oc000164
10.3205/oc000164
urn:nbn:de:0183-oc0001644
Case Report
Acute bilateral serous retinal detachments with spontaneous resolution in a 6-year-old boy
Van Camp
Van Camp
Sophie
S
Department of Ophthalmology, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium, Phone: +32 216332372, Fax: +32 16332367Department of Ophthalmology, University Hospitals Leuven, Belgium
sophie.vancamp@uzleuven.be
author
Vande Walle
Vande Walle
Steffi
S
Department of Ophthalmology, University Hospitals Leuven, Belgium
steffi.vandewalle@uzleuven.be
author
Casteels
Casteels
Ingele
I
Department of Ophthalmology, University Hospitals Leuven, Belgium
ingele.casteels@uzleuven.be
author
Jacob
Jacob
Julie
J
Department of Ophthalmology, University Hospitals Leuven, Belgium
julie.jacob@uzleuven.be
author
Cassiman
Cassiman
Cathérine
C
Department of Ophthalmology, University Hospitals Leuven, Belgium
catherine.cassiman@uzleuven.be
author
Wouters
Wouters
Carine
C
Department of Pediatrics, University Hospitals Leuven, Belgium
carine.wouters@uzleuven.be
author
Schauwvlieghe
Schauwvlieghe
Pieter-Paul
PP
Department of Ophthalmology, University Hospitals Leuven, Belgium
pieter-paul.schauwvlieghe@uzleuven.be
author
German Medical Science GMS Publishing House
Düsseldorf
610
serous retinal detachment
young child
acute exudative polymorphous vitelliform maculopathy
20200825
engl
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).
2193-1496
10
GMS Ophthalmology Cases
GMS Ophthalmol Cases
37
A healthy 6-year-old boy presented with acute bilateral vision loss, multiple serous retinal detachments between the vascular arcades and a thickened choroid. Spontaneous resolution occurred over several weeks.We hypothesize that the clinical constellation in our patient is suggestive of acute exudative polymorphous vitelliform maculopathy (AEPVM) or might be an atypical presentation of Vogt-Koyanagi-Harada (VKH) disease. We propose that it was caused by an autoimmune-mediated activation of inflammatory cells at the level of the choroid, induced by an unknown trigger.
IntroductionAcute exudative polymorphous vitelliform maculopathy (AEPVM) is a rare disorder, first described by Gass et al. in 1988 . Patients usually present with bilateral blurred vision, often associated with headache. The typical fundoscopic findings consist of serous retinal detachments in both eyes, accompanied by scattered yellowish subretinal lesions in a honeycomb-like pattern. These lesions contain lipofuscin, which can be demonstrated on autofluorescence imaging. The clinical features can resolve spontaneously over the course of several months. Thus far no treatment has been found effective, nor has a single etiological hypothesis been proven.
Case descriptionAn otherwise healthy 6-year-old boy with no relevant medical history was referred to our department because of acute onset of bilateral blurry vision, metamorphopsia and scattered scotomas. He has a mother of Turkish descent and a Belgian father. The family history was negative for ophthalmological problems. There was no history of travelling to exotic regions. The patient had suffered from a cold a few weeks before the onset of symptoms.We measured a best corrected visual acuity of Snelle<![CDATA[n 0</PlainText></TextGroup>.6 in the right eye and Snellen 0.16 in the left eye. Slitlamp biomicroscopy of the anterior segment showed no abnormalities and a normal intraocular