Ординатура / Офтальмология / Английские материалы / Atlas of Fundus Autofluorescence Imaging_Holz, Schmitz-Valckenberg, Spaide, Bird_2007

214 Richard F. Spaide

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9.Grossniklaus HE, Gass JD. Clinicopathologic correlations of surgically excised type 1 and type 2 submacular choroidal neovascular membranes. Am J Ophthalmol 1998;126:59–69

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Fig. 16.1  a The normal retinal pigment epithelium (RPE) monolayer has a cor­ responding amount of autofluorescence (b). Inflammatory lesions have an al­ teration in color (c) and are often hyperautofluorescent in the acute phase (d). e, f, g, h, see next page

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Fig. 16.1  (Continued) This increase in autofluorescence may arise from hyper­ trophy or hyperplasia of the RPE cells or increased fluorophores within the RPE. e Later there appears to be shrinkage of the inflammatory lesion, with retraction of the outer aspect of the lesion and formation of a gap between the lesion and the normal RPE monolayer. The gap contains no functional RPE cells and ap­ pears as a black band on autofluorescent photography (f). g In the resolution phase, the darker pigmented regions seen in image e adopt a flat greyish-black color. Along with the change in color, a loss of the hyperautofluorescent charac­ ter occurs as well (h)

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Fig. 16.2  a Color fundus photograph of the right eye shows multiple yellowwhite placoid lesions in a patient with acute posterior placoid pigment epithe­ liopathy. b In the early phase of the fluorescein angiogram, there were many more areas of decreased fluorescence than the number of placoid lesions seen in the color photograph. c The late-phase fluorescein shows staining of some of the lesions (arrow), bordered by an adjacent blocking defect (arrowhead). d The autofluorescence photograph shows a band of hyperautofluorescence (arrowhead) corresponding to the blocking defect in image c. The area of hypoauto­ fluorescence (arrow) corresponded to the area of staining during the fluorescein angiographic evaluation. (From Spaide RF. Autofluorescence imaging of acute posterior multifocal placoid pigment epitheliopathy. Retina 2006;26:479–482)

Fig. 16.3  a The same patient shown in Fig. 16.2, 2 weeks after presentation. The patient had an increase in both the size and number of visible lesions. In addi­ tion, many more of the lesions showed late fluorescein angiographic alterations. Note that the areas of hyperfluorescence (arrows) in the fluorescein angiogram (a) correspond to hypoautofluorescent regions in the autofluorescence pho­ tograph (arrows). The areas of blocking in the fluorescein angiogram (arrowheads) correspond to areas of hyperautofluorescence in the autofluorescence photograph

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Fig. 16.4  a Color fundus photograph 4 weeks after presentation, showing heal­ ing of the lesions with increased pigmentation centrally (arrowheads) and de­ creased pigmentation (arrows). Note the decreased pigmentation forming ha­ loes around the pigmented areas. b The autofluorescence photograph shows that the areas of pigmentation were hyperautofluorescent and the depigmented haloes were hypoautofluorescent. c Color photograph 6 months after presenta­ tion showing alteration in the pigment as seen in image a. Note that some of the pigmentation nearly disappeared, while other areas showed some decrease and other areas consolidated and became more flat-black. d The formerly hy­ perautofluorescent areas have become hypoautofluorescent. Note that the gap of hypoautofluorescence seen initially has tiny dots of autofluorescence, which may indicate repopulation of the atrophic areas