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 Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 32  |  Issue : 2  |  Page : 107-115

Vitrectomy for idiopathic macular hole: outcomes and complications


Department of Ophthalmology, Mansoura University, Mansoura, Egypt

Date of Submission11-Aug-2015
Date of Acceptance29-Nov-2015
Date of Web Publication14-Apr-2016

Correspondence Address:
Amr Mohammed Elsayed Abdelkader
MD, Mansoura Ophthalmic Center, Faculty of Medicine, Mansoura University, Mansoura, 35516
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-208X.180323

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  Abstract 

Purpose
The aim of this study was to determine the anatomical closure rate together with the rate of functional success of idiopathic macular holes following vitreous surgery in different optical coherence tomography (OCT) stages.
Patients and methods
This was a prospective, case series, interventional study. Twenty-two eyes were enrolled in this study conducted at Mansoura University Ophthalmic Center during the period between June 2012 and December 2014 with at least 3 months of follow-up. Eyes with stage 2, 3, and 4 idiopathic macular hole according to the Gass classification were included. All eyes were subjected to 23-G pars plana vitrectomy, inner limiting membrane peeling, fluid-gas exchange, and postoperative positioning.
Results
Idiopathic macular hole closure was achievable in 18 of 22 cases, with overall 81.4% anatomical success. Type 1 closure (U-shaped closure) was achieved in 13 cases (59.1%), type 2 closure (V-shaped closure) in three cases (13.6%), type 3 closure (irregular closure) in one case (4.5%), and type 4 closure was reported in one case (4.5%). The median postoperative log MAR visual acuity at 3 months was 1.0 (0.9445-1.2073). The overall postoperative visual acuity improvement was strongly statistically significant (P = 0.000). The visual acuity improvement at 3 months compared with the preoperative visual acuity was statistically significant (P = 0.000). The delta change in log MAR visual acuity at 3 months was 0.5 (−0.7782 to −0.4331), with greater improvement in log MAR visual acuity in group I (stage 2 OCT) compared with group III (stage 3 and 4 OCT at 3 months; P = 0.05). Retinal breaks were observed intraoperatively in three cases. Retinal detachment was reported in one case 4 months postoperatively.
Conclusion
Macular hole closure rate and visual acuity markedly improved following vitreous surgery for idiopathic macular holes.

Keywords: Inner limiting membrane peeling, macular hole, vitrectomy


How to cite this article:
Abdelkader AM, El-Metwaly MN, Khalaf MA, El Bendary AM, El-Kannishy AM. Vitrectomy for idiopathic macular hole: outcomes and complications. Benha Med J 2015;32:107-15

How to cite this URL:
Abdelkader AM, El-Metwaly MN, Khalaf MA, El Bendary AM, El-Kannishy AM. Vitrectomy for idiopathic macular hole: outcomes and complications. Benha Med J [serial online] 2015 [cited 2017 Oct 22];32:107-15. Available from: http://www.bmfj.eg.net/text.asp?2015/32/2/107/180323


  Introduction Top


No attention was paid to macular hole up to the beginning of the 20th century. Until that time, the pathology was obscure and the cure was unfeasible. Understanding on the pathology of macular hole improved dramatically by the end of last century. Besides, the development of clinical classification of macular hole was a great achievement. The development of the technology of optical coherence tomography (OCT) resulted in a revolution in the diagnosis and management plan of macular hole. The development of effective treatment modalities increased the interest in this disease [1].

Anatomical background

The foveal area refers to the human eye macula and is formed of perifovea, parafovea, foveal slope, and foveal pit. The central yellow-pigmented part is familiar as the macula lutea and represents the reflection of the yellow screening pigments such as lutein, zeaxanthin, carotenoids, and xanthophylls accumulated in Henle fiber layer cone axons. These yellow screening pigments act as a short wavelength filter [2].