pressure. Multiple large serofibrinous detachments with hyperreflective dots below the neurosensory retina were seen bilaterally on fundoscopic examination and optical coherence tomography (OCT) of the retina. These lesions were found to be hyperautofluorescent. A thickened choroid – estimated at 100<TextGroup><PlainText>0 µ</PlainText></TextGroup>m – was detected on enhanced depth imaging optical coherence tomography (EDI-OCT) (Figure 1 <ImgLink imgNo="1" imgType="figure"/>). Infrared imaging showed serous detachments with a center of slightly increased intensity surrounded by decreased intensity (Figure 1 <ImgLink imgNo="1" imgType="figure"/>). Fluorescein angiography (FA) revealed small leakage points at the level of the serous detachments, limited staining of the optic disc in the left eye (without staining in the right eye) and masking effect due to neurosensory detachments (Figure 2 <ImgLink imgNo="2" imgType="figure"/>).</Pgraph><Pgraph>The patient was referred to our department of pediatri<TextGroup><PlainText>cs, w</PlainText></TextGroup>here a total clinical work-up did not show any evidence of systemic inflammation, infection or malignant diseases.</Pgraph><Pgraph>Serology for borreliosis, syphilis, toxoplasmosis, human immunodeficiency virus, herpes simplex, rubella, cytom<TextGroup><PlainText>egaloviru</PlainText></TextGroup>s and Epstein-Barr virus was negative, in the absence of leukocytosis. A chest X-ray and magnetic resonance imaging (MRI) of the brain showed no abnormalities except for a thickened choroid in both eyes.</Pgraph><Pgraph>One week after initial presentation, spontaneous improvement of vision occurred with regression of the lesions on OCT. Minimal inflammation in the anterior chamber (without keratitic precipitates) and vitreous was seen and topical steroids were administered six times per day.</Pgraph><Pgraph>Over the next two weeks, the serous retinal detachments resolved completely in the left eye and decreased markedly in the right eye, with distinct deposition of some yellowish, slightly hyperautofluorescent vitelliform material in the subretinal space (Figure 3 <ImgLink imgNo="3" imgType="figure"/>). Further improvement of visual acuity to Snellen 0.6 in both eyes (OU) occurred. Since intraocular inflammation was no longer present, topical steroids were tapered.</Pgraph><Pgraph>Three months after initial presentation, complete resolution of retinal lesions was noted with recovery of vision to Snellen 0.9 OU (Figure 4 <ImgLink imgNo="4" imgType="figure"/>).</Pgraph></TextBlock>
<TextBlock linked="yes" name="Discussion: differential diagnosis">
<MainHeadline>Discussion: differential diagnosis</MainHeadline><SubHeadline>Acute exudative polymorphous vitelliform maculopathy (AEPVM)</SubHeadline><Pgraph>AEPVM is a rare disorder, with symptoms of (sub)acute bilateral vision loss, frequently – but not always – preceded by headache <TextLink reference="1"></TextLink>, <TextLink reference="2"></TextLink>, <TextLink reference="3"></TextLink>. Usually there are no or very few signs of intraocular inflammation. The fundoscopic findings are remarkable with bilateral multifocal central serous retinal detachments and round to oval white-y<TextGroup><PlainText>ello</PlainText></TextGroup>wish lesions in a peculiar honeycomb-like pattern at the level of the retinal pigment epithelium, between and around the vascular arcades. These lesions