Retinal artery occlusion
Introduction
Introduction to retinal artery occlusion The central retinal artery and its branches belong to the peripheral arteries. In addition to the retinal ciliary artery, it is the only blood vessel that supplies nutrients to the inner layer of the retina. Blood supply disorders can cause retinal ischemia and hypoxia, which seriously impair visual function. Obstruction of the central retinal artery causes acute ischemia of the retina and severe decline in vision, which is one of the blind emergencies. Therefore, early diagnosis should be made and rescued immediately. If there is a retinal ciliary artery, a certain central visual acuity can be retained. basic knowledge The proportion of illness: 0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: glaucoma, neovascular glaucoma, central retinal artery occlusion, optic atrophy
Cause
Cause of retinal artery occlusion
(1) Causes of the disease
The disease mostly occurs in the elderly with hypertension (64%), diabetes (24%), heart disease (28%), carotid atherosclerosis (32%), young patients are relatively rare, the incidence is often accompanied by bias Headache (1/3), abnormal blood viscosity, blood disease, oral contraceptives and trauma, or endocardial neoplasms due to rheumatic heart disease.
(two) pathogenesis
The direct causes of retinal vascular occlusion are mainly vascular embolism, vasospasm, changes in blood vessel wall and thrombosis, and compression of blood vessels from the outside, which may be caused by a single factor, or may be caused by the above factors.
1. Vascular embolization is mainly caused by various types of emboli into the central retinal artery, resulting in vascular obstruction. The embolus is often located at the sieve plate. Because the central retinal artery passes through the sieve plate, the diameter of the tube is narrowed, especially in the elderly. The embolus is more likely to remain here; secondly, the embolus is often located at the bifurcation of the posterior pole. The common emboli have the following categories:
(1) Cholesterol emboli: the most common embolus, accounting for 87%, 67.5% of the embolus originated in the carotid artery, aortic or large blood vessels with progressive atherosclerosis, due to atheroma necrosis The ulcer is exposed to the bloodstream, and the cholesterol-containing substance falls off and becomes an embolus into the central retinal artery. This embolus is relatively small and has a yellow reflection. It is usually located at the bifurcation of the temporal branch artery, especially the upper branch of the iliac crest. Involved, it can be blocked by a single embolus, or it can be a majority. The embolus is located in multiple small arteries around the macula, causing blood flow to be blocked. The degree of obstruction varies with the size of the embolus. After a few days, the embolus migrates to the distal end of the blood vessel. It will disappear completely after about 3 months.
(2) platelet fibrin emboli: common in patients with ischemic heart disease, chronic rheumatic heart disease and carotid embolism, due to hardening of the arteries, endothelial cells are damaged, resulting in loss of smoothness of the inner wall, and proliferation under the endothelium, tube The cavity narrows, platelets and fibrin accumulate on the rough surface of the vascular endothelium to form thrombotic plaque, and the plaque can fall into the retinal blood flow after detachment. This embolus is relatively large, grayish white body, which can completely block the blood flow of the retina. Suddenly complete blindness, the smaller embolus can disappear completely after a few days of fibrinolysis, the blood circulation is restored, and the large embolus can be intravascularized, resulting in the formation of white sheath in the blood vessel wall.
(3) calcification emboli: relatively rare, accounting for 4% of retinal emboli, derived from calcified aortic or mitral valve, or atherosclerotic plaque of ascending aorta and carotid artery, patients often have rheumatic heart disease Or other valvular heart disease, the embolus is mostly single, white and dull, oval, relatively firm, the embolus is located near the sieve plate or enters the first level branch, is not easy to absorb, and is located in the retinal artery for a long time.
(4) Other rare embolisms: including tumor emboli, such as atrial myxoma; fat emboli are found in patients with long bone fracture; sepsis emboli is found in subacute bacterial endocarditis; silicon emboli is found in various molding or beauty Surgical injection of silicon preparation; drug embolism can occur in the injection of cortisone around the eyes; other gas embolism, talcum powder emboli and so on.