The foveal pit is considered as the center of the fovea. It is a highly specialized retinal region different from other central or peripheral retinal areas. This small circular region of retina measures less than a quarter of a millimeter (200 microns) across in radial sections. Retinal layers are displaced concentrically underneath this central 200-micron-diameter foveal pit, leaving only a thin retinal sheet formed of cone cells only and some of their cell bodies. Complete layering of the retina appears along the foveal slope but in a radially distorted manner. Similarly, the second-order and third-order neurons of central cones exhibit the same displacement until the rim of the fovea. The ganglion cells are differentiated into six layers, forming the thickest portion of the entire retina, which is known as the foveal rim or parafovea [3].

The glial cells of the retina comprise radially arranged Muller cells. The adherent junctions between photoreceptor cell inner segments and Muller cells form the outer limiting membrane, whereas the retinal inner limiting membrane (ILM) is formed of laterally contacting end feet of Muller cells and their associated constituents of basement membrane. The outer limiting membrane acts as a barrier between the neural retina proper and the subretinal space. The photoreceptor outer segments project into this subretinal space and come into close contact with the retinal pigment epithelial layer. The ILM forms a diffusion barrier between the vitreous humor and neural retina [3].

The vitreous structure is based on a network of unbranched collagen fibrils including types II, V, IX, and XI collagen. The core of the fibrils is formed of type V and type XI collagen. Type II collagen surrounds this core and type IX forms the outer shell of the fibrils [4].

Glycosaminoglycans, mostly hyaluronan, fill the spaces between collagen fibrils. These collagen fibrils are coated with opticin, which, by its binding to glycosaminoglycans, plays a role in the gel structure of the vitreous and in the vitreoretinal interface adhesion. The nature of the construction of vitreous gel resists both compressive and tractional forces [5].

The vitreoretinal interface is the sheet of adhesion that promotes the connection of the vitreous cortex to the ILM, whereas the vitreomacular interface is the attachment between the retina and vitreous at the macula. The vitreous is firmly adherent to the retina at sites where the ILM is thinnest. These sites are over retinal blood vessels, optic disc, macula, and the vitreous base. The vitreous collagen fibers pass through ILM, interweaving with retinal collagen, and tightly connect the retina and vitreous at the vitreous base. However, at the vitreomacular interface, laminin and fibronectin indirectly connect ILM to posterior vitreous cortex collagen fibrils [6].

For a successful uneventful posterior vitreous detachment to occur as a natural aging process, vitreous liquefaction should be coupled with sufficient vitreoretinal interface weakening. In contrast, if there is no sufficient associated vitreoretinal interface weakening, vitreous fluid will be displaced to the preretinal space and achieve only partial or incomplete posterior vitreous detachment. This condition is known as anomalous posterior vitreous detachment. This attachment is known as vitreomacular adhesion when residual attachment is in the macula [7].

Clinicopathological aspects of macular hole

Many theories have been postulated to explain age-related (idiopathic) macular hole. However, the pathogenesis is not fully defined. Duke-Elder and Dobreein, in 1967, suggested a degenerative process due to vascular insufficiency. Gass, in 1988, postulated the hypothesis of tangential vitreofoveal traction due to muller cell proliferation. Gass [8] suggested a foveal dehiscence followed by centrifugal displacement of photoreceptors. This theory explains vision restoration after removal of tangential traction by means of surgery. In accordance with this, histopathological assessment of the detached operculum showed glial element without photoreceptors. Thus, hole formation is not associated with loss of foveal cones. Pincushion distortion of image confirms the theory of lateral displacement of photoreceptors [9].

The role of the vitreous in the development of the macular hole is emphasized by the low rate of macular hole after complete posterior hyaloid detachment. In cases of impending idiopathic macular holes, OCT studies revealed perifoveal hyaloid detachment with focal attachment of the hyaloid to the umbo and a cystic cleavage starting in the inner part of the umbo. Thus, with more dehiscence in these intraretinal cystic lesions, a full-thickness retinal defect will develop, transforming the macular hole from stage 1 to stage 2. Operculum formation occurs because of anteroposterior vitreofoveal traction and the hole continues to enlarge by centrifugal tangential traction. These changes are facilitated by involutional changes at the fovea [10].