do not occur in every patient, and they usually present after several months <TextLink reference="2"></TextLink>. Fluorescein angiography shows early hyperfluorescence of the multifocal yellow lesions and staining in the late phase. Leakage of dye is minimal to absent. On autofluorescence imaging, lesions are hyperautofluorescent, suggesting the presence of lipofuscin <TextLink reference="4"></TextLink>. Indocyanine green (ICG) angiography shows an affinity of the dye for these yellow lesions, exhibiting involvement of the choriocapillaris. One case reported choroidal thickening measured by EDI-OCT, with striking elevation in the acute phase <TextLink reference="2"></TextLink>, as seen in our patient. The serous retinal detachments typically resolve spontaneously over the course of weeks to months. This tends to occur faster if few or no yellow lesions are visible. These vitelliform lesions can gravitate and form a pseudo-hypopyon of yellow material at the level of the inferior macula, blocking fluorescence on FA. They can persist for years despite complete resolution of symptoms. This is the most typical presentation, although AEPVM can present with a more variable clinical course than initially described. We believe the lesions in our patient are very similar to the subtype ‘bleb-like lesions along vascular arcades’ of AEPVM <TextLink reference="2"></TextLink>.</Pgraph><Pgraph>The etiology of AEPVM remains unclear. Dysfunction of the retinal pigment epithelium (RPE) with decreased phagocytosis of secreted photoreceptor outer segments has been suggested, leading to secondary serous retinal detachment. This can cause precipitation and formation of yellow lesions, consisting of lipofuscin. OCT images have shown thickened outer segments, compatible with this hypothesis. The favorable response to corticosteroid therapy in some patients suggests an inflammatory base for this dysfunction <TextLink reference="1"></TextLink>.</Pgraph><Pgraph>A few cases have been reported following a viral <TextLink reference="5"></TextLink> or bacterial infection <TextLink reference="6"></TextLink>, <TextLink reference="7"></TextLink>, <TextLink reference="8"></TextLink>. These cases were thought to be based on an autoimmune-mediated activation o<TextGroup><PlainText>f i</PlainText></TextGroup>nflammatory cells (presumably T lymphocytes as in Vogt-Koyanagi-Harada disease) at the level of the choroi<TextGroup><PlainText>d, l</PlainText></TextGroup>eading to profound choroidal swelling. This could cause saturation of the choroid with subretinal accumulation of fluid rich in lipofuscin and exudative retinal detachment. A subsequent decrease in choroidal swellin<TextGroup><PlainText>g – eithe</PlainText></TextGroup>r spontaneously or by treatment with corticosteroids – can restore fluid absorption in the choroid with resolution of the retinal detachments. An incomplete clearance of lipofuscin causes yellow subretinal deposits. In our patient, a cold preceded the onset of symptoms, but we could not identify a specific causative micro-organism.</Pgraph><Pgraph>AEPVM has also been reported as a paraneoplastic retinopathy (e.g. metastatic melanoma, small cell lung carcinoma), where antibodies against an extraocular tumor supposedly cross-react with retinal or RPE antigens. Therefore, referral for systemic evaluation is always indicated <TextLink reference="9"></TextLink>, <TextLink reference="10"></TextLink>.