Choroidal neovascularization

Introduction to choroidal neovascularization Choroidal neovascularization refers to proliferating blood vessels from the choroidal capillaries that extend through the rupture of the Bruch membrane, between the Bruch membrane and the retinal pigment epithelium, or between the neural retina and the retinal pigment epithelium, or between the retinal pigment epithelium and the choroid. Proliferation, many diseases involving the RPE-Bruch membrane-choroidal capillary complex can lead to the formation of CNV, also known as subretinal neovascularization. More common in the macula, thus damaging the central vision. The disease has become one of the main causes of blindness. Common in adult eyes, especially those over 60 years old. It should be discovered early and processed in time. basic knowledge The proportion of illness: 0.02% Susceptible people: no special people Mode of infection: non-infectious Complications: edema, cystoid edema

Choroidal neovascular cause

It has been found that many disease processes can affect the retinal pigment epithelium - Bruch membrane - choroidal capillaries, and are often associated with subretinal neovascularization.

Hereditary factors (20%):

Hereditary macular degeneration such as Best disease, Stargardt disease, yellow spotted retinal degeneration, hereditary primary drusen and atrophy of pigmented epithelium in adult macular area affects retinal pigment epithelium-Bruch membrane-choroidal capillaries.

Inflammatory disease factors (20%):

Inflammatory diseases include ocular cytoplasmosis syndrome, toxoplasmosis, purulent choroiditis, rubella retinopathy, sarcoidosis, acute posterior squamous pigment epithelial lesions, central exudation Crohn's disease (Rieger type), Harada disease and Behcet's disease can affect the retinal pigment epithelium - Bruch membrane - choroidal capillaries.

Degenerative factors (30%):

Age-related macular degeneration, degenerative myopia, optic disc palsy and fundus vascular streaks affect the retinal pigment epithelium-Bruch membrane-choroidal capillaries.

Tumor (10%):

Tumor diseases include choroidal pigmented neuritis, choroidal osteoma, choroidal hemangioma, choroidal melanoma, choroidal metastases, retinal and pigment epithelial hamartoma.

Damage factor (10%):

Injuries such as choroidal rupture, argon laser treatment or late complications after retinal condensation injury.

Other (3%):

Idiosyncratics: The cause is still unknown.

Pathogenesis

At present, the pathogenesis of choroidal neovascularization is still unclear. It is generally thought to be related to changes in the retinal pigment epithelium-Bruch membrane-choroidal capillary complex. The macular retina has extremely high metabolic requirements, a large amount of oxygen, and a different blood vessel distribution. Other parts, therefore, degeneration, inflammation and trauma may cause ischemia and hypoxia in the outer layer of the macula, which causes angiogenic factors to stimulate choroidal capillary angiogenesis, forming subretinal neovascularization, Archer photocoagulation causes rhesus retina The inner blood supply is reduced and the Bruch membrane is ruptured, which induces an animal model of choroidal neovascularization. It is believed that there are two main factors affecting choroidal neovascularization: one is the rupture of the Bruch membrane, and the other is the structure or composition of the outer retinal cell. change.

Choroidal neovascularization

The main prevention is to eat more foods rich in vitamins A and C. The most abundant foods of vitamin A are liver and egg yolk. Carotene in plant foods can be converted into vitamin A in the body, so it is also a good source of supplements to prevent this disease.

Choroidal neovascular complications Complications, edema, cystoid macular edema

Cystic macular edema can occur in choroidal neovascular complications. The choroidal neovascularization is gradually stabilized for several months or years, replaced by gray-yellow fibrous vascular membranes, which can then turn white, and finally form a retinal choroidal atrophy zone. Cystoid macular edema (CME) is a common fundus disease, but it is not an independent disease, but a manifestation of many fundus diseases in the macula.

Choroidal neovascular symptoms common symptoms visual impairment retinal hemorrhage visual deformity edema

In the early stage of subretinal neovascularization, there may be no symptoms. As it gradually enlarges, leakage and rupture and bleeding may cause vision loss, visual distortion, central or paracentral dark spots, repeated symptoms, and the macula are affected. Serious damage can cause permanent visual impairment.

Ophthalmoscopy is often not easy to find new blood vessels under the retina. It is often characterized by exudation and hemorrhage during general fundus examination. The more reliable indication is subretinal hemorrhage, which is dark red, blue-gray or dark because the bleeding is deep in the pigment epithelium. Brownish gray, the boundary is relatively clear. If the bleeding breaks through the pigment epithelium to the retina, the nerve epithelium or the neuroepithelium is bright red. In a few cases, the bleeding can break through the retinal neuroepithelial and escape into the vitreous. The other sign is lipid. The appearance of oozing, retinal neuroepithelial detachment is seen in the neovascular area, which is different from the retinal neuroepithelial detachment in central serous chorioretinopathy. The serous turbidity is more turbid, and cystic macular edema can occur in cases with longer course. The choroidal neovascularization is gradually stabilized for several months or years, replaced by a gray-yellow fibrous vascular membrane, which can then turn white, and finally form a retinal choroidal atrophy zone.

Choroidal neovascularization

The necessary laboratory tests can be carried out for the primary disease.

1. Fundus fluorescein angiography: the most valuable method for detecting choroidal neovascularization. The early choroidal phase of fluorescein angiography can identify the morphology of choroidal neovascularization, mostly lace-like or single-wheel-shaped, or fan-shaped. Expanding to the periphery, venous fluorescein leaks outward from the neovascular wall, forming a localized strong fluorescent region. In the advanced stage, fluorescein slowly diffuses from the edge of the neovascular membrane and enters the retinal neuroepithelial detachment zone.

2. Indocyanine green angiography (ICGA): It has obvious superiority in choroidal neovascular membrane imaging. Choroidal neovascularization blocked by blood and turbid fluid or occult neovascular membrane on FFA can often be found in ICGA.

3. Optical coherence tomography (OCT): When the choroidal neovascularization is performed, the retinal tissue structure and neovascularization can be visually displayed, which provides a new examination method for further research.

Diagnosis of choroidal neovascularization

The exact diagnosis is mainly based on fundus fluorescein angiography. In recent years, indocyanine green angiography has deepened its understanding and detection rate. The diagnosis can be determined according to clinical manifestations and typical fundus fluorescein angiography and morphology. The choroid is between the retina and the sclera and is rich in blood vessels and pigment cells. The tolerance to external impact is worse than that of the retina. When the eyeball is transmitted by the external force from the front to the posterior pole, the hard sclera is It is also resistant to the outside, causing rupture and bleeding in the choroid.

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