OSLI Retina

January 2020

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January 2020 · Vol. 51, No. 1 55 choroidal excavation temporal to this lesion. All images were acquired on a Heidelberg Spectralis device (Heidelberg Engineering, Heidelberg, Germany). A diagnosis of an active exudative CNVM was made and treatment was initiated with monthly aflibercept injections. The patient responded well to treatment with resolution of SRF at month 3, better exposing the presence of a conforming-type FCE. During the subsequent years of treatment, the patient was injected with aflibercept as needed when there was recurrent CNVM activity with SRF. Over time, the depth and diameter of the FCE significantly increased, confounding the assessment of recurrent CNVM activity versus the development of nonconforming FCE due to the altered choroidal architecture. At last follow-up 43 months after initial presentation, the patient had visual acuity of 20/25 in the affected eye with last aflibercept injection 11 weeks prior, with marked expansion of the FCE compared with her initial presentation (Figure 4) and some persistent SRF, but relative preservation of the outer retinal architecture. Enhanced depth imaging OCT obtained at more recent follow-up demonstrated choroidal thicknesses of 401 µm underneath an area of excavation of depth 160 µm in the right eye and 501 µm in the left eye, along with notable pachyvessels in both eyes, consistent with an underlying pachychoroid pathophysiology. DISCUSSION This patient presented with features of pachychoroid-spectrum including FCE and thickened choroid with large choroidal pachyvessels. She presented with a symptomatic type 2 CNVM, which has remained active throughout the patient's clinical course. Freund et al. previously described the entity of pachychoroid epitheliopathy, which is typically associated with type 1 CNVM lesions; however, they also described a case of type 1 CNVM associated with a FCE and pachychoroid. 8 In their case, though, the FCE was not noted to change size or character demonstrably following anti-vascular endothelial growth factor (VEGF) therapy. As such, our patient's FCE expansion with anti-VEGF treatment alone represents a novel clinical course in the absence of acute inflammation. 9 Matsubara et al. suggested that some forms of FCE possibly evolve due to an imbalance between intraocular and choroidal pressure, with concurrent RPE and basement membrane weakness. 6 During periods of choroidal inflammation there is engorgement and swelling of the choroid, which, as it resolves, can expose the presence of or expand a Figure 1. Right eye indocyanine green angiography at initial pre- sentation demonstrating hyperfluorescent foci indicative of a cho- roidal neovascular membrane. The fovea and area of choroidal excavation is under an area of hypofluorescence due to a blocking defect from the overlying subretinal hemorrhage. There is no dif- fuse leakage suggestive of inflammation of the choroid. Figure 2. Fluorescein angiography of the right eye 6:23 after dye injection. There is a blocking defect from overlying hemorrhage, with late leakage from a choroidal neovascular membrane supero- nasal to the fovea.

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