</Pgraph><Pgraph>Treatment of AEPVM is controversial. In the first described cases of Gass et al., there was improvement after systemic prednisolone <TextLink reference="1"></TextLink>. However, literature shows little evidence for the efficacy of corticosteroids; resolution of the lesions has been documented in many patients without any form of treatment.</Pgraph><Pgraph>One patient with AEPVM was treated in one eye with an intravitreal implant for sustained corticosteroid release <TextLink reference="11"></TextLink>. There was no difference in the clinical course between both eyes, suggesting corticosteroids affect neither resolution of the lesions nor visual outcome. In another patient, intravenous corticosteroids led to a quick recovery of visual acuity, but the added value of corticosteroids on final visual acuity remains uncertain <TextLink reference="12"></TextLink>.</Pgraph><SubHeadline>Vogt-Koyanagi-Harada (VKH) disease</SubHeadline><Pgraph>An atypical presentation of VKH disease was considered in our case, due to the bilateral presentation of serous retinal detachments in a child of Turkish descent. However, the typical vitelliform lesions in AEPVM do not occur in VKH disease and FA usually shows bilateral hot discs, which in our case was only present in the left eye (due t<TextGroup><PlainText>o s</PlainText></TextGroup>ubretinal fluid – originating from the retinal detachments – in the peripapillary region, which led to staining of the optic disc). Since systemic features (auditory disturbances, skin changes or neurological symptoms) and panuveitis were absent, the diagnostic criteria were not met. Additionally, spontaneous recovery without aggressive treatment (i.e. systemic corticosteroids or other immunosuppressive agents) is not described in VKH disease <TextLink reference="13"></TextLink>, <TextLink reference="14"></TextLink>. However, it must be mentioned that – although rare – VKH disease can be seen in children. There are only few case series describing VKH disease in children, in which a more aggressive course of disease and more frequent sight-threatening complications (e.g. cataract, glaucoma, retinal pigment epithelium atrophy) are noted <TextLink reference="15"></TextLink>, <TextLink reference="16"></TextLink>. Thus, it is incorrect to assume that the disease has the same characteristics as in adult patients. Human leucocyte antigen (HLA) typing could help determine whether there is a genetic predisposition for VKH disease, but it cannot confirm the diagnosis. Therefore it was not tested in our case.</Pgraph></TextBlock>
<TextBlock linked="yes" name="Conclusion">
<MainHeadline>Conclusion</MainHeadline><Pgraph>A 6-year-old boy showed characteristics suggestive of the subtype ‘bleb-like lesions along the vascular arcades’ of AEPVM, but other features – such as a thickened choroid in the acute phase – resembled VKH disease, though as an atypical manifestation. To our knowledge, he is the youngest patient reported with the tentative diagnosis of AEPVM.</Pgraph><Pgraph>We hypothesize that the clinical picture was caused by a transient activation of inflammatory cells at the level of the choroid, resulting in choroidal swelling and subsequent accumulation of lipofuscin-rich fluid in the subretinal space. Spontaneous recovery of choroidal and RPE function occurred. Though asymptomatically, deposition of lipofuscin in the subretinal space, clinically appearing as yellow deposits, remained detectable for a limited period of time.</Pgraph><Pgraph>The underlying pathophysiological mechanism remains unclear. Infectious and paraneoplastic hypotheses have been suggested; we could not confirm any causative m<TextGroup><PlainText>icr</PlainText></TextGroup>o-organism in this case, nor withhold any arguments for RPE dysfunction or involvement of the choriocapillaris.</Pgraph></TextBlock>
