Central retinal artery occlusion is an acute blockade of the central retinal artery or its branches, leading to circulatory disorders and retinal ischemia. Central retinal artery occlusion is manifested by sudden loss of vision or sectoral loss of visual fields in one eye. In the diagnosis of retinal vascular pathology, the data of ophthalmological tests (visometry, perimetry), ophthalmoscopy, tonometry, fluorescence angiography and retinal tomography, electrophysiological studies of the function of the visual analyzer, etc. are taken into account. Detection requires immediate therapy: massage of the eyeball, paracentesis of the anterior chamber of the eye, reduction of IOP, administration of vasodilators and antiplatelet agents.
Central retinal artery occlusion, as a rule, develops in patients older than 60-65 years; at the same time, men are 2 times more likely than women. In most cases, occlusion is unilateral. In 60% of cases, circulatory disorder develops in the central artery of the retina and leads to permanent loss of vision in one eye. In 40% of patients, arterial occlusion affects one of the branches of the retinal artery, which is accompanied by loss of the corresponding part of the visual field.
Depending on the level of blockage of blood flow in ophthalmology, central retinal artery occlusion, occlusion of CRA branches and occlusion of the cilioretinal artery are distinguished. Disease can develop in isolation or be combined with occlusion of the central retinal vein or anterior ischemic optic neuropathy.
The mechanism of acute retinal circulation disorder may be associated with spasm, thrombosis, embolism, collapse of retinal arterioles. Most often, incomplete or complete occlusion is caused by blockage of retinal vessels with cholesterol, calcified or fibrinous emboli. In all cases, central retinal artery occlusion is a consequence of systemic acute or chronic pathological processes.
The main risk factors for the development of this disease in old age are arterial hypertension, atherosclerosis, giant cell arteritis (Horton’s disease). At a younger age, circulatory disorders in the retinal vessels may be associated with infectious endocarditis, mitral valve prolapse, damage to the valvular apparatus of the heart in rheumatism, cardiac arrhythmia, neurocirculatory dystonia, diabetes mellitus, antiphospholipid syndrome. Local provoking factors can be retinovasculitis, edema and druses of the optic disc, increased IOP, compression of the vessels of the orbit by retrobulbar hematoma, tumor, ophthalmological operations, etc.
A potential danger with respect to central retinal artery occlusion is hypercoagulation syndrome, fractures of tubular bones, intravenous injections associated with the danger of thromboembolism, fat or air embolism. The collapse of the retinal arterioles is possible with massive blood loss caused by uterine, gastrointestinal or internal bleeding.
As a result of spasm, thromboembolism or collapse of arterioles, blood flow in the affected vessel is slowed down or completely stopped, leading to acute retinal ischemia. In the event that blood flow can be restored within the next 40 minutes, partial restoration of impaired visual functions is possible. With prolonged hypoxia, irreversible changes develop in the retina – necrosis of ganglion cells and nerve fibers with their subsequent autolysis. The outcome is atrophy of the optic nerve and persistent loss of vision.
In most cases, central retinal artery occlusion develops suddenly and painlessly. At the same time, the patient notes an unexpected loss of vision in one eye, which occurs rapidly, literally within a few seconds. In about 10% of cases, episodes of short-term transient visual impairment occur. With CRA thrombosis, visual impairment may be preceded by photopsy phenomena – light flashes.
Less often, with central retinal artery occlusion, there is a sectoral loss in the field of vision. The degree of decrease in visual acuity varies from the preservation of the distinction of objects in the face to complete blindness.
The diagnosis is facilitated by the analysis of anamnestic data: the presence of cardiovascular, systemic, inflammatory, metabolic diseases, eye injuries, other vascular catastrophes (stroke, myocardial infarction, superficial and deep vein thrombosis of the lower extremities, obliterating endarteritis, etc.). The necessary examination includes ophthalmological tests, examination of the fundus, contrast radiography retinal vessels, laboratory tests.
