Retinal angiospasm is a functional disorder caused by a sharp narrowing of the central retinal artery (CRA) or its branches, without organic changes in the vascular wall. Clinical manifestations are represented by blurred vision, the appearance of “flies”, photo- and metamorphopsies in front of the eyes, discomfort in the ocular region. The main diagnostic methods are ophthalmoscopy, non-contact tonometry, angiography and optical coherence tomography (OCT) of the retina. Treatment tactics are reduced to the appointment of antispasmodics, plasma substitutes, beta-blockers, saluretics and carbonic anhydrase inhibitors.
H35.9 Unspecified retinal disease
Retinal angiospasm is an urgent condition in clinical ophthalmology that requires immediate medical intervention. According to statistics, in 91.2% of cases, an acute violation of blood flow in the central artery occurs against the background of pathologies from the cardiovascular system. The most frequent of them are atherosclerosis and arterial hypertension (60%). In 25-30% of cases, it is not possible to establish the etiology of retinal vascular spasm. The disease occurs at any age, but more often attacks are traced after 40 years. Men get sick 2 times more often than women. Pathology is widespread everywhere.
The etiology of the disease is not fully understood. Idiopathic forms of the disease are often observed when it is not possible to find out the genesis of the pathology. In children, spastic contraction of the middle layer of the arteries is caused by autonomic dysfunction and features of the formation of the peripheral nervous system. In adulthood, the main causes of retinal angiospasm include:
- Hypertension. In response to an increase in blood pressure, reflex vasospasm occurs, including in the orbital region. This phenomenon is associated with the release of catecholamines, which have a pressor effect on the receptors of the vascular wall.
- Diabetes mellitus. People with decompensated form of diabetes mellitus have a high risk of progression of diabetic retinopathy. This pathology is accompanied by frequent episodes of angiospasm.
- Atherosclerosis. With an atherosclerotic lesion of the endothelium, blood pressure increases and perfusion is disrupted. The response to hypoxia is represented by a spastic contraction of the muscle layer of the CRA.
- Bad habits. Narrowing of the retinal artery is a consequence of excessive exposure to nicotine in smokers and ethyl alcohol in people who abuse alcoholic beverages. These substances lead to a temporary narrowing of the vascular lumen, which is replaced by dilation.
- Intoxication. The tone of the vascular wall increases with poisoning by carbon disulfide and lead compounds. Such reactions are typical for people working in harmful production conditions and suffering from chronic intoxication.
Persistent, uncontrolled contraction of myocytes of the middle layer of the vascular wall is caused by a violation of ion transport. With an increase in the concentration of calcium ions and a decrease in sodium and potassium ions, the tone of the smooth muscle layer increases. In turn, with a sharp narrowing of the lumen of the vessels, the blood flow is limited or completely stops. This leads to ischemia of the surrounding tissues and impaired retinal trophic function. With prolonged intoxication, angiospasm develops due to an increase in the tone of the sympathetic nervous system. In patients with diabetes mellitus, insulin resistance is progressing, and at the same time, the degree of stiffness of the vascular wall. The increase in the pulse wave velocity confirms this theory.
Pathology is characterized by bilateral, less often – unilateral lesion. Patients complain about the appearance of “fog” and the flickering of “flies” in front of their eyes. Blurred vision with short-term spasm is transient. It is also possible to distort visual perception in the form of meta- and photomorphopsies. Less often there is a feeling of discomfort in the area of the eye socket on the side of the lesion. Often there is a feeling of pulsation in the temples, dizziness, headache. After the end of the attack, the general condition of the patient is completely normalized, and visual dysfunction is leveled. In severe cases, prolonged ischemia leads to an irreversible decrease in visual acuity.
Prolonged angiospasm causes a sharp irreversible decrease or complete loss of vision. Frequent seizures lead to severe discomfort and impaired performance, because patients cannot anticipate the time of the development of the next episode. Recurrent angiospasm contributes to an increase in intraocular pressure. Over time, patients develop secondary ophthalmohypertension. Periodic spastic contractions of arterioles and small arteries lead to an increase in the clinical picture of ocular migraine. However, short-term attacks of arteriospasm occur without complications.
The diagnosis of retinal angiospasm is established on the basis of anamnestic information, the results of an objective examination and additional diagnostic methods. At the time of the attack, hyperemia and swelling of the conjunctiva are possible. After the end of the angiospasm episode, there are no visual changes in the anterior segment of the eyes. The following studies are used to make a diagnosis:
- Ophthalmoscopy. When examining the fundus, a sharply narrowed CRA and its branches of small caliber are visualized. The veins are full-blooded. The disc of the optic nerve at the time of the attack is pale pink, edematous. The macular and foveolar reflex are not determined.
- Non-contact tonometry. An angiospasm attack is accompanied by a slight increase in intraocular pressure. After the symptoms of the disease are relieved, the ophthalmotonus is normalized. If this does not happen, an additional electronic tonography of the eye should be performed.
- Retinal angiography. The study makes it possible to visualize changes in retinal vessels by studying the features of fluorescein circulation. In patients with angiospasm, the internal hemoretinal barrier remains impervious to contrast.
- OCT of the retina. When scanning the central area of the retina, a sharp thickening of the macula is noted. The foveolar depression is completely smoothed out, and the reactivity of the retina is reduced. The shape of the curve is atypical – straight.
Retinal angiospasm treatment
Etiotropic therapy has not been developed. Pathogenetic treatment is aimed at dilating spasmodic vessels in order to restore retinal blood flow in the ischemic area. It is very important to stop the symptoms of angiospasm in a timely manner, because a prolonged violation of microcirculation leads to complete or partial loss of vision. Therefore, immediately after the examination of the fundus, infusions of antispasmodics and plasma substitutes are prescribed. The next stage of treatment is electrophoresis with peripheral vasodilators and vasodilators.
Saluretics and carbonic anhydrase inhibitors are used to reduce intraocular pressure. If there is no effect, an irrigation system is installed in the retrobulbar space. Instillations of beta-adrenergic receptor blocker solutions are shown. With a concomitant increase in systemic blood pressure, drugs are administered intramuscularly. Peptide bioregulators are used to stimulate the regeneration of the receptor apparatus. In severe pathology, retrobulbar administration of M-cholinolytics is additionally indicated.
Prognosis and prevention
The prognosis for angiospasm depends on the nature of the attack. The short-term narrowing of the small branches of the CRA of the eyeball passes without a trace. Vasospastic reactions lasting more than 15 minutes, when irreversible changes occur on the part of the retina, are considered unfavorable in prognostic terms. Specific preventive measures have not been developed. Nonspecific prevention is reduced to the control of blood pressure and blood glucose levels, taking statins for atherosclerosis, the use of personal protective equipment when working with pesticides in production conditions.