Abstract:Four of the analyzed signs, including early hyperfluorescent stromal vessels, HDDs, fuzzy or lost pattern of large stromal vessels, and disc hyperfluorescence were consistent findings in Japanese VKH patients. Because the primary lesion is situated in the choroid, IA is the method of choice to monitor disease activity in VKH disease.
“…ICGA reveals early choroidal stromal vessel hypercyanescence and vascular leakage, and hypocyanescent dark dots at the level of the choroid in the late phase. Disc hyperfluorescence may also be seen [18, 19]. Fig.…”
The white dot syndromes (WDS) are a diverse group of posterior uveitidies that share similar clinical findings but are unique from one another. Multimodal imaging has allowed us to better understand the morphology, the activity and age of lesions, and whether there is CNV associated with these different ocular pathologies. The “white dot syndromes” and their uveitic masqueraders can now be anatomically categorized based on lesion localization. The categories include local uveitic syndromes with choroidal pathology, systemic uveitic syndromes with choroidal pathology, and multifocal choroiditis with outer retinal/choriocapillaris pathology with uveitis and without uveitis. Neoplastic and infectious etiologies are also discussed given their ability to masquerade as WDS.
“…ICGA reveals early choroidal stromal vessel hypercyanescence and vascular leakage, and hypocyanescent dark dots at the level of the choroid in the late phase. Disc hyperfluorescence may also be seen [18, 19]. Fig.…”
The white dot syndromes (WDS) are a diverse group of posterior uveitidies that share similar clinical findings but are unique from one another. Multimodal imaging has allowed us to better understand the morphology, the activity and age of lesions, and whether there is CNV associated with these different ocular pathologies. The “white dot syndromes” and their uveitic masqueraders can now be anatomically categorized based on lesion localization. The categories include local uveitic syndromes with choroidal pathology, systemic uveitic syndromes with choroidal pathology, and multifocal choroiditis with outer retinal/choriocapillaris pathology with uveitis and without uveitis. Neoplastic and infectious etiologies are also discussed given their ability to masquerade as WDS.
“…Angiographically, choroidal folds, seen in 36.1 % of affected eyes in our series, appear as alternate hyperfluorescent and hypofluorescent bands or more typically as hypofluorescent lines, radiating around the optic disc or passing through the posterior pole [16,17,19]. Although ICGA is more sensitive than FA to evaluate choroidal inflammation, it is yet not used routinely as a diagnostic procedure in typical VKH disease, in which it has been often performed to monitor subclinical choroidal inflammation and guide treatment [23][24][25][26]. Data from our study show that ICGA may provide very important clues for the definitive diagnosis of atypical acute VKH disease that mainly include decrease in the number of large choroidal vessels, fuzzy choroidal vessels, and hypofluorescent dark dots.…”
The purpose of this study was to describe the clinical and multimodal imaging findings in acute Vogt-Koyanagi-Harada (VKH) disease without clinically evident exudative retinal detachment (ERD). We retrospectively reviewed the charts of 18 patients (36 eyes), diagnosed with acute VKH disease without clinically evident ERD. All patients underwent complete ophthalmic examination, fundus photography, optical coherence tomography (OCT), B-scan ultrasonography, fluorescein angiography (FA), and indocyanine green angiography (ICGA). Of 18 patients, twelve (66.7 %) were female and 6 (33.3 %) were male. Mean age was 39 years (range, 23-60). Ten patients had been referred with an erroneous diagnosis of primary optic nerve disorder (8; 44.4 %) or isolated anterior uveitis (2; 11.1 %). Anterior chamber or vitreous inflammatory reaction was noted in 22 eyes (61.1 %), each. Fundus findings included optic disc swelling in 30 eyes (83.3 %), retinal striae in 20 eyes (55.5 %), and yellowish deep lesions in 3 eyes (8.3 %). OCT showed a shallow, localized subclinical ERD in 18 eyes (50 %), and retinal pigment epithelial folds in 23 eyes (63.9 %). B-scan ultrasonography showed diffuse, low- to medium-reflective choroidal thickening in all eyes. FA disclosed delayed choroidal perfusion in at least one eye of all patients (100 %), mild pinpoint leakage in 21 eyes (58.3 %), optic disc hyperfluorescence in 35 eyes (97.2 %) and choroidal folds in 13 eyes (36.1 %). ICGA findings included delayed choroidal perfusion in 24 eyes (66.7 %), decrease in the number of large choroidal vessels in 36 eyes (100 %), fuzzy choroidal vessels in 35 eyes (97.2 %), and hypofluorescent dark dots in 28 eyes (77.8 %). The association of bilateral optic disc edema with retinal striae and intraocular inflammatory reaction highly suggests acute VKH disease. A multimodal imaging approach including fundus photography, OCT, B-scan ultrasonography, FA, and ICGA provides important clues for the definite diagnosis and help differentiate VKH disease from primary optic nerve disorders.
“…However, we know by now that all choroidal inflammation may not be silenced even when clinically apparent disease appears to be under control. ICGA monitoring of VKH patients under treatment has shown that choroidal inflammation is still present in most cases once clinical signs as well as morphological and functional parameters have normalized [28][29][30][31][32][33][38][39][40], and the persistence of this choroidal subclinical disease explains the evolution toward SGF in most insufficiently treated cases [20,22,41].…”
Section: Association Of Steroidal and Non-steroidal Immunosuppressionmentioning
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