List of Abbreviations
BP – blood pressure
ALT – alanine aminotransferase
AST – aspartate aminotransferase
CA – caustic agents
CA – corrosive agents
GGT – gamma-glutamyl transpeptidase
GGT — gamma-glutamyl transferase
GLC – gas-liquid chromatography
GERD – gastroesophageal reflux disease
DIC – disseminated intravascular coagulation
RF – respiratory failure
NLG – nasogastric gastric lavage
IMV – invasive mechanical ventilation
ABDS – acid-base balance status
CK – creatine kinase
LDH – lactate dehydrogenase
ICD-10 – International Statistical Classification of Diseases and Related Health Problems 10th Revision
MRI – magnetic resonance imaging
ARF – acute renal failure
AKI – acute kidney injury
ARDS – acute respiratory distress syndrome
AHF – acute heart failure
BV – blood volume
RCT – randomized controlled trial
RDS – respiratory distress syndrome
SCT – spiral computed tomography
US – ultrasound examination
LCE – level of confidence of evidence
GRS – grade of recommendation strength
FBS – bronchoscopy
CCEs – chemical burn of the esophagus
CVP – central venous pressure
CNS – central nervous system
ALP – alkaline phosphatase
EFGDS – esophagogastroduodenoscopy
ECG – electrocardiography
ETS — exotoxic shock
EEG – electroencephalography
EN – enteral nutrition
** – vital and essential drugs
Terms and Definitions
Detoxification is the process of neutralizing and eliminating an exogenous toxic substance from the body. As a natural defense mechanism against a toxicant, detoxification includes various processes aimed at converting the poison into non-toxic compounds (metabolites), carried out primarily in the liver, and eliminating the poison or its metabolites through various routes – via the kidneys, intestines, liver, lungs, and skin. During natural detoxification, metabolites more toxic than the ingested toxicant may form (lethal synthesis); furthermore, undergoing metabolism in the liver and excretion through the kidneys, the toxicant and its toxic metabolites can cause damage to these organs and lead to acute renal or hepatic failure.
Chemical burn of the esophagus – local damage to the esophageal wall resulting from accidental or intentional ingestion of a caustic chemical substance.
Corrosive agents – chemical substances or mixtures thereof that, upon contact with mucous membranes or skin, cause a chemical burn accompanied by general toxic symptoms.
Poisoning by corrosive agents – a systemic disease, a distinct nosological form of burn disease of chemical etiology.
Toxicant is a broader concept than poison, used not only to designate substances that cause poisoning, but also those provoking other forms of the toxic process, and not only in organisms, but also in biological systems of other levels of organization: cells (cytotoxicant), populations (ecotoxicant).
The term "corrosive substances" is used in the Russian-translated version of ICD-10, as the English-language version designates these substances with the word "corrosive". At the same time, long before the legalized application of ICD-10 in Russia and, accordingly, the terminology in clinical toxicology, the term "caustic agent" was used, and the clinical manifestation of this effect was interpreted as a "chemical burn", including when describing the lesion pattern of the digestive tract mucosa during esophagogastroduodenoscopy (EGD) [3, 5]. Hereinafter, the term "corrosive agent" will be used, as in the International Classification of Diseases, 10th Revision.
1. Brief information on the disease or condition
Acute poisonings by corrosive agents occupy a prominent place in the structure of acute poisonings of chemical etiology. According to the Scientific and Practical Toxicological Center of the FMBA of Russia, 12 to 16% of acute poisonings are caused by corrosive agents. One of the most frequently encountered types of domestic exogenous poisonings by corrosive agents is acute poisoning with acids and alkalis.
Poisoning is a disease developing as a result of external (exogenous) exposure of the human or animal body to chemical compounds in amounts that cause disorders of physiological functions and pose a threat to life [38].
Toxicogenic stage of poisoning – the period of the course of acute chemical illness starting from the moment the toxic substance enters the body at a concentration capable of causing a specific effect [22] and lasting until its elimination. It is characterized by the specificity of clinical manifestations reflecting the chemical and toxicological properties of the toxic substance and its effect on target organs. The severity of this disease period is directly dependent on the dose of ingested poison and its concentration in the blood. The main therapeutic goal in this period is to shorten its duration as early as possible by using various methods of enhanced elimination, antidotal, and symptomatic therapy.
Somatogenic stage of poisoning – the period of the course of acute chemical illness beginning after the elimination from the body or destruction of the toxic substance in the form of residual damage to the structure and functions of various organs and systems of the body [22], manifested, as a rule, by various somatic and psychoneurological complications such as pneumonia, acute renal or hepatic failure, toxic polyneuropathy, anemia, and psycho-organic syndrome. In this stage of poisoning, specific (antidotal) therapy is not required, and detoxification may only be aimed at treating endotoxemia.
Corrosive agents – chemical substances or mixtures thereof that, upon contact with mucous membranes or skin, cause a chemical burn accompanied by general toxic symptoms [3, 35].
Poisoning by corrosive agents – a systemic disease, a distinct nosological form of burn disease of chemical etiology [35].
Condition – changes in the body arising in connection with the impact of pathogenic and (or) physiological factors and requiring the provision of medical care.
Poisonings by corrosive agents are characterized by severe medical, social, and economic consequences (costly treatment, prolonged disability, invalidism, high mortality) [22].
1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)
Corrosive agents belong to the class of the most common etiological factors of acute domestic and suicidal poisonings in the Russian Federation. Suicidal attempts predominate among the causes (65-80%), with poisonings occurring 3 times more frequently among women than among men [26]. Despite a certain downward trend in visits by patients with acetic acid poisonings, the number of patients with severe poisonings is progressively increasing.
The pathogenesis of corrosive agent poisoning consists of local and resorptive effects.
Pathogenesis of the local effect. The pathogenesis of the local effect in acids differs from that in alkalis. With an increase in the number of free H+ ions, the severity of the toxic effect increases. Hydrogen ions withdraw water from tissues, cause protein coagulation with the formation of acid albuminates, and destroy protein, leading to coagulation necrosis. Under the influence of H+ ions, hemoglobin splits due to its resulting derivatives (hematoporphyrin, methemoglobin, acid hematin). Tissues acquire a dark brown or brownish-black color [42].
Coagulation necrosis caused by acid exposure is characterized by the formation of an eschar at the site of exposure, which prevents its further penetration into deeper tissues. The eschar is denser the more free hydrogen ions the acid contains, since it is the hydrogen ions that neutralize alkalis, cause protein coagulation, and thus form this eschar. The thickness of the eschar can vary and involve not only the mucosa, but also the submucosal and even muscular layers of the digestive tract. In this case, the patient's condition will be determined by the extent and depth of tissue destruction, on the one hand, and the impairment of the secretory-evacuatory function of the gastrointestinal tract (GIT), on the other [39, 42]. Organic acids produce a less pronounced coagulation effect, but possess a resorptive action characterized by intravascular hemolysis of erythrocytes and metabolic acidosis, which is most typical for acetic and formic acids. Here, GIT dysfunction plays a lesser role in clinical manifestations. Therefore, poisonings with organic acids differ significantly in their clinical course from poisonings with inorganic acids. The action of the acid is not neutralized in the stomach, and its contact with the gastric wall is practically unrestricted, unlike the esophagus, where alkaline mucus neutralizes the acid to some extent. Therefore, when acid is ingested, the stomach is damaged to the greatest extent.
The degree of acid impact on the body depends not only on their physicochemical properties, but also on the routes of administration, duration of exposure, sensitivity, and reactivity of the body.
Unlike acids, alkalis act on protein with large masses of hydroxyl ions, causing it to swell, followed by melting and liquefaction with the formation of alkaline albuminates that are readily soluble in water. Due to their dissolving action, alkalis easily penetrate deep into tissues, forming a thick layer of moist (colliquative) necrosis. The boundaries of necrosis extend far beyond the direct action of the alkali, so there is no demarcation zone in the damaged tissues.
Strong alkalis dissolve not only the epithelium, muscles, and nervous tissue, but also dense tissues such as skin, hair, and nails. Heated alkalis have an especially powerful destructive effect.
Blood escaping from vessels damaged by the action of alkali does not clot, but its hemoglobin is converted into alkaline hematin, which imparts a greenish-brown color to the affected tissues. If death does not occur as a result of poisoning, the necrotic layers harden and slough off, forming ulcers that heal by scarring.
Alkalis poisonings are characterized by liquefactive (colliquative) necrosis. After ingestion of an alkali, an eschar does not form; the toxic substance penetrates deep into the tissues, causing diffuse destruction of the digestive tract wall. The acidic contents of the stomach significantly mitigate the situation, especially when small doses of the poison are ingested. Esophageal damage may be alleviated only by the speed of swallowing. The mucous secretions of the esophagus and saliva do not play a significant role in mitigating the action of alkali. Therefore, the deepest burns from alkali ingestion often occur in the esophagus. Liquefactive necrosis is caused by hydroxyl ions, which lead to the saponification of fats and the destruction of proteins with the formation of albuminates. Hydroxyl ions freely penetrate deep into the tissues and destroy their structure. Tissues exposed to caustic alkali liquefy, turning into a structureless, gelatinous mass. Burns from alkali exposure are almost always deep and remain aseptic for a very short time—essentially until the chemical reaction is complete. Chemical damage is replaced by purulent-inflammatory transformation on a broader scale due to the loss of local tissue resistance to infection. Strong oxidizing agents cause the same type of necrosis, but the lesions are superficial in the majority of cases [39, 42].
Pathogenesis of the resorptive action. At the site of contact with tissues, acids cause chemical burns (cauterization), leading to pain syndrome and shock. The absorption of acids and tissue breakdown products causes a general toxic effect. The resorptive effect is most pronounced in poisonings with weakly dissociating organic acids; in poisonings with acids having a high dissociation constant, symptoms of local tissue cauterization predominate [9].
Acids dissolve lipid cell membranes and easily penetrate cells. Acid radicals formed during acid dissociation promote lipid peroxidation and further cell destruction both at the site of contact with tissues (skin, oral mucosa, pharynx, stomach, etc.) and after absorption (cell membranes of the vascular wall, membranes of erythrocytes and other formed elements of the blood, and tissue cells). When ingested orally, the mucosa of the oral cavity, esophagus, and stomach suffers the most, and to a slightly lesser extent, the small intestine. This damages not only the mucosal layer but also the submucosal and even muscular layers. The severity of damage depends on the acid concentration, volume, and the presence or absence of stomach contents. Cauterization and damage to the gastric and intestinal mucosa lead to agonizing vomiting with blood, bloody diarrhea, and massive fluid and electrolyte loss. Vascular wall damage promotes the shift of the fluid portion of blood plasma into tissues. Fluid loss and its shift into tissues lead to severe hypovolemia, hemoconcentration, hypercoagulation, elevated hematocrit, decreased circulating blood volume (CBV), deterioration of myocardial contractility, and shock. Undissociated acetic acid entering the bloodstream causes erythrocyte hemolysis and the release of hemoglobin, which in the presence of acetic acid is split into globin and heme, with the latter turning into hemin compounds. The filtration rate and the degree of erythrocyte destruction (hemolysis) correlate closely. Hemoglobin and hemin compounds themselves accelerate the formation of free radicals from unoxidized peroxides, activating further lipid peroxidation and cell damage. Burn-induced tissue destruction and erythrocyte breakdown lead to blood hypercoagulation with increased plasma tolerance to heparin and decreased fibrinolytic activity. Hypercoagulation in moderate poisoning is observed for 5–7 days, after which blood clotting activity returns to normal. In severe cases, the opposite phenomenon occurs: within 10–12 hours, blood clotting factors are consumed (plasma tolerance to heparin decreases, free heparin levels and fibrinolytic activity increase). As a result, profuse secondary bleeding develops, facilitated by necrotic changes in the walls of the esophagus, stomach, and intestines. Vascular thrombosis, foci of necrosis, and simultaneous massive bleeding are characteristic of thrombohemorrhagic syndrome in acetic acid poisoning. The transport of free hemoglobin and erythrocyte membranes through renal tubules and damage to their basement membranes lead to the development of toxic nephropathy, up to acute hemoglobinuric nephrosis and acute kidney injury (AKI), which can be one of the causes of death in patients with acetic acid poisoning. Hemolysis and toxic coagulopathy lead to focal hepatic necrosis, impairing its major functions. The degree of liver damage depends on the poisoning severity. In mild poisoning, only its hemodynamics are impaired, recovering by days 5–7. In moderate poisoning, deterioration of the liver's uptake function joins on days 2–3 and normalizes by days 7–10, while hemodynamics recover by days 20–30. In severe poisoning, both hemodynamics and the uptake-excretory function of the liver are impaired within the first 24 hours. The excretory function recovers in 20–30 days, while hemodynamics and uptake function normalize only after 6 months. In severe liver damage, a sharp increase in the activity of cytoplasmic and mitochondrial enzymes is noted in the blood, indicating severe cytolytic processes in the liver [12].
The absorption of acids and the entry of acidic metabolites into the bloodstream lead to the development of initially compensated and subsequently uncompensated metabolic acidosis.
Oxalic acid poisoning has certain specific features. Oxalic acid binds calcium ions, forming compounds with them that are poorly soluble in water, resulting in a drop in the content of ionized calcium in blood plasma and tissues. Therefore, in poisonings with this acid, hypocalcemia develops very rapidly, combined with severe collapse, leading to tetanic and tonic convulsions. Calcium oxalate crystals can precipitate in the lumen of renal tubules, leading to renal failure manifested by oliguria, and in severe cases, anuria. Protein, calcium oxalate crystals, and isolated casts are found in the urine. Depending on the severity of renal damage, uremia of varying degrees develops, with an increase in residual blood nitrogen [7].
Despite the fact that locally alkalis cause more severe damage than acids, their resorptive effect is relatively small. An excess of OH- ions in the blood causes alkalosis—an increase in the alkalinity of blood and tissues—which leads to impaired cellular metabolism, weakened cardiac activity, and damage to the central nervous system (CNS). Collapse in alkali poisoning is a very significant component of the clinical course [13].
