Hydrogen sulfide poisoning is an acute inhalation intoxication that occurs with a high concentration of gas in the inhaled air. The main clinical symptoms are lacrimation, headache, chest tightness, nausea. In severe cases, seizures, disorders of consciousness, toxic pulmonary edema, hallucinations develop. The diagnosis is established on the basis of anamnesis, the available clinical picture. Laboratory and hardware methods are of auxiliary importance. There is no specific antidote. Treatment consists in the relief of emerging disorders according to generally accepted methods.
ICD 10
59.6 Toxic effect of hydrogen sulfide
General information
Hydrogen sulfide poisoning (H2S, hydrogen sulfide) manifests itself during long-term stay in an area with a toxicant concentration >0.006 g/m3 or short-term stay indoors, where the gas content exceeds 0.3-0.5 g/m3. The risk group includes employees of enterprises using H2S, as well as specialists engaged in mining and oil production. Employees of the railway network, through which tanks with xenobiotic are transported, are exposed to a certain danger. Severe lesions occur mainly in industrial disasters, when a large amount of poison is released into the surrounding space at the same time.
ICD 10
T59.6 Toxic effect of hydrogen sulfide
General information
Hydrogen sulfide poisoning (H2S, hydrogen sulfide) manifests itself during long-term stay in an area with a toxicant concentration >0.006 g/m3 or short-term stay indoors, where the gas content exceeds 0.3-0.5 g/m3. The risk group includes employees of enterprises using H2S, as well as specialists engaged in mining and oil production. Employees of the railway network, through which tanks with xenobiotic are transported, are exposed to a certain danger. Severe lesions occur mainly in industrial disasters, when a large amount of poison is released into the surrounding space at the same time.
Causes
The most common cause of poisoning is accidents at work, accompanied by a spill of a liquid toxicant, which quickly evaporates, turning into gas. Heavier than air, hydrogen sulfide settles at the surface of the earth, forming a toxic cloud. Its greatest concentration is achieved in the lowlands, basements of houses, wells. Gas masks provide full respiratory and eye protection only when the toxic substance content is less than 0.5-0.6 g/m3. Other possible causes:
- The release of gas in the mines. It occurs during the development of coal seams, during the opening of internal cavities filled with H2S and methane. Since this happens in an enclosed space with insufficient ventilation, people experience symptoms of severe poisoning. Self-rescuers used by mine workers make it possible to protect the respiratory organs in cases where the toxicant content is below 1%.
- Non-compliance with safety regulations. Refusal to use respirators when performing laboratory experiments with the release of gas or while working in harmful production can lead to poisoning. Such intoxications occur relatively easily, since at the first signs of a violation of well-being, a person leaves the infected area.
- Hydrogen sulfide baths. They become the cause of exotoxicosis only if the technique of their conduct is violated. A common mistake is mixing excessive amounts of hydrochloric acid and sodium sulfide, which leads to a significant increase in the concentration of H2S. The symptoms of such poisoning are poorly expressed. The mucous membranes of the eyes and nasopharynx are mainly affected.
- Living in the lowlands. It is dangerous only if there is a landfill nearby. Sulfide H2 is formed during the decay of organic substances, spreads in the ambient air, accumulates in areas located below the general level. Residents of such places form chronic hydrogen sulfide poisoning.
Pathogenesis
If the content of the compound does not exceed 50 millionths (ppm), a local toxic effect is observed. The victims develop irritation and swelling of the mucous membranes of the URT, minor areas of necrosis are formed. Inhalation of a high concentration toxicant is accompanied by inhibition of cytochrome C oxidase and disruption of oxidative phosphorylation processes. The amount of cellular adenosine triphosphate is falling. There is a deep lactic acidosis. The brain, heart, nervous tissue, and skeletal muscles are most affected.
Pronounced depression of the respiratory center occurs if the density of the toxic component exceeds 500 ppm. This is due to a violation of the production of neurotransmitters in certain areas of the central nervous system. After 2-4 minutes, the victim develops respiratory paralysis and changes associated with hypoxia. Death occurs from acute respiratory failure of the central type. Before this, generalized seizures are noted. If the gas content does not exceed 30 ppm, exotoxicosis does not occur. The substance is oxidized in the mitochondria and loses its toxic properties.
