Intensive Care of Acute Poisoning - A. V. Hovenko 2010

Main types of acute poisoning and their treatment
Chemical poisoning
Alcohol poisoning

One of the most widespread groups of technical and household substances used by humans is represented by alcohols and alcohol-containing mixtures. In clinical practice, poisoning by substances of this group is classified as alcohol surrogate poisoning. All alcohol surrogates are divided into two categories: those containing ethanol as a base, and those that do not.

The first category includes various solutions and liquids manufactured on The basis of ethyl alcohol or containing a significant amount of it (true alcohol surrogates). Solutions and liquids belonging to this group cause intoxication that is clinically similar to alcohol poisoning. These substances are primarily based on industrial alcohol containing high amounts of fusel oils, along with various specific additives such as Essential Oils, acetone, and colorants. They include: Hydrolysis and sulfite alcohols (obtained from wood via hydrolysis); synthetic ethyl alcohols (obtained by Ethylene Hydration and used mainly for industrial purposes); crude ethyl alcohol (produced from food raw Materials and used both for food-grade alcohol production and industrial purposes); denatured alcohol (industrial alcohol with minor admixtures of methyl alcohol and aldehydes); perfumery and cosmetics such as colognes and lotions (50–60% solutions of food-grade or industrial ethyl alcohol with added Water/23.html">Essential oils and other ingredients); BF glue based on industrial ethyl alcohol, phenol-formaldehyde resin, polyvinyl acetate, and acetone; wood polish (a mixture of industrial ethyl alcohol with acetone, butyl, and amyl alcohols); medicinal plant tinctures (tinctures of hawthorn, zammanicha, hellebore, etc.), water-alcohol plant extracts (extracts of Rhodiola rosea, Eleutherococcus, etc.), alcohol-based plant juices (aloe, kalanchoe juices, etc.); and other solutions containing a considerable amount of ethyl alcohol.

The second category comprises liquids that do not contain ethyl alcohol, yet resemble ethanol in their organoleptic properties or psychoactive effects. The clinical picture of poisoning by these liquids often differs significantly from that of ethanol poisoning. The most common poisonings involve monohydric aliphatic alcohols: methanol, propyl alcohols (n-propanol, isopropanol), butyl alcohols (n-butanol, sec-butanol), amyl alcohol and its isomers, as well as the dihydric alcohol ethylene glycol (a component of automotive brake fluids), ethylene glycol ethers, and tetrahydrofurfuryl alcohol. Liquids of this type are also referred to as false alcohol surrogates.

Alcohols can enter The Human Body through all known routes, though acute poisonings most frequently occur following oral ingestion. Alcohols are rapidly absorbed into the bloodstream and distributed relatively evenly throughout Tissues. The METABOLISM of alcohols takes place primarily in the Liver via the pathway: alcohol → aldehyde → acid. The First stage of this process is catalyzed by Alcohol dehydrogenase (ADH) and, to a much lesser extent, by Other Enzymes such as catalase and the microsomal ethanol-oxidizing system (MEOS). These enzymes belong to the monooxygenase system, whose primary component is cytochrome P-450.

In the second stage, the body eliminates the aldehyde by oxidizing it into an acid with the help of another enzyme, aldehyde dehydrogenase (ALDH). Propanol undergoes oxidation most rapidly in the body, whereas methanol is oxidized more slowly than others. Alcohols are eliminated from the body via urine and exhaled air. Lower aliphatic alcohols are not concentrated in the urine, whereas for dihydric alcohols, The ratio of urine concentration to Blood concentration is 3–5:1.

All alcohols exhibit narcotic (neurotoxic) properties to varying degrees. For monohydric alcohols, the potency of the narcotic effect initially increases, but decreases in alcohols containing six or more carbon atoms due to reduced water solubility. Narcotic effects are less pronounced in dihydric alcohols. During the biotransformation of alcohols, more toxic metabolites are often formed (toxification), which determine the specific Clinical presentation of poisoning by a particular toxin. For instance, toxic damage to the visual Organs is caused by certain primary alcohols—methyl, hexyl, heptylic, and others—with methanol exhibiting the most pronounced toxic effect. Some alcohols also display marked damaging effects on parenchymal organs, specifically The Liver and Kidneys.

