Objective To investigate the clinical features of multifocal choroiditis (MC) and guide the diagnosis and treatment. Methods Retrospective analysis of clinical data of 18 MC cases (28 eyes) who were diagnosed through fluorescein angiography (FFA) or indocyanine green angiography (ICGA) and fundus characteristics. Results Multiple round to oval lesions scattered throughout the posterior pole and peripheral areas of ocular fundi of all of the 28 eyes(binocular in 10 and monocular in 8) were found. Active focal lesions of ocular fundi were seen in 8 patients and inactive lesions in 10 patients. active and 10 cases were inactive. Choroidal neovascularization(CNV) in macular area was found in 7 patients. The images of FFA of the legions showed hypofluorescence in the early phase, with late leakage and gradual staining or window is defect in the late phase. Conclusions MC is a rare disease and often misdiagnosed to other disease and FFA helpful in diagnosis. (Chin J Ocul Fundus Dis, 2005, 21: 367-370)
Objective To explore the clinical manifestations and the characteristics of images of indocyanine green angiography (ICGA) and fundus fluorescein a ngiography(FFA) of multifocal choroiditis. Methods Eight patie nts (10 eyes) with multifocal choroiditis were gathered. The clinical manifestations and the images of ICGA and FFA were analyzed. Results Foci of multifocal choroiditis were found in posterior pole and peripheral areas of ocular fundi of all of the 10 eyes. The images of ICGA revealed hypofluorescence in focal area. The images of FFA showed hypofluorescence at the early phase and fluorescein leakage at the late phase in the active focus, and fluorescein staining and window defect fluor escence in the inactive focus. Conclusions The clinical manife stations of multifocal choroiditis varied with disease course, location and numbers of the lesions. ICGA and FFA can show the development of the disease clearly, which may guide the treatment. (Chin J Ocul Fundus Dis，2004，20：87-89)
Serpiginous choroiditis (SC) is infrequent, chronic and posterior uveitis displaying a geographic pattern of choroiditis easy to recur. Studies reveal that the active lesions of inflammatory processes are mainly localized to the choriocapillaris and retinal pigment epithelium cells. SC may manifest with variable features, although a creeping pattern of choroiditis, extending from the juxtapapillary area, with grayish yellow discoloration. Fundus fluorescein angiography, indocyanine green angiography, fundus auto-fluorescence and optical coherence tomography are helpful to diagnose atypical SC. In addition, these image examinations can evaluate the activity and progression of lesion, and detect any complication that might occur. SC is mainly distinguished from multifocal SC related with tuberculosis or virus and etc. Pathogenesis is unclear, an organ-specific autoimmune inflammation or infection seems likely to be the underlying process. It is mainly using glucocorticoid with immunosuppressant therapy at present. Timely and effectively control inflammation can effectively prevent vision loss, choroidal neovascularization and choroidal scar in SC patients.
Objective To observe multimodality imaging features of different properties in multifocal choroiditis (MFC). Methods Twenty-eight patients (51 eyes) with MFC were enrolled in this study. There were 10 males and 18 females. The patients aged from 31 to 49 years, with the mean age of (41.5±0.8) years. There were 23 bilateral patients and 5 unilateral patients. All patients underwent best corrected visual acuity (BCVA), slit-lamp biomicroscopy, indirect ophthalmoscopy, fundus colorized photography, infrared fundus photography, fundus autofluorescence (FAF), fundus fluorescein angiography (FFA) and optical coherence tomography (OCT) examinations. The lesions were classified as active inflammatory lesion, inactive inflammatory lesion, active choroidal neovascularization (CNV) and inactive CNV. The multimodality imaging features of different properties in MFC was observed. Results In fundus colour photography, the boundaries of active inflammatory lesions were blurry, while inactive inflammatory lesions had relatively clear boundaries. Secondary active CNV showed mild uplift and surrounding retinal edema; Secondary active CNV lesions showed mild uplift, retinal edema around the lesion; Secondary non-active CNV had no retinal exudate edema lesions, but had lesions fibrosis and varying degrees of pigmentation. Infrared fundus examination revealed that both active and inactive inflammatory lesions showed a uniform punctate or sheet-like fluorescence. The fluorescence of CNV lesions was not uniform; there was a bright ring around the strong fluorescence. FAF found that active inflammatory lesions showed weak autofluorescence (AF), surrounded by a strong fluorescence ring; inactive inflammatory lesions showed AF loss. Secondary active CNV lesions showed strong AF with a bright ring along the edge, and obscured fluorescence for co-occurred hemorrhagic edema; secondary non-active CNV lesions were strong AF, surrounded by a weak AF ring. FFA revealed that active inflammatory lesions showed weak fluorescence in the early stage, and fluorescence gradually increased in the late stage with slight leakage. Inactive inflammatory lesions showed typical transmitted fluorescence. Fluorescein leakage secondary to active CNV was significant; lesions secondary to inactive CNV showed scar staining. In OCT, the active inflammatory lesions showed moderately weak reflex signals in the protruding lesions under the retinal pigment epithelium (RPE). The inactive inflammatory lesions showed penetrable RPE defects or choroidal scar, it also showed clear RPE uplift lesions with a strong reflection signal. Secondary active CNV showed subretinal fluid retention; secondary non-active CNV showed RPE defects and choroidal scarring. Conclusions Active inflammatory lesions in MFC have blurred boundary, retinal edema and fluorescein leakage in FFA; inactive inflammatory lesions have clear boundary and typical transmitted fluorescence in FFA, and no retinal edema. Secondary active CNV showed subretinal fluid in OCT; and secondary non-active CNV showed RPE defects and choroidal scarring.