List of Abbreviations
CO – carbon monoxide
FiO2 – fraction of inspired oxygen
HbCO – carboxyhemoglobin
HCl – hydrogen chloride
HCN – hydrogen cyanide
pCO2 – partial pressure of carbon dioxide in arterial blood
pO2 – partial pressure of oxygen in arterial blood
SaO2 – arterial blood oxygen saturation
ALT – alanine aminotransferase
AST – aspartate aminotransferase
ATA – atmosphere absolute
ATP – adenosine triphosphate
HBO – hyperbaric oxygenation
GLC – gas-liquid chromatography
IMV – invasive mechanical ventilation
II – inhalation injury
ABDS – acid-base balance status
CT – computed tomography
CK – creatine kinase
NBO – normobaric oxygenation
CVA – cerebrovascular accident
AKI – acute kidney injury
ICU – intensive care unit
SCT – spiral computed tomography
CO2 – carbon dioxide
FBS – bronchoscopy
TBI – traumatic brain injury
ECG – electrocardiography (electrocardiogram)
Terms and Definitions
Poisoning is a disease developing as a result of external (exogenous) exposure of a human or animal body to chemical compounds in quantities that cause disorders of physiological functions and pose a threat to life.
Inhalation injury (II) – damage to the mucous membrane of the respiratory tract and (or) lung tissue resulting from the effects of thermal and (or) toxic-chemical factors, leading to the development of respiratory failure.
Toxicogenic stage of poisoning – the period during which the toxicant is present in the human body at a concentration capable of exerting a specific damaging effect.
Somatogenic stage of poisoning – the period beginning after the elimination of the toxicant, manifesting as damage to various organs and systems up to the full restoration of their functions or death.
Hemic hypoxia – a pathological state characterized by the inability of systemic blood flow to transport oxygen.
Respiratory hypoxia – a pathological state characterized by the inability of the respiratory organs to perform gas exchange in the lungs.
Tissue hypoxia – a pathological state characterized by impaired oxygen utilization processes in tissues and decreased ATP production.
1. Brief information on the disease or condition
Diagnostic criteria for poisoning by carbon monoxide, other gases, smokes, and vapors are based on anamnestic data: evacuation of victims from the fire source, identification of malfunctions or improper operation of stoves, heating appliances, operation of internal combustion engines in poorly ventilated rooms, as well as on the clinical picture and chemical-toxicological examination [13, 16].
During inpatient care, clinical diagnosis based on anamnestic data and the clinical picture of intoxication is supplemented by chemical-toxicological and clinical-biochemical examinations, instrumental diagnostic methods (electrocardiography, bronchoscopy, spiral computed tomography of the brain, targeted chest radiography, radiography of the entire skull in two projections, etc.).
1.1 Definition of the disease or condition
Carbon monoxide – a colorless, odorless, and tasteless gas (molecular weight – 28.01, boiling point – minus 191.5 °C, vapor pressure – 26,600 mmHg (35 atm)). Poorly soluble in water, not adsorbed by activated carbon, burns in air with a blue flame to form carbon dioxide. Carbon monoxide belongs to hazard class IV (GOST 12.1.007-76) [5, 22, 23, 30]. The maximum permissible concentration of carbon monoxide in the atmospheric air of populated areas is 5 mg/m3, in the working zone air – 20 mg/m3 [26], and the lethal toxic dose of carbon monoxide upon human inhalation is about 11.4 g × min/m3 [5].
It should be noted that the vast majority of victims exposed to carbon monoxide intoxication are currently delivered from fire sources. Therefore, the tactics of diagnosis and treatment of carbon monoxide poisoning must be considered taking into account the toxic effects of combustion products (hydrogen cyanide, hydrogen chloride, carbon dioxide, etc.), aerosols, and the presence of inhalation injury (II) [5, 22, 24].
Along with the treatment of isolated carbon monoxide poisonings, these clinical guidelines consider recommendations for the therapy of patients exposed to the chemical factor of a fire.
Hydrogen cyanide – a colorless gas with the odor of bitter almonds (molecular weight – 27.03, density – 0.68 kg/m3, boiling point – 26.7 °C, vapor pressure – 630 mmHg (0.83 atm)), which is well sorbed by porous materials (including activated carbon) [10, 11, 22, 15]. Hydrogen cyanide belongs to hazard class II (GOST 12.1.007-76). The maximum permissible concentration of hydrogen cyanide in the atmospheric air of populated areas is 0.01 mg/m3, in the working zone air – 0.3 mg/m3 [26], and the lethal toxic dose of hydrogen cyanide upon human inhalation is about 0.8–4.4 g × min/m3 [5].
Hydrogen chloride – a colorless gas with a pungent odor (molecular weight – 36.4, density – 1.5 kg/m3, boiling point – minus 85.1 °C, vapor pressure – 30,780 mmHg (40.5 atm)). Highly soluble in water (up to 500 volumes of gas per one volume of water) with the formation of hydrochloric acid. Hydrogen chloride belongs to hazard class II (GOST 12.1.007-76) [5, 27]. The maximum permissible concentration of hydrogen chloride in the atmospheric air of populated areas is 0.2 mg/m3, in the working zone air – 5 mg/m3 [26], and the lethal concentration of hydrogen chloride upon human inhalation is about 0.7–1.9 g/m3 (exposure time – 30 min) [5, 32].
1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)
Carbon monoxide. The main cause of carbon monoxide poisoning is exposure to the chemical factor of a fire [1, 5, 23, 32]. This is because this toxicant is formed during the combustion of any carbon-containing materials [5]. In addition, acute carbon monoxide intoxication may occur due to violations of safety regulations during the operation of heating systems, exposure to harmful occupational factors, operation of internal combustion engines in poorly ventilated rooms, or suicide attempts [1, 5, 22, 23].
The toxicokinetic parameters of carbon monoxide are well studied. The toxicant enters the body via inhalation. The rate of entry into the body depends on the concentration of carbon monoxide and oxygen in the inspired air. Easily crossing the air-blood barrier, carbon monoxide enters erythrocytes, where it binds to divalent iron of hemoglobin to form carboxyhemoglobin (HbCO) and is distributed throughout the body with the bloodstream. Various factors influence the rate of carboxyhemoglobin dissociation. Thus, the dissociation rate of HbCO increases with a decrease in carbon monoxide concentration and an increase in oxygen concentration in the inspired air, as well as with an increase in the pressure of the inspired mixture. Carbon monoxide is excreted mainly through the respiratory tract with exhaled air [5, 23, 30].
The main mechanism of the acute action of carbon monoxide is due to the formation of carboxyhemoglobin, which is incapable of transporting oxygen. In addition, the interaction between carbon monoxide and hemoglobin causes conformational changes in the latter molecule, which impairs oxyhemoglobin dissociation and reduces oxygen release to tissues. Upon entering muscle tissue, carbon monoxide interacts with myoglobin to form carboxymyoglobin, thereby disrupting its function of supplying muscles with oxygen. When the concentration of carboxymyoglobin exceeds 25%, a significant decrease in the intensity of oxidative phosphorylation in myocytes occurs. Clinically, this manifests as the development of muscle weakness, while victims are unable to independently evacuate from the fire source. The aforementioned mechanisms of the acute action of carbon monoxide lead to the development of mixed hypoxia, which can cause the death of victims [5, 23, 30, 45].
In addition to acute effects, carbon monoxide poisoning leads to long-term functional disorders of the body. To date, a significant number of scientific papers have been published proving that, apart from causing hemic hypoxia, carbon monoxide entering the body triggers other cascades of pathological reactions. It has been experimentally established that carbon monoxide exposure can initiate delayed-onset indirect damage to structures of the central nervous and cardiovascular systems in the late period of intoxication. This is due to the suppression of bioenergetic processes in mitochondria, activation of programmed cell death pathways, inhibition of cellular antioxidant defense and the triggering of oxidative stress, as well as effects on secondary cell signaling systems, and others. These mechanisms of action can explain the variability of clinical symptoms that develop in victims exposed to acute carbon monoxide poisoning [5, 6, 29, 59].