Foveal dehiscence is responsible for central scotoma that gradually enlarges with the development of localized perifoveal retinal detachment or perifoveal cystic changes with intact retina. The presence of epiretinal membrane may also contribute to central vision loss. It is very uncommon to find a rhegmatogenous retinal detachment beyond the macula because of the macular hole. This may happen in the presence of posterior staphyloma or abnormal vitreous traction. Discovery of idiopathic macular hole during vitreous surgery is not an uncommon event [10].

Clinical detection of macular hole is the cornerstone of diagnosis. Slit-lamp biomicroscopy with fundus contact or noncontact lens is very helpful. The Watzke-Allen test is a subjective test for full-thickness retinal defect. The patient was seen to have central positive scotoma after focusing a vertical, thin slit beam on the macula [11].

The Gass classification system

This classification is based on the clinical appearance of macular hole. It is based on the hypothesis that idiopathic hole formation is due to focal shrinkage of the vitreous at the region of the fovea. Gass classified idiopathic macular hole into four stages, which are widely accepted until now and correlate with OCT studies, with the exception of stage 1. The structural retinal changes in stage 1 OCT differ slightly from the Gass clinical stage [12].

Stage 1 idiopathic macular hole

In stage 1 idiopathic macular hole, the photoreceptor layer remains intact. There is no real neuroretinal defect, neither clinically nor on OCT observation. Tangential traction is present and considered as a causative factor, but vitreofoveal separation is not observed in this stage.

Gass subclassified stage 1 idiopathic macular hole on clinical basis into stage 1A (yellow central small spot) and stage 1B (yellow central ring). Stage 1A idiopathic macular hole was considered by Gass as localized foveal detachment. OCT studies corrected this idea and explained stage 1A as cystic changes in the fovea. Muller cell cone or inner retinal layers detach from the photoreceptor layer and form a schisis cavity in stage 1A, whereas in stage 1B there is loss of structural support and subsequent centrifugal displacement of the photoreceptor layer. Stage 1 macular hole carries a good prognosis with 50% spontaneous resolution without any visual sequelae. The spontaneous closure rate is related to the initial visual acuity [12].

Stage 2 idiopathic macular hole

The hallmark of this stage is the appearance of a full-thickness neuroretinal defect due to dehiscence of the roof of the schitic cavity with vitreofoveal traction. The defect is usually small (100-300 μm). Clinically, the defect may be crescentic, slit like, oval, or round. A condensed vitreous and or pseudo-operculum could be present. This stage is characterized by a progressive loss of vision and typical progression to stage 3 macular hole. Visual acuity at presentation varies between 20/50 and 20/400 [12].

Stage 3 idiopathic macular hole

This is the classic stage of fully developed classic macular hole. It is the end process of continuous tangential vitreomacular traction. The hole presents with the classic features of macular hole - rounded defect (350-600 μm), with smooth edges. A cuff of subretinal fluid surrounding the hole gives a characteristic doughnut-shaped appearance. The leading edge of the subretinal fluid may show a demarcation line representing alteration of the retinal pigment epithelium. Incomplete posterior vitreous detachment is present as the vitreous usually remains attached to the optic disc. In pathological terms, there is avulsion of the cyst roof; operculum formation is seen, but with residual parafoveal vitreous attachment. The presenting visual acuity is 20/200 or less. Histopathologically, the opercula in stage 3 macular hole contain Muller cells; however, 40% of cases contain cone photoreceptors, so that the anatomical closure rate is expected to be lower in cases with opercula containing a high cone density [13].

Stage 4 idiopathic macular hole

The base of the defect may show yellow deposits with perifoveal cystic changes. Complete posterior vitreoretinal separation is the landmark of this stage. This could be suggested clinically by the presence of Weiss ring [12].