5.4.1.1. Ethyl Alcohol Poisoning

Among poisonings that lead to severe health consequences and frequently death, ethyl alcohol poisoning occupies one of the leading positions. Ethyl alcohol (C₂H₅OH, wine spirit, ethanol) is a colorless liquid with a characteristic odor. It mixes with water in any proportion and dissolves readily in organic Solvents. It Burns with a blue flame. Its relative density is 0.816 g/cm³, and its boiling point is +78.6 °C.

Ethanol is used as a solvent, a component of specialized fuels, a precursor for the Synthesis of Other compounds, and as an ingredient in certain antifreezes, cosmetics, polishes, and adhesives. So-called hydrolysis and sulfate alcohols, along with denatured alcohol, contain admixtures of methanol, aldehydes, and higher alcohols In addition to ethanol.

Ethyl alcohol is also widely used in its pure form for The production of various alcoholic beverages (vodka, tinctures, liqueurs, etc.).

The current rise in alcohol consumption among the population of Ukraine should be viewed as more than just a biomedical issue. There are compelling reasons to consider ethanol abuse as a serious threat to the Gene pool of Ukrainians and the national security of the country as a whole. In Ukraine, approximately 40,000 people die annually from alcohol-related causes. Most alarmingly, 70% of the 700,000 registered alcoholics in Ukraine are individuals under the age of 35, and 40% of children begin consuming alcoholic beverages during their school years. According to literature, Ukraine ranks first in Europe in terms of pediatric alcoholism. The per capita consumption rate of alcoholic beverages in our country is approximately 12 liters per person per year—1.5 times higher than the threshold deemed hazardous to human health by the WHO (Narodna Armiya, no. 6, Feb. 9, 2008).

Acute alcohol poisonings are typically associated with the ingestion of ethyl alcohol or beverages containing more than 12% ethanol. The lethal single dose of ethanol depends largely on individual sensitivity and ranges from 4 to 12 g/kg of body weight (averaging 300 ml of 96% ethanol in the absence of acquired tolerance). Alcoholic coma develops when blood ethanol concentrations exceed 3 g/L (3‰) (Table 5.3).

Class="center">Table 5.3. Correlation between the degree of intoxication and blood ethanol concentration (according to V. N. Kryukov et al.)

Various additives found in alcoholic beverages deserve special attention, as they can significantly alter the toxicological profile of ethanol.

Aldehydes (acetaldehyde, propionaldehyde, butyraldehyde, etc.) are formed in significant amounts during the distillation of wine into cognac spirit As a result of oxidation processes. Unsaturated aldehydes (acrolein, crotonaldehyde) impart a burning taste and bitterness to alcoholic beverages. At the same time, their combination creates the unique bouquet of wines and cognacs. The toxicity of aldehydes is low; they are actively broken down in the lumen of the Small Intestine upon contact with the mucosa. Their content does not exceed 8 mg/L in rectified spirit, 30–50 mg/L in cognacs, 10–50 mg/L in wines, and up to 250 mg/L or more in sherry.

Fusel oils are a mixture of higher (C₃–C₅) monohydric aliphatic alcohols, esters, and Other Compounds (around 40 constituents) formed during the rectification of crude alcohol. In terms of toxicity, fusel oils significantly surpass ethanol and greatly exacerbate its adverse effects. The content of fusel oils ranges from 250–650 mg/L in wines to 1000–4000 mg/L in rum, brandy, and whiskey.

Methanol is one of the most toxic components of alcoholic beverages. Its Separation during rectification presents considerable difficulty. The lowest concentration of methanol is found in white grape wine (up to 240 mg/L), whereas red wine contains up to 3000 mg/L, cognacs up to 1000 mg/L, and fruit and berry wines up to 6000 mg/L.

Esters (diethyl ether, ethyl formate, ethyl acetate, etc.) are formed through the interaction of alcohols with organic acids. Esters have a minimal impact on the toxicity of ethanol, though they can alter its organoleptic properties. For example, diethyl ether enhances the odor of ethanol, whereas ethyl acetate diminishes it.