Carbon dioxide. In addition to carbon monoxide, combustion products and exhaust gases contain carbon dioxide. Carbon dioxide has low toxicity on its own (the median lethal concentration is about 90 g/m3 with a 5-minute exposure); however, its high concentrations in inhaled air lead to a reflex increase in the respiratory rate and a greater inhalation uptake of other toxic products [5].
Hydrogen cyanide. In fires, hydrogen cyanide is formed during the combustion of certain nitrogen-containing polymers: artificial wool (polyacrylonitrile, etc.), thermal insulation materials (polyisocyanurate foam, chloroprene foam rubber), building materials (polyurethane foam), etc. [1, 11, 22, 31].
Hydrogen cyanide enters the body via inhalation, easily crossing the blood-air barrier. Hydrogen cyanide can penetrate through intact skin. High ambient temperature and increased sweating enhance its percutaneous absorption. The hydrogen cyanide molecule is highly soluble in water, and therefore in the blood it turns into hydrocyanic acid, which rapidly dissociates into a hydronium ion and a cyanide ion. Only the intact hydrocyanic acid molecule passes from the bloodstream into organs and tissues, including across the blood-brain barrier, since the cyanide ion, having a negative charge, cannot cross biological membranes. There are several biotransformation systems for the cyanide ion in the body: reactions resulting in the formation of low-toxicity cyanohydrins and thiocyanate compounds. The cyanide ion is excreted unchanged in exhaled air and as biotransformation products in urine and saliva [5, 8, 11].
Upon entering tissues, hydrocyanic acid releases a cyanide ion, which binds to the ferric iron (Fe3+) of cytochrome c oxidase. The resulting complex of the cyanide ion and cytochrome c oxidase is quite stable, as a result of which ferric iron cannot be reduced by accepting electrons from cytochrome C. Thus, the entire mitochondrial electron transport chain is blocked, leading to decreased ATP production and the manifestation of energy deficiency [5, 11].
Hydrogen chloride. Hydrogen chloride in a fire is formed during the combustion of chlorine-containing polymers: building and finishing materials (polyvinyl chloride), flame retardants (chlorinated paraffin), etc. [20, 27, 32].
Hydrogen chloride enters the body via inhalation. If high concentrations of the toxicant form in the environment, a local irritant effect on exposed skin areas may develop. Hydrogen chloride, interacting with the water of the respiratory mucosal membranes, dissociates into a hydronium ion and a chloride ion. The resulting dissociation products lead to a local change in pH, which accounts for their pronounced irritant effect on the upper respiratory mucosa. Neither hydrogen chloride nor its dissociation products penetrate into the systemic bloodstream, but are cleared from the respiratory tract with the retrograde flow of mucus [5, 56].
Hydrogen chloride is a hydrophilic gas, therefore, as mentioned above, upon interacting with the water of the upper respiratory mucosa, it dissociates into a hydronium ion and a chloride ion. An increase in the hydronium ion content leads to a sharp shift in pH and denaturation of alveolar cell macromolecules. Since the chloride ion has a negative charge, it cannot independently cross the blood-air barrier. Thus, the damaging effect of hydrogen chloride on the components of the blood-air barrier is primarily associated with pH changes and denaturation of alveolar cell macromolecules, which leads to the development of coagulation necrosis [5, 56].
When a large number of chemical compounds contained in combustion products enter the body simultaneously, ambiguous effects of combined action are observed (summation, potentiation, and antagonism), which must be taken into consideration when providing care to victims [5, 22, 30].
1.2.1. Inhalation injury
Inhalation injury is damage to the respiratory mucosa and/or lung tissue resulting from the thermal and/or toxic-chemical factors of a fire.
Upper airway injuries generally develop as a result of inhaling hot air or steam. True burns below the vocal folds practically do not occur because the upper respiratory tract acts as a powerful barrier that prevents high-temperature agents from penetrating into the tracheobronchial tree and lungs for a prolonged time, while effectively lowering the temperature of the inhaled mixture. However, with prolonged exposure to hot gases or gas mixtures, thermal damage to the airways may also spread to the tracheobronchial tree. The most severe airway injuries develop under the action of toxic chemical compounds inhaled along with smoke. Inhalation of hot air, steam, and/or the action of toxic chemical compounds (combustion products) inhaled with smoke can lead to the development of thermal (thermo-inhalation) airway injury, toxic-chemical injury (acute inhalation poisonings by combustion products), or thermochemical (mixed) damage [34, 41].
The pathogenesis of inhalation injury includes the development of inflammation in response to damaging agents, which leads to narrowing of the airway lumen due to mucosal edema, obstruction by desquamated epithelial cells and exudate (mucus), accompanied by bronchospasm. The toxic effect can lead to mucosal ulceration and hemorrhages. Damage to the lung parenchyma causes both epithelial and endothelial injury, leading to pulmonary edema. Reduced barrier function of the lungs due to impaired mucociliary clearance of bronchial epithelial cells, suppression of the cough reflex and the activity of immunocompetent cells leads to secondary infection and the development of purulent respiratory complications, and predisposes to generalized infection [44, 46].
CLASSIFICATION OF INHALATION INJURY [13]
By localization:
a) upper respiratory tract injury:
without laryngeal involvement (nasal cavity, pharynx);
with laryngeal involvement (nasal cavity, pharynx, larynx up to and including the vocal folds).
b) upper and lower respiratory tract injury (trachea and main, lobar, segmental, and subsegmental bronchi).
By etiology:
thermal (thermo-inhalation airway injury);
toxic-chemical injury (airway injury by combustion products);
thermochemical airway injuries.
By the severity of tracheobronchial tree damage based on endoscopic criteria:
mild degree (I) – moderate hyperemia, isolated accumulations of easily washed-off soot in the trachea and bronchi, a small amount of mucous secretion;
moderate degree (II) – hyperemia and mucosal edema, a large amount of soot in the bronchial lumen and isolated accumulations of soot fixed to the mucosa, isolated petechial hemorrhages and erosions in the trachea and main bronchi, a large amount of bronchial secretion mixed with soot;
severe degree (III) – pronounced hyperemia and mucosal edema, friable mucosa, total layer of soot fixed to the mucosa down to the segmental bronchi; when attempting to wash off the soot, a fragile, bleeding mucosa with multiple erosions or a pale-gray "dry" mucosa with no vascular pattern is exposed, scant thick bronchial secretion with a large amount of soot or absence of bronchial secretion, casts of desquamated epithelium obstructing the bronchial lumen (Appendix G2. Scale of Poisoning Severity Grades).
1.3 Epidemiology of the Disease or Condition
According to Rosstat data, in the Russian Federation in 2021, the proportion of victims exposed to carbon monoxide intoxication accounted for 3.2% of the total number of poisonings (about 3.5 thousand people), while in terms of mortality from acute poisonings, carbon monoxide intoxication ranks second, accounting for about 20% [14]. According to the Center for the Treatment of Acute Poisonings of the State Budgetary Institution "I.I. Dzhanelidze Research Institute of Emergency Medicine" (Saint Petersburg), 117 patients with a diagnosis of toxic effect of carbon monoxide (T58, from various sources) were hospitalized in 2021. Mortality was 8.5% [31].
1.4 Features of Coding the Disease or Condition
T58 Toxic effect of carbon monoxide.
T59 Toxic effect of other gases, fumes and vapours.
Under modern conditions, performing a chemical-toxicological analysis of most significant toxicants generated during a fire is not feasible. In routine practice, as a rule, only the carboxyhemoglobin concentration is determined. Consequently, the formulation of the diagnosis will be as follows: Acute poisoning by carbon monoxide and combustion products.
1.5 Classification of the disease or condition
In modern clinical practice, to determine the severity of the condition of victims exposed to carbon monoxide, clinicians are guided by the blood carboxyhemoglobin level, distinguishing mild (blood carboxyhemoglobin concentration less than 30%), moderate (30–50%), and severe (more than 50%) intoxication [23, 45]. Taking into account excretion and therapeutic measures performed at the prehospital stage, the blood carboxyhemoglobin level upon admission to the hospital may be significantly lower than at the scene of the incident. To calculate the initial carboxyhemoglobin concentration, the nomogram by C.J. Clark et al. (1981) can be used, which takes into account the carboxyhemoglobin level at the time of admission, the time elapsed since exposure (in hours), as well as whether normobaric oxygen therapy was administered or not [23].
