Clinical Findings and Management of Central Serous Retinopathy || Sivaletchumi Sigamani

Share on facebook
Facebook
Share on twitter
Twitter
Share on linkedin
LinkedIn
Share on pinterest
Pinterest
eye health optometry education world optometry

Case Study

Sivaletchumi Sigamani, B.Optom (Hons)1 Universiti College Sedaya International (UCSI) University, Kuala Lumpur, Malaysia. Author correspondence: ssheyva@gmail.com

Disclaimers: I hereby declare that the case study is based on my original work has not been previously published or concurrently submitted for consideration by other journals.
Financial support: None.
Statement that patient consent was obtained: A written consent was acquired from the patient after the explanation of the procedures and objectives. The patient was explained in detail regarding the usage of the data and images for case study presentations and scientific publications. The patient acknowledged that the investigator will be responsible to ensure all data or images published are kept confidential.

Abstract: Central Serous Chorioretinopathy (CSR) is an idiopathic disorder characterized by localized serous retinal detachment and retinal pigment epithelial detachment secondary to leakage from the choriocapillaris through one or more hyperpermeable Retinal Pigmented Epithelium (RPE) sites1.  

Central serous chorioretinopathy (CSR) occurs when fluid builds up under the retina. This can cause distortion to the vision similar to the symptoms the patient experience in this case. This is a case report of a 34-year-old male who presented with clinical signs and symptoms of CSR and was managed accordingly. . 

Key words: central serous retinopathy, meibomian gland dysfunction, elevated macular retina,  tigroid fundus, thalasemia.

Introduction: Central Serous Chorioretinopathy (CSR) is an idiopathic disorder characterized by localized serous retinal detachment and retinal pigment epithelial detachment (PED) secondary to leakage from the choriocapillaris through one or more hyperpermeable Retinal Pigmented Epithelium (RPE) sites.1  

Changes are most often confined to the macula and are associated with leakage of fluid through the RPE into the subretinal space. Patients with CSR often experience loss of central vision, central scotoma, micropsia, metamorphopsia, decreased color vision, and abnormalities in contrast sensitivity. Visual acuity may be only moderately reduced, and there may be a hyperopic shift.2

Numerous risk factors have been associated with CSR, the most common being glucocorticoid use. Given the strong association between CSR and steroids, their use should be avoided, whenever possible. Furthermore, patients with CSR should be questioned about their use of all forms of steroids, including products that may contain steroids (e.g., skin creams, joint injections, nasal sprays, inhalants, and other commonly overlooked forms of glucocorticoid), as these could be contributing factors. Pregnancy is a recognized risk factor for CSR. Plasma cortisol levels are elevated during pregnancy, particularly during the third trimester. Pregnancy-associated CSR tends to present as white subretinal exudation that usually resolves spontaneously after delivery.2

Another risk factor traditionally associated with CSR is psychological stress. Other associations include systemic hypertension, gastroesophageal reflux disease, and the use of alcohol or sympathomimetic agents, although the latter requires further confirmation. 2

Case Presentation: Mr. X, a 34-year-old Chinese male presented to University College Sedaya International (UCSI) University Optometry Clinic on 6th August, 2019 with a complaint of distorted vision in the left eye for two years ago. The distortion occurred gradually. Patient reported that the distortion was on and off (intermittently) and persisted for a few months before it resolved. He claimed that there was no treatment done, and that the distortion had occurred previously and was associated with decrease in contrast and brightness in the particular eye. 

Ocular history revealed the patient had an eye examination two years ago at an optical store in Kuala Lumpur, Malaysia. He was prescribed glasses for distance and had no other abnormal findings. The patient was  spectacle lens wearer for more than 20 years, and his current glasses were two years old (he claimed that he was comfortable wearing them). Patient reported that he had no history of wearing contact lenses nor any history of ocular disease/infection, surgery or injury. He was a designer by occupation and often engaged in heavy Visual Display Unit usage. The patient was not under any medications or supplements.

Patient had his medical examination 1 year ago, and no abnormal findings were reported. His overall health history was unremarkable except Thalassemia, which was diagnosed by a physician 20 years ago. Patient had no history of injury, surgery or any infections from head to toe. 

Family history revealed that his mother also had Thalassemia and Retinal Detachment. Both of his parents were myopic without any ocular or systemic diseases.

Examinations and Findings: The distance unaided visual acuity (VA) was 2/36 and 6/36 for right eye (OD) and left eye (OS) respectively. The distance habitual VA was 6/6 and 6/9 for OD and OS respectively. The near unaided VA was N8@36 cm  and the near habitual VA was N5@36 cm for both eyes.

