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ORIGINAL ARTICLE |
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Year : 2015 | Volume
: 14
| Issue : 4 | Page : 163-168 |
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Central serous chorioretinopathy in Benin City, Nigeria
Odarosa Magdiel Uhumwangho, Rita Omoso Momoh
Department of Ophthalmology, University of Benin Teaching Hospital, P.M.B. 1111, Benin City, Edo, Nigeria
Date of Web Publication | 16-Oct-2015 |
Correspondence Address: Odarosa Magdiel Uhumwangho Department of Ophthalmology, University of Benin Teaching Hospital, P.M.B. 1111, Benin City, Edo Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1596-3519.158522
Abstract | | |
Background: Central serous chorioretinopathy (CSCR) is a retinal cause of visual loss. The aim of this report is to describe the pattern of presentation of CSCR in patients presenting to a tertiary hospital in Nigeria within a specified period. Materials and Methods: The case folders of all patients in which a diagnosis of central serous retinopathy (CSR) was made from January 1, 2012 to December 31, 2014 were retrieved, data extracted and reviewed. Results: There were a total of five patients within the study period made of four males and one female. There were two cases of bilateral CSCR and three cases of unilateral CSCR. There was a positive history of underlying anxiety or stress related conditions in all the patients. One patient with bilateral CSCR was on systemic prednisolone for arthritis. Confirmatory investigations were performed in all patients. Four patients had fundus fluorescein angiography which showed smoke stack and ink blot patterns in two patients, respectively. Two patients had optical coherence tomography showing macular neurosensory detachment, with one having associated pigment epithelial detachment. Vision improved in all patients with conservative management, reduction in anxiety/stress related activities and steroid use discontinuation in the patient with chronic steroid use. Conclusion: CSR has a favorable outcome with appropriate intervention. Abstract in French | | |
Résumé Contexte: CRSC (CSCR) est une cause de perte de vision rétinienne. Le but de ce rapport est de décrire le modèle de présentation du CSCR chez les patients présentant un hôpital de soins tertiaires au Nigeria dans un délai déterminé. Matériels et Méthodes: Les dossiers de tous les patients dont le diagnostic de la rétinopathie séreuse centrale (RSE) a été faite à partir du 1er Janvier 2012 au 31 Décembre cas, 2014 ont été récupérés, les données extraites et examinées. Résultats: Il y avait un total de cinq patients pendant la période d'étude, composé de quatre hommes et une femme. Il y avait deux cas de CSCR bilatérale et trois cas de CSCR unilatérale. Il y avait une histoire positive de l'anxiété sous-jacente ou des conditions liées au stress chez tous les patients. Un patient avec CSCR bilatérale était sur la prednisolone systémique pour l'arthrite. Enquêtes de confirmation ont été effectués chez tous les patients. Quatre patients avaient fond angiographie à la fluorescéine a montré que des motifs blot de la pile de fumée et d'encre dans deux patients, respectivement. Deux patients ont eu la tomographie optique de cohérence montrant détachement neurosensoriel maculaire, avec l'un étant associé détachement de l'épithélium pigmentaire. Vision améliorée chez tous les patients avec la direction conservatrice, réduction / stress lié activités de l'anxiété et de l'utilisation de stéroïdes dans l'arrêt du patient avec l'utilisation chronique de stéroïdes. Conclusion: RSE a une issue favorable avec une intervention appropriée. Mots-clés: Chorioretinopathie séreuse centrale, fond d'angiographie, a fluorescéine, tomographie a cohérence optique, stéroïdes, stress Keywords: Central serous chorioretinopathy, fundus fluorescein angiography, optical coherence tomography, steroids, stress
How to cite this article: Uhumwangho OM, Momoh RO. Central serous chorioretinopathy in Benin City, Nigeria. Ann Afr Med 2015;14:163-8 |
Introduction | |  |
Central serous chorioretinopathy (CSCR) also referred to as central serous retinopathy (CSR) wasfirst described by Albrecht von Graefe in 1866 as "relapsing central luetic retinitis."[1],[2] Maumenee [3] described the retinal pigment epithelium (RPE) as the source of the leak and gas documented the findings on fundus fluorescein angiography (FFA).[4],[5] Its pathophysiology is poorly understood, and the predisposing or risk factors implicated varied.[6],[7],[8],[9],[10],[11],[12],[13],[14] Although many treatment modalities have been advocated, it generally has a favorable natural course.[15],[16],[17] There is currently a dearth of information on the presentation of CSCR among Nigerian patients. The aim of the study is thus, to describe the pattern of presentation of CSR in a group of patients presenting to a tertiary hospital in Benin City, Nigeria.