Surgical technique

Gass, in 1988, hypothesized that prefoveal vitreous cortex tangential traction resulted in idiopathic macular hole formation. Consequently, Kelly and Wendel, in 1991, achieved favorable surgical outcomes following vitrectomy for idiopathic macular hole. Since then, the vitrectomy technique has undergone several modulations and improvements to reach better anatomical and functional outcomes. These improvements included adjuvant treatments such as ILM peeling [14],[15],[16],[17],[18], treatment with autologous serum [19] and transforming growth factor-b [20], and dye application [21]. These modulations, especially ILM peeling, achieved better outcomes [22].

Subjects and methods

This thesis is a prospective, case series, interventional study. Twenty-two eyes were included in this study. The study was conducted at Mansoura University Ophthalmic Center during the period between June 2012 and December 2014 with at least 3 months of follow-up. All eyes were subjected to 23-G pars plana vitrectomy, ILM peeling, fluid-gas exchange, and postoperative positioning. Informed consent was obtained from each patient after patient counseling explaining the nature of the disease, surgical procedure, postoperative follow-up, expected outcomes, and possible complications.

Eyes with stage 2, 3, and 4 idiopathic macular hole according to the Gass classification were included. The exclusion criteria were as follows: eyes with past history of vitreoretinal retinal surgery, epiretinal membranes, myopia higher than 8 D, and macular holes secondary to trauma or proliferative vitreoretinopathies.

The preoperative ophthalmic evaluation included data collection (personal information, sex, age, relevant medical history, etc.). Preoperative visual acuity was assessed using Snellen's visual acuity chart and then transformed for statistical analysis to logarithm of minimal angle of resolution units (log MAR).

All patients underwent thorough ophthalmic evaluation using slit-lamp biomicroscopy with special reference to lens status, intraocular tension, and retinal status. Slit-lamp biomicroscopy was used to assess macular hole according to the Gass clinical classification.

The anatomical re-evaluation was carried out using SD-OCT. Two scan types of SD-OCT were acquired for each eye: a 3 D (6.0 × 6.0 mm) cube scan and a 7-line raster scan centered around the fovea. The IS/OS defect was considered to be the lack of a visible IS/OS reflectivity line in spectral OCT. The IS/OS reflectivity line is considered as a 40-μm-block located 20 μm above the retinal pigment epithelium. The IS/OS layer with the largest linear defect was measured [Figure 1].
Figure 1: The boundary of inner segment/outer segment.

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Ultrasonic examination was performed preoperatively in all cases to confirm the clinical assessment of the posterior hyaloid together with ultrasonic biometry regardless of whether the case was scheduled for cataract surgery.

A standard 23-G, three-port pars plana vitrectomy approach was adopted. General anesthesia was used in 20 cases, whereas retrobulbar anesthesia was used in two cases. LUMERA 700 Zeiss operating microscope (Carl Zeiss, MeditecAG, Oberkochen, Germany) was used with the Resight 700 as a fundus viewing system together with Oertli vitrectomy machine (Oertli, Berneck, Switzerland).

Initially, core vitrectomy in addition to separation of the posterior hyaloid in stage 2 and 3 macular hole was performed. Posterior vitreous detachment was performed using the vitrectomy probe in the aspiration mode only. Complete peeling of the posterior hyaloids was confirmed by injection of triamcinoloneacetonide (Kenacort-A 40 Suspension for injection; Bristol-Myers Squibb, New York City, New york, USA). Thereafter, vitreous gel was trimmed toward the periphery. Brilliant blue G (Brillant Peel; DORC, Rotterdam, the Netherlands) was applied after partial fluid-air exchange for 30 s in 15 cases, and without fluid-air exchange for 60 s in eight cases. A 23-G (0.6 mm) symmetrical end-gripping microforceps (Eckardt forceps; DORC) was used to create an edge of the ILM near the arcade and then used to complete the peeling maneuver to create a maculorrexis of about two-disc-diameter centered around the hole.