Preliminary examinations and findings included Stereopsis (Titmus Fly Test): 100”; Hirschberg: Center and Symmetry; Pupil Evaluation: PERRLA with No RAPD present; Cover Test for distance and near: Orthophoria; near point of convergence and accommoation (push up-pull away method): within normal limit. Ocular Motility and Confrontation tests showed no abnormalities. Colour Vision with pseudoisochromatic Ishihara Plates was normal in both eyes.  Keratometry revealed astigmatism of -0.875 × 16 and-0.25 ×7 in the right eye and left eye, respectively. Retinoscopy findings were -3.00DS/-0.50DC × 60 (VA: 6/6) in the right eye and -0.75DS/-0.50DC × 135 (VA: 6/9) in the left eye. Subjective refraction was then conducted over the objective refraction, and it revealed refractive errors of -2.75DS/-0.75DC × 40 (VA: 6/6) in the right eye and -0.75DS/-0.75DC × 150 (VA: 6/9) in the left eye. The present glass prescription of the patient was right eye: -2.75DS/-0.75DC × 40 and left eye: -0.50DS/-0.75DC × 150, with the VAs of 6/6/ and 6/9 respectively. As patient’s primary complaint was distorted vision, Amsler Grid test was performed. The test showed no abnormalities for the right eye, but a distortion on temporal portion of the chart for the left eye.

Slit lamp examination showed Meibomian Gland Blockage Grade (G) 1.0 Upper Lid, G 0.5 Inferior Lid (OD), G 0.5 Superior and Inferior Lid (OS); mild conjunctival concretion on inferior palpebral conjunctiva (OS); Bulbar Conjunctiva redness OD- G 0.5 – G 1, OS- G 0.5 – G 1; Palpebral conjunctiva OD and OS upper and lower lid: G1- G1.5; Limbal Redness G1 (OD); Van Henrick OD: G3/G3, OS: G3/G3; Tear Break Up Time (TBUT): OD: 6 Sec, OS: 5 Sec.

FUNDUS EXAMINATION: Right eye showed Optic nerve head crescent and tigroid appearance of the posterior retina, while left eye showed thickened or elevated macular retina with the presence of drusens. Cup Disc Ratio was 0:3 and Arterial Vein Ratio was 2:3 for both eyes.

eye1 meroeye
eye2 meroeye

Figure 1. Fundus photo of the right eye and left eye.

diagram 2 meroeye

Figure 2. Differential diagnosis based on patient’s complaints and fundus image

Diagnosis and Assessment:

The patient was diagnosed with having low Compound Myopic Astigmatism (OU). Other diagnoses included Meibomian Gland Dysfunction (MGD) OU (OD > OS), moderate dry eye OU, optic nerve head crescent and “tigroid” appearance of the posterior retina (OD), thickened or elevated macular retina with the presence of drusens (OS).

Management and Outcome:

No new prescription was given as there were no significant changes in Rx. The patient was advised for warm compression 3 times a day for meibomian gland blockages and was advised to continue using artificial tears as necessary. Visual hygiene (20-20-20 rule) was suggested to reduce stress due to prolonged VDU usage. The patient was given Amsler Grid to monitor the progression of distortion at home and was referred to Ophthalmologist (Vitreoretinal Specialist) for further evaluation (i.e Optical Coherence Tomography and Fundus Fluorescein Angiography) regarding the changes in the retina with a provisional diagnosis of suspected Central Serous Retinopathy.

Further Evaluation/Diagnosis by Ophthalmologist (Vitreoretinal Specialist):

A vitreoretinal specialist confirmed the diagnosis of central serous retinopathy based on  Optical Coherence Tomography Images and kept the patient under observation for 3 consecutive months. The diagram below presents the management plan for the patient.

diagram 2 meroeye

Figure 3. Management plan for a patient with central serous chorio-retinopathy

Discussion:

Acute classic CSCR is characterized by a short clinical course with spontaneous resolution within 3–6 months with near-normal visual recovery. Recurrences are known in 30–50% of all cases. 3-5 Chronic CSR, also termed diffuse retinal pigment epitheliopathy (DRPE), is seen in a few cases. It is characterized by a chronic course lasting more than 12 months, typically affecting individuals above 50 years of age. Such cases may have permanent visual impairment due to progressive RPE atrophy and photoreceptor degeneration. 3-5

Bullous CSR is a rare presentation characterized by larger and more numerous areas of serous retinal and RPE detachments often confused with bullous retinal detachment.  Differential diagnosis of CSR includes other entities which may produce serous detachment of sensory retina in the macular area. These include optic pit, idiopathic polypoidal choroidal vasculopathy, macular hole with serous detachment, choroidal tumours and pigment epithelial detachment (PED).  5-7

CSR undergoes spontaneous resolution in 80 to 90% of cases. Visual acuity returns to normal or near-normal within 3 to 6 months. Discontinuation of steroids, if possible, should be done at the earliest. Lifestyle changes to reduce stress in life should be adopted. Laser photocoagulation is indicated in long-standing cases (more than 6 months), recurrent CSR with visual loss, and permanent loss of vision in the other eye due to this condition.  8

Contraindications include the cases having leaks near or within the FAZ. Photodynamic therapy (PDT) may be beneficial for those with severe disease not amenable to conventional laser treatment, e.g., with subfoveal leaks and chronic cases. Anti-VEGF can be considered if CNV develops.9-11

Conclusion:

