Macular hole (MH), a small opening in the central macula, can lead to significantly blurred and/or distorted central vision. MHs are thought to develop due to interactions between the vitreous and the retina. Gass was the first to suggest that tangential vitreoretinal traction at the fovea leads to MH formation.1 Further optical coherence tomography (OCT) analysis of MH pathogenesis has supported the importance of anteroposterior traction in MH formation in addition to Gass' original hypothesis of tangential traction.2,3 MHs can develop rapidly or during a period of weeks to months, but regardless of timeline, MHs are frequently identified when the patient has a decrease in visual acuity (VA), metamorphopsia, micropsia, or, rarely, photopsia.4 The management of MHs depends on the stage of the lesion. Early stage lesions are partial thickness and conservative management is recommended, whereas late-stage MHs are full thickness and typically require surgical intervention, usually pars plana vitrectomy (PPV) with or without internal limiting membrane (ILM) peeling.5–10
Although the development of MHs are most often idiopathic, occurring in 0.1% to 0.8% of adults older than 40 years old,11–15 numerous case reports and case series have reported MH formation in 0.24% to 1.9% of patients after undergoing PPV for rhegmatogenous retinal detachment (RRD).16–22 The mechanism by which MHs develop after PPV is unclear and most likely multifactorial; it may include traction from residual vitreous contraction, epiretinal membrane (ERM) formation, a taut ILM, or cystoid macular edema.21 There are currently no published studies reporting MH formation after PPV for diabetic tractional retinal detachment (TRD).
Here, we investigate the incidence and characteristics, as well as the management and outcomes, of full-thickness MH formation after PPV for diabetic TRD at Chicago's Cook County Health and Hospital System (CCHHS).
Patients and Methods
We conducted a retrospective review of the medical records of all PPV cases for diabetic TRD performed by a single vitreoretinal surgeon (DS) at CCHHS between November 2013 and August 2016. Eyes that underwent 23-gauge PPV for primary repair of a diabetic TRD were eligible for inclusion; patients with less than 3 months of postoperative follow-up were excluded. MHs that developed postoperatively in this cohort were diagnosed clinically and confirmed by OCT studies. This study was approved by the institutional review board of CCHHS, and all data handling was in compliance with the Health Insurance Portability and Accountability Act. We calculated the 95% confidence interval (CI) for the incidence of MH after PPV for diabetic TRD based on the binomial distribution using exact methods.
For diabetic TRD repair, 23-gauge PPV was performed using the Alcon Constellation machine (Alcon Laboratories, Fort Worth, TX), with a maximum cut rate of 5,000 cuts per minute and maximum vacuum rate of 650 mm Hg. During diabetic TRD repair, all cases underwent vitrectomy and vitreous base shaving using a wide-angle viewing system and scleral depression during the vitreous base dissection and fibrovascular membrane dissection. Residual adherent hyaloid was removed after visualization with triamcinolone staining. Endolaser photocoagulation was applied in panretinal photocoagulation fashion, including to the anterior retina, and tamponade was utilized in all patients by injection of C3F8 (14% to 16%) or 1,000 cs silicone oil.
Ninety consecutive eyes of 79 patients were included in this case series (Table 1). Four eyes from four male Hispanic patients developed MHs, yielding an incidence of 4.4% (95% CI, 1.2%–11.0%) (Table 2). The mean interval between PPV for diabetic TRD and MH formation was 7.0 months ± 5.5 months (mean ± 1 standard deviation) (range: 1 month to 13 months), and the mean follow-up time was 29.6 months ± 6.9 months (range: 19 months to 37 months). A summary of the four cases that developed MHs is presented in Table 2, and below is a detailed description of each case.
Patient Characteristics (n = 79)
Characteristics, Treatments, and Outcomes of Patients Who Developed MH After PPV for Diabetic TRD
Patient 1 is a 39-year-old Hispanic man who underwent PPV for a macula-off diabetic TRD with severe fibrovascular proliferation (FVP) and vitreous hemorrhage (VH). Vision improved from hand motion (HM) to 20/200 after TRD repair. He developed a MH 12 months after TRD repair, and vision decreased to count fingers (CF). He had PPV with ILM peel and C3F8 injection for MH, and at postoperative month 3, his vision was CF pinhole (ph) 20/200.
Patient 2 is a 66-year-old Hispanic man who underwent PPV for a chronic, macula-off diabetic TRD with severe FVP and chronic VH. His vision improved from light perception (LP) to CF after TRD repair. He developed a MH and ERM 2 months after PPV without significant vision change. Due to a poor visual prognosis, no further surgical intervention was performed.
