Case of the Month I October 2019

Case of the Month
October 29, 2019

The Case

The patient was a 33-year-old healthy man with a history of subretinal fluid in the right eye for which he had laser treatment elsewhere 1 year previously. In April 2018 he presented with a 3-month history of a dark spot in the right eye. The visual acuity was 20/25 OD and 20/30 OS. Anterior segment examination was unremarkable in both eyes. The right fundus had pigmentary mottling and subtle elevation superotemporal to the fovea. The left macula had subtle central pigmentary mottling. In June 2018 he returned with a complaint of a new dark spot in the right eye. The visual acuity was 20/60 and there was a large neurosensory detachment.  The fluorescein angiogram showed leakage into the subneurosensory space from a pinpoint location superotemporal to the fovea resulting in a late “smokestack” appearance. No treatment was done at that time, and close observation was recommended. The next month, the subretinal fluid was substantially reduced and the visual acuity was 20/40-1. He returned in September 2018 with decreased vision to 20/200 and increased subretinal fluid. At this point, what do you think is the underlying disease process, and what treatment would you recommend?

The patient had central serous chorioretinopathy (CSC) with a neurosensory detachment in the right eye in June 2018, and in September 2018 had had deposition of fibrinous material and possible choroidal neovascular membrane activity. He initially presented to us in April 2018 with a superotemporal pigment epithelial detachment (PED), and a small chorioretinal scar from prior laser treatment above the fovea that can be seen on the fluorescein angiogram. The left eye did not have a PED or subretinal fluid, but there was a thickened choroid (pachychoroid) with markedly enlarged deep choroidal blood vessels (pachyvessels), typical of CSC. The fluorescein angiogram of the right eye showed a window defect (indicating loss of RPE pigment) temporal to the fovea and possible late staining.

In June 2018, he had a large neurosensory detachment, as demonstrated on the OCT, and the fluorescein angiogram showed the classic “smokestack” sign of fluorescein leakage into the subneurosensory space. This subretinal fluid usually resolves spontaneously in patients with CSC.  However, in September he manifested central fibrinous material that had retracted and caused retinal folds. The OCT showed a PED, subretinal fluid, and reflective fibrinous material. The fundus photo revealed the central fibrinous material, and the fluorescein angiogram showed leakage into the subneurosensory space. Such fibrinous material is sometimes seen in patients with CSC, particularly if they have been using corticosteroids. He was treated with intravitreal tissue plasminogen activator to alleviate the fibrin and anti-VEGF therapy with Lucentis to address possible choroidal neovascular membrane activity. The fibrinous material diminished and the visual acuity improved to 20/50. He received a second Lucentis treatment one month later. In December he received half-fluence photodynamic therapy with verteporfin for residual subretinal fluid. When seen in January 2019, the subretinal fluid had resolved, the fibrinous material had nearly resolved, and the retinal folds were substantially reduced. The visual acuity was 20/40. Interestingly, there is thickened choroid seen on enhanced depth imaging in June 2019, even though the pachychoroid that typically accompanies central serous chorioretinopathy generally improves markedly after photodynamic therapy. The most likely reason is that only the area with leakage on fluorescein angiography was treated with PDT and the fovea was spared. More extensive PDT would likely have had a greater effect on choroidal thickness. Also of note, there is a persistent PED with reflective material, which is likely scar tissue from a regressed choroidal neovascular membrane.

Case Photos

Click the Images below to enlarge
FA April 2018
FA June 2018
FA September 2018
OCT OD April 9, 2018
OCT OD June 18, 2018
OCT OD September 21, 2018
OCT OD October 15, 2018
OCT OS April 9, 2018
OCT OD June 11, 2019
OCT OD June 11, 2019

The patient had central serous chorioretinopathy (CSC) with a neurosensory detachment in the right eye in June 2018, and in September 2018 had had deposition of fibrinous material and possible choroidal neovascular membrane activity. He initially presented to us in April 2018 with a superotemporal pigment epithelial detachment (PED), and a small chorioretinal scar from prior laser treatment above the fovea that can be seen on the fluorescein angiogram. The left eye did not have a PED or subretinal fluid, but there was a thickened choroid (pachychoroid) with markedly enlarged deep choroidal blood vessels (pachyvessels), typical of CSC. The fluorescein angiogram of the right eye showed a window defect (indicating loss of RPE pigment) temporal to the fovea and possible late staining.

In June 2018, he had a large neurosensory detachment, as demonstrated on the OCT, and the fluorescein angiogram showed the classic “smokestack” sign of fluorescein leakage into the subneurosensory space. This subretinal fluid usually resolves spontaneously in patients with CSC.  However, in September he manifested central fibrinous material that had retracted and caused retinal folds. The OCT showed a PED, subretinal fluid, and reflective fibrinous material. The fundus photo revealed the central fibrinous material, and the fluorescein angiogram showed leakage into the subneurosensory space. Such fibrinous material is sometimes seen in patients with CSC, particularly if they have been using corticosteroids. He was treated with intravitreal tissue plasminogen activator to alleviate the fibrin and anti-VEGF therapy with Lucentis to address possible choroidal neovascular membrane activity. The fibrinous material diminished and the visual acuity improved to 20/50. He received a second Lucentis treatment one month later. In December he received half-fluence photodynamic therapy with verteporfin for residual subretinal fluid. When seen in January 2019, the subretinal fluid had resolved, the fibrinous material had nearly resolved, and the retinal folds were substantially reduced. The visual acuity was 20/40. Interestingly, there is thickened choroid seen on enhanced depth imaging in June 2019, even though the pachychoroid that typically accompanies central serous chorioretinopathy generally improves markedly after photodynamic therapy. The most likely reason is that only the area with leakage on fluorescein angiography was treated with PDT and the fovea was spared. More extensive PDT would likely have had a greater effect on choroidal thickness. Also of note, there is a persistent PED with reflective material, which is likely scar tissue from a regressed choroidal neovascular membrane.

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