Objective To observe the multimodal image features of inflammatory lesions and choroidal neovascularization (CNV) in multifocal choroiditis (MFC). MethodsA retrospective clinical analysis. A total of 90 eyes of 46 patients with MFC diagnosed in the Department of Ophthalmology of Yunnan University Affiliated Hospital from May 2017 to April 2021 were included in the study. Among them, there were 21 males and 25 females; the average age was 38.30±8.97 years old. Twenty-nine cases of MFC were diagnosed in the past, and they visited the doctor again due to new symptoms; 17 cases without a clear past medical history were the first visits. All eyes underwent color fundus photography, fluorescein fundus angiography (FFA), optical coherence tomography (OCT), and OCT angiography (OCTA). With reference to the literature and the results of multimodal fundus imaging examinations, MFC lesions were divided into active CNV lesions, inactive CNV lesions, active inflammatory lesions, and inactive inflammatory lesions, with 31 (34.4%, 31/90), 12 (13.3%, 12/90), 26 (28.9%, 26/90), 90 (100.0%, 90/90) eyes. Nineteen eyes were treated with anti-vascular endothelial growth factor drugs. To summarize and analyze the manifestations of inflammatory lesions and CNV lesions in different imaging examinations. The Wilcoxon rank test was used to compare the detection rate of CNV lesions between FFA and OCTA. ResultsIn eyes with active inflammatory lesions and active CNV lesions, yellow-white lesions, retinal hemorrhage and exudation were seen on fundus color photography; FFA examination showed fluorescein leakage in the lesions; OCT examination showed retinal pigment epithelium (RPE) layer in the lesions was uplifted, the boundary was unclear, combined with subretinal and intraretinal fluid; OCTA examination showed that there was no blood flow signal in each layer of vascular tissue in active inflammatory lesions, and blood flow signals were seen in active CNV lesions. In the eyes of inactive inflammatory lesions and inactive CNV lesions, the fundus color photography showed that the lesions had clear boundaries without bleeding or exudation; FFA examination, the lesions were fluorescently stained, and there was no fluorescein leakage; OCT examination, inactive CNV lesions manifested as raised lesions with clear boundaries, and inactive inflammation manifested as scars formed by mild RPE hyperplasia or depressions in outer structures formed by atrophy; OCTA examination, inactive inflammatory lesions showed patchy loss of blood flow signal or penetrating blood flow signal below, blood flow signal can be seen in inactive CNV lesions. ConclusionMFC active inflammatory lesions and active CNV lesions are often accompanied by retinal hemorrhage and exudation; FFA shows fluorescein leakage; OCT shows that the boundary of raised lesions is unclear; OCTA can identify the nature of CNV or inflammatory lesions.
ObjectiveTo observe and analyze the clinical and imaging features of eyes with cystoid macular degeneration (CMD) secondary to chronic central serous chorioretinopathy (cCSC). MethodsA retrospective clinical study. From February 2018 to June 2023, 9 patients of 15 eyes with cCSC secondary CMD diagnosed by ophthalmology examination in Yunnan University Affiliated Hospital were included in the study. All patients were male. The age was (53.67±3.83) years. The cases of binocular and monocular were 6 and 3 respectively. The visual acuity of the affected eye ranges from 0.02 to 0.1, which cannot be corrected. Visual acuity decreased and the duration of shadow occlusion was ＞1 year. Half dose photodynamic therapy (PDT) was performed on 8 eyes. All the patients underwent the best corrected visual acuity, posterior mydriatic fundus color photography, infrared fundus photography (IR), fundus autofluorescence (AF), fluorescein fundus angiography (FFA), optical coherence tomography (OCT), and multi-wavelength dazzling imaging (MC). The patients who received half dose PDT were followed up until 3 months after treatment. Patients who did not receive treatment were followed up to 2 years after the first diagnosis. ResultsThe light reflection in macular area decreased or disappeared in all eyes, and abnormal macular pigmentation was observed in 12 eyes. IR examination showed diffuse patchy weak fluorescence in the macular area in all affected eyes, and dotted strong fluorescence in the periphery. Fundus AF examination showed disc-like weak AF in the macular area, and scattered small amounts of strong AF in the middle and margins, among which the retinal pigment epithelium (RPE) atrophy trace in the macular area was observed in 7 eyes. By MC examination, the green signal in the macular area of the posterior pole of all affected eyes was uneven and mottled. FFA examination showed that no abnormal fluorescein leakage was observed in 15 eyes and 8 eyes showed strong fluorescence caused by diffuse permeation fluorescence. A small amount of active fluorescein was found in 7 eyes. OCT examination showed that there were several cystic cavities of different sizes in all the affected eyes, RPE atrophied to different degrees, and RPE cell compensatory ridges and tubular structures in the outer retina were seen in 6 eyes; 7 eyes with CMD and active leakage showed signs of subcortical fluid accumulation. Choroidal hypertrophy was seen in all affected eyes, with significant expansion of the great vascular layer and compression of the middle vascular layer and capillary layer. In 8 eyes treated with half-dose PDT, 6 eyes were ineffective at 3 months after treatment. The treatment was effective in 2 eyes. In 7 eyes that did not receive half-dose PDT, CMD structure did not improve significantly after 2 years of follow-up. The visual acuity decreased with the prolongation of the disease. ConclusionsCMD is more common in cCSC with a long course of disease, which has significant effects on vision and poor prognosis. Fundus color photography shows that the reflection in the macular area of the pole is weakened or disappeared, which may be combined with macular abnormal pigmentation. IR and AF examination show uneven fluorescence in macular area. The green signal in macular area is not uniform according to MC inspection. FFA shows strong fluorescence caused by diffuse permeable fluorescence and fluorescein leakage in active lesions. OCT examination shows that multiple small sacs or connections between sacs were broken and fused, and RPE atrophied to varying degrees.