The pathogenesis scheme of acute corrosive substance poisoning is presented in Figure 1.
Figure 1. Pathogenesis scheme of acute corrosive substance poisoning [42].
1.3 Epidemiology of the Disease or Condition
Acute poisonings with caustic and corrosive agents (CCA) continue to attract the attention of toxicologists due to the severity of injuries and high mortality. Only one circumstance mitigates the situation, although not directly related to the professional activity of clinical toxicologists: a significant reduction in the frequency of poisonings by these poisons over the past 10–15 years, as evidenced by statistical data from the I.I. Janelidze St. Petersburg Research Institute of Emergency Medicine (Form No. 64) of the Acute Poisoning Treatment Center [28].
In terms of frequency, patients with acute CCA poisonings at the St. Petersburg Acute Poisoning Center until recently occupied 4th–5th place; however, over the past 10 years, the number of caustic poisonings in the city has decreased and they now occupy 7th–8th place [29].
Acute poisonings with organic acids (acetic, oxalic) account for about 70% of all CCA poisonings, which is associated with the wide availability of these acids in everyday life. Acute poisonings with inorganic acids (sulfuric, hydrochloric, nitric) account for about 7%, with alkalis (ammonia, aqueous ammonia, sodium hydroxide, potassium hydroxide) for about 15%, and with oxidizing agents (potassium permanganate, hydrogen peroxide) for about 7% [30].
It is worth noting that in the countries of the European Union and North America, corrosive poisons occupy a negligibly small place in the overall structure of acute poisonings (0.4–0.5% of the total number of toxicological patients) due to the elementary absence of acetic acid in free retail sale, as well as a high level of compliance with safety regulations in industry and everyday life [45, 61, 62, 66].
1.4 Features of Coding the Disease or Condition
Diagnosis is coded using the International Classification of Diseases, 10th Revision (ICD-10). In the version adapted for Russia, 7 digits are used to formalize the diagnosis of the disorder detected in the patient.
T54 – Toxic effect of corrosive substances:
T54.0 – Phenol and phenol homologs
T54.1 – Other corrosive organic compounds
T54.2 – Corrosive acids and acid-like substances
Acids:
hydrochloric
sulfuric
T54.3 – Corrosive alkalis and alkali-like substances
Potassium hydroxide [caustic potash]
Sodium hydroxide [caustic soda]
T54.9 – Corrosive substances, unspecified.
1.5 Classification of the disease or condition
According to their chemical structure, corrosive poisons can be divided into several groups:
1. Acids:
organic (acetic, oxalic, formic, etc.);
inorganic (sulfuric, nitric, hydrochloric, etc.).
2. Alkalis: sodium hydroxide (caustic soda), ammonia, ammonia solution, etc.
3. Oxidizing agents: potassium permanganate, hydrogen peroxide, Iodine + [Potassium iodide + Ethanol], etc.
4. Complex household chemical products containing corrosive substances («Silit», «Krot» [Mole], etc.).
5. Toxic substances with a corrosive effect (heavy metal compounds (sublimate, etc.)).
1.5.1 Acid Poisoning
Acids are hydrogen compounds (liquid, volatile and non-volatile, oily and solid) whose molecules in aqueous solution dissociate hydrogen ions capable of being replaced by metals to form salts. Aqueous solutions of acids turn blue litmus paper red and have a sour taste. Organic acids are characterized by the presence of the carboxyl group -COOH [13, 15].
INORGANIC ACID POISONING
Inorganic acids. Nitric acid. Pure nitric acid HNO3 is a colorless liquid with a specific gravity of 1.53, boiling at 86 °C, and freezing into a transparent crystalline mass at –41 °C. In air, it "fumes" similarly to concentrated hydrochloric acid, as its vapors form fine mist droplets with air moisture. Nitric acid is miscible with water in any proportion, with the 68% solution boiling at 120.5 °C. Ordinary commercial nitric acid has a specific gravity of 1.4 and this composition. Concentrated acid, containing 96–98% HNO3 and colored red-brown by dissolved nitrogen dioxide, is known as fuming nitric acid. It is consumed in large quantities in the production of nitrogen fertilizers and organic dyes. The lethal dose of a concentrated nitric acid solution upon ingestion is 8–10 mL.
Sulfuric acid. An oily liquid. Transparent and colorless in its pure form, and brown in technical grade. Boiling point 330 °C. Relative density 1.834. Miscible with water in all proportions, releasing a large amount of heat. Several varieties of sulfuric acid are distinguished: 1) monohydrate – a 98% acid solution; 2) oleum, or fuming sulfuric acid – a solution of sulfur trioxide in acid containing 18.5–20% excess sulfur trioxide; 3) crude sulfuric acid, oil of vitriol – a 93–97% acid solution; 4) chamber or Glover acid – a 63–65% acid solution mixed with lead, mercury, copper, zinc, iron, manganese, arsenic, phosphorus impurities; 5) tower acid – a 75% acid solution. Commercial sulfuric acid is often contaminated with arsenic (up to 1%) or selenium; its action on metals can produce highly toxic arsine. When sulfuric acid is heated (starting at 200 °C), sulfur trioxide vapors are released, forming a white mist with water vapor. It actively combines with water and dehydrates many organic compounds, causing their charring. It is used in the production of fertilizers, soaps, nitrocellulose, in non-ferrous and rare metal metallurgy, in the chemical industry for the production of acids and organic substances, in the dyeing and leather industries, for manufacturing batteries, and in the purification of oils, paraffin, and petroleum fractions. In household use, it is utilized for cleaning plumbing fixtures. The lethal dose of ingested sulfuric acid is 5–10 mL [11, 22].
Hydrochloric acid. A colorless or brownish-yellow solution of gaseous hydrogen chloride in water. Boiling point 85 °C. Highly soluble in water, forms a white mist in air. Produced as: 1) synthetic hydrochloric acid, containing at least 31% HC1 with iron, arsenic, and heavy metal impurities; 2) technical hydrochloric acid, containing at least 27.5% HC1 with sulfuric acid and iron impurities; 3) inhibited hydrochloric acid, containing 19–20% HC1 and 0.8–1% inhibitor; 4) food-grade hydrochloric acid, containing at least 31% HC1 with sulfuric and sulfurous acid impurities, and free chlorine. A mixture of 3 parts hydrochloric acid and 1 part nitric acid is called aqua regia and is used for technical purposes. Hydrochloric acid dissolves most metals (except gold, platinum, silver, and some others) with the evolution of hydrogen. Working with hydrochloric acid may result in the formation of other toxic substances, particularly arsine. Hydrochloric acid is produced by the electrolysis of sodium chloride. It is widely used in the production of chlorides, hydrometallurgy, electroforming, and in the canning and textile industries. Diluted hydrochloric acid is used in medical practice. In households, it is used for cleaning enameled and earthenware items and for soldering. The lethal dose of undiluted acid upon ingestion is 15–20 mL [22, 15, 21].
Hydrogen fluoride (hydrofluoric acid). Hydrofluoric acid (HF) is an aqueous solution of hydrogen fluoride. An aqueous solution of hydrogen fluoride is a colorless, strongly fuming liquid. Technical hydrofluoric acid contains 40–70% hydrogen fluoride. It is used for glass etching, engraving, and in the production of matches and phosphate fertilizers. It destroys many organic substances; due to the fluoride ion, it possesses high systemic toxicity [24, 42].
POISONING BY ORGANIC ACIDS
Organic acids. The chemical properties of organic acids are determined both by the properties of the acid group and the nature of the hydrocarbon radical.
Aliphatic organic acids (except formic acid) are weak acids. Their salts are hydrolyzed in aqueous solutions (solutions yield an alkaline reaction).
Aromatic organic acids are significantly stronger. The introduction of halogens into the acid molecule sharply increases the strength of organic acids. Upon direct contact with tissues, strong organic acids act destructively, causing irreversible changes in the state of colloids. This effect is caused by hydrogen ions formed in aqueous solutions during dissociation (the strength of the acid's action is greater the higher its dissociation constant). Organic acid vapors easily dissolve in the fluid lining the upper respiratory tract, where the action of the acids can manifest. The toxicity of organic acid derivatives (acyl halides) is also associated with the formation of acids on moist mucous membranes, which strongly irritate tissues at the moment of release. For most organic acids, a general toxic, resorptive action predominates. Monocarboxylic aliphatic acids change in the body similarly to intermediate products of normal metabolic processes. Dicarboxylic acids (except glutaric and succinic) are inert and undergo little change in the body. Succinic and glutaric acids undergo oxidation. Unsaturated fatty acids are oxidized to the final products of metabolism. Aromatic acids are excreted in a bound state: benzoic acid as hippuric acid, and others as glucuronides [15, 16, 23].
Acetic acid. Relative density 1.05. A weakly dissociating acid, under normal conditions a colorless liquid with a specific odor. Boiling point 118.1 °C. Miscible in all proportions with water, alcohol, ether, glycerin, and organic solvents. Found in the form of: 1) glacial acetic acid, containing 96–98% CH3COOH, freezing into a colorless crystalline mass upon cooling; 2) acetic essence – 40–80%; 3) diluted acid – 30%; 4) table vinegar (3–9% acid solution); 5) wine vinegar (3–4% acid). Wood vinegar contains about 6% acetic acid. Widely used in the food, chemical, and textile industries, and common in everyday life as a condiment. Acetic acid poisoning is among the most frequent domestic poisonings due to its widespread availability. In frequency of poisoning, acetic acid is second only to ethanol and carbon monoxide poisoning. Among fatal acid poisonings, those caused by acetic acid account for 70–90%. Acetic acid is one of the most frequently used substances for suicidal purposes. Accidental ingestion of acetic acid is much less common. The lethal dose of anhydrous acetic acid is 12–15 g, acetic essence – 20–40 mL, table vinegar – about 200 mL.
Formaldehyde (formic aldehyde). A colorless, suffocating gas. Maximum allowable concentration in the workplace air is 0.5 mg/m3. Easily soluble in water. Its 35–40% solution is called formalin and is a colorless, transparent liquid with a specific pungent odor. Common in medical laboratories, used in the pharmaceutical industry, and utilized as a disinfectant.
Technical formalin solutions contain up to 20% methyl alcohol. The lethal dose of formalin upon ingestion is 10–30 g, though death may occur even after smaller doses [16, 22, 42].
1.5.2 Alkali Poisoning
Alkalis are metal oxide hydrates that are highly soluble in water. They are colorless, hygroscopic substances. They have a corrosive effect on most materials in contact with them. Alkalis act via their hydroxyl ions (OH- ions). Similar to acids, alkalis can be strong, releasing large amounts of OH- ions at once, and weak. Mortality from caustic alkali poisoning is high (up to 50%). The lethal dose upon ingestion is considered to be 10–20 g, but cases of recovery after ingesting much larger doses are known. Diluted alkalis are also dangerous. Sometimes 5% solutions cause death. Even a 1% alkali solution can cause severe irritation phenomena, whereas acids at such dilutions no longer exert a toxic effect [13, 22, 24].
Caustic soda (NaOH) (sodium hydroxide) is a strong base. It is a solid white substance in the form of irregular chunks or sticks. Melting point is 320 °C. Boiling point is 1390 °C. It forms hydrates with 1.2 and 3.5 molecules of water. Solubility in water is 42% (at 0 °C). It is readily soluble in glycerol and alcohol. Solid caustic soda binds water and absorbs carbon dioxide from the air. The pH of a 1% solution is about 13. It is produced by the electrolysis of an aqueous sodium chloride solution. It is used in the production of artificial silk, in the aluminum and soap-making industries, as a component of household chemical products («Krot» liquid containing 20% NaOH), etc.
Soluble glass (liquid glass). Soluble glass is the term for alkali metal silicates with the general formula Me2O•SiO2 (Me = Na or K). The sodium salt is more common. A saturated aqueous solution of this salt is called liquid glass. Physical and chemical properties: a gelatinous mass or greenish-gray glassy lumps. It hydrolyzes and has a strongly alkaline reaction (therefore, free caustic soda and colloidal silicic acid are present in the sodium silicate solution). It is decomposed even by weak acids and CO2. It is used as a flotation agent, for the manufacture of acid-resistant cements and putties, as a filler in soap-making, for wood impregnation, in the manufacture of silicate paints, silica gel, matches, paper, silicate glue, etc.
Caustic ammonia (ammonium hydroxide). An aqueous solution of ammonia. A saturated solution contains up to 33% ammonia. The lethal dose is 10-15 ml. A 10% aqueous ammonia solution is known as ammonia water (spirit of hartshorn). The lethal dose of ammonia water is 25-50 ml, although severe disorders may occur when ingesting much smaller doses. Ammonia and its derivatives have wide industrial application for chemical synthesis, in the refrigeration industry, and in silvering. Ammonia water is a component of certain medications and is used as a stimulant. Due to its availability, suicidal poisonings and accidents used to be common. Caustic ammonia is a weak base, its degree of dissociation is much less than 1%, and the effect of hydroxyl ions is weakly manifested [3, 24, 42].
1.5.3 Oxidizing Agent Poisoning
Oxidizing agents. Potassium permanganate (KMnO4). Dark or reddish-purple crystals or fine powder with a metallic luster. Soluble in water (1:18 in cold and 1:3.5 in boiling water); forms a dark purple solution. When interacting with organic substances (coal, sugar, tannin) and easily oxidized substances, an explosion may occur; it is a strong oxidizer. It is used as an external antiseptic in aqueous solutions for washing wounds (0.1-0.5%), for mouth and throat gargling (0.01-0.1%), for lubricating ulcer and burn surfaces (2-5%), and for douches and flushing in gynecological and urological practice (0.02-0.1%). Solutions (0.02-0.1%) are also used for gastric lavage in oral poisonings with morphine, as well as phosphorus. It is ineffective in poisonings with cocaine, atropine, and barbiturates. The oxidation of hydrocyanic acid under the influence of potassium permanganate occurs only in an alkaline medium. When using the solution for gastric lavage, there is a danger of KMnO4 poisoning. The lethal dose upon ingestion is within 15-20 g.