2. Vasospasm occurs in young people with no vascular lesions but unstable vasomotor, patients with early hypertension, but also in elderly patients with arteriosclerosis, mild retinal vasospasm, patients feel short The blurred vision, strong paroxysmal vasospasm can completely block the blood flow, resulting in transient black Mongolian, if the sputum is quickly relieved, vision can return to normal, the frequency and duration of sputum varies with the degree of the disease, can be more 1 time to 1 day, several times, durations ranging from a few seconds to a few minutes, repeated sputum can also impair visual function, vasospasm can often be induced by other reasons, such as flushing the vagina, flushing the paranasal sinus or changing posture It can also occur in a variety of infectious diseases, such as influenza or malaria, or exogenous toxins, such as tobacco, alcohol, quinine and other poisoning, vasospasm often combined with migraine or hearing loss.
3. Vascular wall changes and thrombosis due to arteriosclerosis or atherosclerosis, vascular endothelial cells are damaged, subendothelial proliferation and degeneration, the vascular endothelium is rough, the lumen is narrowed, and thrombus is easily formed, and various inflammations can also directly invade Arteritis occurs in the arterial wall, such as giant cell arteritis, systemic lupus erythematosus, multiple nodular arteritis, scleroderma, and dermatomyositis. Inflammation causes infiltration of blood vessel wall cells, swelling, obstruction of the lumen, inflammation, infection. Or toxins can also irritate blood vessels, causing spasms, contractions and obstructions.
4. External compression of the blood vessels such as glaucoma, optic disc burying drusen, retinal detachment surgery such as scleral cerclage, intraocular injection of inflation gas, orbital surgical trauma, excessive electrocoagulation to stop bleeding, post-ball tumor or traumatic post-ball hemorrhage, etc. Retinal artery occlusion can be induced by various causes of increased intraocular pressure and pressure.
Central retinal artery occlusion is often a multifactorial disease, which is the basis of vascular disease, combined with embolism or other inducement to cause disease.
5. Others, such as trauma, surgery, parasites and tumors, as well as post-balloon bleeding after anesthesia, can cause central retinal artery occlusion.
Prevention
Retinal artery occlusion prevention
The disease is related to systemic vascular disease, and attention should be paid to controlling hypertension, arteriosclerosis, avoiding emotional agitation, paying attention to controlling intraocular pressure during and after eye surgery, and promptly finding timely treatment. Avoid eating too much animal fat and vegetable oils containing saturated fatty acids, such as: fat, lard, bone marrow, cream and its products, coconut oil, cocoa butter, etc., avoid eating more foods with higher cholesterol, such as : liver, brain, kidney, lung and other internal organs, squid, oysters, cuttlefish, caviar, shrimp, crab yellow, egg yolk, etc.
Complication
Retinal artery occlusion complications Complications glaucoma neovascular glaucoma central retinal artery obstruction optic atrophy
Because the inner layer of the retina does not have the ability to induce neovascularization due to ischemic necrosis, neovascularization and neovascular glaucoma are rare. Retinal artery occlusion generally does not produce neovascular glaucoma, unless at the same time combined with internal carotid artery stenosis, resulting in long-term Retinal artery hypoperfusion ischemia, retinal central artery obstruction in the iris may have neovascularization, the incidence rate is 16.6%, chronic ischemia and retinal artery occlusion are two independent features of carotid artery disease, can occur simultaneously, or first After one, the most common complication of central retinal artery occlusion was optic atrophy. After 2 and 3 weeks of onset, optic nerve atrophy began to appear in the central retinal artery. The fundus examination showed pale papillary and narrow retinal artery such as silver. Shape, the visual function of the affected eye is seriously impaired.
Symptom
Symptoms of retinal artery occlusion common symptoms visual field defect light reflex disappearance diabetes optic nerve atrophy retinal artery occlusion angiography abnormal retinal edema
Before occlusion, there may be vasospasm, and the patient has a transient black sputum for a few seconds or a few minutes. If the branch vessel is blocked, the retina supplied by the vertebral artery will have visual field defects due to loss of function, and the occlusion time is very short. Vision and visual field defects can be partially restored.
According to the site of retinal artery occlusion, it is divided into central total trunk obstruction, branch obstruction, anterior capillary arteriolar occlusion and ciliary retinal artery occlusion.
