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BRIEF COMMUNICATION
Year : 2022  |  Volume : 10  |  Issue : 2  |  Page : 85-87

Central serous chorioretinopathy in coronavirus disease-19 patient


Department of Ophthalmology, School of Medical Sciences and Research, Sharda University, Greater Noida, Uttar Pradesh, India

Date of Submission31-May-2021
Date of Decision21-Jul-2021
Date of Acceptance21-Jul-2021
Date of Web Publication18-Jul-2022

Correspondence Address:
Shipra Singh
H-1201, Cloud 9 Towers, Sector 3F, Kamma 1, Vaishali, Ghaziabad - 201 019, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcor.jcor_80_21

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  Abstract 


A 46-year-old male with mild coronavirus disease 2019 (COVID-19) symptoms presented to the emergency department complaining of decreased vision in the right eye (RE). Funduscopic examination revealed serous macular detachment at the posterior pole with loss of foveal reflex in the RE. Fundus fluorescein angiography revealed pinpoint leakage in the early phase, which was enlarged in the late phase to appear like inkblot suggestive of central serous chorioretinopathy (CSCR), which was confirmed on optical coherence tomography as hyporeflective space due to the collection of serous fluid between the neurosensory retina and retinal pigment epithelium. He received COVID-19 directed therapy. The patient became systemically alright and his vision in the RE improved. Severe acute respiratory syndrome coronavirus 2 is associated with thromboembolic events and retinal ischemia may create hyperpermeability of choroid leading to the formation of CSCR.

Keywords: Central serous chorioretinopathy, COVID-19, optical coherence tomography


How to cite this article:
Singh S, Goyal J L, Singh D. Central serous chorioretinopathy in coronavirus disease-19 patient. J Clin Ophthalmol Res 2022;10:85-7

How to cite this URL:
Singh S, Goyal J L, Singh D. Central serous chorioretinopathy in coronavirus disease-19 patient. J Clin Ophthalmol Res [serial online] 2022 [cited 2022 Aug 17];10:85-7. Available from: https://www.jcor.in/text.asp?2022/10/2/85/351301



The pathogenesis of CSCR remains obscure. CSCR is thought to occur due to hyperpermeable choroidal capillaries, which, in association with retinal pigment dysfunction cause a serous detachment of the neurosensory retina. Studies have reported that COVID-19-induced cytokine storm damages the vascular endothelium causing increased permeability.[1] However, these changes were not reported in the macular area in COVID-19 patients. To the best of our knowledge, this is the first case of CSCR in patient who has suffered COVID-19 disease.


  Case Report Top


A 46-year-old male presented to the emergency department complaining of shortness of breath and blurring of vision in the right eye (RE) for 3 days. He had been suffering from flu-like symptoms and fever for 7 days. On investigation, he was tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) at another hospital 2 days earlier.

On examination, his temperature was 36.4°C, pulse was 120 per min, respiratory rate was 24 per min, blood pressure was 126/86 mm Hg, and oxygen saturation was 97%.

His erythrocyte sedimentation rate was 58 mm in 1st h (normal value 0–10), C-reactive protein was 52.0 mg/L (normal value <5.0 mg/L), lactate dehydrogenase (LDH) was 269 U/L (normal 125–220 U/L), fibrinogen was 6.82 g/L (normal 1.70–4.00 g/l), D-Dimer was 625 ng/mL (normal <250.0 ng/mL), and interleukin-6 was 16.0 pg/mL (normal 0.00–7.00 pg/mL) [Table 1]. The remaining blood values including full blood count and serum biochemistry were within the normal limits. Chest X-ray and computed tomographic (CT) imaging of the chest showed normal findings.
Table 1: Inflammatory markers level

