Toxic lesions of the optic nerve: causes, symptoms, diagnosis, treatment
Last reviewed: 23.04.2024
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Many toxic lesions of the optic nerve proceed as retrobulbar neuritis, but at the heart of the pathology is not the inflammatory process, but the dystrophic one. As a result of toxic effects on nerve fibers, their trophicity is disrupted, until the breakdown of the nerve tissue and the replacement of its glial tissue. Such conditions can arise as a result of exogenous or endogenous intoxication.
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Methylalcoholic intoxication
One of the most frequently noted causes of damage to the optic nerve is poisoning with pure methyl alcohol or its derivatives (denatured alcohol, varnishes and other liquids). The toxic dose is very individual - from inhaling vapors to ingesting a significant amount of toxic substance.
In the clinical picture, the manifestations of general intoxication are the foreground: headache, nausea, vomiting, gastrointestinal disorders, coma. Sometimes after a few hours, but more often in 2-3 days, the central vision of both eyes is significantly reduced. When examining a patient, first of all pay attention to wide pupils that do not respond to light. There are no other changes in the eyes. The ocular fundus and the optic disc are not changed.
The further course of the disease may be different. In some cases, the initial decline in vision is replaced by an improvement, in others there is a remitting current: periods of deterioration alternate with periods of improvement.
After 4-5 weeks, descending atrophy of varying degrees of severity develops. Decoloration of the optic nerve disc appears on the fundus. Morphological examination reveals changes in the layer of ganglion cells of the retina and optic nerve, especially expressed in the intracanalicular zone.
When rendering assistance to the victim, first of all, it is necessary to try to remove the poison from the body (gastric lavage, saline laxative) and introduce an antidote - ethyl alcohol. If the patient is in a coma, then 10% solution of ethyl alcohol is administered intravenously at a rate of 1 g per 1 kg of body weight, on average 700-800 ml with a body weight of 70-80 kg. Inside - 50 - 80 ml of alcohol (vodka) every 5 hours (for 2 days). Hemodialysis, infusion therapy (introduction of 4% sodium bicarbonate solution), diuretics are shown. In the first day the introduction of oxidants of methyl alcohol (glucose, oxygen, vitamins) is inexpedient.
Alcohol and tobacco intoxication
Toxic lesions of the optic nerve develop with the abuse of alcohol and smoking. The disease proceeds as a bilateral chronic retrobulbar neuritis. At the heart of its development lies not only the direct toxic effects of alcohol and nicotine, but also the occurrence of endogenous avitaminosis of group B: as a result of damage to the mucous membrane of the gastrointestinal tract and liver, B vitamins are not digested.
The disease begins gradually, imperceptibly. Vision worsens gradually, the sick turn to the doctor, when the vision is already reduced by a few tenths. Blindness usually does not occur, vision is maintained in the range of 0.1-0.2. In the field of vision, a central cattle and an enlarged blind spot are identified. Gradually expanding, they merge, forming a characteristic central cervical cattle. A characteristic complaint of patients is a decrease in vision under bright light: they see better in the twilight and in low light than in the day, which is explained by the damage to the axial beam and greater preservation of peripheral fibers from the ganglion cells located on the periphery of the retina. On the fundus at the beginning of the disease, no changes are detected, later the descending atrophy of the optic nerve develops, a pronounced decoloration of the temporal half occurs, and then the entire disc. In the morphological study, foci of demyelination and fragmentation of the fibers in the zones corresponding to the papillomacular optic nerve bundle (especially in the intracanalicular region), the chiasma, and the optic tract are noted. In the subsequent replacement of the dead fibers of the nervous tissue with glial tissue takes place.
At treatment it is first of all necessary to refuse from alcohol and smoking. Several (2-3) times a year, courses of treatment with the use of B vitamins (parenteral), drugs that improve oxidation-reduction processes, antioxidants and other symptomatic agents.
Toxic lesions of the optic nerve are also observed in case of lead poisoning, quinine, carbon disulfide and overdose or individual intolerance of cardiac glycosides and sulfanilamide preparations.
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