Concentrated hydrogen peroxide solution (Perhydrol). A transparent, colorless liquid, odorless or with a weak, peculiar odor, with a slightly acidic reaction. It slowly decomposes when interacting with alkalis and organic substances, releasing oxygen. Contains 27.5-31% hydrogen peroxide (H2O2). It is commercially available as a 3% or 33% (perhydrol) aqueous solution. It is used as a solution for gargling and lubrication in inflammatory diseases of mucous membranes (stomatitis, tonsillitis), for the treatment of purulent wounds, etc. If necessary, stronger concentrations than the official hydrogen peroxide solution are prescribed. In skin disease clinics, it is used as a depigmenting agent. The lethal dose of perhydrol taken orally is generally considered to be about 100 ml.
Alcoholic solution for external use. In medical practice, various iodine solutions are widely used: iodine + [potassium iodide + ethanol], iodine + [potassium iodide + polyvinyl alcohol], iodine + potassium iodide + glycerol. Iodine solutions are used as local disinfectants and internally (for atherosclerosis, thyroid diseases [13, 15]).
1.6 Clinical presentation of the disease or condition
The rapid development of symptoms and complications makes acute corrosive substance poisoning one of the most severe diseases of chemical etiology. Signs of acute poisoning appear immediately after ingestion of the substance; the severity of clinical manifestations and the severity of poisoning depend on the dose (concentration) of the ingested substance, its exposure time, age, and concomitant pathology.
Clinical syndromes form the basis of the clinical picture of corrosive substance poisoning [20]. The main clinical syndromes:
1. chemical burn of the oropharynx, esophagus, and stomach;
2. toxic encephalopathy;
3. lung damage;
4. cardiovascular system damage;
5. toxic coagulopathy;
6. toxic nephropathy;
7. acute liver failure;
8. chemical burn disease.
1.6.1. Chemical Burn of the GI Tract
The cause of a chemical burn of the gastrointestinal tract (CBGIT) is the ingestion of concentrated solutions of inorganic or organic acids (nitric, sulfuric, hydrochloric, acetic, oxalic), alkali solutions (caustic soda, caustic potash), as well as strong oxidizing agents (potassium permanganate, hydrogen peroxide, and other oxidizing agents found in numerous modern detergents, cleaning agents, and bleaching agents), ammonia, acetone, and iodine + [potassium iodide + ethanol].
The pathogenesis of chemical esophageal burns involves local and general pathological processes.
Local changes: The depth of tissue damage and the extent of the burn depend on the type of cauterizing agent, its concentration, quantity (volume in ml), and contact time with the body's tissues. The clinical and morphological course of chemical esophageal burns includes the following stages:
1) The stage of contact between the cauterizing agent and the esophageal wall. It lasts from a few minutes until medical assistance is provided. With brief contact, a small amount, and low concentration of the chemical agent, as well as with a thermal burn, the contact stage is manifested by edema and hyperemia of the mucosa of the oral cavity, pharynx, and initial sections of the esophagus (degree I burn).
2) The stage of burn phlegmonous or necrotic-ulcerative esophagitis. It lasts from three to six days. This stage of the burn occurs with longer contact with the chemical agent and is manifested by the destruction of the mucosa and submucosa (degree II burn). Taking into account that the destruction of the submucosal layer results in scar tissue formation, some researchers subdivide this degree of burn into IIa (damage only to the mucosa) and IIb (damage to both the mucosa and the submucosa). In this stage, so-called early esophageal bleeding occurs. Necrosis of the mucosa, submucosa, and partially the muscular layer constitutes a degree III burn. At the same time, concentrated acid solutions and oxidizing agents form a dense necrotic scab (coagulation necrosis) and are accompanied by extensive thrombosis of the vessels of the esophageal wall. The action of concentrated alkali solutions produces a loose (colliquative) necrotic layer with deep tissue dissolution.
3) Necrotic tissue rejection stage (from six to ten days post-burn). The rejection of large areas of necrotic tissue leads to late esophageal hemorrhage, which can be profuse and refractory to treatment. In third-degree esophageal burns, the gastric wall is also affected in 18–30% of cases, though less severely than the esophagus, as acid ingestion generally leaves the gastric mucosa more resistant than the esophageal mucosa, while alkali ingestion is partially neutralized by the acidic gastric contents. However, this impairs the barrier function of the cardia, resulting in reflux esophagitis that sustains a prolonged pathological process, particularly when accompanied by a burn of the antrum with impaired gastric emptying. Ingestion of a large volume (more than 100 mL) of a caustic solution and its prolonged exposure lead to extensive damage not only to the esophagus and stomach, but also to the duodenum and jejunum, resulting in rapid death from intoxication (fourth-degree burn). Morphologically, the esophagus in this case appears as a dark crimson or black cord disintegrating in the hands, accompanied by perifocal serous mediastinitis, or suppurative-necrotic anaerobic mediastinitis in cases of ante-mortem perforation. The affected gastric wall in fourth-degree burns resembles "tissue paper"—thinned gray tissue with turbid effusion in the subdiaphragmatic space. In rare instances, limited esophageal necrosis may result in the formation of an esophagomediastinal or esophagorespiratory fistula. Such an outcome is possible when single, undissolved crystals of potassium permanganate, ingested orally, enter the esophagus and become embedded in its wall.
4) Granulation tissue development and scar formation stage (from six days to one year). In third-degree burns, the ulcerated surface becomes covered with granulation tissue, which is partially replaced by thin connective (scar) tissue, leading to deformation and narrowing of the esophageal lumen with impaired patency. The slow subacute inflammatory process subsides within one to two years post-burn.
5) Stage of permanent scar changes. Depending on the extent and depth of the burn, these range from isolated strictures to multiple ones, and occasionally complete obliteration of the lumen. Data on the incidence of post-burn scar strictures of the esophagus vary widely, ranging from 8% to 73% of all observed esophageal burn cases. Long-standing marked narrowing of the esophagus leads to suprastenotic dilation of its lumen; the more distally the stricture is located, the more pronounced the suprastenotic dilation. Complete obliteration of the esophageal lumen leads to the formation of a so-called blind pouch, where chronic esophagitis is sustained due to stasis of infected saliva and food masses. The esophageal wall becomes loose and thinned, and the ingestion of a large volume of fluid can result in a hydraulic rupture of the esophagus in the suprastenotic segment. Scar tissue persisting chronically against a background of esophagitis, subjected to continuous trauma from saliva and food masses (when partial patency is preserved), can lead after 15–20 years to leukoplakia, dysplasia, and ultimately malignant transformation (squamous cell carcinoma), the probability of which is more than 2,000 times higher than in individuals who have not experienced an esophageal burn (Appendix G2. Poisoning severity score).
General toxic (resorptive) effects of toxicants in chemical burns. The degree of general toxic action depends on the duration and rate of resorption. The duration of resorption for organic and inorganic acids ranges from 30 minutes to 6 hours, and for alkalis, from 30 minutes to 2 hours. The rate of resorption, in turn, depends on the burn surface area (amount of caustic agents) and the depth of the burn (concentration of caustic agents). The most frequent and severe consequence of ingesting caustic agents is the development of exotoxic shock following the ingestion of at least 50 mL of the substance. This is fundamentally driven by hypovolemia caused by impaired vascular permeability secondary to severe microcirculatory disorders. As a result of the toxicant's stressor effect on the body, the sympathoadrenal system is activated, causing arteriolar constriction, increased peripheral resistance, and elevated systolic blood pressure (compensated shock phase). Toxic coagulopathy plays a major role in the pathogenesis of toxic shock, being most pronounced in acetic acid poisoning. This is related to erythrocyte hemolysis and the coagulative effect of hemolysates. Furthermore, the release of tissue thromboplastin from destroyed tissues into the bloodstream enhances platelet aggregation and fibrin formation. The decompensated shock phase occurs upon the depletion of catecholamines and arteriolar paralysis, leading to the accumulation of underoxidized metabolic products and decompensated acidosis. Anaerobic metabolism ensues, and hypovolemia progresses against the background of hepatopathy, nephropathy, and disseminated intravascular coagulation (DIC) syndrome. This creates a vicious circle that, without treatment, results in death [42].
1.6.2. Toxic Encephalopathy
Toxic encephalopathy refers to a complex of neurological and psychiatric disorders caused by degenerative-dystrophic and atrophic changes in brain tissue resulting from exogenous intoxication.
The time of onset, nature, and severity of neuropsychiatric disorders in these cases depend on the severity and type of poisoning, exposure duration, age of the victim, effectiveness of prior treatment, and other factors.
In acute poisonings by caustic agents, encephalopathy is toxic-hypoxic in nature (THE) and represents the body's reaction to acute hypoxia of mixed genesis and endogenous intoxication under conditions of chemical trauma.
The primary cause of THE formation is impaired oxygen homeostasis, manifested as a neurosis-like psychosis with anxiety, fear, and restlessness. The clinical presentation of THE is diverse. In the early toxicogenic stage of poisoning, it manifests as neurosis-like psychosis with psychomotor agitation or depression, and inappropriate patient behavior. Subsequently, as cerebral edema progresses, neurological disorders and impaired consciousness ranging from sopor to coma may appear. The clinical picture of encephalopathy is most pronounced in patients with dyscirculatory changes and in those with alcohol or drug dependence. Against this background, cerebrovascular accidents of both hemorrhagic and ischemic types may develop [13, 24].
In the somatogenic phase of intoxication, coma may also develop against the background of impaired liver and kidney function. The clinical picture of central nervous system involvement is manifested by the development of asthenic syndrome in patients, with complaints of weakness, headache, anxiety, and a feeling of fear and restlessness. In the event of intoxication psychosis, patients may exhibit psychomotor agitation, motor restlessness, a sense of panic, and disorientation in place and time.
In severe poisonings, disturbances of consciousness develop up to coma with depression of pain sensitivity, absent or decreased corneal reflexes and pupillary reaction to light, reduced muscle tone, and diminished deep tendon reflexes. In superficial coma, muscle hypertonia and increased tendon reflexes are observed. In some cases, seizure disorders develop with generalized tonic-clonic convulsions (Appendix G2. Poisoning severity score).
1.6.3. Lung Injury
Respiratory failure (RF) is a pathological condition in which the capacity of the lungs and ventilation apparatus to maintain a normal arterial blood gas composition is limited [8, 22].
Currently, there is no universally accepted definition of respiratory failure, nor is there a consensus on its classification.
Since our goal is not to discuss this issue in general, but specifically in relation to respiratory function disorders in acute poisonings by caustic agents, we will limit ourselves to this definition.
According to its pathogenesis, respiratory failure is conventionally divided into two main groups: 1) primarily involving extrapulmonary mechanisms, 2) primarily involving pulmonary mechanisms [26, 39]. In acute poisonings by caustic agents, RF is caused by the involvement of both pulmonary and extrapulmonary mechanisms.
In clinical practice, bronchopulmonary RF is widely divided into ventilatory RF, when the mechanics of breathing are impaired, and parenchymal RF, which is caused by a pathological process in the gas-exchange zone and the interstitial space of the lungs [26, 57]. Both variants of RF occur in acute poisonings by caustic agents.
Depending on the severity of the clinical course, RF is proposed to be divided into three forms: a) latent, b) compensated, c) decompensated [42]. Toxicologists dealing with acute poisonings by caustic agents generally encounter the latter two forms.
Acute respiratory failure (ARF) in acute poisonings by caustic agents is a consequence of the development of major syndromes.
Aspiration syndrome is a critical condition developing as a result of the aspiration of gastric contents. It occurs in various types of poisoning. Aspirated material may include gastric juice, food, blood, various caustic poisons, alcohol, and water (during gastric lavage). It occupies a special place in acute caustic substance poisoning due to the aggressive nature of the aspirated material (acids, alkalis, oxidizing agents), which can cause burns of the upper respiratory tract at various levels and lead to impaired drainage function of the tracheobronchial tree, thereby contributing to the early development of pneumonia. Diagnosis and prevention of its consequences are an important task of intensive care.
The course of the disease and its prognosis depend on the quality and quantity of the aspirated material. The result of aspiration is a burn that leads to the development of acute respiratory distress syndrome (ARDS). In case of bronchial obstruction, atelectasis may form, the extent of which will depend on the caliber of the bronchus, contributing to the development or worsening of acute respiratory failure (ARF). Lung pathology may also be caused by the direct damaging effect of caustic substances on the pulmonary surfactant system.
Respiratory disorders developing immediately after aspiration – airway obstruction, bronchiolospasm, and respiratory rhythm disturbances up to apnea – lead to the development of ARF, and subsequently to pneumonia. Due to laryngeal burns, laryngeal edema and stenosis develop with the onset of ARF [8, 42].
Along with damage to the ventilatory mechanism of respiration, the causes of ARDS can include blood rheology disorders, microcirculation disturbances in the lesser circulation under the action of pro-inflammatory cytokines, as well as decreased surfactant activity.
Patients with severe caustic substance poisoning and exotoxemic burn shock (EBS) develop respiratory distress syndrome (RDS), which is characterized by impaired gas diffusion and the emergence of an intrapulmonary shunt. Clinically, it manifests as hypoxemia unresponsive to oxygen inhalation. Radiologically, it presents with disseminated pulmonary infiltration.
Pneumonia – one of the most frequent causes of respiratory failure in acute caustic substance poisoning – develops in both the toxicogenic and somatogenic stages of poisoning. The causes of pneumonia development may include not only aspiration of gastric contents, but also decreased immune reactivity, impaired cough reflex, disorders of sputum rheological properties upon administration of high doses of anticholinergics, and pathology of the pulmonary surfactant system (Appendix G2. Poisoning severity score).
1.6.4. Cardiovascular System Injury
The most frequent cardiovascular system disorder in acute caustic substance poisoning is EBS. The development of EBS in caustic substance poisoning depends on a number of factors:
patient's age;
patient's baseline status at the time of poisoning;
dose, nature, and concentration of the aggressive substance;
depth and extent of the lesion;
presence of comorbid conditions;
time elapsed from the moment of poison ingestion to the provision of adequate medical care.