2. Diagnostics, medical indications and contraindications for diagnostic methods
Diagnostic criteria for poisoning by carbon monoxide, other gases, smokes, and vapors are based on anamnestic data: evacuation of victims from the fire source, identification of malfunctions or improper operation of stoves, heating appliances, operation of internal combustion engines in poorly ventilated rooms, as well as on the clinical picture and chemical-toxicological examination [13, 16].
During inpatient care, clinical diagnosis based on anamnestic data and the clinical picture of intoxication is supplemented by chemical-toxicological and clinical-biochemical examinations, instrumental diagnostic methods (electrocardiography, bronchoscopy, spiral computed tomography of the brain, targeted chest radiography, radiography of the entire skull in two projections, etc.).
2.1 Complaints and Anamnesis
Diagnosis of acute poisoning is performed comprehensively, taking into account the leading syndromes and symptoms observed in the victim.
It is recommended that all victims with acute poisoning by carbon monoxide, other gases, fumes, and vapours require emergency medical care outside a medical organization by an ambulance team, including either an examination by an ambulance physician (specialist physician) during the provision of emergency medical care, or an examination by an ambulance paramedic (mid-level medical specialist) during the provision of emergency medical care. These medical workers take a detailed history and record complaints from victims with suspected poisoning by carbon monoxide, other gases, fumes, and vapours [3, 29, 63].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C (for adults).
Level of Reliability of Evidence (LRE) – 4, Level of Recommendation Validity (LRV) – C (for children).
It is recommended that upon admission to the hospital, all patients with acute poisoning by carbon monoxide, other gases, fumes, and vapours undergo an initial appointment (examination, consultation) with a clinical toxicologist and/or an initial examination (consultation) with an anesthesiologist-resuscitologist [1, 3, 23, 29, 64].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C (for adults).
Level of Reliability of Evidence (LRE) – 4, Level of Recommendation Validity (LRV) – C (for children).
Comment. The clinical presentation of carbon monoxide intoxication includes typical, syncopal, and euphoric forms of poisoning. The typical form is most frequently encountered. In cases of severe poisoning, taking the medical history and assessing complaints will be difficult due to impaired consciousness. In mild and moderate cases, patients may complain of headache, predominantly in the temporal region, pulsating pain in the occipital region, dizziness, weakness, and nausea [3, 23].
In victims delivered from a fire, in the presence of inhalation airway injury caused by thermal and/or toxic-chemical factors of the fire, there may be complaints of shortness of breath, a feeling of air hunger, burning behind the sternum, voice disorders, and soot on the face or in the oropharynx, with burns localized in the facial area (Appendix G2. Scale for the Severity of Poisoning).
The ambulance team performs diagnosis based on the toxicological situation (exposure to fire factors, being in a car or in a confined space with a running internal combustion engine [box, garage], operation of faulty heating systems, etc.), and a toxicological history aimed at eliciting information about the clinical picture of the poisoning. However, in the case of carbon monoxide poisoning, this is far from always possible to accomplish. This applies to determining such details as the time spent in the exposure zone and the circumstances accompanying the development of the poisoning (for example, the victim might have been in a state of alcohol intoxication, etc.).
Often, these circumstances cannot be ascertained, especially when there are no relatives or acquaintances of the victim, and the victim themselves cannot or will not provide the necessary information about themselves. In such cases, the diagnosis is established based on the leading clinical syndrome [3, 5, 24, 16].
2.2 Physical Examination
It is recommended that all victims with acute poisoning by carbon monoxide, other gases, fumes, and vapours undergo a sequential general examination of systems and organs to confirm the diagnosis:
Examination of the patient's appearance [8, 18, 23];
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Assessment of neurological status [8, 23, 38];
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Assessment of psychoneurological status: state of the level of consciousness (clear, lethargy, stupor, coma). If coma is present, assessment of its depth using the Glasgow Coma Scale (Appendix G1), presence or absence of reflexes, pupil size, pupillary light reflex, presence (absence) of anisocoria, and muscle tone state [8, 18, 23, 65].
Level of Reliability of Evidence (LRE) – 4, Level of Recommendation Validity (LRV) – C.
Assessment of the state of the respiratory system: respiratory rate, depth of breathing, uniform participation of all parts of the chest in the respiratory act, and auscultatory findings in the lungs [8, 18, 23].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Assessment of the state of the cardiovascular system: pulse examination, auscultation in case of heart pathology, measurement of heart rate, cardiac rhythm, and blood pressure on peripheral arteries [8, 18, 23].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended, with the aim of identifying or ruling out traumatic injuries, to pay attention to the presence (absence) of injuries, especially in the face, head, abdomen, and lumbar regions, to confirm or exclude traumatic pathology [5, 9, 16, 23, 24, 28].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. A pathognomonic sign of carbon monoxide poisoning is identified as a pink coloration of the visible mucous membranes of the oral cavity, alae nasi, and earlobes.
In fire victims, it is necessary to assess indirect signs of inhalation injury: localization of burns on the face, neck, and anterior chest wall; traces of soot in the nasopharynx and oropharynx; voice changes (dysphonia, aphonia); cough with sputum containing soot [5, 9, 16, 23, 24, 28].
2.3 Laboratory Diagnostics
When providing care in inpatient settings:
It is recommended for all patients, with the aim of diagnosing carbon monoxide poisoning, to test the level of carboxyhemoglobin in the blood, expressed as a percentage of total hemoglobin [17, 18, 23, 33].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. The main method for diagnosing carbon monoxide poisoning is testing the blood carboxyhemoglobin level. Carbon monoxide easily crosses the blood-air barrier, enters the systemic circulation, interacts with ferrous iron (Fe2+) of hemoglobin to form carboxyhemoglobin, which is incapable of transporting oxygen [5, 16, 17, 18, 19, 23, 57].
It is recommended for all patients, for the purpose of differential diagnosis, to determine ethanol concentration in the blood by gas chromatography and quantitative determination of ethanol in urine by gas chromatography [23, 60, 33].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. The test is performed for differential diagnostic purposes in the presence of impaired consciousness. The test is performed by gas-liquid chromatography [23, 33, 60].
It is recommended for all victims with acute poisoning by carbon monoxide, other gases, fumes, and vapours, with the aim of early diagnosis of potential complications from various organs and systems, to perform a complete blood count (CBC) [7, 23, 26, 29, 46, 58].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended for all patients with acute poisoning by carbon monoxide, other gases, fumes, and vapours, with the aim of early diagnosis of potential complications, to perform a general therapeutic biochemical blood test (testing total bilirubin level in the blood, determining alanine aminotransferase activity in the blood, determining aspartate aminotransferase activity in the blood, determining creatine kinase activity in the blood, testing urea level in the blood, testing creatinine level in the blood, testing total protein level in the blood, testing glucose level in the blood, testing sodium level in the blood) [17, 26, 29, 33, 59].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comments: Myocardial damage marker testing is essential, as the myocardium is a target organ in poisonings with systemic poisons (carbon monoxide, hydrogen cyanide). In severe poisonings, ECG recordings show rhythm and conduction disturbances, as well as signs of myocardial hypoxia. The clinical spectrum of myocardial injury is quite broad and includes cardiomyopathy, angina pectoris, myocardial infarction, arrhythmias, and heart failure, up to cardiogenic shock and sudden death, especially in individuals with coronary artery disease [6, 34].
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors to ensure early diagnosis of potential organ and system complications, performing a general (clinical) urinalysis [7, 23, 50, 59].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors for the timely diagnosis of potential complications and prevention of decompensation in the presence of signs of respiratory and (or) cardiovascular failure, performing a blood coagulation study: (coagulogram (exploratory hemostasis screening)), blood fibrinogen level testing, international normalized ratio (INR) determination, prothrombin (thromboplastin) time determination in blood or plasma, activated partial thromboplastin time (APTT) [61].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Recommended for all moderate and severe patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors for the timely diagnosis of potential complications and prevention of decompensation in the presence of signs of respiratory and (or) cardiovascular failure, performing acid-base balance and blood gas analysis [9, 17, 25, 29, 46, 50, 59].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comments: Acid-base balance and blood gas analysis provide insight into the degree of oxygenation impairment as well as metabolic disorders (metabolic acidosis, indicating tissue hypoxia) [16].