Classification
Hydrogen sulfide poisoning is classified by causes (professional, domestic, disasters), course (acute, chronic), the presence of complications (complicated, uncomplicated). In addition, pathology is divided according to the pathogenetic principle (with predominant damage to the respiratory organs, central nervous system, cardiovascular apparatus). In practice, structuring by severity is used:
- Easy. It is formed by long-term inhalation of hydrogen sulfide of low concentration. It develops in people living in an infected area, as well as in employees of chemical enterprises. It is characterized by damage to the eyes, upper respiratory tract. Significant systemic manifestations are absent or poorly expressed.
- Medium. It occurs in laboratory workers with hydrogen sulfide leakage, miners and employees of the oil industry. Sometimes the symptoms of pathology are detected in diggers after descending into the dungeons. The disease is manifested by a sharp deterioration in well-being, the appearance of a detailed clinical picture.
- Heavy. It is detected during massive leakage of H2S from tanks, release of a toxicant inside mines. The defining criterion is pronounced respiratory depression, which in a short time leads to the death of the patient. Often, victims die by the time they are evacuated from the infection zone.
Symptoms
Symptoms vary depending on the extent of the lesion. With mild forms, local signs prevail. The victim reveals lacrimation, runny nose, eye pain, fullness of the conjunctiva. There are complaints of a metallic taste in the mouth, moderate nausea, headache. The mucous membrane of the nasopharynx and pharynx is hyperemic, edematous. There may be anxiety, slight psychomotor agitation, provoked by a painful condition and fright.
With intoxication of moderate severity, a feeling of tightness in the chest, vomiting, cold sweat is revealed. Patients complain of severe weakness, dizziness. There is a violation of consciousness up to sopor or fainting. The patient is disoriented, agitated, reports a severe headache. Breathing slows down at first, then tachypnea develops, a feeling of lack of air, cough. Toxic pulmonary edema is possible, which leads to the appearance of wheezing and foamy sputum, generalized cyanosis.
Severe hydrogen sulfide poisoning occurs in an apoplectic or convulsively comatose form. The first option is manifested by almost instantaneous loss of consciousness, convulsions, and respiratory arrest. The victim dies in a few minutes. A similar variant occurs when entering a space with an extremely high gas content. Convulsive-comatose course provokes convulsions, which are replaced by a coma. When restoring consciousness, the patient hallucinates, behaves inadequately. At the stage of convalescence, apathy, drowsiness, retrograde amnesia are determined.
Complications
Hydrogen sulfide poisoning causes a decrease in intelligence in 58% of victims. This is due to prolonged oxygen starvation and the toxic effect of the poison on brain tissue. The severity of the lesion depends on the dose of the toxic substance, the severity of the pathology, and the characteristics of the patient’s body. 5-8% of people exposed to H2S are diagnosed with psychosis, 1-2% are disabled due to the formation of paresis and paralysis. It is possible to develop diseases of the gastrointestinal tract, myocardial dystrophy with the subsequent occurrence of heart failure.
Diagnostics
The diagnosis is established according to the data received from witnesses of the incident and the victim himself (with preserved consciousness). The assessment of the environment is important. The ambulance doctor should pay attention to the place where the patient was found. Hydrogen sulfide poisoning occurs more often in wells, mines, cellars, lowlands, where an unpleasant aroma characteristic of H2S is detected. Confirmation of the diagnosis is carried out after hospitalization by a toxicologist and resuscitator. The following methods are used:
- Physical. During the examination of the patient, the smell of rotten eggs present in the exhaled air is detected. Blood pressure is reduced by 10-30 units from normal, in a state of shock, it may not be determined. The pulse is rapid, insufficient tension and filling. Breathing more than 15-20 times / minute, with severe poisoning is absent or sharply weakened. The skin is pale or cyanotic.
- Laboratory. hyperlactatacidemia, a change in the lactate/pyruvate ratio is determined in the blood. The content of bicarbonates is 10-12 mmol / l, pH is below 7.3. A decrease in the partial pressure of oxygen, other changes characteristic of hypoxia are detected. There are electrolyte shifts, a decrease in the concentration of calcium and an increase in the magnesium content of venous blood.