Widespread chemical burn of the gastrointestinal tract is accompanied by EBS in 37% of cases, corresponding to the classical symptomatology of burn shock. Psychomotor agitation is noted, giving way to altered mental status and complete apathy toward the surroundings; the skin becomes pale and cold. Blood pressure (BP) initially rises due to the systolic component up to 150-160 mm Hg, then progressively decreases, and central venous pressure (CVP) decreases as well. Tachycardia, shortness of breath, cyanosis intensify, and urine output decreases [13, 20].
EBS in acute caustic substance poisoning is a pathological process based on massive destruction of digestive tract tissues by chemical substances, leading to hemodynamic disorders with microcirculatory disturbances, changes in water-electrolyte balance, and acid-base balance (ABB). From a pathophysiological standpoint, EBS is hypovolemic, since deep and widespread damage to the digestive tract tissues in severe burns leads to fluid losses so large that they can significantly exceed usual losses and reach 2-4 liters in the first 24 hours following the burn. Severe hemodynamic disturbances with drastic microcirculatory disorders cause impaired oxygen delivery and consumption in tissues. Mortality in shock reaches 70-80%.
Hypovolemia develops very rapidly. It reaches its peak within 5-7 hours. In addition to external fluid losses, the basis of this syndrome includes capillary dilation, increased vascular wall permeability, and marked fluid redistribution in the body. Thus, upon admission to the hospital, the hematocrit in severe burns is 50-55%. Circulating blood volume (CBV) in the first 24 hours after the burn decreases to 45-50 ml/kg of body weight (with a normal range of 70-80 ml/kg).
At the moment of chemical exposure to GI tract tissues, a huge number of cells are destroyed and damaged with the release and enzymatic generation of a mass of various biologically active substances – inflammatory mediators. These include histamine, serotonin, kinins, oxygen and unsaturated fatty acid radicals, complement factors, hydroxyl ions, superoxide anions, hydro- and lipoperoxides, and others. All of them possess vasoactive action and increase vascular wall permeability by disrupting membrane integrity in venules. When edema develops in the first minutes after a burn, a major role is also played by histamine, which is released in large quantities from mast cells immediately after injury. In burned tissues, the amount of hyaluronidase increases, causing depolymerization of hyaluronic acid, which is part of the ground substance of connective tissue and the intercellular substance of endothelial and epithelial membranes. As a result, membrane permeability increases. Destroyed leukocytes serve as a source of specific toxins – leukotrienes, which increase capillary permeability, as well as free radicals that activate the oxidation of arachidonic acid. In damaged tissues, due to an increase in the number of sodium ions, osmolality rises, which leads to an increased fluid flow into this zone and increased edema. The osmotic pressure in the interstitial fluid rises even further due to the subsequent exit of protein from the vascular bed into it, mainly albumin, which has the ability to retain water with a mass 17 times exceeding the mass of the protein itself. With a large loss of protein circulating in the vascular bed, edema also develops in unburned tissues.
In severe burns, due to impaired cell membrane permeability, sodium ions penetrate from the extracellular space into cells and drag water along with them, leading to the development of intracellular edema.
Hypovolemia in burns, and the associated hemoconcentration, significantly alter the dynamic viscosity and suspension stability of blood and the conditions of its passage through the microcirculatory bed [26, 37].
Thus, the pathophysiological basis of EBS is a decrease in capillary bed perfusion caused by four factors: a) a decrease in CBV and, consequently, the volume of circulating plasma due to exogenous causes (outflow of wound exudate) and endogenous causes (pathological pooling of the liquid plasma portion, proteins, and some blood cellular elements in the interstitial sector due to increased capillary permeability and rising colloid-osmotic pressure outside the microcirculatory bed); b) the formation of a low cardiac output syndrome due to decreased venous return to the heart, increased total peripheral resistance, myocardial-depressant effects of lysosomal enzymes, oligopeptides, and myocardial hypoxia; c) constriction of arterioles and postcapillary vessels or opening of arteriovenous shunts (under the influence of increasing tissue metabolic acidosis); d) disorders of capillary blood flow proper due to increased dynamic blood viscosity, increased capillary permeability, and microthrombosis (Appendix G2. Poisoning severity score) [8, 42].
1.6.5. Toxic Coagulopathy
EBS, intravascular hemolysis, and decompensated metabolic acidosis are the main factors in the formation of disseminated intravascular coagulation (DIC) syndrome, which complicates the course of this type of poisoning [20, 28]. Toxic coagulopathy can develop during the course of any severe poisoning by caustic substances, but it most frequently develops in acetic acid poisoning accompanied by hemolysis [5, 37].
In mild and moderate acetic acid poisoning, a tendency toward hypercoagulation is noted on days 1–2: increased plasma heparin tolerance, elevated fibrinogen, and shortened overall coagulation time on the thromboelastogram. In severe poisoning, hypocoagulation is observed: increased plasma heparin tolerance, prolonged recalcification time, decreased fibrinogen concentration, elevated free heparin content and fibrinolytic activity, increased thrombin index, and a decreased maximum amplitude of the thromboelastogram [5, 8].
1.6.6. Toxic Nephropathy
Toxic nephropathy is most characteristic of poisoning with organic acids (acetic, oxalic), occurring in 86.5% of patients with this pathology; its clinical manifestations vary from minor and short-term changes in the urine to the development of stage 3 AKI [13, 22, 40, 42].
Mild nephropathy is characterized by preserved diuresis, microhematuria (up to 6–10 fresh red blood cells per high-power field), moderate leukocyturia, and proteinuria (up to 6.6 g/L); decreased glomerular filtration rate, creatinine concentration index, and a 17% reduction in renal plasma flow compared to normal values are detected. By days 7–15 post-poisoning, normalization of the qualitative and morphological composition of urine, as well as renal functional parameters, is observed [34].
Moderate nephropathy (in 75% of cases) develops against the background of acute hemoglobinuric nephrosis. Over 1–2 days, a moderate decrease in daily diuresis is noted (by an average of 38%). Proteinuria and hemoglobinuria are detected in the urine within the first hours after poisoning. Residual nitrogen and urea levels remain within normal limits. On days 1–3, there is a moderate increase in blood creatinine (0.24 ± 0.01 mmol/L), a 38% decrease in the creatinine concentration index, a 37% decrease in glomerular filtration rate, a 34% reduction in effective renal plasma flow, and a slight decrease in tubular water reabsorption. Normalization of the urine composition occurs by days 10–20, and restoration of renal function parameters occurs by days 15–40 [8, 13].
Severe nephropathy is characterized by the development of the clinical picture of ARF against the background of acute hemoglobinuric nephrosis (in 6.7% of patients). In the first 1–3 hours, changes in urine composition appear: specific gravity ranges from 1026 to 1042 g/L, and proteinuria ranges from 6.6 to 33 g/L. The free hemoglobin content in the urine reaches high figures, with a large number of hemoglobin casts, hyaline and granular casts, renal epithelium cells, fresh, altered, and ghost red blood cells, and a large number (50–80 per high-power field) of leukocytes. Daily diuresis on days 1–3 post-poisoning decreases (to an average of 250 mL). In 25% of patients in this group, anuria develops from day 1 post-poisoning, and azotemia increases. On days 1–4, there is an increase in creatinine (1.47 ± 0.18 mmol/L), a sharp decrease in glomerular filtration rate (22.7 ± 6.2 mL/min), a significant decrease in water reabsorption (95.7 ± 2.1%), and renal plasma flow (131 ± 14.4 mL/min). Examinations on days 10–20 and 25–35 reveal a tendency toward gradual normalization of parameters, with tubular water reabsorption recovering first [7, 37].
AKI is characterized by a severe clinical course, largely driven by concomitant lesions of the lungs, gastrointestinal tract, and liver, with a mortality rate ranging around 60.6% [26].
Nephrotoxicity is determined by the following factors:
severity (depth) and extent of the chemical burn;
severity of shock;
intravascular hemolysis of red blood cells;
decompensated metabolic acidosis;
hemoconcentration;
microcirculatory disorders; mixed-type hypoxia.
At the same time, the combination of these pathological factors characterizes the severity of chemical trauma. Modern capabilities of intensive care, provided the patient seeks medical help in a timely manner, make it possible in some cases to compensate for hemodynamic shifts and homeostasis disorders and prevent the development of renal syndrome, yet fail to positively alter the course of organ burn injuries.
Thus, the root cause of AKI is shock-induced injuries associated with chemical burns and decompensated metabolic acidosis, as well as red blood cell hemolysis with the generation of excess hemoglobin breakdown products that possess membrane-toxic effects. Indirect confirmation of this circumstance may be the damage and ruptures of the basement membrane detected in this type of renal syndrome [7, 20]. If the reality were otherwise, the incidence of AKI in acetic essence poisoning would not be 6.7% [29], but would likely approach 100%. At the same time, free hemoglobin in an acidic environment forms hematin casts that occlude the lumen of the renal tubules (Appendix G2. Poisoning severity score).
1.6.7. Acute Liver Failure
Among organic acids whose poisonings cause liver damage, clinical practice most frequently deals with acetic acid. Poisonings with formic and phosphoric acids are theoretically probable and also possess hepatotoxicity. Given the absence of reliable liver support methods and the poor predictability of the course of liver injury, any deviations in liver function in critical states—both latent and overt—are classified as liver failure. However, it should be noted that latent liver function impairments are nonspecific and usually of a general toxic nature. For this reason, we will characterize only clinically pronounced forms of liver injury [8, 42].
The clinical picture is characterized by jaundice, hepatomegaly, and tenderness of the liver upon palpation; biochemical findings register bilirubinemia, a 3-to-4-fold or greater increase in aminotransferase activity, and a moderate decrease in the prothrombin index. In the first 1–2 days of its appearance, jaundice is predominantly hemolytic in nature. With a favorable course of poisoning, it may subside and resolve within the next few days. However, the early development—within the first and at the beginning of the second day—of intense jaundice and bilirubinemia indicates massive hemolysis and, accordingly, a severe condition. In this case, the shock period is prolonged, indicating an unfavorable prognosis. Typically, jaundice and bilirubinemia are recorded on days 2–3. Already on the first day in severe cases, dyscirculatory and dysmetabolic encephalopathy develops, and with the onset of liver failure, hepatogenic encephalopathy as well. In pronounced liver failure, despite the accompanying anuria and renal failure, there is a tendency toward arterial hypotension. The course of liver failure is aggravated by bleeding from burn-affected sections of the gastrointestinal tract, which accelerates the onset or development of hepatic coma. Gastrointestinal bleeding is particularly dangerous in this regard. The appearance of jaundice after a "lucid interval" in the stabilization period or later may be a manifestation of destructive pancreatitis or sepsis. One should not overlook possible background liver disease and its exacerbation [7, 27].
The examination of patients is conducted according to general rules for liver diseases. Dynamic monitoring of the coagulogram is necessary. In the presence of clinical and anamnestically relevant data, the diagnosis presents no difficulties. In cases of late-onset jaundice, an investigation should be performed to rule out the aforementioned conditions and, if necessary, consult appropriate specialists.
1.6.8. Chemical Burn Disease
Acute poisonings with caustic and corrosive substances in the presence of deep burns can take on the clinical course of chemical burn disease. Several periods can be distinguished in the development of chemical burn disease.
1. Shock or early period (1–3 days).
2. Stabilization period (up to 2 weeks).
3. Complication period (end of the 2nd to beginning of the 3rd week).
4. Recovery period (after 3 weeks), during which the consequences of chemical burns of the digestive tract manifest.
Shock or early period. The shock period is characterized by severe pain in the throat and along the esophagus, dysphagia, abdominal pain, and painful, agonizing, often intractable vomiting. Vomiting, along with plasma loss from the burn surface, contributes to extrarenal fluid and electrolyte losses, leading to a decrease in circulating blood volume and the development of hemoconcentration. Against this background, poisoning with organic acids manifests as their resorptive action in the form of intravascular hemolysis of erythrocytes and metabolic acidosis, which frequently reaches critical figures. All this leads to impaired cardiovascular activity, manifested initially in many patients by a transient increase in blood pressure (BP), tachycardia, and subsequently by arterial hypotension with a decrease in renal glomerular filtration. The urine is dark cherry or even black in color if the poisoning was caused by acetic or formic acid. In this situation, disseminated intravascular coagulation (DIC) syndrome develops, especially in cases of late seeking of medical care by the patient. In some patients poisoned with the indicated organic acids, jaundice appears by the end of the first day, and signs of liver damage are recorded [13, 22, 35].
Poisoning with alkalis also causes metabolic acidosis with corresponding clinical symptoms.
Clinical manifestations of burns caused by inorganic acids are directly due to the depth and extent of damage to the digestive tract, as well as impaired motor-evacuation function of the stomach and intestines, which often forms the clinical picture of an "acute abdomen". Caustic alkalis can produce similar abdominal clinical symptoms. Moreover, in both cases, there is a risk of early perforation of the burned hollow organ (stomach, esophagus, less frequently the small intestine).
Along with burns of the digestive tract, a burn of the upper respiratory tract frequently occurs. As a result of edema of the epiglottis and larynx, there is always a danger of asphyxia developing. The main cause of fatalities in the early period of caustic-substance poisoning is precisely asphyxia caused by the indicated reasons [51]. This mechanism of asphyxia is most commonly observed in poisoning with acetic acid and ammonia solution.
Stabilization period. Depending on the severity of the poisoning, on the second to third day, acute symptoms begin to subside: the pain syndrome eases, vomiting decreases or stops, dysphagia is alleviated, blood pressure stabilizes, heart rate decreases, and the urine becomes clearer. If there is a tendency toward arterial hypertension by this time, attention should be paid to the rate of diuresis and the excretory function of the kidneys should be assessed.
