central retinal artery occlusion
Introduction
Introduction to central retinal artery occlusion The central retinal artery is the only source of retinal lining nutrition. Because the artery belongs to the terminal artery, there is no anastomosis between the branches. Once the obstruction occurs, the blood supply to the inner layer of the retina is interrupted, causing acute ischemia, causing a sharp disorder of visual function. Hurry. Most of them are monocular, and they can also affect another eye in a few days or years. The age of onset is more than 40 years old. There is no significant difference in gender. The disease is extremely serious damage to visual function. Whether it can save part of the visual function depends on whether the treatment and rescue are timely, and also depends on the degree, location and cause of the obstruction. The rescuer is immediately rescued within a few hours after the onset, and the prognosis is good. The prognosis of patients with vasospasm and incomplete obstruction is better; the prognosis of branch obstruction is better than that of trunk obstruction; the obstruction occurs after the central retinal artery enters the optic nerve hard sheath and before entering the optic nerve fiber bundle, so it is easy to establish the lateral branch quickly. Cycling, prognosis is also superior to obstruction occurring at the site of the hard sheath and into the visual fiber bundle. basic knowledge The proportion of sickness: 0.002%-0.003% Susceptible people: more common in the elderly over 50 years old Mode of infection: non-infectious Complications: glaucoma
Cause
Cause of central retinal artery occlusion
Cardiovascular disease (55%)
Most cases of this disease suffer from atherosclerosis, hypertension and other cardiovascular diseases, systemic or local inflammatory vascular diseases (such as temporal arteritis, thrombotic vasculitis, nodular arteritis, behcet disease, Eales disease, Uveitis, etc.) can involve the artery, causing the intimal hyperplasia or edema of the artery, making the lumen narrow, the inner wall rough, due to the blood flow, the stenosis often has a gap, when the gap has the original lumen 1 / At 3 o'clock, there is no clinical manifestation, but under certain factors (such as thrombosis, vasospasm, insufficient blood perfusion pressure or elevated intraocular pressure), this gap can be suddenly closed. In addition, arterial spasm, acute progressive hypertension, arterial spasm such as renal hypertension, and arterial spasm based on extensive hardening of the systemic arterioles may involve the main trunk or branch of the central retinal artery. Over-clogging.
Embolization (5%)
The disease is rarely caused by emboli in the blood circulation. As mentioned above, the embolus is often caused by emboli, and the embolus is often derived from the sputum of the heart valve and the adjacent aorta, such as the aorta of bacterial endocarditis. The valve, the mitral on the mitral valve, the atherosclerotic plaque of the aorta and the thrombus in the aneurysm, etc., the pathological examination of the embolus found: calcium, cholesterol, fat, neutral fat and platelets, in addition, the literature reports There are also: air, fat, tumor fragments, cortisone, pus, parasites and eggs, etc., before the central retinal artery enters the optic nerve and the eyeball, due to the narrow diameter of the optic nerve hard sheath and scleral sieve plate, it is embolism The good part, the smaller embolus, can occur in a certain branch of the artery.
Other factors (5%)
Other post-balloon hemorrhage after anesthesia and post-operative general anesthesia during surgery can also cause central retinal artery occlusion, which may be related to oppression of the eyeball and the patient's blood loss or shock state.
Prevention
Central retinal artery occlusion prevention
The disease is extremely serious damage to visual function. Whether it can save part of the visual function depends on whether the treatment and rescue are timely, and also depends on the degree, location and cause of the obstruction. The rescuer is immediately rescued within a few hours after the onset, and the prognosis is good. The prognosis of patients with vasospasm and incomplete obstruction is better; the prognosis of branch obstruction is better than that of trunk obstruction; the obstruction occurs after the central retinal artery enters the optic nerve hard sheath and before entering the optic nerve fiber bundle, so it is easy to establish the lateral branch quickly. Cycling, prognosis is also superior to obstruction occurring at the site of the hard sheath and into the visual fiber bundle.
Complication
Central retinal artery occlusion complications Complications glaucoma
Patients with neovascularization often have internal carotid artery stenosis, resulting in long-term retinal arterial hypoperfusion and ischemia, inducing neovascularization and glaucoma.
Symptom
Central retinal artery occlusion symptoms common symptoms retinal edema blind spot retinal hemorrhage fundus changes light reflex disappearance angiography abnormalities
Regardless of the trunk or branch obstruction, according to the above clinical manifestations, a diagnosis can be made. When the main artery obstructs the central venous obstruction, the artery can be hidden due to extensive hemorrhage and edema of the Kennedy. It is easy to be misdiagnosed as a separate central vein only by the fundus. Dry obstruction can be identified by a sudden loss of visual function, and clinical manifestations vary depending on the location of the blockage (trunk or branch obstruction) and extent (complete or incomplete obstruction).