This report presents a case of central serous retinopathy. Most people with CSR  regain their vision.  However, having chronic CSR can cause changes to the vision in the long term, but much can be done to help make the most of the remaining vision and adapt to any changes. 12-13 Patients with CSR who are under corticosteroids should discontinue their use if possible, but only after checking with their prescribing physician to ensure it is safe to stop.  14-15 If the affected eye is the eye with better VA, then one may need to make changes by using aids to make the most of the remaining sight. This may mean making things bigger, using brighter lighting or using colour to make things easier to see. 16 A low vision assessment can explore these things. The eye care professional should make a referral to a local low vision service for an assessment. 10

Management of CSR, in particular the chronic one, is challenging. Although focal laser and PDT are current standards of care in chronic CSR, micropulse laser is a good alternative in instances when verteporfin is not available. Some systemic treatments may benefit patients with chronic CSC by decreasing the rate of therapy-induced complications. 19

References 

  1. Nicholson, B., Noble, J., Forooghian, F., & Meyerle, C. (2013). Central Serous Chorioretinopathy: Update on Pathophysiology and Treatment. Survey Of Ophthalmology, 58(2), 103-126. doi: 10.1016/j.survophthal.2012.07.004
  2. Liew, G., Quin, G., Gillies, M., & Fraser-Bell, S. (2012). Central serous chorioretinopathy: a review of epidemiology and pathophysiology. Clinical & Experimental Ophthalmology, 41(2), 201-214. DOI: 10.1111/j.1442-9071.2012.02848.x
  3. Yumnam, C., Laishram, U., & Thangjam, A. (2020). Fundus fluorescein angiography of idiopathic central serous chorioretinopathy in the indigenous population of Manipur.
  4. Wang M, Munch IC, Hasler PW, et al. Central serous chorioretinopathy. Acta Ophthalmol.  2008; 86:126-145.
  5. Haimovici R, Koh S, Gagnon DR, et al; Central Serous Chorioretinopathy Case-Control Study Group. Risk factors for central serous chorioretinopathy: a case-control study. Ophthalmology. 2004;111(2):244-249.
  6. Bowling, B. (2015). Kanski’s clinical ophthalmology (8th ed.). WB Saunders.
  7. Khurana, A., & Khurana, A. (2007). Comprehensive ophthalmology. New Delhi: New Age International.
  8. Sartini, F., Menchini, M., Posarelli, C., Casini, G., & Figus, M. (2020). Bullous Central Serous Chorioretinopathy: A Rare and Atypical Form of Central Serous Chorioretinopathy. A Systematic Review. Pharmaceuticals, 13(9), 221. DOI: 10.3390/ph13090221.
  9. Tittl MK, Spaide RF, Wong, et al. Systemic findings associated with central serous chorioretinopathy. Am J Ophthalmol. 1999;128(1):63-68.
  10. Bouzas EA, Scott MH, Mastorakos G, et al. Central serous chorioretinopathy in endogenous hypercortisolism. Arch Ophthalmol. 1993;111(9):1229-1233.
  11. Cousins L, Rigg L, Hollingsworth D, et al. Qualitative and quantitative assessment of the circadian rhythm of cortisol in pregnancy. Am J Obstet Gynecol. 1983;145(4):411-416.
  12. Chumbley LC, Frank RN. Central serous retinopathy and pregnancy. Am J Ophthalmol. 74;77(2):158-160.
  13. Yannuzzi LA. Type A behaviour and central serous chorioretinopathy. Trans Am Ophthalmol Soc. 1986; 84:799-845.
  14. Michael JC, Pak J, Pulido J, de Venecia G. Central serous chorioretinopathy associated with administration of sympathomimetic agents. Am J Ophthalmol. 2003;136(1):182-185.
  15. Mansuetta CC, Mason JO 3rd, Swanner J, et al. An association between central serous chorioretinopathy and gastroesophageal reflux disease. Am J  Ophthalmol. 2004;137(6):1096-100.
  16. Gemenetzi M, De Salvo G, Lotery AJ. Central serous chorioretinopathy: an update on pathogenesis and treatment. Eye (Lond). 2010;24(12):1743-1756.
  17. Guyer DR, Yannuzzi LA, Slakter JS, Sorenson AJ, Ho A, Orlock D. Digital indocyanine green video angiography of central serous chorioretinopathy. Arch Ophthalmol.  1994;112(8):1057-1062.
  18. Spitznas M. Pathogenesis of central serous chorioretinopathy: a new working hypothesis. Graefes Arch Clin Exp Ophthalmol. 1986;224(4):321-324.
  19. Potsaid B, Baumann B, Huang D, et al. Ultrahigh-speed 1050nm swept source/Fourier domain OCT retinal and anterior segment imaging at 100,000 to 400,000 axial scans per second. Opt Express. 2010;18(19):20029-20048.
Meroeye

Meroeye

Share With

Share on facebook
Facebook
Share on twitter
Twitter
Share on linkedin
LinkedIn
Share on pinterest
Pinterest
Share on whatsapp
WhatsApp

More News, Journal, and Articles

Subscribe now and receive weekly newsletter with educational materials, new courses, interesting posts, popular books and much more!