First Author: T.Fernandes PORTUGAL
Co Author(s): J. Serino
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Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is a typically bilateral inflammatory condition involving the retinal pigment epithelium (RPE), the choriocapillaris and the outer retina. Pathogenesis is still controversial but anomalies in choroidal perfusion may play an important role as evidenced by imaging techniques. Few reports describe choroidal vasculature in APMPPE using optical coherence tomography (OCT) angiography. We report choroidal vasculature changes in an APMPPE patient with the clinical course characterized by OCT-Angiography.
Ophthalmology Department of Centro Hospital Alto Ave, Guimarães, Portugal; Ophthalmology Department of Hospital de Braga, Portugal
We report a clinical case of a 25-year-old male presented himself at the emergency room for acute onset of bilateral photopsias with three days of evolution. Except for a treated gastritis, the patient was otherwise considered healthy. When inquired, the patient stated no occurrence of an influenza-like syndrome, recent vaccination or any systemic findings.
At observation, he recorded 20/20 of best-corrected visual acuity (BCVA) bilaterally. Fundoscopy revealed the presence of several round and confluent cream-coloured, flat lesions with indistinct margins spread throughout the posterior pole. Fluorescein angiography showed early hypofluorescence followed by late hyperfluorecent staining at placoid lesions, a typical pattern of APMPPE. OCT-Angiography demonstrated disruption of the outer perifoveal retinal layers with rarefaction of choroid circulation and choroidal ischaemia.
The diagnosis of APMPEE is essentially clinic, based on examination, course of the disease and imaging findings. This disease normally becomes inactive over a period of weeks without any specific intervention and has a relatively good prognosis. The advent of OCT-Angiography brings new insights on the pathogenesis of APMPEE supporting malperfusion of the choriocapillaris rather than blockage by the RPE edema as the primary pathophysiologic mechanism of disease.