Materials and Methods | |  |
The case folders of all patients in whom a diagnosis of CSR was made from January 1, 2012 to December 31, 2014 were retrieved, data extracted and reviewed. Data retrieved include age, sex, predisposing risk factors, investigations, treatment modality, and outcome. Diagnosis was initially made following detection of the serous macular elevation on clinical biomicroscopic examination with + 78D noncontact lens. Further confirmatory investigations were then advised consisting of FFA and/or optical coherence tomography (OCT).
Results | |  |
There were a total of seven eyes in five patients within the study period made of four males and one female. The mean age of presentation was 45.8 ± 10.5 years. Among the males, the mean age of presentation was 41.3 ± 3.0 years while the only female was aged 64 years. The mean duration of symptoms prior to presentation was 3.8 ± 1.5 weeks. [Table 1] shows the demographic and clinical characteristics of the patients. These were one case of bilateral active CSR, one case of bilateral chronic CSR, and three cases of unilateral active CSR. All patients had presenting complaints of blurring/reduced vision, one patient complained of associated metamorphopsia and the two patients with bilateral involvement also had complaints of associated vague, mild ocular ache. All patients had a positive history of underlying anxiety/stressful conditions. The male patient with bilateral chronic CSR was on prednisolone for arthritis. The female patient was a known hypertensive who though well-controlled, complained of the diuretic effect of her antihypertensive medications which disrupted her sleep pattern. Confirmatory investigations were performed in all patients. All the male patients had FFA, which showed smoke stack pattern in two patients and ink blot pattern in two patients. [Figure 1]a shows the FFA of the male patient with bilateral chronic CSR. The two patients with bilateral involvement had OCT performed. [Figure 1]b and [Figure 1]c is the initial OCT of the right and left eyes, respectively, of the male patient with bilateral CSCR showing neurosensory serous macular detachment, with associated pigment epithelial detachment in the right eye. [Figure 1]d is the repeat OCT 5 months later, showing resolution. [Figure 2] shows OCT of the only female patient also showing neurosensory serous macular detachment but without associated pigment epithelial detachment. Lifestyle modification with minimized stress-related activities was advised in all patients. Steroid use was discontinued in the patient with chronic steroid use and alternative agents for arthritis advised. All patients showed improvement in visual acuity and flattening of the macular elevation on biomicroscopic examination with conservative management. The mean duration for resolution of symptoms in the patients was 16.2 ± 2.9 weeks. Only the male patient with bilateral CSCR performed follow-up investigations following improvement in symptoms. | Figure 1: (a) Fundus fluorescein angiography of the male patient with bilateral central serous chorioretinopathy showing leakage. (b and c) Optical coherence tomography of right and left eyes respectively of the male patient with bilateral central serous chorioretinopathy showing neurosensory macular detachment and pigment epithelial detachment, worse in right eye. (d) Repeat optical coherence tomography of the male patient with bilateral central serous chorioretinopathy showing resolution
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 | Figure 2: Optical coherence tomography of the female patient with bilateral central serous chorioretinopathy showing neurosensory macular detachment
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Discussion | |  |
Central serous retinopathy is a chorioretinal disease with serous detachment of the macular due to focal disruption in the outer blood-retinal barrier. This exudation is due to a hyperpermeable RPE and choriocapillaris with disruption in the choroidal circulation and choroidal vascular congestion.[16],[17] Its pathophysiology is complex, poorly understood with an etiology which is multifactorial and has been associated with many systemic conditions. [4,6-9,12-14] The cause is largely unknown, but factors implicated include venous stasis, ischemia, and inflammation of the choroid. It affects all races but is believed to be most prevalent in Asians and least prevalent in the black population, with blacks having a worse presentation and severity.[17],[18],[19],[20]
In our series, the mean age of presentation was 45.8 years which is similar to previous studies with a mean age of onset between 41 and 45 years.[1],[5] In our study, the mean age of onset in the males was 41.3 years while the female was aged 64 years which agrees with previous studies that women generally have a later age of onset of CSCR.[17],[18] Perhaps, hypertension, a documented risk factor in addition to the stressful state of poor sleep due to nocturia from the diuretic effect of antihypertensive medications may have contributed to having CSCR in the female. There was a male preponderance in this series with a male to female ratio of 4:1. This also agrees with reports which indicate an incidence about 6 times higher in men with about 10 men and 2 women affected per 100,000 people.[17],[21],[22],[23] These patients are usually younger, working-aged individuals with high visual demands with recurrence in about 30–50% of cases.[24],[25] At initial diagnosis, the rate of bilateral involvement occurs in about 4% but could increase to 40%.[17],[26] In our series, there was bilateral involvement in 40% of the cases.
