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Poisoning with nitrates and nitrites

Nitrites are compounds containing N0₂ group, nitrates — NO,.

Nonorganic and organic nitrates and nitrites are included in the composition of fertilizers, explosives, agents for preservation of freshness of flowers, brine (ammonia nitrite and nitrate, potassium nitrate — potassium saltpeter, sodium nitrate — Chile saltpeter, nitroglycerin), serve as medicinal preparations (sodium nitroprusside, sodium nitrite, bismuth nitrite, amylnitrite, nitroglycerin, nitromannite, pentalong, curantyl, apressin, etc.).

They are rapidly absorbed through the oral mucous membrane, GIT, volatile esters of nitric acid are also absorbed through the skin and respiratory tract. They are rapidly excreted in the unchanged form and destroyed down to ammonium, the esters of nitric acid are denitrified in the liver and degraded down to ammonium.

Their effect is characterized by relaxation of vessels and formation of methemoglobin (blood acquires a characteristic chocolate colour).

Clinical picture: bad headache, dizziness, nausea, vomiting, at first hyperemia, later a cyanotic color of the skin, pains in the abdomen, AP decrease, tachy-, more rarely — bradycardia, coma, sometimes, convulsions. Death may come as a result of vascular collapse or asphyxia in methemoglobin formation up to 60-80%. In rare cases hematuria and oliguria are observed. In poisoning with potassium nitrate arises a threat of the cardiac activity disorder.

Treatment consists in immediate gastric lavage, administration of salt laxative, if it gets onto the skin —washing the skin and mucous membranes with a large amount of water. Symptomatic treatment includes vasoconstrictor agents, infusion of salt and colloid plasma substitutes and oxygenotherapy.

Methemoglobinemia deserves a particular attention. It is inherent in the action of all nitrocompounds, but particularly typical for poisoning with those referred to benzene group (aniline, chloraniline, nitrobenzene, tolubin, etc.) that are, therefore, called methemoglobin formers. An oxidation of bivalent iron of methemoglobin occurs, under their action, into trivalent iron with the loss of possibility of reversible binding with oxygen and development of hemic hypoxia of different degrees. In increased methemoglobin content in blood (normally 2%, its increase reaches 60-80%) a color of face, nails and mucous membranes becomes from grey-blue to blue-black, and blood has a chocolate color. A hemic hypoxia is aggravated by hemolytic anemia and added with ventilation hypoxia in connection with the narcotic effect of poisonous substances, and in coma — at the expense of aspiration-obturation factors.

Along with usual methods of urgent detoxication and fight against a hypoxia, a methylen blue is applied to treat methemoglobinemia that cataly2;es methemoglobin restoration. In so doing, methylen blue itself is a weak methemoglobinformer, therefore, in order to avoid an aggravation of patient's condition at the moment of methylen blue administration a total dose of 10 mg/kg is introduced intermittently by 10-15 ml 1% solution with 10-15 min intervals on the background of oxygen inhalation.

It is better to use chromosmon (1% methylen blue solution in 25% glucose soution).

Glucose contributes also to demethemoglobinization. Ascorbic acid (to 60 ml/day of 5% solution), vitamin B₁₂ (600 fig), sodium thiosulfate (100 ml 30% solution) intensify this process.

In development of hepatorenal insufficiency a specific treatment of this syndrome is undertaken.

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