Acid-base balance and blood gas analysis, specifically determining the partial pressure of oxygen in arterial and venous blood (arteriovenous oxygen difference), will help establish the fact of hydrogen cyanide poisoning [5, 8, 9].
Recommended for all moderate and severe patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors to confirm or exclude electrolyte balance disorders, blood potassium level testing, and blood sodium level testing [17, 23, 9].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors when compartment syndrome or systemic rhabdomyolysis is suspected as a complication, to confirm or exclude the development of such complications: blood sodium and potassium testing, acid-base balance and blood gas analysis, creatine kinase activity determination, blood myoglobin, creatinine, and urea testing [2, 9, 17, 23, 33].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: One of the complications of carbon monoxide poisoning is compartment syndrome and systemic rhabdomyolysis (due to prolonged hypoxia). The aforementioned conditions lead to acute kidney injury via myorenal syndrome. Determining blood creatine kinase activity, blood creatinine and urea levels, blood potassium levels, blood sodium levels, and total blood calcium levels has screening value for diagnosing myolysis and acute kidney injury [5, 23, 38]. Detection of myoglobin in the urine is performed when creatine phosphokinase, creatinine, and urea levels are elevated by more than 2 times.
2.4 Instrumental Diagnostics
Instrumental diagnostic methods are an integral part of the diagnostic process and are implemented to monitor the patient's condition.
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors, performing an electrocardiogram, its interpretation, description, and data analysis for the purpose of diagnosing rhythm disorders and detecting signs of myocardial ischemia and injury (including during emergency medical care) [6, 17, 23, 33, 53].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. Carbon monoxide intoxication leads to cardiovascular disorders, including myocardial injury. Performing an electrocardiographic examination is necessary to diagnose rhythm disorders and detect signs of myocardial ischemia and injury [4, 9, 23, 38].
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors, performing targeted chest X-ray for the diagnosis of pathological changes in the pulmonary parenchyma (in moderate and severe poisonings) [7, 9, 17, 23, 46].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. In most cases, patients are poisoned by carbon monoxide in a fire. Fire victims are exposed to the combined effects of gaseous combustion products and aerosols, including those with pulmonotoxic effects (hydrogen chloride, hydrogen fluoride, etc.). Exposure to pulmonotoxicants leads to respiratory system disorders, up to the development of acute pulmonary edema (chemical) [4]. Diagnostic imaging methods allow for the detection of pathological changes in the pulmonary parenchyma [8, 32].
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors presenting with altered consciousness, to identify or rule out traumatic brain injuries and neurological pathology: performing skull radiography in one or more projections, or brain computed tomography [9, 23, 33, 53, 62].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. Diagnostic imaging methods allow for differential diagnosis in patients with altered consciousness to identify brain damage (traumatic brain injury (TBI), acute cerebrovascular accident (ACVA)). They also enable the diagnosis of hypoxic brain injury in carbon monoxide poisoning [49].
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors who show clinical signs of airway damage, including inhalation injury, performing bronchoscopy (FBS) to diagnose them and determine the severity of the lesion [13, 23, 46, 47, 55].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. The combined effect of thermal and chemical factors in a fire can lead to airway damage and the development of inhalation injury. Indications for prescribing FBS include the presence of at least one indirect sign of inhalation injury. Therapeutic FBS is indicated when combustion products are detected in the airways and should aim to restore airway patency, remove secretions, desquamated epithelium, and combustion products [13, 46, 47, 55].
2.5 Other Procedures
Differential diagnosis should be performed with other conditions accompanied by impaired consciousness: TBI, ACVA, ethanol poisoning, neurotropic drug poisoning, narcotic drug poisoning, carbohydrate metabolism disorders, infectious and inflammatory CNS diseases [22, 23, 38].
Recommended upon hospital admission of the patient to also rule out the diseases or conditions listed above, and in the absence of positive dynamics, a more thorough examination is recommended, including chemical-toxicological testing to rule out the combined intake of any drugs of abuse and psychoactive substances or another somatic or infectious disease [2, 9].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
3. Treatment, including drug and non-drug therapies, diet therapy, and pain management
3.1. Provision of emergency medical care outside a medical facility
Recommended for all patients with acute poisoning by carbon monoxide, other gases, smokes, and vapors during the provision of emergency medical care to normalize external respiration function and restore or support adequate hemodynamics [2, 5, 9, 23, 28, 38].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. Starting from the prehospital stage, primary measures should aim at maintaining adequate pulmonary ventilation, restoring and maintaining airway patency, and preventing aspiration-obstructive complications [5, 9, 23].
Treatment should be initiated in all patients by restoring adequate pulmonary ventilation depending on the forms of respiratory impairment.
In cases of aspiration and obturation respiratory disorders, it is necessary to perform oral cavity toilet, aspiration of upper airway contents, use medical tubes in versions for ensuring upper respiratory tract patency, including reusable oropharyngeal airways, laryngeal aspiration tubes, reinforced reusable laryngeal masks and tracheal intubation via direct laryngoscopy.
It is recommended in the event of acute respiratory failure to perform mechanical ventilation using a portable mechanical ventilator, a manual mechanical ventilator for artificial lung ventilation, a portable manual field mechanical ventilator, a motorized field mechanical ventilator, a first-aid manually operated mechanical ventilator, or a portable electronic ventilator for controlled, assisted, high-frequency mechanical ventilation and oxygen therapy. For hemodynamic disorders, as well as for detoxification therapy, intravenous infusion of blood substitutes and perfusion solutions is indicated: albumin, gelatin preparations; solutions affecting water-electrolyte balance: electrolytes, electrolytes in combination with carbohydrates, electrolytes in combination with other agents; irrigation solutions: sodium chloride solution**, combined preparations; other irrigation solutions: dextrose**. Therefore, ensuring venous access is important when providing emergency medical care. [17, 28, 38, 66, 67, 68].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended that all casualties with acute poisoning by carbon monoxide, other gases, smokes, and vapors receive oxygen therapy with 100% oxygen upon provision of emergency medical care [2, 3, 8, 17, 23, 28, 33, 38].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Commentary. The therapeutic effect of oxygen consists in increasing blood pO2 and rapid elimination of carbon monoxide from the body. In the first minutes, inhalation with 100% oxygen is performed, then for 1–3 hours with 80–90% oxygen, followed by a 40–50% oxygen-air mixture. The duration of therapy is determined by the severity of the patient's condition [1, 3, 8, 17, 23, 28, 33, 38].
It is recommended as etiotropic therapy for carbon monoxide poisoning in individuals over 18 years of age to use zinc bisvinylimidazole diacetate** [2, 69].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Commentary. Zinc bisvinylimidazole diacetate** is administered in a volume of 1.0 ml (60 mg) intramuscularly immediately after evacuating the victim from the fire zone [8, 15, 24].
3.2. Provision of specialized medical care
It is recommended for all casualties with acute poisoning by carbon monoxide, other gases, smokes, and vapors who develop acute respiratory failure and/or depressed consciousness to perform tracheal intubation and initiate mechanical ventilation [35, 43, 48, 57].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Commentary. The most dangerous complication of inhalation injury is respiratory failure, which develops against the background of airway obstruction. Clinical manifestations of respiratory failure may not manifest during the first 24–72 hours after injury, which makes the issue of early diagnosis and determining indications for tracheal intubation and respiratory support particularly relevant. Absolute indications for tracheal intubation and respiratory support are signs of respiratory failure and unconsciousness. In patients with inhalation injury, due to the high risk of gas exchange disorders, it is advisable to perform preemptive tracheal intubation and respiratory support when burns are localized on the face and neck with the risk of progressive soft tissue edema, in burns of the upper respiratory tract involving the larynx, and in grade III respiratory tract damage by combustion products. Currently, the criteria for transferring a patient to mechanical ventilation developed by the American Burn Association are considered optimal (sensitivity 77%, specificity 46%) [43]. They include: deep facial burns, stridor or respiratory failure, signs of oropharyngeal soft tissue edema during laryngoscopy, upper airway inhalation injury, altered consciousness, ventilation disorders (hypoxia, hypercapnia), and hemodynamic instability.
