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   Table of Contents      
Year : 1998  |  Volume : 46  |  Issue : 4  |  Page : 185-193

Diagnosis and management of idiopathic macular holes

1 Department of Ophthalmology, King George's Medical College, University of Lucknow, Lucknow, India
2 Barnes Retina Institute, St. Louis, USA
3 Dr. R.P. Centre for Ophthalmic Sciences, AIIMS, New Delhi, India

Correspondence Address:
Sandeep Saxena
G-19, River Bank Colony, Lucknow - 226 018
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Source of Support: None, Conflict of Interest: None

PMID: 10218300

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Modern vitreoretinal surgery is now one of the most effective tools for treating posterior segment diseases. Recent advances in the pathogenesis and classification and better indicators of visual outcome for idiopathic macular holes have led to a renewed interest in this clinical entity. Refinements in the techniques and instrumentation have led to improvement in surgical results. This article reviews the diagnosis and management of idiopathic macular holes.

Keywords: Idiopathic macular holes, diagnosis, management, vitreoretinal surgery

How to cite this article:
Saxena S, Holekamp NM, Kumar A. Diagnosis and management of idiopathic macular holes. Indian J Ophthalmol 1998;46:185-93

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Saxena S, Holekamp NM, Kumar A. Diagnosis and management of idiopathic macular holes. Indian J Ophthalmol [serial online] 1998 [cited 2024 Feb 24];46:185-93. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1998/46/4/185/24164

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Idiopathic macular holes are an important cause of loss of central vision in the elderly. Recent advances in the pathogenesis, classification and surgical intervention have generated a renewed interest in this clinical entity. Better indicators of visual outcome as well as refinements in the surgical technique have led to greater success of macular hole surgery.[1]

  Pathophysiology Top

Clinical characterization and theories on the pathogenesis of macular holes have continued to evolve. It is now recognized that most macular holes occur in the absence of antecedent injury and are referred to as idiopathic. Gass[2] and Johnson and Gass[3] proposed a theory whereby shrinkage of adherent cortical vitreous and subsequent tangential vitreous traction first causes a circumscribed foveolar detachment (stage 1) followed by early retinal dehiscence (stage 2), then enlargement of the macular hole with vitreofoveal separation (stage 3), and finally complete posterior vitreous detachment (stage 4). Guyer and Green[4] proposed three possible mechanisms for the creation of tangential traction on the macula: (i) fluid movements and counter currents;(ii) cellular remodelling of cortical vitreous;and (iii) contraction of a cellular membrane on the inner surface of the tapered cortical vitreous. Gass[2] emphasized the difficulty in distinguishing posterior vitreous detachment (PVD) from a zone of posterior vitreous liquefaction and attached posterior cortical vitreous over the macula. He also emphasized that the diagnosis of PVD is uncertain unless the posterior cortical vitreous contains the vitreous condensation ring (Weiss ring) over the optic nerve, an operculum or a pseudo-operculum. The presence of a thin transparent structure adherent to the retina during vitrectomy for prevention of macular holes provided a correlate to Gass' hypothesis.[5] Proliferation of fibrous astrocytes and Mueller cells occurs with the formation of a macular hole. This reparative tissue, which may be dislodged, has previously been interpreted as an operculum.[6] Cortical vitreous peeling and gas tamponade can allow the macular hole to settle and the edges to reapproximate. The residual defect can be sealed by Mueller cells.[7] Full- thickness macular hole formation in eyes with a pre-existing complete PVD has been documented. It is likely that some mechanism other than tangential by prefoveal vitreous cortex is responsible.[8]