In the pharynx, on the oral mucosa, necrotic fibrinous plaques are detected in cases of organic acid burns; upon exposure to inorganic acids, the mucosa of these sections is wrinkled, lifeless, dark cyanotic, sometimes black (sulfuric acid) or yellow-brown (nitric acid). The abdomen is distended, painful, predominantly in the upper sections, with signs of intestinal paresis, more pronounced in poisoning with mineral acids and strong alkalis. It becomes necessary to rule out possible perforation and destructive pancreatitis, which can also be considered a specific complication of this type of poisoning. Already in this period, bleeding from the burn surface is not uncommon, but in most cases, it is not significant and does not require replacement [42].
Period of complications. This period is not as clearly defined as the others, since the same complications can occur in other periods as well, so this division is somewhat conventional. Nevertheless, most formidable complications occur precisely during this period of the disease, in the second to third week, when the burn scab begins to slough. We are referring to specific complications. Respiratory complications, in particular pneumonia in case of upper respiratory tract burns, and especially when the patient is on mechanical ventilation, can develop as early as the first day, and the same applies to purulent tracheobronchitis.
Specific complications of this type of burn disease include bleeding from the digestive tract, destructive pancreatitis, perforation of a hollow organ with the development of peritonitis and mediastinitis, and purulent-inflammatory transformation, most commonly in the form of phlegmon of the gastric wall.
Gastric, esophageal, and gastroesophageal bleeding is divided into early and late [28]. Early or so-called primary bleeding is bleeding in the first days and hours due to direct damage to the vascular wall, which is frequently discovered during gastric lavage. As a rule, this bleeding is not prolonged, as developing hypercoagulation contributes to rapid hemostasis. If fibrinolysis develops, the formed thrombi undergo lysis, and bleeding recurs (on days 1-2), which is called early secondary bleeding. This bleeding tends to intensify and frequently becomes massive [29, 35].
Bleeding on days 4-14 (sometimes until the end of the 3rd week) is associated with the sloughing of necrotic tissues and the formation of bleeding ulcers and is called late bleeding. According to various authors, the incidence of late bleeding is 1-5%, increasing to 21-50% with the development of acute kidney injury (AKI) [20].
Due to its severity and persistence, late bleeding poses a significant problem. Late bleeding most frequently occurs between days 9 and 11. It is observed during the sloughing of the burn scab, resulting in the formation of an extensive erosive surface, which serves as the source of bleeding. This bleeding is profuse, recurrent, and can last for a week or more. In the case of a purulent-inflammatory process in the burn area, the scab may slough at the end of the first or beginning of the second week, and accordingly, bleeding occurs during this timeframe. Bleeding at these times is more frequently observed in burns caused by strong alkalis: in these cases, a scab does not form, and the purulent-inflammatory reaction begins very early. AKI contributes to bleeding, prolonging the recurrence intervals and making the bleeding more severe.
At the time of scab sloughing, perforation of the burn-damaged organ wall most frequently occurs, often accompanied by bleeding. Just like bleeding, perforation of the hollow organ wall may occur earlier (days 5–7) in poisoning with caustic alkalis, even before purulent-inflammatory destruction. Perforation of the gastric wall occurs most frequently, less often of the esophagus, and in exceptional cases, of the small intestine. In deep burns against the background of a purulent-inflammatory process, microperforation with the formation of subphrenic or subhepatic abscesses is possible. This must be kept in mind in cases of localized upper abdominal pain accompanied by fever and high leukocytosis with a left shift.
The appearance of pain in the upper abdomen, sometimes girdle-like, and recurrent vomiting at later stages necessitates ruling out destructive pancreatitis. Obstructive jaundice arising at this time will be an additional sign of pancreatic damage. Under these circumstances, the presence of left lower lobe pneumonia will point in favor of pancreatitis. Sympathetic pneumonias are observed in the presence of the indicated localized purulent processes [7, 35].
Recovery period. This period can only be called such conditionally, because we can only speak of overall systemic recovery. Local lesions of the digestive tract are characterized by the healing of burn surfaces, which can proceed with scar formation and narrowing of the digestive tract at the burn sites. Areas that undergo scarring are those where deep burns occurred, such as the anatomical constrictions of the esophagus. It is precisely here that the deepest damage occurs. It is generally accepted that superficial burns do not result in scarring, though the development of loose membranous stenoses is possible.
In lesions of the stomach, cicatricial strictures of the pyloric region with impaired emptying function come first. Gastric deformity in the form of an hourglass stomach or total cicatrization of the stomach occurs. Changes in the position of the stomach are observed as a result of the same cicatrization: upward traction of the stomach in lesions of the esophagogastric junction. The frequency of scar formation after burns of the upper digestive tract is noted in the range of 8.3-73.0% [29, 57].
Determination of the severity of acute poisonings with corrosive and caustic substances. Based on the clinical course, mild, moderate, and severe poisonings with corrosive and caustic substances can be distinguished. When determining severity, one must proceed from systemic and local manifestations, which do not always correlate with each other. This is especially true for organic acids. It is often the case that with severe systemic manifestations, gastrointestinal burns are superficial. In poisonings with mineral acids, such a disproportion is quite rare, since systemic signs of poisoning are determined by the extent and depth of the digestive tract burn and, accordingly, the degree of impairment of its functions. The severity of poisoning with a corrosive poison is altered by a burn of the upper respiratory tract. With a relatively mild lesion of the gastrointestinal tract, respiratory lesions can be severe, lead to asphyxiation via the previously specified mechanism, and determine the prognosis. Therefore, finding a universal formula for dividing poisonings by corrosive poisons according to severity is difficult. Consequently, such a classification has to be made for each poison or group of poisons with a similar mechanism of caustic action (Appendix G2. Poisoning severity score) [7, 35, 42].
2. Diagnostics, medical indications and contraindications for diagnostic methods
Diagnosis must be based on the following diagnostic criteria:
evidence of recent use of corrosive and caustic substances (or substances) in toxic doses;
presence of symptoms and signs of poisoning corresponding to the action of corrosive and caustic substances, which must be sufficiently pronounced to lead to clinically significant disorders of consciousness and life support systems (respiration, cardiovascular system) hazardous to the patient's health and life;
the existing symptoms or signs cannot be explained by a disease unrelated to the use of corrosive and caustic substances, nor by another mental or behavioral disorder [22, 42].
2.1 Complaints and Anamnesis
Complaints:
1. Pain — mainly in the upper neck area, burning, stabbing in character, aggravated by swallowing, as well as sharp pains in the esophagus and epigastric region.
2. Vomiting — a frequent symptom in acetic acid poisonings. In grade II-III burns, it is often coffee-ground-colored or blood-tinged.
3. Salivation — develops in all patients with acetic essence poisoning, regardless of the degree of the burn. From 300 ml to 1.0–1.5 liters of saliva are secreted per day.
4. Burning sensation in the throat, along the esophagus, and in the epigastrium — this symptom occurs in all patients with chemical burns of the oropharynx and esophagus and resolves within the same timeframe as the pain syndrome [13, 33, 37].
5. Difficulty swallowing: grade I chemical burn — moderate swallowing disorder, only when consuming solid food; grade II — solid food does not pass, liquid passes with severe pain. Grades III–IV — complete absence of patency for both solid and liquid food. In the absence of adequate treatment, dysphagia worsens on days 2–3 due to an accompanying inflammatory process.
6. Taste disturbance — observed in all patients with acetic acid poisoning [28, 33, 37].
7. Cough, breathing difficulty — develop with a combination of gastrointestinal and respiratory tract burns [38, 40].
8. Fever develops with any degree of burn on days 2–4. Low-grade fever is more commonly observed; patients with severe poisoning, in the absence of adequate therapy, may experience periods of hyperthermia with symptoms of general intoxication [13, 33, 37].
9. Symptoms of general intoxication — chills, dizziness, weakness, shortness of breath develop in moderate and severe poisonings.
10. Bleeding — in patients with chemical burns of the esophagus and stomach of grade II–III. Esophageal and gastric bleeding develop most frequently [33, 34, 35].
It is recommended that all patients with acute poisoning by corrosive and caustic substances receive emergency medical care outside a medical organization by an ambulance team, including either an examination by an ambulance doctor (specialist physician) when providing emergency medical care, or an examination by an ambulance paramedic (mid-level medical specialist) when providing emergency medical care. These medical workers perform a detailed medical history taking in patients with suspected poisoning by corrosive and caustic substances [3, 10, 22].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Identification of the circumstances of the poisoning is carried out at the pre-hospital stage and in the hospital. The emergency ambulance team has a greater opportunity directly at the scene to familiarize themselves with the circumstances of the poisoning and the initial clinical manifestations, and to obtain necessary information not only from the victim, but also from people around them, including those who called the ambulance. When taking the anamnesis, it is necessary to identify the nature of the toxic agent (type, name, purpose), dose, exposure (time from the moment of poisoning to the start of treatment), route of entry into the body, and the cause of poisoning. All this, combined with the patient's complaints and physical examination data, will help establish an accurate or tentative (assuming a group of poisons with a similar mechanism of action) diagnosis, anticipate the expected clinical picture and severity of poisoning, and determine treatment tactics. Pre-hospital and hospital doctors should remember that the patient themselves, as well as their relatives, may intentionally or unintentionally provide false information about the circumstances of the poisoning [3, 10, 22].
It is recommended when constructing the diagnosis of poisoning by corrosive and caustic substances to indicate two nosological forms in the main diagnosis, for example, [22, 42]:
1. Acute oral poisoning with an unidentified corrosive liquid of severe degree.
2. Chemical burn of the oropharynx, esophagus, and stomach. Domestic (occupational). Suicide attempt (accidental).
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended when formulating the diagnosis in the main diagnosis, in addition to the nosological form of poisoning (acids, alkalis, oxidizing agents), to indicate the cause of the poisoning: accidental (occupational or domestic accident) or intentional. Intentional poisonings: suicidal (true, demonstrative), criminal (with intent to kill, with intent to induce a helpless state). The conditions (place) of occurrence (occupational, domestic, iatrogenic) and the route of entry of the poison (oral, percutaneous, parenteral, inhalation, etc.) are also indicated. Following the primary diagnosis, the clinical diagnosis indicates the leading syndromes on which the diagnosis is based: toxic encephalopathy, toxic myocardial dystrophy, toxic hepatopathy, toxic nephropathy, exogenous toxic shock, and others. Then the diagnosis indicates complications and concomitant diseases [22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended that upon admission to the hospital, all patients with acute poisoning by corrosive and caustic substances undergo an admission (examination, consultation) by a toxicologist and/or an anesthesiologist-resuscitologist no later than 10 minutes from the moment of admission to the hospital [22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
2.2 Physical Examination
Clinical diagnosis of poisoning by corrosive and caustic substances is carried out according to the generally accepted principle of diagnosing acute poisonings, but there are certain features associated with the specifics of the toxicant.
It is recommended that all patients with acute poisoning by corrosive and caustic substances undergo a sequential general examination by system and organs to confirm the diagnosis [1, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Appearance of the skin — no specific coloring; in case of respiratory failure, cyanosis of the lips, face, and acrocyanosis are noted; the skin is cold; in deep coma, increased sweating may be noted. It is necessary to identify the presence/absence of rashes, local changes in the form of a chemical burn of the oral cavity, lips, nasolabial triangle, etc., areas of skin hyperemia, which are often regarded as bruises, hematomas, burns, phlebitis, allergic edema, etc.
It is recommended that all patients with acute poisoning by corrosive and caustic substances be assessed for neurological (stupor, sopor, coma) and mental status (psychomotor agitation, hallucinations) to confirm the diagnosis [3, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Assess psychoneurological status: state of consciousness (clear, stupor, sopor, coma, psychomotor agitation, hallucinations). In the presence of a coma, assess its depth using the Glasgow Coma Scale (Appendix G1), the presence or absence of reflexes, pupil width, their reaction to light, presence (absence) of anisocoria, and muscle tone. When detecting anisocoria or pathological reflexes, pay attention to their constancy [13, 22, 37].
It is recommended that all patients with acute poisoning by corrosive and caustic substances be assessed for respiratory status: adequacy, rate, depth, uniform participation of all parts of the chest in the act of breathing, and the auscultatory pattern of the lungs to confirm the diagnosis [3, 39, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Respiratory failure may occur with alveolar hypoventilation, possible aspiration pneumonitis, or non-cardiogenic pulmonary edema [39, 42].
It is recommended that all patients with acute poisoning by corrosive and caustic substances undergo pulse oximetry to confirm the diagnosis [3, 39, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended for all patients with acute caustic substance poisoning to assess the state of the cardiovascular system in order to confirm the diagnosis: pulse examination, therapeutic auscultation for heart and pericardial pathology, heart rate measurement, and blood pressure measurement on peripheral arteries [3, 17, 22].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Toxic damage to the cardiovascular system manifests as circulatory disorders (cardiac arrhythmias, primary toxicogenic collapse, exotoxic shock) and is caused by damage to the mechanisms regulating blood circulation and the cardiovascular system (e.g., due to the progression of hypoxic damage) [3, 21].
It is recommended for all patients with acute caustic substance poisoning to examine visible mucous membranes in order to confirm the diagnosis. Pay attention to the presence/absence of injuries, especially in the face, head, abdomen, and lumbar regions (presence of chemical skin burns). Pay attention to the presence/absence of an ethanol-like odor in the exhaled air [13, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: in some cases, chemical skin burns may be present, particularly in the face, head, and abdominal regions. Pay attention to the presence/absence of an ethanol-like odor in the exhaled air [13, 22, 42].
