Toxic amblyopia is a visual dysfunction caused by acute or chronic intoxication. Common manifestations for all forms are a progressive decrease in visual acuity, the appearance of “fog” or “flies” in front of the eyes, visual discomfort, impaired color perception. Diagnostics is based on visometry, biomicroscopy, perimetry, ultrasound of the eye, ophthalmoscopy, fluorescence angiography. Patients are shown etiotropic treatment, which is based on the introduction of sodium bicarbonate during methanol intoxication. Calcium lactate is used for lead poisoning, keratoprotectors – iodine.
General information
Toxic amblyopia was first described by the Austrian ophthalmologist G. Beer in 1817 in a patient with tobacco intoxication. Every year, about 10-12% of patients hospitalized in the ophthalmology department suffer from this pathology. Most often, the disease can be diagnosed in people of working age. According to statistics, in 16% of cases of methanol poisoning, complete blindness occurs, in 68% of cases, patients react only to the movement of the hand in front of their eyes. In 16% of cases, visual acuity exceeds 0.1 diopters. In ophthalmology, the disease occurs with the same frequency among men and women. Geographical features of the spread of pathology have not been studied.
Causes
The development of toxic amblyopia is provoked by household or industrial poisoning. Tolerance to the action of toxins decreases in patients with diabetes mellitus, atherosclerosis, hypo- and vitamin deficiency. The main causes of pathology:
- Tobacco intoxication. The disease develops in people who consume tobacco by smoking or chewing. In tobacco factory workers, the disease occurs due to inhalation of dust.
- Chronic alcoholism. Wine alcohol does not have a direct cytopathic effect on the optic nerve. However, secondary hypovitaminosis, which is characteristic of people suffering from alcoholism, leads to visual dysfunction.
- Poisoning with methyl alcohol. It is caused by its erroneous consumption instead of alcoholic beverages or inhalation of vapors in production conditions (production of cement, resin solutions, ceramics).
- Chronic lead intoxication. The defeat of the eyeballs occurs during the extraction of metal ore or the manufacture of products from this metal. The cause of poisoning is a violation of safety regulations.
- Iodine poisoning. Prolonged work with iodine leads to damage not only to the eyes, but also to all internal organs. Specific changes in the form of yellow-brown plaque on the conjunctiva or cornea make it possible to diagnose the signs of the disease as early as possible.
Pathogenesis
The development of clinical symptoms in tobacco intoxication is caused by exposure to cyanides, which are contained in large quantities in smoke. A decrease in vitamin B12 in the blood contributes to the progression of pathological changes. It has been proven that cyanides should normally be neutralized by this vitamin. With hypovitaminosis, they accumulate in the tissues of the body and potentiate dystrophic changes in the ganglion cells of the retina. In the pathogenesis of the alcoholic form, the leading importance is assigned not to the effects of alcohol, but to endo- and exogenous hypovitaminosis.
In the case of methyl alcohol poisoning, damage to the optical nerve fibers and retina occurs only at stage 3. The development of pathological changes provokes the effect of formaldehyde, which inhibits cellular respiration and the process of glucose oxidation. Even at a minimal dosage, formaldehyde leads to damage to the inner shell of the eyeball. Initially, ganglion cells are affected, then neurons of the visual pathways. In chronic lead poisoning, clinical symptoms develop only with a significant accumulation of the chemical element. Visual dysfunction is observed in almost all persons who have been in contact with iodine vapors for a long time.
Symptoms
In patients with this syndrome, both eyes are often involved in the pathological process, however, to varying degrees. Patients note a decrease in visual clarity, the appearance of a “veil” or “fog” in front of their eyes. The first manifestations of toxic amblyopia develop suddenly. At the same time, the severity of visual dysfunction during the day can vary widely. Patients complain of a violation of color perception. At first, the ability to perceive shades of the red spectrum decreases, then – white. Very often, patients absolutely do not distinguish the scarlet color. There is increased fatigue when performing visual load (reading books, working at the computer).
This pathology is characterized by the loss of individual areas from the visual field. In persons with tobacco intoxication, when the scotoma spreads to the fixation point, a sudden loss of the ability to see occurs. Visual functions are restored independently. Over time, the density of the scotoma increases. Visual acuity decreases at the same time, but does not reach complete blindness. With the alcoholic nature of the disease, the symptoms slowly progress, and concomitant manifestations are caused by the development of polyneuritis. Specific symptoms of iodine poisoning are swelling of the eyelids, redness of the eyes, the appearance of “floating opacities” in front of the eyes.