<TextBlock linked="yes" name="Notes">
<MainHeadline>Notes</MainHeadline><SubHeadline>Informed consent</SubHeadline><Pgraph>The parents of the patient gave consent to publish this case report.</Pgraph><SubHeadline>Competing interests</SubHeadline><Pgraph>The authors declare that they have no competing interests.</Pgraph></TextBlock>
<References linked="yes">
<Reference refNo="1">
<RefAuthor>Gass JDM</RefAuthor>
<RefAuthor>Chuang EL</RefAuthor>
<RefAuthor>Granek H</RefAuthor>
<RefTitle>Acute exudative polymorphous vitelliform maculopathy</RefTitle>
<RefYear>1988</RefYear>
<RefJournal>Trans Am Ophthalmol Soc</RefJournal>
<RefPage>354-66</RefPage>
<RefTotal>Gass JDM, Chuang EL, Granek H. Acute exudative polymorphous vitelliform maculopathy. Trans Am Ophthalmol Soc. 1988;86:354-66.</RefTotal>
</Reference>
<Reference refNo="2">
<RefAuthor>Barbazetto I</RefAuthor>
<RefAuthor>Dansingani KK</RefAuthor>
<RefAuthor>Dolz-Marco R</RefAuthor>
<RefAuthor>Giovannini A</RefAuthor>
<RefAuthor>Piccolino FC</RefAuthor>
<RefAuthor>Agarwal A</RefAuthor>
<RefAuthor>Lima LH</RefAuthor>
<RefAuthor>Vianna RN</RefAuthor>
<RefAuthor>Yannuzzi LA</RefAuthor>
<RefTitle>Idiopathic Acute Exudative Polymorphous Vitelliform Maculopathy: Clinical Spectrum and Multimodal Imaging Characteristics</RefTitle>
<RefYear>2018</RefYear>
<RefJournal>Ophthalmology</RefJournal>
<RefPage>75-88</RefPage>
<RefTotal>Barbazetto I, Dansingani KK, Dolz-Marco R, Giovannini A, Piccolino FC, Agarwal A, Lima LH, Vianna RN, Yannuzzi LA. Idiopathic Acute Exudative Polymorphous Vitelliform Maculopathy: Clinical Spectrum and Multimodal Imaging Characteristics. Ophthalmology. 2018 Jan;125(1):75-88. DOI: 10.1016/j.ophtha.2017.07.020</RefTotal>
<RefLink>https://doi.org/10.1016/j.ophtha.2017.07.020</RefLink>
</Reference>
<Reference refNo="3">
<RefAuthor>Murtagh P</RefAuthor>
<RefAuthor>Treacy M</RefAuthor>
<RefAuthor>Stephenson K</RefAuthor>
<RefAuthor>Dooley I</RefAuthor>
<RefTitle>Acute Exudative Polymorphous Vitelliform Maculopathy Syndrome; natural history and evolution of fundal and OCT images over time</RefTitle>
<RefYear>2018</RefYear>
<RefJournal>BMJ Case Rep</RefJournal>
<RefArticleNo>bcr2018224241</RefArticleNo>
<RefTotal>Murtagh P, Treacy M, Stephenson K, Dooley I. Acute Exudative Polymorphous Vitelliform Maculopathy Syndrome; natural history and evolution of fundal and OCT images over time. BMJ Case Rep. 2018 Mar;2018. pii: bcr2018224241. DOI: 10.1136/bcr-2018-224241</RefTotal>
<RefLink>https://doi.org/10.1136/bcr-2018-224241</RefLink>
</Reference>
<Reference refNo="4">
<RefAuthor>Vaclavik V</RefAuthor>
<RefAuthor>Ooi KG</RefAuthor>
<RefAuthor>Bird AC</RefAuthor>
<RefAuthor>Robson AG</RefAuthor>
<RefAuthor>Holder GE</RefAuthor>
<RefAuthor>Webster AR</RefAuthor>
<RefTitle>Autofluorescence findings in acute exudative polymorphous vitelliform maculopathy</RefTitle>
<RefYear>2007</RefYear>
<RefJournal>Arch Ophthalmol</RefJournal>
<RefPage>274-7</RefPage>
