Eye damage by arsenic and its compounds

Arsenic and its compounds are used in the manufacture of paints, glass, artificial leather processing, in the manufacture of pesticides, in pyrotechnics.

The main signs of acute poisoning are due to the development of gastrointestinal disorders: vomiting, abdominal pain, diarrhea; in severe cases, a cholera-like state.

Penetration of arsenic and its compounds through the respiratory tract is accompanied by pronounced irritation of the upper respiratory tract.

In the most severe cases, there is a collapse with symptoms of paralysis of the vascular and respiratory centers.

Often, in case of moderate poisoning, arsenic myelopolyneuritis and encephalomyelone neuritis develop in a later period.

Chronic poisoning is characterized by the development of chronic catarrhs ​​of the upper respiratory tract, gastrointestinal disorders, abortive forms of polyneuritis, dystrophic disorders (hypertrichosis, hair loss), liver damage, and anemia.

With the long-term effect of even small doses of arsenic, the change in the eyes is manifested by a lesion of the eyelids in the form of arsenic dermatitis with irritation and peeling of the eyelid skin. Whitish xerotic plaques may form on the surface of the conjunctiva of the eyeball.

In the initial stage of acute intoxication, pain in the eyes, photophobia, tearing, irritation of the conjunctiva are noted. Large bubbles appear on the conjunctiva. Arsenic keratitis may develop with severe pain in the eyes. Edema and erosion of the corneal epithelium are detected.

When biomicroscopy in eroded areas of the cornea can detect dust-like inclusions of arsenides, the color of which corresponds to the color of the effecting arsenic compound. Gradually, these particles dissolve.

Under the influence of long-acting small doses of arsenic, whitish xerotic plaques may form on the surfaces of the conjunctiva of the eyeball.

Arsenic polyneuritis, changes in the skin, nails, digestive tract are observed in cases of arsenic poisoning.

The development of encephalomyelino neuritis in the late period of arsenic poisoning is accompanied by oculomotor disorders, toxic damage to the optic nerve with a significant decrease in visual function. There is a narrowing of the peripheral borders of the visual field, which can be observed in the absence of other signs of intoxication and changes in the fundus. Visual acuity decreases.

In the fundus sometimes indistinctly marked papillitis or retinal hemorrhage, retinal edema. Possible outcome papillitis atrophy of the optic nerve. The most dangerous for the optic nerve is polyvalent arsenic compounds. The process is usually two-way.

In the treatment of acute and chronic poisoning, specific antidotes are used – the British anti-lusitis in the form of intramuscular injections of a 5-10% solution in nut oil at a dosage of 2.5 mg / kg. The first two days administered 4 times a day, in the next 8 days 2 times.

A 5% solution of unitiol is also prescribed in 5–10 ml intramuscularly or orally 0.5 x 2 times a day for 3–4 days. A 30% solution of sodium thiosulfate, 10-15 ml each, is administered intravenously. Apply vitamins B1, B6, B12. The conjunctival cavity is washed with water, instilled indifferent oil. For conjunctivitis and keratitis, a 5% solution of British anti-lunisitis is prescribed in the form of drops. Instilled with a 0.01% citral solution.

Electricity

In industrial and domestic conditions, electric shock is possible, i.e., damage by high-voltage electric current.

Local electric shock effect is manifested by a burn of varying severity. Of the common manifestations in mild cases, functional impairments are observed in the activity of the central nervous system, cardiovascular, endocrine, respiratory, and other systems.

In severe cases, there is a cardiac arrest, respiration, shock.

As a consequence, post-traumatic encephalopathy, vestibular disorders, impaired cardiac activity, etc. often develop. Of the eye symptoms, the most characteristic complication of an electrical injury is clouding of the lens, which usually develops later, that is, after a few months or even years. A cataract can be unilateral and bilateral.

First, under the anterior and posterior lens capsule, as well as in the equatorial region, vacuoles, small, restricted opacities are formed. The number of cloudiness gradually increases, spreading to different layers of the lens, they merge, and the entire lens becomes cloudy (after 1-2 years). But sometimes the cataract is stabilized in the initial stage.

As a result of electrical injury, edema and hyperemia of the conjunctiva, clouding of the cornea, both epithelial and stromal with a decrease in its sensitivity, accommodation paralysis, iridocyclitis develop. Edema, hemorrhage and development of dystrophic changes in the retina may occur. In rare cases, there is atrophy of the optic nerve.

When a high-voltage current is applied directly to the orbit, a burn of the eyelids, conjunctiva, cornea, and sclera of varying degrees occurs.

Changes in the organs of vision caused by exposure to chemical factors

    Benzene and its compounds

Benzene is widely used in the chemical, pharmaceutical, printing, rubber industry, as well as in the production of synthetic rubber, artificial leather, as a raw material for the manufacture of paints, explosives.

It enters the body in the form of vapors through the skin and lungs. It has a toxic effect on the nervous system and blood-forming organs. The main symptoms of acute poisoning are headache, dizziness, confusion, vomiting, seizures, loss of consciousness.

Chronic intoxication is characterized by hematopoietic disorders, hemorrhagic syndrome, functional disorders of the nervous system, and gastrointestinal disorders. In severe cases, toxic encephalopathy.

Eye symptoms are most often observed during acute intoxication.

The early symptoms of intoxication are accommodation disturbance, dilated pupils.

In severe poisoning, retinal hemorrhage is also noted, toxic damage to the optic nerve, which leads to a decrease in visual acuity.

Benzene nitro compounds are used in the production of explosive dyes, artificial resins, in the soap and perfume industry.

They have a hepatotoxic, hematuric, methyl hemoglobin formation effect, they have a toxic effect on the nervous and cardiovascular systems, as well as an irritant effect on the skin and mucous membranes.

