Occlusion of retinal arteries

The retinal artery occlusion has the following types:

1. Occlusion of the branch of the central artery of the retina.
2. Occlusion of the central artery of the retina.
3. Occlusion of the ciliary regulating artery.

[1], [2], [3], [4], [5], [6], [7]

Causes of occlusion of retinal arteries

1. Atherosclerotic thrombosis at the level of the latticed plate remains the most common cause of occlusion of the central artery of the retina (about 80% of cases).
2. Embolism of the carotid originates from the bifurcation area of the common carotid artery. This is the most vulnerable part for atheromatous lesion and stenosis. Embolisms of the retina from the carotid are of the following types:
   • cholesterol emboli (Hollenhorst plaques) - an intermittent cluster of small, bright golden and yellow-orange crystals, which are usually located in the region of arteriolar bifurcations. They rarely cause significant obstruction of the retinal arterioles and often remain asymptomatic;
   • fibrinous emboli - grayish, elongated particles, usually plural, occasionally fill the entire lumen. They can cause transient ischemic attacks followed by amaurosis fugax and less often - complete obstruction. Amuurosis fugax is characterized by
     painless, transient, one-sided loss of vision, described as a "curtain before the eye", more often in the direction from top to bottom, less often - on the contrary. The loss of vision, which can be complete, usually lasts a few minutes. Recovery is also fast enough, but sometimes gradually. The frequency of seizures varies: from several times a day to once in several months. Seizures may be associated with ipsilateral cerebral TIA with manifestations on the contralateral side;
   • The calcified embolus can occur from atheromatous plaques in the ascending aorta or carotid arteries, as well as from calcified heart valves. They are usually single, white, without gloss and are often located near the optic nerve disc. When positioned on the disk itself, they merge with it, and they can be overlooked when viewed. Calcified emboli are more dangerous than the two previous ones, since they can cause permanent occlusion of the central arteries of the retina or one of its main branches.
3. Cardiac embolism accounts for about 20% of occlusion of retinal arterioles and is associated with an increased risk of cerebrovascular disease. Since it is the first branch of the internal carotid artery, embolic material from the heart and carotids easily enters the orbit artery. Emboli, originating from the heart and its valves, can be of 4 kinds:
   • cal cificated from aortic and mitral valves;
   • vegetation (proliferation) of the heart valves in bacterial endocarditis;
   • thrombi from the left ventricle of the heart, arising after myocardial infarction (mural thrombi), mitral stenosis with atrial fibrillation or mitral valve prolapse;
   • Myxomatous material derived from myxoma atrium.
4. Periarteritis associated with dermatomyositis, systemic lupus erythematosus, nodular polyarteritis, Wegener Graiulomatosis and Behcet's disease, can sometimes cause occlusion of branches of the central arteries of the retina, including several.
5. Thrombophilia, such as hyperhomocysteinemia, antiphospholipid syndrome and hereditary defects of natural anticoagulants, can sometimes accompany obstruction of the central retinal arteries in young patients.
6. Retinal migraine very rarely can cause occlusion of the central retinal arteries in young people. However, the diagnosis can be made only after excluding other, more common causes.

[8], [9], [10], [11], [12], [13]

Occlusion of the branches of the central artery of the retina

Occlusion of the branches of the central arteries of the retina is most often caused by embolism, rarely by periarteritis.

The occlusion of the branches of the central arteries of the retina is manifested by a sudden and significant violation of either half the field of vision or the corresponding sector. Deterioration of vision is different.

Ocular fundus

• Blanching of the retina in the field of ischemia due to edema.
• Narrowing of arteries and veins with slowing and intermittent blood flow.
• Presence of one or more emboli.

Foveal angiography reveals arterial filling delay and background fluorescence fuzziness due to retinal edema within the involved sector.

The prognosis is unfavorable, despite the fact that the obstruction takes place within a few hours. Defects of the visual fields and thinning of the affected artery remain. However, sometimes after recanalization of the occluded artery, ophthalmoscopic signs may be hardly noticeable or disappear altogether.