In fatal poisonings from alcoholic beverages, the total dose of the aforementioned impurities generally does not exceed 0.01 of their LD₅₀. This also applies to low-grade alcoholic samples, implying that the primary cause of death is typically the toxic action of ethanol itself.

MECHANISM OF ACTION and Pathogenesis

Toxicokinetics distinguishes Two phases of ethanol distribution: resorption (absorption) and elimination (excretion). During the resorptive phase, the saturation of organs and tissues with ethanol occurs much faster than its biotransformation and excretion, leading to a sharp rise in blood ethanol levels. Ethanol is rapidly absorbed in The Stomach (20%) and the small intestine (80%); on average, its blood concentration peaks within 1–1.5 hours. Alcoholic beverages with an ABV of up to 30% are absorbed more quickly. Carbonated drinks containing carbon dioxide dramatically accelerate alcohol absorption. Food masses in the stomach slow down alcohol absorption due to their sorptive properties. Resorption is significantly faster when alcohol is consumed on an empty stomach, upon repeated intake, or in individuals with stomach pathologies (gastritis, PEPTIC ULCER DISEASE). Up to 10% of ethanol is eliminated from the body over 12 hours via exhaled air and urine. The bulk of the alcohol undergoes metabolism at an average rate of 4–12 g/h (0.1 g/kg per hour).

Determining the aforementioned phases of ethanol distribution is of great diagnostic and forensic significance. To achieve this, the ratio of its concentrations in urine and blood is calculated. During the resorption phase, this ratio is less than one, whereas in the elimination phase, it is invariably greater than one.

Ethanol belongs to the neurotropic and neurotoxic substances of the alcohol-barbiturate group. Several leading factors are distinguished in the pathogenesis of poisoning. Its action occurs at the level of Brain Cell membranes. It has been established that under The Influence of ethanol, the fluidity of the lipid matrix of membrane structures increases, leading to impaired Functions manifested by altered ion fluxes, biophysical receptor characteristics, membrane-bound enzyme activities, and the uptake of certain substances, among other effects. The membrane-Toxic effects of ethanol are facilitated by Lipid Peroxidation induced by these processes.

Processes associated with ethanol metabolism play a significant role in ethanol poisoning.

At least 80% of ethanol is oxidized in the liver with the participation of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Both enzymes utilize oxidized nicotinamide adenine dinucleotide as a hydrogen acceptor:

As a result of ethanol oxidation, reduced NAD accumulates, leading to a corresponding decrease in the concentration of its oxidized form. Given that the majority of oxidative processes in the liver rely on NAD⁺ (such as the metabolism of triglycerides, Fatty acids, and Hormones), severe impairment of hepatocyte function may occur. Furthermore, the resulting acetaldehyde tends to bind to Biomolecules (Amino Acids, Proteins, catecholamines, etc.), disrupting their function and exacerbating metabolic alterations in organs.

A significantly smaller amount of ethanol is metabolized via the microsomal ethanol-oxidizing system (MEOS) of the liver:

The Significance of these last two pathways of ethanol biotransformation gradually increases in cases of chronic alcoholism.

It is well known that The oxidation of ethanol is accompanied by the release of a significant amount of energy (7.1 kcal/g). This energy is actively utilized by tissues. Concurrently, energy supply processes dependent on fats and CARBOHYDRATES are disrupted, as ethanol successfully competes with them, surpassing them in bioavailability. Individuals suffering from chronic alcoholism can obtain up to 50% of their daily caloric intake from ethanol. This phenomenon is referred to as the "calorigenic" effect.

Thus, the toxic action of ethanol is mediated through several mechanisms:

- damage to Introduction/36.html">Biological Membranes;

- depletion of the oxidized nicotinamide adenine dinucleotide (NADH) pool;

- formation of acetaldehyde and its adverse effects;

- the "calorigenic" effect.

