Occupational diseases of the organ of vision. Part 4

Occupational diseases of the organ of vision. Part 4

Damage to eyes with carbon disulfide

Carbon disulfide is used in the rubber, leather and textile industry, agriculture. It is a strong poison of neurovascular action, has the ability to dissolve cellular lipids, which are rich in nervous tissue. When inhaled carbon disulfide fumes it enters the human body. It may be absorbed by the skin and gastrointestinal tract.

The onset of intoxication is manifested by the neurasthenic syndrome, in more severe cases encephalopathy and encephalopolyneuritis develop.

If carbon disulphide fluid gets into the eye, burns occur. Persons who have been in contact with carbon disulfide for a long time have complaints of headache, increased irritability, double vision, and fog before their eyes, which often occurs by the end of the work shift. On the part of the eyes, the development of conjunctivitis, corneal edema and small-point infiltrates in it, the appearance of bubbles in the corneal epithelium, which erupt, accompanied by a sharp pain, are noted. The sensitivity of the cornea and conjunctiva is reduced. In chronic intoxication with carbon disulfide, more than half of the patients show a weakening of convergence.

Patients with chronic intoxication with carbon disulfide and toxic encephalopathy are diagnosed with “eye cramps”, which manifests itself as an involuntary spasm of internal rectus muscles when the subject is fixed close. “Cramp eyes” accompanied by diplopia, dizziness, nausea, increased headache. After the cessation of contact with carbon disulfide for “gaze cramp” for 2–3 years, it may decrease, appear less frequently or disappear altogether.

In severe intoxication with carbon disulfide, the development of oculomotor muscle paralysis, miosis, weakening of the corneal and pupillary reflexes, accommodation paralysis, nystagmus, and optic nerve damage are possible. A typical manifestation of intoxication with carbon disulfide is the central scotoma, primarily, the red color, the concentric narrowing of the peripheral boundaries of the visual field, also red. There is a partial atrophy of the optic nerve. Spasm of the retinal vessels is considered a manifestation of general angiospasm, resulting from the neurogenic influence of the central nervous system in the toxic effects of carbon disulfide. For the early detection of eye lesions with carbon disulfide, an oculosfigmography is recommended, which shows that vascular changes are explained by increased rigidity of the vascular wall. The resulting microaneurysms are visible even with direct ophthalmoscopy, and not only with angiography.

In individuals with chronic intoxication, an increase in blood pressure is also observed.

Electrophysiological examination revealed damage to carbon disulfide, which manifested itself in dysfunction of the outer layers of the retina – the pigment epithelium and photoreceptors, pathways and cortical visual centers, and a decrease in photosensitivity.

Treatment of eye damage with carbon disulfide is not sufficiently developed.


Silver deposition in organs and tissues (argyrosis) can occur in working silver mines, during long-term work with silver alloys and its compounds, long-term use of medicines containing silver (collargol, protargol), silver nitrate, silver grinders, engravers, engravers, photographers.

Silver in the form of dust enters the body through the lungs, gastrointestinal tract and eye mucosa. The silver entering the body combines with proteins and, in the form of silver albuminate, particles of gray-brown color are deposited in the elastic fibers of the skin, the mucous membrane of the eyes and internal organs, dyeing them in a dark (gray-brown) color.

When silver enters the conjunctival cavity, as a result of combining it with tear chlorides, precipitates of silver chlorides are formed. In large quantities, it accumulates directly under the conjunctival epithelium and in the posterior border plate.

Conjunctival staining is observed mainly in the lower half of the eyeball. The lunate fold, the lacrimal caruncle and the lacrimal canaliculi are most strongly stained, which shows the affinity of silver with elastic fibers. The conjunctiva of the eyelids may be colored, more often in the lower fornix, mainly from the inside.

Silver particles accumulate around the sebaceous and sweat glands, hair roots, along the walls of blood vessels, especially along the terminal branches of the eyelid arteries and lymphatic vessels. In the cornea, argyria mainly affects its own tissue. Persons who have used silver medications for a long time may experience staining of the anterior or, less frequently, posterior lens capsule, yellow granules may be found in the vitreous. In severe cases, silver impregnation of retinal and optic nerve tissue is noted.

Visual functions in argyria, as a rule, do not suffer. Some reduction in visual acuity is possible with intensive deposition of silver in the cornea, retina, and optic nerve.

Conjunctival coloration is the first objective sign of general argyria. Eye color occurs earlier than the skin.


Ophthalmometricism – the defeat of organo-mercury compounds.

Mercury and mercury-organic compounds are used in industry and agriculture, in medicine. In agriculture, granosan is used to control pests. Poisoning can occur when used in production, as well as when taking contaminated water, or bread made from grains treated with granozan.

All organo-mercury compounds have pronounced cumulative properties and, acting on the sulfhydryl groups of the enzyme systems, disrupt the course of protein, fat and carbohydrate metabolism. Mercury is excreted by the kidneys, large intestine and oral mucosa. Granozan has a predominant effect on the central nervous system, since it is lipotropic, and as a result, it accumulates in the brain and other parts of the nervous system.

In the clinic of chronic mercury poisoning, functional and organic stages are distinguished.

In the initial stage of acute poisoning, patients complain of headache, dizziness, metallic taste in the mouth, general weakness, fatigue, increased thirst, pain in the heart area, eyelid tremor, fingers, and sleep disturbance.

Memory impairment, emotional dissatisfaction, loss of appetite are noted in severe cases.

In chronic mercury poisoning, patients complain about increased salivation, a metallic taste in the mouth, weight loss, irritability, daytime sleepiness and sleeplessness at night, palpitations, shortness of breath.

On the mucous membrane of the oral cavity, there is loosening, bleeding of the gums appears, and inflammation and burns on the skin.

On the part of the eyes, the muscles of the eyes are affected, there is a tremor in the eyelids, a violation of the size, shape and reaction of the pupils, diplopia, paresis, and paralysis of the eye muscles.

Under production conditions, mercury compounds can irritate the anterior segment of the eyeball. There are conjunctivitis with small hemorrhages in the lower vaults, blepharitis, pingvecula, pterygium. These changes appear in the early years of working with mercury.

Under the influence of prolonged exposure to vapors, mercury dust or with prolonged use of mercury ointment, mercury can be impregnated in the cornea and lens with staining of the cornea and lens in gray-brown or pink-brown. Tactile sensitivity decreases, sometimes corneal clouding in the surface layers is observed, and in case of severe lesions, corneal stroma clouding occurs.

In the lens, the color intensity depends on the degree of intoxication. There may be point opacities of the anterior cortical layers of the lens.

It is believed that the deposition of mercury in the lens is one of the types of deposition. At the same time, visual acuity does not change, but the field of view changes (narrows) both in white and in other colors.

Already in the first years of working with mercury, a decrease in dark adaptation has been observed. An increase in intraocular pressure, which is associated with an increase in the secretion of aqueous humor, is also noted.

In the treatment of the main efforts are directed to the removal of mercury from the places of deposition, antitoxic and stimulating therapy.

In chronic mercury intoxication, D-penicillinamide and unithiol are most effective when used consistently.

The most important preventive measures are: familiarization of toxic chemicals working with toxic properties and methods of safe work with them, preventing the development of severe toxic lesions and identifying the earliest forms of intoxication, and this is possible during periodic examinations by a pathologist, oculist and neurologist.

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