Eye damage with phosphorus compounds

Phosphorus and its compounds are strong poisonous substances. White and yellow phosphorus – waxy mass. In the air, spontaneously ignites. White phosphorus is highly toxic, which, when heated without air, turns into less toxic red.

Under production conditions, phosphorus enters the body through inhalation of vapors, through the gastrointestinal tract and in contact with the skin.

It is excreted by the lungs, intestines and sweat.

Of phosphorus compounds, phosphorous hydrogen is the most toxic, the harmful effect of which can manifest itself in the production of phosphorus, in the production of phosphoric bronze, flammable mixtures, and phosphoric mineral fertilizers.

Phosphorus compounds with chlorine have an irritant effect on the mucous membranes of the respiratory tract, eyes, and phosphoric anhydride leads to severe irritation and burns of mucous membranes.

Three-sulfur phosphate in the form of dust is irritating to the mucous membranes of the respiratory tract and eyes.

With prolonged exposure to vapors of yellow phosphorus, there is a violation of fat, carbohydrate, protein metabolism, impaired liver function, gastrointestinal tract, there is a phosphorus necrosis of the bones, and more often the mandible. Organic compounds of phosphorus, which are part of toxic chemicals, when absorbed through the mucous membranes and skin have a general toxic effect, are strong inhibitors of cholinesterase. Early symptoms of general intoxication are muscle tremor, miosis, spasm of the ciliary muscle.

In chronic phosphorus poisoning there may be retinal hemorrhages, dystrophic foci in the retina, retrobulbar neuritis.

When phosphate gets on the skin, large deep, slow-healing burns are formed, leaving behind rough scars.

In the production of phosphate mineral fertilizers, conjunctivitis and blepharitis were observed, degenerative changes in the form of pterygium and pingveculas, dilation, pigmentation and vascularization of the limbus, expansion and crimpiness of the anterior ciliary vessels.

Certain individuals showed dystrophic changes in the iris, clouding of the cornea and lens, destruction of the vitreous body.

In a large number of cases, a decrease in the sensitivity of the cornea was noted, as well as a violation of color sensation.

Treatment

In case of acute poisoning, frequent and repeated washing of the stomach with 1% copper sulphate solution or 0.4% potassium permanganate solution is recommended; milk, fats in which phosphorus is well dissolved are contraindicated.

Heart remedies, injections of glucose, ascorbic acid, sodium hyposulphite are shown.

When yellow phosphate gets on the skin, it is washed off from the contaminated area of ​​the body with soap, sodium bicarbonate solution, ammonia. Then it is necessary to urgently process these areas with 5% hydrogen peroxide solution, apply lotions of 5% sodium bicarbonate solution and dressings with potassium permanganate solution. Atropine is used as an antidote therapy (1.0-2.0-ml of a 0.1% solution subcutaneously, intravenously).

Assign anesthetics, washing the conjunctival cavity with antiseptic solutions, instillation of sulfanilamide solutions. Ointment dressings are contraindicated.

In chronic poisoning, fortifying treatment is shown, multivitamins, calcium preparations.

Acute organophosphate insecticide poisoning

In our country, organophosphate insecticides are used, according to their chemical composition, in the following groups:

1. Esters of thiophosphoric acid: litofos, trichlormetaphos.
2. Esters of dithiophosphoric acid: karbofos.
3. Amides of pyrophosphoric acid: octomethylamide.
4. Esters of phosphoric acid: chlorophos.

The leading link in the mechanism of action of these drugs on the human body is their ability to inhibit cholinesterase, as a result, there is a significant accumulation of toxic doses of endogenous acetylcholine, which moderately affects the body.

The functions of the central and autonomic nervous system are impaired due to the action on the cholinergic receptors, the activity of the internal organs and the skeletal muscles is disturbed. The toxicity of insecticides depends on the ability to dissolve in lipids, selectivity with respect to cholinesterase, the ability to penetrate hemotoencephalitic and hematoparenchymal barriers.

•     In case of inhalation poisoning and POI contact with eyes, prolonged miosis is characteristic.
•     Muscle fibrillation is characteristic of percutaneous poisoning at the point of contact with poison.
•     For oral poisoning, nausea, vomiting, acute abdominal pain, dyspepsia.

Abundant sweat, solivation, bronchorea, bronchospasm and severe miosis appear due to muscarinic action of the FOI. Nicotin-like effect is manifested in the development of excitation and disorientation, hyperkinesis, choreic and myoclonic types. Curariform – in the development of peripheral paralysis. Central action is manifested in the form of general clonicotonic convulsions and deep coma.

In case of oral poisoning with FOI, a violation of the central nervous system is manifested by impaired mental activity (the development of asthenic syndrome, intoxication psychosis, or coma).

A comatose state is manifested by a sharp inhibition or lack of reaction of the pupils to light, corneal reflexes, pain sensitivity, decreased muscle tone.

Mioz is observed in almost all patients with a severe poisoning clinic.

Complaints about the appearance of the grid in front of the eyes, the feeling of “doubling” in the eyes are characteristic.

In severe poisoning, very narrow pupils persist for a long time, sometimes miosis occurs within a few hours after death. Marked vertical and horizontal nystagmus.