The narcotic effect of ethanol in the initial stage of poisoning is associated with the disruption of inhibitory processes in the higher Divisions of the Central Nervous system and the disinhibition of subcortical structures. This manifests as euphoria, agitation, impaired motor coordination, and similar symptoms. Following the ingestion of large doses of the poison, general depression of brain functions occurs, accompanied by loss of consciousness, suppression of the respiratory center, and thermoregulatory disorders.

Respiratory disorders in ethanol poisoning are caused by the depression of the respiratory center and aspiration-obstructive complications. The genesis of hemodynamic disorders in ethanol poisoning is complex. In addition to the central action of the toxin, a significant role in their development is played by the direct vasodilatory effect of acetaldehyde, as well as its ability to weaken myocardial contractility (myocardiotoxic effect). Clinically, these disorders manifest as a collapse-like state, Cardiac Arrhythmias, and pulmonary edema. A prolonged comatose state developing from poisoning with ethanol and its surrogates may, under certain conditions, lead to the compression of large Muscle masses with The Development of compartment syndrome, and at low temperatures, to hypothermia. Metabolic Disorders, Hypoxia, acidosis, and circulatory disturbances that characteristically develop in severe ethanol poisoning can lead to brain edema and contribute to The formation of diffuse degenerative changes in organs and tissues, impairing their functions.

Clinical Presentation.

Alcohol intoxication and alcoholic coma are distinguished. Alcohol intoxication represents a temporary impairment of bodily functions from which the victim recovers independently, without any medical assistance. The external manifestations of alcohol intoxication depend on the individual's characterological traits and their individual bodily reaction to alcohol (the presence of acquired tolerance). The clinical picture of intoxication is characterized by two distinct effects of alcohol: euphoric and narcotic.

Alcoholic coma has two stages: superficial and deep, with each potentially occurring in uncomplicated or complicated variants. Superficial coma manifests as a loss of consciousness, decreased corneal and pupillary Reflexes, and reduced pain sensitivity. Patients exhibit inconsistent neurological symptoms: preserved or increased deep tendon reflexes, trismus of the masticatory Muscles, muscle rigidity, and myofibrillation; motor agitation, meningeal signs, and seizures may occur. Characteristic features include unstable ocular symptoms ("wandering pupils," primarily manifesting as miosis, less frequently as mydriasis in response to pain or medical Procedures; roving Movements of the eyeballs, transient anisocoria). A flushed facial complexion, tachypnea, tachycardia, and Hypertension are observed. In some cases, asphyxia develops due to glossoptosis (posterior Displacement of the Tongue) or aspiration of vomit.

Deep coma is characterized by profound depression of all types of reflex activity, ophthalmoplegia, signs of meningeal irritation, and the appearance of pathological plantar reflexes. The patient's Skin is pale-cyanotic, cold, and covered in cold sweat. Internal body Temperature is reduced to 36–35 °C.

Impairments of external Respiration manifest as various obstructive-aspiration complications, such as glossoptosis, hypersalivation and bronchorrhea, laryngo-bronchospasm, and aspiration of vomit, leading to Pulmonary Atelectasis or Mendelson's syndrome. Central-type respiratory failure is a rarer complication, encountered only in deep coma.

Cardiovascular disorders are nonspecific. They manifest as tachycardia, and as the depth of the coma increases, they tend to reduce vascular tone, resulting in a drop in blood pressure down to vascular collapse. Microcirculatory disorders are observed, clinically manifested by pallor and marmoration (mottling) of the skin, acrocyanosis, and scleral injection.

Emergence from alcoholic coma occurs gradually with the restoration of reflexes, muscle tone, the appearance of myofibrillation, and shivering-like hyperkinesia. In the majority of poisoned individuals, the restoration of consciousness is preceded by psychomotor agitation with illusory and hallucinatory episodes alternating with periods of Sleep. Epileptiform seizures are possible. Less commonly, emergence from alcoholic coma proceeds without psychomotor agitation and is characterized by somnolence and adynamia.

Diagnostics.