Peripheral retinal indentation and examination for any detected breaks, peripheral holes, lattice degenerations, or localized detachment were carried out. Endolaser photocoagulation was applied accordingly when needed. Fluid-air followed by air-gas exchange was performed with either C3F8, C2F6, or sulfur hexafluoride using a 100-ml syringe to flush the vitreous cavity and ensure adequate air-gas exchange.

Tight closure of the sclerotomies was carried out using a vicryl 7/0 suture to guard against postoperative hypotony. No adjuvants (i.e. platelets, fibrin, etc.) were used during surgery.

In postoperative management, the patients were instructed to maintain a face down position in which they could see the air bubble in the center of the visual field at all times 16 h/day (50 min/h) for 2 weeks. All patients were examined at 1 day, 1 week, and then monthly for at least 6 months. Each time, the visual acuity was recorded using Snellen's visual acuity chart and then transformed for statistical analysis to logarithm of minimal angle of resolution units (log MAR). Any complication (cataract progression, postoperative uveitis, secondary glaucoma or retinal detachment) was recorded and managed accordingly. The anatomical re-evaluation from 1 month to 6 months postoperatively was carried out using SD-OCT.


  Results Top


Patients ranged in age from 49 to 74 years, with a mean of 62.09 ± 7.3 years [Table 1], and included nine (40.9%) male and 13 (59.1%) female patients, which is statistically insignificant.
Table 1: Age distribution

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Patients were divided on the basis of the OCT stage of idiopathic macular hole into three groups: group I included eyes with stage 2 idiopathic macular hole (IMH) [Figure 2]a; group II included eyes with stage 3 IMH [Figure 2]b; and group III included eyes with stage 4 IMH [Figure 2]).
Figure 2: (a) Group I: stage 2 IMH; (b) Group II: stage 3 IMH; (c) Group III: stage 4 IMH.

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The median preoperative log MAR visual acuity was 1.7782 (1.4771-1.7782), and the median preoperative inner segment-outer segment linear defect was 1232 μm (1010-1500 μm).

The three main outcome parameters were the postoperative visual acuity at 3 months as a functional result, besides the anatomical closure rate together with restoration of the photoreceptor layer integrity and reduction of IS/OS segment defect as an anatomical result.

Idiopathic macular hole closure was successfully achieved in 18 of 22 cases (81.4%), which was statistically significant (P = 0.003). Type 1 closure (U-shaped closure) was obtained in 13 cases (59.1%) [Figure 3], type 2 closure (V-shaped closure) was reported in three cases (13.6%) [Figure 4], type 3 closure (irregular closure) was reported in one case (4.5%), and type 4 closure was reported in one case (4.5%) [Figure 5]
Figure 3: Type 1 macular hole closure (U-shaped closure) (a) Preoperative optical coherence tomography (OCT), (b) 3 months postoperatively.

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Figure 4: Type 2 macular hole closure (V-shaped closure with focal retinal nerve fiber layer (RNFL) defect) (a) Preoperative optical coherence tomography (OCT), (b) 9 months postoperative OCT.

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Figure 5: Type 4 macular hole closure (flattening of hole edges) (a) Preoperative optical coherence tomography (OCT), (b) 6 months postoperative OCT.

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In type 4 closure, there was flattening of hole edges and resolution of the cuff of fluid around the hole, but without restoration of the foveal continuity (i.e. residual neurosensory defect with bare retinal pigment epithelium). It is called W-type closure. In contrast, nonclosure was noticed in four cases (18.2%) [Figure 6] and characterized by persistence of cuff of subretinal fluid, bare retinal pigment epithelium, and elevated edges (open macular hole). These data are presented in [Table 2].
Figure 6: Macular hole nonclosure (open macular hole) (a) Preoperative optical coherence tomography (OCT), (b) 6 months postoperatively.