When the trunk is completely blocked, in most cases, the visual function is completely lost within a few minutes or less, the pupil is dilated, and the light reflection disappears directly, but some diseases still retain a narrow light-sensitive area around the side of the visual field. The reason may be that the retinal visual part of the nasal retina extends forward more than the temporal side, while the peripheral full-thickness retinal nutrition is related to the double supply of the choroid and the retinal artery. In some cases, the small island of the visual field may remain in the vicinity of the physiological blind spot. The retina around the optic disc is caused by blood supply through the small branch of the Zinn-Haller ring or the posterior ciliary artery and the retinal blood circulation. Under the ophthalmoscope, the optic disc remains in the original color, the retinal artery is highly narrow, and the blood column color is Darkening, the reflected light in the center of the tube wall becomes very narrow, or even disappears, the small branch of the distal end is not easy to see, the diameter of the vein is also narrowed, and sometimes the blood column breaks into a segmental shape and moves slowly, the entire retina, In particular, the retina of the posterior pole is milky white, and the fovea of the macula has no retinal lining and is not affected by the central blood supply of the retina. The red color, in contrast to the milky white turbidity, is a contrasting round or round red or brownish red spot called cherry redspot, but there are also a few cases, because the edema is particularly strong and wrinkles are formed. Covering the fovea and making the cherry erythema invisible, 1 to 2 weeks after the obstruction, the retinal opacity gradually subsided from the peripheral part to the posterior pole, and the retina recovered transparent, close to the original fundus color, and the inner layer was trapped in necrotic atrophy. The visual function is unlikely to recover, the retinal artery is still extremely narrow, the wall is degenerated and thickened, white sheath or white line can appear, the diameter of the vein is small, and sometimes the parallel white sheath is visible. The fundus of the posterior pole often has pigmentation disorder, that is, pigmentation And the bleaching small dots have a rough granular appearance, and the optic disc is faded and pale, and the boundary is clear, which is called vascular optic atrophy.
The main incomplete obstruction, depending on the function and the change under the ophthalmoscope, also varies according to the degree. The light retinal artery diameter does not change significantly, the retinal opacity is slight, the visual function damage is relatively light, and the severe one is close to the complete obstruction. Occasionally, the blood column in the artery is in a segmental eccentric slow flow.
Branch obstruction, retinal artery branches can be blocked, the upper branch is more common, when the branch is completely blocked, the branch diameter is narrow, the blood supply area retinal edema is cloudy, the corresponding field of view suddenly disappears, if the macula Also included, cherry erythema appears, the central vision drops sharply, the branches are not completely blocked, and the fundus changes and visual function damage vary depending on the degree of obstruction.
When the central retinal artery is obstructed, a few retinal bleeding points are occasionally seen, mostly near the optic disc. This small bleeding point occurs after several weeks of obstruction, which may be due to the expansion and rupture of new small blood vessels or leakage of capillaries due to hypoxia damage. If the fundus has a wide and dense flaky or flaming retinal hemorrhage, it is a combined venous obstruction.
About 15% of people in China have ciliary retinal arteries (Zhang Meixin, 1979). When the central retinal artery is obstructed, if the patient has such an abnormal artery, the optic disc can still be preserved because of the arterial blood supply. A small piece of normal color of the retina (usually including the macula), so that the residual part of the central vision, and vice versa, this abnormal artery can also suddenly block, the retina of the optic disc is pale, edema turbid, central vision drops sharply, and there is a central dark point.
Examine
Examination of central retinal artery occlusion
Because of the interval between angiography and obstruction, the location and degree of obstruction, and the compensatory and reconstructed blood circulation after occlusion are different, so that the angiography can be seen differently. There is no perfusion from the artery, the filling is slow, the small branch is not perfused until the filling is completely normal. All can be seen, in general, there are several performances:
Fluorescence angiography in the early stage of the disease: Clinically, there is no chance of performing fluorescein angiography immediately after the occlusion. The so-called early stage of the disease actually refers to angiographic changes after hours or days.
When the trunk is completely blocked, the retinal artery is not perfused with fluorescent dye, but the capillaries of the optic disc are supplied by the ciliary artery, but the pigment is filled quickly, and the expansion is obvious, forming a side branch anastomosis, and rapidly returning to the central vein root on the optic disc. The dye is accumulated in the proximal end of the vein trunk, and at the same time presents a special countercurrent phenomenon, that is, the dye is retrogradely filled from the vein trunk to the external optic disc branch.
When the main occlusion of the trunk is suddenly relieved, or when the trunk is incompletely blocked, the angiography is different depending on the degree of occlusion at the time of angiography. The heavier occlusion is characterized by a slow fluorescence filling, and the retinal artery completes the circulation time. The normal eye is about 1 ~2s, while the blocked arteries can be extended for 30 ~ 40s, the fluorescence time of the vein is also very slow, the normal arterial phase to the early vein difference is only 1 ~ 2s, and at this time can be extended for 30 ~ 40s, the vein fluorescence is dim or Granulated, suggesting that the blood is severely impaired, the degree of obstruction is mild, and the filling time of the artery and vein is slightly longer or completely normal.
When the branch is completely obstructed, a sudden interruption of blood flow to the obstruction can be seen, where there is fluorescence leakage in the tube wall, and another indication of complete branch obstruction is retrograde filling, due to the relatively low pressure at the distal end of the obstructing branch. It is possible to return blood from the capillaries, so that on the fluorescent sheet at the beginning of the occlusion, it is seen that the dye perfusion at the distal end of the artery is earlier than the proximal end of the obstruction.
The branch is incompletely blocked, and there is no fluorescence leakage in the wall of the obstruction. The fluorescence filling time of the artery branch is slightly longer or completely normal than other normal branches.
Late stage of the disease refers to weeks or even months after the occurrence of occlusion. At this time, the fluorescein angiography in the main or branch-completed obstruction eyes is normal due to the iliac artery circulation, but the venous venous stenosis, vascular sheath The collateral vessels and capillaries without perfusion area can still be seen, and sometimes abnormal fluorescence such as microaneurysms, neovascularization, and retinal proliferative membranes can be found.
Diagnosis
Diagnosis and identification of central retinal artery occlusion
Differential diagnosis should be differentiated from vascular diseases and optic nerve diseases such as diabetic retinopathy, venous obstruction, foveal telangiectasia, ischemic optic disc disease, optic discitis, and the important identification point is the existence of radiotherapy history. Central retinal vein occlusion (CRVO): optic disc edema can occur, veins are obviously distorted, but CRVO is often unilateral, sudden onset, more extensive bleeding, mainly flaming hemorrhage, early no hard exudation. FFA can help with identification.
