Coats disease is a nonhereditary retinal vascular disorder, characterized by retinal telangiectatic vessels and intraretinal or subretinal exudation. It is seen more often in young males and usually involves one eye [1]. Although macular involvement is frequent in Coats disease, the development of a full-thickness macular hole (FTMH) is rare. Only a few pediatric and adult cases have been reported previously [2,3].

This report describes an unusual presentation of adult-onset Coats disease with a FTMH treated surgically, and reviews prior published cases to evaluate the similarities and differences between idiopathic and Coats-related macular holes. Written informed consent for publication of the research details and clinical images was obtained from the patient.

A 61-year-old male patient was referred to our clinic with progressive visual loss in his left eye over the past 10 years. There was no history of ocular surgery or trauma. The visual acuity was 20 / 30 in the right eye and 20 / 500 in the left eye. Fundus examination of the left eye showed circinate exudates, retinal hemorrhages, and a macular hole (Fig. 1A). Wide-field fluorescein angiography demonstrated peripheral telangiectatic vessels with leakage (Fig. 1B), consistent with Coats disease stage 2B [1]. Optical coherence tomography (OCT) of the left eye showed a FTMH, surrounded by intraretinal hyperreflective foci (Fig. 1C). The minimum diameter of FTMH was 257 microns, with a base diameter of 491 microns. The patient underwent 25-gauge pars plana vitrectomy (PPV), internal limiting membrane (ILM) peeling with inverted flap technique, endolaser photocoagulation to exudation sites, and perfluoropropane (C₃F₈) 14% gas tamponade of his left eye. Postoperatively, prone positioning was recommended.

One month postoperatively, the visual acuity of his left eye was 20 / 1,000. The fundus examination of his left eye showed a flat macula with closed macular hole and decreased exudation, which was also confirmed at OCT images (Fig. 1D, 1E). At 6 months postoperatively, the visual acuity of the left eye was 20 / 1,000. Wide-field fundus photography and OCT demonstrated persistent closure of the macular hole with decreased central exudation and slightly increased cystoid macular edema in the temporal retina (Fig. 1F, 1G).

Our case adds to the limited literature on adult-onset Coats disease presenting a FTMH. Idiopathic macular holes mainly occur in older females and are primarily caused by vitreomacular traction. OCT usually shows a round or oval full-thickness defect with well-defined, symmetric edges and relatively normal surrounding retina. Intraretinal cystic spaces and operculum may be present, but exudation is not common. In contrast, FTMH associated with Coats disease occurs in younger males (including adult-onset cases), often in eyes with chronic exudation and retinal vascular abnormalities. In prior studies, OCT findings include intraretinal hyperreflective foci, retinal thinning or atrophy, irregular or asymmetric hole margins, serous macular detachment, and evidence of epiretinal membrane or ILM traction [2-5]. In our case, the FTMH demonstrated irregular, blunted edges of the hole base accompanied by complex intraretinal structural changes. OCT revealed areas of cystic deroofing, asymmetric intraretinal disruption, and multilayered schitic lesions, suggesting that the hole developed not from classic vitreofoveal traction but from chronic exudation and uneven tangential stress within an edematous, lipid-laden macula [2]. Combined with extensive perifoveal exudation and telangiectasia, these features suggest that the FTMH in Coats disease represents a secondary structural breakdown of a chronically compromised fovea, rather than the traction-driven mechanism seen in idiopathic cases. Although a mild epiretinal membrane was present on preoperative OCT, it appeared thin, which would have unlikely produced significant retinal distortion or tractional configuration typically associated with traction-induced macular hole formation.

As described in previous studies, standard PPV with ILM peeling and gas tamponade can lead to anatomical closure of Coats-related FTMH and visual improvement [4,5]. According to Nawrocka et al. [3], the inverted ILM flap technique has been shown to have a favorable outcome for Coats-related FTMH. In our case, the macular hole had a relatively wide basal diameter of 491 microns, and OCT demonstrated irregular, blunted edges of the hole base within a chronic exudative retinal environment. Therefore, the inverted ILM flap technique was selected to facilitate the hole closure. In addition, endolaser photocoagulation was applied to areas of vascular leakage and exudation. Otherwise, the operation procedure followed standard surgical approach for macular hole repair.

Postoperative OCT demonstrated subfoveal exudation and fibrotic changes at the closure site (Fig. 1E). Regarding the chronic exudative environment associated with Coats disease, these findings were considered more likely related to the underlying disease process, rather than a direct effect of the inverted ILM flap technique.

Adult-onset Coats disease may rarely present with a FTMH. In this case, the FTMH associated with Coats disease demonstrated an atypical configuration characterized by irregular, blunted edges of the hole base arising from chronic exudative remodeling, which differs from the steep, sharply angulated edges typically observed in idiopathic macular holes. PPV with inverted ILM flap and gas tamponade can achieve anatomical stabilization. This indicates that despite its unusual architecture, Coats-associated FTMH can respond favorably to conventional repair strategies.