With methanol intoxication, headache, dyspeptic disorders (nausea, vomiting), abdominal discomfort come to the fore in the clinical picture. Vision decreases sharply. In severe cases, consciousness is disturbed early and a coma occurs. Among the manifestations of lead poisoning, common symptoms dominate – pain syndrome, lead colic and peripheral neuritis. A lead border forms on the gums. Visual dysfunction is slowly progressing. At first, only certain areas of the visual field fall out, then there is a persistent violation of visual functions.
Complications
The most common complication of pathology is a toxic lesion of the optic nerve. Persons with chronic iodine vapor poisoning are at risk of developing complicated forms of cataracts, vitreous turbidity. The accumulation of toxic metal compounds in the blood leads to damage to the structures of the uveal tract and contributes to the occurrence of retinopathy. In some cases, degenerative-dystrophic changes of the macula are observed. Damage to the retinal receptor apparatus leads to a violation of dark adaptation up to severe hemeralopia. In severe cases, the outcome of toxic amblyopia is complete blindness.
Diagnostics
The diagnosis is based on anamnesis data, visual examination and the results of specific examination methods. It is often possible to trace the relationship between the development of symptoms and contact with harmful production factors. Instrumental diagnostic methods include:
- Ophthalmoscopy. Examination of the fundus reveals foci of vacuole degeneration of ganglion cells, which are not accompanied by reactive changes from the surrounding tissues. Pale and edematous optic disc (OND), dilated retinal vessels are visualized.
- Visometry. The degree of visual acuity reduction varies significantly. When photoreceptors are affected, visual dysfunction manifests itself only at dusk. If necessary, computer refractometry is additionally performed.
- Perimetry. The technique allows you to diagnose scotomas of different sizes with fuzzy edges. Centrocecal scotomas are observed with the tobacco nature of the pathology and are located between the fixation point and the blind spot. In rare cases, a two-way process is possible. With alcoholic genesis, the location of the scotoma is central.
- Biomicroscopy of the eye. Pathological changes in the anterior segment of the eyeball are characteristic only of iodine intoxication. Patients experience hyperemia and swelling of the conjunctiva, erosive defects and local foci of corneal opacity.
- Fluorescence angiography. The expansion of retinal vessels is determined. When conducting a study with contrast, filling defects are determined. When poisoning with iodine vapors, multiple areas of hemorrhages, perivascular infiltrates are detected.
- Ultrasound of the eyes. When optical media become cloudy, organic changes in the eyes are visualized using ultrasound. It is possible to identify bulky formations and accumulations of toxic deposits on the membranes of the eyeball.
Differential diagnosis is carried out with retrobulbar neuritis, refractive and anisometropic forms of the disease. Unlike neuritis, in this pathology, the location of the scotoma is centrocecal. A differential sign of anisometropic amblyopia is the different refractive ability of the left and right eyes. The mechanism of development of the refractive form is based on anomalies of clinical refraction.
Treatment
First of all, it is necessary to eliminate the impact of etiological factors. In case of methyl alcohol poisoning, etiotropic therapy is reduced to oral or intramuscular administration of sodium bicarbonate in order to prevent the conversion of methanol into formaldehyde. A one-time intake of wine alcohol is also shown. In lead poisoning, calcium lactate is used, which binds the element and prevents its toxic effects. Regardless of the form of the disease, injections of hydroxycobalamin are indicated. Additionally, the introduction of vitamins B, C and PP is recommended. Symptomatic therapy is aimed at prescribing reparants, antihypertensive agents for damage to the trabecular network. Instillations of keratoprotectors are used only for iodine poisoning.
Prognosis and prevention
In most cases, the prognosis for toxic amblyopia is favorable. Often the restoration of visual functions occurs after the elimination of pathogenic factors. Preventive measures are aimed at correcting lifestyle and nutrition. Non-specific prevention is reduced to the rejection of bad habits (smoking, alcohol abuse) and the use of personal protective equipment when working at work (glasses, respirators, gloves). People from the risk group should be examined by an ophthalmologist 1-2 times a year. Patients are shown the consumption of foods rich in vitamins B, PP, A and C.