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The ophthalmic examination was performed because he complained of sudden onset of central blurring in his RE. His best-corrected visual acuity was 6/12 in his RE and 6/6 in the left eye. The anterior segment was within the normal limits in both eyes and intraocular pressure was 17 mmHg in both eyes. Funduscopic examination in the RE revealed loss of foveal reflex and elevated, well-demarcated round area of neurosensory detachment over the posterior pole [Figure 1]a. Spectral-domain optical coherence tomography (OCT) showed bullous elevation of the neurosensory retina with hyporeflective space between the neurosensory retina and retinal pigment epithelium (RPE) with serous fluid in the RE [Figure 1]b and [Figure 1]c. Left eye OCT findings were within the normal limits [Figure 1]d and [Figure 1]e. The characteristic inkblot pattern on fluorescein angiography confirmed the diagnosis of central serous chorioretinopathy (CSCR) [Figure 2]. Left eye showed no alteration of the retina.
Figure 1: Baseline funduscopic examination (a) colored fundus showed the circular neurosensory detachment of the parafoveal region (blue arrow). (b and c) spectral-domain optical coherence tomography hyporeflective space between neurosensory retina and retinal pigment epithelium with serous fluid with a thickness of 338 microns at the foveolar level. Left eye optical coherence tomography findings were within the normal limit (d and e)

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Figure 2: (a-d)-Fluorescein angiographyshows pinpoint leakage in the early phase and characteristic inkblot pattern in the late phase

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The patient remained in the intensive care for 5 days under observation and then transferred to the general medicine ward, where he was given supplemental oxygen through nasal cannula and COVID-19 therapy including ivermectin, azithromycin, and multivitamins. The patient did not receive steroids in any form. The patient was observed and was given supportive treatment in the form of multivitamins and anxiolytics for RE CSCR. He was discharged from the hospital after 10 days. On follow-up visit after 6 weeks, the patient was systemically alright and all blood tests were within the normal limits. OCT imaging showed an almost complete regression of the retinal alteration in his RE [Figure 3]. His vision was back to normal to 6/6 in both eyes.
Figure 3: (a-d) Optical coherence tomography of the right eye 3 months after the acute event showing minimal subretinal (white arrow). Left eye optical coherence tomography was normal

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  Discussion Top


The pathophysiology of CSCR is thought to involve multiple etiologies and mechanisms that lead to hyperpermeability of the choroid which can be due to stasis, ischemia, or inflammation. This can cause widespread choroidal circulatory abnormality and breach in the RPE allowing entry of fluid in the subretinal space.[2] Aldosterone/mineralocorticoid receptor pathway is also thought to be involved in the pathogenesis of CSCR. In one study, intravitreal aldosterone had provoked vasodilation, thickening, and leakage of choroidal vessels with the accumulation of subretinal fluid in preclinical animal models.[3]

The SARS-CoV-2 virus enters the host cells through the angiotensin-converting enzyme 2 (ACE-2) receptors.[4] ACE-2 receptors are expressed in nearly all human organs in varying degrees. In the respiratory system, ACE-2 mainly is expressed in type II alveolar epithelial cells, indicating that the lungs are the primary target of SARS-CoV-2.[5],[6] Moreover, ACE-2 is also highly expressed in myocardial cells, kidney, urinary bladder, and small intestine. ACE-2 has been detected in the human retina,[7] vascularized RPE, choroid,[8] cornea, and conjunctival epithelium.[9] Therefore, this indicates that SARS-CoV-2 infection can cause multiple organ injury depending on the receptor distribution in the body. SARS viral infection induces cytokine storm which damages the integrity of the vascular endothelium causes increased permeability, coagulation activation, and microcirculation disturbances, which contribute to systemic as well as ocular complications.[10]

Previous studies reported that SARS-CoV-2 has been associated with conjunctivitis in humans.[11] In addition, retinal disorders, such as retinal vasculitis,[12] retinal degeneration, and blood-retinal barrier breakdown,[13] had been demonstrated in experimental animal models of coronavirus infection.

Our patient did not suffer from severe systemic complications due to COVID-19 infection although he had evidence of a transient hypercoagulabity with increased fibrinogen, LDH, and raised D-dimer which was on the upper limit of the normal range. COVID-19 can induce a pro-coagulative status.[1] On the other hand, he did not have any known risk factors for CSCR such as type A personality, anti-psychotic medication, psychological stress, hypertension, obstructive sleep apnea, steroids, and Helicobacter pylori infection.[14]

Acute CSCR is self-limiting disease, with reattachment of the neurosensory retina within 4 months in most cases,[15] that is the reason, observation has been considered an appropriate first-line approach. In our patient, vision improved and CSCR resolved after a month and his inflammatory markers and coagulation indices also normalized with COVID-19 directed therapy. The patient did not receive systemic corticosteroids.