2.3 Laboratory Diagnostics
When providing care in inpatient settings:
It is recommended that patients with caustic substance poisoning undergo a complete blood count (CBC), expanded clinical blood count, general clinical urinalysis, and standard general biochemical blood test (determination of total bilirubin in blood, free and conjugated bilirubin in blood, alanine aminotransferase activity in blood, aspartate aminotransferase activity in blood, creatine kinase activity in blood, blood urea, blood creatinine, total protein in blood, blood amylase activity, blood glucose). Assessment of acid-base balance and blood gases, coagulography (exploratory hemostasis screening): blood fibrinogen level, international normalized ratio (INR), activated partial thromboplastin time. Blood sodium level, blood potassium level, blood total calcium level. The frequency of these tests will depend on the severity of the poisoning and the duration of the patient's hospital stay [3, 22, 42, 55].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: in severe acute caustic substance poisoning, water-electrolyte balance (WEB) and acid-base balance (ABB) disorders frequently develop. They manifest as severe disturbances, most commonly in the form of decompensated mixed respiratory and metabolic acidosis, as well as hyperkalemia.
It is recommended at the specialized medical care stage for all patients with acute caustic substance poisoning to diagnose the degree of general resorptive action: assessment of acid-base balance and blood gases for the presence of metabolic acidosis [42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended for all patients with acute caustic substance poisoning to perform a standard biochemical blood test to determine the level of free hemoglobin in blood plasma [42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: The blood free hemoglobin content in mild poisoning is up to 5 g/L, in moderate poisoning – from 5 to 10 g/L, and in severe poisoning – more than 10 g/L. Free hemoglobin appears in the urine when its plasma concentration exceeds 1.0–1.5 g/L and manifests as a change in urine color, which turns red, brown, or cherry-colored depending on the level of hemoglobinuria. In all cases, acetic acid poisoning is accompanied by significant changes in blood coagulation activity [28, 49].
It is recommended to determine blood and urine ethanol and methanol levels in all patients with acute caustic substance poisoning for differential diagnosis no later than 2 hours from admission to the hospital [2, 22, 24, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
2.4 Instrumental Diagnostics
It is recommended for patients with acute caustic substance poisoning to undergo esophagogastroduodenoscopy (EGD) within the first 12–48 hours after injury to assess and determine the presence, location, and extent of the lesion [55, 56].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: It is impossible to determine the depth of the wall lesion and predict the potential risk of organ cicatricial stenosis using standard endoscopic examination [75, 76].
It is recommended to use endoscopic ultrasonography with a 12 or 20 MHz ultrasound miniprobe to determine the depth of the organ wall lesion [77].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Unlike standard endoscopy, ultrasonography allows for the evaluation of the structure of each wall layer and its involvement in the pathological process. The depth of the organ wall lesion is determined by the disruption of differentiation of the contours, boundaries, and echogenicity of the organ wall layers [78, 79].
It is recommended in cases of caustic substance poisoning to perform ultrasound of the abdominal organs and kidneys, targeted chest X-ray, esophageal fluoroscopy if esophageal stenosis is suspected, electrocardiogram recording, and fiberoptic bronchoscopy (FOB) if signs of aspiration are present [9, 22, 31, 38, 42, 58].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended in cases of caustic substance poisoning to perform repeat EGD dynamically to clarify the depth, location, and extent of the organ wall lesion [5].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: In acetic acid poisoning, EGD allows predicting the severity of burn disease and determining intensive care tactics at early stages [31, 42]. Optimal timing for EGD: for mild poisoning on days 1–2 and days 5–7 after poisoning; for moderate poisoning on days 1–2, days 5–7, and days 10–12; for severe poisoning on days 1–2 and days 25–30 [31, 42].
It is recommended for the patient population diagnosed with upper gastrointestinal (GI) tract injuries following caustic ingestion to perform a targeted chest X-ray, double-contrast esophagography, and double-contrast X-ray of the stomach and duodenum [2, 22, 31, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: X-ray examination of the esophagus is performed during the acute period (1–7 days after the burn). Starting from the 2nd and until the end of the 3rd week, there is a period of apparent well-being when inflammatory changes subside, and scarring does not manifest on X-ray control. Examination of patients during this period is undesirable, as it may lead to diagnostic errors. In the 3rd period (end of the 3rd week), the further progression of the process, burn scarring, degree of compensation, and complications can be detected [22, 42].
It is recommended for the patient population diagnosed with upper gastrointestinal (GI) tract injuries following caustic ingestion to perform emergency chest CT (computed tomography of the chest organs with intravenous bolus contrast enhancement, multiplanar, and three-dimensional reconstruction) to clarify the location, volume, and depth of the lesion, provided technical feasibility and adequate renal function [1, 12, 42, 47, 49].
Level of Evidence (LoE) – 2, Grade of Recommendation (GoE) – B.
Comment: Emergency esophageal CT has several advantages over endoscopy in the early diagnosis of chemical injuries to the esophagus and stomach. These include: non-invasiveness, the ability to assess the blood supply to all layers of the esophagus and stomach, and the state of the surrounding adipose tissue and tissues [13, 48, 49, 54]. CT provides a more detailed assessment of transmural damage to the esophageal and gastric walls and the degree of necrosis than early endoscopy [47, 68], and is more valuable than endoscopy in assessing the threat or established perforation of the stomach [51].
It is recommended during inpatient care for all patients with acute caustic substance poisoning to perform a (comprehensive) ultrasound of the abdominal organs and kidneys to obtain information on the state of internal organs [2, 12, 13, 22, 42, 63].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: In mild and moderate poisonings, pathological changes are mild, whereas in severe poisonings, signs of toxic hepatitis and nephritis are observed in the form of diffuse liver compaction, increased renal echogenicity, and pallor of the renal parenchyma [2, 12, 42, 63].
It is recommended for all patients for the early diagnosis of cardiac pathology to record an electrocardiogram with decoding, description, and data interpretation both during emergency medical care and in inpatient settings [2, 12, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: ECG – a study of mathematical heart rhythm analysis using cardiointervalography was performed, revealing the dependence of autonomic nervous system changes on the severity of acetic acid poisoning. Cardiointervalography can be used to assess the severity and prognosis of caustic substance poisoning [12, 22, 24, 42, 72].
Recommended for inpatient medical care in patients with acute caustic substance poisoning when gastric perforation or acute pancreatitis is suspected: initial examination (consultation) by a surgeon [42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Recommended for inpatient medical care in all patients with acute caustic substance poisoning: 24-hour bedside monitoring of vital functions and parameters. Continuous monitoring of an intensive care patient [2, 12, 22, 24, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
2.5 Other Procedures
Recommended for inpatient medical care in patients with impaired consciousness and acute caustic substance poisoning: brain computed tomography to rule out acute neurological or neurosurgical pathology [2, 3, 17, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: The presence of severe injuries, persistent focal neurological symptoms, prolonged coma, and lack of positive dynamics with ongoing treatment indicate acute neurological or neurosurgical pathology and serve as an indication for an advanced examination using brain computed tomography [29, 37, 53].
Recommended for all patients with acute caustic substance poisoning: initial examination (consultation) by an otolaryngologist in patients with airway burns [12, 22, 38].
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
The time factor plays a crucial role in acute caustic substance poisoning; therefore, measures to eliminate the poison from the body and correct organ and system disorders are initiated at the pre-hospital stage.
3.1. Basic Principles of Treatment for Patients with Acute Chemical Poisoning
1. Cessation of further poison intake into the body (gastric lavage and removal of poison from the skin).
2. Pathogenetic and symptomatic therapy (restoration of vital organ functions and management of leading pathological syndromes for emergency indications).
3. Local treatment of chemical burns.
3.2 Provision of Medical Care Outside a Medical Organization
3.2.1 Gastric Lavage
Recommended for all patients with acute caustic substance poisoning, for the purpose of removing poison from the stomach no later than 30 minutes after hospital admission: tube gastric lavage [3, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Recommended prior to tube gastric lavage: take measures to eliminate acute respiratory failure and severe circulatory failure, relieve pain and seizure syndromes [12, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: If the patient shows signs of laryngeal edema and a risk of asphyxia, ice should be administered orally. If ineffective, tracheal intubation is performed using lidocaine** spray for local and topical application; if intubation fails, a temporary tracheostomy is placed. Repeated attempts at tracheal intubation should not be made.
Prior to inserting the gastric tube, medication preparation is mandatory. Administer internally 1–2 tablespoons of a 1% #procaine** solution and a sip of vegetable oil. Wash out the stomach as early as possible via a tube generously lubricated with oil (after anesthesia!) [1, 3, 10, 22, 42].
The lavage procedure is performed using a large-bore tube as early as possible after poisoning. Vomiting blood and traces of blood in the wash water are not contraindications to this procedure.
In caustic substance poisoning, tube gastric lavage should not be performed if marked pharyngeal and esophageal edema is detected at the time of examination, preventing tube insertion. Esophageal bougies should not be used for gastric lavage. The danger lies in the possibility of damaging the edematous mucosa, developing bleeding, and causing perforation.
Tube gastric lavage is preferably performed using the E.A. Moshkin device (not used in children), consisting of a thick gastrointestinal tube, a rubber bulb (for active aspiration of gastric contents and prevention of clogging of the distal tube openings by food particles), and a funnel [3, 42].
If consciousness is preserved, lavage is performed in a sitting position, but the patient's arms must be secured to the chair armrests or behind to the crossbar of the chair to prevent them from removing the tube. The head is positioned strictly along the body's midline and slightly bowed toward the chest, which facilitates the passage of the tube into the esophagus. In children, the length of the inserted gastric tube is determined from the tip of the nose to the base of the xiphoid process of the sternum plus 10 cm.
To prevent wash water containing a high concentration of poison from passing from the stomach into the intestine, as well as to prevent aspiration of vomit, tube insertion and gastric lavage in patients with impaired consciousness are performed in the fixed left lateral position (on the left side without a pillow, left leg bent at the knee and hip joints, right leg straightened. The left arm is extended along the trunk posteriorly, the right hand is placed palm-down under the head). The absence of breathing through the tube and the discharge of gastric contents from it indicate that the tube is in the stomach. If the patient develops coughing or signs of asphyxiation upon introduction of the first portion of liquid, the tube must be removed and the presence of acute respiratory failure assessed. If signs of aspiration are present, proceed in accordance with the aspiration syndrome treatment algorithm.
After insertion, the tube is connected to a funnel, and gastric lavage is performed using a siphon system (the funnel is higher during fluid infusion and lower than the level of the stomach during drainage); classically, for an adult, at least 10–12 liters of room-temperature water is used; in the presence of signs of bleeding, gastric lavage is performed with water at a temperature of 8–10 °C. No more than 300–350 ml of water is injected into the stomach at one time. Clear wash water is the optimal indicator. It is necessary to ensure that the volume of fluid introduced maximally matches the volume recovered. If the patient's condition worsens, the procedure is stopped immediately [3, 42].
Table 1 – Recommended fluid volumes for administration into the stomach in children of various ages
Age | Amount of water | |
|---|---|---|
Single-dose administration (ml) | Total lavage | |
Newborns | 15-20 | 200 ml |
1–2 months | 60-90 | 300 ml |
3–4 months | 90-100 | 500 ml |
5–6 months | 100-110 | < 1 L |
7–8 months | 110-120 | < 1 L |
9–12 months | 120-150 | 1 L |
1–2 years | 150-200 | 1–2 L |
2–3 years | 200-250 | 2–3 L |
4–5 years | 250-300 | 3–5 L |
6–7 years | 250-300 | 6–7 L |
8–11 years | 300-350 | 6–8 L |
12–15 years | 300-350 | 6–8 L |
In children, gastric lavage is performed by 2–5-fold administration of a single dose.
The volume of each extraction is strictly controlled.
The first portion of wash water is collected in a jar for analysis, sealed tightly, and delivered to the hospital along with the patient.
Another calculation method can also be used: newborns are administered 5 ml/kg, 1 month – 8 ml/kg, 2–6 months – 12 ml/kg, 7–9 months – 15 ml/kg, 10 months – 1 year – 20 ml/kg, 2 years – 6 years – 16 ml/kg, 7–14 years – 14 ml/kg.
In caustic substance poisoning, gastric lavage ends with the introduction of 50–70 ml of #Algeldrate + Benzocaine + Magnesium hydroxide into the stomach.
The most frequent and dangerous complications during gastric lavage include aspiration of wash fluid and gastric contents, tears of the pharyngeal, esophageal, and gastric mucosa, tongue injuries, bleeding from damaged areas, and blood aspiration [3, 12, 22, 42].
Not recommended in all patients with acute caustic substance poisoning: tubeless gastric lavage (inducing vomiting) due to the risk of aspiration [42, 58].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Not recommended in all patients with acute caustic substance poisoning: tube gastric lavage with sodium bicarbonate** solutions [42, 63, 70].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comments: The use of sodium bicarbonate** solution as a gastric lavage agent to neutralize acids is unacceptable, as it causes acute gastric dilation due to generated carbon dioxide and increases bleeding. As a neutralizing agent, #Algeldrate + Benzocaine + Magnesium hydroxide may be used orally at 50–70 ml after gastric lavage [10, 13, 56].
3.3 Provision of Specialized Medical Care
3.3.1 Treatment of Respiratory System Injury
Recommended for all patients with acute caustic substance poisoning: start treatment by restoring adequate pulmonary ventilation depending on the forms of respiratory failure. Perform tracheobronchial tree toilet, initiate early oxygen therapy [38, 42, 44].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comments: In aspiration-obstructive respiratory disorders, patent airways must be ensured. Obstructive disorders of external respiration in caustic substance poisoning are often accompanied by hypersalivation and bronchorrhea.
