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Limited macular translocation has been reported to be a promising treatment for some patients with choroidal neovascularisation.1–4 Although this technique has the advantage of being less invasive, there is documentation of various complications that have been experienced with its use.5–8 In this report, we describe an unusual complication associated with limited macular translocation in a patient with long standing choroidal neovascularisation.
A 35 year old woman was referred to our department because of a gradual decrease in visual acuity in her right eye. At the first visit, her best corrected visual acuity was right eye, 20/40, with a refractive error of −17.5 dioptres in the spherical equivalent. Clinical and angiographic examinations showed a juxtafoveal choroidal neovascularisation. During the subsequent follow up period, choroidal neovascularisation and surrounding retinal pigment epithelial atrophy gradually expanded and involved the subfoveal region (Fig 1A). We gave the patient detailed information on the available therapeutic options, including macular translocation, but she chose conservative follow up rather than surgical intervention. Three years after her first visit, the visual acuity in her right eye worsened to 20/100. At that time, the patient decided to have surgical treatment. With her consent, limited macular translocation was performed on her right eye, as described previously.4 Postoperatively, fluorescein angiography showed an extrafoveal neovascular membrane with a foveal shift of 0.7 disc diameter (Fig 1B). Sharply demarcated hypofluorescence in the macular area was also demonstrated. Biomicroscopic examination revealed a slightly hyperpigmented lesion underneath the translocated macula, which corresponded to the area of hypofluorescence. A horizontal optical coherence tomography (Humphrey Systems, San Leandro, CA, USA) section taken through the translocated macula displayed highly reflective double layers (Fig 2A). These findings may indicate that the abnormal subfoveal retinal pigment epithelium, which adhered tightly to the overlying neurosensory retina, probably because of the long history of neovascular maculopathy, was translocated with the macula during surgery. Two reflective bands observed on an optical coherence tomography image may have corresponded to the native retinal pigment epithelium and abnormal retinal pigment epithelium translocated with the macula. Indocyanine green angiography findings supported this speculation (Fig 2B).
Despite sufficient foveal displacement, the patient’s visual acuity has not improved. During a follow up period of 15 months, it has remained at the same level as her preoperative vision.
In many eyes with choroidal neovascularisation, the macula can easily be separated from the subjacent fibrovascular tissue. In some eyes with long standing choroidal neovascularisation, however, the outer portion of neurosensory retina may adhere firmly to the subjacent tissue. In such cases, an inner portion of fibrovascular tissue may be torn off and translocated with overlying neurosensory retina during macular translocation. The underlying healthy retinal pigment epithelium covered with the translocated abnormal tissue may not be able to fulfil its physiological roles on the overlying neurosensory retina, and good functional recovery of the translocated macula is unlikely to be achieved. As documented here, simultaneous translocation of the underlying abnormal retinal pigment epithelium associated with long standing choroidal neovascularisation can occur during limited macular translocation and result in an unsatisfactory visual outcome. When patients are deciding whether to consent to surgical intervention with limited macular translocation in such cases, they should be informed of the benefits and risks of the treatment, with due consideration of this complication.
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