  Clinical Features Top

Idiopathic macular holes occur most frequently in women in the sixth decade of life. [Table - 1] summarizes the biomicroscopic findings of various stages of macular hole. According to Gass,[9] stage 1A and IB lesions represent focal foveal detachments secondary to vitreous traction. A 100-200 μm diameter yellow spot is the earliest change observed. With progression, a 200- 350 μm yellowish ring develops. Fine radiating striae are often seen surrounding the yellow ring. Within several weeks to months, a full-thickness dehiscence develops. This dehiscence often starts eccentrically, then opens in a "can-opener" fashion to form a crescentic retinal defect [Figure - 1], which becomes a horseshoe-shaped hole and finally a round hole with an operculum. In some cases, the dehiscence starts centrally, with gradual enlargement of the hole and no operculum develops. A ring of retinal detachment usually surrounds the hole [Figure - 2]. As the hole enlarges, vision usually decreases and within several months, it progresses to a fully developed hole that measures approximately 500 μm in diameter. When present, the operculum is suspended over the hole by the vitreous cortex. With time the following changes may be observed: round yellow deposits on the central retinal pigment epithelium; epiretinal membranes causing contracture of the internal limiting membrane; depigmentation of the pigment epithelium under the cuff of retinal elevation; and a pigmentary demarcation ring defining the outer margin of the retinal detachment. Posterior vitreous separation from the macula and disc develops in a small percentage of cases. Eyes with idiopathic macular hole lose vision secondary to tissue loss, cystic changes and retinal cuff elevation with photoreceptor degeneration. Clinical observations have led to the impression that the macular hole and cuff enlarge secondary to persistent tangential traction from the vitreous, tangential traction from the epiretinal membranes, and the development of large cystic spaces within the surrounding cuff.

  Natural History Top

The natural history of idiopathic macular hole is well established. Idiopathic macular holes usually cause a decrease in visual acuity to the range of 6/36-3/60.[1] Stage 1 macular holes have a 66% and stage 2 macular holes have a 74% risk of progression to full thickness macular holes.

The incidence of apparent disappearance of idiopathic full thickness macular holes is low.

Improvement in visual acuity is greater in those cases in which macular holes disappear in a relatively short period of time.[10] Foveal detachment and macular break resolution seem to result from the release or weakening of vitreous on the fovea. Reattachment of the fovea may preserve fair to good visual acuity.[11] In patients with an established full thickness-macular hole in one eye, the fellow eye with attached vitreous has a 12% risk of developing macular hole.[1] Baseline characteristics, natural history and risk factors for progression in eyes with stage 2 macular holes has been reported by the Vitrectomy for Treatment of Macular Hole Study Group.[12] The prevalence rates of PVD were 32% and 0% in the centric and eccentric hole groups respectively. The progression rate to stage 3 was 100% in eyes with pericentral hyperfluorescence and 55% in eyes without pericentral hyperfluorescence. They concluded that eccentric and centric holes may have a different pathogenesis. In addition to purely tangential traction, some component of obliquely oriented anteroposterior vitreous traction may be important for the pathogenesis of senile macular holes, particularly stage 2 eccentric macular holes.

  Differential Diagnosis Top

Premacular hole lesions are often misdiagnosed and many conditions may masquerade as full-thickness macular holes.[13] Some of the common misdiagnoses are listed below.

  • An epiretinal membrane with a pseudohole can be confused with a macular hole. The pseudohole usually preserves better vision than the macular hole. In addition, the pseudohole does not have a halo of fluid, an operculum, or yellow deposits at the level of retinal pigment epithelium.

  • A foveal detachment due to central serous retinopathy (CSR) can be mistaken for a premacular hole. Both appear as a yellow spot, but fluorescein angiography can distinguish these two entities. CSR occurs in young to middle-aged men, whereas idiopathic macular holes usually affect elderly women.

  • Cystoid macular edema can also mimic the yellow spot of a stage 1 lesion. Fluorescein angiography and a history of cataract extraction can be useful in differentiating between these two conditions.

  • The early yellow lesion of solar retinopathy can appear similar to a stage 1 lesion. A central druse of retinal pigment epithelium depigmentation with a small amount of subretinal fluid and a central fibrocellular epiretinal membrane with a macular detachment have been described as mimicking an impending macular hole.

