCED was unlikely caused by different operative time between first-year residents and senior residents.

Direct intraoperative injury was a major cause of PCED in our study. We found that most cases of PCED arose from acute-onset (17/21 eyes, 81%) rather than delayed-onset (4/21 eyes, 19%) ED. Apart from the eyes that underwent intraoperative epithelial debridement, the other cases of acute-onset ED were likely caused by direct intraoperative mechanical corneal trauma by the contact viewing lens. Virata et al7 noted that the incidence of corneal ED after PPV can be reduced by avoiding the use of a contact viewing lens. Therefore, we suggest that when training a junior resident in a teaching hospital, a noncontact viewing system may be better to protect corneas in high-risk patients.

Diabetes mellitus has been reported to be a risk factor for corneal ED in previous studies.1,6–9 Our study also demonstrated that diabetes mellitus was significantly associated with the development of PCED. This makes sense mechanistically, because diabetic corneas have previously been reported to have delayed wound healing,10,11 impairment in epithelial barrier function,12–14 abnormalities in epithelial basement membrane,15–17 and abnormalities in the shape of epithelial and endothelial cells.18–26 Thus diabetic eyes may be more vulnerable to corneal injury during surgery. Someone might suspect that increased operative time for more complicated surgeries in patients with diabetes could also increase the risk of PCED. So, we further analyzed our data; there was no significant difference in mean operative time between patients with diabetes and patients without diabetes (120.45 minutes vs. 127.49 minutes, P = 0.495). There was also no significant difference between PCED and non-PCED groups in the mean operative time (120.84 minutes vs. 134.67 minutes, P = 0.278) (Table 2). When we put operative time into the multivariate logistic regression model, it did not show statistical significance (Table 3). Thus, this might imply that the PCED may be more likely to associate with the compromised corneal condition in diabetes rather than longer operative time in these patients.

Our results demonstrated that the occurrence of PCED was significantly greater in the eyes using C3F8 tamponade. However, other tamponade substances such as air, SF6, and silicone oil were not associated with PCED. In subgroup analysis, we found that the association of C3F8 and PCED was only significant in the aphakic or pseudophakic patients (P < 0.001), but not in the phakic patients (P = 0.089). Intraocular tamponade of long-acting expansile gasses in the presence of an open anterior lenticular capsule may induce corneal endothelial cell toxicity22,23,27–31 and corneal abnormalities,6,7 such as corneal edema and corneal opacity. We hypothesize that PCED may result from the direct toxicity of C3F8 when in contact with the cornea. The loss of corneal endothelial cells has also been reported to be significantly greater in eyes with C3F8 than in those with SF6.27 Intraocular C3F8 gas tamponade was a strong predictor of PCED in our study. Taken together, these results indicate that the use of C3F8 should be more conservative in aphakic and pseudophakic patients.

Elevated intraocular pressure may cause corneal edema and increase the risk of corneal complications.24,25 Glaucoma eye drops may also be toxic to the cornea, and this may contribute to the formation of superficial punctate keratopathy and corneal erosions in some patients.26,32 In our study, postoperative ocular hypertension requiring glaucoma medication was a risk factor for PCED in univariate analysis but not in multivariate analysis. This may be, at least in part, explained by the fact that postoperative ocular hypertension was associated with C3F8 tamponade (P = 0.034) in this study, demonstrating that C3F8 tamponade was a much stronger risk factor for PCED compared with previous studies.

In our study, 11/21 eyes (52%) with PCED failed to heal within 4 weeks after conventional medical treatment. These recalcitrant PCEDs tended to have a much higher incidence of serious late complications, such as corneal opacity, infectious keratitis, endophthalmitis, and even phthisis. This suggests that PCEDs persisting for more than 4 weeks is a critical cutoff point for the development of corneal infections and opacity.

To the best of our knowledge, this is the first report showing a high incidence of herpetic keratitis in recalcitrant PCED after PPV. Among 11 eyes with PCED lasting for longer than 4 weeks, 4 eyes (36%) progressed to geographic herpetic keratitis. After vitrectomy, topical corticosteroids are usually prescribed to control intraocular inflammation, and it has been reported that geographic HSV epithelial keratitis is more likely to occur than HSV dendritic keratitis under topical corticosteroid treatment.33 Thus, it may be more difficult to differentiate post-PPV herpetic keratitis from noninfectious PCED. Geographic HSV epithelial keratitis was not initially recognized in one of our patients. This eye had severe corneal melting and required repeated amniotic membrane transplantations. Early diagnosis and aggressive antiviral treatment of geographic HSV epithelial keratitis is important for many reasons. First, geographic ulcers usually take longer to heal.33 Second, when geographic HSV keratitis is associated with stromal inflammation, it usually results in other complications, such as corneal scarring, secondary glaucoma, and cataracts. Third, it also eliminates the beneficial effects of vitrectomy in visual outcomes. Therefore, we suggest that herpetic keratitis should always be taken into consideration in PCEDs that persist for longer than 4 weeks after PPV.

Prolong use of topical corticosteroid after vitrectomy could also potentially retard the corneal epithelial healing and increase the risk of herpetic keratitis. In our hospital, an antibiotic–steroid combination ointment (Tobradex ophthalmic ointment; Alcon Laboratories, Inc) was used twice daily for 3 to 4 weeks after vitrectomy to control postoperative inflammation. However, in patient with corneal ED for 1 week or more, the corticosteroid would either be early tapered or be used with extremely cautious. Because of the retrospective nature in this study, it is difficult to determine whether the topical corticosteroid increased the corneal complications from our data. In the literature, there is still no consensus on the optimal corticosteroid formula and duration of use after vitrectomy.34,35 Also, it needs further studies to determine whether topical corticosteroid would retard the corneal ED after vitrectomy.36 However, to facilitate corneal epithelial healing and prevent herpetic keratitis, it is reasonable to taper the corticosteroid once the anterior chamber is free of cell and flare.

Our study showed that patients with PCED had worse visual outcome than those without PCED. Persistent corneal epithelial defects may lead to further corneal infections and corneal opacity. Although this is a retrospective study with a relatively small sample size, it provides important information on the risk factors, clinical course, and prognosis of PCED after PPV.

The limitations to this study include its retrospective design and that the diagnosis of geographic herpes simplex keratitis from PCED after PPV in four of five infectious keratitis cases was a clinical diagnosis with a lack of laboratory evidence of corneal HSV infection. Furthermore, information on systemic morbidities such as the presence of diabetes mellitus was obtained by questionnaires in some patients without determining the actual level of hemoglobin A1c level or blood sugar.

In conclusion, the incidence of PCED after PPV was 4.6% in this study, and the eyes with PCED had worse visual outcomes. Diabetes, assistance by a first-year resident, and intravitreal tamponade with C3F8 were the risk factors associated with PCED in multivariate analysis. Our results also revealed that a healing time of PCED of more than 4 weeks was a cutoff point for the development of corneal opacity and a high incidence of geographic HSV epithelial keratitis. Early and aggressive management is necessary for patients presenting with PCED after vitrectomy to prevent poor outcomes.

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pars plana vitrectomy; persistent corneal epithelial defect

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