<RefTotal>Vaclavik V, Ooi KG, Bird AC, Robson AG, Holder GE, Webster AR. Autofluorescence findings in acute exudative polymorphous vitelliform maculopathy. Arch Ophthalmol. 2007 Feb;125(2):274-7. DOI: 10.1001/archopht.125.2.274</RefTotal>
<RefLink>https://doi.org/10.1001/archopht.125.2.274</RefLink>
</Reference>
<Reference refNo="5">
<RefAuthor>Zhang W</RefAuthor>
<RefAuthor>Sharma S</RefAuthor>
<RefAuthor>Reichstein D</RefAuthor>
<RefTitle>Possible Herpetic Viral Association in Cases of Acute Exudative Polymorphous Vitelliform Maculopathy</RefTitle>
<RefYear>2018</RefYear>
<RefJournal>J Vitreoretin Dis</RefJournal>
<RefPage>31-5</RefPage>
<RefTotal>Zhang W, Sharma S, Reichstein D. Possible Herpetic Viral Association in Cases of Acute Exudative Polymorphous Vitelliform Maculopathy. J Vitreoretin Dis. 2018 Nov 28;3(1):31-5. DOI: 10.1177/2474126418806830</RefTotal>
<RefLink>https://doi.org/10.1177/2474126418806830</RefLink>
</Reference>
<Reference refNo="6">
<RefAuthor>Singh RS</RefAuthor>
<RefAuthor>Tran LH</RefAuthor>
<RefAuthor>Kim JE</RefAuthor>
<RefTitle>Acute exudative polymorphous vitelliform maculopathy in a patient with Lyme disease</RefTitle>
<RefYear>2013</RefYear>
<RefJournal>Ophthalmic Surg Lasers Imaging Retina</RefJournal>
<RefPage>493-6</RefPage>
<RefTotal>Singh RS, Tran LH, Kim JE. Acute exudative polymorphous vitelliform maculopathy in a patient with Lyme disease. Ophthalmic Surg Lasers Imaging Retina. 2013 Sep-Oct;44(5):493-6. DOI: 10.3928/23258160-20130909-14</RefTotal>
<RefLink>https://doi.org/10.3928/23258160-20130909-14</RefLink>
</Reference>
<Reference refNo="7">
<RefAuthor>Wolff B</RefAuthor>
<RefAuthor>Mrejen S</RefAuthor>
<RefAuthor>Freund KB</RefAuthor>
<RefTitle>A case of neurosyphilis revealed by acute exudative polymorphous vitelliform maculopathy</RefTitle>
<RefYear>2014</RefYear>
<RefJournal>Ophthalmic Surg Lasers Imaging Retina</RefJournal>
<RefPage>e29-e31</RefPage>
<RefTotal>Wolff B, Mrejen S, Freund KB. A case of neurosyphilis revealed by acute exudative polymorphous vitelliform maculopathy. Ophthalmic Surg Lasers Imaging Retina. 2014 Apr 4;45:e29-e31. DOI: 10.3928/23258160-20140331-06</RefTotal>
<RefLink>https://doi.org/10.3928/23258160-20140331-06</RefLink>
</Reference>
<Reference refNo="8">
<RefAuthor>Massaro D</RefAuthor>
<RefAuthor>Pece A</RefAuthor>
<RefAuthor>Pichi F</RefAuthor>
<RefAuthor>Yannuzzi LA</RefAuthor>
<RefAuthor>Gilardoni F</RefAuthor>
<RefAuthor>Carrai P</RefAuthor>
<RefAuthor>Bonsignore F</RefAuthor>
<RefAuthor>Nucci P</RefAuthor>
<RefTitle>A case of acute exudative polymorphous vitelliform maculopathy: follow-up and wide-field spectral-domain optical coherence tomography</RefTitle>
<RefYear>2015</RefYear>
<RefJournal>Eur J Ophthalmol</RefJournal>
<RefPage>e91-e94</RefPage>
<RefTotal>Massaro D, Pece A, Pichi F, Yannuzzi LA, Gilardoni F, Carrai P, Bonsignore F, Nucci P. A case of acute exudative polymorphous vitelliform maculopathy: follow-up and wide-field spectral-domain optical coherence tomography. Eur J Ophthalmol. 2015 Jul 30;25(5):e91-e94. DOI: 10.5301/ejo.5000616</RefTotal>
<RefLink>https://doi.org/10.5301/ejo.5000616</RefLink>
</Reference>
<Reference refNo="9">
<RefAuthor>Li DQ</RefAuthor>
<RefAuthor>Golding J</RefAuthor>
<RefAuthor>Glittenberg C</RefAuthor>
<RefAuthor>Choudhry N</RefAuthor>
<RefTitle>Multimodal Imaging Features in Acute Exudative Paraneoplastic Polymorphous Vitelliform Maculopathy</RefTitle>