Recommended for patients with acute caustic substance poisoning presenting with breathing difficulties and a risk of asphyxia: perform Oropharyngeal suction and prescribe ice orally; if ineffective, tracheal intubation under local anesthesia using a spray for local and topical application containing a 10% lidocaine** solution or placement of a permanent tracheostomy with transition to mechanical ventilation is indicated [42, 44].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Indications for mechanical ventilation (MV) are:
complete absence of spontaneous breathing;
persistent hypoventilation;
pathological respiratory arrhythmia;
tachypnea with a rate of over 36 per minute. [7]
It is recommended for patients with acute poisoning by plant growth regulators (PGRs) who develop acute respiratory failure to undergo mechanical ventilation under sedation and muscle relaxation [3, 4, 22].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: The initial oxygen concentration in the inspiratory mixture should not exceed 50%. Once the mechanical ventilation parameters are adjusted, the oxygen concentration can be gradually reduced to 30%. Optimal mechanical ventilation parameters are those that maintain PaO2 at least 100–110 mmHg and SaO3 at least 95–96% with the minimum oxygen content in the inspiratory gas mixture. In practice, this is not always achievable. In patients with ARDS, pulmonary edema, massive pneumonia, or severe heart failure, even the use of positive end-expiratory pressure may fail to provide adequate arterial blood oxygenation without high oxygen concentrations (100%). Without this, hypoxemia cannot be eliminated. As the patient's condition improves, the oxygen concentration in the inspiratory mixture should be gradually reduced to 30%. In cases of impaired central respiratory regulation—which occurs in patients over 70 years old following IV administration of opioid analgesics—the respiratory center's response to hypocapnia is virtually absent, and hypoxemia acts as the primary central respiratory stimulant. Enriching the inspired air with oxygen reduces hypoxemia, eliminates its stimulating effect, and leads to a further decrease in ventilation and hypercapnia; therefore, in such cases, oxygen therapy should be used solely as a component of mechanical ventilation [3, 4, 22].
3.3.2 Treatment of Cardiovascular System Injury
Main areas of intensive care for acute toxic shock (ATS):
ensuring pulmonary ventilation and gas exchange;
restoration of blood circulation;
correction of microcirculatory disorders;
correction of metabolic disorders;
treatment of hemolysis;
restoration of cell membrane permeability;
treatment of toxic coagulopathy;
management of pain syndrome;
detoxification therapy.
It is recommended to provide patients with acute poisoning by locally caustic substances (LCS) in the acute period of exotoxic burn shock (EBS) with comprehensive intensive therapy aimed at the correction of all major pathogenetic links. Efforts must be directed both at eliminating the most dangerous disorders and their causes, and at preventing the development of life-threatening complications in the subsequent periods of the chemical disease [2, 22, 24, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Correction of hemodynamic disorders involves eliminating BCC deficit, normalizing globular and protein composition of the blood; increasing the pumping function of the heart; eliminating vascular dystonia. The most important area of treatment for hypovolemic exotoxic burn shock in the first hours is restoring BCC with simultaneous rehydration of the interstitial space. This is achieved by intensive administration of solutions affecting the water-electrolyte balance. Vascular wall permeability under adequate intensive therapy usually begins to restore after several hours, so plasma expanders and blood plasma preparations are more appropriate to add during this period of EBS treatment. Ignoring this provision and using agents that increase oncotic pressure (human albumin**, etc.) can lead to their leakage into the interstitium and progression of tissue edema [30]. The volume and duration of volume replacement therapy depend on the nature and depth of the lesion.
The rate of fluid infusion on the 1st day should be such that at least half of the calculated daily volume is administered within the first 8 hours after the burn. This means that if infusion therapy starts 2 hours later, half of the calculated amount of fluid must be administered over 6 hours, which requires using 2 veins. Subsequently, the volume and rate of administration of therapeutic agents are adjusted based on the dynamics of diuresis, hematocrit, hemoglobin, pulse, and BP indicators.
While the volumes of infused media vary individually, their qualitative composition must be relatively constant. In the first 6 hours, the following should be infused: sodium chloride** 0.9% solution, potassium chloride + calcium chloride + magnesium chloride + sodium acetate + sodium chloride + malic acid**, 5-10% dextrose** solution, and solutions affecting water-electrolyte balance containing succinic acid, meglumine sodium succinate** — intravenously by drip at a rate of 1-4.5 ml/min (up to 90 drops per minute) at an average daily dose of 10 ml/kg for adults up to 11 days. Under the influence of solutions affecting the water-electrolyte balance, post-hypoxic metabolic acidosis of various origins is significantly reduced or completely compensated [7, 9, 25, 38, 41].
After 8-10 hours, with stable hemodynamics and sufficient hourly diuresis, the rate of IV infusion can be gradually reduced. At the same time, the administration of solutions affecting the water-electrolyte balance should be initiated. They should account for no more than 20% of the daily balance of administered fluids.
Treatment of hemolysis in organic acid poisoning is carried out by intravenous administration of hypertonic (10-20%) dextrose** solution and KAS correction. To eliminate free hemoglobin, elements of alkaline forced diuresis are used with #furosemide** (1 mg/kg for mild hemolysis, 2 mg/kg for moderate hemolysis, 3-5 mg/kg administered as a single dose for severe hemolysis) [25, 41, 42].
KAS correction is one of the primary therapeutic measures, since in the presence of decompensated KAS disorders and a pH shift towards the acidic or alkaline side, the activity of most enzyme systems—which function only within specific hydrogen ion concentration ranges—is disrupted, and the dissociation of oxyhemoglobin is impaired. To correct metabolic acidosis, it is necessary to normalize oxygen transport and intravenously drip 5% sodium bicarbonate** solution [9, 42].
It is recommended to use intravenous administration of solutions affecting water-electrolyte balance in patients with acute LCS poisoning upon the development of metabolic alkalosis, which may occur in the somatogenic stage of LCS poisoning against the background of hypokalemia and hypochloremia [7, 9, 25, 38, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended for patients with acute LCS poisoning with severe and extremely severe EBS, when prolonged exposure and therapy with solutions affecting water-electrolyte balance make it impossible to maintain blood pressure above 90 mm Hg, not to increase the volume of administered fluids (since they will still escape into the interstitium and cells), but instead to use adrenergic and dopaminergic agents, and glucocorticoids to reduce vascular wall permeability [22, 38, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Severe hemodynamic disorders ultimately lead to renal dysfunction in the form of oliguria or anuria. Therefore, the rate of diuresis, measured using urinary bladder catheterization, is the most informative diagnostic, therapeutic, and prognostic indicator of shock severity and treatment efficacy. Urine output of 0.5-1.0 ml/kg/h is optimal and indicates good renal microcirculation.
Normalization of diuresis, stabilization of blood pressure, decrease in hemoconcentration, increase in body temperature, cessation of dyspeptic disorders, and absorption of ingested fluid are indicators of treatment adequacy and recovery of the patient from the state of EBS.
3.3.3 Treatment of Toxic Coagulopathy
Since DIC syndrome is a secondary pathological process, treating the underlying disease is the decisive factor in its prevention and elimination. Treatment of the underlying pathological process alone can significantly alleviate or even prevent the development of the syndrome.
It is recommended to use drugs for treating acid-related disorders (H2-histamine receptor blockers, proton pump inhibitors, antacids) in patients with acute LCS poisoning for the prevention and treatment of gastrointestinal bleeding associated with gastrointestinal burns [2, 12, 38, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
It is recommended to use transfusion of human blood plasma at 15-20 ml per kg and tranexamic acid** at 10 mg per kg of body weight every 8 hours until bleeding stops in patients with acute LCS poisoning who develop DIC syndrome (approved for children from 1 year of age at 20 mg per kg per day**) in patients with primary fibrinolysis. In patients with DIC and secondary fibrinolysis, antifibrinolytic agents cause thromboembolic complications. These agents must be used in combination with sodium heparin** (contraindications: newborns, especially premature infants) [1, 9, 10, 12, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Along with the correction of the hemostatic system during intensive care, the patient's management should provide for the replacement of circulating blood volume deficit, maintaining hematocrit at the minimum acceptable level; elimination of the consequences of DIC syndrome: acidosis, hypoxia and other disorders (respiratory therapy, diuresis stimulation, metabolic correction); monitoring of the hemostatic system status during treatment using the most informative coagulogram parameters (exploratory hemostasis study).
3.3.4 Treatment of Toxic-Hypoxic Encephalopathy
It is recommended to provide patients with acute corrosive substance poisoning undergoing toxic encephalopathy treatment with adequate syndromic, detoxification therapy and timely correction of hypoxia [22, 24, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: For the treatment of toxic and hypoxic encephalopathy and the normalization of energy metabolism, parenteral administration of medications containing succinic acid is used: meglumine sodium succinate** administered as an intravenous infusion at a rate of 1–4.5 mL/min (up to 90 drops per minute) at an average daily dose of 10 mL/kg for adults (6–10 mL/kg/day for children) for up to 11 days (at a rate of 3–4 mL/min for children over 1 year of age), as well as inosine + nicotinamide + riboflavin + succinic acid** in a single dose of 10 mL twice a day every 8–12 hours for 5 days as an intravenous infusion diluted in 100–200 mL of 5–10% dextrose** (with blood glucose monitoring) or 0.9% sodium chloride solution**. In case of central respiratory disorders, which frequently accompany cerebral edema, mechanical ventilation is inevitable; during the first hours, it is performed in a moderate hyperventilation mode, which helps reduce intracranial pressure in corrosive substance poisoning. Subsequently, mechanical ventilation is performed in a normoventilation mode [3, 7, 10, 22, 25, 38, 42].
To accelerate dehydration, diuretics are used alongside infusion therapy. Dehydration therapy reduces cerebral edema and improves cerebral blood flow conditions. Dehydration therapy will be effective only if the delivery of oxygen to brain tissues is normalized [3, 7, 22].
3.3.5 Treatment of intoxication psychoses
It is recommended for patients with acute corrosive substance poisoning to use psycholeptics (bromdihydrochlorphenylbenzodiazepine**, initial dose for adults is 0.5–1 mg 2–3 times a day; after 2–4 days, taking into account efficacy and tolerability, the dose may be increased to 4–6 mg per day) to eliminate productive psychotic symptoms (irritability, anxiety, nervous tension, emotional lability) [3, 10, 22].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
3.3.6 Diet therapy
It is recommended to provide early enteral nutrition (EN) to patients with acute corrosive substance poisoning [18, 22, 42, 43].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Early enteral nutrition in corrosive substance poisoning serves not only as a physiological component of nutritional support, but also as a means of maintaining esophageal patency. EN is carried out taking into account the degree of chemical burn of the gastrointestinal tract and the stage of the pathological process. Both overly early expansion of the diet and feeding regimen and overly late prescription can have undesirable consequences. However, before prescribing nutritional support, it is necessary to assess liver and kidney function [18].
There are several reasons why patients refuse food: nausea, acute pain during swallowing, impaired esophageal patency, and loss of appetite. In addition, some patients who have attempted suicide refuse food due to a mental illness or developing toxic psychosis. In these cases, coordinated actions between the psychiatrist and the attending toxicologist are essential.
It is recommended for patients with acute corrosive substance poisoning to minimize unpleasant, painful sensations when swallowing and to monitor the correct feeding technique of the patient from the first day [1, 10, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: 20–30 minutes before feeding the patient, administer intramuscularly other analgesics and antipyretics, metamizole sodium** 1000 mg to adults and adolescents over 15 years of age (for children: 100 mg at the age of 3–11 months [body weight from over 5 kg to 9 kg], then in age-appropriate dosages in accordance with the instructions [not used in children under 3 months and with a body weight of less than 5 kg]) and medications for the treatment of functional gastrointestinal disorders; give the patient 50–70 ml of vegetable oil before a meal. Food should be at room temperature. The patient must be fed 4–6 times a day. In severe burns, swallowing is impaired during the first days, and therefore patients should receive parenteral and enteral tube feeding [3, 10, 22].
It is recommended to prescribe an individual diet from the first day to patients with acute corrosive substance poisoning who have preserved swallowing: unboiled sterile milk, vanilla ice cream, kissels prepared using starch (fruit, oatmeal, etc.), jelly, soft-boiled eggs, baby food (porridges) for the age of 6 months to 1 year [18, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Early EN is currently one of the physiological methods for preventing the development of a hypercatabolic reaction to burn stress, allowing the body's increased need for nutrients and calories to be compensated. However, it should not be assumed that prescribing EN is a simple, minimally invasive procedure. Due to the burn, gastrointestinal function is impaired, and its protection with the help of early EN is certainly necessary and improves treatment outcomes [18, 26].
3.3.7 Other treatment
It is recommended to perform hemodialysis in patients who develop acute kidney injury (AKI) if there are indications [6, 14, 34, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
4. Medical Rehabilitation and Sanatorium-Resort Treatment
It is recommended in case of depression or mental disorders after corrosive substance poisoning to undergo rehabilitation in a psychiatric hospital or psychoneurological dispensary (in accordance with the psychiatrist's conclusion) [12, 22, 38, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
In case of organic central nervous system damage resulting from previous toxic encephalopathy, rehabilitation is recommended in a neurology or neurorehabilitation department [12, 22, 38, 42].
Level of Evidence (LoE) – 5, Grade of Recommendation (GoR) – C.
It is recommended to carry out rehabilitation until the function of damaged organs normalizes in patients who have suffered from acute renal failure, gastrointestinal bleeding, acute hepatic failure, or esophageal stenosis in the hospital that provided medical care for the poisoning [22, 42, 64].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
5. Prevention and Dispensary Observation
It is recommended that all corrosive substances for household purposes be correctly labeled indicating the danger to health and life if ingested [12, 22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comment: Corrosive substances must be stored in special places, away from food and beverage storage areas. Children must not have access to these poisons. Caution must be exercised when working with them. Instructions for use of acids and alkalis should indicate the rules for working with them and first aid in case of accidental ingestion or contact with the skin. Educational work should be conducted with the public to raise the general cultural level of the population.
It is recommended that patients who have suffered from acute corrosive substance poisoning undergo mandatory dispensary follow-up [22, 42].
Level of Reliability of Evidence (LRE) – 5, Level of Recommendation Validity (LRV) – C.
Comments: Dispensary follow-up is carried out:
for mild esophageal and gastric burns – for 6 months;
for moderate severity – up to 1 year;
for severe poisoning – at least 5 years [22, 42].
The mainstay of dispensary follow-up is endoscopic control (esophagogastroduodenoscopy [EGD]) [22, 42].