    Eye damage by trinitrotoluene

Trinitrotoluene is the main route of penetration of the skin, but it can also penetrate through the upper respiratory tract and by ingesting dust through the gastrointestinal tract.

For intoxication of trinitrotoluene, the appearance of toxic complicated cataract is associated with the deposition of trinitrotoluene in the lens.

Toxic trinitrotoluene cataract is not only a typical sign of this intoxication, but also the earliest symptom of a common chronic lesion. This cataract is usually bilateral, may progress after cessation of contact with trinitrotoluene.

The features are focal nature of opacities, peripheral and paracentral arrangement of opacification rings, due to which, even with pronounced changes in the lens, visual acuity decreases slightly.

There is a cataract after contact with trinitrotoluene over 5-10 years, and for people working in conditions of significant contact with trinitrotoluene, changes in the lens can appear after 5-6 months, with less prolonged contact – after 2-3 years.

In cases of poisoning with trinitrotoluene, there can be changes in the macular area, toxic damage to the optic nerve.

Trinitrotoluene intoxication leads to pathological changes not only of the organ of vision, but also of other organs and systems.

The development of cataracts is observed with the defeat of the eye by dinitrophenol, nitrocolors.

The effect of high atmospheric pressure

The effect of increased atmospheric pressure is mainly on divers and workers who perform caisson work carried out under water or in saturated soil, during the construction of abutments for bridges, underwater tunnels, subways, etc. The effect of increased pressure on workers engaged in excavation is a difficulty breathing (exhalation), a feeling of constriction and pain in the ears (depressed eardrum), a decrease in the pulse.

Extremely dangerous is the moment of transition from the area of ​​high pressure (caisson) to normal conditions, since the excess amount of nitrogen distributed in the blood and tissue fluids, especially in adipose tissue and white matter of the brain, may not have time to stand out through the lungs and remain as bubbles gas. They are carried by blood throughout the body, can cause embolism.

From the localization of the emboli and the duration of the malnutrition of the tissues caused by vascular occlusion, various manifestations of a disease called decompression sickness depend.

The rupture of the smallest arteries by the embolus may occur, and hemorrhages may occur, even life-threatening ones.

There may be an air embolism of the central retinal artery or its branches, which results in partial or complete loss of vision in one or both eyes. Sometimes there is retinal and vitreous hemorrhage, swelling and atrophy of the optic nerve.

Due to an increase in intracranial pressure, a congestive disc may occur.

Cases of homonymous hemianopsia and complete amaurosis are described. The functions of the external and internal muscles of the eye can be disturbed, which is manifested by nystagmus, paresis of extraocular muscles, and a change in the shape of the pupil.

Of the common symptoms of decompression sickness, itching should be noted and sometimes hemorrhages, pains in the joints, muscles and bones, respiratory disorders and cardiac activity.

As a result of damage to the cerebral vessels, paresis, paralysis, muscle contracture, sometimes aphasia and Meniere’s syndrome are noted.

When ear barotrauma during the period of pressure increase, the eardrum is pulled in and protrudes during the decompression period. Hemorrhage and perforation of the membrane are possible.

Treatment is primarily decompression, followed by a slow decrease in pressure. Oxygen is inhaled to remove nitrogen from the blood, while vascular dilation is used for retinal and optic nerve emboli.

For the prevention of decompression sickness, they limit the residence time under water at one or another depth, replace the nitrogen in the composition of the inhaled air with gases that have significant solubility in the blood — helium, argon, etc.

Careful professional selection and the correct mode of decompression, which ensure complete release of nitrogen from the blood through the lungs, are necessary.

    Atmosphere pressure

Daily fluctuations of atmospheric pressure at the surface of the earth usually do not exceed 4-5, and annual fluctuations – 20-30 mm Hg. Such minor changes in pressure are not felt by healthy people, but some people even respond to such changes in pressure.

A decrease in atmospheric pressure precedes overcast rainy weather due to the inflow of warmer air (cyclone), and an increase in atmospheric pressure portends dry, clear weather with a strong cooling in winter (anticyclone).

Effect of low blood pressure (altitude sickness)

With the rise to a height, a decrease in atmospheric pressure is observed. A person is affected by this factor when flying on airplanes, climbing mountains, and space flights. A drop in atmospheric pressure affects the decrease in the partial pressure of oxygen. A decrease in atmospheric pressure and a partial pressure of oxygen leads to hypoxia. In the pulmonary alveoli, the oxygen content drops particularly noticeably, while the pressure of water vapor and carbon dioxide remains unchanged. Anoxia leads primarily to a decrease in brain function, especially its cortical part.

The first signs of acute altitude sickness appear at an altitude of 3000-4000 m, when there is a feeling of anxiety, some difficulty in breathing.

At an altitude of 5500 m, the atmospheric pressure drops by half, the partial pressure of oxygen — to 79 mm Hg. Art., and people are disturbed by the coordination of movement, memory, the correct assessment of the situation.

At an altitude of 7500 m, death may occur in a few minutes. In the visual analyzer, the cortical region, the visual center in the external cranial body, and the retinal ganglion cells are most sensitive to anoxia. With altitude sickness, visual acuity is reduced, the field of view is narrowed, dark adaptation, color perception, contrast sensitivity worsen; impaired binocular vision is expressed in diplopia, sometimes in marked exophoria.

One of the most dangerous manifestations of altitude sickness in aviation is the appearance of visual illusions.

Ophthalmoscopy shows dilation of retinal vessels, sometimes hemorrhages in the retina.

All these changes can be reversible after returning to the normal oxygen supply conditions of the visual functions, since the impairments are functional.