Central retinal artery occlusion

Occlusion of the central artery of the retina is most often a consequence of atherosclerosis, and can also be caused by calcified embolism.

Occlusion of the central artery of the retina is manifested by a sudden significant loss of vision. Visual impairment is significant, except for cases when the nutrition of a part of the papillomaculary bundle is carried out from the ciliary regulating artery and the central vision remains intact. Afferent pupillary defect - pronounced or total (amaurotic pupil),

Ocular fundus

• Thinning of arteries and veins with slowing and intermittent blood flow.
• Significant blanching of the retina.
• Around the thinned foveola is an orange reflex from an intact choroid, in contrast to the surrounding pale retina, which distinguishes a characteristic symptom of the "cherry bones".
• In the eyes with the ciliary regrowth of the macular area, the color of the retina does not change.

Foveal angiography reveals a delay in the filling of arteries and a weakening of the background fluorescence of the choroid due to retinal edema. However, in the early phase, it is possible to fill a passable ciliary regulating artery.

The prognosis is unfavorable and is caused by a retinal infarction. After a few weeks, the retinal blushing and the symptom of the "cherry stone" disappear, but the arteries remain intact. Internal layers of the retina are atrophied, a gradual atrophy of the optic nerve occurs, leading to a final loss of residual vision. In some cases, development of iris rumenosis is possible, requiring panretinal laser coagulation, in 2% of cases neovascularization occurs in the region of the disk.

[14], [15], [16], [17], [18], [19]

Occlusion of the Ciliary Regeneration Artery

The ciliary regulating artery is found in 20% of people, it occurs from the posterior ciliary arteries and feeds the retina mainly in the area of the macula and the papillomacicular fascicle.

Classification

• Isolated often occurs in young people with concomitant systemic vasculitis;
• in combination with occlusion of the central artery of the retina has a similar prognosis with nonischemic occlusion of the central vein of the retina;
• in combination with anterior ischemic neuropathy is more common in patients with giant cell arteritis and has an extremely unfavorable prognosis.

Occlusion of the ciliary regulating artery is manifested by a sharp, significant loss of central vision.

• Ocular fundus. Blanching of the retina is localized according to the area of artery perfusion.
• Foveal angiography reveals a corresponding filling defect.

Treatment of acute retinal artery occlusion

Treatment of acute occlusion of the retinal artery should be immediate, as it causes an irreversible loss of vision, despite restoration of blood flow in the retina, before retinal infarction develops. It is believed that the vision forecast is worse with occlusions caused by calcified emboli, than cholesterol or platelet. Theoretically, if the embolus of the latter two types breaks down over time, vision loss can be avoided.

In this regard, various mechanical and pharmacological methods are proposed, and a consistent, vigorous and systematic approach within 48 hours after acute occlusion of the retinal artery gives patients a good chance of restoring vision.

Urgent care

1. Massage the eyeball using a three-mirror contact lens for 10 seconds to restore pulsation in the central artery of the retina, then break for 5 seconds with a decrease in blood flow (with occlusion of the branch of the central artery of the retina). The goal is a mechanical slowdown, followed by a rapid change in the arterial blood flow.
2. Sublingually isosorbide dinitrate 10 mg (vasodilator and drag reducing agent).
3. Decreases in intraocular pressure are achieved by administration of acetazolamide 500 mg intravenously, followed by intravenous administration of mannitol 20% (1 g / kg) or oral glycerol 50% (1 g / kg).

Follow-up treatment

If urgent methods are unsuccessful and blood flow is not restored after 20 minutes, the following additional treatment is performed.

• Paracentesis of anterior chamber.
• Streptokinase intravenously 750,000 units for the destruction of the fibrinous embol in combination with methylprednisolone 500 mg is also intravenous to reduce the risk of allergies and bleeding in response to streptokinase.
• Retrobulbar injection of tolazoline 50 mg to reduce the resistance of the retrobulbar blood flow.

[20], [21], [22], [23], [24], [25], [26], [27], [28]