The predominant presenting complaint in all our patients was a history of reduced or blurred vision while some studies report the presence of a central scotoma as the most common presenting symptom in CSCR, occasionally accompanied by metamorphopsia.[17],[21] At presentation, the best corrected visual acuity usually range from 6/6 to 6/60.[17],[21] Other symptoms which could arise from the neurosensory macular detachment include symptoms of micropsia, hypermetropization, dyschromatopsia, reduced contrast sensitivity, and visual acuity. Addition of convex lenses often corrects the reduction in visual acuity.[17],[18],[21],[22],[24],[25]
Corticosteroids lead to an upregulation of transcription and expression of adrenergic receptor genes. This could result in increased adrenergic stimulation on target tissues causing changes in blood pressure and fluid homeostasis in the body including choroidal circulation.[24] Exogenous steroid use in all forms including oral, intravenous, intranasal, intraarticular, intravitreal, topical, inhalational, and dermatologic preparations has been implicated in the etiology of CSCR.[9],[10],[11],[16],[17],[18],[21],[22],[24],[25] The prolonged use of steroids in the male patient with bilateral disease could have contributed to the occurrence of CSCR. Discontinuation of steroids and recourse to other pharmacologic medications for the management of his arthritic condition probably played a role in its resolution. Many cases of CSCR related to corticosteroid use are reported to be bilateral as also found in our case. Onset of CSCR occurs between 1 and a few months following commencement of steroids, with no lower limit on required dose.[9],[17]
In our series, all patients alluded to underlying stressful events. CSCR is a psychosomatic disorder and a common occurrence in people with poor methods of coping with stressful conditions. Type A personality or behavior pattern (quickness to anger, competitiveness, and need to be in control) is an established predisposing risk factor for CSCR.[2],[17] Increased endogenous steroid production occurs in high levels of stress as found in pregnancy, hypertension and Cushing syndrome.[6],[16] CSCR usually occurs in the third trimester of pregnancy, resolving within thefirst 3 months of delivery.
The mean duration for resolution of symptoms was 16.2 weeks. Initial visual acuity is a prognostic factor in determining final visual acuity. The causes of visual loss in CSCR include foveal attenuation, chronic macular edema and damage of the foveal photoreceptor layer which could occur when the condition is prolonged.[16],[17],[22],[25] Photoreceptor atrophy in the fovea, despite successful retinal reattachment, typically occurs after duration of symptoms of approximately 4 months. Thus, treatment should be instituted after 3 months in the presence of angiographic evidence of on-going foveal leakage in recurrent chronic CSC or in a single CSC episode accompanied by signs of chronic CSC alterations.[16],[17],[22],[25]
Treatment modalities utilized in the management of CSCR include observation with the risk factor reduction and exogenous steroid reduction or cessation which was the strategy adopted for the management of CSCR in our study. It also involves lifestyle modification with stress reduction which is useful in patients with a type A personality and includes limiting work hours, increasing vacation time, exercise and adequate sleep, changing attitudes and perceptions about work-life balance, and sometimes professional counseling in order to reduce endogenous hypercortisolism production which occurs during stress.[16],[17],[22],[24],[25] Photodynamic therapy (PDT) with verteporfin with various modifications such as low fluence, half dose verteporfin to minimize its adverse effects on choriocapillaris perfusion and retinal thickness is safe and effective even in chronic CSCR.[16],[17],[24],[25],[27],[28] PDT acts by decreasing choroidal hyperpermeability and tightening the blood–retinal barrier at the level of the RPE. Its complications are rare and can be performed for subfoveal and juxtafoveal leakage, unlike argon laser.[16],[17],[24],[25],[27],[28]
