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CASE REPORT |
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Year : 2023 | Volume
: 5
| Issue : 1 | Page : 15 |
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A misleading case of sudden vision loss: Inflammatory chorioretinopathy superimposed on a diabetic retinopathy
Renato Correia Barbosa, Tiago Maio, Rita Gonçalves
Department of Ophthalmology, Pedro Hispano Hospital, Local Health Unit, Porto, Portugal
Date of Submission | 08-Mar-2023 |
Date of Decision | 20-Mar-2023 |
Date of Acceptance | 01-Apr-2023 |
Date of Web Publication | 11-May-2023 |
Correspondence Address: Renato Correia Barbosa Pedro Hispano Hospital, Local Health Unit, Porto Portugal
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/pajo.pajo_14_23
White dot syndromes are a group of inflammatory chorioretinopathies that share pathologic features involving lesions in the external retinal layers and choroid. This report describes a case of acute visual loss due to a white dot syndrome superimposed on severe diabetic retinopathy (DR), leading to a challenging diagnosis. A 53-year-old man with severe DR was referred with acute unilateral vision loss, with the presumptive diagnosis of diabetic macular edema. The clinical examination and complementary diagnostic tests revealed the absence of diabetic macular edema but showed disruption of the outer retinal layers and choroidal thickening. Laboratory and imaging testing excluded other etiological factors, so an inflammatory chorioretinopathy superimposed on severe DR was considered. Following the initial presentation, without any therapeutic intervention, rapid anatomical and functional improvement was objectified. This case demonstrated that in rare cases, an inflammatory chorioretinopathy may go unnoticed in the presence of preexisting retinopathy, and the true cause of vision loss may initially be misdiagnosed.
Keywords: Chorioretinopathy, diabetic retinopathy, white dot syndrome
How to cite this article: Barbosa RC, Maio T, Gonçalves R. A misleading case of sudden vision loss: Inflammatory chorioretinopathy superimposed on a diabetic retinopathy. Pan Am J Ophthalmol 2023;5:15 |
How to cite this URL: Barbosa RC, Maio T, Gonçalves R. A misleading case of sudden vision loss: Inflammatory chorioretinopathy superimposed on a diabetic retinopathy. Pan Am J Ophthalmol [serial online] 2023 [cited 2023 Jun 3];5:15. Available from: https://www.thepajo.org/text.asp?2023/5/1/15/376674 |
Introduction | |  |
White dot syndromes (WDSs) encompass a group of inflammatory chorioretinopathies that share pathologic features involving chorioretinal lesions located at the retinal pigment epithelium (RPE) and the choriocapillaris. This group of diseases includes multiple evanescent WDS, acute posterior multifocal placoid pigment epitheliopathy, multifocal choroiditis and panuveitis, punctate inner choroiditis, birdshot chorioretinopathy, and acute zonal occult outer retinopathy.[1] They typically affect otherwise healthy adults, and the usual presentation includes vision loss, photopsia, and floaters.[2] The different entities are distinguished by the clinical history, lesion morphology, and fluorescein angiography pattern.
Many cases of WDS are preceded by flu-like symptoms, possibly related to viral infection. The etiology of WDS diseases remains uncertain, but the authors suggest an inflammatory or autoimmune process triggered by an exogenous agent. It is not clear whether the different syndromes are a spectrum of the same disease or are separate disease entities.[3] The fundoscopic appearance consists of discrete, usually white or yellowish lesions, located at various levels of the outer retina, RPE, choriocapillaris, and choroid, depending on the condition.[4]
This clinical report aims to describe a case of WDS superimposed on diabetic retinopathy (DR), which was initially misdiagnosed as a complication of macular diabetic edema.
Case Report | |  |
A 53-year-old man was referred from another hospital with complaints of decreased visual acuity of the right eye (OD) for 3 days. He denied pain, red eye, or trauma and did not have any other ocular complaints. He had a history of known severe nonproliferative DR and was already proposed for panretinal photocoagulation, which was scheduled for the following month. The referring hospital did not have functional optical coherence tomography (OCT), due to a malfunction of the device, and therefore attributed the decreased visual acuity to the potential presence of diabetic macular edema, having referred the patient with this presumptive diagnosis.
