Discussion
Development of an MH during treatment for DME has occasionally been reported. Lecleire-Collet et al. reported a case of concurrent MH and ERM after intravitreal triamcinolone injection for DME; the cause of the MH was the degeneration of Muller cells extended by cystoid macular edema, forming cysts in the retina, yet no retinal vitreous traction was involved [
1]. Hasan et al. reported a case of full-thickness MH following anti-VEGF therapy for DME without vitreomacular traction on OCT imaging [
2]. However, it should be noted that some studies have reported that vitreous traction may be involved in the cause of MH. Yoon et al. reported a case in which the MH occurred after PPV in combination with peeling of the ILM for DME, thus suggesting the possible involvement of mechanical stress at the time of ILM peeling in the development of MH [
3]. Brazitikos et al. reported 8 eyes with an MH following PPV for diabetic retinopathy, 4 of which having concurrent DME. The cause of an MH has been reported to be cystoid changes in the retina due to retinal vitreous traction [
4]. Lee et al. reported a case of MH that developed after intravitreal injection of bevacizumab for DME, speculating that traction by the vitreous body incarcerated at the site of insertion of the vitreous injection and change in the properties of the vitreous body by injection are involved as a trigger in the development of the MH [
5]. Pessoa et al. performed PPV in 46 eyes of 38 patients with DME with vitreous traction, and reported that an MH developed in 1 eye after surgery [
6]. Yamamoto et al. reported that there are two types of MH associated with PDR, i.e., an MH due to traction and an MH due to cystoid macular edema [
7]. In Case 1 in this present study, the patient also had an ERM around the MH, thus suggesting the involvement of traction in the tangential direction of the retina in the development of the MH. Taken together, the findings in these reports suggest that it is highly likely that MH secondary to DME develops when retinal vitreous traction is added to the underlying condition, i.e., macular fragility due to long-term edema.
In our two cases, both patients had SRD, RS, and a thin ERM prior to the development of the MH. The primary cause of RS is generally believed to be a fragileity of the layered structure of the retina due to defective Muller cells [
8], with the presence of SRD due to DME being considered as its background. It has been reported that diseases such as uveitis, high myopia, and glaucoma can cause RS triggered by SRD [
9‐
11]. In the present two cases, persistent SRD attributable to DME may have caused RS, to which retinal vitreous traction was added, thereby causing the development of the MH. In addition, since the RS caused a fragility of the layered structure of the retina, the retina may have formed a convex surface toward the vitreous cavity, unlike the OCT image seen in typical cases of idiopathic MH. The formation of the convex surface of the retina towards the vitreous body implies that outer layer organization of the retina may have progressed much more than the inner layer organization, thus resulting in a relative decrease in the extensibility of the outer layer, although the details remain unknown.
In Patient 1, the MH was closed with PPV, but the central foveal retinal thickness had markedly decreased and the improvement of VA was poor. This may be due to the fact that the function of the outer layer of the retina, including photoreceptor cells, may have decreased due to the long-term effect of SRD.
It has frequently been reported that PPV is effective for treating MH complicated by DME. Kurihara et al. performed PPV with ILM peeling in 3 patients with MH associated with PDR, and reported that the MH was successfully closed in all patients, thereby leading to resolution of the preoperative DME [
12]. On the other hand, some studies have reported that MH closure was possible with pharmacotherapy for DME [
13,
14] and that MH closure was spontaneously attained [
15]. Thus, conservative treatment may be acceptable as the first modality for MH, especially if the diameter of the MH is small. However, and to the best our knowledge, the atypical MH form observed in our 2 cases is very rare in comparison to the form reported in the previous studies. The persistent DME complicated with SRD, RS, and a thin ERM caused the fragility of the layered structure of the retina, which sometimes might result in the development of the atypical MH formation that was observed in our two cases.
In conclusion, the findings in this study show that an MH secondary to DME has various clinical characteristics that are different from those of a typical idiopathic MH, and that the treatment strategy should be determined after fully understanding the pathological condition.
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