  • The vitreomacular traction syndrome can mimic an impending macular hole. Vitreous traction on the macula due to an incomplete vitreous detachment is responsible for this lesion. These disorders can be distinguished by examination of the vitreous.

A full-thickness macular hole is most accurately diagnosed clinically using a fundus contact lens and slitlamp biomicroscopy. Supplemental tests that may assist in or allow for more accurate diagnosis include Amsler grid testing, testing for Watzke-Allen sign, and fluorescein angiography. Amsler grid testing is sensitive in detecting any form of macular abnormality, but is not specific enough to be useful in establishing a diagnosis of macular hole and preoperative testing has not been standardized. The Watzke-Allen test and to a greater degree the laser aiming beam test further improve the accuracy of diagnosis of full-thickness macular holes. The major advantage of these tests is that they are simple to perform, can be done in the office and are easily accessible.[14] Watzke-Allen sign testing in all patients with clinically defined macular holes can show a break or thinning of the slit beam. Thinning of beam is seen in both macular holes and pseudo-macular hole cases. Therefore, thinning is not as specific as a total break in the slit beam in full-thickness macular hole. The laser-aiming beam test may yield similar diagnostic information, allowing the clinician to test focal areas of the retina for a scotoma. A 50 (μm spot laser-aiming beam can be hidden in the macular lesion in all patients with clinically defined full-thickness macular hole. This is thus distinguished from the finding in pseudohole eyes which could detect the 50 μm spot. In addition, the inability to detect a 200 or 500 μam spot size is noted only by patients with macular holes. Thus, the absolute scotoma detected by the laser-beam test is sensitive and specific for full-thickness macular holes. More sophisticated analysis of the absolute and relative scotomas associated with a macular hole can be performed with macular microperimetry using a scanning laser ophthalomscope.[15][16][17] During this technique the retina can be observed while tested in a standardized fashion with kinetic perimetry, similar to the test performed with a Goldmann perimeter. The absolute and relative scotomas can be mapped directly onto the retinal surface. This microperimetry technique has demonstrated that visual loss in eyes with macular holes is due to the absence of retinal function in the area of the hole as well as reduction in retinal function in the area of the surrounding neurosensory retinal detachment.

Echographic features of idiopathic macular hole correlate with clinical features.[18] Optical coherence tomography has been found to be effective in distinguishing full-thickness macular holes from partial thickness holes, macular holes, and cysts.[19] The cross-sectional view provided is an alternative to clinicopathologic correlation and allows lesions to be traced longitudinally over time. The micron scale resolution is useful for quantitatively assessing hole diameter and the amount of retinal thickening and edema surrounding a hole, allowing sensitive monitoring of hole progression or recovery after treatment. It also appears potentially useful in evaluating the vitreoretinal interface [Figure - 3]. Other ancillary tests such as focal electroretinograms,[20] confocal laser tomographic analysis systems,[21] monochromatic photography,[22] and laser biomicroscopy [23,24] have been applied to the study of macular holes with some success, but these modalities are not available or feasible for many clinical practices.

  Surgical Management Top

Careful patient selection is critical to a successful outcome. The ideal candidate would be a patient with bilateral holes of relatively recent onset, with vision in his better eye inferior or equal to 6/36. Patients with unilateral symptomatic holes with recently reduced vision to 6/24 or worse are also good candidates.[25] Both the laser interferometer and the potential acuity meter have been found to be modestly accurate in predicting postoperative visual acuity.[26]

Prospective randomized clinical trials have shown that surgical intervention in stage 2, 3 or 4 macular holes results in some visual benefit.