6. Organization of Medical Care
6.1. Indications for hospitalization
All victims of acute corrosive substance poisoning should expediently be hospitalized in a specialized acute poisoning treatment center. In the absence of an acute poisoning treatment center, patients with severe poisoning and complications, especially with vital function disorders, should expediently be hospitalized in an intensive care unit, followed by transfer to a therapeutic department upon condition stabilization, and, if indicated, to a thoracic surgery department in case of esophageal stenosis development for surgical treatment if necessary [22].
6.2. Indications for patient discharge from the 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.
The duration of hospitalization is determined by the severity of the poisoning.
Average duration of inpatient treatment:
mild severity – from 3 to 7 bed-days;
moderate severity – 10–14 bed-days;
severe degree without complications – 21–28 days;
severe degree (with complications: secondary late hemorrhage, pneumonia, acute renal failure, acute hepatorenal failure) – treatment duration from 28 to 50 bed-days.
7. Additional Information
Possible outcomes of acute corrosive substance poisoning:
in mild chemical burns, the stage of esophageal and gastric mucosal regeneration occurs on days 11–20;
in burns of moderate severity, regeneration of the esophageal and gastric mucosa occurs on days 21–30;
in severe burns, by days 30–60, a thin layer of mucous membrane is formed over a large extent at the burn site, with areas of atrophy. Complete recovery after a severe burn does not occur, creating prerequisites for a chronic, sluggish inflammatory process (chronic esophagitis, gastritis);
The most serious complications of severe upper respiratory tract burns (in 3–5% of cases) include cicatricial strictures of the esophagus and stomach. Cicatricial deformations of the thoracic segment and the lower third of the esophagus are more common. The formation of strictures begins from the 2nd to 4th month after the burn and is completed by the end of the first year, sometimes later. With the progression of strictures (over the course of 1–2 years after the burn), obliteration of the esophageal lumen is possible. In the scarred esophagus with chronic esophagitis, restructuring of the epithelial layer, leukoplastic and dysplastic changes are possible, which are considered precancerous. Against this background, 16–30 years after a chemical burn, squamous cell carcinoma may develop [12, 14, 42].
Severe acute acetic acid poisoning can be fatal. The main causes of death in patients on days 1–2 are intoxication and shock, and at later dates, acute hepatorenal syndrome, pancreatic necrosis, pneumonia, and secondary bleeding [22, 69].
Criteria for Evaluating the Quality of Medical Care
№ | Quality criteria | Evaluation of compliance |
|---|---|---|
1 | An examination by a toxicologist and/or an anesthesiologist-resuscitologist was performed no later than 10 minutes from the moment of admission to the hospital. | Yes/No |
2 | Tube gastric lavage was performed no later than 30 minutes from the moment of admission to the hospital (if this had not been done at the primary health care stage). | Yes/No |
3 | Acid-base status and blood gas analysis performed | Yes/No |
4 | Blood glucose testing performed | Yes/No |
5 | Blood ethanol and methanol levels were tested no later than 2 hours from the moment of admission to the hospital. | Yes/No |
6 | Urine ethanol and methanol levels were tested no later than 2 hours from the moment of admission to the hospital. | Yes/No |
7 | Free plasma hemoglobin level was tested. | Yes/No |
8 | An ECG study was recorded. | Yes/No |
9 | Chest X-ray performed | Yes/No |
10 | Fiberoptic bronchoscopy (FOB) was performed if signs of aspiration were present. | Yes/No |
11 | Ultrasound examination of the abdominal organs and kidneys was performed. | Yes/No |
12 | EGD was performed in the first 12–48 hours after the injury. | Yes/No |
13 | A complete blood count (differential) was performed | Yes/No |
14 | A general (clinical) urinalysis was performed | Yes/No |
15 | General clinical blood chemistry analysis was performed (testing total bilirubin levels 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 levels in the blood, testing creatinine levels in the blood, testing total protein levels in the blood, determining sodium activity in the blood, testing potassium levels in the blood, testing total calcium levels in the blood). | Yes/No |
16 | A coagulogram (exploratory hemostasis study) was performed: testing blood fibrinogen levels, determining the international normalized ratio (INR), and activated partial thromboplastin time. | Yes/No |
17 | Therapy with medicinal products to correct water and electrolyte imbalances was administered. | Yes/No |
18 | Artificial lung ventilation was performed (upon the development of acute respiratory failure). | Yes/No |
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Appendix A1. Working Group Composition
1. Narzikulov, Rustam Abdukhalimovich – Dr. Sc. (Med.), Senior Researcher, Department of Clinical Toxicology, State Budgetary Institution "Saint Petersburg I.I. Janelidze Research Institute of Emergency Medicine".
2. Lodyagin, Aleksey Nikolaevich – Dr. Sc. (Med.), Chief Freelance Specialist Toxicologist of the Northwestern Federal District, Head of the Department of Clinical Toxicology, State Budgetary Institution "Saint Petersburg I.I. Janelidze Research Institute of Emergency Medicine".
3. Batotsyrenov Bair Vasilievich – D.Sc. in Medicine, Chief Researcher, Department of Clinical Toxicology, Saint Petersburg State Budgetary Healthcare Institution "I.I. Dzhanelidze Research Institute of Emergency Medicine".
4. Kuznetsov Oleg Anatolievich – Ph.D. in Medicine, Researcher, Department of Clinical Toxicology, Saint Petersburg State Budgetary Healthcare Institution "I.I. Dzhanelidze Research Institute of Emergency Medicine".
5. Makhnovsky Andrei Ivanovich – Ph.D. in Medicine, Deputy Chief Physician for Emergency Medical Care, Saint Petersburg State Budgetary Healthcare Institution "I.I. Dzhanelidze Research Institute of Emergency Medicine", Saint Petersburg.
6. Teplov Vadim Mikhailovich – D.Sc. in Medicine, Associate Professor, Head of the Inpatient Emergency Department, Professor of the Department of Emergency Medical Care and Injury Surgery, FSBEI HE "Academician I.P. Pavlov First Saint Petersburg State Medical University" of the Ministry of Health of Russia.
7. Makarov Aleksei Vladimirovich – Ph.D. in Medicine, Endoscopist, Department of Endoscopy and Endoluminal Surgery, Sklifosovsky Research Institute of Emergency Care of the Moscow Healthcare Department.
8. Simonova Anastasia Yurievna – Ph.D. in Medicine, Leading Researcher, Department of Acute Poisoning and Somatopsychiatric Disorders, Sklifosovsky Research Institute of Emergency Care of the Moscow Healthcare Department, Chief Freelance Specialist Toxicologist of the Moscow Healthcare Department, Head of the Department of Clinical Toxicology, FSBEI FPE RMACPE MOH Russia.
There is no conflict of interest.
Appendix A2. Methodology for Developing Clinical Guidelines
Target audience of these clinical guidelines:
1. anesthesiologist-resuscitator;
2. gastroenterologist;
3. laboratory geneticist / clinical laboratory diagnostics physician;
4. general practitioner (family physician);
5. otorhinolaryngologist;
6. emergency physician;
7. internist;
8. district internist;
9. toxicologist;
10. functional diagnostics physician;
11. surgeon;
12. endoscopist;
13. psychiatrist-narcologist;
14. Ambulance paramedic.
Methodology for Developing Clinical Guidelines
The working group members independently performed a systematic search and selection of publications. The search was conducted in the PubMed search engine (http://www.ncbi.nlm.nih.gov/pubmed/), the Cochrane Library (http://www.cochranelibrary.com/), the eLIBRARY.ru scientific electronic library (http://elibrary.ru/defaultx.asp), as well as clinical trial registries: https://clinicaltrials.gov/ and https://www.clinicaltrialsregister.eu/ctr search/search. A total of 210 publications were found, of which 105 were selected. Based on the selected publications, consensus recommendations were formulated and assessed using scales for evaluating the levels of evidence reliability and diagnostic methods, the levels of evidence reliability (LER) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions), and the grades of recommendation (GOR) for prevention, diagnostics, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions). (Table 2, Table 3, Table 4) Subsequently, each consensus recommendation was thoroughly discussed at a general meeting of the working group, and consensus was reached in all cases of disagreement.
Table 2 – Scale for assessing levels of evidence (LE) for diagnostic methods (diagnostic interventions)
LoE | 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 (LE) for methods of prevention, treatment, and medical rehabilitation, including those based on natural therapeutic factors (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 (GR) for methods of prevention, diagnosis, treatment, and medical rehabilitation, including those based on natural therapeutic factors (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 are of high or acceptable methodological quality, and/or their conclusions on 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
1. Order of the Russian Ministry of Health No. 298 dated October 5, 1998, "On Analytical Diagnostics of Narcotic Drugs, Psychotropic, and Other Toxic Substances in the Human Body."
2. Order of the Ministry of Health and Social Development of Russia No. 40 dated January 27, 2006, "On Organizing Chemical-Toxicological Research in the Analytical Diagnostics of the Presence of Alcohol, Narcotic Drugs, Psychotropic, and Other Toxic Substances in the Human Body."
3. Order of the Russian Ministry of Health No. 925n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care for Acute Chemical Poisoning."
4. Order of the Russian Ministry of Health No. 919n dated November 15, 2012, "On Approval of the Procedure for Providing Medical Care to Adult Patients Profiled in 'Anesthesiology and Reanimatology'."
5. Order of the Russian Ministry of Health No. 203n dated May 10, 2017, "On Approval of Criteria for Assessing the Quality of Medical Care."
6. Order of the Russian Ministry of Health No. 804n dated October 13, 2017, "On Approval of the Nomenclature of Medical Services."
7. Federal Law No. 489-FZ dated December 25, 2018, "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."
8. Order of the Russian Ministry of Health No. 103n dated February 28, 2019, "On Approval of the Procedure and Timelines for the Development of Clinical Guidelines, Their Revision, the Standard Form of Clinical Guidelines, and Requirements for Their Structure, Composition, and Scientific Validity of Information Included in Clinical Guidelines."
9. Decree of the Government of the Russian Federation No. 2406-r dated October 12, 2019, "On Approval of the List of Vital and Essential Medicines, as Well as Lists of Medicinal Products for Medical Use and the Minimum Assortment of Medicinal Products Necessary for the Provision of Medical Care."
10. Order of the Russian Ministry of Health No. 1165n dated October 28, 2020, "On Approval of Requirements for the Equipping of Medical Kits and Sets with Medicines and Medical Devices for Providing Emergency Medical Care."
11. Order of the Russian Ministry of Health No. 388n dated June 20, 2013, "On Approval of the Procedure for Providing Emergency, Including Specialized Emergency, Medical Care."
Appendix B. Physician Action Algorithms
Appendix C. Patient Information
Information for a patient admitted with impaired consciousness is provided after consciousness is restored and must include details on complications that occurred during the toxicogenic stage of poisoning, as well as planned treatment during the rehabilitation process (if required for the given patient).
In cases of acute mild and moderate poisoning, the patient is informed about the health hazards of these toxic substances, potential complications, long-term consequences of poisoning, planned examinations (chemical-toxicological, clinical-biochemical, instrumental), and treatment (detoxification methods, pathogenetic and specific therapy). The patient (or their legal representatives) signs an informed voluntary consent for the proposed scope of examination and treatment.
Follow-up with a general practitioner (therapist) at the local outpatient clinic is recommended. An otolaryngologist should be consulted if necessary.
A sparing diet and limitation of physical exertion are recommended [10, 65].
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:
Table 5 – Glasgow Coma Scale
Criterion | Possible options | Score |
|---|---|---|
Eye opening | spontaneous | 4 |
to speech – 3 points | 3 | |
to pain | 2 | |
Absent | 1 | |
Verbal response | response to a question is prompt and correct, the patient is oriented | 5 |
confused conversation | 4 | |
response does not make sense in relation to the question | 3 | |
incomprehensible sounds | 2 | |
no speech | 1 | |
Motor response | purposeful movement on command | 6 |
purposeful movement in response to pain (pushing away) | 5 | |
withdrawal of a limb in response to pain | 4 | |
abnormal flexion in response to pain | 3 | |
abnormal extension in response to pain | 2 | |
no response | 1 | |
Total score |
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
Note. According to the Glasgow Coma Scale, the patient's condition is evaluated based on three parameters, each scored individually. The scores are summed. The sum of the three responses ranges from 3 (deep coma) to 15 points (conscious patient).
Appendix G2. Poisoning Severity Score
Table specifications:
Russian title: Poisoning severity score
Original title: Poisoning severity score
Source: https://www.who.int/publications/m/item/poisoning-severity-score
Type: Rating scale
Purpose: for quantitative assessment of the severity of acute poisonings.
Contents:
Organ / organ system | none | 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 | death | |
Gastrointestinal tract | Vomiting, diarrhea, pain; irritation, 1st-degree burns, minimal oral ulcerations Endoscopy: erythema, edema | Severe and prolonged vomiting, diarrhea, pain, ileus, 1st-degree burns in critical locations, localized 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 Paresthesia 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) | 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) | ||
Frequent extrasystoles, atrial fibrillation, first- to second-degree AV block, prolonged QRS or QT, repolarization abnormalities Myocardial Ischemia Pronounced hypo-, hypertension | Life-threatening ventricular dysrhythmia, third-degree AV block, asystole Myocardial infarction Shock, hypertensive crisis | ||||
Metabolic disorders | Mild acid-base disorders ($HCO_3$ 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 | Severe acid-base disorders ($HCO_3$ 10–14 or >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 | Critical acid-base disorders ($HCO_3$ <10 mmol/L, pH <7.15 or >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) Severe 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 <2% of body surface area | 2nd-degree burns covering >50% of body surface area (>30% in children) or 3rd-degree burns covering >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:
asymptomatic, mild: symptoms are mild, rapidly and spontaneously resolving;
moderate: pronounced or persistent symptoms;
severe: severe or life-threatening symptoms;
clinical death.
Note. According to the Poisoning Severity Score, the patient's condition is evaluated based on 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, hematological, and gastrointestinal—as well as organs involved in the elimination of the toxic agent (liver and kidneys), along with the muscular system, local toxic effects on the body, and metabolic disturbances caused by the toxicant. The severity degree is determined by the dominant symptom.