1. Central retinal artery occlusion The obstruction site is near the sieve plate or above the sieve plate. According to the degree of obstruction, it can be divided into complete and incomplete obstruction. The complete symptoms are severe, the attack is rapid, and the visual acuity can be sudden. Loss, or even reduced to no light, some patients (24%) have aura symptoms, that is, there is a sudden black eye in one eye, a history of vision recovery after a few seconds or minutes, repeated attacks, and finally a sudden loss of vision The eye examination is enlarged, and the light reflection disappears or is extremely slow. After the fundus examination, the nerve fiber layer and the ganglion cell layer are thickened by the swelling of the mist, especially in the area where the number of ganglion cells in the macula. Obviously, the retinal milky white diffuse edema is turbid, usually 1 to 2 hours after the obstruction, and also reported to occur 10 minutes after the obstruction. Because the choroidal circulation is normal, the choroidal blood vessels are red through the thin macular tissue, so the yellow spot is cherry red. Point, if there is supply of ciliary retinal artery, the retina of the area is a tongue-shaped orange-red area; if this is the ciliary-like network When the arteries supply the macula, the central vision can be preserved, and the optic disc is light. If the ischemic optic disc disease is combined, the color is lighter, the boundary is blurred, the mild edema, the central retinal artery and its branches become thinner, and the diameter is irregular. The small arteries are almost indistinguishable, the acral pressure can not induce the arterial pulsation, the venous diameter is also thin, the blood flow is stagnant in a segmental shape, and can move back and forth in the blood vessel. Some patients have a little flaming hemorrhage and a small amount of cotton wool spots. The field of view can be completely lost, with a tubular field of view, or a small island-like field of view on the temporal side. The ERG examination is a typical negative phase wave in the complete obstruction. Since the b wave originates from the inner nuclear layer, the b wave is reduced, and the a wave is Originated from the photoreceptor cell layer, it is supplied by choroidal blood vessels, so it presents a negative wave pattern. After 2 to 6 weeks of onset, the retinal edema gradually subsides, the inner layer of the retina recovers transparent and dark red, the red spot of the yellow spot disappears, and depigmentation occurs. Pigment hyperplasia, due to atrophy of the inner retina, retinal edema subsided after the visual function can not be restored, the central retinal artery and veins are thin, may be accompanied by white sheath, and some arteries are silver Filamentous, optic atrophy, pale disc, very few patients with central retinal vein occlusion, visible large retinal hemorrhage, blood vessels hidden in the edema of the retinal tissue, easy to miss the arterial occlusion, according to the patient's visual acuity suddenly dropped to no light Or manually can be identified, venous obstruction is generally not as rapid and severe as visual acuity.
Some patients have incomplete retinal artery occlusion, less severe visual acuity, mild retinal artery stenosis, mild edema of the retina, and a slightly better prognosis than complete.
Fluorescein angiography is different due to the degree of vascular occlusion, location and contrast time. The fluorescence images are very different. The angiography is performed hours or days after occlusion. The retinal circulation time is prolonged, which is characterized by slow filling of arteries and veins. There is no fluorescein perfusion in the lumen of the arteries, and the optic disc from the small branch of the ciliary artery can be filled. Fluorescein is retrogradely filled by the central vein of the optic disc capillary into the optic disc. Due to the low perfusion of the arterial, the lumen of fluorescein in the lumen becomes fine. , or in the form of segments, fluorescein can not enter the small arterial terminals and capillaries to form a non-perfusion area, especially the fluorescein filling of the arterioles around the macula suddenly stops, such as branches broken (Figure 1), small blood vessels around the macular area There may be mild leakage and hemangioma-like changes. After several weeks or in cases of incomplete occlusion, blood flow can be completely recovered. Fluorescence angiography can be found without abnormalities, but in some cases there may still be capillary non-perfusion areas, arteries. The pipe diameter is reduced.