Diagnosing alcohol intoxication is generally straightforward. However, alcohol intoxication is frequently combined with other pathological conditions that can significantly worsen the prognosis: traumatic brain injury, hypothermia, ingestion of sedative-narcotic drugs, stroke, Diabetes Mellitus, etc. The dynamics of the patient's condition are of critical diagnostic importance. The absence of noticeable improvement during intensive Treatment for alcohol intoxication over 3–5 hours indicates undiagnosed complications, predominantly cerebral ones, or a non-alcoholic Etiology of the coma.

Treatment.

Assisting patients in a state of alcoholic coma should begin with the restoration of adequate pulmonary ventilation. In cases of aspiration-obstructive respiratory disorders, the oropharynx is cleared, followed by the insertion of an airway or a laryngeal mask. To reduce salivation and bronchorrhea, atropine (0.5–1.0 ml of a 0.1% solution) is administered parenterally or intratracheally. For central-type respiratory disorders, endotracheal intubation followed by airway suctioning is indicated. Subsequently, oxygen inhalation, postural drainage, and chest vibration massage are performed. If endotracheal intubation has not been performed, the patient must be transported in a fixed lateral position.

Severe hemodynamic disturbances must be corrected prior to gastric lavage. This involves infusion therapy using 5% glucose, isotonic sodium chloride and polyionic solutions, and sodium bicarbonate solution. Administering high doses of analeptics (such as caffeine or cordiamine) in cases of deep coma is inappropriate, as they increase the brain's oxygen demand and can trigger generalized seizures. Once acute respiratory and hemodynamic disorders have been resolved in deeply comatose patients, tracheal intubation is performed followed by gastric lavage.

Gastric lavage is performed via a gastric tube with the patient lying on their left side, using 300 ml portions of water until the wash water runs clear. Special attention should be paid to removing the final portion of the wash water as completely as possible; this is achieved by adjusting the depth of the tube insertion and applying moderate pressure to the patient's epigastric region.

Activated charcoal exhibits poor adsorption of ethanol. Its administration is indicated only when ethanol intoxication is combined with other poisons.

Forced diuresis is employed to eliminate absorbed toxins. In severe cases, particularly with combined poisonings, early hemodialysis (within 6 hours of poisoning) is indicated.

To correct metabolic acidosis, a 4% sodium bicarbonate solution is administered intravenously. To accelerate alcohol oxidation, intravenous infusions of glucose with Insulin, sodium thiosulfate, and a vitamin complex (C, B₁, B₆, nicotinic acid) are given. Intravenous administration of cytoflavin and mexidol solutions is also recommended whenever possible.

Benzodiazepines, barbiturates, and magnesium sulfate are used to treat psychomotor agitation, seizures, and withdrawal syndrome. Barbiturates must be administered with caution due to their depressing effect on the respiratory center.

Staged treatment.

Initial emergency medical care: Management of acute respiratory and cardiovascular disorders — Oral Cavity clearance; insertion of an airway or laryngeal mask; Oxygen therapy, tracheal intubation, and mechanical ventilation (in cases of respiratory failure and comatose state); intravenous administration of glucose (40% — 40 ml) with ascorbic acid (5% — 5-10 ml) or 200 ml of 5% glucose solution with 10 ml of cytoflavin via drip; gastric lavage via tube followed by administration of magnesium sulfate (30 g); warming measures in case of hypothermia. Transport in a fixed lateral position.

Qualified medical care: along with initial emergency measures, tracheal intubation and mechanical ventilation are performed if necessary, alongside infusion therapy with sodium bicarbonate solution (4% — 200-400 ml), glucose (10% — 400 ml), isotonic sodium chloride solution, sodium thiosulfate (30% — 50 ml), aminophylline (2.4% — 10 ml), glucocorticoids, and a vitamin complex; forced diuresis; dehydration therapy for cerebral and pulmonary edema; Antibiotics; and seduxen (0.5% — 4-6 ml) or barbiturates in cases of agitation.

Specialized medical care: the full range of interventions specified for ethanol poisoning is carried out. In severe cases, especially with combined poisonings, hemodialysis is performed.

5.4.1.2. Methanol Poisoning

Methyl alcohol (CH₃OH, methanol, carbinol, wood alcohol) is a colorless, odorless liquid with a taste reminiscent of ethanol. It is readily miscible with water, ether, ethyl alcohol, and other alcohols. Its density is 0.81 g/cm³, and its boiling point is +66 °C. It is used as a solvent, a component of motor and rocket fuels, and in the production of formaldehyde and certain Dyes.