ObjectiveTo observe the clinical evolution process and imaging characteristics of choroidal lesions in different subtypes of serpiginous choroiditis (SC), and to explore the clinical significance of subtype classification. MethodsA retrospective, uncontrolled and observational study. A total of 45 eyes of 25 SC patients diagnosed in Yunnan Eye Hospital from May 2009 to September 2021 were included in the study. According to the initial location of the lesion and fundus images, including fundus color photography, fundus fluorescein angiography (FFA), optical coherence tomography (OCT) and other examination results. SC was divided into peripapillary serpiginous choroiditis, macular serpiginous choroiditis and ampiginous choroiditis. According to the shape of the lesions at the first diagnosis, it can be divided into new lesions with only infiltrating edema, old lesions with only atrophy and recurrent lesions with coexistence of edema and atrophy. the imaging features, development and complications of different subtypes of ocular lesion were observed. ResultsAmong the 45 eyes of 25 cases, 15 cases were male and 10 cases were female, 20 cases of binocular and 5 cases of monocular, age was 42.3±5.7 years old. There were 21 eyes with active lesions, of which 5 eyes were new lesions and 16 eyes with recurrent lesions; 24 eyes were old lesions. Concurrent optic disc edema occurred in 3 eyes; mild vitreitis occurred in 5 eyes; retinal occurred vasculitis in 3 eyes; choroidal neovascularization occurred in 3 eyes. Among the 16 cases (64%, 16/25) of the peripapillary serpiginous choroiditis, 2 cases (2 eyes) were monocular, and 14 cases (28 eyes) were binocular. Active lesions were found in 16 eyes, of which patients with binocular lesions only one had active lesions. The choroidal lesions that were close to the optic disc or around the optic disc, expanded outwards centrifugally with the prolongation of the disease course, and can progress to the macula. The edge of the lesion was tortuous, with a geographic-like, amoeboid-like and finger-like, polypoid or propeller-like shape. Active lesions in FFA showed weak fluorescence in the early stage and strong fluorescence in the late stage; the old lesions showed weak fluorescence in the early stage and mottled fluorescence in the late stage, and mostly strong fluorescence on the edge. OCT showed thickening of active lesions and thinning of old lesions. Among the 4 cases (16.0%, 4/25) of macular type, 2 cases (2 monocular eyes) had active lesions; 2 cases (4 eyes) had lesion in both eyes, among them, 1 case (2 eyes) had old lesion, and the other case had alternate active lesions. The initial lesions were all located in the off-center of the macula, and most of them were disk-shaped and progressing centrifugally to the periphery. The FFA and OCT imaging findings of the lesions were similar to those of the peridisc type. Among the 5 cases (20.0%, 5/25) of ampiginous choroiditis, 1 case (1 eye) was monocular and 4 cases (8 eyes) were binocular. These lesions were multiple old lesions of varying sizes, gray-white with pigmentation, with clear borders in the posterior pole. Among them 4 eyes have new active lesions appeared near the old lesions. The old lesions showed weak fluorescence with clear borders, and the fluorescein leakage at the late edge formed a strong fluorescence ring; the active lesions showed weak fluorescent spots with blurred edges, and the fluorescence was slightly enhanced in the late stage. In old lesions, atrophy of the photoreceptor layer, RPE and choroid can be seen, and RPE hyperplasia in some areas. ConclusionsSC subtype is a classification of the location of the first lesion, but the characteristics of the repeated attack of this disease can lead to the annihilation of each subtype due to the continuous expansion of the lesion. The phenomenon that the fundus active lesions only occur in one eye that can explain the clinical manifestations of asymmetric morphology of binocular lesions. The characteristics of binocular subtype warn that the predilection site of the healthy eye should be paid attention to.