Cyanide poisoning is acute intoxication caused by ingestion or inhalation of cyanide compounds. The clinical picture develops rapidly in 15-30 minutes. There is numbness of the mucous membranes, a metallic taste in the mouth, compression in the chest, general weakness, respiratory disorders, consciousness. Later, seizures, bradycardia, respiratory and cardiac arrest develop. Pathology is diagnosed according to anamnesis, the smell of bitter almonds coming from the victim, a characteristic set of signs. Treatment includes correction of ABB, anticonvulsant measures, the fight against hypoxia and homeostasis disorders, maintenance of the cardiovascular apparatus.
Cyanide compounds are chemicals containing a specific complex of nitrogen and carbon. Upon entry into the body, acute intoxication is caused, which in 85-90% of cases ends with the death of the victim. Timely provision of medical care reduces mortality to 30-32%. The symptoms of cyanide exotoxicosis have been known for a long time. So, in ancient Egypt, “peach punishment” was practiced for the execution of criminals, when the condemned was forced to take prussic acid obtained from the seeds of this plant. At the beginning of the XX century, attempts were made to use hydrogen cyanide as a weapon of mass destruction, but they were unsuccessful.
Cyanide poisoning occurs more often when safety precautions are violated while working with prussic acid, which is used to extract gold and silver from ore, as a fumigant for fumigating citrus and olive trees. In addition, with its help, deratization and disinsection of the holds of ships is carried out. Intoxication is possible if you refuse to use insulating devices, there is no chemical protection suit, an excessively high concentration of the toxicant in the air. Other reasons:
- Military use. The use of cyanides as a chemical warfare agent is limited. Mixtures based on them have high volatility, cannot create a highly concentrated cloud near the earth’s surface for a long time. Nevertheless, prussic acid is considered a reserve BOV, can be used during military campaigns.
- Suicide. Attempts to die independently with the help of cyanide compounds are rarely recorded. The frequency of their occurrence does not exceed 0.2-0.3% of the total number of suicides. Most often, such cases end fatally, since the victim uses high doses of a toxic substance, seeks help late or does not seek it at all.
- Criminal poisoning. Salts of prussic acid (potassium cyanide) are used to kill a person. The lethal dose is 0.7 mg / kg of body weight. Loss of consciousness occurs a few minutes after taking the xenobiotic, death — after 5-15 minutes. The effectiveness of this method is extremely high, the mortality rate for intentional poisoning is close to 100%.
- Fires. During the combustion of nitrogen-containing materials (polyurethane foam, polyamides, wool, polyacrylonitrile) hydrogen cyanide is formed. Penetrating through the skin or respiratory tract, it causes severe poisoning. Usually the symptoms of cyanide intoxication are combined with signs of damage by other gorenje products (carbon monoxide and dioxide, phosgene, sulfur-containing compounds).
- Alternative medicine preparations. There are cases of poisoning with the drug amygdalin (laetrile, vitamin B17). The remedy, developed in 1952, is positioned as an antitumor. It contains components whose metabolite is hydrogen cyanide. Today it is prohibited for use in many countries of the world due to the high risk of toxic effects.
Cyanide poisoning leads to the development of a number of pathological processes. Initially, there is a significant pH shift to the acidic side. Experiments show that when a toxicant is administered at a dose of 1 mg / kg, the hydrogen index decreases to 6.8 at a rate of 7.4. This is accompanied by disruption of the body’s enzymatic systems. There is an inhibition of almost all types of metabolism. Protein metabolism suffers the most. The amount of free amino acids in the blood increases significantly.
The second pathogenetic mechanism is inhibition of the receptor apparatus of the carotid sinus and cytochrome oxidase activity. The result of this phenomenon is a pronounced depression of respiratory activity, almost complete cessation of oxygen uptake by cells. Deep tissue hypoxia occurs. Pathological overexcitation of cholinergic systems leads to myofibrillation, tachycardia, alternating bradycardia, and a decrease in blood pressure. There is a convulsive activity of the brain, a change in photosensitivity.
Pathology is classified according to several parameters: stage (initial manifestations, shortness of breath, convulsions, paralysis), causes (suicide, accidental cyanide poisoning, industrial disasters, military operations), ways of penetration of poison (inhalation, oral, transdermal), type of poisoning agent (prussic acid, hydrogen cyanide). The most common is the division according to the severity of the disease:
- Light form. It is detected with small leaks of cyanide compounds in enterprises, with a concentration of xenobiotic in the air from 0.02 to 0.005 mg/ l. The victims experience a slight deterioration in their well-being, which progresses with prolonged stay in the infected area.
