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    <title>IMC Journal of Medical Science</title>
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                <title><![CDATA[Atypical central serous chorioretinopathy treated with intravitreal injection of bivacizumab – a case report]]></title>

                                    <author><![CDATA[Manash Kumar Goswami]]></author>
                
                <link data-url="https://imcjms.com/public/registration/journal_full_text/74">
    https://imcjms.com/public/registration/journal_full_text/74
</link>
                <pubDate>Tue, 02 Aug 2016 12:14:18 +0000</pubDate>
                <category><![CDATA[Clinical Case Report]]></category>
                <comments><![CDATA[Ibrahim Med. Coll. J. 2015; 9(1): 34-36]]></comments>
                <description>Central serous chorioretinopathy (CSCR) is
common in adult male having sudden dimness of vision in one eye and typical
pattern of leakage in fundus fluorescein angiography. Treatment of typical
central serous chorioretinopathy is conservative and / or focal laser
photocoagulation. But atypical central serous chorioretinopathy is uncommon
having different patterns of clinical presentation and features in fundous
fluorescein angiography. Treatment option of atypical central serous
chorioretinopathy is not yet established. Here, we present a case of atypical
central serous chorioretinopathy successfully treated with intravitreal
injection of anti-vascular endothelial growth factor (anti-VEGF, Bivacizumab).
Ibrahim Med. Coll. J. 2015; 9(1): 34-36
&amp;nbsp;
&amp;nbsp;
Central serous chorioretinopathy is a common
vision lowering disease after age related macular degeneration, diabetic
retinopathy and vascular occlusive disease.1&amp;nbsp;First described
by Vongraefe in 18662&amp;nbsp;and
later OLMSTED study in Minnesota, USA reported that 9.9 per 10000 men and 1.7
per 10000 women were affected by this disease.3&amp;nbsp;Mean age of onset is 41-45
years in case of acute CSCR and for chronic CSCR it is 51yrs.In older
population (age&amp;gt;51 years), CSCR is more likely to have bilateral
involvement.4&amp;nbsp;Risk
factors are type A personality,5&amp;nbsp;Cushing syndrome,6&amp;nbsp;pregnancy,7&amp;nbsp;systemic steroid use8&amp;nbsp;and collagen vascular
diseases.9&amp;nbsp;Psychosomatic factor is also related with
CSCR. In stress, the increased levels of stress hormones and glaucocorticoids
have direct relationship with macular thickness.10&amp;nbsp;Here, we present a case of
atypical central serous chorioretinopathy in a 41 years old male. 
Case presentation
Patient underwent fundus fluorescent
angiography which showed multifocal hyper fluorescence diffusely present in the
macula and perimacular region extending to the temporal retina in both eyes.
The hyper fluorescent increased with time (Fig-1). Optical Coherent Tomography
(OCT) of both maculae showed huge sensory retinal detachment with accumulation
of fluid involving the entire macular region (Fig-2). Blood biochemistry showed
no abnormalities.
Based on the multiple leakage in macula and
perimacular region, elevation of entire macular region with entire sensory
detachment and simultaneous bilateral involvement of both eye, the patient was
diagnosed as a case of acute bilateral atypical CSCR and advised intraviteral
injection of 1.25 mg anti-vascular endothelial growth factor (Bivacizumab). A
total of three doses of Bivacizumab were given over three months period with
non-steroidal anti-inflammatory (NSAID) eye drops twice daily in both eyes. One
injection was given each month in each eye. Vision improved gradually after
each injection of Bivacizumab. One month after the 3rd&amp;nbsp;injection the vision
improved to 6/12 in right eye and 6/9 in left eye. OCT after the third
injection showed normal macular contour (Fig-3). The patient had 6/6 vision in
both eye and normal retinal integrity both clinically and by OCT one year after
the last injection.

&amp;nbsp;
Fig.2: Optical Cohherent Tomography (OCT) of
Maculae shows areas of sensory retinal at maculae of both eyes.
&amp;nbsp; 
Fig.3: OCT of both eyes after treatment with
injection of bivaczumab show normal macular contour
Discussion
In our case, the clinical presentation was
sudden, bilateral with profuse deterioration of vision within a very short
period of time. This is unusual because the usual presentation of typical CSCR
is unilateral with moderate deterioration of vision with a central scotoma.1&amp;nbsp;In our case, diminution of
vision was profound, which was reduced to counting finger close to the eyes.
The findings of multifocal leakage and diffuse appearance in FFA were also
contrary to single smoke steak appearance seen in typical CSCR. In this aspect
the presentation of our case was atypical. Several treatment options have been
described for acute CSCR with variable success. The treatment of CSCR includes
focal argon laser,13&amp;nbsp;photodynamic therapy with verteporfin,14&amp;nbsp;micropulse diod laser15&amp;nbsp;and Anti-VEGF
injection in the intravitreal space.16
In our case the leakages in the FFA are
multifocal and did not have typical smoke stack appearance. Focal laser
photocoagulation could not be done. So intravitreal Bivacizumab was
administered. The visual improvement after multiple intravitreal injection of
Bivacizumab supported the earlier reports of its success in the treatment of
acute CSCR. Acute atypical CSCR with multifocal leakage in the FFA and huge
sensory retinal detachment, involving the whole macula responds well with
intravitreal injection of Bivacizubab in repeated doses. Acute bilateral
extensive CSCR with multifocal leakage and grossly reduced vision can be
treated successfully with intravitreal injection of anti-VEGF instead of laser.
References
2.&amp;nbsp;&amp;nbsp;&amp;nbsp; Yannuzzi LA. Type A behavior and central
serous chorioretinopathy. Retina 1987; 7: 111-31.
4.&amp;nbsp;&amp;nbsp;&amp;nbsp; Spaide RF, Campeas L, Haas A et al. Central
serous chorioretinopathy in younger and older adults. Ophthalmology
1996; 103: 2070-9.
6.&amp;nbsp;&amp;nbsp;&amp;nbsp; Bauzas EA, Scott MH, Mastorako SG, Chrousos
GP, Kaiser Kupfer MI. Central serous corioretinopathy in endogenous hypercortisolism.
Arch Opthalmol 1993; 111: 1229-33.
8.&amp;nbsp;&amp;nbsp;&amp;nbsp; Haimovici R, Koh S, Gagnon DR, Lehrfeld T,
Wellik S. Risk factor for central serous Chorioretinopathy: a case control
study. Opthalmology 2004; 111: 244-9.
10.&amp;nbsp; Garg SP, Dada T, Talwar D, Biswas NR.
Endogenous cortisol profile in patients with central serous chorioretinopathy. Br
J Ophthalmol 1997; 81: 962-4.
12.&amp;nbsp; Yannuzzi LA, Shakin JL, Fisher YL, Altomonte
MA. Peripheral retinal detachment and retinal pigment epithelium atrophic
tracts secondary to central serous pigment epitheliopathy. Ophthalmology
1984; 91: 1554-72.
14.&amp;nbsp; Taban M, Boyer SD, Thomas EL, Taban M, Chronic
central serous chorioretinopalty: Photodynamic therapy. Am J Ophthalmol
2004; 137: 1073-80.
16.&amp;nbsp; Lim JW, Ryu SJ, Shin MC. The effect of
intravitreal bivacizumab in patients with acute central serous
chorioretinopathy. Korean J Ophthalmol 2010; 24: 155-8.
18.&amp;nbsp; Aydin E. The efficacy of intravitreal
bivacizumab for acute central serous Chorioretinopathy. Journal of Ocular
Pharmacology and Therapeutites 2013; 29(01): 10-13.
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