Substantial increase in visual system function has been reported after successful surgery. Objective measures of bilateral visual functions were applied to investigate the benefits of macular hole surgery to overall visual function. Bilateral visual function was improved after macular hole surgery. The improvement rate was markedly better in patients with subnormal vision in the fellow eye.[27]

The objectives for surgical repair of macular holes include relief of all tangential traction and retinal tamponade. Tangential traction is relieved by identification and removal of the cortical vitreous or posterior hyaloid and removal of fine epiretinal membranes around the hole. Tamponade is provided by total gas-fluid exchange with SF and strict face-down positioning.

Most eyes with macular hole have uniform intraoperative vitreous findings. There is usually a zone of collapsed vitreous fibres lying anterior to a posteriorly optically clear cavity. In most instances, the vitreous cortex or posterior hyaloid is invisible and remains attached to the underlying internal limiting membrane of the retina. In some cases, the presence of a focally detached vitreous is suggested by an operculum floating above the macular hole. After surgical removal of the anterior and mid vitreous, it is necessary to develop and/or complete a PVD.

Using active aspiration (150-250 mmHg), a silicone-tipped suction cannula is gently swept over the retinal surface near the major arcades or temporal to the macula. The area immediately around the hole is avoided. The silicone tip is noted to flex once the cortical vitreous is engaged. This has been termed as "fish-strike sign" or "divining rod sign" [Figure - 4]. Once engaged, a PVD can be created with continuous suction with anterior-posterior-tangential traction while moving the tip over the retinal surface. The dissection is carried from the area of initial detachment to adjacent attached areas in an attempt to complete the detachment from the posterior retina to the equatorial zone. The vitreous cortex or posterior hyaloid becomes visible as a translucent sheet, especially with oblique illumination. Occasionally, the disc attachments are so firm that the vitreous cutter (on suction only), tissue forceps or pick manipulation is required to complete the PVD in these areas. A 36-gauge subretinal pick can be useful in engaging the posterior hyaloid near the optic nerve and then pulling off the Weiss ring.[1] Frequently, an operculum is detected as a glial fragment attached to the vitreous cortex. Once the vitreous is completely detached, vitrectomy is completed. If residual vitreous cortex is present, it appears as a gelatinous substance on the surface of the retina during completion of the fluid-air exchange.

Fifty percent of operated eyes have some degree of epiretinal membrane (ERM) proliferation. These ERMs, unlike typical ERMs, tend to be finer and more friable and at times are densely adherent to the retina. The ERMs may be present surrounding the hole or can involve only a few clock hours. A microbarbed myringotomy blade is used to create an edge in the ERM, which is grasped with tissue forceps and stripped. One disc area around the macular hole is checked and liberated from ERMs to ensure relief of traction. During this maneuvre, it is common to create small haemorrhages around the hole. Damage to inner retina is avoided, an early sign of which may be the development of fluffy whitish areas.

Prolonged intense illumination from the light pipe near the macula is avoided to prevent phototoxicity. A total fluid-air exchange is performed and effort is made to dehydrate the vitreous cavity. The shallow fluid in the base of the optic disc cup is aspirated repeatedly, with a soft-tipped cannula, until fluid no longer collects. Frequently, the edges appear to slide closer together, which is considered a good prognostic sign. A nonexpansive concentration of long-acting gas is exchanged for air. A longer-duration intraocular gas tamponade from 16% C3F8 gives a much higher rate of successful closure and improved visual acuity.[28],[29]

Postoperatively, strict prone positioning is prescribed. We now believe that it is an important component to macular hole surgery. In most cases, the anatomic closure rate approaches 90% with two weeks of strict postoperative prone positioning[1] [Figure:5].

At the 1-week visit if the edges of the macular hole are flattened and imperceptible with flattening of the cuff of retinal detachement, anatomic success is assured. However, if the edges are still visible and the cuff elevated, anatomic failure is probable.