It is recommended for subsequent tracheobronchial tree toilet and bronchoscopic examinations to perform tracheal intubation (endotracheal tube, standard, reusable, with a diameter of at least 8 mm) [35, 43, 48, 57, 68].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. Ventilation modes and parameters. The primary goal of respiratory support is to ensure adequate gas exchange while minimizing iatrogenic lung injury, i.e., adherence to the concept of "safe mechanical ventilation." Tidal volume no more than 6 mL/kg of ideal body weight, plateau pressure less than 30 cm H2O, and positive end-expiratory pressure of at least 5 cm H2O, FiO2 0.5-0.6 [57]. Airway pressure release ventilation, based on an extended recruitment maneuver, is considered suitable for patients with acute respiratory distress syndrome. It should be noted that all recommended parameters are relevant for patients with diffuse bilateral lung parenchymal involvement; in many cases, inhalation injury may occur without the development of acute lung injury syndrome and may be predominantly obstructive in nature. High-frequency ventilation modes have been found unsuitable for patients with inhalation injury. [57]. However, there is currently no consensus on the optimal mechanical ventilation modes for patients with inhalation injury [43, 57].
It is recommended for all patients, in order to optimize therapy, to apply a personalized approach taking into account the severity of the injury and concomitant pathology [21].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended in severe hemodynamic disorders to perform anti-shock therapy: infusion of blood substitutes and perfusion solutions: albumin, gelatin preparations; solutions affecting water-electrolyte balance: electrolytes, electrolytes in combination with carbohydrates, electrolytes in combination with other agents; irrigation solutions: sodium chloride solution**, combined preparations; other irrigation solutions: dextrose** [17, 21, 66, 67, 68].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended for all casualties with acute poisoning by carbon monoxide, other gases, smokes, and vapors accompanied by water-electrolyte balance disorders to correct these disorders using solutions affecting water-electrolyte balance: electrolytes, electrolytes in combination with carbohydrates, electrolytes in combination with other agents; irrigation solutions: sodium chloride solution**, combined preparations; other irrigation solutions: dextrose** under the control of pulse examination, blood pressure measurement on peripheral arteries, and central venous pressure (CVP) measurement, hematocrit evaluation, blood total hemoglobin level testing, blood sodium level testing, blood chloride level testing, blood potassium level testing, as well as diuresis monitoring [2, 17, 21, 67, 68].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Commentary: The approach to infusion therapy must be individual. The volume and composition of the infusion program depend on the age, condition of the patient, presence of concomitant pathology, and presence of complications [1, 8, 33, 38]. Casualties with inhalation injury are indicated for infusion therapy with solutions affecting water-electrolyte balance, achieving a stable diuresis rate of at least 1 ml/kg per hour. Blood substitutes and plasma preparations (gelatin preparations, hydroxyethyl starch**) are not indicated. The volume of infusion therapy must not be less than the physiological requirement, which is 30 ml per 1 kg of body weight. Reduction of the infusion volume should be performed under the control of the fluid balance, central venous pressure measurement, and pulse oximetry [2, 13, 34, 38, 44].
It is recommended after relief of respiratory failure and associated hypoxia in patients older than 1 year to use meglumine sodium succinate solution** as an antihypoxic and detoxification agent [2, 23, 28, 70, 71].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. In adults, the drug is administered as an intravenous infusion at a rate of 1–4.5 ml/min (up to 90 drops per minute). The average daily dose is 10 ml/kg. The course of therapy is up to 11 days. In children over 1 year of age, the drug is administered as an intravenous infusion at 6–10 ml/kg per day at a rate of 3–4 ml/min. The course of therapy is up to 11 days. Contraindications: children under 1 year of age, hypersensitivity to meglumine sodium succinate** and/or any of the excipients, conditions following traumatic brain injury accompanied by cerebral edema, acute renal failure, chronic renal failure (glomerular filtration rate (GFR) less than 15 ml/min/1.73 m2), pregnancy and breastfeeding period [23, 71].
It is recommended to use Inosine + Nicotinamide + Riboflavin + Succinic acid** as an antihypoxic and antioxidant agent in patients over 18 years of age after the relief of respiratory failure and associated hypoxia [2, 23, 70].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. The drug is administered in a volume of 10 ml in 100–200 ml of 5–10% dextrose** solution or 0.9% sodium chloride** solution as an intravenous infusion twice daily every 8–12 hours for 5–10 days as part of complex therapy for toxic and hypoxic encephalopathy in acute and chronic poisonings. In comatose states, it is administered in a volume of 20 ml per administration diluted in 200 ml of dextrose** solution [23, 70, 71].
It is recommended to perform targeted antibacterial therapy with systemic antibacterial drugs if infectious respiratory complications develop [7, 17, 47].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. If the infectious process progresses, the administration of empirical antibacterial therapy based on epidemiological monitoring data from the treatment unit is indicated. There are no recommendations for the prophylactic administration of antibacterial drugs in inhalation injury based on sufficient evidence [13, 44, 46].
It is recommended for all patients with acute poisoning by carbon monoxide, other gases, smoke, and vapors complicated by inhalation injury to use proton pump inhibitors or H2-histamine receptor blockers for the prevention or treatment of erosive and ulcerative lesions of the gastrointestinal tract [1, 47, 55].
Level of Reliability of Evidence (LRE) – 4, Level of Recommendation Validity (LRV) – C.
It is recommended for all patients with acute poisoning by carbon monoxide, other gases, smoke, and vapors to undergo oxygen therapy as etiotropic therapy under normobaric oxygenation (NBO) and hyperbaric oxygenation (HBO) regimens, provided there are no contraindications and the medical facility has the technical capabilities [2, 3, 5, 8, 9, 13, 19, 23, 25, 33, 39, 50].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comments. Oxygen therapy is carried out in the form of normobaric oxygenation and hyperbaric oxygenation. The therapeutic effect of normobaric oxygenation consists of faster dissociation of HbCO and rapid elimination of carbon monoxide from the body. The mechanism of action of HBO in carbon monoxide poisoning may be associated with increased tissue oxygen saturation, faster elimination of carbon monoxide from the body, and increased ATP production. The oxygen therapy regimen affects the rate of carboxyhemoglobin dissociation. Thus, the half-life of HbCO during ambient air breathing (FiO2 – 0.21) is about 320 min, upon inhalation of 100% oxygen it decreases to 71 min, and during HBO (30% oxygen, excess pressure of 0.5 ati) it decreases to 21 min.
The working pressure in the hyperbaric chamber is determined in accordance with the severity of poisoning: in moderate intoxication, the pressure should be 0.6–0.9 ati; in severe cases, 1.0–1.5 ati. The total duration of an HBO session is at least 60–90 min, and the duration at the working pressure plateau in the chamber is 30–60 min [2, 3, 5, 8, 9, 19, 23, 25, 50].
It is recommended for pregnant women with carbon monoxide poisoning to undergo an HBO session in all cases, regardless of the severity of the mother's poisoning, given the higher affinity of fetal blood for carbon monoxide compared to adults, good placental barrier permeability, and a higher level of HbCO in fetal blood compared to maternal blood [23, 33, 38].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. In severe carbon monoxide poisoning in patients with respiratory disorders, HBO is performed in a stationary hyperbaric chamber [13].