2. Branch retinal artery occlusion is caused by embolus or thrombosis. The branch of the temporal branch is often involved, especially in the upper branch of the iliac crest. The degree of visual impairment and fundus performance are determined according to the location and extent of the obstruction. The obstruction point is usually at the large blood vessel around the optic disc or at the large bifurcation. It can be seen that there are white or yellowish bright bodies in the obstruction. The retina of the obstruction branch is fan-shaped or quadrant-shaped milky white edema, such as the yellow spot. Cherry red spots may appear, the arteries become thinner, the corresponding veins become thinner, the visual field is quadrant defect or bow-shaped dark spot, ERG is normal or slightly changed, and fluorescein angiography shows that the blocked arteries and corresponding venous filling are delayed compared with the distal obstruction In some cases, fluorescein leakage was observed in the vascular wall blocked by the embolus. Retinal edema subsided after 2 to 3 weeks, the obstructed branch artery became thin and white sheathed, and the fluorescein angiography returned to normal. In a few cases, the obstruction branch and the ciliary vessel Or the obstruction branch forms a collateral circulation.
3. Precapillary arteriole occlusion Preacute anterior capillary arteriolar occlusion may be associated with vascular endothelial damage, thrombosis, vascular inflammation or abnormal erythrocyte occlusion and other factors, which can be seen in hypertension, diabetes or radiation sickness. Caused by retinopathy or systemic lupus erythematosus, sickle cell retinopathy, leukemia and other blood diseases, due to occlusion of the anterior small arteries, leading to ischemia, inhibition of nerve fiber axoplasmic transport, axoplasmic organelle aggregation swelling, fracture formation of cells Cystoid body, under the ophthalmoscope, a cotton-like soft exudate plaque, fluorescein angiography can be seen in the plaque-like non-perfusion area, adjacent to telangiectasia, some dilatation like tumor, late fluorescein leakage, according to anterior small artery occlusion The size and location of the range, visual acuity can be normal or decreased, the visual field is normal or dark spots, cotton-like spots disappear after several days or weeks, small arteries are re-perfused, the reconstructed capillary bed is in a tortuous state, and the late retinal inner layer is locally deformed. Thin, increased transparency, forming a concavity concave reflective area, indicating that the retina There ischemic changes.
4. Ciliary retinal artery occlusion Clinically, ciliary retinal artery occlusion can be seen clinically. Brown reported that 27 cases of young arterial occlusion have 5 cases of ciliary retinal artery occlusion, most of which are located in the macular area of the retinal nipple. The ciliary retinal artery can supply the macula long, and the visual acuity is severely damaged. If the macula is not supplied, the central visual acuity is not affected. The fundus has a tongue-shaped or rectangular milky white edema area, and the corresponding visual field defect is the same as the branch artery occlusion. .
Regardless of the trunk or branch obstruction, according to the above clinical manifestations, a diagnosis can be made. In the case of trunk obstruction combined with central venous obstruction, due to extensive hemorrhage and edema of the fundus, the arterial condition can be concealed, and it is easy to be misdiagnosed as simple by the fundus. Central venous obstruction, but can be identified from a sudden loss of visual function.
Examine
Examination of retinal artery occlusion
Fundus performance: After more than a few minutes of occlusion, anemia necrosis will occur in the fundus, the optic disc will be white, the edges will be blurred, the posterior pole of the retina will be diffuse milky white edema, the macular area will be thin due to retinal tissue, and the choroidal capillaries will reveal "cherry erythema". It is a typical sign of the disease. Generally, the retinal edema subsides after two weeks, but the retinal artery is as small as the line, the optic disc is paler, and the vision cannot be restored.
Fluorescence angiography of retinal artery occlusion is as follows:
1 When the central artery is obstructed, the artery is not perfused, and when the branch artery is blocked, the blood flow is interrupted or retrograde at a certain point of the branch (the dye perfusion at the distal end of the artery is blocked earlier than the proximal point of the arterial obstruction point), and the late obstruction point has high fluorescence. .
2 The filling is slow, the retinal artery completes the circulation time is about 1 to 2 seconds, and the blocked artery can be extended to 30 to 40 seconds.
3 There was no perfusion of small branches of the macular area. After a few days, arterial blood flow reappeared.
Within a few hours after arterial occlusion, the b-wave of the electroretinogram (ERG) rapidly diminished.
Fluorescence angiography showed that the retinal capillary bed was not filled except for the retinal capillaries outside the optic disc area.