Visiometry with central retinal artery occlusion reveals a decrease in visual acuity from 0 to 0.02-0.1. The degree of vision loss depends on the level of occlusion and the area of the ischemia site. With the help of perimetry, peripheral vision defects are detected (sectoral or central scotomas corresponding to the ischemic area of the retina, concentric narrowing of the visual field).
Biomicroscopy allows preliminary assessment of the degree of central retinal artery occlusion. Thus, with incomplete occlusion, an afferent pupillary defect is determined (Markus-Gunn pupil); with total occlusion, the pupil’s reaction to light is absent or sharply reduced.
Visual examination of the fundus by ophthalmoscopy reveals edema, loss of transparency, paleness of the retina and the disc of the optic nerve. Against this background, the central fossa of the macular region (cherry stone syndrome) is clearly distinguished, which has a brighter color due to the choroidal blood supply. Retinal arterioles are narrowed, have an uneven caliber; in the first days after the central retinal artery occlusion has developed, emboli can be seen in them.
Fluorescence angiography makes it possible to clarify the localization of a thrombus or embolus, to find out the degree of blockage of the vessel. Radiographic signs are the slowing or segmental nature of blood flow in retinal arterioles; with complete obstruction of the branches of CRA, it is a symptom of “vessel rupture”.
Electroretinography data are characterized by a decrease or absence of the amplitude of the recorded waves, indicating the destruction of ganglion cells and ischemia of the choroid.
Clarifying diagnostics for central retinal artery occlusion is carried out using ultrasound of the ocular vessels, optical coherence and laser scanning tomography of the retina, tonometry.
It is necessary to conduct a study of coagulogram and lipidogram, blood culture (in case of suspected bacterial embolism), duplex scanning of the carotid arteries, ultrasound of the heart, etc. In addition to an ophthalmologist, if indicated, a patient with central retinal artery occlusion should be examined by a cardiologist, vascular surgeon, rheumatologist, endocrinologist, hematologist, infectious disease specialist.
Treatment of central retinal artery occlusion should be initiated in the first hours from the moment of presenting complaints of decreased vision; otherwise, it will be impossible to restore vision. Emergency primary care includes a massage of the eyeball to restore blood flow to the CRA. In order to reduce IOP, instillation of eye drops is performed, diuretics are administered, corneal paracentesis is performed.
In case of central retinal artery occlusion caused by arteriole spasm, pathogenetic therapy includes the use of vasodilators (sublingual nitroglycerin, intravenous eufillin, intramuscular papaverine, etc.), inhalation with an oxygen mixture or hyperbaric oxygenation.
With CRA thrombosis, the use of thrombolytics and anticoagulants, probing of the branches of the ocular artery through the supraorbital artery, intravenous infusions of dextrans come to the fore.
With any type of occlusion of the central retinal arteries, it is advisable to take antioxidants, local retrobulbar and parabulbar injections of vasodilators, instillation of b-blockers. At the same time, corrective treatment of concomitant systemic pathology is prescribed.
The effectiveness of therapy largely depends on the timing of its initiation and is highest in the first minutes and hours from the moment of central retinal artery occlusion.
Prognosis and prevention
The outcome of central retinal artery occlusion in 1% of patients is neovascularization of the optic disc with the development of secondary neovascular glaucoma. The most frequent and formidable complication of pathology is optic nerve atrophy and blindness.
Restoration of vision is possible only at the beginning of the full volume of treatment during the first 40-60 minutes. from the moment of the development of arteriole occlusion in the event that the pathogenesis of vascular obstruction is due to their spasm. Patients who have undergone central retinal artery occlusion constitute a risk group for the development of acute vascular catastrophes with a fatal outcome.
Prevention is closely related to the need for timely treatment of concomitant pathology, the exclusion of provoking factors (smoking, stressful situations, heavy physical exertion, visiting baths and saunas, taking hot baths, long-term air travel, scuba diving, etc.). Persons who are at risk for the development of occlusion CRA should be regularly examined by an optometrist and receive preventive therapy.