Clinical Analysis of Hypofluorescent Spots in Indocyanine Green Angiography

PURPOSE: We observed many cases which showed hypofluorescent spots in indocyanine green angiography (ICGA) at the late phase as well as white dot syndrome, so we analyzed for types and causes of these. METHODS: we analyzed the color photographs, fluorescein angiographs (FAG) and ICGA of the 21 patients (39 eyes) who have noted hypofluorescent spots at the late phase retrospectively. RESULTS: The hypofluorescent spots in ICGA could be classified into two types. The first is that which seen hypofluorescence from the early phase and clearly to the late phase and the second, relatively lighter dark spots which appeared after midphase and is seen in the late phase. But when we analyze these together with ophthalmologic findings and FAG, we found out that the lesion could not be found in the retina and FAG or that it is noted as hyperfluorescence or hypofluorescence in the early and late phase of FAG. So the causes were thought to be variable. CONCLUSIONS: We could find hypofluorescent spots in the late phase of ICGA in the lesions which were classified as white dot syndrome in the past as well as presented normal finding in the retina and FAG and they had variable morphologies and causes.

The Intracho roidal Changes in Harada`s Disease

The intrachoroidal changes in Harada's disease were studied by indocyanine green(ICG)angiography. ICG angiography using confocal laser scanning ophthalmoscope (Heidelberg Retina Angiograph, HRA)and fluorescein angiography were performed in 12 eyes of 6 patients during the acute stage before the initiation of corticosteroid treatment and recovery stage, and the findings were evaluated retrospectively. During the acute stage, early phase HRA images disclosed a dark background fluorescence in all eyes due to the diffuse filling delay and the vague contour of choroidal vessels. In the midphase, Intrachoroidal hyperfluorescence resulting from vascular leakage and scattered hypofluorescent spots were intermingled, and in some eyes patchy hypofluorescence representing focal filling defect was observed. These choroidal changes could be observed before any visible retinal changes appeared. During the recovery stage, choroidal filling was more rapid and choroidal vessels were more clearly visible. However the scattered hypofluorescent spots due to the blockage by the inflammatory precipitates were still observed in small numbers, and in some eyes focal vascular leakage remained. According to these findings, we hypothesize the pathogenesis of Harada`s disease as follows. Severe inflammatory precipitates and vascular leakage can make the choroid edematous with highly viscous fluid. It adds mechanical damage to choroidal vessels already injured by the inflammatory process, leading to reversible circulatory disturbances. The retinal pigment epithelium and the sensory retina may be damaged secondarily.