1. Blood rheology examination can understand the viscosity of blood.
2. Pathological changes Once the central retinal artery is blocked, the blood flow is interrupted, and the inner layer of the retinal neuroepithelial layer is immediately hypoxic and necrotic. The severity and speed of the retinal nerve epithelial layer are completely consistent with the obstruction. It is reported that the tissue is completely blocked 3 hours after the experiment. Examination, it has been seen that the inner layer of the neuroepithelial membrane is ruptured, nuclear chromatin accumulation, cell autolysis and fluid loss, after which the endothelial cells and inter-wall cells of the capillary wall degeneration, leaving large cells without cells, no functional capillary In the vascular area, after necrosis of the inner layer of the retina is absorbed, it is replaced by glial.
Fluorescein fundus angiography (FFA) examination: due to the interval between angiography and obstruction, the location and degree of obstruction are different. The blood circulation compensation and reconstruction after occlusion are different, so that the angiography is different, and there is no perfusion from the artery, and the filling is slow. Small branches can be seen without filling until the filling is completely normal. Generally, the following types of performance are common:
1. Early in the course of the disease: Clinically, the chance of performing FFA immediately at the beginning of the blockage is arguably absent. The so-called early stage of the disease actually refers to the angiographic changes after hours or even more than 24 hours.
When the trunk is completely blocked, the retinal artery has no fluorochrome perfusion, but the optic disc has capillaries that are supplied by the ciliary artery, but it quickly fills in fluorescence and expands significantly, forming a side branch anastomosis, and rapidly returns to the central venous root of the optic disc. The contrast agent is perfused into the proximal end of the venous trunk, and at the same time presents a special countercurrent phenomenon, that is, the fluorescence is retrogradely filled from the vein trunk to the external optic disc branch.
When the main occlusion of the trunk is suddenly relieved or not completely blocked, the angiography is different due to the degree of obstruction at that time. The more obstructive ones are characterized by slow fluorescence filling, the retinal artery is fully filled, and the normal eye is 1 to 2 s. The obstructed arteries can be extended by 30 to 40 s. Therefore, the time of the fluorescent laminar flow (early venous phase) in the arterial phase to the vein is also very slow. The normal phase difference is only 1 to 2 s, while the time is 30 to 40 s, and the venous fluorescence is dim or Granulated, suggesting that the blood circulation is severely impaired, the degree of obstruction is mild, and the filling time of the movement and vein is slightly extended or completely normal.
Complete branch obstruction During angiography, a sudden interruption of blood flow to the obstruction can be seen, where there is fluorescence leakage in the tube wall, and another indication that the branch is completely blocked is retrograde filling, due to the relatively low pressure at the tip end of the obstruction. It is possible to return blood from the capillaries, so that the fluorescein perfusion at the distal end of the artery is earlier than the proximal end of the obstruction on the initial fluorescent sheet.
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.
2. Late stage of the disease: refers to several weeks or even months after the onset of the disease. At this time, the FFA completely obstructs the eye in the trunk or branch. Although the filling time of the artery returns to normal due to the formation of the collateral circulation, the diameter of the vein is narrow. The vascular sheath, collaterals, and capillaries can still be seen. Sometimes, abnormal fluorescement such as microangioma, neovascularization, and pseudofluorescence of the retinal proliferative membrane can be found. The visual field examination shows quadrant defect or arcuate darkness. Point, ERG is normal or has a slight change.
Diagnosis
Diagnosis and diagnosis of retinal artery occlusion
diagnosis
Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.
Differential diagnosis
1. Anterior ischemic optic neuropathy: frequent bilateral eye disease, the fundus showed obvious papilledema, mild or moderate visual acuity, and the visual field damage was a curved dark spot connected to the physiological blind spot.
2. Ocular artery obstruction: visual function damage is more serious, visual acuity is usually light or no light, intraocular pressure is reduced, retinal edema is more serious, there may be no "cherry red" in the macular area, but the central artery and ciliary of the retina The blood supply of the arteries is interrupted at the same time, so the edema of the retinal edema is more serious than the disease at the time of onset, and the range is also wider. The erythema of the cherry can not be seen (due to choroidal circulation damage), and the late stage of the disease has significant pigmentation in the posterior pole of the fundus. Disorders (pigment hyperplasia and depigmentation), ERG check a, b wave is extinguished or nearly extinguished.