Case 3 (Figure 1)
Patient 3 is a 51-year-old Hispanic man who underwent combined cataract extraction and PPV for a diabetic TRD with severe FVP not involving the macula and VH. Vision improved from HM to 20/50 after TRD repair. Thirteen months later, he developed a small MH with a thin eccentric ERM, and vision decreased to 20/100. The patient refused surgery, and MH was managed with topical 1% prednisolone, 0.5% ketorolac tromethamine, and 1% brinzolamide drops. The MH was almost closed 3 weeks later, but the patient discontinued drops due to travel to Mexico and the MH reopened with focal subretinal fluid (SRF) accumulation. Upon returning from Mexico, all three drops were restarted, and the MH was closed within 1 month. Six months later, the ERM progressed, diabetic macular edema (DME) worsened despite treatment with intravitreal injections, and vision decreased to 20/125, and eventually a small MH recurred, causing VA to drop to CF ph 20/250. A PPV with ERM/ILM peel and C3F8 injection was performed, and VA improved to 20/80.
Case 4 (Figure 2)
Patient 4 is a 49-year-old Hispanic male who underwent PPV for a diabetic macula-off TRD with severe FVP and VH. Vision improved from CF to 20/250 ph 20/200 after repair. Postoperatively, there was shallow, persistently chronic macular SRF that did not resolve with 6 weeks of observation. He underwent repeat PPV for drainage of macular SRF, and 4 weeks after this second PPV, he developed a MH with worsened vision to 20/300. The MH was treated with an intravitreal injection of 0.4 cc 100% C3F8 and face-down positioning, and the MH anatomically closed with a vision of 20/400 and significant cataract progression.
In this case series, we report the incidence of MHs after PPV for diabetic TRD at 4.4% (95% CI, 1.2%–11.0%), which is greater than the incidence of idiopathic MHs (0.1% to 0.8%) and MHs after PPV for RRD (0.24% to 1.9%).11–22 Due to our small sample size and thus wider confidence interval, the interpretation of the incidence must be taken with caution. Despite the well-accepted theory that MHs form due to traction between the vitreous and the retina, here we identify multiple cases of MHs that developed after the vitreous was removed. The incidence of MH formation in our cohort was upward of 5.5 times that of idiopathic MHs and more than double that of reported MH formation after PPV for RRD. Although our sample size is limited, there does not seem to be a temporal relationship between the time intervals from PPV to MH formation here; MHs occurred as soon as 1 month and as late as 13 months post-PPV for diabetic TRD.
Of the four cases, the three who underwent interventions all eventually resulted in MH closure. In Case 1, the traditional approach to MH closure using PPV with ILM peel was employed and resulted in hole closure and improved VA. In case 3, the patient refused to undergo surgery and instead agreed to an off-label trial of topical 1% prednisolone, 0.5% ketorolac tromethamine, and 1% brinzolamide. Drops were administered with the goal of decreasing macular edema by decreasing inflammation and facilitating fluid movement through the retinal pigment epithelium and into the choroid. Gentile has proposed that an important step in MH closure is cystoid dehydration followed by resorption of SRF.23 This topical therapy closed the MH after a few weeks of application, but unfortunately, 6 months later, the patient's ERM progressed with worsening of macular edema and a small MH recurred. The MH was closed surgically with PPV/ERM/ILM peel/C3F8, which improved the patient's VA to 20/80. Although limited literature exists on this technique, a case report in 2009 described full-thickness MH closure using topical nonsteroidal anti-inflammatory drug therapy (topical 0.5% ketorolac tromethamine followed by 1% topical nepafenac).24 In case 4, intravitreal injection of 0.4 cc 100% C3F8 and face-down positioning resulted in MH closure after 5 weeks. This method was used because the patient elected not to undergo surgery but agreed to a trial of gas tamponade. Although not a common technique for MH management, gas tamponade has been used with success in both early MH closure and release of vitreomacular traction in impending macular holes.25–29
Population-based studies have shown that idiopathic MHs occur at female:male ratios between 2.2:1 to 3.3:1.30–32 In nine previous studies investigating MH formation after PPV for RRD (59 patients), the total ratio of male:female patients who developed MHs was 1.2:1.16–22,33,34 An interesting result of our study was that of the 60.8% male and 39.2% female total population, all four patients who developed MHs were male. Although our sample size is small, our data, combined with the data of previous studies, further suggest that males have a higher incidence of MH formation after PPV for RD than females. It is difficult to compare gender ratios of MH formation after PPV for RRD versus TRD due to limited data on MHs post-TRD.