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Table 2: Idiopathic macular hole closure rate and types

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Complete macular closure was achieved in all cases of group I or OCT stage 2 macular (six of six cases, 100% closure rate), whereas seven of 10 cases achieved successful macular hole closure in group II or stage 3 OCT macular hole (70%) and five of six cases of macular hole (83.3%) had been successfully closed in group III or OCT stage 4 macular hole with an overall closure rate of 75% (12 of 16) in group II and III. However, statistical analysis revealed no statistically significant difference between the three groups (P =0.532). These data are presented in [Table 3].
Table 3: Closure rate of idiopathic macular hole in different optical coherence tomography stages

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The median postoperative log MAR visual acuity at 3 months was 1.0 (0.9445-1.2073). The overall postoperative visual acuity improvement was strongly statistically significant (P = 0.000). The visual acuity improvement at 3 months compared with the preoperative visual acuity was statistically significant (P = 0.000). The delta change in log MAR visual acuity at 3 months was −0.5 (−0.7782 to −0.4331).

The median postoperative IS/OS linear defect at 3 months was 0 (0-1448). The overall postoperative IS/OS linear defect reduction was strongly statistically significant (P = 0.000). The IS/OS linear defect reduction at 3 months compared with the preoperative IS/OS linear defect was statistically significant (P = 0.01). The delta change in IS/OS linear defect at 3 months was 809 (88.5-1151) μm. Data are illustrated in [Table 4] and [Figure 7].
Figure 7: Residual IS/OS linear defect in stage II optical coherence tomography (OCT) macular hole.

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Table 4: Postoperative visual acuity and IS/OS linear defect changes (anatomical and functional outcomes)

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The mean delta change in log MAR visual acuity in group I (OCT stage 2 macular hole) was −0.7782 (−1.0198 to −0.6435) at 3 months. Group II (OCT stage 3 macular hole) achieved improvement in log MAR visual acuity of about −0.5880 (−0.9287 to −0.4133) at 3 months. The mean delta change in log MAR visual acuity in group III (OCT stage 4 macular hole) was −0.3891 (−0.4886 to −0.2698) at 3 months. Statistical analysis revealed a significant difference in log MAR visual acuity improvement between the three groups at 3 months (P = 0.044) with a statistically significantly greater improvement in log MAR visual acuity in group I compared with group III at 3 months (P = 0.05).

Complications

Retinal breaks were observed intraoperatively in three cases. They were managed with careful endolaser and thorough follow-up, and there were no reported retinal detachments in any of them. Retinal detachment was a vision-threatening complication. It was reported in one case 4 months postoperatively. Focal nerve fiber layer defect with its resultant visual defects is not an uncommon finding, but there was no associated underlying photoreceptor layer defect [Figure 8].
Figure 8: Postoperative focal nerve fiber layer defects.

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  Discussion Top


The present study reported continuous improvement of visual aacuity, photoreceptor layer segment for at least 3 months postoperative. The limited number of cases was due to the prospective nature of the work, strict patient selection criteria, many patients deferring surgery because of comorbidities, and long waiting period. Age distribution in our study ranged from 49 to 74 years, with a mean of 62.09 ± 7.3 years. Jaycock et al. [23] in a study of 55 cases in 2005 reported a mean age of presentation of 65 years.

In our study, idiopathic macular hole closure was successfully achieved in 18 of 22 cases (81.4%). Larsson et al. (2006) [24] conducted a similar prospective study on 61 eyes of idiopathic full thickness macular hole and achieved successful macular hole closure in 59 of 61 (97%) patients. Jaycock and colleagues (2005) in a retrospective study of 55 cases reported 94.0% closure rate when surgery was performed within 1 year of onset and 47.4% closure rate when surgery was performed after1 year or more. Accordingly, this study encouraged early interference within 1 year [23].