We suggest a possible correlation between the systemic disease and CSCR in this case. In addition, our patient never had a prior attack of CSCR, it only occurred during COVID-19 infection. However, the development of CSCR in a patient without any known risk factor, suggests a possible connection. COVID-induced systemic and local disturbances and autonomic instability of blood vessels have lead to hyperpermeability and leakage of choroidal blood vessels.

An ophthalmologist should be aware about CSCR can be one of the rare ocular manifestations of COVID-19 infection.

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 initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Panigada M, Bottino N, Tagliabue P, Grasselli G, Novembrino C, Chantarangkul V, et al. Hypercoagulability of COVID-19 patients in intensive care unit: A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost 2020;18:1738-42.  Back to cited text no. 1
    
2.
Prünte C, Flammer J. Choroidal capillary and venous congestion in central serous chorioretinopathy. Am J Ophthalmol 1996;121:26-34.  Back to cited text no. 2
    
3.
Zhao M, Célérier I, Bousquet E, Jeanny JC, Jonet L, Savoldelli M, et al.Mineralocorticoid receptor is involved in rat and human ocular chorioretinopathy. J Clin Invest 2012;122:2672-9.  Back to cited text no. 3
    
4.
Li W, Moore MJ, Vasilieva N, Sui J, Wong SK, Berne MA, et al. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 2003;426:450-4.  Back to cited text no. 4
    
5.
Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 2004;203:631-7.  Back to cited text no. 5
    
6.
Zou X, Chen K, Zou J, Han P, Hao J, Han Z. The single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to Wuhan 2019-nCoV infection. Front Med 2020;14:185-92.  Back to cited text no. 6
    
7.
Senanayake PS, Drazba J, Shadrach K, Milsted A, Rungger-Brandle E, Nishiyama K, et al. Angiotensin II and its receptor subtypes in the human retina. Invest Ophthalmol Vis Sci 2007;48:3301-11.  Back to cited text no. 7
    
8.
Wagner J, Jan Danser AH, Derkx FH, de Jong TV, Paul M, Mullins JJ, et al. Demonstration of renin mRNA, angiotensinogen mRNA, and angiotensin converting enzyme mRNA expression in the human eye: Evidence for an intraocular renin-angiotensin system. Br J Ophthalmol 1996;80:159-63.  Back to cited text no. 8
    
9.
Sun LL, Pan X, Jing M. Mechanism of the action between the SARS-CoV S240 protein and the ACE2 receptor in eyes. J Virol 2006;6:783-6.  Back to cited text no. 9
    
10.
Zhou L, Xu Z, Castiglione GM, Soiberman US, Eberhart CG, Duh EJ. “ACE2 and TMPRSS2 are expressed on the human ocular surface, suggesting susceptibility to SARS-CoV-2 infection,” The Ocular Surface, 2020;18:537-44.  Back to cited text no. 10
    
11.
Guan WJ, Ni ZY, Hu Y, Liang WH, Ou CQ, He JX, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med 2020;382:1708-20.  Back to cited text no. 11
    
12.
Marinho PM, Marcos AA, Romano AC, Nascimento H, Belfort Jr R. Retinal findings in patients with COVID-19. Lancet 2020;395:1610. doi: 10.1016/S0140-6736(20)31014-X.  Back to cited text no. 12
    
13.
Vinores SA, Wang Y, Vinores MA, Derevjanik NL, Shi A, Klein DA, et al. Blood-retinal barrier breakdown in experimental coronavirus retinopathy: Association with viral antigen, inflammation, and VEGF in sensitive and resistant strains. J Neuroimmunol 2001;119:175-82.  Back to cited text no. 13
    
14.
Daruich A, Matet A, Dirani A, Bousquet E, Zhao M, Farman N, et al. Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis. Prog Retin Eye Res 2015;48:82-118.  Back to cited text no. 14
    
15.
Gilbert CM, Owens SL, Smith PD, Fine SL. Long-term follow-up of central serous chorioretinopathy. Br J Ophthalmol 1984;68:815-20.  Back to cited text no. 15
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1]



 

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