Argon laser photocoagulation is effective in focal leakage in acute CSCR. It hastens relief of symptoms but does not confer long-term improvement in visual acuity and not suitable for subfoveal leakage.[16],[17],[29] Micropulse diode laser photocoagulation seems to be an effective alternative, avoiding the retinal damage which occurs with the use of focal argon laser photocoagulation. Its results are not superior to PDT and also not suitable for diffuse leakage and diffuse RPE decompensation which occurs in chronic CSR.[16],[17],[30],[31] Glucocorticoid inhibitors are an interesting alternative treatment option such as rifampin, mifepristone, finasteride, ketoconazole and acetylsalicylic acid.[16],[17],[24],[25] The use of other pharmacologic agents with very limited evidence of success includes high dose antioxidants supplementation, intravitreal bevacizumab, and treatment of Helicobacter pylori.[16],[17],[24],[25] Other treatment options include treatment of obstructive sleep apnea and surgical drainage which can be performed in severe cases with exudative detachment.[24],[25],[32],[33]
Conclusion | |  |
Central serous retinopathy has a favorable outcome with appropriate intervention as was the case in our series. A majority of cases have a self-limiting course with spontaneous resolution within a few months, but some may become chronic, lasting 6 months or longer. Perhaps the magnitude among blacks may have been under reported due to previous lack of facilities for investigations which aids its diagnosis such as FFA and OCT but is now becoming increasingly available in the country and other predominantly black communities in developing countries. State of the art facilities and equipment for investigations in retinal conditions should be made readily available in order to improve patient care services.
Source of Support:
Nil
Conflict of Interest:
None declared.
References | |  |
1. | Von Graefe A. Short essays, Notes and Publications of mixed content: VI. About relapsing central luetic retinitis. Albrecht Von Graefes Arch Klin Exp Ophthalmol 1866;12:211-5. |
2. | Yannuzzi LA. Type-A behavior and central serous chorioretinopathy. Retina 1987;7:111-31. |
3. | Maumenee AE. Macular diseases: Clinical manifestations. Trans Am Acad Ophthalmol Otolaryngol 1965;69:605-13. |
4. | Gass JD. Pathogenesis of disciform detachment of the neuroepithelium: II. Idiopathic central serous choroidopathy. Am J Ophthalmol 1967;63:587-615. |
5. | Gass JD. Pathogenesis of disciform detachment of the neuroepithelium: IV. Fluorescein angiographic study of senile disciform macular degeneration. Am J Ophthalmol 1967;63:645-59. |
6. | Bouzas EA, Scott MH, Mastorakos G, Chrousos GP, Kaiser-Kupfer MI. Central serous chorioretinopathy in endogenous hypercortisolism. Arch Ophthalmol 1993;111:1229-33. |
7. | Cotticelli L, Borrelli M, D'Alessio AC, Menzione M, Villani A, Piccolo G, et al. Central serous chorioretinopathy and Helicobacter pylori. Eur J Ophthalmol 2006;16:274-8. |
8. | Giusti C. Association of Helicobacter pylori with central serous chorioretinopathy: Hypotheses regarding pathogenesis. Med Hypotheses 2004;63:524-7. |
9. | Carvalho-Recchia CA, Yannuzzi LA, Negrão S, Spaide RF, Freund KB, Rodriguez-Coleman H, et al. Corticosteroids and central serous chorioretinopathy. Ophthalmology 2002;109:1834-7. |
10. | Jonas JB, Kamppeter BA. Intravitreal triamcinolone acetonide and central serous chorioretinopathy. Br J Ophthalmol 2005;89:386-7. |