The recovery of 6/6 visual acuity, the disappearance of focal hyperfluorescence corresponding with the macular hole angiographically, and the disappearance of absolute central scotomas observed in some patients after macular hole surgery suggest that centripetal movement of paracentral retinal receptors and their xanthophyll may occur after retinal reattachment. [9,30] There does appear to be an inverse relationship between duration of symptoms and both anatomic success and visual improvement. Holes of shorter duration have better anatomic and visual results following surgery compared to long-standing holes. Visual results routinely lag 6 weeks behind anatomical success, with about 75% of the anatomically successful eyes improving by two lines or more. The release of macular traction creates the necessary environment for gas tamponade to reattach cuff surrounding the macular hole in most cases. The role of chorioretinal and epiretinal proliferation in reattachment is unclear.

The etiology of anatomic failure is uncertain. Possible causes are: Patient noncompliance in postoperative prone positioning and subsequent inadequate tamponade, residual ERMs producing traction, and intrinsic retinal changes causing stiffness and preventing retinal reattachment. If failure is believed to be secondary to residual ERMs, reoperation has been successful. If noncompliance with postoperative prone positioning is thought to be the cause of failure, newly motivated patients can be given a second chance. Macular holes can reopen after initial surgical repair. The cells that may lead to the closure of an idiopathic macular hole may also contribute to its recurrence if the reparative process goes away. Anatomically unsuccessful closure of the hole correlates with small enlargements in the diameter of the macular hole and its surrounding subretinal cuff and with a slight decrease in visual acuity.[31] However, visual acuity may improve substantially with reoperation after previously failed surgery.[32]

Bovine and recombinant transforming growth factor (TGF-beta), autologous serum, autologous plasma, thrombin and fibrin, autologous platelet concentrate, and tissucol have been used as adjunctive substances in macular hole surgery [Table - 2]. It appears that closure of a full-thickness macular hole is associated with a limited healing response which may be encouraged by the use of adjunctive substances.[33] Glaser et al[34] proposed using TGF-beta 2 as a pharmacologic adjuvant in surgery on macular holes to increase the anatomic success rate. Single application of TGF-beta 2 had a statistically significant beneficial effect.[35] Despite the initial promising results, a large prospective randomized study did not indicate any additional benefit of TGF-beta 2. The anatomic and visual success rates of vitrectomy using bovine-derived TGF-beta 2 in patients who have failed previous macular hole surgery have been detemined. Visual improvement occurred often although in a lower percentage than has been reported for primary surgical eyes. The only factor associated with better final visual acuity was preoperative visual acuity better than 6/24. Nuclear sclerosis leading to cataract extraction was observed in 30% of initially phakic eyes.[36] Ligget et al[37] proposed the use of human autologous serum. In a small pilot study, resolution of the surrounding fluid and flattening of macular hole occurred in all eyes, but a large randomized controlled study is yet to be reported. In another study[38] where macular hole surgery was done with autologous serum in one group and without autologous serum in the other group, the macular hole closure rates were identical.

  Results Top

  Impending macular holes Top

A prospective multicentred randomized controlled trial was undertaken to study the role of vitreous surgery in impending macular holes. Patients were randomized to surgery or observation. Because of low recruitment, the study was terminated before enough cases were enrolled to achieve statistical significance.[39]

  Stage 2 macular holes Top

A prospective randomized trial of vitrectomy or observation by the Vitrectomy for Macular Hole Study Group reported that compared with observation alone surgical intervention resulted in a significantly lower incidence of hole enlargement and appeared to be associated with better outcome in some measures of visual acuity.[40]

  Stage 3 and 4 macular holes Top

Kelly and Wendel[41] were the first to report successful closure of full thickness macular holes in 58% of 52 patients. Visual improvement was noted in 42% of operated eyes. Subsequent follow-up study[42] of 152 consecutive eyes showed an improved anatomic success rate of 73%. The Vitrectomy for Treatment of Macular Hole Study Group[43] assessed the risks and benefits of vitrectomy surgery for eyes with stage 3 or 4 macular holes. Vitrectomy surgery does hold some benefit for macular holes, despite a notable incidence of adverse events. The large variability in visual acuity outcome in the surgical group may be because of complications or progressive cataract.

