Vitreomacular traction, macular hole formation, and subfoveal choroidal neovascularization in a patient with age-related macular degeneration

Sir,

Vitreomacular attachment (VMA) results from incomplete posterior vitreous detachment (PVD) during ageing with persisting adhesions at the macula, and may cause macular holes (MH) or cystoid macular oedema.¹ The presence of VMA has also been described in patients with age-related macular degeneration (AMD).² Ultrasound studies of patients aged 80–89 years reported 11% with incomplete detached vitreous and determined a higher prevalence of attached vitreous or incompletely detached vitreous in AMD patients compared to age-matched individuals without AMD.³ Meyer and Toth⁴ recently reported the coexistence of incomplete PVD and VMA in AMD patients with RPE tears and postulated that VMA may trigger the progression from pigment epithelial detachment (PED) to an RPE tear. Here, we present a bilateral MH and unilateral VMA with choroidal neovascularization (CNV) in a patient with AMD.

A 78-year-old male complained about reduced visual acuity (VA) OU since 2 years. He experienced an additional loss of vision OD and came to our clinic for further evaluations. He received bilateral cataract surgery 10 years ago and was treated with YAG-laser capsulotomy 3 years later. At presentation, his best-corrected VA was 0.2 OU, the anterior segment appeared normal OU with a well-centred intraocular lens, a moderate opening in the posterior capsule, and no vitreous in the anterior chamber. Fundus examination demonstrated a vascular AMD with subretinal haemorrhages and intraretinal oedema OD. His left eye presented a nonvascular AMD with signs of hypo- and hyperpigmentations as well as signs of a full thickness MH OS (Figure 1c and g). Fluorescein angiography (FA) determined an occult subfoveal CNV OD (Figure 1a and b). On the left fundus, there was a circular well-defined central hyperfluorescence corresponding to the location of the MH OS (Figure 1e and f). An OCT scan in the area of the occult CNV OD delineated hyper-reflective and detached RPE–choriocapillaris complex, corresponding to a fibrovascular PED. The adjacent neuroretina presented clearly an MH stage III with partially attached vitreous (Figure 1d). OCT OS demonstrated the typical signs of an MH stage IV in the neuroretina of approximately 480 μm, a completely detached vitreous, and a freely mobile operculum (Figure 1h).

Figure 1

(a, b) FA OD: During the early phase, there is a delayed filling with partially blocked fluorescence in an area corresponding to the underlying PED. During the late phase, the occult CNV and fibrovascular PED present a progressive diffuse leakage with patchy hyperfluorescence. The irregular elevated RPE demonstrates a speckled hyperfluorescence and diffuse leakage from these areas. Subretinal haemorrhages at the temporal margin block the underlying choroidal fluorescence during all phases. No defined classical neovascularization could be seen in the presence of a thin remaining subretinal haemorrhage. (c) Fundusphoto OD: There is an irregular, subretinal haemorrhage temporal to the subfoveal CNV with adjacent hypo- and hyperpigmentation. The blue circle indicates the presumed size and location of the MH. The green line demonstrates the length, direction, and location of the corresponding OCT scan. (d) Optical coherent tomography OD: The radial OCT scan (5.92 mm in length) delineated a hyper-reflective band corresponding to a complete PVD and central VMA. At the insertion site of the VMA, the inner neuroretinal is missing, presenting the typical contour of an MH stage III. Beneath the neurosensory retina, there is a significant thickening of the hyper-reflective RPE–choriocapillaris complex consistent with the fibrovascular PED and occult CNV on FA. Adjacent to this hyper-reflective lesion is a nonreflective region below the neuroretina, consisting of subretinal fluid. (e, f) FA OS: During the early phase, several focal hyperfluorescent notches at the superior margin become present, corresponding to perifoveal drusen. During the late phase, a central, round-shaped foveal hyperfluorescence becomes evident, corresponding to the location of the MH. (g) Fundusphoto OS: The fovea appears to be located in a reddish area where the neuroretina has been torn away. The adjacent orange patches demarcate soft drusen. The blue circle indicates the visible edge and dimension of the MH. (h) Optical coherent tomography OS: Multiple horizontal OCT scans (2.83 mm in length) confirmed no visible attachments of the posterior vitreous at the macular area and delineated a hyper-reflective intravitreal band with a central mass consistent with a detached posterior hyaloid. There was a broad intraretinal hole in the area of the macular, disclosing an MH stage IV with a diameter of approximately 433 μm.

Although drusen, atrophic RPE changes, and CNV are the continuum of the same disease, the underlying pathogenesis and progression of AMD remain poorly understood. With ageing, there is also a collapse of the collagen network (syneresis) and liquefaction (synchisis) of the vitreous, possibly inducing incomplete PVD and VMA.^{1, 5}

It remains questionable if the underlying aetiology of these MH is idiopathic or possibly associated with age-related degenerative changes of the vitreous or retina itself.⁶ Elsing et al reported five patients with idiopathic MH and CNV. Three eyes presented additional signs of AMD or multifocal choroiditis possibly contributing to the development of the CNV. However, one eye had no additional macular disease, so the cumulative abnormalities of the RPE or Bruch's membrane may have caused the CNV.⁷

Our case demonstrated that it may be difficult to determine small MH in AMD patients using biomicroscopy and/or FA. Smith et al concluded from the clinical presentation of a subsequent CNV developed in an idiopathic MH that the coincidence may be more common than reported owing to the obscuring of details from haemorrhages as part of the disciform lesion.⁸ Cross-sectional OCT scans are very effective in evaluating the vitreoretinal interface and intraretinal architecture. Therefore, OCT should be considered in AMD patients to determine occult VMA and small MH. Unknown full-thickness ‘occult’ MH may induce severe intraoperative complications during subretinal surgery, macular translocation, or photodynamic therapy. The lost integrity of the neuroretina may affect the anatomical prognosis and visual outcome in AMD patients.