- Medium-heavy form. It is observed during long-term stay indoors with a concentration of prussic acid of 0.02-0.06 mg / l. It is characterized by moderate functional changes that can be completely eliminated. It occurs in victims of fire, as well as in people using non-scientific medicine.
- Severe form. It is diagnosed with criminal and suicidal intoxication. Develops with oral or transdermal intake of poison, when its concentration reaches 0.5 mg / liter of blood. The symptoms are expressed as much as possible, the risk of death is high after 30-60 minutes.
- Extremely severe form (lethal). It is detected if the toxicant content in the ambient air is 0.1-0.55 mg / l or after oral administration of 45-70 mg. The rate of onset of life-incompatible effects depends on the dosage of the poison, varies from a few minutes to one hour.
Poisoning occurs in a lightning-fast or slow form. With lightning-fast varieties with inhalation of poison, there is no latent period. When it is swallowed, 120-180 seconds pass before the initial symptoms appear. The picture is characterized by transience and rapid development. After inhaling a toxicant with a high concentration, a person experiences anxiety, psychomotor agitation. This lasts 30-60 seconds. Then the victim falls, loses consciousness.
Transient convulsions are observed, which end in cardiac arrest and respiration. The period from the moment of receipt of the poison to the onset of asystole is 10-15 minutes. When examining the patient, attention is paid to the color of the skin, which retains a scarlet color even after death. There is a smell of bitter almonds around. Shortly before the occurrence of clinical death, a sharp bradycardia, arrhythmia, a critical decrease in blood pressure is determined.
Delayed cyanide poisoning progresses in 4 stages. At first, the patient has a taste of metal in his mouth, numbness of the mucous membranes of the throat, pain and a feeling of heaviness in the projection of the heart. Severe headache, vomiting and nausea, bluntness of attention, tinnitus, a feeling of pulse beating on the temples develops. There is a violation of coordination, dizziness. A person experiences the fear of death. Objectively, symptoms such as hypersalivation, tachycardia, and minor hypertension are determined.
The second stage is dyspnea. It is manifested by an increase in the existing symptoms, a deep violation of breathing. Shortness of breath inspiratory, with long pauses. There is exophthalmos, progressive bradycardia. The latter is considered a bad prognostic sign. Convulsive activity is increasing. The victim is found to have fibrillatory twitching of muscle fibers, rigidity of the muscles of the occiput. The skin acquires a bright pink color, sometimes this leads to diagnostic errors, since similar symptoms occur when carbon monoxide is affected.
The next stage is convulsive. The attack lasts 30-40 seconds, is characterized by clonic-tonic contractions, tongue biting. Breathing is interrupted. Outside of convulsions, respiratory activity is impaired: breathing is difficult, arrhythmic, with long-term delays. Auxiliary muscles are included in the process. This is followed by a paralytic stage, accompanied by general paralysis with loss of reflexes and all types of sensitivity. Involuntary defecation, urination is possible. After a few minutes, breathing stops, and a little later, asystole develops.
A common consequence of cyanide intoxication in surviving patients is toxic encephalopathy, which occurs in 75-80% of cases. With a mild course, the victims complain of cephalgia, dizziness, deterioration of sleep, weakening of working capacity. A serious consequence of the transferred exotoxicosis is a decrease in the level of mental development up to the complete loss of legal capacity. With inhalation poisoning, 20-25% of patients are diagnosed with pneumonia due to a violation of surfactant synthesis and gas exchange in the lungs.
Oxygen starvation and toxic metabolites, which are formed due to a violation of homeostasis, sometimes lead to heart damage. The patient develops conduction blockades, subsequently manifested by the occurrence of arrhythmias. Massive destruction of intracardiac pulse transport pathways requires the installation of a pacemaker. In 0.3-0.4% of cases, myocardial infarction, the formation of an ischemic zone or damage in the coronary muscle layers is diagnosed.
The presumed diagnosis is established by a doctor or paramedic who arrived at the scene of the accident. The exact determination of the toxicant is carried out in a hospital equipped with a toxico-chemical and clinical laboratory. During the examination, a toxicologist and an anesthesiologist-resuscitator work with the patient. You may need to consult a therapist, surgeon, neurologist. The final diagnosis is made based on the results of the following methods:
- Physical. Systolic blood pressure at the initial stages is 140-150, at the final stages – 70-80 mm Hg. The pulse rate is initially above 90, then below 55-60 beats/min. Wheezing or noisy breathing may be heard in the lungs. The skin is bright pink when examined, at the final stages of the slow flow – cyanotic, pale or marble shade.