It is recommended to repeat HBO in the somatogenic stage of carbon monoxide poisoning. According to some studies, this leads to the relief of long-term central nervous system disorders [23, 33, 38]. Given the high risk of upper respiratory tract edema in inhalation injury, HBO sessions are indicated only if airway patency can be maintained [13].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended as etiotropic therapy for carbon monoxide poisoning in individuals over 18 years of age to use zinc bisvinylimidazole diacetate** intramuscularly [2, 5, 8, 9, 69].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. Zinc bisvinylimidazole diacetate** helps reduce heme cooperativity and the relative affinity of hemoglobin for carbon monoxide, thereby inhibiting carboxyhemoglobin formation and normalizing oxygen delivery to tissues. For the prevention of poisonings, zinc bisvinylimidazole diacetate** is administered in a volume of 1 ml (60 mg) 20–30 minutes before anticipated exposure (entering a fire zone, working in smoky conditions, etc.). The protective effect of zinc bisvinylimidazole diacetate** persists for 1.5–2 hours; repeated administration of the drug is permitted 1 hour after the initial injection.
It is recommended as a therapeutic agent in individuals over 18 years of age to use zinc bisvinylimidazole diacetate** for carbon monoxide intoxication as early as possible, regardless of the severity of the injury [2, 5, 8, 9, 69].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. Zinc bisvinylimidazole diacetate** should be used one hour after the first administration (typically during pre-hospital care); repeat administration is permissible, followed by 1 ml 2–4 times a day. The maximum daily dose for an adult is 240 mg (4 ml). The protective effect of zinc bisvinylimidazole diacetate** persists for 1.5–2 hours; repeated administration of the drug is permitted 1 hour after the initial injection [2, 5, 8, 9, 69].
It is recommended as etiotropic therapy for poisoning by combustion products containing hydrogen cyanide in individuals over 18 years of age to use sodium thiosulfate** [2, 5, 8, 9, 10, 11, 69].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. To date, sodium thiosulfate** is the only registered antidote for hydrogen cyanide and other cyanides in the Russian Federation. The use of sodium thiosulfate** facilitates the conversion of cyanide ion and its derivatives into low-toxicity thiocyanate compounds, which are excreted in the urine. Sodium thiosulfate is indicated for use in adults and children from birth as an antidote for cyanide poisoning. Adults are administered a single dose of 50 ml of a 30% sodium thiosulfate** solution. If symptoms of cyanide poisoning recur, administration of the drug must be repeated at a dose equal to 50% of the initial dose. Additionally, it can be used in children from birth at the following doses: The dose of sodium thiosulfate** in children is determined at 250 mg/kg of body weight intravenously. If symptoms of cyanide poisoning recur, administration of the drug must be repeated at a dose equal to 50% of the initial dose [5, 8, 9, 10].
4. Medical Rehabilitation and Sanatorium-Resort Treatment
It is recommended for all patients with acute poisoning by carbon monoxide, other gases, smoke, and vapors presenting with neurological and/or psychiatric disorders to undergo rehabilitation in the hospital that provided medical care for the poisoning [5, 9, 23].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
5. Prevention and Dispensary Observation
It is recommended for all patients with acute poisoning by carbon monoxide, other gases, smoke, and vapors accompanied by depressed consciousness to undergo clinical follow-up (dispensary observation) for 2 years [5, 6, 8, 23, 29].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. This is due to the fact that such patients may develop long-term disorders of the central nervous system (cognitive impairment, emotional lability, sleep disorders, etc.), peripheral nervous system (cervicobrachial plexitis, polyneuritis, etc.) [5, 8, 23, 29], and cardiovascular system (cardiomyopathies) [6], which significantly reduce quality of life.
It is recommended for the entire population to observe fire safety rules, as well as occupational and domestic safety rules when working with potential sources of carbon monoxide (internal combustion engines, heating appliances, etc.) [5, 8, 9, 23].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment. In a fire zone, insulating-type or filtering-type respiratory personal protective equipment equipped with special filtering and absorbing systems (marking: CO, purple color) should be used. Considering that hydrogen cyanide can penetrate intact skin, the use of skin personal protective equipment is required in the fire zone as well as during fire-fighting and rescue operations [5, 8, 9].
6. Organization of Medical Care
6.1. Indications for hospitalization
All patients with acute poisonings caused by carbon monoxide, other gases, smoke, and vapors should preferably be hospitalized in a specialized acute poison treatment center. In the absence of an acute poison treatment center, patients with severe poisoning and complications, especially with vital function impairment, should preferably be hospitalized in hospitals with technical capabilities for hyperbaric oxygen therapy, in an intensive care unit, or in an emergency hospital department (in an intensive care ward), followed by transfer to an acute poison treatment center or, upon condition stabilization, transfer to a therapeutic department of the given medical organization.
6.2. Indications for patient discharge from the inpatient hospital
Treatment in the intensive care unit is carried out until vital function impairments stabilize and detoxification measures are completed, followed by rehabilitation measures in the acute poison treatment center, therapeutic, and pediatric departments.
7. Additional Information
It is important to ensure observation of the behavior of patients with neurological and (or) neuropsychiatric disorders in the form of toxic encephalopathy. It is difficult to calculate the frequency of providing these services in advance; however, based on data from toxicology center reports, these disorders occur regularly.
Criteria for Evaluating the Quality of Medical Care
№ | Quality criteria | Evaluation of compliance |
|---|---|---|
1 | Initial examination (consultation) by a toxicologist and (or) initial examination (consultation) by an anesthesiologist-resuscitologist performed upon hospital admission | Yes/No |
2 | Blood carboxyhemoglobin level test performed | Yes/No |
3 | Blood ethanol concentration determination by gas chromatography performed (in case of impaired consciousness) | Yes/No |
4 | Quantitative determination of urine ethanol by gas chromatography performed (in case of impaired consciousness) | Yes/No |
5 | Acid-base status and blood gas analysis performed | Yes/No |
6 | Blood glucose testing performed | Yes/No |
7 | Complete blood count performed | Yes/No |
8 | General clinical blood chemistry analysis performed | Yes/No |
9 | Coagulogram (exploratory assessment of hemostasis) performed | Yes/No |
10 | Electrocardiogram recording performed | Yes/No |
11 | Chest X-ray performed | Yes/No |
12 | X-ray of the entire skull in one or more projections, or computed tomography of the brain was performed | Yes/No |
13 | Oxygen therapy was administered via normobaric oxygenation (NBO) and hyperbaric oxygenation (HBO), provided there are no contraindications and the medical institution has the technical capabilities | Yes/No |
14 | Administration of zinc bisvinylimidazole diacetate** was performed in individuals over 18 years of age | Yes/No |
15 | Intravenous administration of solutions affecting water-electrolyte balance was performed: electrolytes, electrolytes in combination with carbohydrates, electrolytes in combination with other agents; irrigation solutions: sodium chloride** solution, combination drugs; other irrigation solutions: dextrose** in case of water-electrolyte balance disorders | Yes/No |
16 | Artificial lung ventilation was initiated (in case of depressed consciousness and/or acute respiratory failure) | Yes/No |
17 | Bronchoscopy (FBS) was performed when clinical signs of respiratory tract damage, including inhalation injury, were detected | Yes/No |
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Appendix A1. Working Group Composition
Kuznetsov Oleg Anatolyevich – Candidate of Medical Sciences, Researcher at the Department of Clinical Toxicology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Lodyagin Alexey Nikolayevich – Doctor of Medical Sciences, Chief Freelance Specialist Toxicologist of the Northwestern Federal District, Head of the Department of Clinical Toxicology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Batotsyrenov Bair Vasilyevich – Doctor of Medical Sciences, Chief Researcher at the Department of Clinical Toxicology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Balabanova Olga Leonidovna – Candidate of Medical Sciences, Senior Researcher at the Department of Clinical Toxicology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Makhnovsky Andrey Ivanovich – Candidate of Medical Sciences, Deputy Chief Physician for Emergency Medical Care, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Narziculov Rustam Abdukhalimovich – Doctor of Medical Sciences, Senior Researcher at the Department of Clinical Toxicology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Teplov Vadim Mikhailovich – Doctor of Medical Sciences, Head of the Emergency Medical Care Department, Professor at the Department of Emergency Medical Care and Surgery of Trauma, Pavlov First Saint Petersburg State Medical University.
Tolkach Pavel Gennadyevich – Doctor of Medical Sciences, Lecturer at the Department of Military Toxicology and Medical Defense, Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation.