  Complications Top

The most common complication of a vitrectomy for macular hole is the occurrence or progression of nuclear sclerotic cataract [Table - 3]. Nuclear sclerotic cataracts progress substantially after macular hole surgery with long-acting intraocular gas tamponade. Visual acuity often decreases 12 or more months after vitrectomy because of cataract progression.[44] Posterior segment complications have been noted in 23% of surgical cases. These include peripheral retinal breaks, rhegmatogenous retinal detachment from a peripheral retinal break, enlargement of the hole, late reopening of the hole, retinal pigment epithelium loss under the hole, phototoxicity and endophthalmitis.[45] Iatrogenic retinal breaks tend to be in the inferior and temporal retina which establishes the need for greater intraoperative surveillance in these areas.[46] Peripheral retinal tears may develop during stripping of cortical vitreous. Retinal pigment epitheliopathy after macular hole surgery may portend a guarded visual prognosis. This may be the result of individual patient sensitivity to manipulation, direct trauma or a prolonged exposure to the endoilluminator.[47] Late reopening can complicate initially successful macular hole surgery. Reopening has been documented to occur between 2 and 22 months and it has been hypothesized that the growth of an ERM plays a part in at least some of the eyes. Repeat vitrectomy with gas injection may result in reclosure of the hole and improvement in vision.[48] Some eyes develop increased intraocular pressure (IOP) after macular hole surgery. The increase occurs most frequently between 2 days and 2 weeks postoperatively. The risk of increased IOP is somewhat greater in eyes treated with bovine/ recombinant TGF-beta 2.[49]

Dense wedge-shaped temporal and/or inferior visual field deficits have been noted upon gas resorption. Proposed origins of this visual field include ischaemia of or direct trauma to the optic nerve head, posterior segment ischaemia and transient intraoperative/postoperative raised IOP.[50-52]

  Future horizons Top

The benefits of macular hole surgery are reasonably well established. The more exciting "instruments" are the pharmacologic agents. Chondroitinase-ABC, an agent that disinserts vitreous and/or preretinal membranes from the neurosensory retina, has been developed. This holds tremendous promise and Phase I FDA-approved clinical trials are underway.

  Addendum Top

The following important studies have appeared recently on this subject: Leonard et al[53] reported long-term visual outcomes in patients with successful macular hole surgery. They found that visual acuity in patients after anatomically successful macular hole surgery continues to improve even beyond one year after surgery. Although substantial improvement occurs soon after cataract extraction, further improvement in visual acuity continues for two years thereafter. Banker et al[54] reported that retinal pigment epitheluim (RPE) alterations and retinal detachments are common after macular hole surgery and result in significantly reduced postoperative visual acuity. The RPE changes may be related to trauma or light toxicity. Tornambe et al,[55] in a pilot study, suggested that successful macular hole closure is possible without face-down positioning. Leonard et al[56] reported that after macular hole surgery, anatomically unsuccessful closure of the hole correlates with small enlargement of the diameter of the macular hole and a slight decrease in visual acuity. Miller et al[57] reported that in selected cases, a combination of cataract surgery with intraocular lens implantation and macular hole surgery offers advantage.

  References Top

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Smiddy WE, Sjaarda RN, Glaser BM, Flynn HW Jr, Thompson JT, Hanham A, et al. Reoperation after failed macular hole surgery. Retina 1996;16:13-18.  Back to cited text no. 36
Liggett PE, Skolik SA, Horio B, Saito Y, Alfaro V, Mieler W. Human autologous serum for the treatment of full-thickness macular holes: a preliminary study. Ophthalmology 1995;102:1071-76.  Back to cited text no. 37
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Kelly NE, Wendel RT. Vitreous surgery for idiopathic macular hole: results of a pilot study. Arch Ophthalmol 1991;109:654-59.  Back to cited text no. 41
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  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]

  [Table - 1], [Table - 2], [Table - 3]


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