Toxic lesions of the optic nerve: causes, symptoms, diagnosis, treatment

Many toxic lesions of the optic nerve occur as retrobulbar neuritis, but the pathology is based not on an inflammatory process, but on a dystrophic one. As a result of the toxic effect on nerve fibers, their trophism is disrupted up to the disintegration of nerve tissue and its replacement with glial tissue. Such conditions can arise as a result of exogenous or endogenous intoxication.

Methyl alcohol intoxication

One of the most frequently noted causes of optic nerve damage is poisoning with pure methyl alcohol or its derivatives (denatured alcohol, varnishes and other liquids). The toxic dose is very individual - from inhalation of vapors to ingestion of a significant amount of toxic substance.

In the clinical picture, manifestations of general intoxication come to the fore: headache, nausea, vomiting, gastrointestinal disorders, coma. Sometimes after a few hours, but more often after 2-3 days, the central vision of both eyes is significantly reduced. When examining the patient, first of all, attention is paid to wide pupils that do not react to light. No other changes in the eyes are detected. The fundus and optic disc are unchanged.

The further course of the disease may vary. In some cases, the initial decrease in vision is replaced by improvement, in others, a remittent course is observed: periods of deterioration alternate with periods of improvement.

After 4-5 weeks, descending atrophy of varying severity develops. Decolorization of the optic nerve disc appears on the fundus. Morphological examination reveals changes in the retinal ganglion cell layer and the optic nerve, especially pronounced in the intracanalicular zone.

When providing assistance to the victim, first of all, it is necessary to try to remove the poison from the body (gastric lavage, saline laxative) and administer an antidote - ethyl alcohol. If the patient is in a coma, then a 10% solution of ethyl alcohol is administered intravenously at the rate of 1 g per 1 kg of body weight, on average 700-800 ml for a body weight of 70-80 kg. Orally - 50-80 ml of alcohol (vodka) every 5 hours (for 2 days). Hemodialysis, infusion therapy (administration of a 4% solution of sodium bicarbonate), diuretics are indicated. In the first day, the introduction of methyl alcohol oxidizers (glucose, oxygen, vitamins) is inappropriate.

Alcohol-tobacco intoxication

Toxic lesions of the optic nerve develop with alcohol abuse and smoking. The disease occurs as bilateral chronic retrobulbar neuritis. Its development is based not only on the direct toxic effects of alcohol and nicotine, but also on the occurrence of endogenous vitamin B deficiency: due to damage to the mucous membrane of the gastrointestinal tract and liver, vitamins of group B are not absorbed.

The disease begins gradually, unnoticed. Vision deteriorates gradually, patients seek medical attention when vision is already reduced by several tenths. Blindness usually does not occur, vision remains within 0.1-0.2. In the visual field, a central scotoma and an enlarged blind spot are detected. Gradually expanding, they merge, forming a characteristic centracecal scotoma. A typical complaint of patients is decreased vision in bright light: in the twilight and in dim light they see better than during the day, which is explained by damage to the axial bundle and greater preservation of the peripheral fibers coming from the ganglion cells located on the periphery of the retina. At the onset of the disease, no changes are detected in the fundus, later descending atrophy of the optic nerve develops, pronounced decolorization of the temporal half occurs, and then the entire disk. Morphological examination reveals foci of demyelination and fragmentary disintegration of fibers in areas corresponding to the papillomacular bundle of the optic nerve (especially in the intracanalicular section), chiasm, and optic tract. Subsequently, the replacement of dead fibers of the nervous tissue with glial tissue occurs.

During treatment, it is necessary to first of all give up alcohol and smoking. Several (2-3) times a year, courses of treatment are carried out using B vitamins (parenterally), drugs that improve oxidation-reduction processes, antioxidants and other symptomatic agents.

Toxic damage to the optic nerve is also observed in cases of poisoning with lead, quinine, carbon disulfide, and overdose or individual intolerance to cardiac glycosides and sulfonamide drugs.

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