Epiretinal membrane-induced intraretinal neovascularization





Abstract


Purpose


To report a 71-year-old male patient diagnosed with epiretinal membrane-induced intraretinal neovascularization.


Observations


The presence of an epiretinal membrane (ERM) was confirmed by Optical Coherence Tomography (OCT), fluorescein and indocyanine angiography. Optical coherence tomography angiography (OCT-A) revealed a neovascular membrane within the ERM. Intravitreal ranibizumab injections were administered three times at four-week intervals. Imaging revealed a stable membrane with no leakage. Five months after the third injection, OCT revealed intraretinal fluid. OCT-A showed a new branch of the neo-vascular membrane at the superficial capillary plexus. Following an additional ranibizumab injection, the membrane stabilized.


Conclusions and importance


It is conceivable that neovascularization developed due to, or in close conjunction with an epiretinal membranes already in place.



Introduction


Idiopathic epiretinal membranes are macular disorders with an incidence of 2–20 %, frequently diagnosed in the elderly. ERMs are thought to result from fibroglial proliferation on the inner retinal surface secondary to small internal limiting membrane (ILM) breaks occurring during posterior vitreous detachment (PVD). ERM contraction or shrinkage may create irregular folds in the membrane itself, and exert anteroposterior or tangential tractional forces on the retina and retinal vasculature. Anteroposterior forces produce vertical traction and increases retinal thickness whereas tangential forces pull the superficial retinal layers away from their original position, causing retinal deformation and displacement.


ERMs also alter the morphology, location and permeability of the retinal vasculature. Morphological abnormalities include straightening and curling of retinal blood vessels and shrinkage of the foveal avascular zone (FAZ). Eyes with ERMs often have macular edema and tortuous vessels with abnormal hemodynamics in the perifoveal capillaries and disturbance of the macular microcirculation. Some reports suggest a partial similarity between idiopathic ERM and central retinal vein occlusion (CRVO) , and venous outflow from the macula can be impeded in eyes with ERM. Patients may experience metamorphopsia, micropsia, monocular diplopia, and, depending on the location, decreased visual acuity.



Case report


A 71-year-old Caucasian male, presented with gradual vision loss in his right eye (OD) over the past four months. Snellen best-corrected visual acuity (BCVA) was 20/50 OD and 20/20 in his left eye (OS). Fundus examination revealed an epiretinal membrane OD as well as sub-hyaloid and intraretinal hemorrhage inferior to the foveola ( Fig. 1 A) without any apparent PVD or any other rhegmatogenous, vascular, inflammatory or hamartomatous findings. No findings were observed in OS. Fluorescein angiography (FA) revealed leakage in both early and late phases, corresponding to the intraretinal neovascularization inferior to the foveola OD ( Fig. 1 B and C). Indocyanine green angiography confirmed the fluorescein angiography results.




Fig. 1


a. Fundoscopic view at presentation; Subhyaloid and intraretinal hemorrhage inferior to the foveola.

b. Fluorescein angiography showing the intraretinal neovascular membrane, early arteriovenous phase, c. peak phase angiogram. d.-e. OCT scans of the right eye showing ERM and hyperreflective foci in the intraretinal edema in the macula.


Optical Coherence Tomography (OCT, Heidelberg Engineering, Ltd., Heidelberg, Germany) confirmed the presence of an epiretinal membrane in the macula OD with intraretinal cystic macular edema and a hyperreflective area in the inner retinal layer corresponding to the intraretinal hemorrhage ( Fig. 1 D). Optical coherence tomography angiography (OCT-A) revealed increased flow only in the retinal superficial capillary plexus, corresponding to an area of intraretinal neovascularization, a dense and apparently active membrane. There were no apparent changes in the deep capillary plexus, outer retina and choriocapillaris ( Fig. 2 ). Intravitreal ranibizumab (0.5 mg, Lucentis, Novartis AG) injections were given OD three times at four-week intervals. One month after the third intravitreal injection, BCVA was stable with no intraretinal edema and only remnants of the neovascular tissue remained at the level of the epiretinal membrane in OCT-A ( Fig. 3 ). OCT, OCT-A and clinical examination were repeated monthly for the next four months with no signs of intraretinal fluid. BCVA remained unchanged. Five months after the third injection, OCT revealed intraretinal fluid. OCT-A showed a new branch of the neovascular membrane at the superficial capillary plexus. One month after a fourth intravitreal ranibizumab injection, there was no intraretinal fluid while the OCT-A showed a stable membrane ( Fig. 4 ). BCVA was 20/30 OD and 20/20 OS.


Jan 3, 2022 | Posted by in OPHTHALMOLOGY | Comments Off on Epiretinal membrane-induced intraretinal neovascularization
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