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To describe six patients (six eyes) who developed an eccentric macular hole after surgery for idiopathic epimacular proliferation.
Review of records from six patients who developed eccentric macular holes postoperatively following vitrectomy in 107 consecutive cases with peeling of the epimacular proliferation and internal limiting membrane (ILM) from June 2004 to January 2009
Eccentric macular holes were developed from nine days to eight months (mean, 3.1 months) after epimacular proliferation peeling. The ILM was peeled in addition to the epimacular proliferation in five of the six cases. Of the six eccentric macular holes, four were located temporal to the fovea, one was located superior to the fovea, and one was located nasal to the fovea. Final visual acuities after a mean follow-up period of 17.3 months were 20/20 in two eyes, 20/25 in one eye, 20/40 in two eyes, and 5/200 in one eye. The eye with the eccentric macular hole nasal to the fovea had the poorest final visual acuity of 5/200.
Eccentric macular holes occurring after vitrectomy to remove epimacular proliferation is an uncommon postoperative finding. Various explanations have been suggested for the etiology of these holes, but there is no consensus. We suggested that the ILM tear should be initiated with a diamond dusted knife to reduce the likelihood of injury to the underlying Muller cells that may contribute to the formation of eccentric macular holes.
Epimacular proliferation (or macular pucker) is a well known cause of decreased visual acuity. Vitreoretinal surgeons have been successful in removing visually significant epiretinal membranes for many years.1–5 Various complications of pars plana vitrectomy with the removal of epimacular proliferation are known, which include cataract, retinal breaks, retinal detachment, recurrent epiretinal membranes, retinal pigment epithelial abnormalities, and infection.1–6 Rarely, postoperative eccentric macular holes have been observed. To our knowledge, only one case series of four such holes by Rubenstein et al,7 has been reported in the literature, and these were thought to be iatrogenic in nature. In addition, these holes developed after vitrectomy with internal limiting membrane (ILM) peeling for idiopathic macular holes and not for epimacular proliferation as in this series. The purpose of this case series was to describe the characteristics and outcomes of these eccentric macular holes as well as to discuss plausible explanations as to their etiology.
A retrospective chart review was performed for 107 consecutive patients (107 eyes) who underwent vitrectomy for epimacular proliferation between June 2004 and January 2009. Indocyanine green (ICG) dye was used in all cases to ensure that all foveal traction was removed. The ILM was peeled in 99% of the patients. Six eyes of six patients were identified as having developed an eccentric macular hole postoperatively and were included in the study. All patients were scheduled to have postoperative visits after one day, one week, four weeks, six weeks to eight weeks, four months, six months, and one year of the surgery. Characteristics of the eccentric macular holes were studied using the clinical description, color photography, and optical coherence tomography images. Figure 1 represents the appearance of one such hole in the temporal macula with color photography and optical coherence tomography. Data were collected on age, sex, date of surgery, preoperative as well as postoperative best-corrected visual acuity, ocular history, characteristics of surgical techniques used, time of onset of eccentric macular hole, any necessary subsequent interventions, and duration of follow up. Each of the six eyes had undergone traditional 3-port 20-gauge pars plana vitrectomy with peeling of the epimacular pucker. No patient required air or gas tamponade. In all six cases, ICG dye was used to stain the underlying ILM, which was also removed in five of the cases. Informed consent was obtained from all patients prior to surgery and photography.
The mean age of the patients was 63 years (range, 34-77 years), and 50% were females. In these six cases, eccentric macular holes were first observed at a mean of 3.1 months (range, nine days to eight months) after surgery. All patients were asymptomatic. As noted above, the ILM was peeled in addition to the epimacular proliferation in five of the six cases, while ICG dye was used in all six cases. ILM was not peeled in one case secondary to the epimacular proliferation being easily removed with no residual traction remaining on the fovea. Of the six eccentric macular holes, four were located temporal to the fovea, one was located superior to the fovea, and one was located nasal to the fovea. Final visual acuities after a mean follow-up period of 17.3 months were 20/20 in two eyes, 20/25 in one eye, 20/40 in two eyes, and 5/200 in one eye. The eye with the eccentric macular hole nasal to the fovea had the poorest final visual acuity of 5/200. Table 1 outlines detailed characteristics of each individual case. Optical coherence tomography was performed to image the holes. Optical coherence tomography showed the holes to be full thickness and flat. Two of the six eyes underwent subsequent intervention in the form of laser retinopexy to the eccentric macular holes, and their final visual acuities remained unchanged at 20/20 and 20/40. Once the eccentric macular holes were diagnosed in all six cases, none were noted to increase in size or lead to any deleterious sequelae (e.g., loss of visual acuity, retinal detachment, or choroidal neovascular membrane) during the follow-up period.