In our study, complete macular closure was achieved in all cases of group I or OCT stage 2 macular hole (six of six cases, 100% closure rate), whereas seven of 10 cases achieved successful macular hole closure in group II or stage 3 OCT macular hole (70%) and five of six cases of macular hole (83.3%) had been successfully closed in group III or OCT stage 4 macular hole, with an overall closure rate of 75% (12 of 16) in groups II and III.

In a meta-analysis of the outcomes of 389 cases, Kang and colleagues found an anatomical closure rate of 97.6% for stage 2 holes when surgery was performed within 4 months of onset compared with 88.9% when surgery was performed later on. However, the anatomical closure rates in stage 3 and 4 macular holes were 82.5% when surgery was performed within 4 months of onset compared with 88.9% when surgery was performed later on [25].

According to the national database of vitreo-retinal surgery study in the UK report 2 that included an analysis from a multicentre database in the UK, 1078 eyes from 1045 patients had undergone pars plana vitrectomy (PPV) for IMH with 94% had ILM peeling. A total of 119 of 476 eyes (48.6%) had achieved success that was defined as more than 0.3 log MAR visual acuity units improvement (i.e. 2 or more Snellen's lines) by 12 weeks after surgery; this proportion increased to 58.3% at 24 weeks, and 8% had deteriorated by more than 0.30 log MAR units [26].

In our study, the postoperative visual acuity improvement was strongly statistically significant (P=0.000). The median postoperative log MAR visual acuity at 3 months was 1.0 (0.9445-1.2073). These results were comparable to the meta-analysis of the outcomes of 389 cases by Kang and colleagues, who found a postoperative log MAR visual acuity of 0.5 or better for stage 2 holes in 78.6% of cases when surgery was performed within 4 months of onset compared with 55.6% of cases when surgery was performed later on. However, they reported postoperative log MAR visual acuity of 0.5 or better in stage 3 and 4 macular holes in 33.3% of cases when surgery was performed within 4 months of onset compared with 18.2% of cases when surgery was performed later on. The overall cases that achieved postoperative log MAR visual acuity of 0.5 or better was less than 40% [25]. Jaycock and colleagues (2005) in a retrospective study of 55 cases reported a postoperative log MAR visual acuity of 0.5 or better in 43% of cases. In our study, a postoperative log MAR visual acuity of 0.5 or better was achieved in 25% of cases only. This could be explained by the long latency of patient presentation [23].

Complications

Superficial retinal hemorrhages are not infrequent following ILM peeling. However, they were not usually visually significant in most cases [27]. Such superficial retinal hemorrhages were observed in our study, with subtle effect on the visual outcomes. In our study, retinal breaks were observed intraoperatively in three cases. They were managed with careful endolaser and thorough follow-up and there were no reported retinal detachment in any of them. The reported incidence in the literature on iatrogenic retinal breaks was variable, from 6 to 36% [27],[28],[29]. Retinal detachment was a vision-threatening complication. The reported incidence of retinal detachment following PPV for IMH ranged from 2 to 6% [27],[30],[31]. It was reported in our study in one case 4 months postoperatively.

In our study, observation of focal nerve fiber layer defect with its resultant visual defects is not an uncommon finding after macular hole surgery. This complication had been reported in several studies, as far back as in the study by Ezra and colleagues (1996). However, these focal nerve fiber layer defects had subtle effect on the visual outcomes as they are not associated with underlying photoreceptor layer defects [32].


  Conclusion Top


The study reported continuous improvement in visual acuity and photoreceptor layer segment defects for at least 3 months postoperatively. Besides, subtle complications that were not infrequent following ILM peeling were reported. However, they were not usually visually significant in most cases.

Acknowledgements

This work is a genuine one and has never been submitted before. All surgeries were performed by Dr Kannishy at Mansoura University Ophthalmic Center during the period between June 2012 and December 2014 with at least 6 months of follow-up. The research adhered to the tenets of the Declaration of Helsinki. Written informed consent was obtained from all participants after explanations of possible consequences.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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