<RefYear>2016</RefYear>
<RefJournal>Ophthalmic Surg Lasers Imaging Retina</RefJournal>
<RefPage>1143-6</RefPage>
<RefTotal>Li DQ, Golding J, Glittenberg C, Choudhry N. Multimodal Imaging Features in Acute Exudative Paraneoplastic Polymorphous Vitelliform Maculopathy. Ophthalmic Surg Lasers Imaging Retina. 2016 Dec 1;47(12):1143-6. DOI: 10.3928/23258160-20161130-09</RefTotal>
<RefLink>https://doi.org/10.3928/23258160-20161130-09</RefLink>
</Reference>
<Reference refNo="10">
<RefAuthor>Koreen L</RefAuthor>
<RefAuthor>He SX</RefAuthor>
<RefAuthor>Johnson MW</RefAuthor>
<RefAuthor>Hackel RE</RefAuthor>
<RefAuthor>Khan NW</RefAuthor>
<RefAuthor>Heckenlively JR</RefAuthor>
<RefTitle>Anti-retinal pigment epithelium antibodies in acute exudative polymorphous vitelliform maculopathy: a new hypothesis about disease pathogenesis</RefTitle>
<RefYear>2011</RefYear>
<RefJournal>Arch Ophthalmol</RefJournal>
<RefPage>23-9</RefPage>
<RefTotal>Koreen L, He SX, Johnson MW, Hackel RE, Khan NW, Heckenlively JR. Anti-retinal pigment epithelium antibodies in acute exudative polymorphous vitelliform maculopathy: a new hypothesis about disease pathogenesis. Arch Ophthalmol. 2011 Jan;129(1):23-9. DOI: 10.1001/archophthalmol.2010.316</RefTotal>
<RefLink>https://doi.org/10.1001/archophthalmol.2010.316</RefLink>
</Reference>
<Reference refNo="11">
<RefAuthor>Scupola A</RefAuthor>
<RefAuthor>Abed E</RefAuthor>
<RefAuthor>Sammarco MG</RefAuthor>
<RefAuthor>Traina S</RefAuthor>
<RefAuthor>Villano A</RefAuthor>
<RefAuthor>Grimaldi G</RefAuthor>
<RefAuthor>Blasi MA</RefAuthor>
<RefTitle>Intravitreal dexamethasone implant for acute exudative polymorphous vitelliform maculopathy</RefTitle>
<RefYear>2014</RefYear>
<RefJournal>Eur J Ophthalmol</RefJournal>
<RefPage>803-7</RefPage>
<RefTotal>Scupola A, Abed E, Sammarco MG, Traina S, Villano A, Grimaldi G, Blasi MA. Intravitreal dexamethasone implant for acute exudative polymorphous vitelliform maculopathy. Eur J Ophthalmol. 2014 Sep-Oct;24(5):803-7. DOI: 10.5301/ejo.5000477</RefTotal>
<RefLink>https://doi.org/10.5301/ejo.5000477</RefLink>
</Reference>
<Reference refNo="12">
<RefAuthor>Grenga PL</RefAuthor>
<RefAuthor>Fragiotta S</RefAuthor>
<RefAuthor>Cutini A</RefAuthor>
<RefAuthor>Vingolo EM</RefAuthor>
<RefTitle>Acute exudative polymorphous vitelliform maculopathy: To bolus or not to bolus?</RefTitle>
<RefYear>2018</RefYear>
<RefJournal>Oman J Ophthalmol</RefJournal>
<RefPage>280-3</RefPage>
<RefTotal>Grenga PL, Fragiotta S, Cutini A, Vingolo EM. Acute exudative polymorphous vitelliform maculopathy: To bolus or not to bolus? Oman J Ophthalmol. 2018 Sep-Dec;11(3):280-3. DOI: 10.4103/ojo.OJO_12_2017</RefTotal>
<RefLink>https://doi.org/10.4103/ojo.OJO_12_2017</RefLink>
</Reference>
<Reference refNo="13">
<RefAuthor>Chan CK</RefAuthor>
<RefAuthor>Gass JD</RefAuthor>
<RefAuthor>Lin SG</RefAuthor>
<RefTitle>Acute exudative polymorphous vitelliform maculopathy syndrome</RefTitle>
<RefYear>2003</RefYear>
<RefJournal>Retina</RefJournal>
<RefPage>453-62</RefPage>
<RefTotal>Chan CK, Gass JD, Lin SG. Acute exudative polymorphous vitelliform maculopathy syndrome. Retina. 2003 Aug;23(4):453-62. DOI: 10.1097/00006982-200308000-00002</RefTotal>
<RefLink>https://doi.org/10.1097/00006982-200308000-00002</RefLink>
</Reference>
<Reference refNo="14">
<RefAuthor>O’Keefe GA</RefAuthor>
<RefAuthor>Rao NA</RefAuthor>
