American journal of ophthalmology case reports · 2024
Cystoid macular edema as a complication of central retinal artery occlusion.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Estawro Rania, Abraham Neda, Fouad Yousef, Bousquet Elodie, Sarraf David
Аннотация
PURPOSE: To describe the development of cystoid macular edema (CME) as a complication of central retinal artery occlusion (CRAO) in 2 cases.
OBSERVATIONS: The first patient was a 51-year-old female who presented with acute loss of vision in the left eye. Multimodal retinal imaging revealed a CRAO with a perfused cilioretinal artery. CME acutely developed one week after presentation. Cystoid spaces predominantly involved the outer nuclear layer (ONL) on optical coherence tomography (OCT) and completely resolved in two weeks. The second case was a 50-year-old man who presented with acute vision loss in the right eye for 3 weeks. Multimodal retinal imaging illustrated an acute CRAO of the right eye. Four weeks later, visual acuity spontaneously improved to 20/20 and was maintained at 20/20 for more than 2 years. After 28 months, the patient returned with a recurrent drop of vision in the right eye. Cross sectional and en face OCT revealed CME in the right eye without leakage on FA. Cystoid spaces predominantly involved the inner nuclear layer (INL) and resolved with intravitreal anti-VEGF injection combined with carbonic anhydrase inhibitor (CAI) and steroid topical drop therapy.
CONCLUSIONS AND IMPORTANCE: CME can rarely complicate both the acute and chronic phase of CRAO. In the acute phase, cystoid spaces were transient and confined to the ONL on OCT. While in the chronic phase, cystoid spaces were confined to the INL on OCT and angiographically silent on FA. Further studies are needed to identify the incidence, underlying pathophysiology and visual prognosis of CME in cases of CRAO.
OBSERVATIONS: The first patient was a 51-year-old female who presented with acute loss of vision in the left eye. Multimodal retinal imaging revealed a CRAO with a perfused cilioretinal artery. CME acutely developed one week after presentation. Cystoid spaces predominantly involved the outer nuclear layer (ONL) on optical coherence tomography (OCT) and completely resolved in two weeks. The second case was a 50-year-old man who presented with acute vision loss in the right eye for 3 weeks. Multimodal retinal imaging illustrated an acute CRAO of the right eye. Four weeks later, visual acuity spontaneously improved to 20/20 and was maintained at 20/20 for more than 2 years. After 28 months, the patient returned with a recurrent drop of vision in the right eye. Cross sectional and en face OCT revealed CME in the right eye without leakage on FA. Cystoid spaces predominantly involved the inner nuclear layer (INL) and resolved with intravitreal anti-VEGF injection combined with carbonic anhydrase inhibitor (CAI) and steroid topical drop therapy.
CONCLUSIONS AND IMPORTANCE: CME can rarely complicate both the acute and chronic phase of CRAO. In the acute phase, cystoid spaces were transient and confined to the ONL on OCT. While in the chronic phase, cystoid spaces were confined to the INL on OCT and angiographically silent on FA. Further studies are needed to identify the incidence, underlying pathophysiology and visual prognosis of CME in cases of CRAO.