creeping choroidal atrophy
Introduction
Introduction to choroidal choroidal atrophy Serviginous choroidal atrophy (serpiginous choroidal trophy), also known as geographical helicoidal choroidal choroidal lesion (geographichelicoids peripapilltary choroidopathy), is a chronic recurrent disease of the choroidal capillaries and retinal pigment epithelium (RPE) in the posterior pole of the fundus. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious complication:
Cause
Causes of purulent choroidal atrophy
(1) Causes of the disease
The cause has not yet been elucidated. The possible pathogenic factors mentioned are: infection, choroidal vascular occlusion caused by immune response, and primary choroidal sclerosis. Duke-Elder believes that it may belong to primary choroidal atrophy, which Yanaff thinks is a kind. Malnutrition (dystrophy).
(two) pathogenesis
Schlaegel believes that the disease mainly invades the choroidal capillaries and causes atrophic changes in RPE. If the visual acuity is caused by the invasion of the macula, the pathogenesis may be related to ischemia. The scarring phase of the disease shows choroidal blood vessels and RPE damage, the morphology of the lesions and The range is likely to be related to the distribution of choroidal capillary units. Fundus fluorescein angiography shows the non-perfused segment of choroidal capillaries during the active phase of the lesion. During the quiescent period of the lesion, the choroidal atrophy also shows strong fluorescence of the segmental distribution. The lesion mainly occurs in the choroidal capillary layer.
Prevention
Claudication choroidal atrophy prevention
Prevention: The cause of the disease is not clear and there are no effective preventive measures.
Complication
Claudication choroidal atrophy complications Complication
Generally no special complications
Symptom
Claudication choroidal atrophy Symptoms Common symptoms of retinal edema
1. The main symptom of visual function change is vision loss, the shadow of the eye, the degree of vision loss depends on the location and size of the lesion. If the posterior pole or macular fovea is not involved, the visual impairment is lighter. Normal field of view, absolute or relative center or side center dark spots can appear, visual electrophysiological examination can find ERG and EOG abnormalities in a small number of patients.
2. Fundus changes
(1) Acute phase: The main fundus features in the early stage are multiple under the retinal blood vessels of the posterior pole, with unclear borders, large yellowish white, irregular lesions, and a map-like morphology with the optic disc as the center to the macula and equator. The expansion of the lesions can be repeated again and again. In the acute lesions, the retinal choroidal atrophy is entrapped. The lesions are surrounded by yellow and white edges, and the deep retinal tissue invading the lesions around the lesions is invasive, and the lesions are shallow. Retinal vascular filling and expansion, optic disc edema, it has been reported that inflammatory cells in the vitreous, but there are also those who believe that there is no inflammation, the macula and other parts of the subretinal may have bleeding, accompanied by the posterior pole serous retina or Pigment epithelial detachment and yellow-white exudate (Fig. 1), recurrence after 6-8 weeks after the lesion subsided or recovered, the lesion extended to the periphery on the basis of the old lesion, and there was retinal choroidal atrophy in the center of the lesion. Limb, invading deep tissue under normal retinal blood vessels.
(2) Subacute phase: After 6-12 months of onset, RPE and retinal edema subsided, yellow-white exudate was absorbed under the retina, and the retinal pigment epithelium and choroidal capillary destruction in the lesion area were replaced by gray-scarred scar tissue. There are pigmentation and deposition in the lesion and margin. The scar can be isolated. It can also be fused into a map. The old choroidal vessels are exposed, the boundary of the atrophy is clear, and there is a clear boundary with the normal fundus. New blood vessels can appear underneath, and the lesion sometimes stops for a period of time, and then the activity progresses.
(3) Chronic phase: the lesion stops completely progressing, and the RPE and choroidal capillaries shrink, forming subretinal scars, and the large choroidal vessels are common. The lesions have clear boundaries, and each lesion is the same size during the lesion. No inflammatory response, no retinal neovascularization and RPE detachment.
Examine
Examination of purulent choroidal atrophy
1. Histopathology: The choroid and the retina are separated from the lesion, and there are significant edema. The tissue thickening can reach 5 times of the thickness of the normal tissue. There is tissue necrosis in the choroid, optic ganglion cell layer and nerve fiber layer, and in the outer layer of the retina. The outer membrane has bleeding and organizing granuloma.
2. In the early stage of fundus fluorescein angiography, the lesions in the arterial phase showed weak fluorescence, which was due to tissue edema obscuration, or the choroidal capillaries were slowly filled or not filled, but the marginal part of weak fluorescence showed strong fluorescence, and the late stage of the angiography Tissue staining, strong fluorescence, optic disc vasodilation and fluorescence leakage, retinal vein filling, thickening of the wall, and leakage, angiography in the lesion area, choroidal capillaries and RPE disappeared under the retina There is scar tissue occlusion, irregular fluorescent dark areas appear, but the choroidal large vessels and surrounding choroidal capillaries develop normally, due to the diffusion from normal choroidal capillaries near the edge to the scar area, late imaging, tissue staining of the lesion area , showing uniform and strong fluorescence.
3. Indocyanine green angiography showed obvious persistent weak fluorescence in the acute phase of the disease, and the late lesions had sharp and clear edges. In some cases, focal strong fluorescence areas were observed outside the active inflammation area. In the subacute phase, the choroid is large, the middle blood vessels are visible in the lesion, the choroidal capillaries and the smaller choroidal vessels are delayed or unperfused, and the general staining and strong fluorescence in the lesion area are seen in the late stage. Due to the onset of old RPE and choroidal capillary atrophy after inflammation, angiography in the early filling phase showed delayed or no filling of the choroidal filling. With the loss of RPE and choroidal choroid, weak fluorescence was observed (Fig. 3), when choroidal neoplasia was present. When the blood vessels are seen, strong fluorescence of the new blood vessels is visible.
Diagnosis
Diagnosis and diagnosis of choroidal atrophy
The diagnosis is mainly based on the fundus manifestation and fundus fluorescein angiography. The early lesions are weakly fluorescent, the edges are strongly fluorescent, and the lesions are irregularly distributed in a map.
The disease should be differentiated from multiple posterior squamous pigment epithelial lesions, acute pigment epithelium, retinal choroiditis, age-related macular degeneration, and choroidal atrophy around the optic disc.