- Hardware. When measuring SpO2, its decrease to 90-92% is detected. On the ECG there are signs of tachycardia, later — the phenomena of myocardial dystrophy: ST segment depression, negative T wave. With pulmonary edema, diffuse focal-drain changes are visible on X-rays, a symptom of “butterfly wings”.
Differential diagnosis is carried out with poisoning with other inhaled poisons, drug overdose, epilepsy. To exclude the narcotic effect, the patient is prescribed a toxic-chemical blood test. A characteristic feature of seizures in epilepsy is the short duration of the attack, followed by the onset of sleep. Exposure to other gases is excluded based on the available clinical manifestations.
Treatment
Poisoning requires immediate medical attention. Before the arrival of the SMP brigade, the victim should be taken out into the fresh air, laid down, and unbuttoned the restraining clothes. Symptoms of pulmonary edema are an indication for a semi-sitting position, this helps to relieve shortness of breath and improve ventilation. Transportation of the patient from the infected area should be carried out in insulating respiratory protective equipment. With a low concentration of toxic gas, the use of respirators is permissible.
First aid
Regardless of the level of the lesion, oxygen inhalation through a facial mask or nasal cannula is indicated. The volume of gas is calculated according to Darbinyan’s formula. An assessment of the general condition is necessary. With a sharp suppression of respiratory function, the doctor ensures the patency of the respiratory tract with a laryngeal mask or a combitube, after which he begins ventilating. If the eyes are affected, lotions with boric acid are made, binocular bandages are allowed. Symptoms of alveolar pulmonary edema are treated by passing a respiratory mixture through a defoamer, which can be ethyl alcohol.
In convulsions, the introduction of relanium and other drugs with anticonvulsive activity is indicated. Lowering blood pressure requires a titrated infusion of dopamine, norepinephrine. Pronounced bradycardia is stopped by intravenous administration of atropine. Hospitalization of the victim is carried out in a toxicological hospital if his condition allows for long-term transportation. If there is a high risk of death, the patient should be placed in the nearest medical facility equipped with an ICU.
Hospital treatment
The therapy started at the prehospital stage continues. In order to correct electrolyte disorders, salt solutions are prescribed. The ventilator is maintained. For its implementation, the patient is intubated or a tracheostomy is applied. An infusion of buffers (sodium bicarbonate) is required. Hyperbaric oxygenation is considered an effective method of therapy, which minimizes tissue hypoxia. With pulmonary edema, diuretics, bronchodilators, hormones are prescribed.
Antiplatelet agents and antibiotics are administered for preventive purposes. Convulsions are stopped by anticonvulsants. If the patient is on full respiratory support, an infusion of peripheral muscle relaxants is allowed. General restorative therapy is indicated: multivitamin complexes, medications that improve cerebral circulation and microcirculation, sedatives. For timely diagnosis of changes, round-the-clock hardware monitoring is carried out.
Rehabilitation
At the recovery stage, therapy is aimed at minimizing the effects of exotoxicosis. The patient necessarily receives nootropic drugs, is examined by a neurologist, a psychiatrist. With paresis, medications are prescribed that improve neuromuscular conduction, physical therapy. It is recommended to visit sanatorium-resort institutions. The choice of rehabilitation measures depends on which complications of intoxication are present in the victim.
Prognosis and prevention
Severe hydrogen sulfide poisoning has a sharply unfavorable prognosis. About 70% of people die before the arrival of doctors from respiratory arrest and cardiac activity. Moderate intoxication can be stopped in 90-95% of cases. 5% of the situations are due to pulmonary edema, in which acute respiratory failure develops, and exotoxic shock. The survivors have a weakening of mental abilities, somatic changes. Symptoms of mild poisoning are eliminated completely within a few hours or days, there is no decrease in the quality of life.
Prevention of poisoning consists in compliance with safety regulations when working in laboratories, mines, and in production. Employees working in high-risk areas should be provided with respirators, gas masks or self-rescuers. The means of protection must be chosen in accordance with the level of risk and the volume of possible release of the toxicant.