Basharin Vadim Alexandrovich – Doctor of Medical Sciences, Professor, Head of the Department of Military Toxicology and Medical Defense, Kirov Military Medical Academy – Chief Toxicologist-Radiologist of the Ministry of Defense of the Russian Federation.
Afonchikov Vyacheslav Sergeyevich – Candidate of Medical Sciences, Head of the Clinical Center of Anesthesiology and Reanimatology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Orlova Olga Viktorovna – Candidate of Medical Sciences, Senior Researcher at the Department of Anesthesiology and Reanimatology, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Oksakovsky Alexander Alexandrovich – Anesthesiologist-Resuscitator, Dzhanelidze St. Petersburg Research Institute of Emergency Medicine.
Conflict of interest.
All members of the Working Group have confirmed that they have no financial support or conflicts of interest to disclose.
Appendix A2. Methodology for Developing Clinical Guidelines
Target audience of these clinical guidelines:
anesthesiologist-intensivist;
gastroenterologist;
infectious disease physician;
immunologist;
cardiologist;
clinical laboratory diagnostics physician;
neurologist;
neurosurgeon;
general practitioner (family physician);
otorhinolaryngologist;
ophthalmologist;
emergency physician;
forensic medical expert;
internist;
district general practitioner;
toxicologist;
transfusiologist;
functional diagnostics physician;
surgeon;
endoscopist;
psychiatrist-narcologist;
radiologist;
emergency medical technician (paramedic).
Methodology for developing clinical guidelines:
Information resources used to develop the clinical guidelines:
electronic databases (MEDLINE, "POISON" computerized information and poisons toxicological system, version 3.1, INCHEM IPCS WHO);
consolidated clinical experience of leading specialized centers for the treatment of acute chemical poisonings, clinical toxicologists of St. Petersburg, Moscow, and Yekaterinburg;
thematic monographs, textbooks, guidelines published between 1999 and 2024.
Based on the selected publications, recommendation statements were formulated and evaluated using scales for assessing levels of evidence (LoE) for diagnostic methods (diagnostic interventions), levels of evidence for prevention, treatment, and rehabilitation methods (preventive, therapeutic, rehabilitation interventions), and grades of recommendation (GoR) for prevention, diagnostics, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, rehabilitation interventions). (Table 2, Table 3, Table 4) Subsequently, each recommendation statement was thoroughly discussed at the general meeting of the working group, and consensus was reached in all cases of disagreement.
Table 2 – Scale for assessing levels of evidence (LoE) for diagnostic methods (diagnostic interventions)
Definition | |
|---|---|
1 | Systematic reviews of studies with reference standard control or systematic reviews of randomized controlled trials with meta-analysis |
2 | Individual studies with reference standard control or individual randomized controlled trials and systematic reviews of studies of any design, except randomized controlled trials, with meta-analysis |
3 | Studies without consecutive reference standard control or studies with a reference standard not independent of the test method, or non-randomized comparative studies, including cohort studies |
4 | Non-comparative studies, case report |
5 | Only justification of mechanism of action or expert opinion is available |
Table 3 – Scale for assessing levels of evidence (LoE) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, rehabilitation interventions)
LoE | Definition |
|---|---|
1 | Systematic review of randomized controlled trials (RCTs) with meta-analysis |
2 | Individual RCTs and systematic reviews of studies of any design except RCTs, with meta-analysis |
3 | Non-randomized comparative studies, including cohort studies |
4 | Non-comparative studies, case reports or case series, case-control studies |
5 | Only justification of the mechanism of action of the intervention (preclinical studies) or expert opinion is available |
Table 4 – Scale for assessing grades of recommendation (GoR) for prevention, diagnostics, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, rehabilitation interventions)
GoR | Definition |
|---|---|
A | Strong recommendation (all considered efficacy criteria (outcomes) are important, all studies are of high or acceptable methodological quality, and their conclusions on the outcomes of interest are consistent) |
B | Conditional recommendation (not all considered efficacy criteria (outcomes) are important, not all studies have high or satisfactory methodological quality and/or their conclusions regarding the outcomes of interest are inconsistent) |
C | Weak recommendation (lack of adequate quality evidence (all considered efficacy criteria (outcomes) are unimportant, all studies are of low methodological quality, and their conclusions on the outcomes of interest are inconsistent) |
Procedure for updating clinical guidelines.
The clinical guidelines update mechanism provides for their systematic revision—at least once every three years, as well as upon the emergence of new evidence-based data regarding the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.
Appendix A3. Reference Materials
Toxic effect of substances of predominantly non-medical use (T51-T65) / World Health Organization // International Statistical Classification of Diseases and Related Health Problems. Tenth Revision. Volume 1 (Part 2). – Moscow: Meditsina, 1995. – P. 337-344. (In Russ.)
Order of the Ministry of Health and Social Development of the Russian Federation No. 40 dated January 27, 2006, "On the organization of chemical-toxicological studies in the analytical diagnosis of alcohol, narcotic drugs, psychotropic, and other toxic substances in the human body." (In Russ.)
Order of the Ministry of Health of the Russian Federation No. 925n dated November 15, 2012, "On approval of the Procedure for providing medical care to patients with acute chemical poisonings." (In Russ.)
Order of the Ministry of Health of the Russian Federation No. 388n dated June 20, 2013, "On approval of the Procedure for providing emergency, including specialized emergency, medical care." (In Russ.)
Order of the Ministry of Health of the Russian Federation No. 203n dated May 10, 2017, "On approval of criteria for assessing the quality of medical care." (In Russ.)
Order of the Russian Ministry of Health No. 804n dated October 13, 2017, "On Approval of the Nomenclature of Medical Services".
Federal Law No. 489-FZ dated December 25, 2018 (as amended on June 11, 2021) "On Amendments to Article 40 of the Federal Law 'On Compulsory Medical Insurance in the Russian Federation' and the Federal Law 'On the Fundamentals of Protecting the Health of Citizens in the Russian Federation' Regarding Clinical Guidelines".
Order of the Russian Ministry of Health No. 103n dated February 28, 2019, "On Approval of the Procedure and Deadlines for the Development and Revision of Clinical Guidelines, Their Standard Template, and Requirements for Their Structure, Composition, and Scientific Validity of Information Included in Clinical Guidelines".
Order of the Russian Ministry of Health No. 1165n dated October 28, 2020, "On Approval of Requirements for the Equipment of First Aid Kits and Packs with Medications and Medical Devices".
Appendix B. Physician Action Algorithms
Appendix C. Patient Information
Information for a patient admitted in a state of poisoning with carbon monoxide, other gases, smoke, and vapors is provided after the recovery of consciousness; it must contain information on complications that occurred in the toxicogenic stage of poisoning, and planned rehabilitation treatment (if required for the given patient).
In cases of mild to moderate carbon monoxide, other gas, smoke, and vapor poisoning, the patient is informed about the health hazards of this toxic substance, potential complications, long-term effects of the poisoning, planned examinations (chemical-toxicological, clinical-biochemical, instrumental), and treatment (detoxification methods, cerebroprotective therapy).
The patient (or their legal representatives) signs an informed voluntary consent for the proposed scope of examination and treatment.
Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools
APPENDIX G1. Glasgow Coma Scale
Table specifications:
Russian name: Glasgow Coma Scale
Original name: Glasgow Coma Scale
Source: https://www.glasgowcomascale.org
Type: Rating scale
Purpose: For the quantitative assessment of the severity of coma and neuropsychiatric disorders related to impaired consciousness of any etiology.
Contents:
Eye opening | Verbal response (non-verbal children) | Verbal response | Motor response |
|---|---|---|---|
Spontaneous – 4 points To speech – 3 points To pain – 2 points No response – 1 point | Child smiles, orients to sound, tracks objects, interactive – 5 points Child can be calmed when crying, interactivity is incomplete – 4 points Calms down when crying, but not for long, moans – 3 points Does not calm down when crying, restless – 2 points No crying and no interactivity – 1 point | Oriented, answers questions quickly and correctly – 5 points Disoriented, confused speech – 4 points Word salad, answer does not make sense in relation to the question – 3 points Inarticulate sounds in response to the question – 2 points No speech – 1 point | Executes movements on command – 6 points Purposeful movement in response to painful stimulus (pushing away) – 5 points Withdrawal of limbs in response to painful stimulus – 4 points Pathological flexion in response to painful stimulus (decortication) – 3 points Pathological extension in response to painful stimulus (decerebration) – 2 points No movement – 1 point |
Key:
15 points – clear consciousness
10–14 points – moderate and deep obtundation
8–10 points – stupor
6–7 points – moderate coma
4–5 points – terminal coma
3 points – brain death
Explanation: A patient's condition according to the Glasgow Coma Scale is assessed based on three parameters, each scored in points. The points are summed up. The sum of the three responses ranges from 3 (deep coma) to 15 points (conscious patient).