In addition to being male, the four patients in this study who developed MHs were all Hispanic. Although our cohort was primarily Hispanic (62.0% Hispanic, 32.9% African-American, 3.8% white, and 1.3% Asian), this finding posed the question if certain races are at increased risk for MHs. A 2017 study of 659,357 participants was the first to report an association between race / ethnicity and the risk of MHs.31 Of the 144 (0.2%) individuals who developed idiopathic MHs requiring vitrectomy, the only race that had a significantly increased incidence as compared to white individuals were Asian Americans (adjusted hazard ratio, 2.77; 95% CI, 1.27–6.02; P = .01). Hispanic participants did not have a significant increase in idiopathic MHs requiring vitrectomy (adjusted hazard ratio, 0.94; 95% CI, 0.35–2.58; P = .91). The authors of this study postulate that the increased incidence of MHs in Asian Americans is due to the greater proportions of myopia, a known risk factor for MH, in this population. Although Hispanic individuals have a greater prevalence of some MH risk factors, such as ERMs, no studies to date have shown an increased prevalence of MHs in this population.35 The increased prevalence of MHs in Hispanics in this study may be due to proliferative diabetic retinopathy (PDR) severity in these patients, the possibility that Hispanics have an increased tendency to develop MHs post-PPV for TRD but not idiopathic MHs, or statistical chance given the majority of patients in this study were Hispanic and the sample size was small. Further studies are necessary to fully understand the associations between race and MH risk post-PPV for RD.
The mechanism of MH formation at a higher incidence in this study is not certain but may be related to diabetic pathology / macular edema, a taut ILM, ERM formation, and vitreous remnant contraction. We will explore these speculative mechanisms below.
The severe diabetic retinal pathology present here helps distinguish this study from previous studies investigating MH formation after PPV.16–22 All 79 patients (90 eyes) in this study had significant PDR that led to VH and TRD formation. The pathophysiology of increased MH formation in diabetic eyes may be due to a higher incidence of macular edema. Gentile's “hydration” theory proposes that increased cyst formation contributes to MH formation.36 This cystic fluid accumulation may compromise retinal integrity, especially in these cases of severe PDR with underlying diabetic macular pathology, and could contribute to increased MH formation.22,37
A taut ILM, which has been noted in diabetic patients and is occasionally associated with macular edema resistant to medical management, may contribute to increased MH formation after diabetic TRD repair. Gentile et al. described that a taut ILM can cause diffuse DME after PPV, and its removal can restore the normal foveal contour and improve VA.38 Thus, the presence of a taut ILM after PPV for TRD may increase tangential forces within the macula and, when combined with diffuse DME, could lead to MH formation.
Dikopf et al. described that ERM formation is a common complication of PPV for diabetic TRD and reported ERM formation in 24% of 70 eyes after PPV for diabetic TRD.39 Here, cases 2 and 4 developed ERMs after PPV and before MH formation. Previous literature has shown that ERMs lead to retinal traction and are a cause of MH formation and reopening.40,41 Because ERM formation is a common complication of PPV for TRD, it is likely that ERMs contribute to MH formation by increasing traction on the retina. In addition to retinal traction from ERMs, the presence of residual cortical vitreous after diabetic vitrectomy with subsequent contraction may also be a source of retinal traction and another possible etiology of MH formation post-PPV for diabetic TRD.
Although limited by our small sample size, this study suggests that the incidence of MHs after PPV for diabetic TRD may be greater than the incidence in eyes post-PPV for RRD or in cases of idiopathic MHs. Further studies are necessary to understand the pathophysiology of our observations and to further elucidate the best treatment methods for patients with MHs post-PPV for diabetic TRD.
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Patient Characteristics (n = 79)
|Patient Characteristics||Number of Patients (%)|
| Range||21 to 65|
| Male||48 (60.8)|
| Female||31 (39.2)|
| Hispanic||49 (62.0)|
| Black||26 (32.9)|
| White||3 (3.8)|
| Asian||1 (1.3)|
Characteristics, Treatments, and Outcomes of Patients Who Developed MH After PPV for Diabetic TRD
|Patient||Age at MH, Sex||Ocular Hx||BCVA at TRD Dx||Fovea off RD?||Type of RD Repair||BCVA Post-TRD|
|1||39 M||PDR, FVP, TRD||HM||Yes||PPV, MP, C3F8||20/200|
|2||66 M||PDR, FVP, TRD||LP||Yes||PPV, MP, SO||CF|
|3||51 M||PDR, FVP, chronic TRD||HM||No||PPV, MP, C3F8||20/50|
|4||49 M||PDR, FVP, TRD||CF||Yes||PPV, MP, C3F8||20/250 ph 20/200|
|Patient||Time to MH After PPV for TRD (Months)||BCVA With MH||ERM?||MH Repair Method||BCVA After Repair||Outcome|
|1||12||CF||No||PPV, ILM Peel, C3F8||CF ph 20/200||MH closure|
|2||2||CF||Yes||No repair||No repair||MH present|
|3||13||20/100 (first MH), CF ph 20/250 (second MH)||Yes||Topical 1% prednisolone QID, 0.5% ketorolac tromethamine QID, and 1% brinzolamide TID followed by PPV and ERM/ILM peel||20/50 (first closure with drops), 20/80 (second closure)||MH closure|
|4||1||20/300||No||Intravitreal injection of 0.4 cc 100% C3F8 and face-down positioning||20/400 with 3+ NS and 2+ PSC||MH closure|