Acta ophthalmologica · 2009
Electrophysiological evaluation and visual outcome in patients with central retinal vein occlusion, primary open-angle glaucoma and neovascular glaucoma.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Wittström Elisabeth, Ponjavic Vesna, Lövestam-Adrian Monica, Larsson Jörgen, Andréasson Sten
Аннотация
PURPOSE: To evaluate patients with central retinal vein occlusion (CRVO) and neovascular glaucoma (NVG) using electrophysiology in order to gain better understanding of visual outcome and risk factors, such as previously diagnosed primary open-angle glaucoma (POAG).
METHODS: Eighty-three patients (83 eyes) initially presenting with CRVO and examined with full-field electroretinography (ERG) within 3 months of the thrombotic event were analysed retrospectively regarding treatment, risk factors and visual outcome. In addition, 30 patients initially presenting with NVG caused by CRVO were also investigated regarding risk factors using electrophysiology in order to determine the cause of their visual impairment.
RESULTS: Nineteen (23%) of the 83 patients initially presenting with CRVO had been diagnosed previously with POAG. Ninety-five per cent (18/19) of all the patients with previously diagnosed glaucoma developed ischaemic CRVO. Thirty-four per cent of the patients initially presenting with CRVO (28/83) developed NVG. Sixty-eight per cent (13/19) of the patients with previous glaucoma developed NVG, compared to 23% (15/64) of the patients without previous POAG. In the patients who initially presented with NVG, full-field ERG demonstrated a remaining retinal function of both cones and rods, indicating that the main cause of visual impairment is ischaemia of the ganglion cell layer.
CONCLUSION: Glaucoma is a significant risk factor for developing ischaemic CRVO and subsequent NVG. The presence of POAG in CRVO worsens visual outcome. NVG is associated with preserved photoreceptor function, thus indicating ischaemia of the ganglion cell layer as the primary cause of visual impairment. This emphasizes the importance of prompt treatment of ischaemia and elevated intraocular pressure in these patients.
METHODS: Eighty-three patients (83 eyes) initially presenting with CRVO and examined with full-field electroretinography (ERG) within 3 months of the thrombotic event were analysed retrospectively regarding treatment, risk factors and visual outcome. In addition, 30 patients initially presenting with NVG caused by CRVO were also investigated regarding risk factors using electrophysiology in order to determine the cause of their visual impairment.
RESULTS: Nineteen (23%) of the 83 patients initially presenting with CRVO had been diagnosed previously with POAG. Ninety-five per cent (18/19) of all the patients with previously diagnosed glaucoma developed ischaemic CRVO. Thirty-four per cent of the patients initially presenting with CRVO (28/83) developed NVG. Sixty-eight per cent (13/19) of the patients with previous glaucoma developed NVG, compared to 23% (15/64) of the patients without previous POAG. In the patients who initially presented with NVG, full-field ERG demonstrated a remaining retinal function of both cones and rods, indicating that the main cause of visual impairment is ischaemia of the ganglion cell layer.
CONCLUSION: Glaucoma is a significant risk factor for developing ischaemic CRVO and subsequent NVG. The presence of POAG in CRVO worsens visual outcome. NVG is associated with preserved photoreceptor function, thus indicating ischaemia of the ganglion cell layer as the primary cause of visual impairment. This emphasizes the importance of prompt treatment of ischaemia and elevated intraocular pressure in these patients.