|Year : 2021 | Volume
| Issue : 3 | Page : 529-531
Recurrent central serous chorioretinopathy in a surgically closed traumatic macular hole
Manoj Soman, KR Sheera, Unnikrishnan Nair
Department of Ophthalmology, Vitreoretinal Services, Chaithanya Eye Hospital and Research Institute, Kesavadasapuram, Thiruvananthapuram, Kerala, India
|Date of Submission||10-Sep-2020|
|Date of Acceptance||11-Feb-2021|
|Date of Web Publication||02-Jul-2021|
Dr. K R Sheera
Vitreoretinal Services, Department of Ophthalmology, Chaithanya Eye Hospital and Research Institute, Kesavadasapuram, Thiruvananthapuram, Kerala
Source of Support: None, Conflict of Interest: None
A 36-year-old gentleman with history of central serous chorioretinopathy (CSCR) developed full thickness macular hole in the right eye with recurrence of CSCR 2 weeks after blunt trauma to his right eye. Vitrectomy resulted in complete closure of the macular hole and resolution of the subretinal fluid. Post macular hole surgery he developed two episodes of CSCR recurrence with no reopening of the hole. This report hypothesises the possible mechanisms underlying this unusual association and explains how a surgically manipulated macular tissue could endure significant submacular fluid accumulation.
Keywords: Central serous chorioretinopathy, macular hole, optical coherence tomography, traumatic macular hole, vitrectomy
|How to cite this article:|
Soman M, Sheera K R, Nair U. Recurrent central serous chorioretinopathy in a surgically closed traumatic macular hole. Indian J Ophthalmol Case Rep 2021;1:529-31
|How to cite this URL:|
Soman M, Sheera K R, Nair U. Recurrent central serous chorioretinopathy in a surgically closed traumatic macular hole. Indian J Ophthalmol Case Rep [serial online] 2021 [cited 2021 Sep 24];1:529-31. Available from: https://www.ijoreports.in/text.asp?2021/1/3/529/320019
Full-thickness macular holes are mostly of idiopathic origin. Vitreomacular traction is the widely accepted mechanism for formation of macular holes. Central serous chorioretinopathy (CSCR) is the serous detachment of the neurosensory retina. We report a case in which macular hole developed over CSCR following trauma and recurrences of CSCR after surgical closure of the macular hole without its reopening.
| Case Report|| |
A 36-year-old gentleman presented to the outpatient clinic with diminished vision two weeks after blunt trauma to his right eye. He was diagnosed to have CSCR in the right eye one month prior to the trauma. There was history of CSCR in the left eye also four years back with spontaneous resolution [Figure 1]a and [Figure 1]b. He had no co-morbid medical illnesses or history of any relevant drug intake.
|Figure 1: Fundus photographs showing CSCR in the right eye (panel 1a). There are retinal pigment epithelial alterations in the left eye (panel 1b). Fundus autofluorescence images showed mottled autofluorescence in the right eye with hyperfluorescence corresponding to the macular hole (panel 1c) and foci of hyper auto fluorescence in the left eye extending nasally (panel 1d)|
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The best-corrected visual acuity (BCVA) was 20/40N8 in the right eye and 20/20N6 in the left eye. The intraocular pressure was 12 mmHg in both eyes. Anterior segment was normal in both eyes. Dilated fundus examination revealed a full-thickness macular hole in the right eye with an area of subretinal fluid and retinal pigment epithelium alteration. Left eye showed macular retinal pigment epithelial alterations, consistent with resolved CSCR. Autofluorescence imaging of the right eye showed patchy hyper autofluorescence in the peripapillary area and in the macular hole region. Left eye showed scattered foci of hyper autofluorescence in the perifoveal region extending nasally [Figure 1]c and [Figure 1]d.
Spectral-domain optical coherence tomography (OCT) of the right eye showed a full-thickness macular hole with neurosensory detachment with photoreceptor segments stuck to the inner surface of detachment. The underlying retinal pigment epithelium showed irregularity. Few hyperreflective spots were seen in the choroid, subretinal space, and intraretinally. Left eye showed normal outer retina though some foci of palisading were seen in the outer plexiform layer – outer nuclear layer region nasally corresponding to the altered autofluorescence signals. Choroidal thickness was increased in both eyes with pachychoroid appearance [Figure 2]a and [Figure 2]b.
|Figure 2: OCT of the right eye shows full-thickness macular hole and neurosensory detachment with photoreceptor segments stuck to the inner surface of detachment (arrowhead). The underlying RPE showed irregularity (asterisk). Few hyperreflective spots were seen in the choroid, subretinal space and intraretinally (white arrows) (panel 2a). Left eye showed normal outer retina though some foci of palisading seen in the outer plexiform layer – outer nuclear layer region nasally (red arrow) (panel 2b). Choroidal thickness was increased in both eyes with pachychoroid appearance|
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Fundus fluorescein angiography (FFA) [Figure 3]a and [Figure 3] cand indocyanine green angiography (ICG) [Fig. 3b and d] of both eyes did not demonstrate any typical leaking points though some areas of patchy fluorescence and macular hole fluorescence were seen.