Idiopathic macular hole formation is generally thought to be secondary to tangential vitreous traction on the macula as proposed by Gass.8 The fact that all the macular holes in this series occurred after vitrectomy that seems to eliminate vitreomacular traction as the causative factor. Two separate case series by Smiddy9 and Kimura et al,10 demonstrated the formation of an eccentric (temporal) full-thickness macular hole occurring after vitrectomy for epimacular proliferation. Both studies support the theory of glial cell migration along the outer retinal surface with underlying inner retinal degeneration and spontaneous dehiscence of the umbo.10,11 Although all the holes in our study were located eccentrically, there may likely be a shared mechanism. Although the ILM was not removed in every case (five of six cases), ICG dye was used in all six cases. ICG toxicity has been reported to cause retinal pigment epithelium degeneration12–17 but, to our knowledge, has never been linked to retinal hole formation. Alternatively, peeling of the ILM and/or epiretinal membrane could traumatize the underlying Muller cells that are enough to cause secondary delayed degeneration of the adjacent retinal neurons.18 Ultrastructural studies have shown remnants of Muller cell processes attached to the removed ILM with signs of necrosis. ILM removal may result in glial apoptosis and reduced retinal function due to removal of Mueller cell plates19 and may be responsible for glial structure weakening of the macula leading to retinal hole development. A different and perhaps more plausible explanation of hole formation with eccentric location is iatrogenic trauma to the retina while grasping the macular pucker and/or ILM with ILM forceps. This could occur with the initial membrane elevation or subsequent regrasps. In fact, this explanation was favored by Rubenstein et al,7 in their series of eccentric macular holes after ILM peeling for repair of idiopathic macular holes. However, there were no comments in the operative reports or in the immediate postoperative notes of retinal whitening or hemorrhaging that suggested such trauma. In addition, the formation of a nasal hole in one of the cases seems less likely to be from forceps-related damage because initial elevation of the membrane is never performed there and regrasping is very limited. Furthermore, the initial point of pucker and ILM removal was superior in most cases, while only one case of eccentric macular hole was superior. Nevertheless, this explanation cannot fully be discounted in the pathogenesis of some of our cases. Yet another potential cause of eccentric macular hole formation may be contracture at the edge of the peeled epiretinal membrane or ILM. Clearly, there is a propensity for epiretinal scar tissue formation with subsequent traction in eyes with macular puckers. It is then reasonable to speculate that the ILM and overlying epiretinal membrane left behind at the edge of the peel could continue to contract with secondary hole formation. Perhaps ICG exposure could further lead to changes conducive to residual membrane contracture. In fact, Wollensak et al,20 demonstrated increased biomechanical stiffness of ILM after ICG and light exposure.
In summary, eccentric macular holes occurring after otherwise successful epimacular proliferation peeling are uncommon. These holes appear to have minimal impact on the patient’s vision unless they are located either close to the fovea or in the nasal macula. We believe the likely etiologies of these holes may be due to contracture of the remaining edge of epimacular proliferation and/or ILM causing expansion of a previously undetectable iatrogenic defect. Therefore, perhaps it would be best for surgeons to peel the membranes to the edge of the macula using a diamond dusted knife, thereby limiting the visual impact of any future holes. As is evident by our discussion, several theories exist as to the etiology of these postoperative eccentric macular holes, but there remains no consensus.
Source of Support: Nil
Conflict of Interest: None declared.