One of the objective symptoms of damage to the peripheral nervous system are fibrillar muscle twitching, including the tongue, tibia; sometimes they extend to the muscular muscles of the face, the region of the pectoralis major muscles, and the upper and lower limbs. Respiratory disorder in patients with acute poisoning FOI develops obturator-aspiration, central and mixed type. Disorders of the cardiovascular system are manifested by early hypertensive syndrome (systolic pressure up to 200-250 mm Hg. Due to severe hyperadrenalinemia), rhythm and conduction disturbance of the heart, toxic shock.

From the gastrointestinal tract, due to pronounced spasm, nausea, vomiting, cramping abdominal pain, diarrhea. If pregnancy is possible abortion or premature birth.

In oral poisoning, FOI has three stages.

The first stage is arousal, after 15-20 minutes the patient notes dizziness, headache, nausea and decreased visual acuity. Patients experience a sense of fear, refuse treatment. Objectively observed moderate miosis, sweating, salivation, sometimes the effects of bronchorea, tachycardia (moderate) and an increase in blood pressure.

The second stage is hyperkinesis and convulsions. Characterized by pronounced miosis, with no reaction of pupils to light. There is a sharp sweating, salivation, bronchorea, hyperkinesis of the choreic and myoclonic types in the area of ​​the eyelids, facial muscles, muscles of the chest and lower leg, sometimes fibrillation of all muscles.

Appear bradycardia or severe tachycardia, an increase in blood pressure to 250/160 mm Hg. Art., then the fall of the heart.

The third stage is paralysis. Patients are in a deep coma. Pronounced miosis. Determined by hyperhidrosis.

The central form of respiratory depression predominates, bradycardia or tachycardia increases, blood pressure drops.

Complications include: pneumonia, late intoxication psychosis and polyneuritis, occurring within a few days from the moment of poisoning. Pneumonia is the main cause of death in late poisoning.

Treatment. Specific: antidote therapy – the combined use of anticholinergics (such as atropine) and cholinesterase reactivators (oximes).

During the first hour, all patients are prescribed intensive atropinization until dry skin and mucous membranes appear, moderate tachycardia, and pupil dilation.

Doses for intensive atropinization are different in different stages. In the first stage of poisoning – 2-3 mg, in the second – 20-25 mg, in the third stage – 30-50 mg IV. This condition is supported by the introduction of atropine in doses: for the first stage – 4-6 mg, for the second – 30-50 mg, for the third stage – 100-150 mg.

In parallel, during the first days after the poisoning, cholinesterase reactivators should be administered.

In the first stage, dipyroxime is used at 150 mg i / m (a total of 150-450 mg per course of treatment).

In the second stage, the therapeutic dose is administered in 1-3 hours after the poisoning in the total dose for a course of treatment of 1.2-2.0 grams.

For mental disorders in / in or in / m injected 3 ml of 40% solution of isonitrosine. If necessary, after 30-40 minutes, the injection is repeated.

In the third stage, isonitrazine 1.2 grams in 30-40 minutes is administered in parallel with dipyroxime IM or IV is administered after 30-40 minutes (the total dose does not exceed 3-4 grams).

Specific therapy is carried out under the constant control of the activity of cholinesterase enzymes.

To remove insecticides from the gastrointestinal tract, gastric lavage is performed through a probe with 10–15 liters of cold water (12–15 °) to clean wash waters, followed by 300–500 ml of sulfuric acid magnesia through a probe of vaseline oil, diluted in 100-150 ml of water.

In the second and third stages, repeated gastric lavages are shown at intervals of 4-6 hours until the insecticide smell from the washings disappears.

Further, gastric lavage and siphon enemas are performed daily until the elimination of severe symptoms. To remove the FOI from the bloodstream and excrete with urine soluble hydrolysis products of FOI, polyglucine, reopolyglucine, isotonic sodium chloride solution and 5% glucose solution are injected in an amount of 1.5-2.5 liters for 2-3 hours, after which Furosemide, lasix at a dose of 40–200 mg or osmotic diuretics (urea in the form of a 30% solution on glucose, mannitol in the form of a 10% solution in a dose of 60–90 g) are injected intravenously.

Hemosorption, hemodialysis, and peritoneal dialysis are performed. It is advisable to carry them out from the first hours from the moment of poisoning.

Extracorporeal methods of blood purification should be used after normalization of the central venous pressure to 40-120 mm of water column and elimination of hypovolemia by intensive infusion therapy with plasma-substituting solutions.

The most effective is hemosorption. If it is possible to conduct it, then it is advisable to use hemodialysis with the help of the “artificial kidney” apparatus.

Clinical criteria for the effectiveness of hemosorption and hemodialysis can be the disappearance of myofibrillation, the regression of toxic disorders, persistent tachycardia and mydriasis, the termination of the decrease or increase of ache.

In the presence of a very severe clinical picture with a pronounced manifestation of exotoxic shock that is not amenable to treatment, peritoneal dialysis is shown.

Resuscitation and symptomatic therapy of patients with acute poisoning with FOI should be aimed at eliminating severe respiratory and hemodynamic disorders, arresting convulsive status and psychomotor agitation, treatment of complications. In case of respiratory disorders, tracheal intubation should sometimes be performed; antibiotics are prescribed to prevent pneumonia. With symptoms of acute heart failure, cardiovascular agents, blood and blood substitutes transfusions, hormones are indicated.

For the prevention of psychomotor agitation, sedative therapy is carried out (10 ml each of a 25% solution of magnesia sulphate, 2-4 ml of a 2.5% solution of aminazine). For severe delirium and convulsive status, sodium hydroxybutyrate (40-60 ml of a 20% solution), viadryl (500-1000 mg)