|Figure 3: Baseline Fundus fluorescein angiography (FFA) showed areas of punctate hyper fluorescence in the perifoveal region without any active leak in both eyes (panel 3a, 3c). Indocyanine green angiography (ICG) showed focal areas of hyperfluorescence in both eyes and hypofluorescent dots in the left eye (panel 3b, 3d). Subsequent angiography; FFA showed extrafoveal leak (arrow) in the right eye. (panel 3e) and left eye with punctate hyperfluorescence (panel 3g). ICG showed focal areas of hyperfluorescence in both eyes and hypofluorescent dots in the left eye (panel 3f, 3h)|
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After 2 months of conservative management, as there was no resolution, he underwent 25G vitrectomy with internal limiting membrane (ILM) peeling and SF6 tamponade of the right eye. A gentle silicon-tipped flute SRF drainage was done at the hole area. Inverted flap technique was not used. Post-operative OCT showed complete resolution of CSCR with closure of the macular hole [Figure 4]a.
|Figure 4: OCT of the right eye after vitrectomy (panel 4a) showed complete resolution of the SRF and type 1 closure of the macular hole. OCT during first recurrence of CSCR (panel 4b) showed subretinal fluid involving the inferior macula and the preservation of closed macular hole configuration. OCT during second recurrence (panel 4c) showed subretinal fluid involving the fovea and superior macula with preservation of a closed macular hole configuration. Laser resulted in complete resolution of the SRF and preservation of macular hole closure at 1st month (panel 4d) and 12th month (panel 4e)|
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He developed posterior subcapsular cataract in the right eye ten weeks after vitrectomy and needed phacoemulsification and intraocular lens implantation and the BCVA improved to 20/40N8.
He developed recurrent CSCR three weeks following cataract surgery in the right eye. The pocket of subretinal fluid predominantly involved the inferior macula and the closed macular hole configuration was preserved. [Figure 4]b. Topical steroid use was attributed as the likely cause for the recurrence, and was withdrawn. Spontaneous resolution of the CSCR with stable closed-hole configuration was documented by five weeks. Twelve months after cataract surgery, he had a second recurrence of CSCR in the right eye. The new pocket of subretinal fluid was significant (Central foveal thickness: 396 μm) and involved the superior macula with preserved closed macular hole configuration [Figure 4]c and was associated with ipsilateral decline in BCVA to 20/80. As there was no significant improvement over the next two months, angiography was done and the extrafoveal leak [Figure 3]e was treated with laser photocoagulation. There was good resolution [Figure 4]d and he had no recurrences thereafter. Twelve months after laser [Figure 4]e, the visual acuity in the right eye remained 20/40N8.
| Discussion|| |
While most cases of full-thickness macular holes are idiopathic, it can occasionally occur following trauma resulting from a countercoup mechanism. CSCR and macular hole can rarely develop simultaneously following blunt trauma. The pathophysiology of CSCR following trauma is not clear but is thought to involve choriocapillaris hyperpermeability and/or retinal pigment epithelium dysfunction resulting in subretinal fluid accumulation. Predisposed patients may develop CSCR triggered by blunt trauma as noted in our case. Tornambe's hydration theory suggests that the progression of full-thickness macular hole follows a defect in the inner retina and depends on the fluid balance created by the fluid entering the retina and the rate of fluid removed by the RPE cells. Our case did not demonstrate an active vitreomacular traction process. Pachychoroid and abnormal RPE noted on fundus autofluorescence support the hydration theory in macular holes. While traumatic macular holes may close spontaneously, recent data supports the role of vitrectomy in achieving better anatomical results. While reopening of a surgically closed macular hole is not uncommon, cataract surgery and foveal pathologies like epiretinal membrane, intact ILM, and cystoid macular edema are potential risk factors for reopening. We however documented two recurrences of CSCR after successful macular hole surgery in the same eye without reopening of the closed hole.
| Conclusion|| |
This unique case illustrates the elastic and stable nature of a surgically closed-hole especially when ILM peeling has been done in the advent of significant subretinal fluid collection. The peeled ILM (Mullers base plate) probably loosens up the z-shaped perifoveal and parafoveal mullers fibers allowing more elasticity to the retina thereby preventing opening of the closed hole. There could be other mechanisms at play and a clinicopathological study may yield more knowledge.
The study was approved by the Chaithanya Eye Hospital and Research Institute Ethics Committee and was conducted in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its amendments. Patient detail privacy has been taken care of and identity particulars have not been disclosed.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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