Acute poisonings predominantly result from the accidental (unintentional) ingestion of methyl alcohol. Inhalational and percutaneous intoxications occur only under exceptional circumstances (spilling a large volume over the body surface without prompt decontamination, or prolonged exposure to an atmosphere containing high concentrations of the toxin). Severe percutaneous poisonings in infants have been documented when methanol was used for alcohol compresses.

According to literature, the lethal dose of methyl alcohol for adults upon ingestion varies over a wide range. In some cases, death occurs after ingesting 10-30 ml of the poison, whereas in others, 250-300 ml or more is required. The average lethal dose of methyl alcohol is considered to be 100 ml. In group poisonings, mortality can reach 30-40%.

Mechanism of action and pathogenesis.

Following ingestion, methanol is rapidly absorbed and distributed across biological fluids. Average plasma lethal concentrations are 1 g/L in adults and 0.4 g/L in children. Methanol is primarily metabolized in the liver (94%), with 5% excreted unchanged by the kidneys and 1% eliminated via respiration. The half-life (T0.5) of methanol taken in small doses ranges from 14 to 27 hours, increasing to up to 30 hours following large doses.

The metabolism of methanol has been studied in considerable detail (Fig. 3). The primary metabolites of methanol are formaldehyde and formic acid (formate). While The conversion of formaldehyde to formate occurs rapidly, The breakdown of formic acid into carbon dioxide and water is very slow. Consequently, significant amounts of formate accumulate in biological fluids.

Fig. 3. Scheme of methyl alcohol metabolism involving alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)

The biological action of the unchanged methanol molecule is limited to a narcotic effect. The toxicity of methyl alcohol is driven by formaldehyde and formic acid. These metabolites exert a primary and multifaceted impact on the body's biochemical systems. The Morphology/3.html">MAIN DIRECTIONS OF this action include:

- inhibition of Oxidative Phosphorylation AND development of ATP deficiency;

- metabolic acidosis (resulting from both impaired oxidation and the accumulation of formate);

- decreased reduced Glutathione levels and sulfhydryl group deficiency;

- formation of conjugates with BIOLOGICALLY ACTIVE SUBSTANCES — amines, vasoactive compounds, Neurotransmitters, NUCLEOTIDES, etc.

Methanol is a potent neurovascular toxin. Its primary targets are the brain, retina, and Optic nerve, which are highly sensitive to ATP depletion. The oculotoxic effect manifests at varying intervals following ingestion (ranging from 40 minutes to 72 hours). Ophthalmoscopy reveals optic disc edema developing secondary to demyelination. The underlying cause of visual organ damage is the disruption of phosphorylation processes within the cytochrome oxidase system (cytochrome a). This impairs energy production, subsequently altering mass Transport of substances across the axolemma, which leads to demyelination and overall optic nerve atrophy. These lesions are exacerbated by metabolic acidosis, impaired metabolism of vasoactive substances and neurotransmitters, systemic and cerebral hemodynamic disorders, increased membrane permeability, and fluid redistribution resulting in cerebral edema. General cerebral disorders with disruption of vital functions are the primary cause of death in patients with methanol poisoning.

Clinical Picture

The progression of methanol poisoning is characterized by distinct stages. The periods of intoxication include the initial stage, the latent period, the stage of pronounced manifestations, and the recovery and sequelae stage. Based on severity, poisonings are classified into mild, moderate (ophthalmic), and severe (generalized) forms.

Some time after ingestion of the poison, a state of intoxication occurs, lasting up to several hours. Characteristically, the degree of intoxication is usually less than what would be expected from consuming a comparable amount of ethanol. The euphoric component is less pronounced; quite often, lethargy, headache, and nausea are observed already in this stage. Intoxication caused solely by methanol typically does not reach an advanced degree with a rapid onset of the narcotic phase, although somnolence is a very characteristic sign in these patients.