Appendix G2. Poisoning Severity Score
Original title:
Original name (if any): The European Association of Clinical Poison Centres and Clinical Toxicologists Poisoning Severity Score.
Source (official developer website, validation publication): Persson H.E., Sjöberg G.K., Haines J.A., Pronczuk de Garbino J. Poisoning severity score. Grading of acute poisoning. (Eng.) // Assessment of coma and impaired consciousness. A practical scale. (Eng.) // J. Clin. Toxicol. – 1998. – Vol. 36, №3. – P. :205-213. doi: 10.3109/15563659809028940.
- rating scale
- index
- questionnaire
Purpose: For the quantitative assessment of acute poisoning severity.
Contents:
Organ / Organ system | No | Mild | Moderate | Severe | Fatal / terminal |
|---|---|---|---|---|---|
0 | 1 | 2 | 3 | 4 | |
No signs of poisoning | Mild and spontaneously resolving symptoms (signs) of poisoning | Pronounced and prolonged symptoms (signs) of poisoning | Life-threatening signs of poisoning | Dead | |
Gastrointestinal tract | Vomiting, diarrhea, pain Irritation, 1st degree burns, minimal oral ulceration Endoscopy: erythema, edema | Pronounced and prolonged vomiting, diarrhea, pain, ileus 1st degree burns in critical locations, limited areas of 2nd degree burns dysphagia Endoscopy: ulcerative transmural lesions | Massive bleeding, perforations Widespread 2nd and 3rd degree burns Severe dysphagia Endoscopy: ulcerative transmural lesions, perforations | ||
Respiratory system | Irritation, cough, shortness of breath, mild dyspnea, mild bronchospasm Chest X-ray: minimal changes | Prolonged cough, bronchospasm, dyspnea, stridor, hypoxia, need for oxygen therapy Chest X-ray: moderate changes | Manifestations of respiratory failure (due to severe bronchospasm, airway obstruction, laryngeal edema, pulmonary edema, ARDS, pneumonia, pneumothorax) Chest X-ray: severe abnormalities | ||
Nervous system | Drowsiness, dizziness, tinnitus, ataxia Restlessness Mild extrapyramidal disorders Mild cholinergic syndrome Paresthesias Minimal visual and auditory impairments | Superficial coma with preserved response to pain (pain localization, purposeful movement in response to pain) Transient bradypnea Confusion, agitation, hallucinations, delirium Infrequent generalized or focal seizures Pronounced extrapyramidal syndrome Pronounced cholinergic syndrome Localized paralysis not affecting vital functions Visual and auditory hallucinations | Deep coma with no response to pain or inappropriate response to pain Respiratory depression with respiratory failure Pronounced agitation Frequent generalized seizures, status epilepticus, opisthotonos Generalized paralysis or paralysis affecting vital functions Blindness, deafness | ||
Cardiovascular system | Single isolated extrasystoles Mild hypo-, hypertension | Sinus bradycardia (HR 40-50 in adults, 60-80 in children, 80-90 in newborns) Sinus tachycardia (HR 140-180 in adults, 160-190 in children, 160-200 in newborns) Frequent extrasystoles, atrial fibrillation, first- to second-degree AV block, prolonged QRS or QT, repolarization abnormalities Myocardial Ischemia Pronounced hypo-, hypertension | Pronounced sinus bradycardia (HR less than 40 in adults, less than 60 in children, less than 80 in newborns) Pronounced sinus tachycardia (HR greater than 180 in adults, greater than 190 in children, greater than 200 in newborns) Life-threatening ventricular dysrhythmia, third-degree AV block, asystole Myocardial infarction Shock, hypertensive crisis | ||
Metabolic disorders | Mild acid-base disorders (HCO3 15-20 or 30-40 mmol/L, pH 7.25-7.32 or 7.5-7.59) Mild electrolyte and fluid disorders (K+ 3.0-3.4 or 5.2-5.9 mmol/L) Mild hypoglycemia (2.8-3.9 mmol/L in adults) Short-term hyperthermia | Pronounced acid-base disorders (HCO3 10-14 or greater than 40 mmol/L, pH 7.15-7.24 or 7.6-7.69) More pronounced electrolyte and fluid disorders (K+ 2.5-2.9 or 6.0-6.9 mmol/L) More pronounced hypoglycemia (1.7-2.8 mmol/L in adults) Prolonged hyperthermia | Severe acid-base disorders (HCO3 less than 10 mmol/L, pH less than 7.15 or greater than 7.7) Severe electrolyte and fluid disorders (K+ less than 2.5 or greater than 7.0 mmol/L) Severe hypoglycemia (less than 1.7 mmol/L in adults) Dangerous hyperthermia | ||
Liver | Slight enzyme elevation (AST, ALT within 2-5 times the upper limit of normal) | Elevated serum enzymes, but no other biochemical criteria (e.g., ammonia, clotting factors) or clinical evidence of hepatic dysfunction | Elevated liver enzymes (more than 50 times the upper limit of normal) or presence of biochemical or clinical evidence of liver failure | ||
Kidneys | Minimal proteinuria/hematuria | Massive proteinuria/hematuria Renal dysfunction (e.g., oliguria, polyuria, serum creatinine greater than 200-500) | Renal failure (e.g., anuria, serum creatinine greater than 500) | ||
Blood | Mild hemolysis Mild methemoglobinemia | Hemolysis More pronounced methemoglobinemia (metHb 30-50%) Coagulation disorders without bleeding Anemia, leukopenia, thrombocytopenia | Massive hemolysis Severe methemoglobinemia Coagulation disorders with bleeding Severe anemia, leukopenia, thrombocytopenia | ||
Muscular system | Mild pain, weakness CK 250-1,500 IU/L | Pain, rigidity, spasms, and fasciculations Rhabdomyolysis, CK 1,500-10,000 IU/L | Severe pain, pronounced rigidity, extensive spasms and fasciculations Rhabdomyolysis with complications Crush syndrome / Positional compartment syndrome | ||
Local effects on the skin | Irritation, 1st degree burns (erythema) or 2nd degree burns covering less than 10% of body surface area | 2nd degree burns covering 10-50% of body surface area (30-50% in children) or 2nd degree burns covering less than 2% of body surface area | 2nd degree burns covering more than 50% of body surface area (more than 30% in children) or 3rd degree burns covering more than 2% of body surface area | ||
Local effects on the eyes | Irritation, redness, lacrimation, mild conjunctival edema? | Severe irritation, corneal abrasion Minor, punctate corneal ulcers | Corneal ulcers (other than punctate), perforation Permanent damage | ||
Local effect of the bite | Local tumor, pruritus Mild pain | Edema of the entire limb Moderate pain | Edema of the entire limb and a significant part of the adjacent area Extensive necrosis Critical localization threatening airway edema Severe pain |
Key:
1 – asymptomatic, mild: symptoms are mild, rapidly and spontaneously resolving;
2 – moderate – pronounced or persistent symptoms;
3 – severe – severe or life-threatening symptoms;
4 – clinical death.
Explanation: The patient's condition, according to the Poisoning Severity Scale, is assessed by the degree of organ and system damage. The occurrence of a specific symptom is checked against a scale that lists vital systems: cardiovascular, respiratory, nervous, circulatory, and gastrointestinal tract, as well as organs involved in the elimination of the toxic agent: liver and kidneys; the muscular system, local toxic effects on the body, and metabolic disorders associated with the toxicant are also evaluated. The severity grade is determined by the dominant symptom.