The clinical observation revealed an OD best-corrected visual acuity of 6/30 (there was a recent record of 6/6). The anterior segment examination was unremarkable, without anterior chamber reaction or rubeosis iridis, and the fundoscopy revealed characteristic lesions of severe nonproliferative DR, with microaneurysms and microhemorrhages in all four quadrants, pathological arteriovenous crossing, and macular exudates without the involvement of the central macula [Figure 1]. A spectral-domain OCT (SD-OCT) was promptly made, which revealed the absence of macular edema. However, it showed hyperreflective changes of the outer layers of the central retina, at the level of the RPE, with loss of definition of the ellipsoid layer, and apparent choroidal thickening [Figure 2]. A fluorescein angiography was performed, which showed central and peripheral ischemia, with peripheral but not central diffusion [Figure 3]. An angio-CT of the brain and neck vessels was requested, to exclude the presence of macrovascular occlusion, which showed the presence of partially calcified carotid atheromatous plaques, leading to stenosis of <50% of the vessels. A systemic infectious and immunological study was also carried out, which was unremarkable. Considering the absence of macrovascular ischemic causes, a more detailed anamnesis was carried out, and the patient revealed that he had recently suffered from an acute upper respiratory infection, with mild flu-like symptoms. Therefore, despite the severe DR, the possibility of an overlapping inflammatory chorioretinitis was considered, taking into account the structural alterations of the external retina layers and the recent viral infection. | Figure 2: SD-OCT of the macular of the right eye at presentation showing the absence of macular edema and hyperreflective changes of the outer layers of the central retina, at the level of the RPE, with loss of definition of the ellipsoid layer and choroidal thickening. SD-OCT: Spectral-domain optical coherence tomography, RPE: Retinal pigment epithelium
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Only 1 week after the initial admission, without any therapeutic intervention, the patient presented at a re-evaluation consultation with an uncorrected visual acuity (UCVA) of 6/6. The fundoscopic appearance was similar, and SD-OCT now showed a better definition of the retinal external layers, with clearer delineation of the RPE and ellipsoid layers [Figure 4]. On subsequent re-evaluations, months after the initial presentation, the patient maintained a 6/6 UCVA and an OCT without the external layer changes. He remains under follow-up and has undergone panretinal photocoagulation due to the DR. | Figure 4: SD-OCT of the macula of the right eye 1 week after presentation showing better definition of the retinal external layers, with clearer delineation of the RPE and ellipsoid layers. SD-OCT: Spectral-domain optical coherence tomography, RPE: Retinal pigment epithelium
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Discussion | |  |
Inflammatory chorioretinopathies are a group of diseases with predominant pathological manifestations in the outer layers of the retina, RPE, and choroid. Despite having in common a similar presentation, it is often difficult to differentiate the individual entities. The distinction between the various diseases is based on the clinical history, the form of presentation, lesion morphology, and appearance in complementary diagnostic tests.[5] While they are conventionally recognized as different identities, some suggest that they represent a spectrum of chorioretinal disease.[6] Laboratory testing should be done to exclude alternative etiologies to the differential diagnosis.[7]
In the presented case, the diagnostic challenge was due to the fact that the disease was superimposed on a severe DR. The fundoscopic appearance of WDS is heterogeneous on its own and many times difficult to differentiate from other pathologies.[8] In this case, the fact that it occurred on a fundus that already had many alterations due to the severe diabetic retinopathy (DR) made the diagnosis more difficult and less apparent. The tool that proved to be essential was the SD-OCT, as it showed the disruption of the outer layers of the retina, distinct from the predominantly vascular changes of the inner layers of the retina, typical of RD.[9] In retrospect, the fact that the anatomical and functional changes resolved rapidly and spontaneously also shows that an overlying condition was the true cause of the vision loss. Although the inflammatory condition improved promptly, the presence of severe DR with central and peripheral ischemia still required urgent treatment. The execution of urgent panretinal photocoagulation and close patient monitoring remained paramount.
This report aimed to demonstrate that in rare cases, an inflammatory retinal disease may go unnoticed if an underlying retinal disease is already present. The fact that the vast majority of fundoscopic changes were due to DR initially led to the presumption of the wrong diagnosis. It was only through a detailed clinical history and careful complementary tests that the true cause of the vision loss was detected.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
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9. | Curtis TM, Gardiner TA, Stitt AW. Microvascular lesions of diabetic retinopathy: Clues towards understanding pathogenesis? Eye (Lond) 2009;23:1496-508. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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