The intoxication is immediately followed by a latent period, which averages 12–16 hours, though it can range from as short as 2–5 hours to as long as 1–4 days. A prolonged latent period does not indicate a mild poisoning.

The severity of intoxication is determined by the prominence of symptoms in the subsequent stage, which is characterized by encephalopathic disorders, visual disturbances, and gastrointestinal syndrome.

In mild poisoning, patients complain of general weakness, headache, dizziness, a feeling of haze, a veil, or flickering before the eyes, abdominal pain, nausea, and vomiting. Objective Examination reveals moderate pupillary dilation with a sluggish light reflex. The duration of these symptoms typically does not exceed 3–4 days, while asthenic phenomena persist for up to a week. Vision is fully restored, and no long-term sequelae are observed.

Moderate poisonings initially present with the same symptoms as mild intoxications, but in a more pronounced form. Subsequently, symptoms involving the visual organs come to the fore—specifically, a progressive decrease in visual acuity leading to complete blindness. In some cases, after a sharp drop in visual acuity, vision may temporarily recover within 3–4 days, only to deteriorate again after 1–2 weeks, usually irreversibly. Methanol poisoning is characterized by a combination of these visual impairments with mydriasis and loss of the pupillary light reflex.

Early ophthalmoscopy reveals edema of the retina and the optic disc, venous dilation, and occasionally small hemorrhages; later on, pallor of the disc, arterial constriction, and signs of acute optic neuritis and optic atrophy are observed.

During the acute stage of moderate poisoning, other complications may develop, such as myocardial dystrophy, Pneumonia, pancreatitis, and peripheral neuritis. Severe abdominal pain experienced by some patients can lead to an unnecessary exploratory laparotomy. Asthenia persists for 2–3 weeks following the intoxication. The most serious consequence is blindness or varying degrees of visual impairment that cannot be corrected with optics.

The severe form of poisoning is characterized by a rapid and stormy onset of symptoms. Following the latent period, there is sudden weakness, severe headaches, abdominal and calf muscle pain, repeated vomiting, and visual disturbances. Psychomotor agitation is observed, progressing to stupor and coma. The skin of the face and neck is purplish-cyanotic. The pupils are markedly dilated and unresponsive to light. Respiration is frequent and labored (acidotic). Muscle rigidity, signs of meningeal irritation, and centrally mediated respiratory and Circulatory Disorders are observed. In the acute stage, severe alterations in vital organs and systems may manifest: myocardial dystrophy with cardiac arrhythmias, pneumonia and pulmonary edema, pancreatitis, and hepatonephropathy. However, hepatic and renal involvement, even in severe methanol poisonings, is moderately expressed, and acute liver and Kidney failure typically does not have time to develop.

Death in fatal cases generally occurs within 1–2 days as a result of central respiratory and circulatory failure. In more favorable courses, consciousness gradually returns, and visual disorders along with systemic and organ complications come to the forefront. Asthenia persists the longest, frequently combined with signs of micro-organic brain damage and persistent visual impairments.

Diagnostics

The Diagnosis of methanol poisoning takes into account history data, the staged course of the disease, the odor of methanol on the breath, early visual disturbances combined with mydriasis and a sluggish light reflex, symptoms of metabolic acidosis, findings of methanol in biological media, and the results of toxicological and chemical Analysis of the remaining ingested fluid.

As a rapid test for remaining poison, the glowing copper wire test can be used; when immersed in methanol, a characteristic formaldehyde odor is released. The primary method for toxicological and chemical analysis is Gas-Liquid Chromatography. Methyl alcohol can be detected in biological media for 3–5 and even up to 7 days after poison ingestion.

Treatment

In acute oral methanol poisonings, unabsorbed poison must be removed from the gastrointestinal tract as quickly as possible. For this purpose, vomiting is induced, non-tube followed by tube gastric lavage is performed, saline laxatives are administered, and the bowels are cleansed. Gastric lavage is performed using a 1–2% sodium bicarbonate solution or a weak potassium permanganate solution. Administering activated charcoal internally is ineffective because it does not adsorb methanol. Repeated lavages or prolonged gastric irrigation with a sodium solution are indicated for 2–3 days to remove methanol eliminated by the mucous membrane.

