Purpose:To determine the proportion of patients with central serous chorioretinopathy (CSCR) mistaken for posterior uveitis and to identify the deleterious consequences.Methods:Charts of 1,657 patients admitted in the section of inflammatory eye diseases at the Center for Ophthalmic Specialized Care (COS) in Lausanne, Switzerland from 1995 to 2013 were reviewed. CSCR cases misdiagnosed as posterior uveitis or those with superimposed disease due to steroid therapy for uveitis were studied. Delay in diagnosis, specific erroneous uveitis diagnosis and evolution of the disease were also evaluated. Retrospectively, the most useful means for a correct diagnosis of CSCR were the original fluorescein angiography (FA), indocyanine green angiography (ICGA) and optical coherence tomography (OCT) when available.Results:Out of a total of 1,657 patients, 15 (0.9%) cases with CSCR were identified. These included 12 subjects misdiagnosed as posterior uveitis and 3 uveitis subjects with superimposed CSCR following corticosteroid therapy for uveitis. The presentation of the disease was largely influenced by improper and continued use of corticosteroids.Conclusion:CSCR is a rare but not negligible misdiagnosis in posterior uveitis representing approximately 1% of subjects from a collective series of uveitis cases at a referral center. Investigative measures such as FA, ICGA and OCT are crucial for reaching a correct diagnosis and avoiding disease aggravation due to corticosteroid therapy.
The present appraisal of Birdshot retinochoroiditis (BCR) is based on obsolete criteria that only represent advanced disease. Early diagnosis of BC can only be done using indocyanine green angiography (ICGA) showing the typical choroidal involvement. The aim of this study was to investigate long‐term follow ups of BRC patients regarding the impact of early treatment on the phenotype of BRC, both on ICGA findings as well as fundus appearance. 13 patients had sufficient data to be included in the study. Out of 13 patients, 8 showed typical birdshot lesions at presentation according to the presently used criteria. A significant proportion of the “no lesions” group did not develop typical birdshot lesions throughout the course. Mean treatment delay was 45.50 ± 33.39 months in the “typical lesions” group and 5.80 ± 2.95 months in the “no lesions” group. Early treatment can avoid the apparition of typical BRC lesions in the same fashion as early and heavy treatment can avoid the development of “sunset glow” fundus in Vogt‐Koyanagi‐Harada disease (VKH). Early diagnosis relies heavily on ICGA, that together with FA, visual field testing and presence of HLA‐A29 antigen allows the diagnosis before typical birdshot lesions can be seen.
SummaryCentral serous chorioretinopathy (CSC) can sometimes be mistaken for posterior uveitis. Its diagnosis is of utmost importance as CSC as failure to do so will worsen when steroid therapy is erroneously given. The situation is even more tricky when CSC is complicating IST including steroids given for uveitis. In a collective of 1739 patients seen from 1995 to 2014 at the COS, 16 patients (0.9%) with CSC were misdiagnosed as posterior uveitis of which the development of CSC was missed in 4 uveitis patients under IST including corticosteroids. The mean diagnostic delay in the latter group was 2.4 ± 1.9 months, substantially shorter than the group of patients misdiagnosed at the onset (56.3 ± 60.6 months). The key to rapid diagnosis of a decrease of VA due to CSC in uveitis, is to search on one side whether inflammatory parameters such as laser flare photometry and dual fluorescein (FA) and indocyanine green angiography (ICGA) are improving combined with the search of CSC signs including serous detachments and/or small PEDs on OCT as well as typical CSC angiographic signs on dual FA/ICGA angiography. Although CSC complicating uveitis treatment is rare, prompt diagnosis is of utmost importance to avoid deleterious consequences.
Purpose Inflammation of the choroid evolves mostly unnoticed when only clinical examination and/or only classical investigational methods are used. In some cases such occult inflammation, when it is finally noted has already caused irremediable damage. Methods Inflammatory cases are presented that showed minimal or no signs on clinical examination/investigational tests, where significant occult choroïdal inflammation was detected by ICGA and that responded to therapy initiated on the base of ICGA findings. In parallel, patients that were treated with delay or received no therapy and suffered irremediable damage will be presented. Results Primary inflammatory choriocapillaropathies PICCPs (MEWDS, APMPPE, multifocal choroiditis) known to be caused by inflammatory choriocapillaris non perfusion can only be meaningfully investigated for activity by ICGA as non‐perfused areas are not seen otherwise. If active disease (non‐perfusion) is suspected, PICCPs have to be evaluated and followed by ICGA and in case of persistence of non‐perfusion and worsening of function, therapy has to be introduced to avoid irremediable damage. For stromal choroiditis such as Vogt‐Koyanagi‐Harada (VKH) disease, persisting choroiditis after alleged clinical recovery needing continued therapy can only be shown by ICGA, so avoiding complications due to smouldering occult disease. Conclusion ICGA in the work‐up of posterior uveitis should be part of a routine investigation for those case where angiographic work‐up is deemed necessary.
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