11. | Bouzas EA, Karadimas P, Pournaras CJ. Central serous chorioretinopathy and glucocorticoids. Surv Ophthalmol 2002;47:431-48. |
12. | Chumbley LC, Frank RN. Central serous retinopathy and pregnancy. Am J Ophthalmol 1974;77:158-60. |
13. | Eckstein MB, Spalton DJ, Holder G. Visual loss from central serous retinopathy in systemic lupus erythematosus. Br J Ophthalmol 1993;77:607-9. |
14. | Kloos P, Laube I, Thoelen A. Obstructive sleep apnea in patients with central serous chorioretinopathy. Graefes Arch Clin Exp Ophthalmol 2008;246:1225-8. |
15. | Rahbani-Nobar MB, Javadzadeh A, Ghojazadeh L, Rafeey M, Ghorbanihaghjo A. The effect of Helicobacter pylori treatment on remission of idiopathic central serous chorioretinopathy. Mol Vis 2011;17:99-103. |
16. | Gemenetzi M, De Salvo G, Lotery AJ. Central serous chorioretinopathy: An update on pathogenesis and treatment. Eye (Lond) 2010;24:1743-56. |
17. | Liew G, Quin G, Gillies M, Fraser-Bell S. Central serous chorioretinopathy: A review of epidemiology and pathophysiology. Clin Experiment Ophthalmol 2013;41:201-14. |
18. | Spaide RF, Campeas L, Haas A, Yannuzzi LA, Fisher YL, Guyer DR, et al. Central serous chorioretinopathy in younger and older adults. Ophthalmology 1996;103:2070-9. |
19. | How AC, Koh AH. Angiographic characteristics of acute central serous chorioretinopathy in an Asian population. Ann Acad Med Singapore 2006;35:77-9. |
20. | Desai UR, Alhalel AA, Campen TJ, Schiffman RM, Edwards PA, Jacobsen GR. Central serous chorioretinopathy in African Americans. J Natl Med Assoc 2003;95:553-9. |
21. | Wang M, Munch IC, Hasler PW, Prünte C, Larsen M. Central serous chorioretinopathy. Acta Ophthalmol 2008;86:126-45. |
22. | Ross A, Ross AH, Mohamed Q. Review and update of central serous chorioretinopathy. Curr Opin Ophthalmol 2011;22:166-73. |
23. | Kitzmann AS, Pulido JS, Diehl NN, Hodge DO, Burke JP. The incidence of central serous chorioretinopathy in Olmsted County, Minnesota, 1980-2002. Ophthalmology 2008;115:169-73. |
24. | Colucciello M. Update on central serous chorioretinopathy. Retin Physician 2012;9:42-76. |
25. | Fine HF, Ober MD, Hariprasad SM. Current concepts in managing central serous chorioretinopathy. Ophthalmic Surg Lasers Imaging Retina 2014;45:9-13. |
26. | Gäckle HC, Lang GE, Freissler KA, Lang GK. Central serous chorioretinopathy. Clinical, fluorescein angiography and demographic aspects. Ophthalmologe 1998;95:529-33. |
27. | Chan WM, Lai TY, Lai RY, Liu DT, Lam DS. Half-dose verteporfin photodynamic therapy for acute central serous chorioretinopathy: One-year results of a randomized controlled trial. Ophthalmology 2008;115:1756-65. |
28. | Reibaldi M, Cardascia N, Longo A, Furino C, Avitabile T, Faro S, et al. Standard-fluence versus low-fluence photodynamic therapy in chronic central serous chorioretinopathy: A nonrandomized clinical trial. Am J Ophthalmol 2010;149:307-15.e2. |
29. | Ficker L, Vafidis G, While A, Leaver P. Long-term follow-up of a prospective trial of argon laser photocoagulation in the treatment of central serous retinopathy. Br J Ophthalmol 1988;72:829-34. |
30. | Chen SN, Hwang JF, Tseng LF, Lin CJ. Subthreshold diode micropulse photocoagulation for the treatment of chronic central serous chorioretinopathy with juxtafoveal leakage. Ophthalmology 2008;115:2229-34. |
31. | Gupta B, Elagouz M, McHugh D, Chong V, Sivaprasad S. Micropulse diode laser photocoagulation for central serous chorio-retinopathy. Clin Experiment Ophthalmol 2009;37:801-5. |
32. | Kim JT, Eichling PS, Wang M. Central serous chorioretinopathy associated with narcolepsy. Retin Cases Brief Rep 2011;5:302-5. |
33. | John VJ, Mandelcorn ED, Albini TA. Internal drainage for chronic macula-involving serous retinal detachment in idiopathic central serous chorioretinopathy. Int Ophthalmol 2014;34:91-5. |
[Figure 1], [Figure 2]
[Table 1]
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