<RefTitle>Vogt-Koyanagi-Harada disease</RefTitle>
<RefYear>2017</RefYear>
<RefJournal>Surv Ophthalmol</RefJournal>
<RefPage>1-25</RefPage>
<RefTotal>O’Keefe GA, Rao NA. Vogt-Koyanagi-Harada disease. Surv Ophthalmol. 2017 Jan-Feb;62(1):1-25. DOI: 10.1016/j.survophthal.2016.05.002</RefTotal>
<RefLink>https://doi.org/10.1016/j.survophthal.2016.05.002</RefLink>
</Reference>
<Reference refNo="15">
<RefAuthor>Tabbara KF</RefAuthor>
<RefAuthor>Chavis PS</RefAuthor>
<RefAuthor>Freeman WR</RefAuthor>
<RefTitle>Vogt-Koyanagi-Harada syndrome in children compared to adults</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Acta Ophthalmol Scand</RefJournal>
<RefPage>723-6</RefPage>
<RefTotal>Tabbara KF, Chavis PS, Freeman WR. Vogt-Koyanagi-Harada syndrome in children compared to adults. Acta Ophthalmol Scand. 1998 Dec;76(6):723-6. DOI: 10.1034/j.1600-0420.1998.760619.x</RefTotal>
<RefLink>https://doi.org/10.1034/j.1600-0420.1998.760619.x</RefLink>
</Reference>
<Reference refNo="16">
<RefAuthor>Rathinam SR</RefAuthor>
<RefAuthor>Vijayalakshmi P</RefAuthor>
<RefAuthor>Namperumalsamy P</RefAuthor>
<RefAuthor>Nozik RA</RefAuthor>
<RefAuthor>Cunningham ET Jr</RefAuthor>
<RefTitle>Vogt-Koyanagi-Harada syndrome in children</RefTitle>
<RefYear>1998</RefYear>
<RefJournal>Ocul Immunol Inflamm</RefJournal>
<RefPage>155-61</RefPage>
<RefTotal>Rathinam SR, Vijayalakshmi P, Namperumalsamy P, Nozik RA, Cunningham ET Jr. Vogt-Koyanagi-Harada syndrome in children. Ocul Immunol Inflamm. 1998 Sep;6(3):155-61. DOI: 10.1076/ocii.6.3.155.4041</RefTotal>
<RefLink>https://doi.org/10.1076/ocii.6.3.155.4041</RefLink>
</Reference>
</References>
<Media>
<Tables>
<NoOfTables>0</NoOfTables>
</Tables>
<Figures>
<Figure format="png" height="525" width="669">
<MediaNo>1</MediaNo>
<MediaID>1</MediaID>
<Caption><Pgraph><Mark1>Figure 1: OCT and infrared images show multiple serofibrinous retinal detachments in the right (A, C) and left (B, D) eye and a thickened choroid measured with EDI-OCT (A). </Mark1></Pgraph></Caption>
</Figure>
<Figure format="png" height="316" width="675">
<MediaNo>2</MediaNo>
<MediaID>2</MediaID>
<Caption><Pgraph><Mark1>Figure 2: Late-phase fluorescein angiography shows tiny leakage points with limited leakage in the subretinal space (A, B) and discrete staining of the left optic disc (B). </Mark1></Pgraph></Caption>
</Figure>
<Figure format="png" height="519" width="603">
<MediaNo>3</MediaNo>
<MediaID>3</MediaID>
<Caption><Pgraph><Mark1>Figure 3: Fundoscopic images three weeks after initial presentation show multiple yellow deposits scattered around the vascular arcades (A and B, see arrows), with corresponding mild hyperautofluorescence (C, D). </Mark1></Pgraph></Caption>
</Figure>
<Figure format="png" height="724" width="606">
<MediaNo>4</MediaNo>
<MediaID>4</MediaID>
<Caption><Pgraph><Mark1>Figure 4: Three months after initial presentation, there was total resolution of the exudative retinal detachments in the right (A) and left (B) eye with normalization of choroidal thickness and an almost complete resorption of the vitelliform lesions (C, D). Autofluorescence was normal (E, F). </Mark1></Pgraph></Caption>
</Figure>
<NoOfPictures>4</NoOfPictures>
</Figures>
<InlineFigures>
<NoOfPictures>0</NoOfPictures>
</InlineFigures>
<Attachments>
<NoOfAttachments>0</NoOfAttachments>
</Attachments>
</Media>
</OrigData>
</GmsArticle>]]></plaintext></textgroup></pgraph></textblock></origdata></gmsarticle>