- Hardware. The ECG determines the lengthening of the PQ interval, the loss of ventricular complexes, the increase in the gap between the vertices of R. Depression or ST segment elevation is possible with the development of focal ischemic disorders in the myocardium. On the EEG – activation of theta rhythms, gamma potentials, rapidly increasing convulsive discharges. On CT, the cerebral membranes are edematous, full-blooded, circulatory and ischemic disorders are detected.
- Laboratory. According to the results of the blood test, pronounced acidosis (pH 7-7.2), electrolyte imbalance is detected. The content of free amino acids increases significantly, this indicator exceeds the norm by 1.66 times. The concentration of cystine, lysine, histidine, arginine increases especially strongly.
Differential diagnosis is carried out with exotoxicosis by carbon monoxide and organophosphorus compounds. Cyanide poisoning has such distinctive features as a short hidden interval, extremely rapid development of clinical symptoms, tachycardia, followed by bradycardia. A characteristic phenomenon is mydriasis, deep and frequent breathing, scarlet blood color (high saturation with oxyhemoglobin).
Therapy at all stages should be aimed at maintaining vital functions. Correction of water-electrolyte changes and hemostasis, normalization of gas exchange is shown. The introduction of anticonvulsants and cardiac agents is required. Hospitalization is carried out by the forces of the ambulance brigade in the nearest intensive care unit. Transportation to a general hospital is possible only with mild variants of the course of the disease. Acute manifestations are stopped directly at the scene of the incident.
The specific antidote of cyanide compounds is amyl nitrite. It temporarily binds toxicant ions, forming non-toxic complexes. In addition, the drug prevents the blockade of cytochromes, prevents the occurrence of tissue hypoxia. The remedy should be given as early as possible, as symptoms develop, its effectiveness decreases. With parenteral administration of xenobiotic in the extremities, a tourniquet must be applied. As experiments show, prussic acid and its salts are completely destroyed in tissues in 1 hour.
Symptomatic therapy consists in maintaining vital functions. Anticonvulsants and sedatives, drugs that improve tissue circulation, respiratory analeptics are used. With severe respiratory insufficiency, the introduction of a combitube or laryngeal mask is indicated, followed by the transfer of the patient to a ventilator. Bradycardia is stopped by intravenous infusion of atropine, titrated supply of pressor amines through an injectomat is used to eliminate hypotension. Hospitalization is carried out under the control of blood pressure, pulse, respiratory rate.
HCN neutralization in hospital conditions is carried out using methemoglobin converters, carbohydrates, cobalt or sulfur compounds (amyl nitrite, sodium thiosulfate, glucose, cobalt chloride). Benzodiazepines, derivatives of gamma-aminobutyric acid, are used to relieve seizures. To eliminate hypoxia, a ventilator with increased inhalation pressure, hyperbaric oxygenation is indicated. Stimulation of tissue respiration with methylene blue or high doses of ascorbic acid is considered a promising direction.
Cyanide poisoning causes activation of the blood coagulation system, while inhibiting the enzymatic fibrinolytic apparatus. To eliminate hypercoagulation, heparin is prescribed. Atropine is recommended to normalize the work of the heart. An infusion of cordiamine, adrenaline may be required. In order to prevent infectious complications, all patients receive sulfonamide preparations. Infusions of crystalloid solutions are carried out to restore the water-salt balance.
The destruction of the toxic component in the body proceeds relatively quickly, about 60% of the toxicant is removed in an hour. After 4-5 hours, there are no traces of it in the blood. There comes a somatic stage that requires rehabilitation measures. To normalize brain activity, nootropic medications are prescribed to the patient. With the development of paresis of the limb, means should be used to improve neuromuscular conduction. Sometimes the use of oxygen therapy is required. It is recommended sanatorium-resort treatment, a gentle regime of work and rest, rest.
Prognosis and prevention
Severe cyanide poisoning has an unfavorable prognosis, it is almost never possible to save a patient with a lightning course. Delayed variants of the disease are amenable to therapy, with its timely onset, 70-78% of cases end safely. Mild pathology is completely eliminated. Symptoms disappear by day 4-6 without any residual effects. Moderate-severity lesions require longer-term treatment, however, they are also amenable to medication.
Prevention consists in observing safety precautions when working with chemicals. It is necessary to use gas masks, and at high concentrations of prussic acid in the air – chemical protection suits and insulating life support systems. If characteristic symptoms appear, ambulance should be called. Contamination can be determined by the specific aroma of bitter almonds. The rejection of medicines that have not passed clinical trials and have a potential toxicogenic ability is recommended.