The specific antidote for methyl alcohol is ethanol, which competes with methanol for alcohol dehydrogenase and other alcohol-metabolizing enzymes, thereby preventing the formation of formaldehyde. Ethanol is administered orally; the initial loading dose is 100–150 ml of a 30% solution, followed by ethyl alcohol at 50–100 ml of the same solution every 3–4 hours for 3–4 days. The daily dose of ethanol is 1.5–2 ml per kg of body weight. In addition to oral administration, ethanol is given intravenously (as a 5–10% solution diluted in 5% glucose for peripheral Veins, while a 30% solution can be used for central veins) at a daily dose of 1–1.5 ml/kg. Regular repeat administrations of ethyl alcohol are crucial to maintain its blood concentration at approximately 1 g/L (corresponding to mild intoxication), which ensures effective competition with methanol. If ethanol levels in biological media drop below this threshold, the toxicity of methyl alcohol resumes. It must be noted that antidote therapy should be initiated no later than 18 hours after poisoning.

To neutralize the metabolites of the poison, high doses of Folic acid are prescribed at a daily dose of 1–1.5 mg/kg for 2–3 days.

Pyrazole derivatives (4-methylpyrazole, 4-bromopyrazole), which act as alcohol dehydrogenase inhibitors, may also be used as antidotes.

To eliminate absorbed poison and its metabolites from the body, forced diuresis with alkalinization, hemodialysis, and peritoneal dialysis are employed. Hemodialysis is the most effective method, providing a methanol blood clearance of up to 140 ml/min. During hemodialysis, the dose of ethanol must be increased twofold. The optimal timing for these interventions is the first to second day. Hemoperfusion is ineffective in methanol poisoning.

Pathogenetic and symptomatic therapy should begin with the correction of metabolic acidosis. For this purpose, sodium bicarbonate is administered (3–5 g orally every 2–3 hours, or 100–150 ml of a 4% solution intravenously) under the control of blood acid-base balance parameters or until the urine becomes alkaline. In the event of cerebral edema, which is frequently observed in severe methanol poisonings, dehydration therapy is performed (glycerol orally, Diuretics intravenously, craniocerebral hypothermia, therapeutic lumbar punctures). To combat hypoxia, circulatory disorders, and metabolic disturbances, oxygen therapy, plasma expanders, glucocorticoids, piracetam and aminophylline solutions are administered, along with a complex of Vitamins (C, B₁, B₆, PP, B₁₂), ATP, cardiovascular agents, and antibiotics.

For progressive visual deterioration, retrobulbar injections of atropine, prednisolone, etc., are indicated. Treatment of methanol poisoning must be carried out in conjunction with an ophthalmologist and a neurologist. All patients must be hospitalized in specialized centers or departments.

Staged Treatment

Initial medical aid: tube gastric lavage followed by intragastric administration of sodium bicarbonate (5–6 g), a saline laxative (30 g), ethyl alcohol (30% 150 ml), folic acid (20–30 mg); oxygen inhalation. Urgent evacuation from the accident site following safety regulations and utilizing protective equipment (gas masks, respirators, etc.).

Qualified medical care: repeated tube gastric lavage, administration of ethyl alcohol (50–100 ml of a 30% solution orally every 4 hours or 300–500 ml of a 5% solution in 5% glucose intravenously); folic acid (20–30 mg); forced diuresis with alkalinization (occasionally up to 1 L of a 4% sodium bicarbonate solution is administered intravenously). Glucose (40% 40–60 ml), aminophylline (2.4% 10 ml), prednisolone (60–90 mg), vitamins (C, B₁, B₆, PP, B₁₂), and ATP (1% 2–4 ml) are continued. Oxygen therapy, cardiovascular medications, and antibiotics are also administered, alongside dehydration measures in cases of cerebral edema. Evacuation to a specialized center.

Specialized care: Structure/175.html">Implementation of the measures specified in the previous section, administration of hemodialysis, retrobulbar drug administration, measures for the Prevention and treatment of complications, and rehabilitation measures.